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Anesthesia for cardiac surgery

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    Anesthesia for cardiac surgery Anesthesia for cardiac surgery Document Transcript

    • Anesthesia for Cardiac Surgery
    • DedicationTo my wife Denée for her love, support and wisdom.To my daughter Isabel and her limitless potential.To my mother Josephine Ann who taught me the value of honesty and perseverance. James A. DiNardoTo my wife, Bharathi, and daughters, Alexandra, Jessica, Gracie and Olivia: each of you have inspiredme in ways that you will never know. I love you and dedicate this book to you and your life’s dreams.Go confidently in the direction of your dreams. Live the life you have imagined. (Henry David Thoreau) David A. Zvara
    • Anesthesia forCardiac SurgeryThird EditionJames A. DiNardo, MDClinical Co-Director of Cardiac AnesthesiaDepartment of AnesthesiaChildren’s Hospital Bostan300 Longwood AvenueBoston, MA, 02115USADavid A. Zvara, MDJay J. Jacoby Professor and ChairDepartment of AnesthesiologyThe Ohio State University410 West 10th AvenueColumbus, Ohio, 43210USA
    • © 1990 and 1997 James A. DiNardo© 2008 James A. DiNardo and David A. ZvaraPublished by Blackwell PublishingBlackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USABlackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UKBlackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, AustraliaThe right of the Author to be identified as the Author of this Work has been asserted inaccordance with the Copyright, Designs and Patents Act 1988.All rights reserved. No part of this publication may be reproduced, stored in a retrievalsystem, or transmitted, in any form or by any means, electronic, mechanical,photocopying, recording or otherwise, except as permitted by the UK Copyright, Designsand Patents Act 1988, without the prior permission of the publisher.First published 1990Second edition 1997Third edition 20081 2008Library of Congress Cataloging-in-Publication DataDiNardo, James A. Anesthesia for cardiac surgery/James A. DiNardo, David A. Zvara. – 3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4051-5363-8 (alk. paper) 1. Anesthesia in cardiology. 2. Heart–Surgery. I. Zvara, David A. II. Title.[DNLM: 1. Cardiac Surgical Procedures. 2. Anesthesia. WG 169 D583a 2007] RD87.3.H43D5 2007 617.9’67412–dc22 2007001204ISBN: 978-1-4051-5363-8A catalogue record for this title is available from the British LibrarySet in 9/12pt Meridien byNewgen Imaging Systems (P) Ltd, Chennai, IndiaPrinted and bound in Singapore by Fabulous Printers Pte LtdCommissioning Editor: Stuart TaylorEditorial Assistant: Jennifer SewardDevelopment Editors: Adam Gilbert and Victoria PittmanProduction Controller: Debbie WyerFor further information on Blackwell Publishing, visit our website:http://www.blackwellpublishing.comThe publisher’s policy is to use permanent paper from mills that operate a sustainableforestry policy, and which has been manufactured from pulp processed using acid-free andelementary chlorine-free practices. Furthermore, the publisher ensures that the text paperand cover board used have met acceptable environmental accreditation standards.Blackwell Publishing makes no representation, express or implied, that the drug dosages inthis book are correct. Readers must therefore always check that any product mentioned inthis publication is used in accordance with the prescribing information prepared by themanufacturers. The author and the publishers do not accept responsibility or legal liabilityfor any errors in the text or for the misuse or misapplication of material in this book.
    • ContentsPreface, vii 1 Introduction, 1 2 Myocardial Physiology and the Interpretation of Cardiac Catheterization Data, 20 3 Monitoring, 42 4 Anesthesia for Myocardial Revascularization, 90 5 Anesthesia for Valvular Heart Disease, 129 6 Congenital Heart Disease, 167 7 Anesthesia for Heart, Heart-Lung, and Lung Transplantation, 252 8 Pericardial Disease, 289 9 Anesthesia for Surgery of the Thoracic Aorta, 30410 Management of Cardiopulmonary Bypass, 32311 Mechanical Circulatory Support, 37512 Myocardial Preservation during Cardiopulmonary Bypass, 40913 Special Considerations during Cardiac Surgery, 425Index, 439 v
    • PrefaceAnesthesia for Cardiac Surgery originally published in Acknowledgements1989, and revised in 1998, was written with the The authors would like to acknowledge Adela S.F.intention of filling the perceived void in cardiac Larimore at the Wake Forest University School ofanesthesia reference material between definitive, Medicine, Department of Anesthesiology for herheavily referenced texts and outline-based hand- editorial support in the preparation of this textbook.books. The updated 3rd Edition strives to do the Without her assistance this work would not besame. This book is intended to provide practi- possible.cal recommendations based on sound principlesof physiology. The text provides a comprehensiveoverview of the contemporary practice of cardiacanesthesia. There is a place for this work as a compo-nent of a core curriculum in cardiac anesthesiologytraining as well as in the library of the busy, practic-ing clinician. We hope this work helps you in caringfor your patients. JAD DAZ vii
    • CHAPTER 1IntroductionA complete evaluation of the patient’s medical conditions discovered in the process help definehistory, physical examination, and review of per- the anesthetic plan and are often associated withtinent laboratory and supportive tests is necessary strong prognostic value. For example, a history ofprior to any elective cardiac surgical procedure. The myocardial infarction, unstable angina, congestiveintention of the preoperative evaluation is sever- heart failure, dyspnea, obstructive sleep apnea, andalfold: define the status of the patient’s medical any number of other conditions may directly affectcondition, identify areas of uncertainty that require the course of the preoperative evaluation, operativefurther evaluation, consultation or testing, devise outcome, and patient satisfaction. There are manya strategy to improve or stabilize ongoing medi- algorithms for quantifying patient risk, includingcal conditions prior to surgery, determine a prog- the American Society of Anesthesiologists Physi-nostic risk classification, and provide information cal Status Classification. The Revised Cardiac Riskto formulate an intraoperative and postoperative Index is a clinically useful example of a preopera-plan. The anesthesiologist must clearly understand tive scoring system to define perioperative cardiacthe intended surgical procedure. This chapter will risk (Table 1.1).present a systems review of the common and sig- In most cardiac surgical procedures, the preanes-nificant features found preoperatively in the cardiac thetic evaluation should take place prior to thesurgical patient. There will be a special emphasis on day of surgery. This will allow time for additionalthe methodology, limitations, and accuracy of the testing, collection, and review of pertinent pasttests used most commonly in evaluation of cardiac medical records, and appropriate patient counsel-surgical patients. ing. The examination can be obtained on the day of surgery for procedures with relatively low sur-Cardiovascular evaluation gical invasiveness. The history provides insight into the severity of the pathologic condition. For exam-A directed history and physical examination are ple, a history consistent with heart failure is mostessential before any cardiac surgical procedure. alarming and requires careful deliberation beforeThe information obtained, in the context of proceeding (Table 1.2). In evaluating a patient withthe anticipated surgical procedure, will deter- angina, it is essential to determine if the symp-mine the requirement for subsequent evaluation, toms represent unstable angina (Table 1.3). Theconsultation or testing. Canadian Cardiovascular Society Classification ofHistory and physical examination Angina defines anginal symptoms (Table 1.4).There are no controlled trials evaluating the effec- At a minimum, the physical examination musttiveness of the history and physical; however, include the vital signs and an evaluation of 1
    • 2 Chapter 1Table 1.1 The Revised Cardiac Risk Index. Electrocardiogram A preoperative electrocardiogram (ECG) should beIschemic heart disease: Includes a history of myocardial obtained in all cardiac surgical patients. There is noinfarction, Q waves on the ECG, a positive stress test, consensus on the minimum patient age for obtain-angina, or nitroglycerine use ing an ECG, although ECG abnormalities are moreCongestive heart failure (CHF): Includes a history of CHF, frequent in older patients and those with multiplepulmonary edema, paroxysmal nocturnal dyspnea, rales, cardiac risk factors. The ECG should be examinedS3 gallop, elevated β-naturetic peptide, or imaging study for rate and rhythm, axis, evidence of left and rightconsistent with CHF ventricular (RV) hypertrophy, atrial enlargement,Cerebrovascular disease: Includes a history of transient conduction defects (both AV nodal and bundleischemic attack or stroke branch block (BBB)), ischemia or infarction, andDiabetes mellitus treated with insulin: metabolic and drug effects.Renal dysfunction (serum creatinine >2) Rate and rhythm abnormalitiesHigh-risk surgery: Includes any intraperitoneal, There are a large number of rate and rhythm abnor-intrathoracic or suprainguinal vascular procedures malities which may be present in the cardiac surgical patient. Tachycardia may be a sign of anxiety, drugCABG, coronary artery bypass surgery; ECG, electrocardio-gram. effect (i.e. sympathomimetics, β-adrenergic ago-0–2 risk factors = low risk. nists, and cocaine intoxication), metabolic disorder3 or more risk factors = high risk. (hypothyroidism), fever, sepsis or other condi- tions. Bradycardia is typically due to medications (β-adrenergic blocking agents), although a slowthe airway, lungs and heart. Auscultation of the heart rate may by indicative of other pathol-chest may reveal wheezing, rales, or diminished ogy (hypothyroidism, drug effect, hypothermia,breath sounds. Auscultation of the heart is critical in conduction defects). Arrhythmias are potentiallyuncovering new murmurs, S4 gallops, and rhythm more serious and require immediate evaluation.abnormalities. In patients older than 40 years, new Electrolyte abnormalities are common in cardiacheart murmurs are found in upwards of 4% of surgical patients and may lead to premature ven-patients. Further screening with echocardiography tricular contractions (PVCs). The actively ischemicreveals significant valvular pathology in 75% of patient may present with ventricular irritability, fre-these patients. Arterial hypertension is common quent or multifocal PVCs, or ventricular tachycardiain the cardiac surgical patient; however, there is (VT). Atrial fibrillation is frequently observed inlittle evidence for an association between admis- the elderly cardiac surgical patient. The diagnosission arterial pressures less than 180 mmHg systolic of new atrial fibrillation requires evaluation prior toor 110 mmHg diastolic and perioperative compli- surgery if time and the clinical condition permit.cations. In patients with blood pressures abovethis level, there is increased perioperative ischemia,arrhythmias, and cardiovascular lability. Axis Once the history and physical examination are Axis refers to the direction of depolarization incomplete, attention turns to what additional eval- the heart. The mean QRS vector (direction ofuation, consultation or studies are indicated prior depolarization) is normally downward and to theto the operative procedure. The decision regard- patient’s left (0–90◦ ). This axis will be displaceding which test to order should be based upon with physical relocation of the heart (i.e. extrinsican analysis of value of the information obtained, cardiac compression from a mass effect), hypertro-resource utilization and timeliness in regards to phy (axis moves toward hypertrophy), or infarctionthe scheduled procedure. Several common tests are (axis moves away from infarction). In the normalreviewed below. condition, the QRS is positive in lead I and aVF .
    • Introduction 3Table 1.2 American College of Cardiology/American Heart Association Classification of chronic heart failure.Stage DescriptionA. High risk for developing heart failure Hypertension, diabetes mellitus, coronary artery disease, family history of cardiomyopathyB. Asymptomatic heart failure Previous myocardial infarction left ventricular dysfunction, valvular heart diseaseC. Symptomatic heart failure Structural heart disease, dyspnea and fatigue, impaired exercise toleranceD. Refractory end-stage heart failure Marked symptoms at rest despite maximal medical therapyStage A includes patients at risk of developing heart failure but have no structural heart disease at present. A highdegree of awareness is important in this groupStage B includes patients with known structural heart disease but no symptoms. Therapeutic intervention withangiotensin converting enzyme inhibitors or adrenergic beta-blocking agents may be indicated for long-term chronictreatment in this groupStage C includes patients with structural heart disease and symptomatic heart failure. Operative risk is increased in thisgroup. Medical therapy may include diuretics, digoxin, and aldosterone antagonists in addition to ACE inhibitors andbeta-blockers depending upon the severity of symptoms. Cardiac resynchronization therapy also may be considered inselected patientsStage D includes patients with severe refractory heart failure. These patients frequently present for heart transplantationor bridging therapy with ventricular assist devices. Acute decompensation is managed with inotropes and vasodilatortherapyACE, angiotensin-converting enzyme.Table 1.3 The principal presentations ofunstable angina. Rest angina Angina occurring at rest and usually prolonged greater than 20 minutes New onset angina Angina of at least CCSC III severity with onset within 2 months of initial presentation Increasing angina Previously diagnosed angina that is distinctly more frequent, longer in duration or lower in threshold (i.e. increased by at least one CCSC class within 2 months of initial presentation to at least CCSC III severity) CCSC, Canadian Cardiovascular Society Classification.Left atrial enlargement the stenotic mitral valve. In aortic stenosis andIn adults, left atrial enlargement (LAE) may be systemic hypertension, an elevated left ventricu-found in association with mitral stenosis, aortic lar (LV) end-diastolic pressure results in left atrialstenosis, systemic hypertension, and mitral regur- hypertrophy. In mitral regurgitation, LAE occursgitation. In mitral stenosis, LAE occurs secondary to because of the large volumes of blood regurgitatedthe increased impedance to atrial emptying across in the left atrium during systole.
    • 4 Chapter 1 Table 1.4 The Canadian Cardiovascular Society Classification System of angina pectoris. Class I: Ordinary physical activity, such as walking and climbing stairs does not cause angina. Angina occurs with strenuous, rapid, or prolonged exertion Class II: Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in the cold or wind, under emotional stress or only during the few hours after awakening. Angina occurs on walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and under normal conditions Class III: Marked limitations of ordinary physical activity. Angina occurs on walking one or two blocks on the level ground and climbing one flight of stairs in normal conditions and at a normal pace Class IV: Inability to carry on any physical activity without anginal discomfort. Symptoms may be present at restRight atrial enlargement Ischemia and infarctionRight atrial enlargement (AAE) may be seen with New findings of active ischemia require immedi-RV hypertrophy secondary to pulmonary outflow ate attention. In the patient with known coro-obstruction or pulmonary hypertension. RAE also nary artery disease (CAD) and unstable angina,may be observed in patients with tricuspid stenosis, ST segment abnormalities may be observed.tricuspid atresia, or Epstein’s abnormality. In patients with diabetes, there may be episodes of silent ischemia during which the heart is ischemic,Left ventricular hypertrophy but due to autonomic dysfunction and a dimin-In adults, left ventricular hypertrophy (LVH) com- ished ability to perceive nociceptive signals, themonly occurs in LV pressure overload lesions such patient does not experience pain. The presence ofas aortic stenosis and severe systemic hypertension. Q waves indicates an old transmural myocardialIn children, LVH may be present with coarctation of infarction. Determining the timing of the Q wavethe aorta and congenital aortic stenosis. finding may be clinically relevant. For example, a Q wave not seen on an ECG 6 months priorRight ventricular hypertrophy to the evaluation suggests a myocardial infarctionRight ventricular hypertrophy (RVH) is a common sometime during this recent interval. Periopera-finding in patients with congenital heart disease tive cardiac morbidities are related to timing ofand may be seen in pulmonic stenosis, tetralogy surgery after a myocardial infarction, and there-of Fallot and transposition of the great arteries. fore this information requires attention and clinicalIn adults, RVH frequently results from pulmonary resolution.hypertension. Metabolic and drug effectsConduction defects Elevated serum potassium will flatten the P wave,Similar to rate and rhythm abnormalities, there are widen the QRS complex, and elevate the T wave.a wide variety of conduction defects which may Low serum potassium will flatten of invert thebe observed in the cardiac surgical patient. Atrio- T wave. A U wave may appear. With elevated serumventricular (AV) block may be innocuous (1st and calcium the QT interval shortens; whereas with2nd degree type 1) or clinically significant requir- hypocalcemia, the QT interval is prolonged. Digi-ing immediate evaluation of pacemaker placement talis toxicity will cause a gradual down sloping of(2nd degree type 2 and 3rd degree). BBB delay the ST segment. There may also be atrial and junc-depolarization in the effected ventricle and may lead tional premature beats, atrial tachycardia, sinus, andto ineffective ventricular contraction. AV nodal blocks.
    • Introduction 5 It must be emphasized that a normal ECG does septal or atrial septal defect), the pulmonary arterynot preclude the presence of significant cardiac dis- and pulmonary vasculature is prominent. In con-ease in the adult, child, or infant. The ECG is normal trast, patients with reduced pulmonary blood flowin 25–50% of adults with chronic stable angina. (as with tetralogy of Fallot or pulmonary atre-Likewise, the ECG may be normal in children with sia) may manifest a small pulmonary artery andLV pressure overload (aortic stenosis) and volume diminished vascularity. Some congenital lesions areoverload (patent ductus arteriosus or ventricular associated with classic radiographic cardiac silhou-septal defect) lesions. ettes: the boot-shaped heart of tetralogy of Fallot, the “figure 8” heart of total anomalous pulmonaryChest radiograph venous return, and the “egg-on-its-side”-shapedObtaining a Chest radiograph (CXR) should be heart seen in D-transposition of the great arteries.based upon the necessity for the planned clini-cal procedure (i.e. a lateral chest film is essen- Stress testingtial in a repeat sternotomy), or in assessing the Patients presenting for cardiac surgery frequentlypatient’s clinical condition. Clinical characteristics undergo stress testing to establish the diagnosis ofsuggesting a benefit to obtaining a CXR include CAD, assess the severity of known CAD, establisha history of smoking, recent respiratory infection, the viability of regions of myocardium, or eval-chronic obstructive pulmonary disease (COPD), or uate anti-anginal therapy. Stress testing may usecardiac disease. The posterior–anterior and lateral exercise or pharmacological agents. Pharmacolog-CXR provide a wealth of information including an ical agents are useful for patients with physicalassessment of pulmonary condition and maybe car- disabilities that preclude effective exercise. It alsodiovascular status. For example, radiographic evi- is useful for patients who cannot reach an optimaldence of pulmonary vascular congestion suggests exercise heart rate secondary to their medicationpoor systolic function. For patients with valvu- regimen (i.e. patients on beta-blockers).lar heart disease, a normal CXR is more usefulthan an abnormal radiograph in assessing ventricu- Pharmacological stress testinglar function. The presence of a cardio-to-thoracic Pharmacologic stress testing uses dipyridamole,ratio less than 50% is a sensitive indicator of an adenosine, or dobutamine. Pharmacologic stressejection fraction greater than 50% and of a car- testing can be performed in conjunctiondiac index greater than 2.5 L/min/m2 . On the other with myocardial perfusion scintigraphy orhand, a cardio-to-thoracic ratio greater than 50% is echocardiography.not a specific indicator of ventricular function. For Adenosine and dipyridamole are potent coro-patients with CAD, an abnormal CXR is more useful nary vasodilators that increase myocardial bloodthan a normal radiograph in assessing ventricu- flow three to fivefold independent of myocardiallar function. Cardiomegaly is a sensitive indicator work. Adenosine is a direct vascular smooth muscleof a reduced ejection fraction, whereas a normal- relaxant via A2 -receptors; whereas, dipyridamolesized heart may be associated with both normal and increases adenosine levels by inhibiting adenosinereduced ejection fractions. deaminase. Dobutamine increases myocardial work As with the ECG, efforts should be made to corre- through increases in heart rate and contractility vialate radiographic findings with the clinical history. β1 -receptors. The increased work produces propor-LAE is expected in mitral stenosis and regurgitation. tional increases in myocardial blood flow. In thisEnlargement of the pulmonary artery and right ven- sense, dobutamine stress testing is similar to exercisetricle occurs with disease progression. Eccentric LV stress testing.hypertrophy results from mitral and aortic regur- The hyperemic response to adenosine and dipyri-gitation. Aortic stenosis results in concentric LV damole produce increased myocardial blood flowhypertrophy. In infants and children with increased in regions supplied by normal coronary arteries.pulmonary blood flow (as with a large ventricular In regions of myocardium supplied by steal prone
    • 6 Chapter 1anatomy or diseased coronary arteries, myocardial All exercise tests increase metabolic rate andblood flow increases will be attenuated or decreased oxygen consumption (V O2 ). Isometric exercisebelow resting levels. may be used to increase the workload, but more Dipyridamole is infused at 0.56–0.84 mg/kg for commonly, dynamic exercise using either a tread-4 minutes, followed by injection of the radiophar- mill or a bicycle is used. V O2max is the maximalmaceutical for myocardial perfusion scintigraphy amount of oxygen a person can use while per-3 minutes later. If infusion produces headache, forming dynamic exercise. V O2max is influencedflushing, gastrointestinal (GI) distress, ectopy, by age, gender, exercise habits, and cardiovascu-angina, or ECG evidence of ischemia, the effect lar status. Exercise protocols are compared by usingcan be terminated with aminophylline 75–150 mg metabolic equivalents (METs). One MET is equal tointravenously (IV). Adenosine is infused at a V O2 of 3.5 mL oxygen(O2 )/kg/min and represents140 µg/kg/min for 6 minutes with injection of resting oxygen uptake. Different exercise protocolsthe radiopharmaceutical for myocardial perfu- are compared by comparing the number of METssion scintigraphy 3 minutes later. Side effects consumed at various stages.are similar to dipyridamole and are termi- The Bruce treadmill protocol is the most com-nated by stopping the infusion (the half-life of monly used protocol for exercise stress testing.adenosine is 40 seconds). Dobutamine is infused at This protocol uses seven 3-minute stages. Each5 µg/kg/min for 3 minutes and then is increased to progressive stage involves an increase in both10 µg/kg/min for 3 minutes. The dose is increased the grade and the speed of the treadmill. Dur-by 5 µg/kg/min every 3 minutes until a maximum ing stage 1 the treadmill speed is 1.7 miles/h onof 40 µg/kg/min is reached or until significant a 10% grade (5 METs); during stage 5 the tread-increases in heart rate and blood pressure occur. mill speed is 5 miles/h on an 18% grade (16 METs).Injection of the radiopharmaceutical for myocar- The patient progressively moves through thedial perfusion scintigraphy takes place 1 minute stages until either exhausted, a target heart rateafter the desired dose is reached, and the infusion achieved without ischemia, or the detection ofis continued for 1–2 minutes after injection. Side ischemic changes on the ECG. Exercise stress test-effects of dobutamine (headache, flushing, GI dis- ing can be performed in conjunction with tradi-tress, ectopy, angina, or ECG evidence of ischemia) tional ECG analysis, myocardial perfusion scintig-can be terminated by discontinuing the infusion raphy, or echocardiography. The details of stress(the half-life of dobutamine is 2 minutes). myocardial perfusion scintigraphy, stress radionu- cleotide angiography, and stress echocardiographyExercise stress testing are discussed below.Exercise stress testing increases in myocardial The following factors must be considered inoxygen consumption to detect limitations in coro- interpretation of an ECG exercise stress test:nary blood flow. Exercise increases cardiac out- • Angina. Ischemia may present as the patient’sput through increases in heart rate and inotropy. typical angina pattern; however, angina is not aDespite vasodilatation in skeletal muscle, exercise universal manifestation of ischemia in all patients.typically increases arterial blood pressure as well. Ischemic pain induced by exercise is stronglyAs a result, exercise is accompanied by increases in predictive of CAD.the three major determinants of myocardial oxygen • V O2max . If patients with CAD reach 13 METs,consumption: heart rate, wall tension, and contrac- their prognosis is good regardless of other fac-tility. To meet the demands of exercise, the coronary tors; patients with an exercise capacity of less thanvascular bed dilates. The ability of the coronary 5 METs have a poor prognosis.circulation to increase blood flow to match exercise- • Dysrhythmias. For patients with CAD, ventricu-induced increases in demand is compromised in the lar dysrhythmias may be precipitated or aggravateddistribution of stenosed coronary arteries because by exercise testing. The appearance of reproduciblevasodilatory reserve is exhausted in these beds. sustained (>30 seconds) or symptomatic ventricular
    • Introduction 7tachycardia (VT) is predictive of multivessel disease expertise and patient-specific attribute. In eitherand poor prognosis. case, angiography should be considered in patients• ST segment changes. ST segment depression is the with moderately large defects.most common manifestation of exercise-induced Limitations of exercise ECG testing are the inabil-myocardial ischemia. The standard criterion for an ity to accurately localize and assess the extentabnormal response is horizontal or down sloping of ischemia. Furthermore, no direct information(>1 mm) depression 80 ms after the J point. Down regarding left ventricle function is available. Stresssloping segments carry a worse prognosis than hor- myocardial perfusion scintigraphy, radionuclideizontal segments. The degree of ST segment depres- angiography, and echocardiography provide thission (>2 mm), the time of appearance (starting with information. On the other hand, these methods are<6 METs), the duration of depression (persisting more expensive and technically more demanding>5 minutes into recovery), and the number of than exercise ECG testing.ECG leads involved (>5 leads) are all predictive ofmultivessel CAD and adverse prognosis. Myocardial perfusion scintigraphy• Blood pressure changes. Failure to increase systolic Myocardial perfusion scintigraphy assesses myocar-arterial blood pressure to greater than 120 mmHg, dial blood flow, myocardial viability, the numberor a sustained decrease in systolic blood pressure and extent of myocardial perfusion defects, tran-with progressive exercise, is indicative of cardiac sient stress-induced LV dilatation, and allows forfailure in the face of increasing demand. This finding risk stratification. Myocardial perfusion scintigra-suggests severe multivessel or left main CAD. phy is performed most commonly in conjunc- tion with stress testing. Stress testing can beComparison of stress test methods accomplished with exercise or pharmacologicallyThe sensitivity of detection of CAD with exer- with dipyridamole, adenosine, or dobutamine. Withcise myocardial perfusion scintigraphy or exercise this technology, it is possible to determine whichechocardiography is superior to that of exercise regions of myocardium are perfused normally,ECG testing. The superiority of these two modal- which are ischemic, which are stunned or hibernat-ities over ECG testing in detecting CAD is great- ing, and which are infarcted. The technique is basedest for patients with single vessel CAD. When on the use of radiopharmaceuticals that accumulatecomparing myocardial perfusion scintigraphy to in the myocardium proportional to regional bloodstress echocardiography, the data suggest a trend flow. Single-positron emission computed tomogra-toward greater sensitivity with myocardial per- phy (SPECT) or planar imaging is used to imagefusion scintigraphy, particularly for patients with regional myocardial perfusion in multiple viewssingle-vessel disease. Moderate to large perfusion and at various measurement intervals. Patients withdefects by either stress echocardiography or thal- small fixed perfusion defects have reduced periop-lium imaging predicts postoperative myocardial erative risk profiles, whereas patients with multipleinfarction or death in patients scheduled for elec- larger defects are at higher risk.tive noncardiac surgery. Negative tests assure the The radiopharmaceuticals currently in use areclinician of a small likelihood of subsequent adverse thallium-201 and technetium-99m methoxyiso-outcome (negative predictive value = 99%). Unfor- butyl isonitrile (Sestamibi). Thallium has biologictunately, however, the positive predictive value properties similar to potassium and thus is trans-(i.e. the chance that a patient with a positive test ported across the myocardial cell membrane bywill have an adverse cardiovascular event) is poor the sodium–potassium adenosine triphosphataseranging from 4% to 20%. In a meta-analysis com- (ATPase) pump proportional to regional myocar-paring the two techniques, stress echocardiography dial blood flow. Sestamibi is not dependent onis slightly superior to thallium imaging in predicting ATP to enter myocardial cells because it is highlypostoperative cardiac events. The choice of which lipophilic but its distribution in myocardial tissue istechnique should be made based upon institutional proportional to blood flow.
    • 8 Chapter 1Thallium these regions exhibit transient postischemic dys-Thallium-201 is injected at the peak level of a mul- function in the setting of normal coronary bloodtistage exercise or pharmacological stress test. Scin- flow. Stunned myocardium is detected by identify-tillation imaging begins 6–8 minutes after injection ing regions of dysfunctional myocardium in which(early views) and is repeated again 2–4 hours after no perfusion defect exists.injection (delayed or redistribution views). Identi- Some regions of myocardium that do notcal views must be used so the early and delayed exhibit redistribution at 2.5–4.0 hours exhibit redis-images can be compared. During stress, myocardial tribution in late images at 18–24 hours. Thisblood flow and thallium-201 uptake will increase in late redistribution represents areas of hibernatingareas of the myocardium supplied by normal coro- myocardium. Another approach to detecting hiber-nary arteries. Subsequently, thallium redistributes nating myocardium is reinjection of thallium at restto other tissues, thus clearing from the myocardium after acquisition of the 2.5–4.0-hour stress images.slowly. Areas of myocardium supplied by diseased Persistent defects that show enhanced uptake afterarteries are prone to ischemia during stress and reinjection represent areas of viable myocardium.have a reduced ability to increase myocardial blood Finally, serial rest thallium imaging has proved use-flow and thallium-201 uptake. These areas will ful in detecting hibernating myocardium. Imagesdemonstrate a perfusion defect when compared are obtained at rest after injection of thalliumwith normal regions in the early views. In the and then are repeated 3 hours later. Regionsdelayed views, late accumulation or flat washout of myocardium that exhibit rest redistributionof thallium-201 from the ischemic areas compared represent areas of viable myocardium.with the nonischemic areas results in equalization Increased lung uptake of thallium is related toof thallium-201 activity in the two areas. These exercise-induced LV dysfunction and suggests mul-reversible perfusion defects are typical of areas of tivessel CAD. Because increased lung uptake ofmyocardium that suffer transient, stress-induced thallium is due to an elevated left atrial pressureischemia. Nonreversible perfusion defects are present (LAP), other factors besides extensive CAD andin both the early stress and delayed redistribution exercise-induced LV dysfunction (such as mitralimages. These defects are believed to represent areas stenosis, mitral regurgitation, and nonischemic car-of nonviable myocardium resulting from old infarc- diomyopathy) must be considered when few or notions. Reverse redistribution is the phenomenon in myocardial perfusion defects are detected. Transientwhich early images are normal or show a defect and LV dilation after exercise or pharmacologic stressthe delayed images show a defect or a more severe also suggests severe myocardial ischemia.defect. This is seen frequently in patients who haverecently undergone thrombolytic therapy or angio- Sestamibiplasty and may result from higher-than-normal Sestamibi, unlike thallium, does not redistribute.blood flow to the residual viable myocardium in the As a result, the distribution of myocardial bloodpartially infarcted zone. flow at the time of injection remains fixed over Modified thallium scintigraphy protocols are use- the course of several hours. This necessitates twoful in detecting areas hibernating myocardium. separate injections: one at rest and one at peakHibernating myocardium exhibits persistent stress. The two studies must be performed so thatischemic dysfunction secondary to a chronic reduc- the myocardial activity from the first study decaystion in coronary blood flow, but the tissue remains enough not to interfere with the activity from theviable. Hibernating myocardium has been shown second study. A small dose is administered at restto exhibit functional improvement after surgical with imaging approximately 45–60 minutes later.revascularization or angioplasty and restoration of Several hours later, a larger dose is administeredcoronary blood flow. Stunned myocardium, in con- at peak stress, with imaging 15–30 minutes later.trast, has undergone a period of transient hypop- Reversible and fixed defects are detected by com-erfusion with subsequent reperfusion. As a result, paring the rest and stress images. As with thallium,
    • Introduction 9late imaging after Sestamibi stress imaging may be After equilibrium of the labeled red cells in thehelpful in detecting hibernating myocardium. cardiac blood pool, gated imaging with a scintil- Sestamibi allows high-count-density images to be lation camera is performed. A computer dividesrecorded, providing better resolution than thallium. the cardiac cycle into a predetermined number ofIn addition, use of Sestamibi allows performance of frames (16–64). Each frame represents a specificfirst pass radionuclide angiography (see below) to time interval relative to the ECG R wave. Databe performed in conjunction with myocardial perfu- collected from each time interval over the coursesion scintigraphy. Use of simultaneous radionuclide of several hundred cardiac cycles are then addedangiography and perfusion scintigraphy has proved together with the other images from the same timeuseful in enhanced detection of viable myocardium. interval. The result is a sequence of 16–64 images,Viable myocardium will exhibit preserved regional each representing a specific phase of the cardiacperfusion in conjunction with preserved regional cycle. The images can be displayed in an endlesswall motion. loop format or individually. The procedure can then be repeated with the camera in a different position.Radionuclide angiography Below is a summary of the relative advantagesRadionuclide angiography allows assessment of and disadvantages of first-pass and equilibrationRV and LV performance. Two types of cardiac studies. Both types of studies currently are used forradionuclide imaging exist: first-pass radionuclide adults, infants, and children.angiography (FPRNA) and equilibrium radionu- • With both FPRNA and ERNA studies, the num-clide angiography (ERNA), also known as radionu- ber of radioactive counts during end systole andclide ventriculography or gated blood pool imaging. end diastole can be used to determine strokeERNA is also known as multiple-gated acquisition volume, ejection fraction, and cardiac output.(MUGA) or multiple-gated equilibrium scintigraphy • Both types of studies allow reliable quantification(MGES). of LV volume using count-proportional methods FPRNA involves injection of a radionuclide bolus that do not require assumptions to be made about(normally technetium-99m) into the central circu- LV geometry.lation via the external jugular or antecubital vein. • Although both studies allow determination of RVSubsequent imaging with a scintillation camera in a and LV ejection fractions, determination of RV ejec-fixed position provides a temporal pictorial presen- tion fraction is more accurate with a first-pass studytation of the cardiac chambers as the radiolabeled because the right atrium overlaps the right ventriclebolus makes its way through the heart. First-pass in equilibrium studies.studies may be gated or ungated. Gated studies • First-pass studies allow detection and quantifica-involve synchronization of the presented images tion of both right-to-left and left-to-right intracar-with the patient’s ECG such that systole and dias- diac shunts, whereas shunt detection is not possibletole are identified. Ungated studies simply present a with equilibration studies.series of images over time. • First-pass studies allow sequential analysis of ERNA involves use of technetium-99m-labeled right atrial (RA), RV, left atrial (LA), and LV size,red cells, which are allowed to distribute uniformly whereas equilibration studies do not. Abnormalitiesin the blood volume. Radiolabeling of red cells is in the progression of the radioactive tracer throughaccomplished by initially injecting the patient with the heart and great vessels assist in the diagnosis ofstannous pyrophosphate, which creates a stannous- congenital abnormalities.hemoglobin complex over the course of 30 minutes. • Equilibration studies provide better analysis ofSubsequent injection of a technetium-99m bolus regional wall motion abnormalities than first-passresults in binding of technetium-99m to the studies due to higher resolution.stannous-hemoglobin complex, thus labeling the • Both types of studies can be used with exer-red cells. cise. First-pass studies can be performed rapidly
    • 10 Chapter 1but do not allow assessment of ventricular wall shunts, enhancement of Doppler signals, andmotion at different exercise levels, nor do they allow improved assessment of regional and global LVassessment of wall motion from different angles. function.• Mitral or aortic regurgitation is detectable with • Stress echocardiography. Stress echocardiography isboth first-pass and equilibration studies by analysis based on the concept that exercise or pharmacolog-of the stroke volume ratio. This method tends to ically induced wall motion abnormalities developoverestimate regurgitant fraction and is not reliable early in the course of ischemia. Stress-inducedfor detection of minor degrees of regurgitation. wall motion abnormalities occur soon after perfu- sion defects are detected by radionuclide imaging because, in the ischemic cascade, hypoperfusionEchocardiography precedes wall motion abnormalities. ComparisonTransthoracic and transesophageal echocardiogra- of resting and stress images allows resting abnor-phy has revolutionized the noninvasive structural malities to be distinguished from stress-inducedand functional assessment of acquired and con- abnormalities. Resting abnormalities indicate priorgenital heart disease. Transthoracic echocardiogra- infarction, hibernating or stunned myocardium;phy (TTE) and transesophageal echocardiography whereas, stress-induced abnormalities are spe-(TEE) often play a major role in the evaluation cific for ischemia. Furthermore, dobutamine stressof cardiac surgical patients. Routine use of two- echocardiography may be useful in determin-dimensional imaging, color flow Doppler, contin- ing myocardial viability. Regions that are hypo-uous wave Doppler, pulsed wave Doppler, and kinetic, akinetic, or dyskinetic at rest and improveM-mode imaging allows the following: with dobutamine administration probably contain• Assessment of cardiac anatomy. Delineation of the areas of stunned or hibernating myocardium. Suchmost complex congenital heart lesions is feasi- areas demonstrate functional improvement afterble. In many instances, information acquired from myocardial revascularization.a comprehensive echocardiographic examinationis all that is necessary to undertake a surgical Computerized tomography and magneticrepair. resonance imaging• Assessment of ventricular function. A comprehen- Advances in imaging techniques have played asive assessment of RV and LV diastolic and systolic major role in defining anatomy in cardiac surgi-function is feasible. cal patients. Computerized tomography (CT) and• Assessment of valvular abnormalities. Assessment magnetic resonance imaging (MRI) now allow theof the functional status of all four cardiac valves clinician detailed anatomy, three-dimensional ren-is possible. In addition, quantification of valvular dering, and functional assessment of myocardialstenosis and insufficiency is accurate and reliable. performance and blood flow (Fig. 1.1). It is likelyAssessment of prosthetic valves also is feasible. that new advances in imaging techniques will con-• Characterization of cardiomyopathies. Hypertrophic, tinue to improve the quality and the anatomic detaildilated, and restrictive cardiomyopathies can be afforded by these techniques. Molecular imaging,identified. i.e. imaging of cellular function, is a developing area• Assessment of the pericardium. Pericardial effusions, in cardiac imaging. The applications of these newcardiac tamponade, and constrictive pericarditis are technologies remain to be seen.reliably identified.• Assessment of cardiac and extracardiac masses. Vege-tations, foreign bodies, thrombi, and metastatic and Cardiac catheterizationprimary cardiac tumors can be identified. Cardiac catheterization remains the gold standard• Contrast echocardiography. Contrast solutions con- for evaluation of acquired and congenital hearttaining microbubbles enhance the image allowing disease. Cardiac catheterization is covered in detailassessment of myocardial perfusion, intracardiac in Chapter 2.
    • Introduction 11 (FEV1 ), the forced vital capacity (FVC), and the forced mid-expiratory flow (FEF 25–75%). Arterial blood gases should be obtained for patients in whom carbon dioxide (CO2 ) retention is suspected and for those with severe pulmonary dysfunction as deter- mined by history, physical examination, PFTs, or cardiac catheterization. Pulmonary assessment and congenital heart disease Lesions that produce excessive pulmonary blood flow (large ventricular septal defect, truncus arte- riosus, dextrotransposition of the great arteries, and patent ductus arteriosus) are associated with pulmonary dysfunction. Occasionally, large airway compression occurs in response to enlargement of the pulmonary arteries. More commonly, how-Fig. 1.1 Three dimension reconstruction of the heart ever, these lesions produce pulmonary vascularand aorta changes that affect pulmonary function. The pul- monary vascular smooth muscle hypertrophy that accompanies increased pulmonary blood flow pro- duces peripheral airway obstruction and reducedRespiratory evaluation expiratory flow rates characteristic of obstructiveA preoperative assessment of pulmonary function lung disease. In addition, smooth muscle hypertro-(other than CXR) is required in all cardiac surgi- phy in respiratory bronchioles and alveolar ductscal patients. The evaluation must include a history in patients with increased pulmonary blood flowof known pulmonary disease, current respiratory contributes to this obstructive pathology. Thesesymptoms, and a physical examination. Evalua- changes predispose the patient to atelectasis andtion may include consultation with specialists and pneumonia. Children with Down syndrome havespecific pulmonary testing (pulmonary function a more extensive degree of pulmonary vasculartesting, spirometry, pulse oximetry, arterial blood and parenchymal lung disease than other childrengas analysis). The history should determine the with similar heart lesions. This predisposes patientsextent and length of tobacco use, the presence of with Down syndrome to greater postoperativeCOPD, asthma, recurrent or acute pulmonary infec- respiratory morbidity and mortality.tions, and the presence of dyspnea. Physical exam- Patients with lesions that reduce pulmonaryination should focus on the detection of wheezes, blood flow (pulmonary atresia or stenosis, tetralogyflattened diaphragms, air trapping, consolidations, of Fallot) also have characteristic pulmonary func-and clubbing of the nails. A CXR is indicated in tion changes. These patients have normal lung com-nearly all cardiac surgical patients. Pulmonary func- pliance as compared with the decreased compliancetion tests (PFTs) play a limited role in preoperative seen in patients with increased pulmonary bloodassessment. If there is confusion about whether flow. However, the large dead space to tidal volumeintrinsic pulmonary disease exists, its cause, and ratio in these patients greatly reduces ventilationits appropriate treatment, then pulmonary func- efficiency, and large tidal volumes are required totion testing may help guide the clinician. Spirom- maintain normal alveolar ventilation. Finally, 3–6%etry measures lung volumes, capacities, and flow. of patients with tetralogy of Fallot will have anSpirometry of expiratory flow rates allows measure- absent pulmonary valve and aneurysmal dilata-ment of the forced expiratory volume in 1 second tion of the pulmonary arteries. This aneurysmal
    • 12 Chapter 1dilatation produces bronchial compression and complications include respiratory failure, unantic-respiratory distress at birth. ipated intensive unit admission, pneumonia, air- way events during induction of anesthesia (cough, laryngospasm), and increased need for postopera-Pulmonary assessment and acquired tive respiratory therapy. Smoking increases mucusheart disease secretion, impairs tracheobronchial clearance, andPulmonary dysfunction ranks among the highest causes small airway narrowing. For patients under-predictors of postoperative pulmonary complica- going coronary revascularization, abstinence fromtions. Pulmonary dysfunction is defined as a pro- smoking for 2 months may reduce the incidenceductive cough, wheeze, or dyspnea. Pulmonary of postoperative respiratory complications. Absti-function testing consistent with pulmonary dys- nence for less than 2 months is ineffective infunction shows a FEV1 < 70% of predicted reducing the incidence of postoperative respiratoryor FEV1 /FVC < 65% of predicted, plus either complications. Similar studies of patients under-vital capacity (VC) < 3.0 L or maximum volun- going other surgical procedures have confirmedtary ventilation (MVV ) < 80 L/min. For patients the necessity of a 4–6-week abstinence period.undergoing valvular surgery, the presence of pul- Typically, tobacco-using patients presenting for car-monary dysfunction is associated with up to a diac surgery will not have had the recommended2.5-fold increase in perioperative mortality and a abstinence period required to reduce complications.2.5-fold increase in postoperative respiratory com- Acute cessation of smoking during the perioperativeplications. For patients undergoing only coronary period is not associated with elevated risk. Thererevascularization, pulmonary dysfunction is less is no added cardiovascular risk for patients usingpredictive of postoperative morbidity and mortality. nicotine replacement therapy (NRT).Pulmonary assessment and tobacco use Pulmonary assessment and asthmaChronic tobacco use has several physiologic effects Asthma is characterized by paroxysmal or persis-that may complicate anesthetic management. tent symptoms of wheezing, chest tightness, dys-Smoking accelerates the development of atheroscle- pnea, sputum production, and cough with airflowrosis. Further, smoking reduces coronary blood flow limitation. There is hyper-responsiveness to endo-by increasing blood viscosity, platelet aggregation, genous or exogenous stimuli. Preoperative evalua-and coronary vascular resistance. Nicotine, through tion of asthma confirms the diagnosis and evaluatesactivation of the sympathetic nervous system and the adequacy of treatment. Adequate control iselevated catecholamine levels, increases myocardial demonstrated when the patient reports normaloxygen consumption by increasing heart rate, blood physical activity, mild and infrequent exacerba-pressure and myocardial contractility. Furthermore, tions, no missed school or work days, and lessthe increased carboxyhemoglobin level, which may than four doses of β2 -agonist therapy per week.exceed 10% in smokers, reduces systemic and Long-term treatment is largely preventive in nature.myocardial oxygen delivery. This is particularly First-line pharmacologic treatment often incorpo-detrimental to the patient with CAD due to the high rates inhaled corticosteroids (ICSs). Beclometha-extraction of oxygen that normally occurs in the sone significantly improves FEV1 , peak expiratorymyocardium. The threshold for exercise-induced flow, and reduces β-agonist use and exacerba-angina is reduced by carboxyhemoglobin levels as tions. Leukotriene receptor antagonists (LTRAs) arelow as 4.5%. Short-term abstinence (12–48 hours) sometimes used as first-line therapy; however, theiris sufficient to reduce carboxyhemoglobin and nico- role is less clearly established when compared totine levels and improve the work capacity of the the ICS agents. Long-acting β2 -agonists are safe andmyocardium. effective medications for improving asthma control There is an increased incidence of postoperative in older children and adults when ICSs therapy doesrespiratory morbidity in patients who smoke. These not adequately control the disease. Theophylline is
    • Introduction 13less effective than ICSs and LTRAs in improving Table 1.5 Risk factors for acute renal failure afterasthma control. cardiac surgery. For patients in whom bronchospasm is well con- Female gendertrolled preoperatively, it is essential to continue Congestive heart failuretherapy during the perioperative period. Beta-2- LV ejection fraction <35%agonist metered-dose inhaler or nebulizer therapy Preoperative use of an intraaortic balloon pumpcan be continued until arrival in the operating room Chronic obstructive pulmonary diseaseand can be restarted soon after emergence from Previous cardiac surgeryanesthesia. Metered-dose inhalation therapy can be Emergency surgerydelivered via the endotracheal tube. For patients not Valve or valve + CABG surgeryon bronchodilator therapy who present for surgery Elevated preoperative creatininewith bronchospasm, a trial of bronchodilators withmeasurement of PFTs before and after therapy is CABG, coronary artery bypass graft.often helpful. An increase in the FEV1 of 15% ormore after inhalation of a nebulized bronchodilator Dialysis will correct or improve the abnormalities insuggests a reversible component of bronchospasm. potassium, phosphate, sodium, chloride, and mag-Surgery should be delayed until the asthma is con- nesium. In addition, the platelet dysfunction thattrolled. If this is not possible, acute therapy with accompanies uremia will be improved. L-deamino-steroids and β2 -agonists is indicated. Therapy for 8-D-arginine vasopressin (DDAVP) administrationthe cardiac surgical patient should be initiated with may improve uremia-induced platelet dysfunctiona β2 -selective metered-dose inhaler or nebulized and should be considered if clinically significantsolution. post-dialysis platelet dysfunction exists. Dialysis will not favorably affect the anemia, renovascu- lar hypertension, or immune-system compromiseRenal function associated with chronic renal failure.Patients presenting for cardiac surgery may pos- For nondialysis-dependent patients, preoperativesess varying degrees of renal dysfunction ranging hydration is necessary to prevent prerenal azotemiafrom mild elevations in creatinine to dialysis depen- from complicating the underlying renal dysfunc-dence. Assessing renal function preoperatively is tion. This is particularly important after proceduresvitally important in the cardiac surgical patient. such as cardiac catheterization with arteriography.Renal dysfunction after cardiac surgery is associ- Creatinine clearance falls after contrast arterio-ated with increased mortality, morbidity, resource graphy; in patients with preexisting azotemia, thisutilization and intensive care unit stay. Depending reduction is much more likely to result in ARF.on the definition of acute renal failure (ARF), any- Hydration ameliorates contrast-induced renal dys-where from 5% to 30% of patients demonstrate function. Treatment with acetylcysteine and sodiumrenal dysfunction after cardiac procedures. Renal bicarbonate reduce post-contrast ARF.dysfunction requiring dialysis is associated with a Patients with renal transplants occasionally50–80% increased risk of death. ARF is among the present for cardiac surgical procedures. The extra-strongest predictors for death with an odds ratio renal component of renal blood flow autoregula-of 7.9 (95% confidence interval 6–10) in cardiac tion is absent in the denervated kidney. Therefore,surgical patients. Identification of high-risk can- preoperative hydration and maintenance of sys-didates remains important for appropriate patient temic perfusion pressure are particularly importantconsent, risk-benefit analysis, and hospital resource to maintain renal perfusion. Sterile technique isutilization planning (Table 1.5). mandatory in these immunocompromised patients. The dialysis-dependent patient will require dial- Renal dysfunction often results in electrolyteysis preoperatively. If dialysis is unobtainable imbalance. Potassium regulation is often difficultpreoperatively, it can be managed intraoperatively. in the cardiac surgical patient. Hyperkalemia
    • 14 Chapter 1(>5.5 mEq/L) is uncommon in patients with normal approximately 300 mEq of total body potassiumrenal function; however, it may occur with injudi- deficiency. In preparing the cardiac surgical patientcious potassium administration. The major causes of for surgery, it is reasonable to maintain serumhyperkalemia result from diminished renal excre- potassium higher than 3.5 mEq/L for patients ontion of potassium secondary to reduced glomerular digitalis, those at high risk for myocardial ischemiafiltration rate (acute oliguric renal failure, chronic and those who have suffered acute reductions inrenal failure). Reduced tubular secretion may lead serum potassium. Potassium replacement is notto hyperkalemia as seen in Addison’s disease, without risk (iatrogenic hyperkalemia). In gen-potassium-sparing diuretics and angiotensin con- eral, potassium replacement should not exceedverting enzyme inhibitors. Other causes include 10–20 mEq/h or 200 mEq/day. Serum potassiumtranscellular shifts of potassium as seen in acido- must be closely monitored during the replacementsis, trauma, burns, beta-blockade, rhabdomyolysis, therapy.hemolysis, diabetic hyperglycemia, and depolar-izing muscle paralysis with succinylcholine. Theclinical manifestations relate to alterations in car- Endocrine evaluationdiac excitability. Peaked T waves will appear with apotassium level of 6.5 mEq/L. At levels of 7–8 mEq/L A careful evaluation for endocrine abnormalitiesthe PR interval will prolong and the QRS complex should be sought in the history and physical exami-will widen. At 8–10 mEq/L sine waves appear and nation. Diabetes mellitus (DM) and hypothyroidismcardiac standstill is imminent. Treatment is multi- deserve special consideration.modal and includes glucose, insulin, bicarbonateand β-agonists (shifting potassium to the intracel-lular compartment), diuretics, exchange resins and Diabetes mellitusdialysis (enhancing potassium elimination), and cal- Diabetes mellitus is a risk factor for developmentcium (no change in serum potassium concentra- of CAD; therefore, perioperative management oftion, but calcium counteracts the cardiac conduction DM is a common problem facing those who anes-effects of hyperkalemia). thetize patients for cardiac surgery. Patients with Hypokalemia (<3.5 mEq/L) is not uncommon in insulin-dependent diabetes have reduced or absentthe cardiac surgical patient. The most common eti- insulin production due to destruction of pancre-ology is chronic diuretic therapy, but other causes atic beta cells. Patients with noninsulin-dependentsuch as GI loss (nasogastric suction, diarrhea, vom- diabetes have normal or excessive production ofiting), mineralocorticoid excess, acute leukemia, insulin but suffer from insulin resistance. Thisalkalosis, barium ingestion, insulin therapy, vita- resistance may be due to a reduction in insulinmin B12 therapy, thyrotoxicosis and inadequate receptors, a defect in the second messenger onceintake must be considered. The clinical manifesta- insulin binds to receptors, or both. Patients withtions of hypokalemia are observed in skeletal mus- noninsulin-dependent diabetes may be managedcle, heart, kidneys, and the GI tract. Neuromuscular with diet, oral hypoglycemic agents (agents thatweakness is observed with levels of 2.0–2.5 mEq/L. increase pancreatic insulin production), or exoge-Hypokalemia leads to a sagging of the ST segment, nous insulin. Patients with insulin-dependent dia-depression of the T wave, and the appearance of a betes must receive exogenous insulin.U wave on the ECG. In patients treated with digi- Cardiopulmonary bypass (CPB) is associated withtalis, hypokalemia may precipitate serious arrhyth- changes in glucose and insulin homeostasis in bothmias. Treatment of hypokalemia involves either diabetic and nondiabetic patients. During normoth-oral or parenteral replacement. A deficit in serum ermic CPB, elevations in glucagon, cortisol, growthpotassium reflects a substantial total body deficit. hormone, and catecholamine levels produce hyper-A decrease in plasma potassium concentration of glycemia through increased hepatic glucose produc-1 mEq/L with a normal acid-base balance represents tion, reduced peripheral use of glucose, and reduced
    • Introduction 15insulin production. During hypothermic CPB, hep- Table 1.6 Recommendations for insulin administration.atic glucose production is reduced and insulin pro- Blood Insulin Rate induction remains low such that blood glucose lev- glucose infusion 100 kgels remain relatively constant. Rewarming on CPB (mg/dL) rate patientis associated with increases in glucagon, cortisol, (U/kg/h) (U/h)∗growth hormone, and catecholamine levels and isaccompanied by enhanced hepatic production of 150–200 0.02 2glucose, enhanced insulin production, and insulin 200–250 0.03 3resistance. The transfusion of blood preserved with 250–300 0.04 4acid-citrate-dextrose, the use of glucose solutions in 300–350 0.05 5the CPB prime, and the use of β-adrenergic agents 350–400 0.06 6for inotropic support, further increase exogenous ∗The actual rate of administration will vary from patientinsulin requirements. For nondiabetic patients, to patient and should be titrated against measured serumthese hormonally mediated changes usually result glucose levels and patient response.in mild hyperglycemia. For diabetic patients, thesechanges may produce significant hyperglycemiaand ketoacidosis. periods. On the morning of surgery, the usual Management of perioperative glucose is directly insulin dose is withheld. On arrival in the operatingrelated to perioperative outcome. Uncontrolled, or room, the patient’s blood glucose is measured. Forpoorly controlled, perioperative glucose is associ- tight control, a continuous regular insulin infu-ated with increased mortality, wound infection, and sion can be started and adjusted to maintain bloodintensive care unit length of stay. This relationship glucose between 100 and 150 mg/dL during theis true in cardiac and noncardiac surgical patients operative procedure. Determinations of blood glu-admitted to an intensive care unit setting. The ideal cose are made every 15–30 minutes. Table 1.6level of glucose is unknown; however, if a target provides guidelines for insulin administration. Itof 130 mg/dL can be achieved, this is associated must be emphasized that the alterations in glucosewith improved clinical outcome. Administration of homeostasis and the insulin resistance that accom-exogenous insulin should be administered early in pany hypothermic CPB may necessitate alterationthe perioperative period to achieve this goal. The in infusion rates, and therefore insulin must beclinician must remember that achieving this goal titrated against demonstrated patient response bymay be impossible in some patients. Insulin resis- measuring serial serum glucose levels.tance and the physiologic conditions encouraging Patients taking oral hypoglycemic agents shouldhyperglycemia may be too great in some patients. discontinue them at least 12 hours before surgery.Similarly, the clinician must exercise caution when For patients managed with these agents andadministering insulin. Serum glucose levels should patients managed with diet, blood glucose deter-be checked as frequently as every 15–30 minutes minations should be made every 30–60 minutesperioperatively while insulin therapy is utilized. during the operative procedure. These patientsUnrecognized hypoglycemia can adversely affect frequently require insulin infusions to maintainpatient outcome. glucose homeostasis during surgery. Because of the varying insulin requirements dur-ing cardiac surgery and the unreliable absorption Hypothyroidismof subcutaneously administered insulin in patients Hypothyroidism is characterized by a reduction inundergoing large changes in body temperature the basal metabolic rate. In patients with hypothy-and peripheral perfusion, insulin is best delivered roidism cardiac output may be reduced by up toIV for patients undergoing cardiac surgery. The 40% due to reductions in both heart rate and strokegoal of therapy should be maintenance of normo- volume. In addition, both hypoxic and hypercapnicglycemia during the pre-CPB, CPB, and post-CPB ventilatory drives are blunted by hypothyroidism.
    • 16 Chapter 1Furthermore, hypothyroidism may be associated in age. Serum chemistry (i.e. potassium, sodium,with blunting of baroreceptor reflexes, reduced drug glucose, renal and liver function studies) are indi-metabolism, renal excretion, reduced bowel motil- cated in patients anticipating invasive surgery withity, hypothermia, hyponatremia from syndrome of possible metabolic alterations, diabetic patients andinappropriate antidiuretic hormone (SIADH), and other patients at specific risk of renal or liver dys-adrenal insufficiency. The hypothyroid patient may function. Plasma N-terminal pro-brain natureticnot tolerate usual doses of antianginal drugs such as peptide (NTproBNP) is secreted by the left ven-nitrates and β-adrenergic blocking agents. Hypothy- tricle in response to wall stress. It is elevated inroid patients on beta-blockers typically require very patients with LV dysfunction and heart failure. Pre-low anesthetic drug requirements. operative NTproBNP levels greater than 450 ng/L Despite these problems, thyroid replacement are predictive of cardiac complications with a sen-for cardiac surgical patients, particularly those sitivity of 100% and a specificity of 89%. Hence,with ischemic heart disease, is not always desir- an NTproBNP level may assist in preoperative riskable. For hypothyroid patients requiring coronary assessment and resource management in selectedrevascularization, thyroid hormone replacement patients. A urinalysis is usually not indicated unlessmay precipitate myocardial ischemia, myocar- there are specific urinary findings. A pregnancydial infarction, or adrenal insufficiency. Coronary test should be considered in all female patientsrevascularization may be managed successfully in of childbearing age. Coagulation studies are indi-hypothyroid patients with thyroid replacement cated depending on the invasiveness of the proce-withheld until the postoperative period. Mild to dure, a history of renal or liver dysfunction, and inmoderate hypothyroid patients undergoing cardiac patients on anticoagulant medications.surgery have perioperative morbidity and mortality Medical management of acute coronary syn-similar to euthyriod patients. Hypothyroid patients dromes, myocardial infarction, peripheral vascularmay experience delayed emergence from anesthe- disease, atrial fibrillation, and stroke often includessia, persistent hypotension, tissue friability, bleed- antithrombotic medications such as aspirin, clopido-ing and adrenal insufficiency requiring exogenous grel bisulfate, heparin, coumadin, and others. Thesesteroids. Hypothyroidism is preferentially treated medications are common in patients presenting forwith levothyroxine (T4). In healthy adults without cardiac surgery and may have a major impact onCAD, a starting dose of 75–100 µg/day is appro- the management and preoperative evaluation of thepriate. In elderly patients, and those with CAD, patient. Patients may present with a long history ofthe initial dose is 12.5–25.0 µg/day and is increased aspirin or clopidogrel use. In the acute setting, hep-by 25–50 µg every 4–6 weeks allowing for a slow arin or shorter acting IIb/IIIa inhibiting agents suchincrease in metabolic rate thereby avoiding a mis- as integrelin may be in use. These agents are ben-match in coronary blood supply and metabolic eficial in reducing the incidence of stent occlusion,demand. myocardial infarction, or other thrombotic sequaela of peripheral vascular disease or hyper-coagulation. A thoughtful plan regarding the continued admin-Hematologic evaluation istration of these medications is required prior toBy the nature of the surgery, and the associated the operative procedure. In the case of clopido-cardiovascular medications (heparin, clopidogrel), grel, stable patients presenting for elective surgerycardiac surgical patients are at higher periopera- may be advised to stop the medication for 5 daystive risk of bleeding. A hemoglobin and hema- to reduce the risk of excessive bleeding duringtocrit is indicated based on the invasiveness of the operation. All of the agents, including aspirin,the procedure (i.e. relative risk of blood loss and are associated with increased blood loss duringtransfusion), the history of liver disease, anemia, surgery. The relative risk of stopping the agentbleeding, other hematologic disorders or an extreme versus the increased risk of excessive bleeding must
    • Introduction 17be weighed in each patient. Consultation with factor VIII activity level by 2%. The 12-hour half-lifesurgeon and cardiologist are recommended before of factor VIII requires that factor VIII be re-infuseddiscontinuing antithrombotic therapy. every 12 hours during the perioperative period. In addition to the medication history, all patients Factor VIII may be provided with cryoprecipitate,scheduled for cardiac surgical procedures require a which contains 100 units of factor VIII per bagcareful bleeding history with emphasis on abnor- (10–20 mL). Factor VIII concentrates that containmal bleeding occurring after surgical procedures, 1000 units of factor VIII in 30–100 mL also maydental extractions and trauma. Signs of easy bruis- provide factor VIII.ing should be sought on physical examination.All patients should undergo laboratory screening Factor IX deficiency (hemophilia B)for the presence of abnormalities in hemostasis. The half-life of factor IX in plasma is 24 hours; nor-A platelet count, partial thromboplastin time (PTT), mal persons have approximately 1 unit of factorand prothrombin time (PT) should be obtained. IX activity per 1 mL of plasma (100% activity).Time permitting, all abnormalities should be eval- Factor IX deficiency is clinically indistinguishableuated prior to surgery so that post-CPB hemostasis from factor VIII deficiency. Diagnosis is made byis not complicated by unknown or unsuspected factor assay. Safe conduct of cardiac surgery requiresmedical conditions. 60% factor IX activity during the operative pro- cedure, with maintenance of activity levels in thePT and PTT elevations 30–50% range for 7 days postoperatively. An infu-Elevations in PT and PTT should be investigated sion of 1.0 unit of factor IX per kilogram of bodyfor factor deficiencies, factor inhibitors, and the weight will increase the patient’s factor IX activ-presence of anticoagulants such as warfarin and ity level by 1%. The 24-hour half-life of factor IXheparin. It is important that documentation of a requires that factor IX be re-infused only everynormal PTT and PT existing before warfarin or 24 hours during the perioperative period. Freshheparin administration is initiated so that other frozen plasma (FFP) contains 0.8 units of all ofcauses of an elevated PTT and PT are not over- the procoagulants per milliliter and generally islooked. Deficiencies of factors VIII, IX, and XI used to replace factor IX. A 250-mL bag of FFPare most commonly encountered. These deficien- will provide 200 units of factor IX. For patients incies and their management are summarized in the who factor IX replacement with FFP will requirefollowing sections. infusion of prohibitively large volumes, factor IX concentrates are used.Factor VIII deficiency (hemophilia A)The half-life of factor VIII in plasma is 8–12 hours; Factor XI deficiency (Rosenthalnormal persons have approximately 1 unit of syndrome)factor VIII activity per 1 mL of plasma (100% activity). The half-life of factor XI in plasma is 60–80 hours;Patients with severe hemophilia A will have as normal persons have approximately 1 unit oflittle as 1% factor VIII activity, whereas mildly factor XI activity per 1 mL of plasma (100% activity).affected patients will have up to 50% activity. Factor XI deficiency is most common amongPatients present with an elevated PTT and varying patients of Jewish descent and is associated withdegrees of clinical bleeding. The diagnosis is made a prolonged PTT. Many of these patients haveby a factor assay. Safe conduct of cardiac surgery no symptoms or have a history of bleeding onlyrequires 80–100% factor VIII activity during the with surgery or major trauma. The diagnosis isoperative procedure, with maintenance of activity made by factor assay. FFP administration replen-levels in the 30–50% range for 7 days postopera- ishes factor XI. It is recommended that 10–20 mLtively. An infusion of 1.0 unit of factor VIII per of FFP/kg/day be used during the preoperative andkilogram of body weight will increase the patient’s postoperative periods to manage this deficiency.
    • 18 Chapter 1Platelet dysfunction with unfractionated heparin with good result. InThrombocytopenia should be evaluated and treated the preoperative setting, identification of patientsas necessary to avoid excessive operative bleeding. who have experienced HITT is paramount. If HITTA platelet count and platelet function monitoring is diagnosed, then the surgery should either beare important laboratory evaluations. The bleed- delayed long enough to clear the heparin antibodiesing time is not a reliable predictor of perioperative (usually 90–100 days), or an alternate anticoagu-or postoperative bleeding. Other measurements of lation strategy devised. If heparin re-exposure isplatelet dysfunction include thromboelastography considered, testing for the presence of HITT anti-and assays of activated platelet aggregation (aggre- bodies, generally by enzyme-linked immunosobentgometry). These evaluations provide information assay (ELISA), is required.on the functional integrity of platelet action. In thecase of thromboelastography, clot formation and Qualitative platelet defectsfibrinolysis are observed. The information gained Abnormalities in platelet function are observed withprovides insight into both factor content and platelet some medications, renal failure, hepatic failure,function. The activated platelet aggregation assays paraproteinemias (i.e. multiple myeloma), myelo-provide both a total platelet count and a percent- proliferative disorders, and hereditary disorders ofage of active platelets. Platelet dysfunction can result platelet function. In the cardiac surgical patient,from a variety of causes. medication related dysfunction, uremic dysfunction are most common.Thrombocytopenia There is an ever growing list of medicationsThrombocytopenia may due to dilution (i.e. with that inhibit platelet function. Some medicationsmassive fluid replacement), increased peripheral altering function and commonly observed in thedestruction (sepsis, disseminated intravascular coag- cardiac surgical patient include aspirin, nonsteroidalulation, thrombotic thrombocytopenic prupura, anti-inflammatory drugs (NSAIDs), thienopyridineprosthetic valve hemolysis or platelet antibodies) adenosine diphosphate (ADP) receptor antago-or sequestration (splenomegaly, lymphoma). In nists (clopidogrel, ticlopidine) and GP IIb/IIIathe cardiac surgical patient, dilutional thrombo- antagonists (abciximab, integrelin, and tirofiban),cytopenia is common. Thrombocytopenia is also dextran, dipyridamole, heparin, plasminogen acti-frequently the result of platelet destruction from the vators, and beta-lactam antibiotics. NSAIDs inhibitCPB circuit and from activation of heparin induced platelet function by blocking platelet synthesis ofplatelet antibodies. prostaglandins and platelet function is normalized Heparin-induced thrombocytopenia and throm- when these drugs are cleared from the blood.bosis (HITT) occurs due to the presence of an anti- Aspirin irreversibly acetylates prostaglandin syn-heparin-platelet factor 4 antibodies. The condition thase (cyclooxygenase) impairing platelet functioncan be terminated by withdrawal of heparin ther- for the life of the platelet (7–10 days). Like aspirin,apy. Ideally, heparin therapy should not be restarted the effects of clopidogrel are present for the lifeuntil in-vitro platelet aggregation in response to of the platelet. It is recommended that for elec-heparin no longer occurs. Heparin induced throm- tive surgery, clopidogrel should be held for 5 daysbocytopenia may re-occur up to 12 months after the allowing adequate time to reestablish a normalinitial episode. Patients with HITT requiring CPB platelet response to bleeding. Integrelin inhibitsbefore the antibody can be cleared present a man- fibrinogen from binding to the platelet surfaceagement problem. These patients may be treated GP IIb/IIIa receptor. Integrelin should be discon-by a variety of alternate anticoagulation agents. tinued 12 hours before surgery to ensure adequateDirect thrombin inhibitors such as danaparoid, lep- return of platelet function.irudin, bivalirudin, and argatroban have all been Renal dysfunction with uremia inhibits plateletused with success. Other agents such as tirofiban function. The cause of this effect is unknown. Inand epoprostenol have been used in combination addition to the qualitative defect there is often
    • Introduction 19thrombocytopenia in these patients. The bleed- In addition to the defects induced by cyanosis,ing time is usually prolonged and there is asso- defects inherent to normal infants and to childrenciated anemia. Bleeding may be treated with with congenital heart disease are present. Neonatalplatelet transfusion or administration of DDAVP, platelets are hypo-reactive to thrombin (the mostor cryoprecipitate. DDAVP and cryoprecipitate raise potent platelet agonist), epinephrine/ADP, colla-the levels of factor VIII (antihemophilic factor/ gen, and thromboxane A2 . In addition, neonatalvon Willebrand factor). When DDAVP is used, fibrinogen is dysfunction as compared to older chil-0.3 µg/kg is infused IV over 15 minutes and the dren and adults. An acquired deficiency of thehalf-life of its activity is 8 hours. large von Willebrand multimers has been demon- strated in patients with congenital heart disease.Coagulopathy and congenital heart Finally, factors synthesized in the liver may bedisease reduced in both cyanotic and acyanotic patientsCoagulopathies in children with congenital heart in whom severe right heart failure results in pas-disease are common. The etiology of these coag- sive hepatic congestion and secondary parenchymalulopathies is multifactorial. Cyanosis has been disease.implicated in the genesis of coagulation and fib-rinolytic defects particularly in patients where Suggested readingsecondary erythrocytosis produces a hematocritgreater than 60%. Thrombocytopenia and qualita- Ashley EA, Vagelos RH. Preoperative cardiac evaluation: mechanisms, assessment, and reduction of risk. Thoractive platelet defects are common. Defects in bleeding Surg Clin 2005;15:263–75.time, clot retraction, and platelet aggregation to Katz RI, Cimino L, Vitkun SA. Preoperative medical con-a variety of mediators have all been described. sultations: impact on perioperative management andPlatelet count and platelet aggregation response to surgical outcome. Can J Anaesth 2005;52:697–702.ADP are inversely correlated with hematocrit and Maurer WG, Borkowski RG, Parker BM. Qualitypositively correlated with arterial oxygen satura- and resource utilization in managing preoperativetion. In cyanotic patients, generation of platelet evaluation. Anesthesiol Clin North America 2004;22:microparticles, hypofibrinogenemia, low-grade dis- 155–75.seminated intravascular coagulation (DIC), defi- Practice Advisory for Preanesthesia Evaluation. A reportciencies in factors V and VIII, and deficiencies in by the Society of Anesthesiologists Task Forcethe vitamin-K-dependent factors (II, VII, IX, X) have on Preanesthesia Evaluation. Anesthesiology 2002;96: 485–96.all been implicated in the genesis of coagulapathy. Schmiesing CA, Brodsky JB. The preoperative anesthesiaIn patients who are cyanotic and erythrocytotic, evaluation. Thorac Surg Clin 2005;15:305–15.the plasma volume and quantity of coagulation fac- Thakar CV, Arrigain S, Worley S, Yared JP, Paganini EP.tors are reduced, and this may contribute to the A clinical score to predict acute renal failure after cardiacdevelopment of a coagulopathy. In some instances, surgery. J Am Soc Nephrol 2005;16:162–8.erythrophoresis with whole blood removed and Wesorick DH, Eagle KA. The preoperative cardiovascularreplaced with fresh frozen plasma or isotonic saline evaluation of the intermediate-risk patient: new data,may be justified. changing strategies. Am J Med 2005;118:1413.e1–9.
    • CHAPTER 2Myocardial Physiology andthe Interpretation ofCardiac Catheterization DataThe ability to interpret cardiac catheterization data the foramen ovale. Right atrial, right ventricular,is essential to the cardiac anesthesiologist. Catheter- and pulmonary angiography may be performedization data provide information about the extent on infants and children to delineate congenitaland distribution of coronary stenosis, the type and lesions.extent of valvular lesions, the location and quantifi-cation of intracardiac shunts, congenital lesions, and Left heart catheterizationan assessment of systolic and diastolic function. Thisinformation contributes to a complete preoperative A fluid-filled catheter capable of making high-evaluation and serves as a predictor of postoperative fidelity systolic, diastolic, and mean pressure mea-functional status. surements and capable of allowing angiographic dye injection is used. The catheter may be passed retro- grade via the brachial or femoral artery to the aorticRight heart catheterization root under fluoroscopic guidance where pressuresA fluid-filled catheter capable of making high- are recorded. In infants and children the femoralfidelity pressure measurements in the right atrium, artery is the preferred route. The umbilical arteryright ventricle, pulmonary artery, and pulmonary is small and its course is tortuous; therefore, is notartery occlusion position is passed antegrade via useful except for pressure monitoring and angiogra-a basilic, cephalic, or femoral vein under fluoro- phy of the descending aorta. Left heart catheteriza-scopic guidance. In addition, the catheter may have tion can be performed antegrade via the right atriumthe capability of making thermodilution cardiac in patients in whom the atrial septum can be crossedoutput and mixed venous oxygen saturation mea- via a patent foramen ovale or an atrial septal defect.surements. Angiography is performed by recording This is a common approach in infants and children.several cardiac cycles on cine film while radio- In patients in whom the retrograde approach tographic contrast material is injected into the right the left ventricle is undesirable, and where an atrialheart chambers. or ventricular level communication does not exist, For infants and children, the femoral vein is the the atrial septum can be intentionally punctured tousual access site; however, right heart catheteri- gain access to the left atrium using a Brockenbroughzation via the umbilical vein may be possible in needle.the first few days after birth. Catheterization of the Pressures in the aorta, left ventricle, and leftright ventricle and pulmonary arteries may be diffi- atrium are recorded. Aortography may be per-cult via the umbilical route because umbilical vein formed by recording on cine film the injection ofcatheters tend to pass directly into the left atrium via radiographic contrast material into the aortic root.20
    • Myocardial Physiology 21 Ao (a) (b) Ao 1 2 LA LA mv mv 3 5 4 Diastole SystoleFig. 2.1 Left ventriculogram in right anterior oblique (RAO) projection. End-diastolic image is shown in (a) whileend-systolic image is shown in (b). For purposes of comparison, end diastole is represented by dotted outline onend-systolic image. Numbers 1–5 refer to five segments analyzed for wall motion in RAO projection (see Fig. 2.12).Ao, aorta; LA, left atrium; mv, mitral valve.This will allow detection of aortic regurgitation,congenital aortic arch abnormalities such as coarcta-tion or aortic arch interruption, and acquired aorticlesions such as aortic dissection. Left atrial and ven-tricular angiography allows detection of congenitalanomalies. Left ventriculography is performed byrecording several cardiac cycles on cine film asradiographic contrast material is injected into themid left ventricle. The left ventriculogram allowsdetection of mitral regurgitation as well as com-parison of both regional and global wall motion insystole and diastole (Fig. 2.1a,b). The left ventricu-logram also allows calculation of left ventricularend-diastolic volume (LVEDV) and left ventricu-lar end-systolic volume (LVESV). The innermostmargin of the left ventricular (LV) silhouette in sys- Fig. 2.2 Left anterior oblique (LAO) projection of aortatole and diastole is determined. Computer assisted illustrating use of Judkin’s technique to catheterize theplanimetry calculates LV volumes from these two- right coronary ostia retrograde via femoral artery.dimensional pictures based on the assumption thatventricular shape is approximated by an ellip-soid. Angiographic stroke volume (SV) is then cannulization of the ostia and are advanced underdefined as LVEDV – LVESV. Ejection fraction (EF) fluoroscopic guidance via the same artery used foris defined as (LVEDV – LVESV)/LVEDV, which is left heart catheterization (Figs 2.2 & 2.3).SV/LVEDV. Cardiac output determinationCoronary angiography Two complimentary methods are used to deter-Cine recordings of radiographic contrast material mine cardiac output: the thermodilution techniqueselectively injected into the coronary ostia are made. and the Fick determination. Both methods measureSpecial catheters are used for the selective forward cardiac outputs. Forward cardiac output
    • 22 Chapter 2 Oxygen uptake or consumption (Vo2 ) can be determined from calculations made on a 3-minute expired air sample collected in a Douglas bag. The bag contents are analyzed for carbon dioxide and, using the respiratory quotient, VO2 is calculated. More commonly, an estimate of VO2 is obtained from tables that relate VO2 to body surface area or to heart rate and age. Arterial–venous oxygen content difference (A–VO2 difference) is calculated from the difference between the arterial and mixed venous oxygen contents where: Content = (O2 saturation of arterial or mixed venous blood×Hb concentration×(1.38)) +(0.003×PO2 of arterial or mixed venous blood) This method measures systemic blood flow;Fig. 2.3 Left anterior oblique (LAO) projection of which equals forward left heart output. It also can beaorta illustrating use of Judkin’s technique to used to measure pulmonary blood flow or forwardcatheterize the left coronary ostia retrograde viafemoral artery. right heart output, when oxygen consumption is divided by pulmonary arterial content subtracted from pulmonary venous content. The method isand total cardiac output are equal only if there are more accurate at low cardiac outputs, where theno regurgitant lesions or shunt fractions. arterial to venous oxygen difference is great. It also Thermodilution cardiac output is a modification is accurate in the presence of intracardiac shuntsof the indicator dilution method, in which flow is when the mixed venous oxygen content and pul-determined from the following relationship: monary venous oxygen content are properly deter-Known amount of indicator injected mined. This will be discussed further in the section × time on intracardiac shunts.Measured concentration of indicator In the thermodilution method, cold water is theindicator. A predetermined volume of indicator Resistancesof known temperature is injected into the right Systemic and pulmonary vascular resistances areatrium, where the temperature of the blood also made using hemodynamic and cardiac output datais known. The subsequent change in temperature as follows:over time is measured by a thermistor in the pul- • Systemic vascular resistance (SVR)monary artery. This method measures pulmonary • Pulmonary vascular resistance (PVR)blood flow, which is equal to forward right heart • Transpulmonary gradient (TPG)output. It is not accurate at low cardiac outputs, • Mean arterial blood pressure (MAP)in the presence of tricuspid regurgitation, or where • Mean pulmonary artery pressure (mPAP)an intracardiac left-to-right shunt exists. Thermo- • Pulmonary artery occlusion pressure (PAOP)dilution cardiac outputs are discussed in detail in • Central venous pressure (CVP)Chapter 3. • Cardiac output (CO) The Fick determination is based on the rela-tionship: (MAP − CVP)80 SVR =O2 consumption/arterial − venous O2 content CO difference nl = 700–1600 dynes/s/cm5
    • Myocardial Physiology 23 (MAP − CVP)SVR = CO D C nl = 9–20 Wood units (mPAP − PAOP)80PVR = SW = ∫ PdV CO Pressure nl = 20–130 dynes/s/cm5 (mPAP − PAOP)PVR = CO B nl = 0.25–1.6 Wood units ATPG = mPAP − PAOP nl = 5–10 mmHg The use of these parameters in evaluation of Volumepatients is discussed in detail in Chapters 4–9. Fig. 2.4 Schematic representation of ventricular pressure–volume loop. Crosshatched area representsSaturation data stroke work (SW) or total external mechanical work. Curve AB, diastolic filling; BC, isovolumicThe oxygen saturation (%) of blood in the low contraction; CD, systolic ejection; DA, isovolumicsuperior vena cava (SVC), the main pulmonary relaxation.artery, and the aorta are obtained to screen forintracardiac shunts. If an intracardiac shunt is sus-pected, multiple samples from locations in the great is illustrated in Fig. 2.4. Curve AB represents thevessels and cardiac chambers are necessary to local- diastolic pressure–volume relationship. Ventricularize the shunt and determine its magnitude and filling begins when left atrial pressure (LAP) exceedsdirection. left ventricular pressure at point A and the mitral valve opens. Point B represents LVEDP and LVEDV.Assessment of valve lesions LVEDV is also known as Ved. Point B also repre-Analysis of the pressure data from right and left sents the onset of isovolumic contraction at whichheart catheterization, in combination with anal- LV pressure exceeds LAP and the mitral valve closes.ysis of ventriculography and aortography data, Changes in diastolic function can be represented bywill delineate the extent and nature of valvular changes in the position and shape of the curve ABlesions. and will be discussed later. Curve BC represents isovolumic contraction. LV pressure increases while LV volume remains con-Assessment of pulmonary vascular stant. At point C, LV pressure exceeds aortic diastolicanatomy pressure and the aortic valve opens.For infants and children with congenital heart Curve CD represents the ejection phase ofdisease, special procedures may be necessary to ventricular contraction. At point D, aortic pres-assess the pulmonary vasculature and the extent of sure exceeds LV pressure and the aortic valvepulmonary vascular disease. closes. Point D represents the left ventricular end-systolic pressure (LVESP) and the left ventric- ular end-systolic volume (LVESV). LVESP is alsoPressure–volume loops known as Pes.To fully understand catheterization data, it is Curve DA represents isovolumic relaxation. Atnecessary to be familiar with ventricular pressure– this time there is constant LV volume and rapidlyvolume loops. A normal LV pressure–volume loop decreasing LV pressure.
    • 24 Chapter 2 The area encompassed by ABCD represents the Eastroke work (SW) that is external mechanical work. Ees EaPreload is defined as the end-diastolic fiber length Pesor volume and is represented by point B on the LV pressure (mmHg)curve AB. Augmented preload produces an increasein end-diastolic muscle fiber length represented bya point B further to the right on the curve AB. PesThis increased fiber length enhances the velocityof muscle shortening for a given level of afterload(Frank–Starling mechanism). A family of pressure–volume loops exists for anyventricle. Experimentally these loops are generated Vedby altering preload over a physiologic range using Vedpartial inferior vena cava (IVC) occlusion. Whenthe ventricular end systolic pressure volume points LV volume (mL)(point D) from each loop are connected a straight Fig. 2.5 A family of four ventricular pressure–volumeline is created. The slope of this line is ventric- loops have been generated by varying preloadular elastance (Ees) and it uniquely defines the (ventricular end diastolic volume or Ved ) in a ventriclecontractile state of the ventricle (Fig. 2.5). with fixed contractility (Ees ) and fixed afterload (Ea ). Afterload in this model can be defined simply Joining the ventricular end-systolic pressure (Pes ) andas Pes (point D) or as the stress (force per unit volume points from the four loops defines the slope Ees. The ventricular end-systolic pressure and volume pointsarea) encountered by ventricular fibers after the correspond to point D in Fig. 2.4. Ea is the slope of theonset of shortening as represented by moving from line defined by joining Ved to Pes for each loop. Sincepoint C to D. afterload is fixed in this example the slope Ea is the same pressure × radius for each loop. This can be seen in loops 2 and 4. DespiteStress = fixed afterload and fixed contractility, augmentation of 2hwhere h is wall thickness. Afterload, defined as preload results in an elevation of Pes . The intersectionwall stress, is constantly changing during ventric- point of Ees and Ea uniquely define Pes for each loop. Pes will remain constant with an augmentation ofular ejection because ventricular pressure, radius, preload only if Ea simultaneously decreases (shallowerand thickness are all changing during ejection. slope). These definitions of afterload are incompletebecause they do not directly describe the charac-teristics of the arterial system. Because the ventricle resistance. The pulsatile component of afterloadproduces pulsatile ejection of a viscous fluid (blood) is measured as frequency-dependent aortic inputinto a viscoelastic reservoir (the arterial system), it is impedance, which is determined by the elasticworth considering the characteristics of the arterial properties of the proximal aorta and by the reflec-system and of the blood, both of which consti- tion of pulse waves from the peripheral arterial tree.tute impedance to ventricular ejection. Pulsatile and Effective arterial elastance (Ea ) is defined as thenonpulsatile flow must be considered because both ratio of LVESP/SV (Pes /SV) and is the line that con-exist in the intact arterial system. The nonpulsatile nects point B to D (see Fig. 2.5). This relationshipcomponent of afterload is measured as peripheral incorporates peripheral resistance, characteristicvascular resistance. This is a familiar concept and is impedance, and lumped total arterial compliance.defined as Thus Ea can be used to define the hydraulic loadMean arterial pressure − central venous pressure (afterload) of the LV. cardiac output In the pressure–volume loop scheme, LVESV Blood viscosity and the caliber of the arterioles and Pes (point D) are uniquely determined by theare the major determinants of peripheral vascular intersection point of the contractile state (Ees ) and
    • Myocardial Physiology 25the afterload (Ea ). Normally, the ratio of Ea /Eesis 0.7–1.0. In this range, SW (external mechani- Eescal work) and efficiency (ratio of SW/myocardialoxygen consumption) are optimized. In heart fail- Pes′ Ea′ LV pressure (mmHg)ure patients the ratio may be as high as 4.0 due Ves′ Eato simultaneous decreases in Ees and increasesin Ea . Pes For a given Ees with Ea constant an increase inpreload (LVEDV or Ved ) will produce an increase inSV and an increase in LVESP (Pes ) (see Fig. 2.5).This increase in the area ABCD is known as preloadrecruitable stroke work (PRSW). In reality the only Vedway in which LVESP (Pes ) could remain con-stant for a given Ees with an increase in preload LV volume (mL)would be for the slope of Ea to decrease. Statedanother way, an increase in preload for a given Fig. 2.6 Two ventricular pressure–volume loopsEes will cause a parallel (no change in slope) shift illustrating the effect of increased afterload (Ea ) with preload (Ved ) and contractility (Ees ) fixed. Increasedin Ea to the right resulting in an increase in Pes afterload is represented by the line Ea which has aand LVESV. With enhanced contractility (steep Ees steeper slope than line Ea . Increased afterload (Ea )slope) the rise in Pes will be great and the reduc- results in an increase in Pes (from Pes to Pes ) andtion in LVESP will be small; PRSW will be high. an increase in end-systolic volume (from Ves to Ves ),With diminished contractility (shallow Ees slope) which causes a reduction in SV (from Ved –Ves tothe rise in Pes will be small and the reduction in Ved –Ves ). EF = Ees /(Ees + Ea ) and therefore EF falls asLVESP will be great; PRSW will be limited. This is Ea increases to Ea with Ees constant.consistent with the clinical observation that in thepresence of reduced contractility preload augmen- an increase in Ea as evidenced by a greater increasetation does not substantially improve SV and cardiac in LVESV.output. Figure 2.8 serves to unify these concepts. Loop 1 For a given contractile state with fixed preload, represents the control situation. Loop 2 representsan increase in afterload (steeper Ea slope) results an abrupt increase in afterload with contractilityin an increase in Pes and LVESV; represented constant. The result is an increased LVESV and anby moving upward and to the right on the line unchanged LVEDV. The result is a reduction in SV.A decrease in afterload (shallower Ea slope) results In subsequent beats (loop 3) of a normal heart,in a decrease in Pes and LVESV; represented by LVEDV is increased such that the original SV ismoving downward and to the left on the line now maintained at the new increased afterload.(Fig. 2.6). Increased contractility is represented by The ability of the ventricle to maintain SV in thean Ees that is steeper and shifted upward to the left. face of increasing afterload by increasing preloadAn increase in contractility with preload and after- is defined as preload reserve. Preload reserve isload fixed obviously augments SV because of the exhausted when the sarcomeres are stretched tomarked decrease in LVESV with LVEDV (preload) their maximum diastolic length. When this occurs,constant (Fig. 2.7). Decreased contractility is rep- there will be no further augmentation of the veloc-resented by an Ees that is shallower and shifted ity of shortening and the ventricle behaves as ifdownward to the right. With fixed preload (Ved ) preload is fixed. For a given level of contractil-and afterload (Ea ), SV is diminished when contrac- ity, after preload reserve is exhausted, additionaltility decreases (see Fig. 2.7). It is also obvious that increases in afterload will be accompanied by par-the shallower the Ees slope (more depressed con- allel decreases in SV (loop 4). This is defined as atractility) the more sensitive the ventricle will be to state of afterload mismatch. Afterload mismatch is
    • 26 Chapter 2 Ees Ea Ees′ 240 4 LV pressure (mmHg) Ea Pes Pes′ Ves Ves′ SV LV pressure (mmHg) 180 3 2 120 1 Ved′ SV Ved 60 LV volume (mL) 30Fig. 2.7 Two ventricular pressure–volume loops Limit ofillustrating effect of decreased contractility (Ees ) with Pes reserveand afterload (Ea ) constant. Decreased contractility is 50 100 150represented by the line (Ees ) that has a shallower slope LV volume (mL)than line Ees and is shifted downward to the left. Sinceafterload is fixed in this example, the slope Ea is the same Fig. 2.8 Ventricular pressure–volume loops illustratingfor both loops. Decreased contractility (Ees ) results in an the compensation of an intact ventricle for progressiveincrease in end-systolic volume (from Ves to Ves ) while increases in afterload with contractility fixed. StrokePes = Pes . Since Pes and Ea are constant in this example, volume (SV) can be maintained in the face of progressivestroke volume (SV) must be constant as well as afterload increases until preload reserve is exhausted.SV = Pes /Ea . As a result Ved increases by an amountequal to the increase in Ves . With Pes fixed SV willonly decrease with a decrease in contractility if (Fig. 2.9a–d). Any or all of these abnormalities mayafterload (Ea ) simultaneously increases (steeper slope). exist in a given patient.Progressive increases in Ea will result in a greaterincrease in Ves for Ees as compared to Ees . AlthoughSV is constant in this example EF decreases because ComplianceEF = Ees /(Ees + Ea ). Compliance or distensibility is defined as the ratio of a volume change to the correspond- ing pressure change or as the slope of thethe inability of the ventricle at a given level of con- volume–pressure ( V / P) relationship. Elastancetractility to maintain SV in the face of an increased or stiffness is the inverse of compliance ( P/ V ).wall stress. Decreased compliance or increased stiffness is thus defined as an increase in the steepness of the pressure–volume plot (see Fig. 2.9c). Strictly speaking, diastolic compliance is determinedDiastolic function by the intrinsic volume–pressure relationship ofNormal diastolic function is dependent on normal completely relaxed myocytes. There are two causesventricular diastolic compliance, distensibility, and of poor diastolic compliance.relaxation. Both extrinsic and intrinsic factorsaffect ventricular diastolic function. It is necessary Increased chamber stiffnessto differentiate between compliance, distensibil- This occurs in aortic stenosis or systemic hyper-ity, and relaxation, and this is best accomplished tension. In these cases, there is an increase inby examining diastolic pressure–volume diagrams the amount of myocardial tissue due to concentric
    • Myocardial Physiology 27 (a) Abnormal (b) Pericardial maintain SV may function on the steep portion of an relaxation restraint otherwise normal compliance curve (see Fig. 2.9d). Distensibility Decreased ventricular distensibility is defined as an increased diastolic pressure at a given volume.LV pressure This would be represented in a diastolic pressure– volume diagram by a parallel upward shift of the entire pressure–volume relation (see Fig. 2.9b). (c) Increased (d) Chamber chamber stiffness dilatation Decreased distensibility can occur from intrinsic and extrinsic causes. Intrinsic causes It has been demonstrated clearly that pacing- induced ischemia in humans with coronary artery disease (CAD) is responsible for diminished dia- LV volume stolic distensibility. Although impaired relaxation certainly plays a role in diastolic dysfunction withFig. 2.9 A series of diastolic pressure–volume curves.The solid curve in each example represents a normal ischemia, the pressure–volume relation in ischemiadiastolic pressure–volume relationship, whereas the more closely resembles the pattern seen withdotted curve represents the altered diastolic pericardial restraint (see Fig. 2.9b). This dimin-pressure–volume relationship. (a) The diastolic ished diastolic distensibility often precedes systolicpressure–volume relationship when ventricular dysfunction. In addition, pacing-induced ischemiarelaxation is impaired. (b) The diastolic pressure–volume elicits diminished diastolic distensibility in humansrelationship when distensibility is reduced as with with aortic stenosis without CAD. Differencespericardial restraint. (c) The diastolic pressure–volumerelationship when ventricular chamber stiffness is in the diastolic behavior of ischemic and non-increased or ventricular chamber compliance is reduced. ischemic segments of the same ventricle subjected(d) The effect of chamber dilatation on a normal diastolic to pacing-induced ischemia have been demon-pressure–volume relationship. strated. An upward shift (diminished distensibility) in the pressure–length relationship is observed inLV hypertrophy. Diastolic compliance of the ven- ischemic segments. For a given diastolic volume thistricle is diminished despite that fact that the results in an increase in diastolic pressure, whichcompliance of the individual muscle units is causes the nonischemic segments to move to anormal. steeper (less compliant) portion of their original pressure–length relationship.Increased muscle stiffnessThis occurs in restrictive cardiomyopathies due to Extrinsic causesamyoidosis and hemochromatosis. In these cases, Decreased distensibility may be caused by extrin-the compliance of the individual muscle units is sic limitations to ventricular expansion in diastole.diminished due to an infiltrative process. Diminished distensibility occurs due to ventricular interdependence via an intact ventricular septum The diastolic pressure–volume relationship is and the restraining effect of the pericardiumdynamic. There is high compliance at low volumes (see Fig. 2.9b). For example, distension of theand diminished compliance at higher volumes. As right ventricle with a leftward septal shift willa result, reduced diastolic compliance is not limited result in diminished distensibility of the leftto ventricles with altered pressure–volume slopes. ventricle. In addition, reduced distensibility mayA ventricle forced to make use of preload reserve to occur due to restrictive pericarditis or pericardial
    • 28 Chapter 2tamponade a diseased or fluid-filled pericardium and mean pressures of the RAP and PAOP tracing,(see Chapter 7). the RVEDP and LVEDP, and the left ventricular end- systolic and end-diastolic volume indices (LVESVIRelaxation and LVEDVI) are provided. The LVESVI and theVentricular relaxation is an energy consumptive LVEDVI are simply the LVESV and LVEDV obtainedprocess. Adenosine triphosphate (ATP) is required by planimetry of left ventricular end-systolic andfor calcium sequestration back into the sarcoplas- end-diastolic angiograms divided by the patient’smic reticulum and for detachment of actin–myosin body surface area (BSA). Pressure and volume datacross-bridges. When isovolumic relaxation is delayed, from a representative catheterization report areearly diastolic filling is impeded. When relax- reproduced in Figs 2.10 and 2.11.ation is incomplete, filling is impeded through- One point on the LV diastolic pressure–volumeout diastole (see Fig. 2.9a). Relaxation is impaired curve is obtained if the pressure and volume mea-during myocardial ischemia and in patients with surements are made under identical conditions ofhypertrophic and congestive cardiomyopathies. preload, heart rate, and ischemia. Thus, incomplete Normally, the right ventricular end-diastolic pres- information must be used to draw inferences onsure (RVEDP) is 1–2 mmHg greater than the mean overall diastolic performance. Clinically, a dilatedright atrial pressure (RAP), and the left ventric- heart would be expected in patients who are depen-ular end-diastolic pressure (LVEDP) is 2–3 mmHg dent on a large LVEDV to maintain an adequategreater than the mean PAOP and the LAP. These forward SV. Patients with chronic volume over-small differences in pressure are due to the volume load valvular lesions such as mitral regurgitationadded to the ventricle by atrial systole. When LV and aortic insufficiency are good examples. In thesecompliance is poor, the A wave produced by atrial patients, a large LVEDV is needed because only asystole will be large and the additional volume pro- portion of the total SV becomes forward SV. Earlyvided by the atrial kick in end-diastole will result in the disease, these patients operate on the flatin a large increase in LVEDP. In these patients, the portion of a diastolic pressure volume curve andpeak A-wave pressure in the LAP or PAOP trace have enormous preload reserve. As the disease pro-is a better measure of LVEDP than the mean LAP gresses and systolic function deteriorates, a largeror PAOP because the mean LAP or PAOP pressure LVEDV is needed to maintain SV. Eventually, thesewill underestimate LVEDP. Even large A waves only patients operate on the steep portion of the diastolicslightly elevate mean LAP because their duration is pressure–volume relationship and are unable toshort. Thus, well-timed atrial contraction results in augment preload without large increases in diastolica large elevation of LVEDV with only a small ele- pressure and subsequent pulmonary congestion. Invation of mean LAP and limited pulmonary venous patients with mitral regurgitation, this analysis ofcongestion. For patients who chronically function diastolic function is complicated by the presenceon a steep portion of the compliance curve, a large of regurgitant V waves in the LAP or PAOP traceA wave, left atrial enlargement on electrocardio- during ventricular systole. The electronically deter-gram (ECG) and an S4 on physical examination are mined mean LAP or PAOP will be increased in directexpected findings. proportion to the height and duration of the regurgi- tant V wave. This will cause the mean LAP or PAOP to overestimate LVEDP. An estimate of the LVEDPAnalysis of diastolic can be obtained by examining a calibrated PAOP orpressure–volume curves LAP trace and determining the A-wave amplitude.Ideally, the diastolic pressure–volume curve should In patients without atrial systole, the best estimatebe examined over its entire range and under of LVEDP will be the PAOP or LAP at end diastolebaseline and stress conditions. Unfortunately, this (see Chapter 3).information is not routinely available from cardiac A normal LVEDV and diminished ventricularcatheterization data. Typically, the A wave, V wave, compliance is seen most commonly in patients with
    • Myocardial Physiology 29Fig. 2.10 Reproduction of portion ofcardiac catheterization report from61-year-old woman with severethree-vessel coronary artery disease(CAD) and systolic dysfunction. Rightand left ventricular pressuremeasurements, Fick cardiac output(CO) determination, and derivedhemodynamic variables are reported.Fig. 2.11 Reproduction of portion ofcatheterization report from the patientdescribed in Fig. 2.10. Section reportsinformation obtained from leftventriculography. Left ventricularend-diastolic volume index (LVEDVI),left ventricular end-systolic volumeindex (LVESVI), stroke volume index(SVI) and ejection fraction (EF) arereported. In addition, qualitativedescriptions of left ventricular wallmotion in five wall segments seen inright anterior oblique (RAO) projectionare reported.
    • 30 Chapter 2LV pressure overload valve lesions such as aortic EF = Ees /(Ees + Ea )stenosis and, to a lesser degree, in patients with sys- Normal Ees and Ea are 1–3 mmHg/mLtemic hypertension. In these patients, the LVEDVnecessary to maintain an adequate SV is maintained These equations are consistent with a number ofat the expense of a high LVEDP because compliance clinical observations:is poor. The volume contributed by atrial systole • In the range of normal contractility (Ees ), EF isrepresents a larger proportion of the LVEDV than it largely insensitive to changes in afterload (Ea ) anddoes in ventricles with normal compliance because preload (Ved ).the early diastolic filling is compromised by low • EF is increasingly inversely related to afterloadcompliance and is compensated for by a well-timed (Ea ) as contractility (Ees ) decreases with fixedforceful atrial systole. Loss of atrial systole in these preload (Ved ). In addition this inverse sensitivity ispatients is disastrous because LVEDV can only be enhanced in the setting of reduced preload (Ved ).maintained by large elevations of mean LAP with • EF is increasingly inversely related to preloadconsequent pulmonary venous congestion. (Ved ) as contractility (Ees ) decreases with fixed A ventricle with abnormal LVEDV and dimin- afterload (Ea ).ished distensibility is characteristic of patients with • When preload (Ved ) is very low, EF will besevere CAD in which the energy requirements nec- reduced in presence of normal contractility (Ees )essary to guarantee complete ventricular relaxation and afterload (Ea ).at rest are not met. Such diastolic dysfunction • If the Ea /Ees ratio is 1.0 (ideally matched) thenprecedes the development of systolic dysfunction. EF = 50%. • EF is most useful as screening tool with low EF identifying those patients most likely to be sus-Systolic function ceptible to alteration in preload, afterload, andSystolic function is not synonymous with contrac- contractility.tility. Normal systolic function is the ability of the As an example, an increase in LVEDVI fromventricle to perform external work (generate a SV) 75 to 90 mL/m2 with LVESVI constant at 25 mL/m2 ,under varying conditions of preload, afterload and as would occur with afterload and contractilitycontractility. Any assessment of systolic function constant, would result in an increase in EF frommust take the contribution of these three factors 66% to 72%. Thus, a 20% increase in preloadinto account. results in a 9% increase in EF. EF is not a very sensitive index of CAD becauseEjection fraction areas of regional myocardial dysfunction secondaryDefined as {(LVEDV – LVESV)/LVEDV} × 100, the to ischemia may exist without depression of globalEF is an ejection-phase index and the most com- systolic function. EF separates patients with normalmonly used assessment of global systolic function. LV function from those with LV dysfunction andThe LVEDV and the LVESV are obtained from is reliable in following changes in systolic functionplanimetry of LV end-diastolic and end-systolic in individual patients. An EF lower than 40% inangiograms (see Fig. 2.1). The normal value is the absence of acute afterload elevations represents50–80%. Determination of EF is dependent on vari- depressed systolic function and corresponds clin-ations in preload, afterload, and contractility (see ically with New York Heart Association class 3Figs 2.5–2.7). This becomes obvious when EF is symptoms. An EF lower than 25% represents severedescribed mathematically using the concepts of Ees , depression of LV systolic function and correspondsEa , stroke volume (SV), and LVEDV (Ved ): to New York Heart Association class 4 symptoms (see Chapter 1).EF = SV/Ved EF may overestimate systolic function in mitral Pes /Ved (Ea ∗ SV)/Ved regurgitation because of the unique systolic loadingEF = 1 − =1− Ees Ees conditions in this lesion. The left ventricle is
    • Myocardial Physiology 31presented with two outflow tracts in systole: the LWSW is used in conjunction with Ved to describeaortic valve and the incompetent mitral valve. The PRSW where PRSW = LWSW/Ved. PRSW is a mea-mitral valve provides a low impedance outflow tract sure on myocardial contractility that is independentand the aortic valve provides a normal-impedance of preload and afterload. This method requires theoutflow tract. EF may remain near normal in the ability to simultaneously record LV pressures andface of depressed systolic function due to this low volumes and is not in routine clinical use.mean afterload state. With mitral valve replace-ment and the elimination of the low-impedance Left ventriculographyoutflow tract, the ventricle is presented with more Qualitative analysis of regional wall motion bynormal systolic loading conditions. EF may actu- left ventriculography is another index of systolically decrease substantially postoperatively in such function. Ventriculography is performed by mak-patients because depressed systolic function is now ing cine recordings as contrast material is injectedunmasked. directly into the mid-left ventricle. Left ventricu- lography is performed in the 30◦ right anteriorStroke work oblique (RAO) projection or in the right and 60◦ leftAnother ejection-phase index of systolic function anterior oblique (LAO) projections. The ventricle isis stroke work (SW), or external LV work, repre- divided into segments (Fig. 2.12) and visual analy-sented by the area ABCD in Fig. 2.4. When the sis of regional wall motion is made by comparisonshape of the LV pressure–volume loop is normal, of end-diastolic and end-systolic cineangiogramsas is true in the absence of pressure or volume (see Fig. 2.1). Five segments are generally analyzedoverload conditions, left ventricular stroke work in the RAO projection: anterobasal, anterolateral,(LVSW) is a good measure of systolic function. apical, diaphragmatic (inferior), and posterobasal.Chronic volume and pressure overload conditions Five segments also may be analyzed in the LAOalter the shape of the pressure–volume loop and projection: basal septal, apical septal, apical infe-the calculated LVSW is increased above the normal rior, posterolateral, and superior lateral. These areasvalue of 60–120 g-m/beat. LVSW is defined as: are graded qualitatively for wall motion. Normal areas exhibit concentric inward movement in sys-(Mean LV systolic pressure tole. Hypokinetic areas exhibit reduced concentric − mean LV diastolic pressure) × SV × 0.0136 inward motion in systole. Akinetic areas exhibit no motion with systole. Dyskinetic areas exhibit a para-When aortic and mitral regurgitation are absent, this doxical outward bulging with systole. Aneurysmalcan be simplified to: areas exhibit characteristic dilation with either(Mean arterial pressure − mean pulmonary artery hypokinesis or akinesis. Areas of hypokinesis generally are composed of occlusion pressure) × SV × 0.0136 ischemic myocardium, whereas akinetic areas arebecause mean arterial pressure approximates mean composed of infracted or hibernating myocardium.LV systolic pressure and mean pulmonary artery Improvements in wall motion occur in hypokineticocclusion pressure closely approximates mean LV and akinetic areas when ischemic tissue has beendiastolic pressure. In direct contrast to EF, alter- salvaged by revascularization or by pharmacologications in afterload have little effect on calculated interventions to improve perfusion. The presenceSW. SV declines or increases in proportion to the of collaterals, the absence of surface ECG Q waves,afterload elevation or reduction such that the area of and the presence of an associated proximal coro-the loop remains unchanged. SW, unlike EF, is very nary stenosis less than 90% improve the likelihoodsensitive to changes in preload. The area of the loop that medical or surgical intervention will improveis increased or decreased by increases or decreases the wall motion abnormalities. Dyskinetic andin preload. LVSW can be converted to LVSWI by aneurysmal areas, respectively, represent regionsdividing SV by BSA to get SVI. with little or no viable myocardium and rarely
    • 32 Chapter 2 LA Basal septal Superior lateral Anterobasal 10 Anterolateral 6 1 2 LV LA LAO LV 9 Posterolateral RAO 3 Apical 5 4 7 8 Posterobasal Diaphragmatic Apical septal Apical inferiorFig. 2.12 Schematic delineation of the five wall or distal RCA; PDA. 6. Basal septal – LMCA; proximal orsegments seen in right anterior oblique (RAO) and left mid-LAD, 1st septal. 7. Apical septal – LMCA; proximal,anterior oblique (LAO) projections during mid, or distal LAD. 8. Apical inferior – proximal, mid, orleft ventriculography. The following is a summary of distal RCA. 9. Posterolateral – LMCA; proximal or distalcoronary arterial supply to these regions: CIRC marginals. 10. Superior lateral – LMCA; proximal1. Anterobasal – LMCA; proximal LAD; 1st diagonal. CIRC marginals. CIRC, circumflex artery; LAD, left2. Anterolateral – LMCA; proximal or mid-LAD; anterior descending artery; LMCA, left main coronary1st diagonal. 3. Apical – LMCA; proximal, mid, or distal artery; PDA, posterior descending artery; RCA, rightLAD; 2nd diagonal. 4. Diaphramatic (inferior) – proximal, coronary artery.mid, or distal RCA; PDA. 5. Posterobasal – proximal, mid,show improvement in wall motion with surgical or requires knowledge of the regional blood supplypharmacologic intervention. pattern. The right and left coronary anatomy is illus- Regional wall motion abnormalities are a more trated in Figs 2.13 and 2.14. Most patients (85%)sensitive indicator of CAD than is a reduction in a have a right dominant system of coronary circu-global ejection-phase index of systolic function such lation. Here, the right coronary artery extends toas EF. This is because global systolic function can be the crux cordis in the atrioventricular groove andmaintained in the presence of regional dyssynergy gives rise to the posterior descending branch, leftby compensatory increases in wall shortening in atrial branch, atrioventricular (AV) nodal branch,areas of normal wall motion as long as large areas and one or more posterior LV branches. In a leftof myocardium are not dyssynergic. dominant system (8%), these branches are supplied by the left circumflex artery and the right coronary artery supplies only the right atria and ventricle. InCoronary angiography 7% of patients, the system is balanced, with the rightCoronary angiography delineates the normal and coronary artery supplying the posterior descend-pathologic features of the coronary circulation. ing, left atria, and AV nodal branches, whereasNormally, angiography is performed in the 60◦ LAO the left circumflex artery supplies the posterior LVprojection and the 30◦ RAO projection with caudal branches.or cranial angulated views if necessary. There is variation in the blood supply to various regions of myocardium, but some generalizationsCoronary anatomy can be made. This information is summarized inDetermination of the areas of myocardium at risk Fig. 2.12. Normally, a proximal branch of the leftwith a particular stenotic or vasospastic lesion circumflex artery supplies the anterobasal region.
    • Myocardial Physiology 33 posterior descending arteries supply the posterior one-third. A branch of the right coronary artery sup- SA nodal Conus plies the sinoatrial (SA) node in 55% of patients Proximal and by a branch of the left circumflex artery in the RCA other 45%. RV branch The bulk of the right ventricle is located in the diaphragmatic and posterobasal regions supplied AV nodal Mid-RCA by the right coronary artery in a right dominant RCA distal to posterior system. Small portions of the right ventricle also descending are included in the apical and septal areas. It is for Acute marginal LV branch this reason that involvement of the LAD results in compromise of perfusion to the anterior right ven- Distal RCA Posterior tricular wall near the ventricular septum and to the descending right ventricular apex. Conversely, involvement ofFig. 2.13 Anatomy of right coronary artery. the right coronary artery in a right dominant systemAV, arterioventricular; LV, left ventricle; RCA, right results in compromise of perfusion to the portionscoronary artery; RV, right ventricle; SA, sinoatrial. of the left ventricle located in the diaphragmatic and posterobasal regions. How severely the posterior Left main portion of the left ventricle will be compromised inProximal circumflex Proximal LAD 1st diagonal this setting will depend on how much of this region Atrial branch is supplied by the distal branches of the circumflex1st septal perforator Mid-LAD artery.Obtuse marginal 2nd diagonalDistal circumflex Anatomic coronary lesions Coronary atherosclerotic stenotic lesions are quan- Distal LAD Posterior lateral titated visually from moving cineangiograms in several projections. Coronary arteriography from a representative catheterization report is repro-Fig. 2.14 Anatomy of left coronary artery (right duced in Fig. 2.15. Stenotic areas of artery areoblique). LAD, left anterior descending. compared with adjacent normal areas and the per- cent reduction in lumen diameter caused by theThe anterolateral region is supplied by contributions stenosis is quantified. Thus, a 90% lesion refers tofrom both the diagonal branch of the left anterior a stenosis that causes a 90% reduction in lumendescending (LAD) artery and the obtuse marginal diameter. It is generally acknowledged that rest-branch of the left circumflex. The terminal por- ing coronary blood flow does not decrease untiltion of the LAD artery supplies the apical region. there is an 85% reduction in lumen diameter. ThisThe inferior region is a combination of the poste- corresponds to a greater than 90% reduction inrior lateral and diaphragmatic regions, which are lumen cross-sectional area. By contrast, a 50%best seen in an LAO projection. The posterior lat- diameter reduction corresponds to a 75% reductioneral branch of the left circumflex artery supplies the in cross-sectional area. Maximal coronary flow inposterior lateral region. The diaphragmatic region is response to a stimulus for vasodilation is bluntedsupplied by the posterior descending artery, which, when there is a 30–45% reduction in lumen diam-as previously discussed, is either a branch of the eter and is absent when the lumen diameter isright coronary or left circumflex artery. The poster- reduced 90%. Inter-observer variability exists in theobasal region is supplied by the proximal right coro- grading of stenotic lesions. In addition, coronarynary artery. The septal branches of the LAD artery angiography typically underestimates the severitysupply the anterior two-thirds of the ventricular of stenotic lesions and may not accurately predictseptum, and branches of the right coronary and the physiologic significance of a particular lesion.
    • 34 Chapter 2 thrombolytic therapy, percutaneous transluminal coronary angioplasty, or both. Coronary collaterals An extensive network of coronary collaterals is nor- mally present at birth. However, these collaterals are not demonstrable by angiography in normal hearts due to their small diameter. It is only when the collateral channels enlarge secondary to regional myocardial oxygen deprivation that they are visi- ble angiographically. The development of collateral pathways in patients with comparable degrees of coronary insufficiency is variable in both extent and time course. The presence of collaterals has been identified as a determinant of reversible wall motion abnormalities. LV function in the region of an occluded coronary artery is better main- tained in the presence of collaterals than in their absence. Interpretation of coronary angiography data To properly interpret the coronary angiograms it is necessary to integrate data from the angiogramsFig. 2.15 Reproduction of a portion of a catheterization with data from the right and left heart catheteri-report from patient described in Fig. 2.10. This section zations and from the left ventriculograms. Severalreports information obtained from coronary questions should be answered:angiography. Morphology of stenoses, percent reduction • What is the status of systolic function? Globalin lumen diameter, and sources of collaterization are function in the absence of mitral regurgitationreported. A pictorial representation of coronary arterialanatomy also is given. is best evaluated with EF. Regional function is assessed by analysis of the ventriculogram. Patients with an EF greater than 55% would be expected toCoronary spasm have limited areas of dyssynergy and no history ofTrue coronary spasm is diagnosed at the time of a prior myocardial infarct. Patients with a historycoronary angiography with a provocation test utiliz- of prior myocardial infarction or three-vessel coro-ing methylergonovine, acetylcholine, or hyperven- nary disease would be expected to have a reducedtilation. The test is considered positive if focal spasm EF and more extensive areas of dyssynergy. EFsoccurs in the presence of clinical symptoms or ECG in the range of 40% are common in this subsetchanges. of patients. Patients with three-vessel disease and a history of myocardial infarction have EFs in theCoronary thrombus formation range of 35%. More extensive areas of dyssynergyA thrombus superimposed on an obstructive coro- would be expected. Patients with an EF lower thannary lesion is often the pathogenesis of unsta- 25% have poor ventricular function and will haveble angina and is the direct cause of an acute large areas of akinesis and dyskinesis.transmural myocardial infarction in most patients. • What is the status of diastolic function? It is nec-Currently, protocols designed to intervene in the essary to determine whether myocardial ischemia isearly stages of myocardial infarction incorporate responsible for diminished ventricular distensibility
    • Myocardial Physiology 35as discussed in the section on diastolic function. allows a determination of valve area. For theAn elevated LVEDP is characteristic of diastolic mitral valve, then, the equation is: valve area = √dysfunction; although this also may exist in con- flow/37.7 × mean pressure gradient. For the aorticcert with systolic dysfunction, an elevated LVEDP is valve, the equation is: valve area = flow/44.5 × √not synonymous with systolic dysfunction. mean pressure gradient. Obviously, flow occurs• What regions of myocardium are jeopardized? across the mitral valve only in diastole and acrossSignificant stenotic lesions jeopardize the myocar- the aortic valve only in systole. Therefore, car-dium in specific regions as discussed previously. diac output cannot be substituted for flow in theA region is at high risk of developing ischemic equations. The time per heartbeat during whichdysfunction if it is poorly collaterized and distal blood flows across the mitral valve is defined as theto a severe stenosis. It also is necessary to deter- diastolic filling period. The diastolic filling period ismine whether the regional myocardium distal to measured from mitral valve opening to end dias-a stenosis is viable. If the area of myocardium is tole. The time per heartbeat during which blooddyskinetic or aneurysmal with evidence of sur- flows across the aortic valve is defined as the sys-face Q waves, pharmacologic and surgical efforts tolic ejection period. The systolic ejection period isto salvage the area will likely be of no benefit. measured from aortic valve opening to aortic valveIf the myocardium is viable, however, (hibernat- closure.ing myocardium), then revascularization may leadto a dramatic improvement in regional systolic Mitral valve flow (cm3 /sec)function. = {Cardiac output (cm3 /min)}• What are the consequences of deteriorating func- × {diastolic filling period (sec/beat)tion in a given region? Deteriorating function × heart rate (beat/min)}−1in a given region may cause major managementproblems. Continued compromise of flow to the Mitral valve area (cm2 )AV node may cause progressive heart block with = {mitral valve flow (cm3 /sec)} √subsequent hemodynamic compromise. A patient × {37.7 × mean pressure gradient (cm/sec)}−1with depressed global systolic function whose hypo-kinetic anterior lateral wall becomes akinetic may Aortic valve flow (cm3 /sec)develop cardiogenic shock. = {cardiac output (cm3 /min)} × {systolic ejection period (sec/beat)Evaluation of valvular lesions × heart rate (beat/min)}−1The impressive technological advances in Doppler Aortic valve area (cm2 )echocardiography and nuclear cardiac imaging = {aortic valve flow (cm3 /sec)} √ × {44.5 × mean pressure gradient (cm/sec)}−1now allow noninvasive assessment of valvularpathology. Evaluation via cardiac catheterization,however, provides important information. The mean pressure gradient for mitral stenosis is obtained by using planimetry to determine the areaStenotic lesions between simultaneous tracings of the left atrial orThe analysis of stenotic valve lesions is based on PAOP and the LV pressure during the diastolic fillingobtaining a valve orifice area from flow and period and then dividing this area by the length ofpressure–gradient data. The Gorlin equation uses the diastolic filling period. Figure 2.16 illustrates thisthe basic hydraulic formula: area = flow/velocity. area during one diastolic filling period. Normally,Combining this with an equation that relates the pressure gradients for several beats are deter-velocity to mean pressure gradient: velocity = mined and the average is taken. For aortic stenosis, √k × mean pressure gradient, where k is a spe- analogous measurements are made using planime-cific constant for either the aortic or mitral valve try to determine the area between simultaneous
    • 36 Chapter 2 150 ECG LV 100 mmHg 40 LA mmHg 30 Ao 50 20 LV 10 0 0 SecondsFig. 2.16 One diastolic filling period in a patient with Fig. 2.17 One systolic ejection period in a patient withsevere mitral stenosis. Simultaneous tracings of severe aortic stenosis. Simultaneous recordings ofelectrocardiogram (EGG), left atrial (LA) pressure, and proximal aortic pressure and LV pressure are recorded.left ventricular (LV) pressure are shown. The pressure The pressure gradient across the aortic valve isgradient across the mitral valve is crosshatched and seen crosshatched and seen to vary during systolic ejectionto vary during diastolic filling period. The length of the period. Time scale for length of systolic ejection perioddiastolic filling period can be seen in seconds. not shown. Ao, aorta; LV, left ventricular.tracings of the proximal aortic pressure and the It is important when evaluating stenotic lesionsLV pressure during the systolic ejection period. that the pressure gradient alone is not evaluated.Figure 2.17 illustrates this area during one ejec- At low flows (low cardiac output), it is possi-tion period. The gradients for several beats are ble for a valve to be critically stenotic with adetermined and averaged. small transvalvular pressure gradient. Several other It is essential that proper assessment of flow relationships should be kept in mind. The meanbe used for lesions in which stenosis and regur- pressure gradient is directly related to the squaregitation coexist. A thermodilution or Fick cardiac of flow. Thus, if cardiac output doubles, the meanoutput determination is an assessment of forward pressure gradient will increase by a factor of four.flow across a valve orifice. If regurgitation exists, The mean pressure gradient is inversely related tototal flow across the valve orifice will be for- the square of the valve area. Thus, if valve area isward flow plus regurgitant flow. If forward flow reduced by one-half, the mean pressure gradientinstead of total flow is used, the valve area for will increase by a factor of four.a given gradient will be underestimated and the The normal mitral valve area in an adult isdegree of stenosis will be exaggerated. Total flow 4–6 cm2 . The mitral valve area must be reducedis best obtained from angiographic determination to 2.6 cm2 before symptoms occur. A valve areaof cardiac output. Left ventriculography is used to of 1.5–2.5 cm2 is considered mild mitral stenosis,determine SV (as described previously) and SV is with symptoms occurring during exercise. A valvemultiplied by heart rate. area of 1.1–1.5 cm2 is considered moderate mitral
    • Myocardial Physiology 37stenosis. In these patients an elevated LAP neces-sary to maintain cardiac output. A valve area of1.0 cm2 is considered severe mitral stenosis. A LAPof 25 mmHg is necessary to maintain even minimalcardiac output. The normal aortic valve area is 2.6–3.5 cm2 . Theaortic valve area must usually be reduced to 0.8 cm2before angina, syncope, and congestive heart fail-ure occur. A valve area of 0.5–0.8 cm2 is consid-ered moderate aortic stenosis. Severe aortic stenosisexists when the valve area is less than 0.5 cm2 . For adults, valve areas usually are not normalizedfor body surface area (BSA). As a result, extremesof body size must be taken into consideration whendeciding whether a stenotic lesion is significant.A large person with higher cardiac output demandsmay have a large gradient and symptoms with avalve area that would be adequate for a smallerperson with reduced cardiac output requirements. Fig. 2.18 Long-axis cross-sectional view of left atrium,Valve areas commonly are normalized for BSA in left ventricle, and aorta in severe mitral regurgitation.infants and children. Injection of contrast material into left ventricle demonstrates regurgitation of contrast into left atrium and pulmonary veins.Regurgitant lesionsQuantification of regurgitant lesions with catheter-ization techniques is more difficult and less accu- The quantitative method of assessing regurgi-rate than for stenotic lesions. Two approaches are tation is based on calculation of the regurgitantavailable. One method is qualitative; the other is fraction:quantitative. Qualitative analysis is based on assess- regurgitant stroke volumeing the amount of contrast material regurgitated Regurgitant fraction = total stroke volumeinto the left atrium during left ventriculographyfor mitral regurgitation (Fig. 2.18) or into the left Regurgitant stroke volumeventricle during aortography for aortic regurgita- = total stroke volume − forward stroke volumetion (Fig. 2.19). The degree of regurgitation is gradedfrom mild to severe (1+ to 4+). In mild aortic regur- Angiographic or total SV is determined from leftgitation, a small amount of contrast enters the left ventriculography as described previously and for-ventricle during diastole but clears with each sys- ward SV is determined by the Fick method. Atole. In mild mitral regurgitation, a small amount regurgitant fraction lower than 30% indicates mildof contrast enters the left atrium during systole but mitral regurgitation, 30–60% indicates moderateclears in diastole. In severe aortic regurgitation, the mitral regurgitation, and higher than 60% indicatesleft ventricle is filled with contrast after the first dias- severe mitral regurgitation. A regurgitant fractiontole and it remains opacified for several systoles. In of 10–40% indicates mild aortic regurgitation, 40–severe mitral regurgitation, the left atrium is filled 60% indicates moderate aortic regurgitation, andwith contrast after the first systole and becomes more than 60% severe aortic regurgitation.progressively opacified with each beat. In addition, It is important to note that the height and dura-contrast is seen refluxing into the pulmonary veins. tion of V waves are not a direct assessment of theSimilar qualitative analysis is used to grade tricuspid degree of mitral regurgitation. Severe mitral regur-regurgitation. gitation can exist in the absence of a significant
    • 38 Chapter 2 mitral valve. An increase in the impedance to aortic ejection will favor increased outflow through the lower impedance of the incompetent mitral valve. With all other variables constant, this will increase the magnitude of the V wave. • The inotropic state of the left ventricle. An increase in LV contractility will tend to decrease LV dimensions, decrease the size of the valvular annu- lus, and thus decrease the amount of regurgitant flow. • The length of ventricular systole. A decrease in the length of ventricular systole will reduce the time available for regurgitant flow to take place. However, forward SV may be compromised as well. Analysis of the V wave in tricuspid regurgitation is hampered by similar considerations. Nonethe- less, with severe tricuspid regurgitation, the right atrial pressure trace takes on the shape of the right ventricular pressure trace.Fig. 2.19 Long-axis cross-sectional view of leftventricle, right ventricle, and aorta in severe aorticregurgitation. Injection of contrast material into proximal Evaluation of cardiac shuntsaorta demonstrates regurgitation of contrast into left A comprehensive discussion of the physiology ofventricle. shunts is provided in Chapter 6. Oxygen saturation measurements in multiple cardiac chambers andV wave. It has been stated that, for an individual the great vessels are used to localize and quantifypatient, the height of the V wave correlates with the cardiac shunts. Additionally, angiography duringdegree of regurgitation under conditions of chang- cardiac catheterization may be used to locate cardiacing afterload. Such conclusions must be drawn shunts.carefully however, as there are several factors thataffect the height and duration of V waves:• The degree of mechanical mitral valve impair- Shunt locationment. Mechanical impairment occurs with a rup- Shunt localization is usually accomplished using atured papillary muscle, a torn prosthetic valve combination of angiography and measurement ofleaflet, or a perivalvular leak. oxygen saturations in the pulmonary veins, SVC• The degree of functional mitral valve impair- and IVC, right heart chambers, left heart chambers,ment. Functional impairment occurs with papil- aorta, and pulmonary artery. Oxygen saturationlary muscle ischemia or ventricular dilation with sampling is used to detect an oxygen saturationdeformation of the valvular annulus. step-up in the right heart in the case of a left-to-• The compliance characteristics of the left atrium right shunt or an oxygen saturation step-down inand pulmonary veins. For a given regurgitant vol- the left heart in the case of a right-to-left shunt.ume, a dilated, compliant left atrium will exhibit A step-up is defined as an increase in the oxygen sat-a smaller V wave than a small, noncompliant left uration of blood in a particular location that exceedsatrium. the normal variability in that location; whereas,• The relative impedance to ejection through the a step-down is a greater-than-expected decrease inaortic valve versus that through the incompetent saturation for a given location.
    • Myocardial Physiology 39Shunt quantification This formula may be used to determine MVO2Shunt quantification is based on comparison of in the catheterization laboratory when left-to-rightsystemic and pulmonary blood flows. Systemic (QS ) shunts exist. More commonly, particularly in chil-and pulmonary (QP ) blood flows are calculated by dren, SVC oxygen content is commonly used as athe Fick method previously described. surrogate for MVO2 content. SVC blood has a lower oxygen content than IVC blood and a higher con-QP = VO2 /(PVO2 content − PAO2 content) tent than coronary sinus blood and thus SVC blood provides a very close estimate of the mixture of PAO2 content is the pulmonary arterial oxygen the three samples. In addition, streaming of bloodcontent. PVO2 content is pulmonary venous oxygen of varying oxygen contents in the IVC hamperscontent. Sampling blood from the left atrium (when accurate IVC oxygen content sampling.the pulmonary veins return to the left atrium) will After QP and QS have been calculated, shuntsprovide a weighted average of the four pulmonary can be quantified. For an isolated left-to-right shunt,veins oxygen content. If a right-to-left atrial level the magnitude of the shunt is QP − QS . For an iso-shunt is present this sampling site will not provide lated right-to-left shunt, the magnitude of the shuntan accurate assessment of pulmonary vein oxygen is QS − QP . The ratio QP :QS is also useful. It can becontent. Each of the four pulmonary veins can be calculated from content data alone because the Vo2entered and sampled separately. When this is done terms cancel out:segmental areas of intra-pulmonary shunt and V /Q (SAO2 content − MVO2 content)mismatch can be detected. The PaO2 or saturation QP :QS = (PVO2 content − PAO2 content)of pulmonary venous blood from a lung segmentwith V /Q mismatch will improve with an increase Furthermore, if the blood is sampled using ain FiO2 while there will be no improvement if an low FiO2 , the dissolved oxygen portion of theintra-pulmonary shunt is present. content equation (PO2 × 0.003) can be ignored. The hemoglobin × 1.34 term cancels out andQS = VO2 /(SAO2 content − MVO2 content) the equation can be simplified to one using just saturation data from the four sites: SAO2 is systemic arterial oxygen content. MVO2 (SAO2 saturation − MVO2 saturation)content is mixed venous oxygen content. True QP :QS = (PVO2 saturation − PAO2 saturation)mixed venous blood is a mixture of desaturated A QP :QS >2.0 constitutes a large shunt, whereasblood from the IVC, SVC, and coronary sinus. In a QP :QS <1.25–1.5 constitutes a small shunt. Obvi-a normal heart a mixed sample of venous blood ously, a QP :QS <1.0 indicates a net right-to-leftfrom these three locations can be obtained from shunt.the pulmonary artery. In the presence of an intra For bidirectional shunts, it is necessary to cal-cardiac left-to-right shunt, PAO2 saturation will culate effective pulmonary blood flow (QPeff ) andoverestimate true MVO2 saturation because pul- effective systemic blood flow (QSeff ). QPeff is themonary arterial blood will be a mixture of mixed quantity of desaturated systemic venous blood thatvenous blood and oxygenated pulmonary venous traverses the pulmonary capillaries to be oxy-blood from the left heart. In this setting, true mixed genated. QSeff is the quantity of oxygenated pul-venous saturation must be determined from sam- monary venous blood that traverses the systemicples taken from the SVC and IVC. If the very low capillaries to deliver oxygen to tissue. QSeff and QPeffoxygen content low volume blood from the coro- are always equal. This concept is discussed in detailnary sinus is ignored then a weighted average of in Chapter 6.oxygen content of SVC and IVC blood can be usedto determine MVO2 content: Qseff = QPeff = VO2 /(PVO2 content−MVO2 content)(3/4 × superior vena cava O2 content) The left-to-right shunt is defined as QP − QPeff + (1/4 × inferior vena cava O2 content) while the right-to-left shunt is defined as QS −QSeff .
    • 40 Chapter 2The net shunt is the difference between these two vein. When antegrade pulmonary blood flow iscalculated shunts. severely diminished, retrograde filling of even the main pulmonary artery can occur.Evaluation of the pulmonary Assessment of pulmonary arterialvasculature hypertensionMarked increases or decreases in pulmonary blood Assessment of pulmonary arterial hypertensionflow routinely occur in patients with congenital (PAH) is defined as a PA systolic pressureheart disease. Obstructive pulmonary vascular dis- >35 mmHg or mean pulmonary artery pressureease may occur as a consequence of increased pul- (PAP) >25 mmHg at rest or mean PAP >30 mmHgmonary blood flow in patients with congenital heart with exercise. While the causes of PAH are myr-disease. The extent of pulmonary vascular disease iad the etiology of pulmonary hypertension relatedwill greatly influence the type of corrective or pal- to cardiac disease can be divided into four generalliative operative procedure performed. For patients categories:with diminished pulmonary blood flow, an evalu-ation of the extent and caliber of the pulmonary LA hypertensionvessels is necessary to choose the proper corrective Elevated LAP can result from a number of causesor palliative operative procedure. (mitral valve disease, LV diastolic dysfunction, LV systolic dysfunction, loss of AV synchrony). This isPulmonary artery wedge angiogram the by far the most common cause of elevated PAPThe pulmonary artery wedge angiogram is recorded in adults with acquired heart disease.on cine film while radiocontrast material is injectedinto a catheter that is in the pulmonary artery Pulmonary venous obstructionwedge position. Generally, the artery to the pos- This may be the result of obstruction to pulmonaryterior basal segment of the right lower lobe is vein entry into the venous circulation as with totalstudied. As obstructive pulmonary vascular disease anomalous pulmonary venous return or as withprogresses, the wedge angiogram demonstrates pro- cor triatriatum, or the result of obstructive diseasegressive increases in the diameter and tortuosity of inherent to the veins themselves.the pulmonary arteries, a diminution in the blushseen as capillaries fill, and the abrupt termination of Pulmonary vascular occlusive diseasethe dilated, tortuous arteries with a marked decrease (PVOD)in the number of supernumerary arterial branches. Chronic exposure of the pulmonary arterial bed to high flow and/or pressure leads to extensive struc-Pulmonary vein wedge angiogram tural changes. There is progressive muscularizationIn many congenital cardiac lesions with reduced of peripheral arteries, medial hypertrophy of mus-pulmonary blood flow, the pulmonary vasculature cular arteries and gradually reduced arterial numbermay be well visualized with injection of contrast due to occlusive neointimal formation with fibrosis.into collaterals that arise off the aorta. For patients Chronic LA hypertension can lead to developmentwith pulmonary atresia, pulmonary blood flow is of a similar process thru chronic elevation of PAP.markedly diminished and the pulmonary arteriesmay not be well visualized with contrast injec- High QP :QStions into collateral vessels. In this instance, the When a large nonrestrictive intracardiac communi-pulmonary vein wedge angiogram may be used to cation exists, particularly at the ventricular level,delineate the pulmonary vasculature. Retrograde PAP may be systemic or just sub-systemic. Thefilling of the parenchymal pulmonary vessels can be question that must be answered is whether theseen on cine recordings when contrast is hand elevated PAP is due to high flow into a low resis-injected into a catheter wedged in a pulmonary tance pulmonary bed (high QP :QS , normal PVR,
    • Myocardial Physiology 41 Table 2.1 Characteristics findings in pulmonary hypertension from different etiologies. Etiology Pressures LAP TPG PVR QP LA hypertension PAD ≈ PAOP ≈ LAP ↑↑ ↔ ↔ ↔ (acute) PAD > PAOP ≈ LAP ↑↑ ↑ ↑ ↔ (chronic) Pulmonary vein PAD ≈ PAOP LAP ↔ ↑↑ ↑↑ ↔ obstruction sl ↓ Pulmonary vascular PAD PAOP ≈ LAP ↔ ↑↑ ↑↑ ↔ occlusive disease sl ↓ Large L–R shunt PAD ≈ PAOP ≈ LAP sl ↑ ↔ ↔ ↑↑ sl ↑ sl ↑ LAP, left atrial pressure; PAD, pulmonary artery diastolic pressure; PAOP, pulmonary artery occlusion pressure; PVR, pulmonary vascular resistance (TPG/cardiac output) nL < 2 Wood units; QP , pulmonary blood flow; TPG, transpulmonary gradient (mPAP–LAP) nL 5–10 mmHg.large L–R shunt) or normal/low flow into a high Izzo JL, Jr. Arterial stiffness and the systolic hypertensionresistance pulmonary bed (normal/low QP :QS , high syndrome. Curr Opin Cardiol 2004;19:341–52.PVR, PVOD). Lock JE, Keene JF, Perry SB (eds). Diagnostic and Inteven- Determination of the etiology of pulmonary hy- tional Catheterization in Congenital Heart Disease, 2nd edn.pertension requires measurement of the PAP, LAP, Boston: Kluwer Academic Publishers, 2000. Maughan WL, Sunagawa K, Burkhoff D, Sagawa K.PAOP, TPG, and PVR as summarized in Table 2.1. Effect of arterial impedance changes on the end- systolic pressure–volume relation. Circ Res 1984;54: 595–602.Suggested reading Robotham JL, Takata M, Berman M, Harasawa Y. EjectionChemla D, Antony I, Lecarpentier Y, Nitenberg A. Contri- fraction revisited. Anesthesiology 1991;74:172–83. bution of systemic vascular resistance and total arterial Segers P, Stergiopulos N, Westerhof N. Relation of effec- compliance to effective arterial elastance in humans. tive arterial elastance to arterial system properties. Am J Physiol Heart Circ Physiol 2003;285:H614–20. Am J Physiol Heart Circ Physiol 2002;282:H1041–6.
    • CHAPTER 3MonitoringBasic monitoring of cardiopulmonary function is To ensure oxygenation, the standard prescribes thatessential to the safe conduct of any anesthetic. inspired oxygen concentration will be monitoredFor patients undergoing cardiac surgery, advanced with an oxygen analyzer with a low oxygen concen-monitoring of cardiac, pulmonary, renal, and cere- tration limit alarm in use. The patient’s oxygenationbral function will allow measurement of the phys- will be assessed using a quantitative method such asiologic variables necessary to make sound clinical pulse oximetry. Further, when a pulse oximeter isdecisions. The extent of monitoring required for used, the variable pitch pulse tone and a low thresh-a given case should be individualized and based old alarm shall be audible. Adequate exposure andupon the relative advantages and risks present. illumination is required to assess patient color.The consideration for advanced monitoring should Ventilation shall be continually evaluated forinclude patient characteristics, the anticipated surgi- adequacy. Means to determine adequacy includecal procedure, and the postoperative requirements chest excursion, observation of the reservoir bag,for advanced monitoring. This chapter will provide auscultation, expired end-tidal carbon dioxide con-an overview of the monitoring systems used most centration monitoring and qualitative monitoringcommonly in the management of cardiac surgical of the volume of expired gas. Airway manipulationpatients. involving a laryngeal mask airway or endotracheal tube shall have the device position confirmed with carbon dioxide monitoring. When ventilation isStandard American Society of controlled by a mechanical ventilator, there shallAnesthesiologists (ASA) monitors be a disconnection device in place with an audi-The ASA approved the Standards for Basic Anesthetic ble alarm. During regional anesthesia or monitoredMonitoring in 1986 and last amended the document anesthesia care, ventilation shall be evaluated byin 2005. This standard outlines the basic require- continual observation of qualitative clinical signsments for all anesthetics including cardiothoracic and/or monitoring for the presence of end-tidaland vascular procedures. There are two essential carbon dioxide.standards outlined in the text: Circulation will be assessed with the use of on• Standard I. Qualified anesthesia personnel shall be electrocardiogram (ECG) continuously displayedpresent in the room throughout the conduct of all during the duration of the anesthetic. An arterialgeneral anesthetics and monitored anesthesia care. blood pressure and heart rate will be determined• Standard II. During all anesthetics, the at least every 5 minutes. Every patient shall fur-patient’s oxygenation, ventilation, circulation, and ther have at least one of the following continuallytemperature shall be continually evaluated. monitored: palpation of a pulse, auscultation of42
    • Monitoring 43heart sounds, intra-arterial monitoring, ultrasound 50peripheral pulse monitoring, or pulse plethysmog-raphy or oximetry. Single lead sensitivity (%) Finally, every patient shall have their tem- 40perature monitored when clinically significantchanges in temperature are intended, anticipated,or suspected. 30 These monitoring standards form the basis uponwhich all advanced monitoring of the cardiothoracicpatient occurs. Advanced monitoring in the cardio- 20thoracic patient involves both invasive and non-invasive strategies to assess circulation. In addition,the cardiothoracic patient may require advanced 0cerebral function monitoring. Finally, the cardio- I II III aVR aVL aVF V1 V2 V3 V4 V5 V6thoracic anesthesiologist is required to monitor ECG leadadvanced coagulation function monitoring. The Fig. 3.1 The lead sensitivity in detecting myocardialremainder of the chapter will review the various ischemia is displayed. The combination of lead II and V5components of this advanced monitoring stratagem. provides the greatest ability to detect ischemia and rhythm disturbances. (From London MJ, Hollenberg M, Wong MF, et al. Anesthesiology 1988;69:232–41, withAdvanced electrocardiographic permission.)(ECG) monitoring a 12-French esophageal stethoscope for pediatricThe Advanced electrocardiographic is a standard patients or a 15-French esophageal stethoscope formonitor during cardiac surgical procedures for mon- adults. Alternatively, two of the three atrial elec-itoring heart rate, rhythm, and ischemia. A five- trodes from a pacing pulmonary artery catheterelectrode ECG system capable of monitoring seven (PAC) can be used to obtain a bipolar intra-atrialleads (I, II, III, aVR , aVL , aVF , and V5 ) is typi- ECG. The two leads from these electrodes are con-cal. In most operating room (OR) environments, nected to the right arm and left arm jacks of aleads II and V5 are simultaneously monitored. The standard three-lead ECG system. The third lead ofcombination of these two leads provides the best the three-lead ECG is connected to the patient viasurveillance for ischemia and arrhythmia detection a skin electrode and lead I monitored. Because the(Fig. 3.1). esophageal and intra-atrial ECG place electrodes so proximal to the atria, there is augmentation of atrialDysrhythmia detection activity such that the P wave is often larger than theLead II usually allows P-wave identification and QRS complex.morphology allowing for easy dysrhythmia iden-tification. In some tachydysrhythmias (paroxysmal Ischemia detectionatrial tachycardia, nodal rhythm, ventricular tachy- The presence of ECG changes is useful in the detec-cardia), the P wave may be difficult or impossible tion of myocardial ischemia. Specifically, ischemiato see in any of the standard leads. In other tachy- alters repolarization causing either downslopingdysrhythmias (atrial fibrillation, atrial flutter), the or horizontal ST-segment depression. Transmu-P wave is absent. In some cases of AV nodal block ral ischemia and myocardial injury are associatedor AV dissociation, the relationship between the with ST-segment elevation. In the case of coro-P waves and the QRS complex may be difficult to nary spasm, ST-segment elevations are likely to bediscern with standard ECG leads. In such instances, the initial manifestation seen on ECG. For ECGthe bipolar esophageal or intra-atrial ECG may be monitoring to be effective in detecting ischemia,useful. Two electrodes are incorporated in either the appropriate leads must be monitored. Exercise
    • 44 Chapter 3treadmill testing has demonstrated that 89% of Radial artery cannulationthe significant ST-segment depressions occurring Radial artery cannulation can be accomplished induring exercise can be detected in lead V5 . The infants, children, and adults. A 24-gauge Teflonaddition of leads II, AVF , V3 , V4 , and V6 to lead or polyurethane catheter is appropriate for infantsV5 increases the sensitivity of ischemia detection <4–5 kg. A 22-gauge catheter is appropriate forto 100% during exercise testing. Combining leads infants and children weighing less than 30 kg,V5 and II increase the sensitivity for detecting whereas a 20-gauge catheter is used in larger chil-ischemic changes to 90%. This combination allows dren and adults. The wrist is dorsiflexed over a rollthe most sensitive dysrhythmia and ischemia detec- of towel or gauze and secured on a short arm board.tion and is therefore the preferred lead selection in The thumb is taped back to reduce the mobilitymost OR environments. of the artery. Neither the dorsiflexion of the wrist It is important to understand ECG mode selec- nor the taping of the thumb should be so severe astion and ischemia analysis. The monitoring mode to compromise the radial pulse. The puncture site(0.5–40.0 Hz) filters out high and low frequency should be approximately 2 cm proximal to the sty-artifacts thereby attenuating the effects of extrane- loid process of the radius. After appropriate sterileous interference from 60 cycle interference, elec- prepping, the area of proposed puncture is anes-trocautery, respiratory variation, and movement. thetized with 1–2 mL of 1% lidocaine in the awakeUnfortunately, this mode makes analysis of sub- patient. When using a 22-gauge catheter it is help-tle ST segment changes unreliable. The diagnostic ful to nick the skin with a needle directly over themode (0.05–100.00 Hz) reflects the true extent of artery prior to catheter placement. The skin nickST segment changes but is more prone to interfer- helps prevent deformation of the catheter tip.ence. The monitoring mode is best selected when The catheter is introduced at an angle of 30◦ tothere is a low risk of ischemia; whereas, the diag- the artery with the bevel of the needle directednostic mode should be employed when ischemia is upward. When blood flows freely out the end ofsuspected or anticipated. the catheter, the angle between the catheter and Automated ST-segment software is currently the artery is reduced and the catheter and needleavailable on many intraoperative monitoring sys- are advanced approximately 1–2 mm. At this point,tems. These ST-segment analysis systems identify both the catheter and needle should be within thethe QRS complex and then identify the isoelectric vessel lumen, and the catheter can be advanced for-point in the P–R interval and a measurement point ward over the needle into the vessel. If there is noalong the ST-segment (80 ms from the J-point). blood flow out the needle, it is likely that the pos-Most monitors analyze of two to three leads simulta- terior wall of the artery has been punctured. Theneously allowing a more complete examination for needle and catheter are then intentionally advancedischemia. Alarms may be set for specific amounts of through the posterior wall. The needle is withdrawnST-segment deviation. partly from the catheter and the catheter is then withdrawn until its tip is located within the lumen of the artery and free flow of blood is noted. At thisArterial pressure monitoring point, the catheter is advanced into the artery. Alter-Arterial access allows beat-to-beat monitoring natively, a small guide wire (0.018) can be passedof arterial blood pressure as well as the ability to up a 24-, 22-, or 20-gauge catheter into the arteryobtain arterial blood samples for analysis of partial and often will facilitate advancement of the catheterpressure of oxygen (PO2 ), partial pressure of carbon (Fig. 3.2a–c).dioxide (PCO2 ), pH, bicarbonate, and other elec- Radial arterial cannulation is associated with atrolytes. The most common sites of arterial cannula- very low incidence of morbidity. An Allen’s test totion are the radial and femoral arteries in adults and assess collateral circulation to the hand via the ulnarchildren. In newborns the umbilical artery serves as artery and palmar arch is frequently performedan alternative to the radial or femoral arteries. before cannulation of the radial artery. There is
    • Monitoring 45 (a) radial artery contralateral to the subclavian artery being used must be used for monitoring. Like- wise, for children with pre-existing Blalock–Taussig shunts, accurate arterial blood pressure will be obtained only in the contralateral arm. • Coarctation repair. Arterial blood pressure is best monitored in the right radial artery for a variety of reasons: arterial blood pressure in the left arm may be lower than that in the right arm in the presence of hypoplasia of the aortic isthmus, a left subclavian artery patch may be used to repair the coarcta- (b) tion, or left subclavian artery circulation may be 30° compromised by placement of aortic cross-clamps during the coarctation repair. • Thoracic aortic surgery. Left subclavian artery flow may be compromised by surgical procedures on the distal arch or descending aorta; there- fore, blood pressure should be monitored in the right radial artery. For procedures involving the ascending aorta, the left radial artery is a better choice. (c) Femoral artery cannulation 10° A 22-gauge, thin-wall needle to puncture the artery in infants and children weighing less than 30 kg can be used for femoral artery cannulation. After free flow of blood is obtained, a straight wire is passed through the needle up into the artery. For infants, a 2-inch 20-gauge catheter is passed into the artery over the wire. For children, a 3-inch 20-gaugeFig. 3.2 Radial artery cannulation. (a) The wrist is catheter can be employed. For children weighingpositioned. (b) The artery is cannulated approximately more than 30 kg, an 18-gauge thin-wall needle for2 cm proximal to the styloid process of the distal radius.(c) The needle angle is reduced and the catheter arterial puncture and a 4-inch 18-gauge catheteradvanced. (From Lake CL. Cardiovascular Anesthesia. is appropriate. For larger children and adults, anNew York, Springer-Verlag, 1985:54, with permission.) 18-gauge thin-wall needle for arterial puncture and a 6-inch 16- or 18-gauge catheter is used. Femoral artery catheters have been used withcontroversy regarding the specificity and sensitivity a low complication rate for infants, children andof an Allen’s test, however, and this examination is adults. Hesitation to use femoral artery cathetersnot universally applied. The radial artery catheter is in children stems from concern that damage tomost often placed into the wrist of the nondominant the poorly encapsulated hip joint may occur eitherhand for patient comfort and convenience. In some directly, from sepsis or arterial occlusion and throm-instances, however, the radial artery catheter must bosis. This does not seem to be a problem forbe introduced preferentially into one radial artery infants and children when proper insertion tech-or the other, as specified below: niques and catheter sizes are used. However, for• Blalock–Taussig shunts. For children undergoing infants younger than 1 month of age, the inci-these subclavian to pulmonary artery shunts, the dence of transient perfusion-related complications
    • 46 Chapter 3(loss of distal pulse, limb coolness) has been Internal jugular cannulationreported to be 25% when a 20-gauge catheter is Three general approaches to the internal jugularused. This is higher than the rate associated with using anatomical landmarks have been described:radial or umbilical artery catheterization in this age central, anterior, and posterior. The centralgroup. approach involves localization of the internal jugu- lar vein at the apex of the triangle formed by theUmbilical artery cannulation two heads of the sternocleidomastoid muscle. TheThe umbilical artery cannulation may be obtained apex is lateral to the carotid pulse and generally is atin the catheterization laboratory or in the inten- the level of the cricoid cartilage (2–3 finger-breadthssive care unit (ICU) in neonates requiring invasive above the clavicle in adults). This approach appliesarterial pressure monitoring. A 3.5- or 5-French to infants and children. The anterior approachcatheter is used for arterial monitoring. The catheter involves localization of the vein at the lateral bordertip should lie just above the aortic bifurcation but of the medial head of the sternocleidomastoid at abelow L3, or alternatively, above the diaphragm at point halfway between the clavicle and the mastoid.the T7–T8 level. The posterior approach involves localization of the vein under the lateral border of the medial head of the sternocleidomastoid at the level of the cricoidCentral venous access cartilage. Regardless of the approach, extreme careAccess to the central venous circulation is essential must be exercised to ensure that the jugular veinfor cardiac surgical patients for a variety of reasons is cannulated and not the internal carotid arteryincluding secure intravenous (IV) access for volume (CA). Ultrasound imaging of the internal jugularand medication administration and advanced mon- vein demonstrates large anatomic variability in theitoring of volume status and cardiac function. The relationship between the jugular vein and the CAinternal and external jugular veins and the sub- (Figs 3.3 & 3.4). In about half of children and adults,clavian veins are commonly used for central venous more than 75% of the right CA is overlaid by theaccess in infants, children, and adults. The right right internal jugular vein when the head is rotatedinternal jugular vein offers fairly constant anatomy to the left. This overlap can be reduced somewhatwith a straight course to the right atrium and a by rotating the head less than 40% from the neu-low complication rate. Attempts at left internal tral position. Ultrasonic guidance facilitates catheterjugular venous cannulation may lead to injury to placement and may reduce the complication ratethe thoracic duct, and for patients with congenital of central venous catheter placement. The follow-heart disease, the left internal jugular may drain ing is recommended for cannulation of the internalinto a persistent left superior vena cava. The left jugular vein:subclavian vein provides an alternative for patients 1 The patient is positioned with the head turnedwith difficult or impossible internal jugular cannu- away from the intended cannulation site. Sup-lation. For patients with communication between plemental oxygen is supplied to nonanesthetizedthe right and left heart chambers, all peripheral and patients.central venous lines must be kept clear of air bubbles 2 For adults and older children, the pillow isto avoid potential systemic air embolization. removed from beneath the head to produce a A wide variety of central venous catheters are slightly extended neck position. For elderly patientsavailable for use. For adults and large children, with limited neck mobility, removal of the pil-7- and 8-French double- and triple-lumen catheters low may not be possible. For children, infants, andare available. For infants and children weighing neonates, it may be necessary to place a small roll<4 kg, 4-French double-lumen catheters 5 cm in under the shoulders to prevent cranial hyperflexionlength are available. For children weighing >4 kg, due to the larger head size.5-French double-lumen catheters 5 or 8 cm in 3 The anatomic outline of the clavicle and of thelength are used. two heads of the sternocleidomastoid muscle are
    • Monitoring 47 RIJ RIJ ICA ICAFig. 3.3 The internal carotid artery (ICA) is well Fig. 3.4 In this same patient with a Valsalva maneuver,visualized. In this patient with spontaneous respiration, the right internal jugular vein (RIJ) is now engorged andthe right internal jugular vein is collapsed (RIJ). prominent, anterior and lateral to the internal carotid artery (ICA).identified (some prefer to mark these structureswith a pen). In nonanesthetized patients, lifting with caution because the vein is not very deepthe head off the bed will help define these land- below the skin. The patient is placed in a 10–15◦marks. An ultrasonic probe (5.0–7.5 MHz) is placed Trendelenberg position. This positioning increaseson the neck using ultrasonic gel. The relationship of the size of the internal jugular and reduces the riskthe internal jugular and CA relative to each other of air embolus. It is best to wait until the last minuteand to the anatomic markings is noted. The depth to do this for patients with pulmonary venousof the vein below the skin surface also is deter- congestion or poor ventricular function becausemined. Head position can be altered to provide prolonged periods in the Trendelenberg positionthe least amount of overlap of the internal jugular may exacerbate pulmonary venous congestion andand CA without compromising access to the neck. heart failure. In nonanesthetized patients, this mayUltrasonography further allows one to determine result in patient discomfort, dyspnea, agitation andwhether the internal jugular is small, absent, throm- lack of cooperation.bosed or compressed from extravascular structures 5 A 25-gauge 5/8-inch needle is used to locate the(i.e. hematoma from previous attempts). This may center of the vein in all but the largest of adults.prompt a look at the contralateral internal jugular A 1 1 -inch 22-gauge needle rarely is needed to 2or move to a subclavian vein cannulation. localize the internal jugular. There is no need to4 The neck is prepped and draped using sterile keep a hand on the CA after the vein position hastechnique. The operator is gowned and gloved. For been localized with ultrasound. This maneuver onlyawake patients, local anesthesia is accomplished serves to compress the internal jugular.with 1% lidocaine in the area of the intended needle 6 After the vein is localized, the finder needle canpuncture. Deeper infiltration should be performed be left in place or removed. The appropriate-sized
    • 48 Chapter 3thin-wall needle is inserted through the skin in the made with the knife. The dilator is passed over thesame orientation as the finder needle. The thin-wall wire. The dilator should only be passed once andneedle is advanced. If the skin is depressed or dim- only deep enough to pass through skin, soft tissue,pled inward, the vein is at least partially compressed. platysma, and into the vein. The dilator is removedWhen dimpling occurs, the skin should be allowed and gentle pressure is held over the dilated punctureto “rebound.” This does not mean pulling the nee- site until the central venous pressure (CVP) catheterdle back out of the skin, it means relieving pressure or PAC introducer is placed.to allow the skin to return to a neutral position. 10 For instances in which venous access is difficultSome compression of the vein by the larger thin- or large transfusion requirements are anticipated,wall needle is inevitable, but when the needle is two catheters can be placed in the same inter-advanced without compressing the skin, it is more nal jugular. In this “double-stick” technique, onelikely that the vein will be entered on the way in and guidewire is placed and then a second guidewire isless likely that the vein will be transfixed and the CA placed through a second puncture site 1–2 cm abovewill be punctured. Often, when the skin is allowed or below the first one. The cannulation process isto rebound, free flow of internal jugular blood is then the same as described previously.obtained without any further advancement of the The most common complication of the inter-needle. nal jugular approach is carotid puncture (4%).7 When free flow of internal jugular blood is Other potential complications of the internal jugu-obtained, the thin-wall needle is fixed in place with lar approach include pneumothorax, thoracic ductthe fingers of the left hand while the hypothenar injury, brachial plexus injury, and air embolism.eminence rests on the patient. A flexible J-wire isadvanced into the thin-wall needle and vein. If thewire goes a short distance out the end of the nee- External jugular cannulationdle and resistance is met, advancement of the wire The external jugular approach is complicated bywhile spinning it with the right hand should be the presence of a system of venous valves, whichattempted. If resistance is still met, the wire can can make the placement of a guidewire and, sub-be left in place and the thin-wall needle can be sequently, a catheter into the central circulation,removed. An appropriate-sized IV catheter is then difficult. The advantage of this approach is thatplaced over the wire and advanced into the vein. there is little or no risk of carotid puncture, pneu-The guide wire is removed and a syringe is attached mothorax, thoracic duct injury, or brachial plexusto the catheter. The syringe is aspirated and the injury. For adults, the use of a guidewire with acatheter is withdrawn until free flow of blood is flexible J-shaped tip increases the success rate ofobtained. The catheter is then advanced into the this approach to 75–95%, compared with 95% forvein and the guide wire is reintroduced. the internal jugular route. In children, the success8 If there is any doubt that the thin-wall needle rate of this approach is approximately 60%. Clini-or catheter is in the internal jugular, the needle cally silent venous thrombosis in pediatric patientsor catheter should be connected to the monitor is high when the external jugular catheter does notand the venous (or arterial) waveform identified. reach the central circulation.Checking the color of the blood or the blood flowthrough the catheter are unreliable indicators ofarterial cannulation. Central circulation pressure9 When the guide wire is in place in the internal monitoringjugular (it is reassuring and common to see someventricular ectopy as the wire is advanced), a skin Pulmonary artery catheter monitoringnick is made with a knife. The skin nick should be PACs are multilumen, multipurpose catheterscontiguous with the wire; that is, there should not available in a variety of sizes (5-, 7-, andbe a skin bridge between the wire and the incision 7.5-French). A typical PAC contains the following
    • Monitoring 49components: c Atrial and ventricular pacing electrodes for bipo-1 A proximal lumen that terminates in a port lar endocardial atrial, ventricular, and atrioventric-located 30 cm (7- and 7.5-French) or 15 cm ular (AV) sequential pacing. These catheters contain(5-French) from the distal end of the catheter. three atrial electrodes and two ventricular elec-When the catheter is positioned properly, this prox- trodes. Two electrodes must be in contact withimal port will be located in the right atrium. This the endocardium for successful pacing. Consider-lumen is used to measure right atrial pressure (RAP) ing the variations in patient size and the length ofand to inject fluid of a known volume and temper- catheter necessary to properly position a PAC, theature for determination of a thermodilution (TD) presence of three atrial electrodes increases the like-cardiac output. lihood that two electrodes will be in contact with the2 A distal lumen that terminates in a port located at atrial endocardial surface. These catheters are 80%the distal end of the catheter. This lumen measures effective in establishing atrial, ventricular, and AVpressures as the catheter is advanced into position sequential pacing.and, when the catheter is properly positioned, is d The addition of fiberoptic bundles, which allowused to measure pulmonary artery systolic pressure continuous determination of mixed venous oxygen(PASP), pulmonary artery diastolic pressure (PADP) saturation by reflective spectrophotometry. Light ofand pulmonary capillary wedge pressure (PCWP). selected wavelengths is transmitted down a fiber-3 A balloon located 1 mm from the distal end of optic bundle, the tip of which is located in thethe catheter. This balloon is connected to the proxi- pulmonary artery. This light is transmitted throughmal end of the catheter by a lumen that runs the blood flowing past the fiberoptic bundle and islength of the catheter. The balloon can be filled reflected back to be transmitted down anotherwith air from a syringe located at the proximal fiberoptic bundle to be analyzed by a photodetector.end. The 7- and 7.5-French catheters have a 1.5-mL The differential absorption of known wavelengthsballoon, and the 5-French catheter has a 1-mL bal- of light by oxyhemoglobin and deoxyhemoglobin isloon. When the balloon is inflated, the catheter is used by a computer to determine mixed venous oxy-directed forward in the flow of blood. Balloon infla- gen saturation. The use of continuous mixed venoustion is used whenever the catheter is advanced. oxygen saturation measurements will be discussedWhen the catheter is positioned properly in the pul- in detail later.monary artery, inflation of the balloon will result in e The ability to perform continuous cardiac outputthe balloon occluding a branch of the pulmonary determinations using a thermal filament.artery. The pressure tracing obtained from the dis- f The ability to measure right ventricular ejec-tal port at this point will be a measure of the tion fraction using a rapid-response thermistor PACPCWP. As described in Chapter 2 it is technically (discussed in detail later).the pulmonary artery occlusion pressure (PAOP)that is measured. PAC placement4 A thermistor is located at the distal end of the In cardiac surgery, PACs usually are introduced per-catheter just proximal to the distal port and the bal- cutaneously into the right heart and pulmonaryloon. The thermistor is connected to one or more artery via an introducer placed in the right inter-plugs at the proximal end of the catheter, which nal jugular vein. For adults and large children, 7-,are used to interface the thermistor with a cardiac 7.5-, and 8.0-French catheters are used and areoutput computer. placed through an 8.5- or 9.0-French introducer.5 The catheter is labeled in 10-cm increments from The 5-French catheter is used in smaller chil-the distal end of the catheter. dren (weighing 15–40 kg) and is placed through a6 Optional features in PACs include: 6-French introducer.a An additional lumen for drug infusion. During placement, the patient should be moni-b An additional lumen for placement of a bipolar tored with a continuous ECG display. A defibrilla-right ventricular endocardial pacing wire. tor should be in the room and in working order.
    • 50 Chapter 3The defibrillator should be capable of being syn- If the catheter is advanced more than 10–15 cmchronized with the ECG signal to allow cardiover- (5–10 cm for smaller children) before the trace fromsion as well as defibrillation. The catheter must be the next expected chamber or vessel is noted, theplaced under sterile conditions by the operator. The catheter may be coiling in the right atrium or ven-catheter is placed in a sterile sheath, and the proxi- tricle. At this point, the balloon should be deflated,mal end of the catheter is handed off to an assistant, the catheter should be drawn back into the sheath.who uses the syringe to test balloon inflation. The The catheter can then be advanced again afterfully inflated balloon should protrude out over the inflation of the balloon. Catheter coiling maydistal end of the catheter and inflate symmetrically. ultimately lead to catheter knotting.The assistant also should connect the proximal and If coiling occurs, several things can be tried todistal lumens to their respective transducer/flush advance the catheter out of the RA or RV:systems. The proximal lumen will be used to mea- 1 Remove the catheter from the introducer andsure the RAP while the distal lumen will be used make certain that the balloon inflates properly.to measure the PASP, PADP, and PCWP. The distal 2 Orient the curve of the catheter so that it is morelumen trace must be visible on the monitor screen anterior than medial as it enters the introducer. Thisas the catheter is advanced. Finally, the TD car- may help direct it toward the tricuspid valve orifice.diac output computer should be connected to the 3 After multiple attempts, the catheter may soften.appropriate jack and the correction factor for the This can be remedied by flushing the distal portcatheter being used should be programmed into with 2–3 mL of iced saline or by gently twisting thethe computer. catheter as it is advanced. The catheter is held, loosely coiled, in the opera- 4 For awake patients, taking a deep breath maytor’s hand with the tip pointed toward the patient’s enhance blood flow out the RA and the right ven-left (toward the right ventricle and pulmonary out- tricular outflow track. For anesthetized patients,flow tract). The catheter is placed into the introducer release of a Valsalva maneuver may accomplish theand advanced 20 cm for older children and adults same thing.and 10 cm for smaller children. At this point, the 5 Putting the patient in the head-up positionballoon is inflated and the catheter is advanced and/or rotating the bed left or right may helpwith a smooth motion. For adults and older chil- as well.dren, a RAP trace will be seen on the distal lumen Most patients with congenital heart disease aretrace at approximately 20–30 cm. For smaller chil- not candidates for percutaneous placement of PACs.dren, this will occur at approximately 10–15 cm. Some of the reasons and considerations in theseSmooth catheter advancement with the balloon patients include:inflated continues until the right ventricular trace 1 Some patients (less than approximately 15 kg)is seen, followed by the PASP trace and finally the are too small for the 5-French catheters.PCWP trace. 2 In some patients, percutaneous placement of a Catheter advancement stops when the PCWP PAC may be difficult or impossible. For example,trace is seen. For adults and older children, the the presence of a large atrial septal defect or aPCWP trace will be seen at approximately 45–55 cm. ventricular septal defect may make placement dif-In smaller children, the PCWP trace will be seen at ficult without the use of fluroscopy. Similarly, theapproximately 25–35 cm. Deflation of the balloon presence of tricuspid atresia, pulmonary atresia, orat this time should result in reappearance of the pulmonary stenosis make percutaneous placementPASP trace. If the PCWP trace remains after bal- impossible.loon deflation, the catheter should be pulled back. 3 The PAC may interfere with the surgical repairThe catheter should not remain in the PCWP posi- and may have to be removed intraoperatively.tion for any longer than it takes to measure PCWP. 4 If necessary, catheters can be placed directlyExcessive balloon inflation can lead to pulmonary into pediatric patients by the surgeon imme-artery rupture or pulmonary infarction. diately before termination of cardiopulmonary
    • Monitoring 51bypass (CPB). A thermistor probe (2.5-French) ora thermistor probe combined with a distal lumen I 5s I(4-French) may be placed directly into the pul-monary artery via the right ventricular outflowtract. When combined with a directly placed right ECGatrial catheter (3.5-French), these will allow deter-mination of TD cardiac outputs. Because these 40catheters do not allow determination of PCWP, a leftatrial pressure (LAP) line may be placed by the sur- AX 20 V Y Cgeon as well. These lines may be placed directly intothe left atrium or into the left atrium via the right 0 Left atrial pressuresuperior pulmonary vein. Caution must be exer-cised with left atrial lines to avoid introduction of Fig. 3.5 Left atrial pressure (LAP) obtained from aair into the systemic circulation. patient undergoing left atrial pacing. Arrow shows pacer spike. The paper speed is 50 mm/s and clearly shows the A, C, and V waves as well as the X and Y descent.Central venous and pulmonary artery (From DiNardo JA. Monitoring. In: DiNardo JA (ed).pressure (PAP) measurements Anesthesia for Cardiac Surgery, 2nd edn. Stamford, CT: Appleton & Lange, 1998:37–80, with permission.)Right and left atrial pressureRight atrial pressure (RAP) is monitored directlythrough the proximal lumen, whereas LAP is not follows the peak of the P wave on the ECG bydirectly measured by the PAC. The PCWP will be 80 ms when simultaneous RAP and ECG traces arean accurate assessment of LAP, except for instances compared. The peak of the left atrial A wave followsin which there is pulmonary venous obstruction the peak of the P wave by 240 ms due to the later(rare) or in which the pulmonary alveolar pres- depolarization of the left atrium compared withsure exceeds pulmonary venous pressure. In these the right atrium. The peak A-wave pressure is theinstances, PCWP will reflect pulmonary alveolar best estimate of ventricular end-diastolic pressure,pressure (Palv). Pulmonary alveolar pressure will particularly when ventricular compliance or disten-exceed pulmonary venous pressure (Pv) when the sibility is poor (Fig. 3.6). Obviously, no A wave willdistal port lies in zone one (PAP < Palv > Pv) or be present when atrial systole is absent, as in atrialzone two (PAP > Palv > Pv) of the lung. Fortu- fibrillation and atrial flutter. For instances in whichnately, most catheters (93%) reside in zone three atrial systole is not synchronous with ventricular(PAP > Palv < Pv) portions of the right middle and diastole, atrial contraction may occur in the pres-lower lobes. ence of a closed tricuspid or mitral valve during The RAP trace usually is of higher quality than ventricular systole. This will result in productionthe PCWP trace because the LAP changes are of a large A wave (cannon A wave) because thedamped as they are transmitted through the pul- atrium cannot empty via the closed tricuspid ormonary vasculature to be detected by the distal mitral valve. Cannon A waves may be seen duringport. The RAP and LAP traces normally contain A, nodal rhythms with retrograde atrial depolarizationC, and V waves as well as X and Y descents (Fig. 3.7), re-entrant supraventricular tachycar-(Fig. 3.5). dia in which ventricular activation precedes atrial activation, and heart block with nonconductedA wave atrial activity occurring during ventricular systole.The A wave reflects the atrial pressure increase seen Cannon A waves also may be seen in instances induring atrial systole. Atrial systole occurs at ven- which atrial and ventricular contraction are syn-tricular end diastole and is commonly called the chronous but in which atrial outflow is preventedatrial kick. The peak of the right atrial A wave by tricuspid or mitral atresia.
    • 52 Chapter 3 C wave I 1s I The C wave reflects movement of the tricuspid or mitral valve annulus into the atrium during the iso- volumic phase of ventricular systole and is often not well seen. The C wave follows the A wave by a time ECG interval equal to the P–R interval and is seen best40 when the P–R interval is prolonged. V wave20 A V The V wave represents passive atrial filling while the X Y tricuspid and mitral valves are closed during ven- 0 PCWP tricular systole. The peak V-wave pressure will be determined by the compliance of the atrium andFig. 3.6 Pulmonary capillary wedge pressure (PCWP) the volume of blood that enters the atrium duringtrace from a patient with aortic stenosis and concentric passive filling. In the right atrial trace, the V waveleft ventricular hypertrophy. A large A wave is clearly peaks near the end of the ECG T wave, whereas theseen. The peak A-wave pressure at end-expiration is18 mmHg; this is the best estimate of left ventricular left atrial V wave peaks after the T wave.end-diastolic pressure. (From DiNardo JA. Monitoring. A large V wave may be produced by tricuspidIn: DiNardo JA (ed). Anesthesia for Cardiac Surgery, or mitral regurgitation (Figs 3.8 & 3.9). In this set-2nd edn. Stamford, CT: Appleton & Lange, 1998:37–80, ting, the V wave represents a combination of passivewith permission.) atrial filling and regurgitation of blood into the atrium via the incompetent valve during ventric- ular systole. Commonly, the height and duration of the V wave is used to quantitate tricuspid or mitral regurgitation. Such conclusions must be drawn carefully, however, because the duration of systole, the extent of mitral or tricuspid valve impairment, atrial compliance, the systolic performance of the ECG ventricle, and the impedance to ejection via the pul- monary artery or aorta all contribute to the height200 and duration of V waves. It is important to note that other factors may be100 responsible for production of a large V wave. A large volume of blood returning to the atrium and poor 0 Radial artery pressure atrial compliance will both produce large V waves. 40 For example, in the presence of a ventricular sep- A tal defect with a two-to-one left-to-right shunt, left 20 X CY atrial venous return will be twice that of right atrial return. Likewise, in the presence of poor ventric- PCWP ular systolic performance, preload reserve may be 0 exhausted to meet baseline cardiac output demands.Fig. 3.7 Pulmonary capillary wedge pressure (PCWP) In both instances, the large preload requirementsobtained from a patient in a nodal rhythm with will result in atrial distension, with the atrium func-retrograde atrial activation. Cannon A waves are present. tioning on the steep portion of its compliance curve.(From DiNardo JA. Monitoring. In: DiNardo JA (ed). This reduced atrial compliance will result in theAnesthesia for Cardiac Surgery, 2nd edn. Stamford, CT:Appleton & Lange, 1998:37–80, with permission.) production of a large V wave during passive atrial filling.
    • Monitoring 53 I 1s IFig. 3.8 Pulmonary artery pressure(PAP) and pulmonary capillary wedgepressure (PCWP) from a patient withmitral regurgitation. The presence of ECGthe large V wave may makedistinguishing PAP from PCWP 150difficult. Close examination shows thatthe peak of the PAP trace occurs muchearlier in the electrocardiogram (ECG) Radial artery pressure 0cycle than the V wave in the PCWPtrace. (From DiNardo JA. Monitoring.In: DiNardo JA (ed). Anesthesia for 50 A VCardiac Surgery, 2nd edn. Stamford, CT: X YAppleton & Lange, 1998:37–80, with 25 0 Pulmonary artery pressure PCWPpermission.) artery pressure or ECG traces can be used to differ- entiate the two traces. It has been demonstrated that the peak of the pulmonary artery trace normally occurs approximately 130 ms after the upstroke of a simultaneously recorded systemic arterial trace, ECG whereas the peak of the V wave occurs approxi- mately 350 ms after the systemic arterial upstroke. Similarly, the peak of the V wave will occur later in50 the ECG cycle than the peak of the PAP wave.25 0 Pulmonary artery pressure X and Y descent The X descent follows the A and C waves andFig. 3.9 Pulmonary artery pressure (PAP) and reflects a combination of the downward displace-pulmonary capillary wedge pressure (PCWP) in a patient ment of the tricuspid and mitral valve with thewith mitral regurgitation. The PCWP V wave is clearlyseen. The arrow points to the end-diastolic pressure in onset of ventricular systole and atrial relaxationthe PCWP trace. This pressure is approximately 18 mmHg following atrial systole. The Y descent follows theand is the best estimate of left ventricular end-diastolic V wave and reflects rapid atrial emptying afterpressure (LVEDP). (From DiNardo JA. Monitoring. In: opening of the tricuspid and mitral valves. Thus,DiNardo JA (ed). Anesthesia for Cardiac Surgery, 2nd edn. the Y descent also reflects early diastolic filling ofStamford, CT: Appleton & Lange, 1998:37–80, with the ventricle. In the presence of pericardial tam-permission.) ponade, the X descent usually will remain visible while the Y descent will be attenuated. In pericardial tamponade, diastolic filling of the heart chambers is Differentiating the PAP trace from the PCWP impeded because the potential space available forcan be difficult in the presence of large V waves expansion of the heart in the pericardium is largelybecause of the similarity of the two traces. Fail- eliminated when the pericardium is filled with fluid.ure to recognize the V wave of the PCWP can For this reason, passive filling and expansion of theresult in over advancement of the PAC into a dis- ventricle as reflected in the Y descent is attenuated.tal pulmonary artery, increasing the likelihood of To the contrary, the X descent is preserved becausea catheter-induced pulmonary artery perforation. it reflects a decrease in pericardial volume as atrialUse of simultaneously obtained PAP and systemic relaxation and ventricular systole begin.
    • 54 Chapter 3 For patients with constrictive pericarditis, early of ventricular end-diastolic pressure will be the RAPdiastolic filling of the ventricle is not compromised or PCWP at end diastole. This can be determinedas it is in pericardial tamponade. Constrictive peri- by obtaining simultaneous ECG and RAP or PCWPcarditis is characterized by impairment of ventric- paper traces. End-diastolic pressure in the RAP traceular filling in late diastole. Because early diastolic is determined at a point approximately 40 ms beforefilling is not impaired and because atrial pressure the start of upstroke of the QRS complex. End-is elevated, the Y descent is more prominent than diastolic pressure in the PCWP trace is determinednormal in constrictive pericarditis. As in pericardial at the QRS ST-segment junction.tamponade, the X descent remains prominent. Thiscombination of prominent X and Y descents givesa characteristic shape to the atrial pressure curve, Changes in pleural pressurewhich is often referred to as the M or W sign. Transmural pressure, i.e. the pressure acting to distend a heart chamber, is determined by thePulmonary artery pressure pressure–volume relationship of the chamber.A determination of systolic, mean, and diastolic Intracardiac pressures (such as RAP and PCWP) arePAP can be made with a PAC. In the presence of equal to the transmural pressure plus the juxtacar-normal pulmonary vascular resistance, the diastolic diac pressure. Transmural and intracardiac pressurePAP will overestimate the PCWP by 2–3 mmHg. In will be equal as long as juxtacardiac pressure is zero.the presence of increased pulmonary vascular resis- Pleural pressure is a major determinant of juxtac-tance, the diastolic PAP will overestimate PCWP and ardiac pressure. Pleural pressure will be negativecannot be used as a substitute measurement. during spontaneous inspiration and positive dur- ing controlled inspiration and forced exhalation.Limitations Large fluctuations in pleural pressure will causeThere are major limitations to accurate measure- intracardiac pressure to over- and underestimatement and interpretation of intracardiac and PAPs. transmural pressure and preload. Ideally, all intra-Common errors include a failure to properly zero cardiac pressure determinations should be made atthe transducers, placement of the transducer at an passive end-expiration, when pleural pressure isinappropriate level relative to the patient (trans- close to zero (atmospheric pressure).ducer too low reports a spuriously high pressure), If positive end-expiratory pressure (PEEP) iscatheter whip, and catheter dampening. added to the ventilation circuit, the juxtacardiac pressure at end expiration may be greater thanDetermination of mean pressure atmospheric pressure; this will cause intracardiacMonitor systems designate systolic, diastolic, and pressure to overestimate transmural pressure andmean pressures as the average highest, lowest, and preload. How much a given quantity of PEEPmean pressures obtained during a preset time inter- will elevate juxtacardiac pressure depends on theval or a series of such intervals. The electronically relationship of lung and thoracic compliance. Underdetermined mean RAP and PCWP will be skewed normal circumstances, the juxtacardiac pressure isupward by the presence of large V waves. This will expected to rise by approximately one half the valuecause mean RAP or PCWP to overestimate ven- of the added PEEP. Thus, if 10 cm H2 O of PEEP istricular end-diastolic pressure. A device to provide added, the juxtacardiac pressure can be expectedcalibrated paper printout of pressure traces is use- to increase by 5 cm H2 O. When lung compliance isful in analysis of pressure traces. These paper traces high (emphysema) and thoracic compliance is lowcan be used for accurate determination of A- and (obesity), a larger proportion of the added PEEP willV-wave pressures as well as systolic and diastolic be added to the juxtacardiac pressure. A smallerPAP. The best estimate of ventricular end-diastolic proportion will be added in cases where lung com-pressure will be the peak A-wave pressure. For pliance is poor (acute respiratory distress syndrome)patients without an atrial systole, the best estimate and thoracic compliance is high (muscle relaxation).
    • Monitoring 55Ventricular preload and pressure the equation:measurements Cardiac output = V1 × S1 × C1 × (TB − T1 )Ventricular preload is defined as the ventricu-lar end-diastolic volume. Unfortunately, methods × 60/SB × CB TB (t) dtof obtaining measurements of ventricular end-diastolic volume are not possible in a clinical envi- where V1 is the volume of the injectate; S1 andronment. In the absence of tricuspid or mitral SB are the specific gravity of the indicator and thestenosis, the A wave of the RAP and LAP (as mea- blood, respectively; C1 and CB are the specific heatsured by PCWP) traces are good estimates of the of the indicator and the blood, respectively; and T1right and left ventricular end-diastolic pressures. If and TB are the temperature of the indicator and thewe assume that the ventricular pressure–volume blood, respectively. (S1 ×C1 )/(SB ×CB ) = 1.08 whenrelationship does not vary, then measurement of isotonic saline or 5% dextrose is injected. TB (t)dtventricular end-diastolic pressure is as good an is the temperature–time curve measured by the pul-assessment of preload as ventricular end-diastolic monary artery thermistor after indicator injection.volume. Unfortunately, the shape of the ventricular TB (t) dt is the area under the temperature–timepressure–volume relationship is not linear. Fur- curve.thermore, changes in ventricular distensibility and A computer extrapolates the exponential downcompliance alter the relationship between ventric- slope of the temperature–time curve to the base-ular pressure and volume. It is not surprising, then, line and then determines the area under thethat changes in PCWP and LAP have been shown curve. With all variables thus known or mea-to correlate poorly with changes in left ventricular sured the computer solves the equation for cardiacend-diastolic volume in both the pre- and post-CPB output.periods. Two recent modifications of the bolus TD tech- nique deserve attention: continuous cardiac outputThermodilution cardiac output (CCO) monitoring and RV ejection fraction (EF)determination catheters.Thermodilution (TD) cardiac output is a modifica- The CCO technique makes use of a thermal fil-tion of the indicator dilution method in which flow ament located between the 15- and 25-cm gra-is determined from the following relationship: dations on the PAC. No injectate is necessary. This filament infuses, on the average, 7.5 W ofKnown amount of indicator injected heat, heating the blood as it passes by. Although × time/measured concentration of indicator warmed, the blood temperature always remains below 44◦ C. The resulting temperature change isIn the bolus TD method, the indicator is a crys- detected downstream in the pulmonary artery andtalloid injectate (usually 5% dextrose in water or cross-correlated with the input sequence to produceisotonic saline) at a temperature lower than the a TD washout curve. This requires use of a signalblood temperature. Blood temperature is measured processing system with an enhanced signal-to-noiseby a thermistor in the pulmonary artery. Crys- ratio because the thermal input is low relative to thetalloid temperature is measured by separate ther- background PA thermal activity. The monitor dis-mistor. A predetermined volume of crystalloid is plays the average cardiac output from the previousinjected into the right atrium. Adequate mixing 3–7 minutes updated every 30 seconds. In the Statof the crystalloid and blood occurs before passage mode, a new cardiac output can be obtained everyinto the pulmonary artery, and the change in blood 45–60 seconds. In this mode, fast trend estimates oftemperature over time after injection of the crys- cardiac output can be obtained when an unstabletalloid is measured by the thermistor in the pul- thermal signal is present. These catheters also canmonary artery. Cardiac output in liters per minute be used to obtain standard bolus injectate cardiaccan be calculated with the aid of a computer and outputs.
    • 56 Chapter 3 Clinical studies have demonstrated a close cor- • Stroke volume (SV), right ventricular end-relation between TD cardiac output determinations diastolic volume (RVEDV), and right ventricularmade with the bolus and CCO techniques in a rel- end-systolic volume (RVESV) are calculated asatively stable ICU environment. A major advantage follows:of the CCO technique would be the ability to mon- SV = CO/HRitor acute changes in cardiac output (CO) as theyoccur in real time. In the Stat mode, these changes RVEDV = SV/EFcan be tracked approximately every minute; in the RVESV = RVEDV − SVstandard mode, changes are averaged over timeand show data more consistent with a trend over The normal RVEF = 0.4. Good correlations betweentime. In either mode, the changes in CCO lag PAC determined RVEF and radionuclide determinedbehind those seen with mixed venous saturation RVEF have been reported.monitoring. • Several points regarding TD CO techniques Right ventricular ejection fraction (RVEF) (bolus, RVEF, and CCO) are worth emphasizing:catheters are another modification of the bolus a TD CO is a measure of pulmonary blood flow,injectate catheter. RVEF catheters incorporate: which in the absence of shunting (both intracar-• a rapid response thermistor, which has a reac- diac and systemic to pulmonary artery), is equal totion time of 50 ms compared with the 300–1000 ms forward right heart output.response time of standard bolus injectate PACs. b Cardiac output is inversely proportional to the• a multi-hole injectate port located 21 cm from area under the pulmonary artery temperature timethe catheter tip to ensure complete mixing of the curve.injectate in the RV. c There are large cyclical variations in the TD deter-• two ECG electrodes, which enable the computer mination of cardiac output during the differentto detect the R wave. phases of mechanical ventilation. This seems to be• This arrangement allows beat-to-beat determina- due to cyclic variations in pulmonary blood flow andtion of PA temperature changes. The injectate mixes temperature. For this reason, bolus measurementsand equilibrates with RV blood within two beats. obtained at random during the ventilatory cycle willThere is an exponential decrease in the amount exhibit a great deal of variability, whereas thoseof indicator ejected with each subsequent beat. PA obtained during the same phase of the ventilatoryconcentrations of indicator for each beat are equal cycle will have the greatest reproducibility. It hasto the RV end-diastolic concentration of indicator been demonstrated that multiple cardiac output val-for that beat. This produces a series of diastolic ues obtained at end expiration or peak inspirationtemperature plateaus that are identified by the com- in ventilated patients have high reproducibility. Theputer. The RVEF is calculated as follows from three highest measured TD CO occurs at peak inspiration,diastolic plateaus using the equation: whereas the lowest occurs at end expiration. Tripli- cate TD CO determinations are commonly made atEF = 1 − RFmean end-expiration because end-expiration is the easiestwhere phase of respiration to detect clinically. This prac- tice provides excellent reproducibility but tends toRFmean = (RF1 − RF2 )/2 underestimate the average cardiac output over oneRF1 = (T2 − TB )/(T1 − TB ) full cycle of mechanical ventilation. d Injectate temperatures from 0◦ C to room temper-RF2 = (T3 − TB )/(T2 − TB ) ature are used. The lower temperatures are obtainedwhere T1 , temperature at first diastolic plateau; T2 , by placing the injectate in an ice bath. The accuracytemperature at second diastolic plateau; T3 , tem- and variability of TD CO in adults is similar withperature at third diastolic plateau; and TB , blood either 10 mL of room temperature or iced injectate.temperature. Sinus bradycardia and atrial fibrillation have been
    • Monitoring 57reported in conjunction with iced injectate for car- is questionable. Bolus TD COs have been showndiac output determination. The slowing of the sinus to underestimate true cardiac output by approx-rate is likely due to cooling of the sinus node. imately 0.5 L/min in the first 10 minutes after• TD cardiac output is inaccurate in the termination of CPB due to a downward drift ofpresence of: the temperature baseline in the pulmonary artery.a Low cardiac outputs. Cardiac output is overesti- Another source of bolus TD CO error in the firstmated because low flow allows the cold injectate to 30 minutes after termination of CPB is the presencewarm and reduces the area under the TD curve. of respiratory variations or thermal noise in the pul-b Left-to-right intracardiac shunts (atrial septal monary artery blood temperature. These thermaldefect, ventricular septal defect). Computer analysis variations in pulmonary artery blood temperatureof the temperature–time curve often is not possi- may cause large variations in the bolus TD COble due to recirculation of indicator (cold water) determinations made at the various points in thethrough the pulmonary vasculature, which results respiratory cycle. This problem can be minimized byin interruption of the exponential downslope of measuring bolus TD CO at the same point in the res-the temperature–time curve with a prolonged, flat piratory cycle or eliminated by holding ventilationdeflection. The larger the shunt, the earlier the recir- during bolus TD CO determination.culation curve interrupts the normal downslope. Similar considerations may exist for the CCOManual planimetry has been used to determine the technique. In theory, the data processing of the CCOarea under the two portions of these curves. The system should minimize the effects of baseline tem-ratio of the area under the terminal deflection of perature shift and of thermal noise and improvethe curve to the area under the entire curve has performance. There is a poor correlation betweenbeen shown to be an accurate estimate of the ratio bolus TD CO and CCO during the first 45 minutesof pulmonary to systemic blood flow. after termination of CPB. The “stat” mode should bec Tricuspid regurgitation. Regurgitation of a frac- used during this interval.tion of the cold injectate results in delayed clearanceof the indicator from the right heart. This causesthe TD curve to be broad and of low amplitude, Continuous mixed venous oxygenwhich results in inaccurate assessment of forward saturation (SvO2 ) monitoringcardiac output. In the presence of TR TD cardiac SvO2 monitoring is available with some PACs. Theoutput tends to underestimate true cardiac output SvO2 is measured in the main pulmonary artery byat high cardiac outputs and to overestimate it at low oximetry. The main pulmonary artery is the loca-cardiac outputs. Similar problems are encountered tion of the most reliable site of true mixed venouswith CCO catheters. (SVC, IVC, and coronary sinus) blood. In infants andd Rapid infusion of volume via peripheral IV children where SVC saturation is used as a surrogatecatheters. Abrupt increases in the infusion rate of for mixed venous saturation surgically placed oxi-IV solutions within 20 seconds of a bolus TD CO metric SVC catheters can be used. In either case, thedetermination have been shown to result in vari- SvO2 is used to determine total tissue oxygen bal-ations of up to 80% in TD CO. The precise timing ance. It will not reflect regional oxygen imbalanceof the infusion rate increase relative to the TD CO (Table 3.1). Several definitions are in order:measurement determines whether the output will • Oxygen (O2 ) delivery (DO2 ) = cardiac outputbe an over- or underestimate. It is recommended (CO) × O2 content.that volume infusions be terminated or held at a • Arterial oxygen content (CaO2 ) = (hemoglobinconstant rate for at least 30 seconds before a TD CO (Hgb) × 13.8) (SaO2 ) + (0.003 × PaO2 ).determination. Likewise, rapid infusions of cold IV • Mixed venous oxygen content (CvO2 ) = (Hgb ×solutions affect the accuracy of CCO catheters. 13.8) (SvO2 ) + (0.003 × PvO2 ).The accuracy of bolus TD CO determinations in the • Oxygen consumption (VO2 ) = the metabolic rateperiod immediately following termination of CPB or the amount of oxygen consumed by the body.
    • 58 Chapter 3Table 3.1 Limitations of mixed venous oxygen a reflection of the adequacy of systemic oxygensaturation monitoring. (From Marx G, Reinhard K. Curr delivery. A reduced SvO2 indicates inadequateOpin Crit Care 2006;12:263–8, with permission.) systemic oxygen delivery and increased peripheral oxygen extraction and should prompt an evalu-SvO2 level Consequences ation of SaO2 , Hgb, VO2 , and CO. Similarly, aSvO2 > 75% Normal extraction; low CO in the setting of a normal SvO2 indicates O2 supply > O2 demand that systemic oxygen delivery is adequate to meet present metabolic needs and that, in reality, the75% > SvO2 > 50% Compensatory extraction; CO is not low for the metabolic demand. Although increasing O2 demand or a high CO is reassuring, it does not guarantee decreasing O2 supply adequate systemic oxygen delivery under condi-50% > SvO2 > 30% Exhaustion of extraction; tions of reduced Hgb and SaO2 or increased VO2 . beginning of lactic acidosis; A SvO2 measurement allows this determination to O2 supply < O2 demand be made.30% > SvO2 > 25% Severe lactic acidosis Hemodynamic profilesSvO2 < 25% Cellular death The information obtained from a PAC can be used in conjunction with arterial blood pressure moni- toring to obtain a number of derived hemodynamic parameters. The most commonly used parameters,This is equal to the amount of oxygen delivered sys- their formula, and their units of measurement aretemically (CO) (CaO2 ) minus the amount of oxygen given in Table 3.2.returned to the heart (CO) (CvO2 ).• If we ignore the small dissolved component of Efficacy and complications ofoxygen in arterial (0.003 × PaO2 ) and venous blood pulmonary artery catheterization(0.003 × PvO2 ) then (CO) (CaO2 ) − (CO) (CvO2 ) = Remarkably, demonstrating the efficacy of pul-[(Hgb × 13.8) (SaO2 ) (CO)] − [(Hgb × 13.8) (SvO2 ) monary artery catheterization is difficult. There are(CO)] = (Hgb × 13.8) (CO) × (SaO2 − SvO2 ). several studies indicating that PAC is not associatedThis is simplified to: with improved outcome. Unfortunately, each studySvO2 = SaO2 − [VO2 /(Hgb × 13.8)(CO)] carries certain limitations making a broad recom- mendation against use in specific patient popula-Thus, mixed venous oxygen saturation as measured tions impossible. Published guidelines for PAC usecontinuously by a mixed venous saturation PAC indicate that PAC risk and benefit must be weighedvaries directly with CO, Hgb, and SaO2 and varies in each patient in view of the specific patient char-inversely with VO2 . If SaO2 , Hgb, and VO2 remain acteristics, intended surgical procedure, and theconstant, then SvO2 will directly reflect changes in practice setting. PACs are indicated in patients atCO. Under these circumstances, continuous mea- increased risk of hemodynamic disturbance, clinicalsurement of SvO2 is analogous to a continuous CO evidence of cardiovascular disease, pulmonary dys-measurement. The response time of SvO2 to acute function, hypoxia, renal insufficiency, or other con-changes in CO under conditions of constant SaO2 , ditions associated with hemodynamic instability.Hgb, and VO2 has been demonstrated to be more Surgical procedures associated with increased riskrapid than CCO measurements. This is a reliable and include those with anticipated hemodynamic insta-sensitive indicator of function in the cardiac surgical bility, damage to the heart, vascular tree, kidneys,patient. liver or brain. The decision to use a PAC should be A normal SvO2 is 75%, which corresponds to based upon the individual hemodynamic risk char-a mixed venous PO2 of 40–45 mmHg. SvO2 is acteristics of the individual case rather than the type
    • Monitoring 59Table 3.2 Hemodynamic parameters,derivation, and measurement. Formula Units Normal value(From DiNardo JA. Monitoring. In:DiNardo JA (ed). Anesthesia for Cardiac SV = CO/HR × 1000 mL/beat 60–90Surgery, 2nd edn. Stamford, CT: SI = SV/BSA mL/b/m2 40–60Appleton & Lange, 1998:37–80, with LVSWI = [1.36 × (MAP − PCWP)/100] × SI [g-m/m2 ]/beat 45–60permission.) RVSWI = [1.36 × (PAP − CVP)/100] × SI [g-m/m2 ]/beat 5–10 SVR = (MAP − CVP/CO) × 80 dynes s/cm5 900–1500 PVR = (PAP − PCWP/CO) × 80 dynes s/cm5 50–150 BSA, body surface area; CO, cardiac output; CVP, central venous pressure; HR, heart rate; LVSWI, left ventricular stroke work index; MAP, mean arterial blood pressure; PAP, pulmonary artery; PCWP, pulmonary capillary wedge pres- sure; PVR, pulmonary venous return; RVSWI, right ventricular stroke work index; SI, stroke index; SV, stroke volume, SVR, systemic vascular resistance.of procedure. Finally, PAC use may be indicated after the sternum and pericardium are opened andfor postoperative management depending upon direct access to the heart obtained.the practice setting which should consider factors The incidence of pulmonary artery rupture, asuch as technical support and nursing training and potentially lethal complication, is less than 0.07%.skills. The risk of pulmonary artery rupture is increased PAC insertion carries all the risks of central line by anticoagulation, pulmonary hypertension, distalplacement. There can be arterial injury, pneumoth- catheter placement, and eccentric balloon inflation.orax, arrhythmias, pulmonary artery hemorrhage, Pulmonary infarction is rare (<0.07%) and can bethromboembolism, sepsis, and endocardial dam- avoided by preventing the catheter from remainingage. In addition, there may be misinterpretation of in a continuous wedge position. Placement of pul-information resulting in inappropriate patient care. monary catheters has resulted in direct tricuspid andFinally, unnecessary PAC placement is expensive. pulmonary valvular damage as well as tricuspid and The incidence of catheter-induced transient pre- pulmonary valvular endocarditis.mature ventricular contractions (PVCs) duringadvancement of PACs is approximately 65%;whereas, the incidence of persistent PVCs during Transesophageal echocardiographycatheter advancement is only approximately 3.0%. Transesophageal echocardiography (TEE) is anThese persistent PVCs are generally self-limited. intraoperative diagnostic and monitoring modal-Removal of the catheter nearly always stops the per- ity with wide use among cardiovascular anesthesi-sistent PVCs. If persistent, pharmacologic therapy ologists. The esophagus lies in direct proximity towith lidocaine (1.0–1.5 mg/kg) may suppress these the heart and great vessels allowing extraordinarilyPVCs. The prophylactic use of lidocaine does clear imaging windows. Furthermore, TEE allowsnot reduce the incidence of these benign, tran- intraoperative use without disrupting the surgicalsient catheter-induced PVCS. The incidence of procedure. It is a valuable tool in the ICU and incatheter-induced right bundle branch block is less the evaluation of trauma or other hemodynamicallythan 0.05%. Although frequently mentioned, the unstable or poorly responsive patients. Every car-risk of complete heart block in a patient with a diovascular anesthesiologist should be familiar withpre-existing left bundle branch block is rare. If con- the basic applications, advantages, and limitationscerned about arrhythmias, the PAC can be floated of TEE.
    • 60 Chapter 3(a) (b) (c)Fig. 3.10 Generation of longitudinal ultrasound echocardiography (TEE) imaging typically employswave front production. (a) Single small element. phased array ultrasound wave generation. (From(b) Multiple small elements (phased array). (c) Single Feigenbaum H. Echocardiography, 5th edn. Philadelphia:large element. The ultrasound waves travel in circular Lea & Febiger (Lippincott Williams & Wilkins), 1994:4,fashion away from a single element. Transesophageal with permission.)Basics of ultrasound signal. Because the wavelength, the frequency, andUltrasound is defined as sound waves above the the speed of the transmitted and reflected wavesaudible range in humans (above 20 000 cycles/s). In are known, the time it takes for the signal to beechocardiographic equipment, piezoelectric crystals transmitted and reflected back can be used to deter-in the distal transducer head generate and receive mine the depth of the reflecting object (remember,the ultrasound waves (Fig. 3.10a–c). A high fre- ultrasound travels at a constant 1540 m/s throughquency electrical current is applied to the crystal soft tissue). With proper amplification and pro-causing vibration and sound wave formation. As the cessing, these signals are converted to display thegenerated sound waves pass through tissue, they are real-time reflected wave activity (the image).either absorbed, reflected, refracted, or scattered. Doppler echocardiography is based on theThe degree of ultrasound wave reflection (return Doppler principle, which states that when a wave ofto the transducer) is enhanced when the struc- a given frequency strikes a moving target it will beture of interest is perpendicular to the ultrasound reflected with a frequency shift proportional to thewave. In order to identify two contiguous struc- velocity of the target parallel to the path of the emit-tures, there must be a difference in density and ted wave. If the target is moving toward the emittedimpedance between them altering beam absorption, wave, the frequency of the returning reflected wavereflection, refraction and scattering. will be higher. If the target is moving away from The frequency of the ultrasound waves produced the emitted wave, the frequency of the reflectedby the piezoelectric crystals is important. Recall returning wave will be lower. Red blood cell mass isthat wavelength equals velocity (V ) divided by fre- an excellent reflector in the heart and vascular sys-quency (F): 1 = V /F. Because ultrasound travels tem. Measuring the red blood cell flow velocity inat 1540 m/s through soft tissue, there is a constant the heart is the application of Doppler technologyrelationship between frequency and wavelength. As in echocardiography. The Doppler principle, whenthe frequency of the vibrations of the piezoelectric used to calculate the velocity of red blood cell mass,crystals increases, the length of the waves produced can be summarized in the following equation:decreases. A smaller wavelength signal allows betterimage resolution but is prone to greater signal atten- V = c fd /2fo cos θuation with increasing distance from the transducer.Likewise, greater wavelength will reduce resolu- where V , velocity of red cells; c, speed of sound intion, but will enhance visualization of structures at tissue (1540 m/s); fd , shifted or Doppler frequency;greater depth from the transducer. fo, transmitted frequency; θ, the angle of incidence When the piezoelectric crystal receives a reflected between the transmitted wave and the velocitysound wave, it vibrates and generates an electrical vector being interrogated.
    • Monitoring 61 Recall that cosine 90◦ and cosine 270◦ = 0, the transducer, and time is on the horizontal axis.the cosine 0◦ = 1 and cosine of 180◦ = −1; Blood-filled chambers with little or no reflectedtherefore, detection of velocity is most accurate wave activity appear black, whereas valve tissue andwhen the transmitted beam and the velocity vec- myocardium with high wave reflectivity are gray ortor are parallel (cosine 0◦ and 180◦ ). The detec- white.tion of velocity is impossible when the transmitted Ultrasound waves through a single beam pathbeam and the velocity vector are perpendicular are transmitted and received in 0.001 seconds. As(cosine 90◦ and 270◦ ). In practice, aligning the a result, the display is a real-time repetitive dis-Doppler beam and the velocity vector within 20◦ play of cardiac activity along this single beam lineproduces acceptable results (6% underestimation of at 1000 frames/see. This M-mode feature allowsvelocity). By convention, flow away from the trans- very high-resolution images of moving cardiacducer (cosine 180◦ ) has a negative value and flow structures.toward the transducer (cosine 0◦ ) has a positivevalue. Two-dimensional (2-D) echocardiography Two-dimensional imaging is the display of reflectedM-mode echocardiography images obtained for transmission of waves not alongM-mode echocardiography is the simplest echo- a single beam line but across a multiple beam linecardiographic imaging technique. Ultrasonic waves sector. This sector usually is 60–90◦ wide (Fig. 3.12).of known frequency and wavelength are trans- Sector scanning is accomplished most frequentlymitted in a single beam path and recorded over by use of a phased-array technology. In 2-D imag-time. This provides a linear (“ice pick”) view of ing, a set of piezoelectric crystals are activated inthe imaging sector through which the beam passes phased sequences to create a single beam through(Fig. 3.11). M-mode is used in conjunction with a defined sector. An analogy may help: For M-two-dimensional (2-D) imaging and the cursor line mode, imagine a man holding a flashlight in oneis used to direct the beam path through the desired position, looking at one object; in 2-D, imaginearea. The reflected waves are displayed in real time the same man moving the flashlight beam backas a time-motion study. The vertical axis displays and forth across the horizon and putting the com-the distance and intensity of the reflected from bined images together to create a picture of the objects in the night. The resulting sector sweep inFig. 3.11 M-mode image through the left ventriclewith a measurement of fractional shortening (FS).The left ventricular internal dimension is measured Fig. 3.12 Two-dimensional (2-D) mid-esophageal fourin both systole (LVIDs) and diastole (LVIDd). The chamber view of the heart. There is left ventricular septalFS = LVIDd – LVIDs/LVIDd. Normal is 0.25–0.45. hypertrophy.
    • 62 Chapter 32-D contains approximately 100 single scan lines.The computer assembles these scan lines and dis-plays the processed information as the echocardio-graphic image. Obviously, obtaining 100 scan linesis more time consuming than obtaining one scanline, as in M mode (hence, diminished spatial res-olution). Two-dimensional images are presented inreal time with the sector scan updated 30–60 times/sas opposed to the 1000 times/s of M mode. As withM mode, distance of the reflected wave from thetransducer is displayed from the top of the scandown and the displayed brightness of the reflectedwave is proportional to its amplitude. Fig. 3.13 Pulse wave Doppler at the distal tips of the mitral valve demonstrating an E and A wave.Pulsed-wave (PW) DopplerPW Doppler analyzes frequency shifts in a time-gated manner. The transducer intermittently trans- PRF must decrease as the distance from the trans-mits and then waits a specified time (t) to receive ducer to the sampling site increases. This must occurreflected ultrasonic signals. This pulse and receive because it takes longer for the emitted wave to reachpattern allows depth localization because the dis- the increased depth and for the reflected wave totance of the reflecting object from the transducer is return.defined by: Exceeding the Nyquist limit causes aliasing or wraparound. The signal literally wraps around thed = ct/2 velocity scale in the other direction. It then becomes difficult or impossible to determine red cell velocitywhere d, distance of the reflecting object from the or direction. The trade-off is unambiguous distancetransducer; c, 1540 m/s; t, time between emission information but ambiguous velocity and direc-and reception of signal. tion information. An analogy may help: recall old In practice, the PW Doppler cursor and sample Western movies in which the wagon wheels appearvolume are positioned on an updated 2-D image. to be rotating backwards as the wagon moves for-After the Doppler cursor and sample volume are ward. This is due to the frame capture rate of thepositioned, only reflected signals from that position film as the spokes on the wagon wheel turn. Appro-are analyzed (Fig. 3.13). The sample volume also priate film capture (altering the PRF) will capturecan be selected (usually from 2 to 6 mm). This allows the forward progression of the spokes allowing thethe interrogated area to be expanded or contracted. image to portray the reality. There are two strategiesData are displayed as spectra, which are a real-time to deal with aliasing during PW Doppler interroga-presentation of velocity over time. tion. The first is to increase the available scale. The There are limitations with PW Doppler. In order second is to shift the baseline. If wraparound stillto reliably detect the frequency shift (and hence the occurs, then continuous-wave (CW) Doppler mustvelocity) of a reflecting object, the reflected ultra- be used to determine peak velocity and direction.sound wave must be sampled at a frequency at PW Doppler is useful for measuring low velocitiesleast twice that of the object (Nyquist criterion). The at very specific locations such as mitral and tricuspidsampling frequency of PW Doppler is the pulse repe- inflow or in the pulmonary and hepatic veins.tition frequency (PRF). Thus, the maximal detectedvelocity for a given PRF is PFR/2. This is the Nyquist Continuous-wave Dopplerlimit. Thus, the maximum velocity that can be In CW Doppler, one transducer continuously emitsdetected is limited. An additional problem is that the signals and a separate transducer continuously
    • Monitoring 63receives reflected signals. These transducers are not called packets. The average velocity and directionthe same ones used to obtain 2-D images. This for the spectra in a sample volume are deter-arrangement allows reliable measurement of very mined and assigned a predetermined color. Gener-high velocities because there is no lag between ally, 8–16 samples per frame determine the averageemission and reception of signals. In other words, object velocity. The set of velocities that are aver-the PRF is extremely high. Because reflected sig- aged in a sample volume for a single frame is callednals returning from all points along the Doppler a packet or packet size. Object velocities are assignedbeam are recorded, the location of returning sig- specific colors. A popular presentation is BART (bluenals is ambiguous. In addition, lower velocity signals away, red toward). In this scheme, velocities towardare buried in the higher velocity signals. Therefore, the transducer are red and those away are blue. AsCW Doppler provides unambiguous peak velocity velocity increases, the intensity of color increasesand direction information but ambiguous distance as well. The CF Doppler image is presented in realinformation. time as a sector displayed over a real-time 2-D image In practice, the CW Doppler cursor is positioned (Fig. 3.15).on an updated 2-D image just like PW except that CF Doppler has some of the same limitations asthere is no sample volume. A spectrum of data is PW Doppler. There is no position ambiguity, butdisplayed demonstrating a real time presentation the peak velocity is limited and decreases with theof object velocity over time. CW Doppler is use- distance from the transducer. Aliasing occurs andful for measuring high velocities such as those seen is presented as a color mosaic. Because the colorwith aortic stenosis (Fig. 3.14) or with intracardiac image is presented over the real-time 2-D image,shunts. With the baseline shifted, velocities up to the direction of the aliased signal can be deter-600–800 cm/s are obtainable. mined easily. This is an obvious advantage when comparing CF to PW Doppler. Because the averag-Color-flow Doppler ing process loses valuable spectral data, CF DopplerColor-flow CF Doppler is a modification of PW is useful for detection of abnormal flows and theDoppler called multigated PW Doppler. Sampling direction and spatial extent of these flows. Reliableof object velocity occurs at several locations along determination of peak velocities requires PW or CWmany lines in a sector. The sample volumes are Doppler spectral analysis.Fig. 3.14 Continuous wave Doppler across the aortic Fig. 3.15 This color compare image shows thevalve in the deep transgastric long-axis view. The peak two-dimensional (2-D) image on the left and thevelocity is approximately 3 m/s yielding a peak gradient color-flow Doppler image on the right. There is aof 36 mmHg. central jet of mitral regurgitation that is severe.
    • 64 Chapter 3 50% accuracy 94% accuracy desired portion of the cardiac cycle (systole or dias- tole). Machine software integrates the area under the traced spectra to determine VTI in centimeters. 0% VTI can be used to determine the mean gradient, the 20% stroke volume, and orifice area using the continuity 60% equation. Mean velocity (cm/s) is determined by the machine software by dividing the VTI (cm) by the A duration of flow (seconds). Mean velocity cannot be used to calculate the mean gradient because B the mean gradient is actually the average of mul- tiple instantaneous gradients within the VTI trace.Fig. 3.16 The angle of interrogation has a great impact Machine software determines, totals, and averageson the accuracy of Doppler measurement. (From these individual pressure gradients to determine theObeid AI. Echocardiography in Clinical Practice. mean gradient.Philadelphia: Lippincott Williams & Wilkins, 1992, Stroke volume and cardiac output are determinedwith permission.) using the VTI as follows. The VTI can be used to determine stroke volume (cm3 ) by multiplying theDoppler spectra measurements VTI (cm) obtained at a given location by the areaAs discussed previously, Doppler spectra represent of the location (cm2 ). Cardiac output is then strokeobject velocity data over time. Velocities toward the volume multiplied by heart rate (HR). This determi-transducer are presented above the zero velocity nation can be done in the main pulmonary artery,line or baseline and are assigned positive values. in the right ventricular outflow tract (RVOT), at theVelocities away from the transducer are presented mitral valve annulus, in the left ventricular outflowbelow the zero line or baseline and are assigned tract (LVOT), or at the level of the aortic valve. Thenegative values. Accurate Doppler measurements feasibility depends on two factors:are dependent on the Doppler beam being paral- • obtaining a Doppler spectra from the desired arealel (or within 20◦ of parallel) to the interrogated with the Doppler beam within 20◦ of parallel toflow (Fig. 3.16). Several important Doppler spectra blood flow, andmeasurements are discussed below. • obtaining an accurate measure of the area fromPressure gradients which the Doppler sample was obtained.A velocity measurement (m/s) can be converted to Diameter (D) is easily measured with ultrasound cana pressure gradient (mmHg) using a modification be converted to area using the equation:of the Bernoulli equation 4V 2 where V = velocity Area = π(r)2 = π(D/2)2 = 0.785(D)2in meters per second. Peak instantaneous pressuregradients are determined by identifying the peak Alternatively, a direct measurement of area can bevelocity (Max V ) of the desired Doppler spectra obtained using planimetry.and using the equation 4V 2 . In practice, machine The continuity equation makes use of the VTIsoftware will calculate the peak pressure gradient to calculate valve areas. The conservation of massusing a peak velocity identified by the operator (see demands that a stroke volume remain equal imme-Fig. 3.14). Peak instantaneous gradients are always diately upstream and downstream of a stenoticgreater than the peak-to-peak gradients determined valve. Although the velocities may be different, theat catheterization. mass of ejected blood must be the same. Thus, (A1 ) × (VTII ) = (A2 ) × (VTI2 )Velocity–time integralVelocity–time integral (VTI) is determined by trac- where A1 , area of region 1; A2 , area of region 2;ing (planimetry) the entire Doppler spectra over the VTI1 , VTI from area 1; VTI2 , VTI from area 2.
    • Monitoring 65 The concept can be extended to state that the TEE probesflows across all valves in the heart must be equal, TEE probes consist of an echocardiographic trans-but this is true only in the absence of regurgitant ducer or combination of transducers fitted to thelesions or shunts. Thus, in theory, the continuity distal, flexible end of a gastroscope. The trans-equation could be used to determine aortic valve ducer consists of an array of piezoelectric crys-area using mitral valve or pulmonary artery flows tals. Most current adult TEE transducers have aor vice versa. 64-crystal element, whereas pediatric probes have a 48-crystal element. Adult TEE transducers gen-Deceleration time, acceleration time, erally operate at 5 MHz, whereas pediatric probespressure half-time operate at 7.5 MHz. Some adult TEE probes pos-Deceleration time (D1) is the time it takes (ms) sess frequency agility or the ability to functionfor the peak velocity of a Doppler spectra to fall at 3.7 and 5 MHz, whereas some pediatric probesto the zero baseline (Fig. 3.17). In instances in can function at 7.5 and 5.5 MHz. The higher fre-which the zero baseline is not reached, the natu- quency transducers can be used without significantral slope of the Doppler spectra is extended to the signal attenuation because of the proximity of thebaseline. transducer to the heart. TEE probes allow 2-D, The acceleration time (A1) is the time it takes (ms) M-mode, PW Doppler, CW Doppler, and CF Dopplerfor the Doppler spectra to reach peak velocity from imagining.the zero baseline. Hand controls allow flexion of the transducer The pressure half-time (PHT) is the time it takes both side to side and anterior and posterior. These(ms) for the peak velocity gradient of a Doppler controls allow 70◦ of lateral mobility in each direc-spectra to decrease by one-half. In other words, it tion (right and left) and 90◦ of anteflexion andis the time it takes for the peak velocity to decline retroflexion (Fig. 3.18). Presently, there are single- √ plane, biplane, and multiplane adult TEE probesto the peak velocity divided by 2. In addition, thePHT (ms) is always 0.29 × DT. The PHT is impor- available. Pediatric single plane and biplane probestant because it can be used to calculate mitral valve can be used for neonates and infants as small asarea (MVA) over a wide range of values using the 2–3 kg. With care, adult probes can be used forformula: MVA = 220/PHT. children as small as 15–20 kg.Fig. 3.17 Schematic of a CW Doppler Max V = 250 cm/s Mean V = 185 cm/sspectra across a stenotic mitral valve. The VTI = 200 cmvelocity–time integral (VTI) is the shaded Max PG = 25 mmHgarea inside the spectra. The values Mean PG = 13.7 mmHgcalculated from the VTI are shown in the DTupper left hand corner. The deceleration PHT 0time is obtained by extending the slope ofthe spectra to the zero baseline. Thepressure half time (PHT) can bedetermined by calculating V2 and − 100measuring the time between V1 and V2 .The values calculated from the DT areshown in the bottom right corner. DT,deceleration time; MVA, mitral valve area.(From DiNardo JA. Monitoring. In: − 200 V2 DT = 600 msDiNardo JA (ed). Anesthesia for Cardiac PHT = 174 msSurgery, 2nd edn. Stamford, CT: MVA = 1.26 cm2Appleton & Lange, 1998:37–80, with V1permission.) − 300
    • 66 Chapter 3 this. Activation of multiplane capability is obtained with a switch on the handle of the probe. Turn to the left Insertion of the TEE probe Turn tothe right Insertion of the TEE probe in the anesthetized adult 0° or pediatric patient with an endotracheal tube (ET) Withdraw in place is usually easy. The patient should have an 180° orogastric tube placed and the stomach should be Rotate emptied as well as possible. Even a small volume Rotate forward of air in the stomach can interfere with imaging Advance back 90° from the transgastric position. The orogastric tube should be removed before probe insertion. The Anterior Posterior Right Left presence of a tube in the esophagus will interfere with imaging. The endotracheal tube should be well secured. The TEE probe is left in the unlocked posi- tion and is lubricated with ultrasonic gel. A bite block is essential for TEE examinations in nonanes- thetized patients, but in anesthetized patients it is only required in patients with jagged teeth or at theAnteflex Retroflex Flex to Flex to the left operator’s discretion. the right The operator stands in the same position as ifFig. 3.18 Movement of the transesophageal to perform direct laryngoscopy. The patient’s headechocardiography (TEE) probe allows extensive and neck should be in a neutral position. Theresectioning and imaging of the heart in a two-dimensional(2-D) plane. (From Shanewise JS, Cheung AT, should be no positioning rolls under the patient’sAronson S, et al. Anesth Analg 1999;89:870–84, with shoulders. The thumb of the left hand is placedpermission.) on the patient’s tongue and the left hand is used to pull the jaw upward. The right hand is used to insert the probe into the pharynx to the left side Single-plane probes have a single transducer that of the ET with the probe transducer facing ante-transmits and receives ultrasonic signals in the rior. The remainder of the probe can be looped0◦ plane (transverse or horizontal plane). Biplane around the operator’s neck and shoulder, held byprobes have two transducers mounted one above an assistant, or rested on the head of the bed nearthe other. One transducer transmits and receives the patient. The probe is advanced with steadyultrasonic signals in the 0◦ plane and the other gentle pressure using a slight left to right rotatingtransmits and receives ultrasonic signals in the 90◦ motion. The unlocked probe will follow the natural(longitudinal or sagittal) plane. Changing planes curve of the pharynx. At the pharyngeal-esophagealrequires switching from one transducer to the other. junction (10 cm from the lips in neonates, 20 cmBecause the transducers are at different levels, sub- from the lips in adults), some mild resistance willtle (1.0–1.5 cm) advancement or withdrawal of the characteristically be met. This can be overcomeprobe is necessary after transducers are switched with gentle, steady pressure. If undue resistance isto ensure imaging at the same anatomic level. encountered, it is possible that the probe is in theMultiplane (omniplane) probes have the ability to piraform sinus or the vallecula. It should be with-transmit and receive ultrasonic signals in any plane drawn and advancement tried again. If there is anyfrom 0 to 180◦ . These probes use either mechan- doubt regarding probe position, the probe should beical rotation or phased-array activation (varying placed under direct vision using a laryngoscope. Insequential activation of the piezoelectric crystals in some rare instances, it is impossible to place the TEEthe transducer) of a single transducer to accomplish probe.
    • Monitoring 67TEE views in both the transverse (0◦ ) and longitudinal (90◦ )The American Society of Echocardiography and planes. Multiplane views are all of the viewsthe Society of Cardiovascular Anesthesiologists from 0 to 180◦ . In fact, most of the viewsrecommended views for a comprehensive TEE obtainable with a multiplane probe are obtain-examination are shown in Fig. 3.19. able with a biplane probe. The difference is Views available with a single-plane probe are that use of a biplane probe requires significantlythose obtained in the 0◦ plane. The basic views more probe manipulation than a multiplane probe.available with a biplane probe are those obtained The following is useful when using a biplane (a) (b) (c) (d) ME four chamber ME two chamber ME LAX TG mid SAX (e) (f) (g) (h) TG two chamber TG basal SAX ME mitral commissural ME AV SAX (i) (j) (k) (l) ME AV LAX TG LAX deep TG LAX ME bicaval (m) (n) (o) (p) ME RV inflow–outflow TG RV inflow ME asc aortic SAX ME asc aortic LAX (q) (r) (s) (t) desc aortic SAX desc aortic LAX UE aortic arch LAX UE aortic arch SAXFig. 3.19 The 20 recommended views for a comprehensive transesophageal echocardiography (TEE) examination bythe American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. (From Shanewise JS,Cheung AT, Aronson S, et al. Anesth Analg 1999;89:870–84, with permission.)
    • 68 Chapter 3probe: detection of a patent ductus arteriosus (PDA). Gen-• Angles 0–45◦ : flex the transverse probe to the tle anteflexion may be necessary to get good contactpatient’s left. with the esophagus at this level.• Angles 45–90◦ : flex the longitudinal probe to the Figure 3.21 shows views obtained with slightpatient’s right. advancement of the probe from the previous level.• Angles 90–135◦ : flex the longitudinal probe to the This level provides excellent views of the pulmonarypatient’s left. veins and allows Doppler interrogation. At 0◦ the• Angles 135–180◦ : flex the transverse probe to the left lower pulmonary vein (LLPV) is lateral to andpatient’s right. seen at a slightly deeper level (10–50 mm) thanIn this text, rotation to the right always means the left upper pulmonary vein (LUPV). The LLPVto the patient’s right (clockwise) and rotation usually is seen in conjunction with the descendingto the left always means to the patient’s left aorta. At 0◦ , the right lower pulmonary vein is pos-(counterclockwise). terior to and at a slightly deeper level (10–50 mm) Figure 3.20 shows views from the upper esopha- than the right upper pulmonary vein (RUPV). Thegus. At this level, there can be interference from air RUPV is seen in conjunction with the superior venain the right and left main stem bronchi. Good views cava (SVC). The LUPV and LLPV usually can beof the proximal ascending aorta can be obtained. seen in the same image at 100–110◦ while theThe view at 0◦ is useful for Doppler interrogation of RUPV and RLPV can usually be seen in the samethe main pulmonary artery. For some patients, the image at 50–60◦ . A persistent left superior venapulmonic valve and a small portion of the RVOT can cava would appear as a vascular structure (circularbe seen as well. in the sulcus between the left atrial appendage and CF Doppler interrogation just above this level but the LUPV).at a level just below the aortic arch is useful for Figure 3.22 shows views obtained at a slightly deeper level in the upper esophagus. Some of the most valuable views are obtained at this level. Both RPA 0° long- and short-axis views of the aortic valve are LPA SVC seen. In the short-axis views, the right coronary Ao cusp is anterior, the noncoronary cusp is next to the MPA right atrium, and the left coronary cusp is next to the left atrial appendage (LAA). In the long-axis views, 30–40° two cusps are seen: the right coronary cusp is ante- RPA LPA rior and the noncoronary cusp is in continuity with the anterior mitral valve leaflet. A good long-axis Ao MPA view of the main pulmonary artery and two leaflets of the pulmonic valve are seen. Views of the tricus- 110–120° 90–110° pid valve suitable for Doppler interrogation are seen LA as well. RA Ao Ao Figure 3.23 shows views obtained at the mid- RA RV esophageal level. Varying amounts of retroflexion are needed to prevent foreshortening of the leftFig. 3.20 Transesophageal echocardiography (TEE) ventricle (LV) and right ventricle (RV). The clas- sic four-chamber view is seen at 0◦ . These viewsviews at the base of the heart. Ao, aorta; LA, left atrium;LPA, left pulmonary artery; MPA, main pulmonaryartery; RA, right atrium; RPA, right pulmonary artery; allow good alignment for Doppler interrogation ofSVC, superior vena cava. (From DiNardo JA. Monitoring. the mitral valve. The anterior mitral valve leafletIn: DiNardo JA (ed). Anesthesia for Cardiac Surgery, is seen in continuity with the ventricular septum2nd edn. Stamford, CT: Appleton & Lange, 1998:37–80, at 0◦ and in continuity with the noncoronary cuspwith permission.) of the aortic valve at 130–150◦ . The LAA also
    • Monitoring 69Fig. 3.21 Transesophageal 0° 0–30° RLPVechocardiography (TEE) views of the SVC LA LA LLPVpulmonary veins at the base of the heart. Ao RUPV LVAo, aorta; LA, left atrium; LAA, left atrial RAappendage; LLPV, left lower pulmonaryvein; LPA, left pulmonary artery; LUPV, left 35–40° 0–30° LAupper pulmonary vein; MPA, main RLPV LAApulmonary artery; RA, right atrium; Ao LUPV PA PARLPV, right lower pulmonary vein; Ao RV RUPVRPA, right pulmonary artery; RUPV, right SVCupper pulmonary vein; SVC, superior 70–80° 100–110°vena cava. (From DiNardo JA. Monitoring. LA RUPVIn: DiNardo JA (ed). Anesthesia for Cardiac LA LPA RLPV LLPV LUPVSurgery, 2nd edn. Stamford, CT: Appleton &Lange, 1998:37–80, with permission.) 0–30° 130–150° LA MV Ao RV AV LV RVFig. 3.22 Transesophageal 40–60° 110°echocardiography (TEE) views obtained LA LA AV LAAfrom the upper esophagus. Ao, aorta; AoAV, aortic valve; LA, left atrium; LV, left RA RV RVventricle; MV, mitral valve; PA, pulmonaryartery; PV, pulmonic valve; RA, rightatrium; RV, right ventricle. (From 60–75° 90–100°DiNardo JA. Monitoring. In: DiNardo JA LA LA(ed). Anesthesia for Cardiac Surgery, 2nd edn. RA RAStamford, CT: Appleton & Lange, PA PV RV RV1998:37–80, with permission.)is seen. Slight withdrawal and anteflexion will give or atrial septal defect. Good visualization of the righta short-axis view of the aorta. The coronary arter- atrium/superior vena cava and right atrium/inferiories can be seen at this level. The left coronary vena cava (IVC) junctions also is obtained.artery often can be seen dividing into the left ante- Figure 3.25 shows views obtained at the gas-rior descending (LAD) and circumflex branches in troesophageal junction (36–38 cm from the teeth).the area near the LAA. The right coronary artery Gentle anteflexion usually is needed to obtain theseis anterior and usually requires very slight probe views. The coronary sinus (CS) is seen entering theadvancement to be seen. Slight off angles (20–30◦ ) right atrium. A large CS should alert one to theoften will allow better visualization. possibility of a persistent left superior vena cava Figure 3.24 shows views also obtained at the or anomalous pulmonary venous return. The rightmidesophageal level. The probe is rotated to atrium/inferior vena cava junction and eustachianthe patient’s right to obtain these views from valve are seen as is the right atrial appendage.the previous angles. These views provide excellent Figure 3.26 shows transgastric views of the leftvisualization of the atrial septum, which makes heart structures. Varying degrees of anteflexion arethem useful for detection of a patent foramen ovale required to obtain these views. These provide the
    • 70 Chapter 3 0° 0° RA LA RV CS RA LV LV RV 30–60° 50° LA Ao LV RA RV 130–150° LA 110° 90° 90° LA Ao LAA IVC RV RA RAA RA LV Ao LV RVFig. 3.23 Transesophageal echocardiography (TEE) Fig. 3.25 Transesophageal echocardiography (TEE)views obtained from the mid-esophagus. Ao, aorta; LA, views obtained at the gastroesophageal junction.left atrium; LAA, left atrial appendage; LV, left ventricle; Ao, aorta; CS, coronary sinus; IVC, inferior vena cava;PA, pulmonary artery; RA, right atrium; RV, right LA, left atrium; LV, left ventricle; RA, right atrium; RAA,ventricle. (From DiNardo JA. Monitoring. In: DiNardo JA right atrial appendage; RV, right ventricle; SVC, superior(ed). Anesthesia for Cardiac Surgery, 2nd edn. Stamford, CT: vena cava. (From DiNardo JA. Monitoring. In:Appleton & Lange, 1998:37–80, with permission.) DiNardo JA (ed). Anesthesia for Cardiac Surgery, 2nd edn. Stamford, CT: Appleton & Lange, 1998:37–80, with permission.) 0° LA 0–30° IAS RA LV RV 30° 40–60° IVC LA Ao LV RA 0° 120° 90° 115–130° 90° LA LA IVC SVC LA MV MV LV LV MV LA Ao RV Ao RA RA RV LAA Fig. 3.26 Transesophageal echocardiography (TEE)Fig. 3.24 Transesophageal echocardiography (TEE) views at the transgastric position. Ao, aorta; IVC, inferiorviews obtained from the mid esophagus. Ao, aorta; IAS, vena cava; LA, left atrium; LAA, left atrial appendage;interatrial septum; IVC, inferior vena cava; LA, left LV, left ventricle; MV, mitral valve; RA, right atrium;atrium; RA, right atrium; SVC, superior vena cava. (From RV, right ventricle; SVC, superior vena cava. (FromDiNardo JA. Monitoring. In: DiNardo JA (ed). Anesthesia DiNardo JA. Monitoring. In: DiNardo JA (ed). Anesthesiafor Cardiac Surgery, 2nd edn. Stamford, CT: Appleton & for Cardiac Surgery, 2nd edn. Stamford, CT: Appleton &Lange, 1998:37–80, with permission.) Lange, 1998:37–80, with permission.)
    • Monitoring 71 0° 0° LV LV RV RV AV RA Ao 30° 120–140° RA TV TV SVC Ao Ao PA 110–130° 90–100° 0° RV TV LV RA SVC RV RV PA Ao PAFig. 3.27 Transesophageal echocardiography (TEE) Fig. 3.28 Transesophageal echocardiography (TEE)views of the right ventricle from the transgastric position. views from the deep transgastric position. Ao, aorta;Ao, aorta; IVC, inferior vena cava; LV, left ventricle; IVC, inferior vena cava; LA, left atrium; LV, left ventricle;PA, pulmonary artery; RA, right atrium; RV, right PA, pulmonary artery; RA, right atrium; RV, rightventricle; SVC, superior vena cava; TV, tricuspid valve. ventricle; SVC, superior vena cava. (From DiNardo JA.(From DiNardo JA. Monitoring. In: DiNardo JA (ed). Monitoring. In: DiNardo JA (ed). Anesthesia for CardiacAnesthesia for Cardiac Surgery, 2nd edn. Stamford, CT: Surgery, 2nd edn. Stamford, CT: Appleton & Lange,Appleton & Lange, 1998:37–80, with permission.) 1998:37–80, with permission.)short-axis views of the LV and RV used in regional felt. Flexion of the probe to the left and rotation towall motion analysis. The anterior and posterior the patient’s right helps align the image so that thepapillary muscles are seen. With manipulation, the LVOT, aortic valve, and proximal ascending aortaview at or around 1200 can provide views of the are vertical. This location reliably provides views ofLVOT and aortic valve amenable to Doppler interro- the LVOT and aortic valve and of the RVOT and pul-gation. A short-axis view of the mitral valve suitable monary valve amenable to Doppler interrogation.for planimetry often is obtainable either by with- These views also provide images equivalent to thedrawing the probe slightly or ante-flexing it to a those obtainable with subcostal transthoracic imag-greater degree. ing which are valuable in children with congenital Figure 3.27 shows transgastric views of the right heart lesions.heart structures. Varying degrees of anteflexion are Figure 3.29 shows the probe set in the transverserequired to obtain these views. They are obtained by plane and positioned as depicted in Fig. 3.23. Next,rightward rotation of the probe from the previous the probe is rotated 90–100◦ to the patient’s left andposition. These views provide excellent visualiza- the descending thoracic aorta is visualized. Once it istion of the RVOT, which is very useful in the located, it can be viewed from the arch (see below)congenital heart disease patient. They also provide to just below the diaphragm. Inability to see thegood visualization of wall motion in the RV inferior descending aorta to the left should arouse suspicionwall and free wall. that there is a right aortic arch. This can be localized Figure 3.28 shows the deep transgastric views. by rotating the probe to the patient’s right from theThese views are obtained by passing the probe in original position.a neutral position all the way into the stomach. Figure 3.30 shows, with the descending tho-At this point, the probe is maximally flexed and racic aorta visualized, the probe being withdrawn,withdrawn until contact is made and resistance is keeping the image of the aorta in the center of
    • 72 Chapter 3 0–30° the screen. As the arch is approached in the upper esophagus, the probe is rotated slightly to the patient’s right. At this point, the inferior portion of the aortic arch is seen. At 90◦ , a short-axis view of the arch is obtained. With slight further withdrawal 30–60° and rotation to the patient’s right, the left CA can be seen. With rotation to the left, the left subclavian artery can be seen curving off inferiorly. TEE examination 80–110° There is no one way to conduct a comprehensive TEE examination. Each examiner has a particular protocol. What is important is that the examiner conducts the same examination on every patient in a consistent format. This is the only way toFig. 3.29 Transesophageal echocardiography (TEE) avoid missing what may turn out to be critical find-views of the descending thoracic aorta. (From ings. The examiner should concentrate on knownDiNardo JA. Monitoring. In: DiNardo JA (ed). Anesthesiafor Cardiac Surgery, 2nd edn. Stamford, CT: Appleton & diseases, but not to the exclusion of a completeLange, 1998:37–80, with permission.) examination. This should include complete 2-D imaging with a comprehensive Doppler examina- tion. When the TEE probe is not being used, it should be left in the unlocked position and the image should be frozen. Freezing the image will ter- minate ultrasound transmission. Some examiners 0–30° advocate advancing the probe to the stomach when it is not being used to prevent undue pressure on Ao arch the esophagus from the probe tip. LV systolic function, ejection fraction, 90° and preload LCA One of the most powerful applications of periop- erative TEE is the quick assessment of LV systolic function and regional wall motion abnormalities. LV systolic function can be determined by gross observation or it can be calculated using several 90° different parameters. Intraoperative changes in the shape and posi- LSCA tion of the LV pressure–volume relationship make the traditional pressure measurements used to assess LV preload unreliable, whereas hemody-Fig. 3.30 Transesophageal echocardiography (TEE) namic assessment of LV ejection fraction is not pos-views of the aortic arch. Ao, aorta; LCA, left carotid sible. Both qualitative and quantitative assessmentartery; LSCA, left subclavian artery. (From DiNardo JA. of LV end-diastolic area (EDA), end-systolic areaMonitoring. In: DiNardo JA (ed). Anesthesia for Cardiac (ESA), and fractional area change (FAC) are possibleSurgery, 2nd edn. Stamford, CT: Appleton & Lange, using TEE.1998:37–80, with permission.) Quantitative assessment of EDA using TEE pro- vides an accurate assessment of preload in adults
    • Monitoring 73and children. Quantitative assessment of LV EDA is by increases in contractility or decreases in after-frequently performed using the short-axis view of load. The clinician may also be fooled if using onlythe LV at the mid-papillary muscle level, although one view to render an opinion or form judgment.the most accurate assessments are derived from a Remember that the TEE slice represents only a lim-combination of several views. EDA is determined ited view of the heart. One area may appear grosslyby one of two ways: hypokinetic, while the remainder of the heart func-1 Computer planimetry – this method requires tions normally. With experience, clinicians canfreezing the LV end-diastolic TEE image and trac- estimate FAC or ejection fraction area (EFA) toing the endocardial border using a trackball. The within 10% of offline values in 75% of cases.computer then calculates EDA. The short-axis EDA The assessment of EDA as either low or normalfor several cardiac cycles are obtained and averaged. corresponds well with offline assessment of EDAThis method also can be used to determine ESA as well.using the frozen end-systolic echocardiographicimage. ESA and EDA can be used for the FAC, which Regional wall motion analysisis analogous to EF. TEE analysis of regional wall motion abnormalitiesFAC% = (EDA − ESA)/EDA × 100 (RWMA) can be used to detect myocardial ischemic and has predictive value concerning adverse clinical2 Automated border detection (ABD) – also called outcomes.acoustic quantification (AQ), this method makes Intraoperative assessment of RWMA involvesuse of backscattered signals from the blood–tissue imaging the heart in several planes to view all ofinterface to outline the endocardial borders in real the 17 wall segments (Table 3.3). The most pop-time. When the data are gated to the ECG, a beat- ular view for general surveillance, perhaps, is theto-beat display of EDA, ESA, and FAC is provided. transgastric short-axis view of the LV at the level ofBoth methods can be performed online, but obvi- the mid-papillary muscle level. This view is obtainedously, the first method is more time consuming and easily and contains regions of myocardium suppliedis not a continuous real-time assessment. ABD is a by all three coronary arteries. Most data regardingcontinuous real-time assessment but is cumbersome intraoperative use of TEE to monitor for ischemiaand, for 20–30% of patients, is unreliable because of uses this view with analysis that has been performedpoor image quality. FAC obtained by both methods offline. One should not forget to assess RV wallhas been shown to correlate well with EF obtained motion. The RV is imaged in many planes includ-by radionuclide angiography. ing the RV inflow–outflow view, the four-chamber Qualitative assessment of EDA, ESA, and FAC view, and the transgastric short axis view.requires no special techniques except a trained eye. Wall motion is graded both on excursion and wallIn practice, clinicians must often make quick judg- thickening. Excursion is defined as inward move-ments for treatment plans based on limited informa- ment along an imaginary radius to the center oftion. TEE allows the ability for clinicians to quicklylook at the heart and determine if it is hypokinetic,normal or empty and hyperdynamic is invaluable. It Table 3.3 Left ventricular 17 segment anatomic model.is quick and can be as continuous as desired. Severalcautions are in order, however. The development of Base Mid Apexend-systolic cavity obliteration commonly is usedas one of the visual signs of a reduced EDA. How- Anterior Anterior Anteriorever, it has been demonstrated that although many Anterio-lateral Anterio-lateral Lateral Infero-lateral Infero-lateral Inferiorof the episodes of end-systolic cavity obliteration Inferior Inferior Septalare associated with reduced EDA, end-systolic cav- Infero-septal Infero-septal Apical capity obliteration does not always indicate reduced Anterio-septal Anterio-septalEDA. End-systolic cavity obliteration may be caused
    • 74 Chapter 3the ventricular cavity. Both assessments are neces-sary because it is possible for an infarcted segment Mitralof myocardium to move passively by surround- Normal Abnormal “Pseudo- Restriction relaxation normalization”ing areas of normal myocardium; however, the D D Sinfarcted myocardium will not thicken. By concen- Pulmonary S S D Dtrating on both excursion and thickening, it is pos- vein AC AC ACsible to account for the translation (lateral motion Fig. 3.31 Schematic of the relationship between mitralof the entire heart) and rotation of the echocar- inflow and pulmonary venous flow patterns. (Fromdiographic image during contraction. Wall motion DiNardo JA. Monitoring. In: DiNardo JA (ed). Anesthesiais graded as follows: 1, normal; 2, hypokinetic; for Cardiac Surgery, 2nd edn. Stamford, CT: Appleton &3, akinetic; and 4, dyskinetic. Lange, 1998:37–80, with permission.) A new wall motion abnormality is defined whenthe wall motion score changes two or more grades. Table 3.4 Normal values for mitral inflow parametersThe recognition of a new RWMA is more diffi- as well as those encountered with impaired relaxationcult than it sounds, particularly in the presence and restriction. (From DiNardo JA. Monitoring. In:of a preexisting RWMA. Furthermore, recogni- DiNardo JA (ed). Anesthesia for Cardiac Surgery, 2nd edn.tion of mild degrees of RWMAs are more diffi- Stamford, CT: Appleton & Lange, 1998:37–80, with permission.)cult than recognition of normal wall motion orsevere RWMA. Abnormal Normal Restriction relaxationLV diastolic functionLV diastolic function is characterized using an inte- DT >240 ms 160–240 ms <160 msgrated approach, involving analysis of the mitral E ↓ 0.8–1.5 M/s ↔↑inflow pattern, the pulmonary venous blood flow A ↑ 0.75 M/s ↓pattern and tissue Doppler. Diastole commences E/A E<A E > A (>1.0) E Awith isovolumic relaxation. As ventricular relax- IVRT ↑ 55–90 ms <70 msation continues, LV pressure falls. LAP eventuallyexceeds LV pressure and the mitral valve opens,allowing early (E) rapid filling of the LV. Next, a leaflets. The spectra will contain E and A veloci-period of diastasis occurs as LA and LV pressure ties, which correspond to passive (E) and atrial (A)equilibrate. Finally, atrial contraction (A) occurs filling of the LV (Fig. 3.31). Normal values for theand augments LV filling as diastole terminates. All parameters derived from the spectra are shown inof these events are detectable with Doppler spectra. Table 3.4.Isovolumic relaxation time Pulmonary venous flowIsovolumic relaxation time (IVRT) is the time from Pulmonary venous flow is measured by placing theaortic valve closure to the commencement of flow PW sample volume 1.0–2.0 cm into the pulmonaryacross the mitral valve. IVRT can be detected by vein from its junction at the left atrium. Typically,placing the CW Doppler cursor across the mitral the LUPV or LLPV is used. A typical pulmonaryinflow and aortic outflow tracts. The time from the vein spectra is shown in Fig. 3.31. The systolic (S)aortic valve closure click to the commencement of velocity occurs as a result of LA filling during LV sys-mitral flow is the IVRT. tole, whereas the diastolic (D) velocity occurs as the result of LA filling during LV diastole. There is flowMitral inflow reversal seen with atrial systole (A). The D velocityMitral inflow can be assessed with the PW Doppler usually mirrors the E velocity of mitral inflow. Thesample volume placed at the tips of the mitral S velocity often is seen to have an early (S1) and
    • Monitoring 75late (S2) velocity with S1 < S2. S1 is the result of Pseudonormalization occurs due to an eleva-LA relaxation, whereas S2 is the result of movement tion in mean LAP. This normalizes the passiveof the mitral annulus toward the LV apex during LV mitral filling, mitral DT, and IVRT by increasing thecontraction. pressure gradient between the LA and LV and masking the impaired relaxation. This pattern isAbnormalities of LV diastolic function distinguished from the normal pattern by analysisThe range of LV diastolic abnormalities is summa- of the pulmonary venous blood flow and the tis-rized in Fig. 3.32. With impaired relaxation, the sue Doppler pattern. The systolic component (S)E velocity is reduced, the A velocity is increased, of pulmonary venous return is reduced becauseand the mitral DT and IVRT are increased. The pul- of the elevated LAP. In addition, the flow reversalmonary venous spectra mirror these changes with a with atrial contraction is more prominent because ofreduction in the velocity and an increase in the DT of enhanced atrial contraction in the expanded atriumthe diastolic component (D) of pulmonary venous and reduced ventricular compliance.return. These changes all are a consequence of pro- Rapid mitral DT and IVRT characterize the restric-longed ventricular filling during early diastole. This tive pattern. In this pathology, ventricular fillingpattern is very common in patients with coronary is restricted resulting in rapid equilibration of LAPartery disease and in patients with left ventricular and LV pressure. The velocity of early filling (E)hypertrophy. is high because of an elevated LAP. There is little Transmitral flow velocity Normal Delayed Pseudonormal Restrictive E ≥A relaxation E<A E A DT 140–220 E<A DT 140–220 DT < 140 IVRT 60–100 DT > 200 LAP increased IVRT < 60 IVRT >100 Pulmonary vein flow velocity Normal Delayed Pseudonormal Restrictive S≥D relaxation S <D S<D Ar < 25 cm/s S>D Ar > 25 cm/s Ar > 25 cm/s Ar < 25 cm/s LAP increased LAP increased Mitral annular velocity (lateral wall) Normal Mild dysfunction Moderate Severe EM/AM > 1 (delayed dysfunction dysfunction EM > 8 cm/s relaxation) (pseudonormal) (restrictive) EM ≤ 8 cm/s EM < 8cm/s EM 8 cm/sFig. 3.32 Transmitral Doppler imaging, pulmonary view Doppler imaging, and tissue Doppler imaging profilescorresponding to normal, delayed relaxation, pseudonormal, and restrictive filling patterns. (From Groban L,Dolinsky SY Chest 2005;128:3652–63, with permission.)
    • 76 Chapter 3contribution to LV filling from atrial contraction, Valvular heart diseaseand thus, atrial filling velocity (A) is low The pul- All four heart valves are well visualized with TEE.monary veins exhibit marked reduction of the sys- Although most cardiac surgical patients will presenttolic component (S) of filling due the high LAP. The to the operating room with a complete diagnosticvelocity of the diastolic component (D) is high as it work up of anatomic structure, a comprehensivecorresponds to the early filling (E) velocity across examination is required in all patients when a TEE isthe mitral valve. There is pronounced flow reversal performed. Heart valve structure and function mustwith atrial contraction because of enhanced atrial be observed and documented. It is not uncommoncontraction and minimal antegrade flow across the to find new pathology or new information that willmitral valve with atrial systole. This restrictive pat- help steer the planned operative procedure. Theretern is common in patients with dilated cardiomy- are many excellent textbooks detailing the variousopathies and in patients with ventricular volume techniques and anatomic findings seen with TEE.overload. In this next section, disease of the mitral, aortic and Unfortunately, the velocity patterns are load tricuspid valve are briefly reviewed.dependent, which can make application difficult.A normal pattern can be converted to an impaired Mitral valverelaxation pattern with hypovolemia or afterload The mitral valve separates the LV from the leftincreases. Similarly, an impaired relaxation pattern atrium, pulmonary circulation and entire right sidecan be pseudonormalized with volume expansion. of the heart. The valve is bicuspid with an anterior and posterior leaflet. The anterior leaflet is the largerTissue Doppler of the two leaflets, accounting for two-thirds of theTissue Doppler is the application of a PW Doppler in surface area of the valve. The posterior leaflet wrapsthe annular ring of the mitral valve and sampling around the anterior leaflet, accounting for only one-for the velocity of the heart tissue during relax- third of the valve’s surface area and two-thirds ofation. There are two measured components: the the annular circumference. The mitral annulus is aearly diastolic movement (E ) and the atrial con- fibrous ring surrounding the mitral valve. Duringtraction component of ventricular filling (A ). The ventricular systole, the contraction of the papillaryE and A correspond to the mitral inflow velocities muscles prevent mitral leaflet prolapse. Rupturedof E and A. An E less than 8 cm/s is abnormal and chordae are a common cause of mitral insufficiency.indicates diastolic dysfunction. The Carpentier classification divides the three scal- Figure 3.33 provides an easy step-by-step lops of the posterior leaflet into P1, P2, and P3;algorithm to determine the degree of diastolic and the anterior leaflet into the three segments A1,dysfunction. A2, and A3, which oppose the corresponding scal- lops of the posterior valve. The coaptation of A1/P1Right ventricular function at the annulus form the anterolateral commissure.Global RV function is assessed using the same tech- The coaptation of A3/P3 at the annulus form theniques as described for the LV to determine EDA, posteromedial commissure.ESA, and FAC. This usually is performed in a short-axis view, the four-chamber view, and the transgas-tric view. This allows all five wall segments of the Mitral stenosis (MS)RV to be analyzed: inferior wall, septal wall, lateral Normal mitral valve areas range from 4–6 cm2 ,wall, anterior wall, and anterior wall of the RVOT. and symptomatic stenosis is seen when the valveUse of the biplane and multiplane probes allows a approaches 1.5 cm2 . Rheumatic heart disease is along view of both the RV inflow and outflow tracts common cause of MS and it is characterized by com-and of the RV inferior wall and anterior wall of missural fusion with doming of the valve leaflets.the RVOT. This view is valuable for assessing RV Leaflet tip thickening and chordae tendineae thick-size and systolic function. ening, fusion, and calcification result in restricted
    • Monitoring 77 To do EF ≥ 45% Diagnosis Doppler mitral inflow E<A E>A E A DT > 140 ms DT > 140 ms DT < 140 ms TDI TDI TDI EM ≤ 8 cm/s EM > 8 cm/s EM ≤ 8 cm/s EM > 8 cm/s EM ≤ 8 cm/s E/EM≤ 8 8 ≤E/EM≤ 15 E/EM>15 E/EM ≤ 8 8 ≤E/EM ≤ 15 E/EM >15 E/EM <8 E/EM >15 Impaired Restrictive relaxation Impaired Normal diastolic Pseudonormal High myocardial normal filling relaxation suspicion of increased filling function disease pressures pericardial pressures disease Doppler Valsalva Valsalva pulmonary and and vein mitral inflow mitral inflow Ar wave Ar wave E >A E<A E >A E A < 25 cm/s ≥ 25 cm/s (unchanged) Impaired relaxation Impaired Normal Reversible, Fixed, normal filling relaxation diastolic Pseudonormal restrictive restrictive pressures increased filling function pressures And/or Doppler pulmonary vein Ar wave Ar wave < 25 cm/s ≥ 25 cm/s Normal PseudonormalFig. 3.33 An algorithm to determine the degree of diastolic dysfunction using transesophageal echocardiography(TEE). A, atrial peak velocity; Ar, retrograde velocity; E, early filling peak velocity; EM , early filling; TDI, tissueDoppler imaging. (From Groban L, Dolinski SY. Transechocardiographic evaluation of diastolic function. Chest2005;128:3652–63, with permission.)leaflet motion. MS increases transvalvular pres- Two-dimensional (2-D) anatomysure gradients leading to increased left atrial (LA) Two-dimensional imaging of the stenotic mitralpressures and LA distention. Increased LA pres- valve typically demonstrates thickening and fibro-sures can lead to pulmonary hypertension with sis of the mitral valve leaflets, restricted leafletright ventricular dysfunction and tricuspid regur- motion, and mitral annular calcification. The MVgitation. The left atrium will be enlarged and hypo- area can be estimated directly with planimetry inkinetic and may be filled with spontaneous contrast the transgastric basal short-axis view.(swirling, smoke-like contrast). Spontaneous con-trast is indicative of a low flow state and is predictive Dopplerof subsequent development of left atrial thrombus. CW Doppler is used to determine the mean velocityThe left atrium should be examined carefully for and mean grade using the VTI. Because the meanthrombus, particularly in the left atrial appendage. gradient can underestimate the severity of MS withIf there is atrial fibrillation or flutter, the atrium will low cardiac outputs and overestimate the severityappear akinetic. in the presence of mitral regurgitation, the valve
    • 78 Chapter 3Table 3.5 Severity estimation of mitral stenosis. MR is significantly different from the preoperative assessment.Grade Mild Moderate SevereMean gradient (mmHg) <6 6–10 >10 Two-dimensional (2-D) anatomyPHT (ms) 100 200 >300 Mitral leaflet motion is well visualized with TEEDHT (ms) <500 500–700 >700 and will direct the echocardiographer to the cor- rect diagnosis. There can be excessive leaflet motion,MVA (cm2 ) 1.6–2.0 1.0–1.5 <1.0 restricted leaflet motion, or normal leaflet motion with poor coaptation. Excessive leaflet motion can be classified as billowing, prolapse or flail. A billow-area should be determined. MVA can be calculated ing mitral leaflet demonstrates bowing of part ofusing the PHT method. The summary of mean gra- the mitral valve leaflet above the level of the mitraldients, PHT, deceleration time, and MVA in MS are annulus. The leaflet edge, however, still coapts well,seen in Table 3.5. Color flow Doppler can be used to and there is no MR. Prolapse occurs when thecalculate valve area using the proximal isovolemic leaflet edge extends above the level of the annulus.surface area (PISA) equation. The PHT will overesti- Flail leaflet occurs when the supporting structures,mate MVA (underestimate severity) in conditions in the papillary muscle or chordae tendinae rupture,which LV pressure rises quickly in diastole, such as allowing leaflet movement into the left atrium dur-aortic insufficiency (AI) or reduced LV compliance. ing systole. MR due to excessive leaflet motion willPHT is unreliable when there is merging of the E and result in a regurgitant jet directed away from theA waves or an alteration in the E wave decay pat- affected valve leaflet. Conversely, MR caused bytern due to tachycardia, atrioventricular (AV) block, restricted leaflet motion results in a regurgitant jetor atrial flutter. In these instances, the continuity directed towards the affected valve leaflet. Severeequation using the MVVTI and the LVOTVTI and MR is associated with a dilated left atrium andLVOTAREA can be used to calculate MVA assuming elevated pulmonary pressure.there is no MR. Details of the use of LVOTVTI andLVOTAREA are explained in the section on aorticstenosis. Doppler Comprehensive quantitative evaluation of MR should be performed intraoperatively. Color flowMitral regurgitation (CF) Doppler analysis of the regurgitant jet (seeMitral regurgitation is commonly seen in the Fig. 3.15) is performed in combination with PWcardiac surgical patient. There are a myriad of Doppler interrogation of the pulmonary veins. Thecauses including has including myxomatous degen- area of the regurgitant jet relative to the area of theeration, rheumatic disease, endocarditis, Marfan LA is a useful CF Doppler technique. This shouldsyndrome, infiltrative diseases (amyloid, sarcoid, be performed in as many planes as possible to gainmucopolysaccharidosis), collagen-vascular disor- a good understanding of the extent of the MR. Itders (SLE, rheumatoid arthritis), papillary muscle should be performed at the level of the mitral valverupture or dysfunction (ischemia), and cardio- using a full 180◦ sweep with a multiplane probe or atmyopathies. General anesthesia, changing hemo- multiple angles using a biplane probe. Table 3.6 listsdynamic conditions and volume status greatly affect several measures one can use to assess MR severity.measured mitral regurgitation. It is important for Regurgitant jets, which hug the atrial wallthe echocardiographer to quantify the degree of MR (Coanda effect), are considered constrained jets andunder physiologic conditions if possible. It may be will be 30–40% smaller than a free jet (such as anecessary to use phenylephrine to elevate afterload central jet) under the same conditions of regurgi-and attempt to duplicate preoperative conditions for tation. Jets that exhibit the Coanda effect usuallypatients in whom the intraoperative assessment of are associated with moderate to severe MR. When
    • Monitoring 79 Table 3.6 Grading of mitral regurgitation severity. Method Mild Moderate Severe Jet area (cm2 ) <3 3–6 >6 Vena contracta (cm) <0.3 0.3–0.55 >0.55 Regurgitant fraction (%) <30 30–50 >50 Mitral orifice area (cm2 ) <0.2 0.2–0.39 ≥0.4 Regurgitant volume (mL) <30 30–59 ≥60 Pulmonary vein flow Blunted S wave S wave < D wave Systolic reversalthe MR jet width at the mitral leaflet (vena con- three categories by valve area as follows: mildtracta) is greater than 0.6 cm, MR usually is severe. (1.5–1.0 cm2 ), moderate (1.0–0.8 cm2 ), or severeQuantitative methods to classify MR exist, such (<0.8 cm2 ). The classic triad of syncope, angina andas regurgitant fraction calculations and proximal congestive heart failure are associated with the lateisovelocity surface area (PISA), but they generally stages of aortic stenosis and are ominous signs atare cumbersome and time consuming. their onset. Technical factors such as CF Doppler gain andNyquist limit will affect the imaging of the regur- Two-dimensional (2-D) anatomygitant jet. Proper technique calls for turning the A number of views of the aortic valve are avail-color gain up all the way, then reduce it until able, but the short- and long-axis views of the aorticthe “sparkling” disappears, and starting with the valve are most useful. Leaflet mobility should bevelocity scale peak at 50–60 cm/s. Both right and observed. A stenotic valve will have limited openingleft pulmonary veins should be examined because and heavy calcification may be present in the leafletseccentric jets may reverse flow in the pulmonary and commissures. A bicuspid aortic valve can beveins on only one side of the atrium. identified easily in a short-axis view. Unfortunately, 2-D imaging is limited by the occasional inabilityThe aortic valve to evaluate the stenotic valve in the correct plane,The aortic valve consists of three semilunar valves thereby underestimating the true area of valvularnamed according to their relationship to the coro- stenosis. Therefore, it is imperative to examine thenary arteries: the right coronary cusp, the left valve until the narrowest area of stenosis is iden-coronary cusp, and the noncoronary cusp. At the tifiable and the stenotic area is reproducible withcenter of the free-edge of each cusp is a tiny, ele- multiple measurements. A secondary sign of aorticvated nodule commonly referred to as the nodule stenosis is left ventricular hypertrophy.of Arantius. The aortic valve complex is composedof the sinotubular junction, the sinuses of Valsalva, Dopplerthe valve cusps, the junction of the aortic valve Severity can also be quantified using Doppler mea-with the ventricular septum, and the anterior mitral surements of the peak and mean gradients and thevalve leaflet. All of these structures are imaged easily calculated aortic valve area. The mean gradient andwith TEE. peak instantaneous gradient are determined with the VTI obtained by using CW Doppler aligned par-Aortic stenosis allel (or within 20◦ ) to the LVOT, aortic valve, andAortic stenosis occurs when there is a fixed obstruc- proximal ascending aorta. If the peak aortic veloc-tion to left ventricular ejection of blood into the ity is greater than 4.5 m/s, the aortic stenosis isaorta. Normal aortic valve area is 2.5–3.5 cm2 . severe. Either the peak or the mean aortic veloc-The severity of aortic stenosis is divided into ity can be substituted into the simplified Bernoulli
    • 80 Chapter 3equation that is used to calculate the transvalvular examine the secondary effects on other heartpressure gradient. The simplified Bernoulli equation structures (i.e. left ventricle, mitral valve). In gen-for the peak gradient is calculated with the follow- eral, the etiology of aortic regurgitation is classi-ing equation: Peak Gradient (mmHg) = 4 (Aortic fied into two major groups: leaflet abnormalitiesPeak Velocity)2 . Based on the peak aortic gradient and aortic root abnormalities. Leaflet abnormalitiesvalue, the severity of aortic stenosis is graded as mild include congenital bicuspid valves, calcific valve dis-(<36 mmHg), moderate (>50 mmHg), or severe ease, rheumatic valve disease, myxomatous valve(>80 mmHg). The simplified Bernoulli equation for disease, endocarditis, and nonbacterial thromboticthe mean gradient is calculated with either of the endocarditis. Aortic root abnormalities are the mostfollowing equations: Mean Gradient (mmHg) = common cause of aortic regurgitation. Aortic root4 (Mean Velocity)2 or 2.4 (Vmax)2 . The value abnormalities include annular dilatation, hyper-of the mean aortic velocity grades the severity tensive aortic root dilation, cystic medial necrosis,of aortic stenosis as mild (<20 mmHg), moderate Marfan syndrome, and aortic dissection.(20–50 mmHg), or severe (>50 mmHg). Unfortu-nately, this technique is sometimes difficult because Two-dimensional (2-D) anatomythe deep transgastric long-axis view can be very Similar to the evaluation of aortic stenosis, 2-Delusive even for an experienced echocardiographer. examination of the aortic valve will yield informa-Remember that gradients will underestimate the tion on the etiology and extent of aortic regurgi-severity of the stenosis when output is low and may tation. In severe AR there may be fluttering of theoverestimate it when output is high. If there is suspi- anterior mitral valve leaflet in diastole when the ARcion that the gradient is misleading, the aortic valve jet is directed along it. There may be enlargementarea should be calculated or the dimensionless index of the ascending aorta and aortic root causing poor(DI) should be used: coaptation of the aortic leaflets and AR. RetrogradeDI = peak velocity LVOT/peak velocity AoV or aortic dissection can cause mechanical deformation of the aortic valve annulus and AR. The AR may LVOTVTI /AoVVTI . be associated with vegetations and leaflet perfora-A DI < 0.2 indicates severe aortic stenosis. Because tion. The presence of AR may alter the manner inthe peak velocity in the LVOT and across the aor- which cardioplegia is delivered as infusion into thetic valve will change proportionally, this index is aortic root may not be effective when moderate orindependent of cardiac output. severe AR is present. The LV may exhibit eccentric Doppler information can be used to calculate the hypertrophy.aortic valve area using the continuity equation:AoVAREA = (LVOTAREA ) × (LVOTVTI )/AoVVTI . DopplerThe LVOT area is determined using the diame- CF Doppler imaging of the aortic valve in the longter method. The long-axis view of the aortic valve axis is used to measure the minimum width of thecan be used to measure the diameter at the point regurgitant jet (usually at the origin of the jet at theat which the aortic valve cusps abut the LVOT. leaflets) relative to the width of the LVOT. AR isAoVVTI is obtained with CW Doppler across the aor- graded, based on this assessment, as follows:tic valve in systole with the views used to obtain VTI. • Trace: jet area/LVOT width <0.25LVOTVTI is obtained with PW Doppler in the LVOT • Mild: jet area/LVOT width 0.25–0.46just below the aortic valve leaflets in systole with • Moderate: jet area/LVOT width 0.47–0.64the views used to obtain VTI. • Severe: jet area/LVOT width >0.65 CF Doppler imaging of the aortic valve in the shortAortic regurgitation (AR) axis at or just below the level of aortic valve leafletsTEE can identify the presence of regurgitation, is used to measure the regurgitant jet area relativequantify its severity, determine the etiology, and to the circular LVOT area at this level (Fig. 3.34).
    • Monitoring 81Fig. 3.34 M-mode color Doppler image just below the Fig. 3.35 Pulse wave Doppler in the hepatic veinsaortic valve in the left ventricular outflow track of a patient with severe tricuspid regurgitation (TR).demonstrating aortic regurgitation. There is reversal of hepatic venous flow indicating severe TR.AR is graded, based on this assessment, as follows: not as well defined as those of the mitral valve. The• Trace: jet area/LVOT width <0.20 orifice is larger than that of the mitral valve and• Mild: jet area/LVOT width 0.20–0.40 is triangular in shape, as compared to the saddle-• Moderate: jet area/LVOT width 0.40–0.60 shape of the mitral valve. The pulmonic valve is• Severe: jet area/LVOT width >0.60 anterior and superior to the aortic valve. Similar CW Doppler is useful for quantifying AR by deter- to the aortic valve, it is trileaflet and semilunar,mining the PHT of the regurgitant spectra. A PHT consisting of anterior, left and right leaflets. The<300 ms is indicative of severe AR; whereas, a PHT plane of the valve is roughly perpendicular in ori->800 ms is associated with mild AR. This occurs entation to the aortic valve. The pulmonic valve isbecause, in severe AR, there is more rapid equili- isolated from the other three heart valves by thebration between aortic and LV pressure in diastole infundibulum.and thus a more rapid decay in the velocity of the Insignificant tricuspid insufficiency is very com-regurgitant spectra. In severe AR, the CW Doppler mon and is often seen in patients with transvenousspectra will be dense, whereas in mild AR, it will be pacemaker leads and/or PACs. Moderate to severefaint. CF Doppler will help guide positioning of the tricuspid insufficiency is most frequently the resultCW cursor. of dilation of the right ventricle and the tricuspid PW Doppler of the mitral inflow will reveal annulus. Any condition resulting in elevated righta restrictive pattern in severe or acute AR. PW ventricular pressure (>55 mmHg) or right ventricu-Doppler of the proximal descending thoracic aorta lar dilation can cause tricuspid insufficiency. Com-will reveal holodiastolic flow reversal in severe AR. mon causes observed in surgical patients includeIt is impossible to align the Doppler beam parallel to myocardial ischemia, cor pulmonale, pulmonarythe descending aorta, but it still may be possible to embolism, left heart failure, pulmonic valve steno-detect diastolic flow reversal. sis and pulmonary hypertension. Significant mitral insufficiency is a common cause of right ventric-Tricuspid and pulmonic valves ular dilation and secondary tricuspid insufficiency.The tricuspid valve consists of anterior, posterior Reversal of flow in the hepatic veins is associatedand septal cusps tethered by chordae tendinae and with more severe tricuspid regurgitation (Fig. 3.35).papillary muscles all suspended by a fibromuscular Tricuspid stenosis is much less common thanannulus. The commisures of the tricuspid valve are tricuspid insufficiency. Rheumatic heart disease
    • 82 Chapter 3is the most common cause of tricuspid stenosisand results in thickened, immobile valve leafletswith commissural fusion. Diastolic doming of theleaflets is usually present. In these cases, the mitralvalve is usually also involved. Other causes oftricuspid stenosis, although rare, include congeni-tal anomalies, endocarditis, carcinoid heart diseaseand endomyocardial fibrosis. Tricuspid valve areais estimated by the pressure half-time method orplanimetry. Pulmonary insufficiency is commonly observedin cardiac surgical patients, especially if a PAC isin place. Severe pulmonary insufficiency is always Fig. 3.36 Zoom view of a perivalvular leak after a mitralpathologic and usually the result of dilation of valve replacement. Transesophageal echocardiographythe main pulmonary artery as seen in patients (TEE) evaluation after all valve repair and replacementwith pulmonary hypertension from any etiology. procedures must include an examination for regurgitation, perivalvular leak, and gradients across theThe causes of pulmonary insufficiency include valve.fenfluramine–phentermine valvulopathy and car-cinoid syndrome. These lesions result in short and either directly by planimetry or indirectly with thethickened valves which fail to properly coapt. Infec- PHT method. Systolic anterior motion (SAM) lead-tious endocarditis can affects the tricuspid and ing to LVOT obstruction should be evaluated. Dis-pulmonic valves and presents as mobile masses cussion of all types of prosthetic valves is beyondattached to the valve leaflets. the scope of this presentation. However, several Pulmonic stenosis is categorized as valvular, sub- important points deserve discussion. All mechani-valvular, or peripheral (supravalvular). Ninety per- cal valves have some small quantity of regurgitantcent of the lesions are valvular in nature and the flow built into their design to prevent thrombus for-majority of pulmonary stenosis in the adult popu- mation. This regurgitant flow is characterized by lowlation is from untreated or recurrent congenital dis- velocity, small area, and location within the annulusease, such as tetralogy of Fallot. Pulmonary stenosis of the valve. If a leaflet is stuck in the open posi-is more commonly seen as individuals with complex tion, the amount of regurgitation present will becongenital heart disease increasingly survive into large. Tissue valves are not regurgitant unless theyadulthood. Pressure gradients using CW Doppler have degenerated. Perivalvular leaks generally haveacross the stenotic valve allow the quantification a high velocity and are located at the outer marginof pulmonary stenosis as follows: Peak gradients of the annulus or sewing ring (Fig. 3.36).<30 mmHg are associated with mild stenosis, peak Prosthetic valves should have transvalvular gradi-gradients between 30 and 65 mmHg indicate mod- ents that are physiologic for the particular position.erate stenosis, and gradients >65 mmHg are seen If the gradient across a prosthetic valve is high,with severe pulmonary stenosis. The continuity an aggressive examination to determine whetherequation can be used to determine the area of the the leaflets are opening is warranted. A leafletpulmonary valve to further assess disease severity. may be stuck closed because of impingement on surrounding tissue.TEE after valve repair or replacementAfter any valvular surgery, the repair or replace-ment must be assessed for both regurgitation and Removing air from the heartstenosis. The presence of trace to mild MR after MV All procedures in which the heart is openedrepair does not confer increased morbidity or mor- have potential to introduce air into the systemictality. The valve should be evaluated for stenosis circulation. In addition, closed procedures have
    • Monitoring 83the potential to introduce air because of the place- than RAP and the atrial septum is bowed towardment of vents to decompress the left side of the the RA. During the passive, expiratory phase ofheart. TEE can detect intracardiac air and guide air mechanical ventilation, there is a transient mid-evacuation before termination of CPB. Air is par- systolic reversal of inter-atrial septum position withticularly likely to be retained in the LV apex, left bowing of the atrial septum into the LA fromatrium, right coronary sinus, and the pulmonary the RA. This finding is highly predictive of aveins, particularly the right upper pulmonary vein. pulmonary capillary wedge pressure (PCWP) less than 15 mmHg. Conversely, absence of this find-Estimation of intracardiac pressures ing is highly predictive of a PCWP greater than 15 mmHg.Peak pressure gradients The observation of an atrial septum continuouslyThis method requires the presence of a regurgitant shifted to the left would predict elevated RAP.valve or a communication between cardiac cham-bers. It is based on the premise that the peak velocity Pulmonary and hepatic venous bloodof a regurgitant jet can be used to determine the flow velocitiespressure gradient between two cardiac chambers Reductions in the systolic portion of the hepaticduring either systole or diastole. Peak velocity is venous Doppler spectra relative to the diastolicconverted to the peak pressure gradient using 4V2 . portion are strongly correlated with increases in For example, if there is a TR jet with a peak RAP. In fact, progressive decreases in the ratiovelocity of 3.0 m/s, then a peak pressure gradient VTIsystolic/(VTIsystolic + VTIdiastolic) are associ-of 36 mmHg exists between the RV and RA during ated with increasing RAP. Similar observationssystole because TR is a systolic event. If we measure have been made regarding pulmonary venousthe central venous pressure (CVP) to be 10 mmHg Doppler spectra and PCWP and LAP. When LVEDP(or assume that it is 10 mmHg), then RV systolic >15 mmHg the flow duration of pulmonary versuspressure must be 36 + 10 = 46 mmHg. If we know atrial flow reversal is more than 30 ms longer than(or assume) that there is no RVOT obstruction, then the duration of the mitral A wave.PA systolic pressure is also 46 mmHg. Pulmonary regurgitation (PR) Doppler spectra Thoracic aortacan be used in the same way. The peak PR veloc- TEE is useful for examination of the ascending aorta,ity (velocity at the beginning of diastole) is used aortic arch, and descending thoracic aorta. The dis-to calculate the pressure difference between the tal ascending aorta and proximal aortic arch arepulmonary artery (PA) and the RV at the time of poorly visualized because of interposed interfer-pulmonary valve closure in diastole which gives a ence from air in the trachea and/or left main stemgood estimate of mean PA pressure (PAP). bronchus. Unfortunately, this area encompasses the Mean PAP = 4(peak PR velocity)2 + RV end- region in which the aortic cannula, aortic cross-diastolic pressure (EDP); RV EDP = CVP, which clamp, and proximal ends of the saphenous veinagain is measured or assumed. If the PR velocity grafts are typically placed. Because of the higherat the end of diastole is used, PA EDP can be calcu- incidence of stroke seen in patients with atheromalated. PA EDP = 4(end-diastolic PR velocity)2 + RV in the ascending and descending aorta undergoingEDP; RV EDP = CVP, which again is measured or undergo cardiac surgery with CPB, there is con-assumed. cern about manipulation of the aortic if it contains The same arguments can be used with MR and atheroma. Presently, only epiaortic scanning (place-AR velocities. ment of a transducer directly on the aorta) can reliably visualize this area.Movement of the atrial septum Atheromatous disease of the aorta is graded IThe shape of the atrial septum is determined by the to V as follows: I, normal; II, extensive intimalatrial pressure gradient. Normally, LAP is greater thickening; III, sessile atheroma protruding <5 mm
    • 84 Chapter 3 can be detected using CF Doppler in conjunction with 2-D images of those vessels. TEE also is used extensively to diagnosis aneurysm, dissection, and disruption of the ascending aorta, aortic arch, and descending aorta. Ultrasound artifacts are found in 50–60% of patients and may result in misdiagnosis. There are two classes of artifacts: linear and mirror image. Linear artifacts occur in the ascending aorta and are the result of reflections from either the left atrium (LA) or right pulmonary artery (RPA). They can be distinguished from intimal flaps because they do not display rapid oscillatory motion, do not dis- rupt the CF Doppler flow pattern, are parallel toFig. 3.37 Moderate plaque in the descending aorta. the posterior aortic wall, have movement (best seenSuch an image may prompt an epiaortic examination of with M mode) parallel to that of the posterior aorticthe ascending aorta. wall, and are located twice as far from the posterior wall of the LA or RPA as from the posterior wall of the aorta. Mirror image artifacts occur in the arch and descending aorta and give the appearance of a double barrelled aorta. They are caused by reflec- tions from the lung–aorta interface. They can be distinguished from intimal flaps or false lumens by the double-barrelled mirror image appearance and by the lack of interruption of the CF Doppler flow pattern. Congenital heart disease A comprehensive treatment of the use of TEE of the wide variety of congenital lesions the pediatric car- diac anesthesiologist is likely to encounter is beyond the scope of this chapter. However, by becom-Fig. 3.38 An epiaortic scan of the ascending aortareveals grade III atheromatous disease. ing familiar with some basic principles, the reader should be able to begin conducting a good quality examination in patients with congenital heart dis-into the aorta; IV, sessile atheroma protruding ease. With a biplane or multiplane probe, a compre->5 mm into the aorta; and V, mobile atheroma hensive 2-D and Doppler examination of the heart,(Figs 3.37 & 3.38). including the LVOT and RVOT can be obtained. Observation of atheroma in the aorta should The LVOT and RVOT are not well-oriented forprompt attention to placement of the aortic cannula. performance of a Doppler examination with stan-Although TEE can rarely be used to visualize the dard single-plane imaging. If only a single-planesite of aortic cannulation, it can be used to visualize probe is available, the deep transgastric position willthe jet out of the aortic cannula. This is accom- allow visualization of the LVOT and RVOT and theplished using CF Doppler in conjunction with a 2-D ventriculo-arterial connections. In some situations,image of the aortic arch. The direction of the jet deep transgastric imaging may provide superiorout of the aortic cannula is important because the delineation of anatomy than biplane examination.jet can dislodge plaque. Misdirection of the cannula From a practical point of view, deep transgastricjet down the left subclavian artery or left CA also imaging with a biplane probe is difficult and much
    • Monitoring 85less satisfactory because the extra transducer ele- c the RV has a triangular shape and a trabeculatedment makes the distance from the tip of the probe endocardial surface.to the flexion point longer. This makes good tis- d the RV has the moderator band, a band of tissuesue contact difficult, particularly in small infants. that stretches from lower intraventricular septumThe following issues should be addressed while per- to the anterior RV wall and is best seen in theforming an examination of a patient with congenital four-chamber view with retroflexion of the TEEheart disease. probe. 2 LV:Atrial identity and location a has the mitral valve (two leaflets) with no chordalIdentity of the atrial chamber by examining the attachment to the septum; there are two papillaryappendage is helpful. The right atrial appendage muscles that are located at the junction of the apical(RAA) is best seen in the transverse plane at and middle two-thirds of the chamber.the level demonstrated in Fig. 3.22. Flexion of the b has an ellipsoidal shape and a smooth endocardialprobe will allow better visualization. The RAA has surface.a broad junction to the RA which is short andblunt (Snoopy’s nose). The LAA is seen in multi- Great vessel orientation and identityple views. The LAA has a narrow junction to the Normally, the great vessels are oriented at 45◦ toLA, it is long, narrow, and crenulated (Snoopy’s each other when they leave the heart with the pul-ear). The IVC almost always returns to the RA; monary artery (PA) anterior to the aorta. Whenwhereas, the return patterns of the SVC and pul- they are viewed with echocardiography, one vesselmonary veins are much less reliable. The RA will will be observed in the short axis and the other willhave a eustachian valve and the LA septal surface have a sausage shape. This is seen in the transversehas the flap of the fossa ovalis. The atrial situs soli- plane image. When the great vessels are transposed,tus is the normal condition: the RA on the right side they are oriented parallel to each other when theyof the heart, LA on the left side of the heart. Atrial leave the heart. When they are viewed by TEE,situs inversus occurs when the RA is on the left side both vessels will be observed in the same axis. Theof the heart, and the LA on the right side of the rule of thumb when viewing transposed vessels inheart. the short axis is that the anterior vessel is invari- ably the aorta. When the vessels are aligned side toVentricular size and identity side, the determination is more difficult and usuallyA chamber is considered a ventricle if it receives requires finding the arch of the aorta or the branchmore than 50% of the ventricular inlet or fibrous pulmonary arteries to make the determination.ring of an AV valve. The AV valve need not be patent After the great vessels are identified, their rela-for the chamber to be considered a ventricle, as is tionship to the ventricles must be delineated. Thisthe case with tricuspid or mitral atresia. Likewise, requires creativity in finding the views that allowthe chamber does not need to be large to be consid- this to be seen. This is an instance in whichered a ventricle, as is the case with hypoplastic left deep transgastric views are useful, although biplaneheart syndrome. The right and left ventricles have imaging also works well.different morphologies:1 RV: Presence of intracardiac shunts anda has the tricuspid valve (three leaflets) with one obstructive lesionsthe leaflets having a chordal attachment to the CF Doppler is indispensable in identifying intra-septum; there are three papillary muscles that are cardiac shunts, including those not seen with 2-Dlocated apically. imaging. CW Doppler is useful in determiningb the septal leaflet of the tricuspid valve inserts velocities and gradients across restrictive commu-slightly lower on the intraventricular septum than nications or valves, whereas PW Doppler assessesthe anterior leaflet of the mitral valve. less restrictive orifices as well as hepatic and
    • 86 Chapter 3pulmonary venous blood flow. The RVOT must and diastole. CF Doppler will help position the CWbe examined carefully for both dynamic and fixed Doppler beam.obstructive lesions. Two-dimensional echocardio-graphy in combination with Doppler will clearly Saline-contrast echocardiographydelineate dynamic obstructive lesions. The use of Saline-contrast echocardiography is a techniqueCW Doppler to determine intracardiac pressures as that can be used to detect intracardiac shunting. Thedescribed previously is also valuable. basis of the technique is opacification of the right heart chambers using agitated saline injected rapidlyEvaluation of the surgical repair into a catheter. Microbubble formation occurs as theA comprehensive preoperative intraoperative study solution leaves the catheter orifice as dissolved gasis the foundation of repair assessment. This allows escapes from solution. The presence of micro bub-the operator to focus the examination on the bles in high concentrations opacifies the RA andrepaired lesions. Look for the common things: RV. The amount of opacification with a properly1 Patch leaks. After ventricular septal defect (VSD) performed procedure is impressive.and atrial septal defect (ASD) repairs, detection Saline-contrast studies are used most commonlyof residual VSD leaks can be more difficult than in conjunction with a provocative maneuver toit sounds, because the VSD patch produces areas detect right-to-left flow patency of the foramenof echo attenuation in the RV and RVOT that ovale. Agitated saline is produced by vigorouslymay mask leaks. The use of multiplane imaging transferring 10 mL of saline with a small amountimproves detection but does not completely resolve of air between two syringes connected by a stop-this problem. cock. Alternatively, 8 mL of saline and 2 mL of the2 Regurgitant valves. After valvuloplasty but also patient’s blood can be used. The agitated mixtureafter transvalvular approaches to the lesion (such can be injected peripherally or centrally.as approach to a VSD via the tricuspid valve). Detection of the right-to-left flow patency of the3 Stenotic anastomoses. Pulmonary vein anasto- patent foramen ovale (PFO) is dependent on tran-mosis to LA in total anomalous pulmonary venous siently increasing RAP above that of LAP. The easiestreturn (TAPVR). SVC to PA in bidirectional cavopul- way to accomplish this is by applying a Valsalvamonary connections (bidirectional Glenn) and total maneuver (actually sustained positive inspiratorycavopulmonary connections (Fontan). PW Doppler pressure) during positive-pressure ventilation. Thisinterrogation of these cavopulmonary connections transiently impedes venous return to the right heartwill reveal a phasic venous blood flow pattern with and subsequently to the left heart. Upon release ofrespiratory variation. the Valsalva, the rapid increase in venous return4 Residual outflow tract gradients. After tetralogy to the right heart will precede the increase in returnof Fallot repairs and repair of subaortic membranes. to the left heart and the result will be a transient ele-5 Residual gradients across ASD or VSD left open vation in RAP above that of LAP. The atrial septumin the course of a staged repair (tricuspid atresia, must bow into the LA for the test to be effective. Thedouble outlet RV, hypoplastic left heart syndrome). test is accomplished by injecting the saline contrast6 Ventricular function assessment. After all repairs. during the Valsalva maneuver. After opacificationParticular attention paid to patients with reim- of the RA occurs, the Valsalva is released and theplanted coronary arteries such as vessel switch for TEE is observed for appearance of saline contrast intransposition of the great vessels or Ross procedure the LA. Appearance of three or more microbubbles(transplantation of the pulmonic valve to the aortic in the LA within three cardiac cycles is indicative ofposition and creation of an RV-to-PA conduit) and a flow-patent PFO.to patients who may have had air in the coronaryarteries during the surgical process. Intracardiac and endovascular catheters7 Patency of aortopulmonary shunts. CW Doppler TEE can be used in a wide variety of ways towill detect a high velocity signal with flow in systole image intracardiac and endovascular catheters and
    • Monitoring 87devices. A few of the most common and important The complications reported in infants and chil-are summarized here: dren involve hemodynamic or respiratory compro-• Intra-aortic ballon pump (IABP). TEE views of the mise. Vigilance is required when using TEE probesdescending thoracic aorta can and should be used in a small child, even with the availability of pedi-to document that the tip of the IABP is below the atric probes. Airway obstruction may occur duelevel of the aortic arch and the takeoff of the left to compression of the small trachea or bronchussubclavian artery. In addition, inflation and defla- between surrounding tissue and the rigid probe.tion can be observed, which may aid in detection of Likewise, aortic or aortic arch vessel compressiona ruptured balloon. may occur.• Coronary sinus cannula for cardioplegia. The coro- Prophylactic antibiotic coverage for patientsnary sinus is easily seen in most patients and is undergoing TEE examinations is debated because itobliterated when the catheter is placed properly. carries a risk of inducing bacteremia like any other• Ventricular assist devices. The inflow and outflow endoscopic procedure. Most patients undergoingcannulas to the devices can be seen and should be cardiac surgery receive prophylactic antibiotics ofchecked to rule out obstruction. some kind, and many consider this sufficient• Venous cannulas for CPB. Position in the IVC and prophylaxis for endocarditis.SVC can be checked. In particular, the IVC cannulashould not impinge on any hepatic veins. Diffi- Coagulation monitoringculty in placing an IVC cannula can be caused by By necessity, cardiac anesthesiologists must bea prominent eustachian valve. familiar with coagulation monitoring. CPB requires• PACs. The position of a PAC can be documented anticoagulation, and reversal of the anticoagulatedby sequential views of the RA, RV, and PA. This may condition. In addition, the patient is often pronehave some use if catheter placement is difficult. to bleeding disorders wither through their pre- operative medication regimen, thrombocyptope-Contraindications and complications nia or the inflammatory response associated withThe relative and absolute contraindications to use surgery. Whether at the beginning of the case withof a TEE probe are summarized below: heparinization or at the end of the case when there• Relative: may be excessive bleeding from an unknown cause,a Recent gastroesophageal operation the anesthesiologist must be familiar with the toolsb Esophageal varicies to treat the patient.c Upper gastrointestinal bleedd Cervical disk disease Activated coagulation timee Severe cervical arthritis The Activated coagulation time (ACT) is most com-f Unexplained dysphagia or odynophagia monly used to monitor for heparin effect. Whole• Absolute: blood is added to a test tube containing eithera Esophageal obstruction (stricture, neoplasm) diatomaceous earth (celite) or kaolin. This activatorb Esophageal fistula, laceration, or perforation induces thrombosis which is measured in seconds.c Esophageal diverticulum Normal ACT values range between 80–120 seconds.d Cervical spine instability When aprotinin is used as an antifibrinolytic agent,A number of complications have been reported in kaolin ACT cartridges should be used; celite ACTassociation with use of TEE probes. Most complica- cartridges are associated with falsely elevated ACTtions in adults involve trauma to the upper gastro- values (thereby making the patient appear fullyintestinal (GI) tract ranging from minor lacerations anticoagulated when, in fact, this is not the case).to perforation of the esophagus. The incidence of The ACT test can be modified by adding hepari-swallowing complications after cardiac surgery in nase to one of the chambers. In this situation,adults having undergone intraoperative TEE also heparin is revered with the heparinase, and there-may be higher. fore any abnormality in ACT value is likely due to
    • 88 Chapter 3some factor other than inadequate heparin reversal for unknown reasons. In these patients, stan-with protamine. The ACT is subject to variability, dard tests of coagulation are indicated. These testsand there are elevated ACT values seen with both include a prothrombin time (PT), activated partialhemodilution and hypothermia. Nonetheless, the thromboplastin time (aPTT), fibrinogen and plateletACT is the standard monitor of coagulation in most count. The PT (normal 12–14 seconds) measuresoperating rooms. The ACT should be checked at the extrinsic and common coagulation pathways.least every half-hour while on CPB. It is prolonged with factor VII deficiency, warfarin treatment, vitamin K deficiency and in the pres-Heparin dose–response test ence of large heparin doses. The aPTT measuresThe Heparin dose–response test (HDR) allows the the intrinsic and final common pathway of coagula-clinician to fine tune the patient variability in tion. It is extremely sensitive to heparin, deficienciesresponse to a heparin dose by constructing an indi- of factors XII, XI, IX and VIII, and kallikrein. Nor-vidualized heparin dose–response curve. The HDR mal aPTT is 28–32 seconds. Fibrinogen and plateletuses a known quantity of heparin in an ACT deter- levels measure the quantitative amount of thesemination, and an algorithm using the baseline ACT substances in the blood. Normal fibrinogen levelsand the estimated blood volume to construct a dose– range from 180 to 220 mg/dL.response curve. The advantage of this system is the Cryoprecipitate (a source of concentratedgreater accuracy in dosing eliminating both under fibrinogen) is indicated when the fibrinogenand over dosing with heparin. Further, this test level is below 150 mg/dL. Thrombocytopenia isprovides information on individualized protamine encountered when the platelet count falls belowdoing at the termination of CPB. 100 000/µL. Platelet counts greater than 50 000/µL have no correlation with bleeding time or observedHeparin concentration testing postoperative bleeding in cardiac surgical patients.Heparin concentration can be measured using a Qualitative defects in platelet function are oftendevice that automatically titrates protamine in more important than the platelet count.known quantities in whole, heparinized blood.Protamine neutralizes heparin in the ratio of1 mg/100 units of heparin. With this information, Fibrin degradationa protamine–heparin titration can yield the circu- Evidence of normal or abnormal fibrinolysis islation concentration of heparin. When monitoring obtained by measuring the end products of fib-heparin concentration, higher doses of heparin are rin degradation. When plasmin cleaves fibrin,typically administered than when the ACT is mon- dimeric units are released into the blood, anditored likely because of the effects of hypothermia these “d-dimers” can be quantified. The presenceand hemodilution on the ACT. In side-by-side com- of d-dimers in the blood signifies fibrin cross-parisons between ACT and heparin concentration link degradation and may represent a condition ofmonitoring, the additional heparin administered abnormal fibrinolysis.seems to have little effect on blood loss or bloodadministration outcomes.High dose thrombin time Bleeding timeThe High dose thrombin time (HiTT) measures the The bleeding time is obtained by performing aconversion of fibrinogen to fibrin by thrombin. HiTT precisely measured incision in the patient’s fore-is not altered by hemodilution, hypothermia or arm above which a cuff is inflated to 40 mmHg.aprotinin. The wound is dabbed with an absorbent tissue and the time until clot formation is measured.Standard blood tests of coagulation The bleeding time has no predictive value in car-After CPB and reversal of heparin with protamine, diac surgical patients and has largely fallen out ofthere are some patients that continue to bleed favor.
    • Monitoring 89(a) (b) (c) (d) (e) takes between 15–30 minutes to complete and allows diagnosis of a variety of pathologic conditions including coagulation factor deficiency, platelet and fibrinogen function and fibrinolysis. In clinical prac- tice the TEG has been shown to function well as a predictor of abnormal bleeding. In some centers, TEG use is associated with a reduction in mediastinal exploration for bleeding and transfusion of blood products.Fig. 3.39 Thromboelastograph tracings. (a) Normal.(b) Coagulation factor deficiency. (c) Platelet dysfunctionor deficiency. (d) Fibrinolysis. (e) Hypercoagulability. Suggested reading(From Mallett SV, Cox DJ. Br J Anaesth 1992;69:307–13, American Society of Anesthesiologists. Standards forwith permission.) Basic Anesthetic Monitoring. Available online at: http:// www.asahq.org/publicationsAndServices/standards/ 02.pdf. Accessed June 28, 2006.Platelet aggregometry Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC;Activated platelets aggregate. Aggregometry mea- AHA; ASE. ACC/AHA/ASE 2003 Guideline Update forsures platelet responsiveness to various agonists and the Clinical Application of Echocardiography: sum-provides information on the quality of the circulat- mary article. A report of the American College ofing platelets to respond to various stimuli. Various Cardiology/American Heart Association Task Forceagonists include epinephrine, adenosine diphos- on Practice Guidelines (ACC/AHA/ASE Committee tophate and collagen. Impaired aggregation is seen in Update the 1997 Guidelines for the Clinical Appli- cation of Echocardiography). J Am Soc Echocardiogrpatients taking aspirin and after exposure to CPB. 2003;16:1091–110. Groban L, Dolinski SY. Transesophageal echocardio-Thromboelastography graphic evaluation of diastolic function. Chest 2005;128:Thromboelastography (TEG) is a method of mon- 3652–63.itoring blood viscosity that can be used to evalu- Practice Guidelines for Pulmonary Artery Catheteriza-ate various components of the coagulation system. tion. American Society of Anesthesiologists, Inc. Avail-The device usually contains two identical chan- able online at: http://www.asahq.org/publicationsAndnels so that two blood samples can be run at Services/pulm_artery.pdf. Accessed June 28, 2006. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCAonce. Each channel consists of a disposable cylin- Guidelines For Performing a Comprehensive Intraop-drical plastic cup mounted in a base. The cup is erative Multiplane Transesophageal Echocardiographyfilled with a blood and maintained at 37◦ C dur- Examination: recommendations of the American Soci-ing testing. A piston is attached to a torsion wire ety of Echocardiography Council for Intraoperativethat generates a signal as the blood clots. With Echocardiography and the Society of Cardiovascularthis presentation, the real-time development of Anesthesiologists Task Force for Certification in Peri-the TEG pattern can be assessed. A TEG sam- operative Transesophageal Echocardiography. Anesthple trace is shown in Fig. 3.39. The test usually Analg 1999;89:870–84.
    • CHAPTER 4Anesthesia for MyocardialRevascularizationCoronary artery bypass graft (CABG) surgery is the summation of factors that tend to collapseaccounts for approximately 500 000 operative microvessels, is important in determining coro-procedures per year in the United States. Although nary perfusion pressure (CPP). In clinical practice,there is great interest and development in alterna- myocardial back-pressure is equal to myocardialtives to CABG, this operative procedure remains an tissue pressure. The best estimate of myocardialappropriate, indicated therapy for a large number of tissue pressure is the ventricular pressure. In dias-patients. Patient outcome after percutaneous coro- tole, this will be the ventricular end-diastolic pres-nary intervention (i.e. stent placement, atherec- sure. The best clinical estimate of left ventriculartomy, angioplasty, other) remains a moving target end-diastolic pressure (LVEDP) is the pulmonaryas new therapies and technologies are developed capillary wedge pressure (PCWP); whereas the bestand employed. Similar to this, outcome after CABG estimate of right ventricular end-diastolic pres-is evolving. The indications for CABG are period- sure (RVEDP) is the central venous or right atrialically reviewed by the American College of Cardi- pressure (RAP).ology (ACC) and the American Heart Association In the absence of obstruction to flow within(AHA) (Tables 4.1 and 4.2). The reader is referred the coronary arterial system, left ventricular (LV)to the ACC’s website (www.acc.org) for the latest CPP is the driving force for blood going intoupdate. the myocardium – the resistance to blood flow. A firm understanding of the dynamics of coronary Physiologically, in the left ventricle, this relation-blood flow, the determinants of myocardial oxygen ship translates as CPP = aortic root diastolic bloodbalance, and the consequences and treatment of pressure – PCWP (Fig. 4.1). CPP will differ duringischemia are necessary to care for patients under- systole and diastole. In the left ventricle, ventriculargoing coronary revascularization. This chapter will pressure during systole is equal to or, as in the casereview the physiology of coronary blood flow, the of aortic stenosis, greater than aortic root pressure.elements of myocardial oxygenation, the care and For this reason, most coronary blood flow to the lefttreatment of patients with active ischemia, and the ventricle occurs during ventricular diastole. In theanesthetic care of patients presenting for CABG. right ventricle, in which right ventricular (RV) sys- tolic and diastolic pressures are both considerably less than aortic root pressure, coronary blood flowControl of coronary blood flow is distributed evenly between systole and diastole.Coronary perfusion pressureCoronary perfusion can only occur when aortic Autoregulationroot pressure exceeds subepicardial and subendo- Changes in coronary vascular resistance are nec-cardial pressure. Myocardial back-pressure, which essary for the myocardium to regulate coronary90
    • Anesthesia for Myocardial Revascularization 91Table 4.1 The list of indications for coronary artery bypass graft surgery for patients with stable angina and unstableangina/Non-ST-segment elevation myocardial infarction (MI). The indications are assigned class and the level ofevidence provided for the recommendation. (From Eagle KA, Guyton RA, Davidoff R et al. ACC/AHA 2004Guideline Update for Coronary Artery Bypass Graft Surgery: summary article. A report of the American College ofCardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999Guidelines for Coronary Artery Bypass Graft Surgery). Circulation 2004;110:1168–76.)Stable anginaClass I1 CABG is recommended for patients with stable angina who have significant left main coronary artery stenosis (Level ofevidence: A)2 CABG is recommended for patients with stable angina who have left main equivalent: significant (≥70%) stenosis ofthe proximal LAD and proximal left circumflex artery (Level of evidence: A)3 CABG is recommended for patients with stable angina who have 3-vessel disease. (Survival benefit is greater whenLVEF is <0.50) (Level of evidence: A)4 CABG is recommended in patients with stable angina who have 2-vessel disease with significant proximal LAD stenosisand either EF < 0.50 or demonstrable ischemia on noninvasive testing (Level of evidence: A)5 CABG is beneficial for patients with stable angina who have 1- or 2-vessel CAD without significant proximalLAD stenosis but with a large area of viable myocardium and high-risk criteria on noninvasive testing (Level ofevidence: B)6 CABG is beneficial for patients with stable angina who have developed disabling angina despite maximal noninvasivetherapy, when surgery can be performed with acceptable risk. If the angina is not typical, objective evidence of ischemiashould be obtained (Level of evidence: B)Class IIa1 CABG is reasonable in patients with stable angina who have proximal LAD stenosis with 1-vessel disease.(This recommendation becomes Class I if extensive ischemia is documented by noninvasive study and/or LVEF is <0.50)(Level of evidence: A)2 CABG may be useful for patients with stable angina who have 1- or 2-vessel CAD without significant proximal LADstenosis but who have a moderate area of viable myocardium and demonstrable ischemia on noninvasive testing(Level of evidence: B)Class III1 CABG is not recommended for patients with stable angina who have 1- or 2-vessel disease not involving significantproximal LAD stenosis, patients who have mild symptoms that are unlikely due to myocardial ischemia, or patients whohave not received an adequate trial therapy and the following:a Have only a small area of viable myocardium (Level of evidence: B) orb Have no demonstrable ischemia on noninvasive testing (Level of evidence: B)2 CABG is not recommended for patients with stable angina who have borderline coronary stenoses (50–60% diameterin locations other than the left main coronary artery) and no demonstrable ischemia on noninvasive testing (Level ofevidence: B)3 CABG is not recommended for patients with stable angina who have insignificant coronary stenosis (<50% diameterreduction) (Level of evidence: B)Unstable angina/non-ST-segment elevation MIClass I1 CABG should be performed for patients with unstable angina/non-ST-segment elevation MI with significant left maincoronary artery stenosis (Level of evidence: A)2 CABG should be performed for patients with unstable angina/non-ST-segment elevation MI who have left mainequivalent: significant (≥70%) stenosis of the proximal LAD and proximal left circumflex artery (Level of evidence: A) Continued p. 92
    • 92 Chapter 4 Table 4.1 (Continued). 3 CABG is recommended for unstable angina/non-ST-segment elevation MI in patients in whom revascularization is not optimal or possible and who have ongoing ischemia not responsive to maximal nonsurgical therapy (Level of evidence: B) Class IIa 1 CABG is probably indicated in patients with unstable angina/non-ST-segment elevation MI who have proximal LAD stenosis with 1- or 2-vessel disease (Level of evidence: A) Class IIb 1 CABG may be considered for patients with unstable angina/non-ST-segment elevation MI who have 1- or 2-vessel disease not involving the proximal LAD when percutaneous revascularization is not optimal or possible. (If there is a large area of viable myocardium and high-risk criteria are met on noninvasive testing, this recommendation becomes Class I) (Level of evidence: B) Table 4.2 The classification ofClass I: Conditions for which there is evidence and/or general agreement that a recommendations and level ofgiven procedure or treatment is useful and effective evidence used by the AmericanClass II: Conditions for which there is conflicting evidence and/or a divergence College of Cardiology and theof opinion about the usefulness/efficacy of a procedure or treatment American Heart Association Guidelines for Coronary Artery BypassIIa: Weight of evidence/opinion is in favor of usefulness/efficacy Graft Surgery. (From Eagle KA,IIb: Usefulness/efficacy is less well established by evidence/opinion Guyton RA, Davidoff R et al. ACC/AHAClass III: Conditions for which there is evidence and/or general agreement 2004 Guideline Update for Coronarythat the procedure/treatment is not useful/effective and in some cases may be Artery Bypass Graft Surgery: summaryharmful article. A report of the American College of Cardiology/American HeartLevel of Evidence Association Task Force on PracticeLevel of Evidence A: Data are derived from multiple randomized clinical trials Guidelines (Committee to Update theor meta-analyses 1999 Guidelines for Coronary ArteryLevel of Evidence B: Data are derived from a single randomized trial, or Bypass Graft Surgery). Circulationnonrandomized studies 2004;110:1168–76.)Level of Evidence C: Only consensus opinion of experts, case studies, orstandard of careblood flow in response to changes in myocardial (diastole for the left ventricle, systole and diastoleoxygen consumption. Coronary autoregulation is for the RV).the intrinsic ability of the myocardium to main- Autoregulation is dependent on changes in coro-tain coronary blood flow constant over a variety nary vascular resistance. The arterioles are theof perfusion pressures. As illustrated in Fig. 4.2, primary source of resistance in the coronary arte-coronary autoregulation maintains coronary blood rial system. Autoregulation is tied to myocardialflow constant between perfusion pressures of oxygen metabolism and coronary venous partial60 and 140 mmHg. Below and above these pres- pressure of oxygen PO2 , although the exact medi-sures, myocardial blood flow is pressure-dependent; ators at the vascular level are unknown. Duringthat is, myocardial blood flow varies linearly with exercise, reductions in coronary vascular resis-pressure and with the time available for perfusion tance result in increased coronary blood flow
    • Anesthesia for Myocardial Revascularization 93 MADBP 150 Autoregulatory Coronary blood flow (mL/min/100 g) vasodilator 100 Aortic blood reserve pressureBP (mmHg) Systole 100 50 LAP or PCWP 0 TimeFig. 4.1 Left ventricular coronary perfusion pressure 0(CPP) is the difference between aortic diastolic blood 0 40 80 120 160pressure and left ventricular end-diastolic pressure Coronary perfusion pressure (mmHg)(LVEDP). Clinically, LVEDP is estimated by left atrial Fig. 4.2 Coronary blood flow is seen to be constantpressure (LAP) or pulmonary capillary wedge pressure (autoregulated) over coronary perfusion pressures from(PCWP). Diastolic CPP is represented by cross-hatched 60–140 mmHg. When coronary perfusion pressurearea and can be seen to decrease as diastole progresses. reaches 60 mmHg, there will be maximal autoregulatoryAverage diastolic CPP can be obtained by taking vasodilation to maintain coronary blood flow. Furtherdifference between mean aortic diastolic blood pressure decreases in coronary perfusion pressure will result in(MADBP) and LAP or PCWP. Length of time available for decreases in coronary blood flow. At pressures higherperfusion of left ventricle is dependent on length of than 60 mmHg, maximal autoregulatory vasodilation willdiastole. Shortening diastole by increasing length of provide autoregulatory vasodilator reserve. This reservesystole per beat or by increasing heart rate will decrease provides the increased coronary blood flow necessarythe time available for left ventricular perfusion. (From to meet increases in myocardial oxygen consumptionDiNardo JA. Anesthesia for myocardial revascularization. such as those induced by exercise. (From DiNardo JA.In: DiNardo JA (ed). Anesthesia for Cardiac Surgery, Anesthesia for myocardial revascularization. In:2nd edn. Stamford, CT: Appleton & Lange, 1998:81–108, DiNardo JA (ed). Anesthesia for Cardiac Surgery, 2nd edn.with permission.) Stamford, CT: Appleton & Lange, 1998:81–108, with permission.)(up to six-times normal). Likewise, as CPP falls,coronary vascular resistance decreases to main- if perfusion pressure at the origin of the collateral istain coronary blood flow. At pressures <60 mmHg, reduced.there is a progressive loss of autoregulation. At There is evidence that coronary collateral flowsome point, the coronary arteries dilate maximally improves the outcome in patients with an acuteand coronary blood flow now decreases linearly myocardial infarction (MI). This same relationshipwith CPP. Autoregulation in the subendocardium is also true after CABG surgery. In a review ofis exhausted before that of the subpericardium. 561 patients with a low-risk profile, the presence of collaterals protects against cardiac death and MICollateral blood flow at 1 year after coronary revascularization (Fig. 4.3).The development of collateral blood flow inhumans is dependent on enlargement of pre-existing anastomoses between coronary arteries. Causes of increased myocardialThese anastomoses may be either serial (pre- oxygen demandstenosis to post-stenosis in the same artery) or Three factors are primarily responsible for deter-parallel (one artery to another). Collateral pathways mining myocardial oxygen consumption (MVO2 ):enlarge in response to pressure gradients. After the wall tension, contractility, and heart rate (HR).collateral pathways have enlarged, the direction andmagnitude of collateral blood flow remain pressure Wall tensiondependent. For this reason, collateral blood flow to Myocardial wall tension is determined by the rela-a post-stenotic segment can be significantly reduced tionship between ventricular radius (r), ventricular
    • 94 Chapter 4 (a) 6.0 preload, afterload, and hypertrophy. Increases in end-diastolic volume (EDV) (preload) will increase 5.0 Collaterals absent: 5.3% ventricular radius and will reduce wall thickness if Cardiac death or MI (%) 4.0 dilation is severe. These changes will increase wall tension. Increases in the impedance to ventricular 3.0 P = 0.01 ejection (afterload) will necessarily increase ventric- ular pressure and increase wall tension. Concentric 2.0 Collaterals present: 1.1% ventricular hypertrophy will increase wall thickness 1.0 and reduce wall tension. There are important differences between the 0.0 increase in MVO2 induced by increases in preload 0 60 120 180 240 300 360 420 Time since randomization (days) and by those induced by increases in afterload. No. at risk 0 19 21 22 22 22 22 23 Work done in the isovolumic phase of ventricular Collaterals − Collaterals + 0 1 1 2 2 2 2 2 contraction is very energy-consumptive. Increases (b) in the impedance to ventricular ejection increase 14.0 the pressure required to begin ventricular ejection, 12.0 and thus increase the work done in the isovolumic contraction phase. The ejection phase of ventric- All cardiac events (%) 10.0 Collaterals absent: 13.5% ular contraction, on the other hand, is a more 8.0 energy-efficient process. Increases in preload induce 6.0 Collaterals present: 5.7% ejection of a larger stroke volume (SV) and an increase in the work done in the ejection phase. 4.0 For these reasons, when comparing equal work, the 2.0 increase in MVO2 induced by an increase in preload P < 0.01 (volume work) is much less than that induced by 0.0 0 60 120 180 240 300 360 420 an increase in afterload (pressure work). Time since randomization (days)Fig. 4.3 Kaplan–Meier estimates of proportion of first Contractilityclinical events at 1 year after coronary revascularization Contractility is the state of myocardial performanceas stratified by collaterals. The P-values were calculated (inotropy) independent of preload and afterload.using the log–rank test. (a) Cardiac death or nonfatal Increasing the contractile state of the heart willmyocardial infarction (MI). (b) All-cause death, nonfatal increase MVO2 . However, an increase in contrac-stroke, nonfatal MI, or repeat coronary revascularization. tility may actually result in a reduced or unchanged(From Nathoe HM, Koerselman J, Buskens E et al.Determinants and prognostic significance of collaterals MVO2 under certain conditions. For example, ifin patients undergoing coronary revascularization. ventricular dilation (increased ventricular radius)Am J Cardiol 2006;98:31–5, with permission.) exists to maintain cardiac output (CO), wall ten- sion and MVO2 will be high. Improving contractilitypressure (P), and ventricular wall thickness (h) through use of an inotropic agent can reduce ven-according to Laplace’s law: T = Pr/h. Ventricular tricular radius while maintaining CO. The reductionwall tension constantly changes during the cardiac in MVO2 that accompanies the reduction in ventric-cycle. For example, during isovolumic contrac- ular radius may more than offset the increase thattion, ventricular pressure and wall thickness accompanies an increase in contractility.will be increasing while ventricular radius remainsunchanged. During ventricular ejection, ventricular Heart ratepressure will remain relatively constant while radius Heart rate directly affects myocardial oxygen bal-decreases and wall thickness increases. Inherent in ance. Tachycardia increases myocardial oxygenthe analysis of wall tension are the concepts of demand and reduces supply by diminishing the time
    • Anesthesia for Myocardial Revascularization 95in diastole. Perhaps more importantly, one must (a) 1000consider the imbalance on a beat-to-beat basis.Myocardial ischemia does not occur with tachycar- 800 R–Rdia simply because there are more beats per minute;rather, ischemia occurs with tachycardia because Total 600supply per beat is inadequate to meet demand diastolic Time (ms) periodper beat. Increases in HR increase MVO2 per beat (R–R)–(QS2) 400by increasing contractility via the Bowditch effect. QS2Normally, increasing HR decreases EDV. This reduc- 200tion in preload reduces wall tension and MVO2per beat. Thus, with tachycardia, the increase in 0MVO2 per beat caused by enhanced contractility 30 40 50 60 70 80 90 100 110 120 130 140 150is offset by the reduction in MVO2 per beat that Heart rateaccompanies reduced wall tension. On the other (b) 80hand, oxygen delivery is sometimes compromisedby tachycardia-induced reductions in the length of 70diastole per beat (discussed later). 60 % DiastoleCauses of reduced myocardialoxygen delivery 50Adequate myocardial oxygen supply is dependent 40on delivery of the appropriate volume of oxy-genated coronary blood flow. The following sections 30describe factors that may compromise myocardial 30 50 70 90 110 130 150oxygen delivery. Heart rate Fig. 4.4 (a) Increases in heart rate cause decreases inReduction in CPP length of each cardiac cycle (R–R interval). DecreasesLV CPP falls with either a reduction in diastolic in length of systole (OS2 ) with increases in heart rate areblood pressure (DBP) or an increase in LV end- far less dramatic than decreases in length of diastolediastolic pressure. A commonly overlooked cause (R–R–OS2 ). (b) Percent of each cardiac cycleof reduced CPP is bradycardia. Bradycardia encour- (R–R interval) spent in diastole at various heart rates.ages diastolic runoff from the proximal aorta and Small changes in heart rate are seen to cause large decreases in percent of time spent in diastole. (Frommay result in a wide pulse pressure and reduced Boudoulas H. Changes in diastolic time with variousDBP. Furthermore, maintenance of CO with brady- pharmacologic agents. Circulation 1979;60:165, withcardia requires an increased SV. The increased SV permission.)occurs primarily by an increase in left ventricularend-diastolic volume (LVEDV) and pressure. This remains constant. Because MVO2 per beat is min-further reduces CPP. imally affected by tachycardia, the primary dis- advantage of tachycardia is a reduction in diastolicReduction in time available for perfusion time per beat.coronary perfusionThe left ventricle receives most its perfusion dur- Obstruction to flowing diastole; therefore, reductions in diastolic time Any obstruction to flow in a coronary arteryare potentially detrimental. Figure 4.4 illustrates results in a pressure drop across the obstruction.that as HR increases the length of time per beat The high velocity of blood flow in the area ofspent in diastole falls while the length of systole a stenosis (either stable, i.e. plaque disease; or
    • 96 Chapter 4dynamic, i.e. coronary spasm) necessarily results forces. Plaque rupture may result in exposure ofin the conversion of pressure energy to kinetic superficial vascular wall elements or of deep fibrillarenergy. On the distal side of the obstruction, tur- collagen.bulent eddies form and dissipate. The transfer of • Thrombosis. Exposure of vascular wall elements iskinetic energy to this turbulent energy and the sub- a stimulus for thrombus formation. Platelet depo-sequent dissipation of the turbulence reduce the sition occurs at the site of disruption. Superficialquantity of kinetic energy available for conver- plaque disruption is a much milder thrombogenicsion to pressure energy. This results in a pressure stimulus than deep plaque disruption. Thrombusdrop across the obstruction. The pressure drop will formation at the site of a superficial injury is likelyincrease in direct proportion to any increase in to be labile and transient, whereas thrombus forma-flow across the obstruction as a greater propor- tion associated with deep plaque disruption is likelytion of kinetic energy dissipates as turbulence. For to be stable and permanent. This is often the causethis reason, requirements for increased coronary of acute coronary syndromes.blood flow, such as those that accompany exercise, • Vasoconstriction. Transient vasoconstrictionwill increase the hemodynamic significance of any accompanies plaque disruption and thrombusobstructive lesion. formation. Injury to the endothelium produces Arteriolar dilatation distal to the obstruction will thrombin-mediated vasoconstriction; whereas,help compensate for this pressure loss until the subsequent platelet deposition mediates vasocon-stenosis becomes critical. A stenosis is “critical” striction via release of thromboxane-A2 and sero-when the vasodilator reserve distal to the stenotic tonin. In addition, endothelial injury may impairlesion is exhausted. This occurs with stenosis >90%. the release of nitric oxide (NO).In the absence of autoregulation, coronary blood Using these concepts, one can understand theflow distal to a stenotic lesion will fall linearly with spectrum of coronary artery disease (CAD) fromdecreases in perfusion pressure. This places the dis- chronic stable angina to acute MI. Chronic stabletal subendocardium at risk for ischemia. It follows stenotic lesions that cause angina develop as thethat in the presence of an obstructive coronary result of progression of atherosclerotic lesions.lesion, coronary perfusion is critically dependent on Progression of early lesions is more rapid in patientsaortic DBP. The factors described in the following with coronary risk factors. Progression is the resultsections deserve attention. of mural thrombus formation and fibrotic orga- nization, which follows minor plaque disruption.Atherosclerotic disease Initially, platelet thrombi form on the disruption.Atherosclerosis is a complex, heterogeneous dis- This is followed by migration of smooth muscleease often starting in the very young and evolving cells from the media into the intima. During theover several decades. There are both acute and final phase, intimal thickening and progression ofchronic manifestations of the disease, the most the lesion occur. Repetition of this process leadssignificant of which, involves the development of to gradual progression of the lesion. Ultimately, itcoronary occlusive disease, unstable coronary syn- may lead to a chronic vessel occlusion. The slowdromes, MI, and death. Other systemic manifes- progression of the lesion allows time and providestations include progressive neurologic dysfunction stimulus for distal arteriolar collateral formation.(dementia), renal impairment, claudication, mesen- This explains why thrombotic occlusion is frequentteric ischemia, hypertension, and stroke. The dis- in patients with high-grade stenoses but does notease is progressive in nature with a defined pattern lead to infarction.of morphologic evolution (Fig. 4.5). In unstable angina, a small plaque disruption The fate of atheromatous lesions is dependent on may change plaque morphology such that coro-three additional factors: nary blood flow is acutely reduced and angina• Plaque disruption. Atheromatous lesions are lipid intensifies. Alternatively, plaque disruption may berich, soft, and prone to disruption from mechanical associated with labile thrombus, temporary vessel
    • Anesthesia for Myocardial Revascularization 97 Foam cell Smooth muscle mitogens 8 1 LDL Cell Vascular 6 apoptosis Monocytes Scavenger receptor endothelium 4 Macrophage 7 Cell adhesion Smooth muscle molecule proliferation Internal elastic lamina 5 IL-1 MCP-1 2 Oxidized LDL Smooth muscle 3 migrationFig. 4.5 Schematic of the evolution of the anion (O− ), and matrix metalloproteinases. 6. Smooth 2atherosclerotic plaque. 1. Accumulation of lipoprotein muscle cells in the intima divide other smooth muscleparticles in the intima. The modification of these cells that migrate into the intima from the media.lipoproteins is depicted by the darker color. Modifications 7. Smooth muscle cells can then divide and elaborateinclude oxidation and glycation. 2. Oxidative stress, extracellular matrix, promoting extracellular matrixincluding products found in modified lipoproteins, accumulation in the growing atherosclerotic plaque.can induce local cytokine elaboration. 3. The cytokines In this manner, the fatty streak can evolve into athus induced increase expression of adhesion molecules fibrofatty lesion. 8. In later stages, calcification can occurfor leukocytes that cause their attachment and (not depicted) and fibrosis continues, sometimeschemoattractant molecules that direct their migration accompanied by smooth muscle cell death (includinginto the intima. 4. Blood monocytes, upon entering the programmed cell death, or apoptosis) yielding aartery wall in response to chemoattractant cytokines relatively acellular fibrous capsule surrounding asuch as monocyte chemoattractant protein 1 (MCP-1), lipid-rich core that may also contain dying or dead cellsencounter stimuli such as macrophage colony stimulating and their detritus. IL-1, interleukin-1; LDL, low-densityfactor (M-CSF) that can augment their expression of lipoprotein. (From Libby P. The vascular biology ofscavenger receptors. 5. Scavenger receptors mediate the atherosclerosis. In: Zipes DP, Libby P, Bonow RO,uptake of modified lipoprotein particles and promote the Braunwald E (eds). Braunwald’s Heart Disease: A Textbookdevelopment of foam cells. Macrophage foam cells are of Cardiovascular Medicine, 7th edn. Philadelphia:a source of mediators such as further cytokines and Elsevier–Saunders, 2005:921–37, with permission.)effector molecules such as hypochlorous acid, superoxideocclusion, and angina at rest. Coronary blood flow In a Q-wave MI, plaque disruption is associ-is further compromised by release of vasoconstrictor ated with formation of a fixed, persistent occlusionsubstances and impaired endothelial relaxation. (usually by a thrombus, although this may occur In non-Q-wave MI, the process is similar to that in with an embolized vegetation or other material).unstable angina, except that the duration of vessel This leads to cessation of blood flow and myo-occlusion by labile thrombus is longer and there is cardial necrosis. The coronary lesion involvedresultant muscle injury and necrosis. Spontaneous usually is mild to moderate in severity with lim-thrombolysis or resolution of arterial spasm ulti- ited distal collateralization. Thus, it is the intensitymately limits occlusion and prevents Q-wave MI of plaque disruption and subsequent thrombus for-(full thickness, or transmural MI). This process is mation rather than the severity of the lesion that isresponsible for 75% of non-Q-wave MIs. The other the determining factor.25% occur when there is complete occlusion of the Further discussion is necessary to explain theinfarct-related vessel with distal collateralization. spectrum of anginal symptoms that can accompany
    • 98 Chapter 4a chronic, stable, stenotic coronary lesion. The main in Fig. 4.6, a normal change in coronary vasomotorcoronary artery epicardial branches have lumens tone resulting in a 10% circumferential shorteningthat are 2–4 mm in diameter. In the absence of of the outer arterial wall can convert an insignificantcollaterals, exertional angina occurs when lumen 49% eccentric stenosis to a 76% stenosis, whicharea is reduced to 1.0 mm2 (50–60% reduction in will result in rest ischemia. Likewise, Fig. 4.6 illus-lumen diameter or 75% reduction in cross-sectional trates that a normal increase in arterial tone canarea) and angina at rest occurs when lumen area convert an eccentric stenosis, which causes ischemiais reduced to 0.65 mm2 (75% reduction in lumen on exertion (60% stenosis), to one that also causesdiameter or 90% in cross-sectional area). ischemia at rest (76% stenosis). Figure 4.6 illustrates how changes in coronary Atheromatous lesions may be static if the athero-vascular tone can alter the clinical characteristics matous changes involve the entire circumferenceof a chronic, stable stenotic lesion. Atheromatous of the arterial wall. In this instance, the luminallesions may be localized to one area of the arterial area is fixed and is unaltered by changes in arte-wall. As these eccentrically located lesions enlarge, rial vasomotor activity. Figure 4.6 illustrates thatthey encroach upon the arterial lumen. Because a lesion that occupies the entire circumference ofthe remainder of the arterial wall is free of plaque, the arterial wall and causes exertional ischemiait remains responsive to vasoactive stimuli and is (60% stenosis) will be unaffected by changes incapable of contraction. Such contraction will cause arterial vasoconstriction.the fixed atheromatous lesion to occupy a greaterportion of the arterial lumen and will result in a Variations in coronary vasomotor tonelarger pressure drop across the lesion. Therefore, There is a large variation in the extent of coro-the severity of the stenosis is not static but is nary vasomotor activity across a population. At onedynamic and dependent on the vasomotor activ- end of the spectrum is the normal 10% reduc-ity of the free arterial wall. This phenomenon is tion in outer arterial wall circumference that occursknown as dynamic coronary stenosis. As illustrated with α-adrenergic stimulation. At the other end of Normal Morphologic variants of atherosclerosis Young, thin Diffuse intimal Moderate sized Small eccentric Circumferential intima smooth muscle eccentric lumen plus lumen atheroma proliferation intimal proliferation central lumen Resting lumen cross-section 47% 49% 60% 60% 1/3 fixed 2/3 fixed 100% fixed circumference “Normal” vasoconstriction 17% 76% 76% 76% 60% (0% outer circumferential shortening) Clinical syndrome: Asymptomatic Rest pain only Rest pain only Rest and Exertional exertional pain pain onlyFig. 4.6 Cross-sections of normal and diseased associated with both resting and vasoconstricted state ofcoronary arteries. Morphologic state of arteries is normal and diseased arteries are summarized at bottomillustrated. Percent reduction in lumen diameter for each of diagram. (From Brown BG. Dynamic mechanisms inmorphologic state at rest and following normal degree of human coronary stenosis. Circulation 1985;70:921, withvasoconstriction is also shown. Clinical syndromes permission.)
    • Anesthesia for Myocardial Revascularization 99the spectrum, is the intense vasoconstriction that reduce myocardial perfusion, true coronary stealoccurs with variant or Prinzmetal’s angina. The does not occur when CPP is maintained. Furtherexaggerated coronary spasm seen in these patients studies demonstrate that the volatile agentsresults in total or near total occlusion in response do not abnormally reduce or redistribute coronaryto stimuli that cause only minimal constriction in collateral flow.individuals who do not have variant angina. For In contrast to these initial concerns regardingpatients with coronary spasm, myocardial ischemia isoflurane, recent evidence suggests a myocardialmay develop in the absence of coronary stenosis. protective benefit with volatile agent use (Fig. 4.8).For patients with normal coronary vasoconstriction, These protective benefits extend beyond a favor-myocardial ischemia will occur only if coronary able alteration in the oxygen supply and demandstenoses also exist. balance. The benefits may be related to physiologic alterations in response to ischemia and reperfu-Coronary steal sion. Many of these actions are similar to thoseCoronary steal refers the physiologic condition found with ischemic preconditioning, and are inwhereby blood flow is directed away from ischemic fact, termed, anesthetic-induced preconditioningprone areas of the myocardial dependant upon (discussed later).upstream coronary artery anatomy (Fig. 4.7).Coronary steal occurs in some patients with specific Anemiacoronary artery lesions upon the exposure of coro- Myocardial oxygen delivery is the product ofnary vasodilators. Approximately one-fourth of coronary blood flow and the oxygen content ofpatients with CAD meet these anatomical criteria. the transported blood. Anemia reduces myocardialIn these patients, the administration of an arterio- oxygen delivery by reducing the oxygen-carryinglar dilator, such as dipyridamole or adenosine, may capacity of blood. The degree of anemia that an areaproduce a steal. of myocardium can tolerate without developing In the mid-1980s a series of reports suggested ischemia is dependent on the relationship betweenthat isoflurane induced coronary steal by abnor- regional MVO2 and regional coronary blood flow.mally redistributing flow away from ischemic areas In the absence of coronary stenoses, hematocritof the myocardium. Subsequent work and clinical levels <15% result in subendocardial ischemiaexperience, however, have refuted this proposition. in anesthetized canines. In the presence of theAlthough isoflurane-induced hypotension may increased MVO2 that accompanies large increases Blocked Stenosis epicardial > 50% Coronary coronary arteriolar vasodilator Preferential Collateral flow vasodilatation Reduced collateral increases flow to flow nonischemic area Area A Area B Area A Area B Dependent on collaterals Normal autoregulation Ischaemic as collateral Normal regulation lost No autoregulatory reserve perfusion diverted away Luxury perfusion Maximally dilatedFig. 4.7 Schematic diagram illustrating coronary steal. Arrows represent coronary blood flow. (From Agnew NM,Pennefather SH, Russell GN. Isofurane and coronary heart disease. Anaesthesia 2002;57:338–47, with permission.)
    • 100 Chapter 4 Propofol Desflurane Sevoflurane 10 10 10 Troponin I (ng/mL) 8 8 8 6 6 6 4 4 4 2 2 2 0 0 0 Control T0 T3 T12 T24 T36 Control T0 T3 T12 T24 T36 Control T0 T3 T12 T24 T36 14 14 14 12 12 12 Troponin I (ng/mL) 10 10 10 8 8 8 6 6 6 4 4 4 2 2 2 0 0 0 Control T0 T3 T12 T24 T36 Control T0 T3 T12 T24 T36 Control T0 T3 T12 T24 T36Fig. 4.8 Coronary artery patients (n = 45) were with 95% confidence intervals. The lower panels showrandomly assigned to receive either target controlled the evolution of the individual values. Concentrationsinfusion of propofol or inhalational anesthesia with were significantly higher with propofol anesthesia. (Fromdesflurane or sevoflurane. After coronary artery bypass De Hert SG, Cromheecke S, ten Broecke PW et al. Effects(CPB), the cardiac index was lower in the propofol of propofol, desflurane, and sevoflurane on recovery ofgroup. Cardiac troponin I concentrations in the three myocardial function after coronary surgery in the elderlygroups before surgery (control), at arrival in the intensive high-risk patients. Anesthesiology 2003;99:314–23, withcare unit (T0), and after 3 (T3), 12 (T12), 24 (T24), and permission.)36 (T36) hours. The upper panel show the median valuesin afterload, hematocrit levels <30% producesubendocardial ischemia in the same canine model. Myocardial ischemia There is great debate about the ideal hematocrit Regional or global imbalances in myocardial oxygenin any patient and especially in the patient with supply and demand result in myocardial ischemia.known CAD. Recent investigation in a medical pop- The metabolic consequences of ischemia are dis-ulation after MI reveals that a hematocrit of at cussed in detail in Chapter 12. The clinical manifes-least 33% is associated with improved outcome. tations of myocardial ischemia are varied. AnginaHematocrit levels must be individualized for each pectoris, with or without signs of ventricular fail-patient; however, low hematocrit levels (<30%) are ure or dysrhythmias, is the classic manifestationpotentially dangerous in awake patients with CAD of myocardial ischemia. However, it is importantfor the following reasons: to remember that angina is not a universal mani-• Increased CO necessarily accompanies normo- festation of ischemia. In fact, myocardial ischemiavolemic anemia to maintain systemic oxygen may present as ventricular failure or dysrhyth-transport; this CO increase results in an increased mias without angina. In some individuals, especiallyMVO2 . diabetics, ischemia may remain clinically silent. Fur-• Increases in coronary blood flow to main- thermore, patients have varying thresholds for thetain coronary oxygen delivery result in increased development of ischemia during the course of a day.pressure drops across stenoses and potential for The dynamic nature of coronary stenoses accountssubendocardial hypoperfusion. for the changes in the caliber of a stenosis that
    • Anesthesia for Myocardial Revascularization 101may produce rest pain at one time and angina with product (RPP) (the product of HR and systolic BP).varying degrees of exercise at other times. In fact, most episodes are clinically silent. The same Despite these varied clinical presentations, the is true in cardiac surgical patients in the preopera-progression of hemodynamic and electrocardio- tive period. Approximately 40% of cardiac surgicalgraphic changes with ischemia tends to follow a patients will experience ST-segment evidence ofconsistent pattern in a given patient. Myocardial ischemia sometime in the 48 hours prior to elec-ischemia is heralded by a decrease in regional tive cardiac surgery. Less than one-fourth of theseventricular diastolic distensibility (see Chapter 2), episodes are preceded by a HR increase of 20%which usually results in an elevation in LVEDP or or more. In addition, most of these episodes areRVEDP, and central venous pressure (CVP). This clinically silent.is followed by systolic dysfunction, electrocardio- As with preoperative ischemic events, approxi-gram (ECG) changes, and finally by angina during mately half of intraoperative ischemic events aresymptomatic episodes. Patients manifesting eleva- unrelated to changes in HR and BP. This unpro-tions in PCWP with symptomatic episodes are likely voked ischemia suggests that decreases in myocar-to do so with asymptomatic episodes as well. Some dial oxygen supply may be important in the genesispatients will not manifest wedge pressure changes of intraoperative ischemia. In the cardiac sur-with either symptomatic or asymptomatic episodes. gical patient, ischemia consists of a background of hemodynamically unrelated silent ischemia,Symptomatic versus asymptomatic upon which is superimposed episodes of hemo-myocardial ischemia dynamically related ischemia. Rigorous intraoper-Ambulatory Holter monitoring of patients with ative hemodynamic control will not worsen thechronic stable angina demonstrates that 83% of preoperative ischemic pattern and may actuallyischemic episodes with ST-segment depression of improve it.1–2 mm are asymptomatic, and 63% of ischemic In the noncardiac surgical population, the post-episodes with ST-segment depression of 3 mm operative period is the most common time foror more are asymptomatic. Of the ischemic ECG ST-segment myocardial ischemia. In addition tochanges seen in elective CABG surgery patients the underlying propensity towards silent ischemiamonitored for 48 hours in the preoperative period, (as described above), the postoperative period isup to 80% are asymptomatic. The reasons why subject to increasing metabolic demands, increasedsome episodes of ischemia are symptomatic while MVO2 , and a hypercoagulable state. There may beothers are not remain unclear. There is some evi- plaque fissure and subsequent thrombus formation.dence that asymptomatic episodes are of shorter In the patient recovering from CABG, one antic-duration and lesser severity than symptomatic ipates a reduction in the incidence of ischemia.episodes, but this is not consistently true. There is After all, the coronary artery stenoses are bypassed,also evidence to suggest that patients with asymp- and myocardial blood flow normalized. In reality,tomatic episodes have a higher pain tolerance, however, CABG patients may suffer postoperativebut this is not uniformly true. Diabetic patients ischemia for a number of reasons including acutewith autonomic dysfunction are at higher risk for graft occlusion, coronary air or debris embolism,asymptomatic ischemia. technical anastomoses failure or disruption, tam- ponade with graft obstruction, or myocardialIncidence of perioperative ischemia oxygen supply–demand mismatch. CABG patientsEfforts to prevent myocardial ischemia usually require close monitoring for ischemia in the hourstarget control of the readily obtainable hemody- after surgery.namic determinants of myocardial oxygen demandsuch as HR and blood pressure (BP). Contrary to Outcome after myocardial ischemiathis practice, however, most ischemic episodes are The most significant consequence of pre- andnot preceded by increases in HR or rate-pressure intraoperative ischemia is postoperative myocardial
    • 102 Chapter 4infarction (PMI). The risk of PMI is approxi- will reflect LVEDP. LV ischemia, which produces LVmately 7% in CABG patients who had preoper- dilation or papillary muscle dysfunction, may causeative ischemia, intraoperative ischemia, or both, mitral regurgitation with generation of a prominentand 2.5% in patients who did not have ischemia. V wave. If there is inferior ischemia with RV dys-The risk of PMI correlates with the severity of function, some of these same observations may beischemia. In patients with ST-segment depressions seen on the CVP waveform.>2 mV, the PMI incidence is 9%; whereas those The PCWP trace is a reflection of LAP. However,with ST-segment depressions between 1.0–1.9 mV, because the PCWP waveform is transmitted throughthe incidence is 6%. the compliant pulmonary venous system, it is a There are many factors well beyond the control of damped version of the LAP. In particular, the leftthe anesthesiologist that are responsible for increas- atrial A wave may be poorly seen. As a result, it hasing the incidence of PMI. An aortic cross-clamp time been demonstrated that mean PCWP reflects meanin excess of 40 minutes increases the incidence of LV diastolic pressure and may underestimate LVEDPPMI from 2.6 to 10.9%. PMI occurs in 14.3% of by 10–15 mmHg during ischemia.patients in whom the distal anastomoses were rated Changes in PCWP and the PCWP waveform haveby the surgeon as poor as compared with 3.4% of poor sensitivity and specificity in detecting episodespatients in whom the anastomoses were considered of myocardial ischemia. This is true for a number ofof good quality. reasons: • PCWP does not necessarily reflect LVEDP asDiagnosing myocardial ischemia previously described. • When only a small region of LV wall developsECG changes diminished compliance with an ischemic episode,The gold standard for diagnosis of myocar- overall LV function may be only minimally affected.dial ischemia is the presence of ECG changes. This will reduce the observed changes in LVEDP asUnfortunately, ECG changes occur relatively late in reflected by the PCWP.the temporal sequence of myocardial ischemia after • The quantitative change in PCWP and the qual-deterioration of ventricular diastolic and systolic itative change in the PCWP waveform neces-function. Lead selection greatly enhances ischemic sary to define an ischemic event have not beendetection. Simultaneous monitoring of leads II and systematically defined.V5 is commonly used because of the high sensi- • Acute elevations in afterload in the absence oftivity of this combination in detecting myocardial ischemia can produce elevations in PCWP. This mayischemia. lead to a false positive interpretation of the PCWP tracing.PCWP trace Myocardial ischemia does not result in PCWPThe PCWP trace of the pulmonary artery catheter chances in all patients, and therefore, PCWP cannot(PAC) can assist in the early diagnosis of LV be relied upon as the sole indicator of ischemia. Forischemia. Reduction in LV compliance occurs in this reason, it is important to emphasize that sus-the early stages of LV ischemia because of dias- picious ECG or transesophageal echocardiographytolic dysfunction. In particular, LVEDP is elevated. (TEE) changes cannot be ignored simply becauseUnder these circumstances, left atrial pressure (LAP) there is no change in the PCWP or the PCWPwill be elevated to maintain LV diastolic filling. waveform.Movement of the left atrium (LA) to a steeperpotion of its pressure–volume relationship will Transesophageal echocardiographyresult in magnification of the normal LAP wave- Regional wall motion abnormalities (RWMA)forms. In addition, dilation of the LA may result in during systole (diminished inward excursion anda more forceful atrial contraction and production thickening) occur with ischemia. These RWMAof an enlarged A wave. The peak of this A wave precede ECG changes. The development of severe
    • Anesthesia for Myocardial Revascularization 103hypokinesis, akinesis, or dyskinesis is more specific avoidance of events initiating ischemia. Unfortu-for ischemia than mild hypokinesis. Changes in nately, the diverse nature of myocardial oxygenwall thickening are more sensitive for detecting imbalance in patients leaves the anesthesiolo-ischemia than changes in wall excursion. Typically, gist with no predictor of myocardial ischemiawall motion abnormalities and ECG changes occur that is reliable in all circumstances. The indiceswithin 60 seconds of each other. However, in a sit- described in the next sections all have limiteduation in which ischemia is less severe, RWMA usefulness.may precede ECG changes by several minutes. Infact, numerous studies have shown intraoperative Rate-pressure product and triple indexTEE qualitative analysis of regional wall excursion The RPP is the product of HR and systolic BP,and thickening to be a more sensitive detector of whereas the triple index (TI) is the product ofmyocardial ischemia than ECG changes and to be HR, systolic BP, and PCWP. The RPP provides acapable of detecting ischemia before ECG changes. useful assessment of MVO2 and predicts ischemia As with all monitors, there are occasional dis- in patients undergoing stress testing. Most patientscrepancies between ischemia detected by ECG experience the onset of ischemia at an RPP ofand that detected by TEE. There are both TEE- 20 000. However, its usefulness in assessing MVO2detected ischemic episodes not detected by ECG and predicting ischemia in anesthetized patients isand ECG-detected ischemic episodes not detected not reliable. In fact, it is common for a patient underby TEE. This may be due to several factors: anesthesia to have a low RPP and yet be at high• Normally, the TEE probe is placed at the mid-LV risk for ischemia (tachycardia and hypotension withlevel (level of the papillary muscles), at which wall acute blood loss).segments in the distribution of all three coronary The TI is subject to the same criticisms as thearteries can be monitored. Because a short-axis view RPP. The addition of PCWP to the product adds theof the left ventricle can only be obtained at one level variable of wall radius to the assessment of MVO2 .at a time, ischemic changes occurring in the basal or However, the TI still fails to account for large reduc-apical ventricular levels will be missed. Obtaining tions in myocardial oxygen delivery in the genesismultiple TEE windows, allowing visualization of all of ischemia.17 segments of the heart will reduce or eliminatethis as a source of error. Myocardial supply–demand ratio• Ischemic episodes may be missed because qual- (DPTI:SPTI)itative wall motion analysis is difficult for patients Efforts to account for beat-to-beat variations in bothwith preexisting wall motion abnormalities. myocardial supply and demand in the genesis of• Some RWMA (particularly in areas tethered to ischemia led to development of the supply–demandscar) may not be ischemic in origin. Changes in ratio. In this evaluation, supply is defined by theafterload may unmask areas of previous scarring. diastolic pressure time index (DPTI): DPTI = (mean• Ventricular pacing or a bundle-branch block may diastolic pressure – LVEDP) × duration of diastole.make detection of RWMA more difficult because of Demand is defined as the systolic pressure timeasynchronous contraction. index (SPTI): SPTI = (mean arterial pressure) ו Stunned myocardium may exhibit continued duration of systole. Ratios below 0.5 may result inRWMA despite adequate perfusion. subendocardial ischemia. Unfortunately, use of this• The ECG may detect ischemia with small areas of ratio is also unreliable for several reasons:subendocardial ischemia undetectable by TEE. • Increases in MVO2 due to increased contractil- ity are not reflected in BP and HR changes andPredicting myocardial ischemia therefore are not accounted for by SPTI.The ability to predict hemodynamic alterations that • A higher ratio is required in the presence of ane-are likely to result in myocardial ischemia in indi- mia to compensate for the reduced oxygen carryingvidual patients would allow prompt treatment and capacity of blood.
    • 104 Chapter 4• The presence of pressure drops across coronary Treatment of ischemiastenoses makes the DPTI an unreliable index of The most effective ischemic therapy involvesdistal coronary perfusion. identification of the cause of ischemia and tar-• Changes in coronary vascular resistance make geted treatment of this causative factor or factors.DPTI an unreliable index of distal coronary In some cases, the specific cause for new ischemiaperfusion. is unclear.• Use of the ratio is cumbersome because it requirescalculation of the areas under the diastolic and Tachycardiasystolic pressure curves, respectively. No single value of HR is uniformly detrimental to myocardial oxygen balance in a given patient.Mean arterial blood pressure–heart rate As already discussed, the HR at which ischemia is(BP–HR) quotient likely to occur will vary with mean arterial BP andAnimal work demonstrates that ischemia occurs the other determinants of myocardial oxygen bal-in the distribution of a critical coronary stenosis ance. When an increase in HR results in ischemiaand in collateral-dependent myocardium when the or is likely to result in ischemia, immediate therapypressure rate quotient (PRQ), defined as mean arte- is necessary.rial pressure (MAP)/HR, is <1. This relationship Eliminating inadequate anesthetic depth as ais valid over a wide range of pressures and HRs. cause is among the first and immediate steps inAn increase in HR can cause or worsen ischemic the patient undergoing surgery. Preload must bedysfunction at any mean arterial BP; however, the adequate. This is particularly important for patientsabsolute HR at which ischemia occurs is dependent with diminished ventricular compliance. In theseon the pre-existing MAP. In other words, higher patients, a higher-than-normal end-diastolic pres-HRs are tolerated without ischemia at higher MAPs. sure is necessary to ensure an adequate ventricularFor patients undergoing coronary revascularization, EDV. Once anesthetic depth and volume status arePRQ < 1.0 has poor sensitivity and specificity in eliminated as a cause of the tachycardia, treat-predicting myocardial ischemia as detected by both ment with a beta-blocker may be necessary. ManyECG and TEE. patients taking beta-blockers preoperatively may In summary: have plasma concentrations that are too low to• The combination of hypertension and tachycar- blunt the hemodynamic responses to surgery anddia may result in myocardial ischemia by increasing will require supplemental medication. Propranololmyocardial oxygen demand. in incremental doses of 0.5–1.0 mg IV to a total of• The combination of hypotension and tachy- 0.1 mg/kg may be used for patients without severecardia is particularly detrimental to myocardial ventricular systolic dysfunction. For patients with aoxygen balance because it reduces both the time history of bronchospasm or reactive airway disease,and the pressure gradient available for myocardial a β1 selective agent such as metoprolol is useful.perfusion. Incremental doses of 2.5–5.0 mg IV to a total of• Tachycardia, in and of itself, is detrimental to 0.5 mg/kg can be used. Because elevations in PCWPmyocardial oxygen balance. Experimentally, tachy- will reduce CPP, concomitant intravenous (IV) ther-cardia causes or worsens ischemic dysfunction at apy with nitroglycerin 0.5–1.0 µg/kg/min is indi-any given mean arterial BP. Clinically, tachycar- cated in the presence of an elevated PCWP. Thedia is associated with the development of ischemia clinician must titrate drug use against anticipatedin patients undergoing coronary revascularization or observed hypotension.whereas hypertension per se is not a risk factor. In some instances, the ultra-short-acting beta-In particular, HRs > 110 b/min are associated with blocker esmolol may be useful. Esmolol has ana dramatically increased incidence of intraoper- elimination half-life of 9 minutes due to metabolismative ischemia in patients undergoing coronary by red-cell esterases and is β1 selective. Esmololrevascularization. is started with a bolus of 0.5 mg/kg given over
    • Anesthesia for Myocardial Revascularization 105several minutes followed by an infusion of Hypertension50 µg/kg/min and titrated up to 300 µg/kg/min Hypertension is classically associated with tachy-as necessary. In a patient under general anesthe- cardia in the genesis of myocardial ischemia.sia, however, the initial dose should be signifi- Treatment, in this instance, is directed towardcantly reduced (10–50 µg). Esmolol is useful in deepening of anesthesia. If hypertension is persis-patients with poor ventricular function or bron- tent despite adequate anesthetic depth, vasodilatorchospastic disease. A striking advantage to this therapy is warranted. Many agents reduce systemicmedication is the short half-life. If the drug is BP. Sodium nitroprusside is an easily titrated, potentpoorly tolerated, therapy can be quickly termi- arteriolar dilator that effectively treats hyperten-nated. Furthermore, unlike longer-acting beta- sion. An infusion can be started at 0.25 µg/kg/minblockers, esmolol can be used aggressively in the and titrated upward. However, because sodiumpre-cardiopulmonary bypass (CPB) period with- nitroprusside is a potent arteriolar dilator, it has theout fear that it will compromise termination potential to induce a coronary steal in the presenceof CPB. of the appropriate anatomy. Another concern is over treating the patient and inducing acute, severeHypotension hypotension.Many patients with coronary disease will toler- Nitroglycerin preferentially dilates large coronaryate brief episodes of hypotension without ischemic vessels and is not implicated in the steal phe-sequelae, but others will not. The extent of hypoten- nomenon. Nitroglycerin has its greatest dilatingsion that can be tolerated before ischemia develops effect on the venous beds and arterial dilatationis dependent on several variables. For example, occurs only at higher doses. Despite this, when useda reduction in arterial BP may reduce MVO2 in appropriate doses, nitroglycerin and nitroprus-by reducing afterload (decreasing demand); how- side have been shown to be equally effective inever, at the same time, aortic perfusion pressure treatment of hypertension associated with coronarymay fall to a critical level (decreasing supply). artery bypass surgery. Both agents have comparableFurthermore, as discussed previously, at higher effects on HR, CO, and PCWP. With compara-HRs, hypotension adversely effects perfusion. In any ble reductions in systolic BP, nitroglycerin causescase, the source of hypotension must be quickly and less reduction in diastolic BP than does nitroprus-accurately determined. Determination of CO and side. Therefore, CPP may be better preserved withsystemic vascular resistance (SVR) will help direct nitroglycerin than with nitroprusside. For these rea-therapy. sons, nitroglycerin may be the preferred agent for When hypotension is due to a reduction in treatment of hypertension associated with myocar-CO, HR and preload should be optimized. If dial ischemia. For treatment of hypertension,these measures fail to correct the fall in CO, one start nitroglycerin at 0.5 µg/kg/min and titrate toshould consider starting an inotrope and eliminat- effect.ing or reducing any inhalational anesthetic agents(eliminating their negative inotropic properties). Dynamic stenosisA fall in SVR can be treated with an α-adrenergic Evidence of myocardial ischemia may occur withagonist such as phenylephrine in incremental doses little or no initial change in HR or BP. In theseof 40–100 µg IV. It should be kept in mind instances, acute reductions in coronary blood flowthat α-adrenergic agonists may constrict coronary may occur due to vasoconstriction in the area of aarteries with dynamic stenoses and should there- coronary stenosis or due to true coronary spasm infore be titrated carefully. Because elevations in an area free of a stenosis. The mainstays of ther-PCWP will reduce CPP (increasing ventricular wall apy are nitroglycerin and calcium channel blockerstension), concomitant therapy with nitroglycerin to reduce coronary vasomotor tone. Nitroglycerin0.5–1.0 µg/kg/min is indicated in the presence of can be started at 0.5 µg/kg/min and titrated upward.an elevated PCWP. When an elevated PCWP accompanies the ischemic
    • 106 Chapter 4episode, nitroglycerin effectively reduces PCWP diminished ventricular compliance. Patients func-through both vasodilation (reducing preload) and tioning on the steep portion of their diastolictreatment of the underlying ischemia. Nifedipine is pressure–volume curve will be dependent on aa calcium channel blocker and systemic vasodilator well-timed atrial systole (the A wave in the atrialthat can be administered sublingually in a 10-mg pressure trace) to adequately fill the ventricle at enddose to reduce coronary vasomotor tone. diastole. Systemic hypotension may occur with adminis- Echocardiography offers another avenue for eval-tration of these agents. CPP improves when the uation of diastolic dysfunction. This noninvasivepressure drop across the stenosis diminishes with modality allows precise quantification of dias-vasodilation in the area of the stenosis and when tolic parameters. The function can be character-vasodilation reduces PCWP. However, extreme ized as normal, delayed relaxation, pseudo-normaldiastolic hypotension offsets any potential improve- and restrictive. These quantifications represent ament of CPP. For this reason, administration of continuum of disease (Figs 4.9 and 4.10).phenylephrine in addition to nitroglycerin acts to For patients undergoing repeat coronary revascu-preserves diastolic BP and CPP. larization procedures, elevated right heart pressures increase the risk of inadvertent right atriotomies and ventriculotomies during sternotomy. Similarly,Anesthetic management for if the pericardium was left open after the origi-CABG surgery nal surgical procedure, the anterior surface of theGoals RV is more likely to be adherent to the sternum• Avoid increases in myocardial oxygen (Fig. 4.11). The hemorrhage induced by these trau-consumption. matic atriotomies, and ventriculotomies can be life• Avoid tachycardia; it compromises oxygen threatening. A femoral vein and artery are oftendelivery at any MAP. exposed before sternotomy in redo patients so that• Appreciate that the patient’s baseline ischemic partial bypass can be initiated emergently if hem-pattern will continue into the preoperative and orrhage occurs with sternotomy. Partial bypass pro-intraoperative periods; these episodes must be vides the circulatory support and the decompressiontreated when recognized. of the right heart that may be necessary for surgical repair.Preoperative cardiac assessmentPreoperative evaluation is discussed in detail in Systolic functionChapter 1. Careful review of the cardiac catheteriza- Ejection fraction (EF) and assessment of walltion data is also an essential part of the preoperative motion are the most commonly obtained assess-visit. The important features of the catheterization ments of systolic function (Fig. 4.12). Because EFreport are reviewed here and discussed in detail in is an ejection-phase index, it is dependent on load-Chapter 2. ing conditions. For this reason, the presence of a low-impedance outflow tract, such as that whichDiastolic function exists via the mitral valve in mitral insufficiency,To varying degrees, many patients with CAD man- will cause the EF to overestimate systolic func-ifest diminished ventricular compliance. In many tion. EF is an assessment of global systolic functionpatients with diastolic dysfunction, an elevated and will not be depressed until a relatively largeLVEDP is necessary for adequate LVEDV. The mea- portion of ventricle exhibits compromised systolicsurement of LVEDP at the time of cardiac catheter- function. An EF lower than 40% is abnormal. Wallization will provide some index of the degree of motion abnormalities are seen with ventriculogra-diastolic impairment. In addition to diminished phy, advanced magnetic resonance imaging (MRI)distensibility, patients with long-standing systemic or computed tomography (CT) imaging, or com-hypertension may have concentric hypertrophy and monly, with echocardiography. When large areas of
    • Anesthesia for Myocardial Revascularization 107 Transmitral flow velocity Normal Delayed Pseudonormal Restrictive E ≥A Relaxation E<A E A DT 140–220 E<A DT 140–220 DT < 140 IVRT 60–100 DT > 220 LAP increased IVRT < 60 IVRT >100 Pulmonary vein flow velocity Normal Delayed Pseudonormal Restrictive S≥D relaxation S <D S<D Ar < 25 cm/s S>D Ar > 25 cm/s Ar > 25 cm/s Ar < 25 cm/s LAP increased LAP increased Mitral annular velocity (lateral wall) Normal Mild Dysfunction Moderate Severe EM/AM > 1 (Delayed Dysfunction Dysfunction EM > 8 cm/s relaxation) (Pseudonormal) (restrictive) EM ≤ 8 cm/s EM < 8cm/s EM 8 cm/sFig. 4.9 Transmitral Doppler imaging, pulmonary view Doppler imaging and tissue Doppler imaging (TDI) profilescorresponding to normal, delayed relaxation, pseudonormal, and restrictive filling patterns. (From Groban L,Dolinski SY. Transechocardiographic evaluation of diastolic function. Chest 2005;128:3652–63, with permission.)akinesis and dyskinesis exist, systolic function will The coronary angiograms guide the surgeonbe severely compromised. in target vessel location. Distal disease in small RV EF and wall motion analysis generally are not vessels makes the technical success of the operativeobtained at the time of catheterization. For patients procedure less likely. Furthermore, bypassingwith suspected RV systolic dysfunction, either first- a vessel supplying a dyskinetic or aneurysmal areapass or equilibrium noninvasive radionuclear imag- of ventricle may yield little in terms of improveding can be used to determine EF. systolic function postoperatively because such areas have little salvageable myocardium. There areCoronary anatomy and coronary lesions strong data to suggest that bypassing areas of hiber-The surgeon and anesthesiologist must know the nating myocardium result in improved LV func-extent of coronary disease and the presence or tion at 1 year after surgery. In some patients, theabsence of collateral flow. This will allow intelligent EF% may dramatically improve from 20 to 40% orassessment of the areas most at risk for developing better.ischemia. This knowledge will help guide monitor- The term “left main equivalent” is commonlying decisions (i.e. ECG monitoring selection and TEE used and deserves clarification. A high-grade leftwindow). main coronary artery lesion potentially jeopardizes
    • 108 Chapter 4 = To do EF ≥ 45% = Diagnosis Doppler mitral inflow E<A E>A E A DT > 140 ms DT > 140 ms DT < 140 ms TDI TDI TDI EM ≤ 8 cm/s EM > 8 cm/s EM ≤ 8 cm/s EM > 8 cm/s EM ≤ 8 cm/s E/EM≤ 8 8 ≤E/EM≤ 15 E/EM>15 E/EM ≤ 8 8 ≤E/EM ≤ 15 E/EM >15 E/EM <8 E/EM >15 Impaired Restrictive relaxation Impaired Normal diastolic Pseudonormal High myocardial normal filling relaxation suspicion of increased filling function disease pressures pericardial pressures disease Doppler Valsalva Valsalva pulmonary and and vein mitral inflow mitral inflow Ar wave Ar wave E >A E<A E >A E A < 25 cm/s ≥ 25 cm/s (unchanged) Impaired relaxation Impaired Normal Reversible, Fixed, normal filling relaxation diastolic Pseudonormal restrictive restrictive pressures increased filling function pressures And/or Doppler pulmonary vein Ar wave Ar wave < 25 ≥ 25 Normal PseudonormalFig. 4.10 Algorithm for the assessment of diastolic function in the patient with a normal or near-normal ejectionfraction (EF) (i.e. ≥ 45%). A, atrial peak velocity; Ar, retrograde velocity; E, early filling peak velocity; EM , early filling;TDI, tissue Doppler imaging. (From Groban L, Dolinski SY. Transechocardiographic evaluation of diastolic function.Chest 2005;128:3652–63, with permission.) Fig. 4.11 Lateral and posterior/anterior chest radiographs of a woman presenting for a re-do sternotomy. Note the sternal wires and the heart adherent to the sternum. This woman has a thoracoabdominal aortic aneurysm.
    • Anesthesia for Myocardial Revascularization 109(a) of lesions occurs when collaterals from a vessel with a high-grade stenosis supply myocardium dis- tal to an occluded vessel. An example would be myocardium distal to an occluded LAD supplied by collaterals from a right coronary artery (RCA) with a high-grade proximal stenosis. In this setting, complete occlusion of the remaining vessel (RCA) compromises most of the LV. For patients undergoing redo procedures, evalua- tion of the extracardiac conduits (internal mammary arteries and reverse saphenous veins) is required.(b) These grafts may now have varying degrees of stenosis. Inadvertent compromise (i.e. transec- tion, laceration, kinking) of these conduits dur- ing the difficult dissection that often accompa- nies a redo procedure may severely compromise myocardial perfusion. Likewise, surgical manipula- tion of these conduits may result in embolization of atherosclerotic plaques into the distal coronary vas- cular bed with subsequent transmural myocardial ischemia. PremedicationFig. 4.12 Systolic function is easily assessed with Reassurance and allowing time to address thetransesophageal echocardiography (TEE). (a) Ejectionfraction (EF) is determined by the modified method of patient’s concerns are perhaps the best anxiolytic.disk. Capturing the image in both end systole and end This is especially import when one considers thediastole allows the echocardiographer to trace the relative risk CABG surgery involves. In the veryendocardial border and determine ejection fraction. best of hands, the risk of mortality is approximatelyThe EF in this patient is normal (65%). (b) M-mode 1–3%, and there is a further risk of neurocognitiveDoppler allows determination of wall motion and deficit, stroke, renal failure and respiratory failure.fractional shortening. In this patient, there is significant Our patients are facing a major risk which inducesinferior wall hypokinesis as evidenced by a lack ofthickening and movement during systole. Compare significant anxiety. It is our obligation to treat themthe thickening and movement of the anterior wall with care, compassion and patience.(far field) to that of the inferior wall. There are a number of safe premedication pre- scriptions than a clinician may chose. Patients withmost of the LV muscle mass. Likewise, high-grade preserved ventricular function can be premedicatedstenoses of both the left anterior descending (LAD) with morphine 0.10–0.15 mg/kg intramuscularlyand circumflex arteries jeopardize the same ter- (IM), scopolamine 0.005 mg/kg IM, and diazepamritory. As a result, this combination of lesions is 0.15 mg/kg or lorazepam 0.04 mg/kg orally (PO)functionally the same as a left main lesion; hence, approximately 1.5 hours before scheduled induc-the designation left main equivalent. The difference tion time. Alternatively, morphine 0.10–0.15 mg/kgis that with the true left main lesion, only one vessel IM and midazolam 0.03–0.05 mg/kg IM may be(the left main) must become completely occluded used. The dysphoric effects of scopolamine may beto compromise LV blood flow. In the case of the troublesome for elderly patients. For elderly patientsLAD and circumflex lesions, both vessels would or patients with poor ventricular function, the doseshave to be occluded simultaneously to produce can be reduced and supplemental premedicationthe same effect. Another high-risk combination can be given in the operating room holding area
    • 110 Chapter 4under direct observation. Supplemental oxygen an infusion of 2–6 units/h). The antiplatelet med-with a face mask should be started at the time ications pose an unusual management problem.of premedication. Most prudently, premedication Patients on clopidogrel should have the medicationcan be held until the patient arrives in the pre- held for 3–5 days before elective surgery. Surgeryoperative holding area. At this time, the physician in patients on clopidogrel is associated with exces-or nurse anesthetist can administer either fen- sive bleeding and transfusion of blood and bloodtanyl or midazolam under direct supervision and products.observation. All cardiac medications should be continued Preinductionon schedule until the time of surgery. Preop- After arrival in the operating room, all patientserative beta-blocker therapy has been shown to should be attached to an ECG system capable ofblunt the hemodynamic responses to surgical stim- monitoring leads I, II, III, aVR , aVL , AVF , andulation during coronary revascularization and to V5 . Baseline recording of all seven leads shouldreduce the incidence of HR-related intraoperative be obtained for comparative purposes. Normally,ischemic events. Continuation of preoperative beta- two leads (II and V5 ) are monitored simultane-blockade therapy does not compromise myocardial ously intraoperatively. However, if the areas ofperformance during the post-CPB period. Further- myocardium at risk are better assessed in othermore, abrupt withdrawal of beta-blockade therapy leads, then those leads should be monitored.has been associated with myocardial ischemia, All patients should have a radial arterialhypertension, and tachydysrhythmias secondary catheter and adequate peripheral IV access (14- orto a beta-blockade induced increase in β-receptor 16-gauge). Alternatively, if peripheral IV accessdensity. In fact, continuation of beta-blockers in is poor, a peripheral IV suitable for inductionpatients undergoing surgery who are receiving the can be started and a large-bore multilumen (16- ormedication for angina, symptomatic arrhythmias, 14-gauge) central venous line can be placed at thehypertension or other ACC/AHA class I indications same time as the PAC. For patients who are to havecarries a class I level recommendation. an internal mammary artery (IMA) harvested, the Some preoperative medications require addi- arterial waveform obtained in the ipsilateral radialtional comment. Patients treated with diltiazem or brachial artery may be compromised during IMAand nifedipine preoperatively demonstrate a dimin- dissection. This occurs when the patient’s arm isished response to phenylephrine. Thus, treatment tucked at the side and is compressed between theof intraoperative hypotension may require higher body and the retractor used for IMA dissection. Thisthan usual doses of phenylephrine for patients con- results in compression of the brachial artery againsttinued on preoperative calcium channel blockers. the humerus and is particularly common in largeThe incidence of perioperative ischemia during patients. The arterial line may be placed in the con-coronary revascularization is greater in patients tralateral arm or the ipsilateral arm can be abductedreceiving just calcium channel blockers (nifedipine, to avoid this problem. When the arm is tucked at thediltiazem, or verapamil) preoperatively than in side, care should be taken to provide ample paddingpatients receiving beta-blockers or a combination of between the arm and the retractor. Many surgeonscalcium channel and beta-blockers. This is probably harvest the radial artery for additional arterial con-due to better attenuation of tachycardia-induced duit. In these cases, the nonsurgical arm is onlyischemia in patients receiving beta-blockers. The site available for radial artery cannulation. If can-angiotensin converting enzyme inhibiting drugs are nulation is impossible, a femoral artery catheter isassociated with refractory hypotension after CPB required.in some patients. These medications should be The use of PACs for all patients undergoing coro-held on the morning of surgery. If hypotension is nary revascularization is controversial. PACs allowencountered, treatment is most effective using IV measurement of thermodilution CO; pulmonaryvasopressin (2 units IV bolus titrated to effect or artery, right atrial, and PCWPs; systemic and
    • Anesthesia for Myocardial Revascularization 111pulmonary vascular resistances (PVRs); and LV and reductions in SV and CO. Because poor systolicRV stroke work. Some PACs monitor continuous function associated with ischemic heart diseaseCO, mixed venous oxygen saturation, right heart is accompanied by reduced diastolic distensibility,EF, and RV diastolic volume. Analysis of the PCWP maintenance of an adequate preload will requireand RAP traces may be helpful in the early diag- a PCWP in the range of 12–18 mmHg.nosis of ischemia. There are several reviews of All episodes of ischemia in the preinduc-outcome and pulmonary artery catheterization. It is tion period require aggressive therapy. Therapyextremely difficult to demonstrate a benefit in plac- should be directed toward the specific cause of theing a PAC, and in many studies, the PAC is associ- ischemic episode. A high proportion of ischemicated with worse outcome. Nonetheless, PAC use is episodes are likely to be asymptomatic and to occurcommon during cardiac surgery. in the absence of hemodynamic changes, the ECG, The PAC may be safely placed either before or RAP, and PCWP traces are important in diagnosingafter the induction of anesthesia. If placed before, ischemia in these patients.the information can be used during the inductionsequence. However, some patients may experience Induction and maintenanceundue anxiety, or if sedated, potential respira- No one anesthetic technique is superior to anothertory compromise during line placement. If placed for patients presenting for coronary artery bypassafter induction, the patient will be under gen- grafting. Two types of techniques are discussed:eral anesthesia and paralyzed thereby facilitating a traditional high-dose narcotic technique and arapid and safe placement. As with any central line “fast-track” technique geared toward shorter post-placement, certain precautions are required. All operative ventilation and earlier discharge from theof the equipment and medications for treatment intensive care unit (ICU).of dysrhythmias should be on hand before place-ment of the catheter is attempted. In particular, a High-dose narcotic techniquedefibrillator with demonstrated consistent synchro- Fentanyl and sufentanil generally provide the stablenization to the patient’s ECG signal must be in the hemodynamics essential in preventing imbalanceroom in case cardioversion is necessary. In addi- in myocardial oxygen supply and demand. Thesetion, strict sterile technique is required to reduce agents have no effect on myocardial contractilitythe incidence of perioperative line colonization and and cause a reduction in peripheral vascular resis-sepsis. tance only through a diminution in central sym- The information obtained at cardiac catheteriza- pathetic tone. In a high-dose narcotic technique,tion about LV diastolic function and LV end-diastolic 50–75 µg/kg of fentanyl, or 10–15 µg/kg of sufen-pressure can be used in conjunction with the tanil serve as the primary anesthetic for inductionPCWP to optimize LV preload. Patients with reduced and maintenance before CPB. A benzodiazepinecompliance may require a PCWP in the range must be included to avoid awareness.of 12–15 mmHg to ensure an adequate preload Sufentanil is associated with greater decreases in(LVEDV). When preload is inadequate, SV and CO arterial BP and SVR on induction than fentanyl.will be reduced and systemic BP and CPP will However, sufentanil is more effective than fen-be maintained by increases in SVR. Subsequent tanyl in blunting the hypertensive responses toreductions in SVR (as with induction) may lead to skin incision, sternotomy, sternal spread, and aor-hypotension and potentially to tachycardia. In this tic manipulation. To avoid hypotension on induc-setting, any advantage of a low PCWP in terms of tion with either narcotic, adequate preload isCPP is offset by systemic hypotension. essential. For patients with poor systolic function, preload The choice of muscle relaxant influences thereserve will be limited or exhausted to meet baseline hemodynamic stability of a high-dose narcotic anes-CO demands. Any increase in afterload will pro- thetic. Pancuronium has a vagolytic effect as wellduce afterload mismatch and result in progressive as the capacity to enhance sympathetic outflow by
    • 112 Chapter 4blockade of sympathetic postganglionic muscarinic Bradycardia with hypotension requires promptreceptors, inhibition of catecholamine reuptake, treatment. A small dose of pancuronium (1–3 mg) isand stimulation of release of catecholamine from often effective if vecuronium or cisatracurium hasnerve terminals. Vecuronium and cisatracurium are been used. Glycopyrrolate, ephedrine, or atropinedevoid of these effects. Induction with fentanyl– may be appropriate alternatives. Atropine should bepancuronium provides stable induction hemo- used cautiously. Atropine administration may ini-dynamics without ischemia. In some patients, tiate tachycardia. Atropine, unlike β1 -adrenergicinduction with fentanyl–vecuronium or sufentanil– agents, increases HR without any reduction in thevecuronium results in bradycardia and hypoten- duration of systole. Thus, for equal increases insion. Induction with sufentanil–pancuronium HR, atropine will cause a greater reduction in theprovides stable induction hemodynamics and HR. duration of diastole and will compromise suben-Caution is urged in any case in a patient receiv- docardial perfusion to a greater degree than willing beta-blocking agents preoperatively. In these a β1 -adrenergic agent. Ephedrine (a direct- andpatients, a high-dose narcotic is more likely to be indirect-acting β- and α-agonist), 5 mg, is a reli-associated with significant bradycardia. able agent to increase HR without compromising Preoxygenation is important in cardiac surgical diastole. In addition, the augmentation in dias-patients. The induction sequence must be tailored tolic BP obtained is beneficial when hypotensionto the individual patient. A system of graded stimu- accompanies bradycardia.lation is used to individualize the narcotic dose for Tachycardia requires aggressive treatment toeach patient. After loss of consciousness, the hemo- avoid subendocardial ischemia and hemodynamicdynamic response to insertion of an oral airway, fol- compromise. The first strategy should be to termi-lowed by insertion of a urinary catheter, can gauge nate any noxious stimuli, assure proper intravas-the need for additional narcotic to blunt the antic- cular volume and increase the depth of anesthesiaipated hemodynamic response to tracheal intuba- when necessary. Failing this, a short- or long-actingtion. If an upward trend in HR or BP is noted during beta-blocker is usually appropriate therapy.laryngoscopy, additional narcotic should be admin- Should hypotension due to reduced SVR occur,istered. If there is poor visualization of the trachea, small doses of phenylephrine (40–120 µg) andlaryngoscopy should be terminated and intubating volume infusion to increase preload to preinduc-conditions should be improved by changing head tion levels usually will correct the problem. A doseposition, using a stylet, or changing blades. This of phenylephrine reliably causes an increase in SVRapproach will help prevent long, stimulating laryn- with a concomitant increase in wall stress and agoscopies that compromise hemodynamics. After reduction in ejection phase indices of contractility inthe airway is secure, the stomach should be evac- CABG patients. The peak effect of a phenylephrineuated with an oral-gastric tube, after which, a TEE dose occurs 30–40 seconds after injection.probe can be placed. If surgical stimulation (skin incision, sternotomy, It is sometimes helpful to administer a priming sternal spreading, and aortic manipulation) pro-dose of muscle relaxant prior to the narcotic admin- duces hypertension, additional doses of sufentanilistration. Vecuronium or pancuronium 0.02 mg/kg (1–5 µg/kg) or fentanyl (5–25 µg/kg) may be nec-or cisatracurium 0.04 mg/kg are appropriate approx- essary. If this fails to control the hypertension, theimately 1–2 minutes before starting the narcotic use of additional agents will be necessary. As dis-infusion. As the patient loses consciousness, the cussed previously, treatment of hypertension withremainder of the total dose of 0.1 mg/kg of vecuro- vasodilator therapy must take into account thenium or pancuronium or 0.2 mg/kg of cisatracurium effect of these agents on regional myocardial bloodis administered and controlled ventilation with flow and on their ability to improve concomitant100% oxygen is initiated. This technique minimizes ischemia.the risk of narcotic-induced rigidity without undue As mentioned, this technique requires thestress to the patient. administration of benzodiazepines and possibly
    • Anesthesia for Myocardial Revascularization 113inhalational anesthetics to reduce the incidence the clinician will soon master a technique suitableof operative recall. Diazepam, midazolam, and for his or her practice.lorazepam administered in conjunction with fen- • Premedication with midazolam 1–2 mg IV in thetanyl or sufentanil may decrease peripheral vascu- preoperative holding area.lar resistance resulting in subsequent hypotension. • Fentanyl 15–20 µg/kg and etomidate 0.20–Therefore, they must be titrated with caution. Mida- 0.30 mg/kg for induction in combination withzolam in increments of 1–2 mg or lorazepam in cisatracurium or vecuronium. The considerationsincrements of 0.5–1.0 mg are reasonable. used in choosing a relaxant are the same used in Nitrous oxide (N2 O), in association with high- the high-dose narcotic technique.dose opiates, causes systolic dysfunction in patients • Maintenance of anesthesia with isofluranewith CAD, particularly those with an LVEDP 0.5–1.0%.>15 mmHg. N2 O combined with high-dose opiates • Either Propofol 75–100 µg/kg/min, or isofluranealso elevates PVR, particularly in the presence of is administered while on CPB.pre-existing pulmonary hypertension. The potent • Intermediate-acting neuromuscular blockinginhalational agents, isoflurane, sevoflurane and agent (Fig. 4.13).desflurane are safe in patients undergoing coronaryrevascularization. The role of anesthetic precondi-tioning with inhalational agents is discussed later inthis chapter. 120 Rocuronium PancuroniumFast-track technique 100The “fast track” is a comprehensive program TOF fade ratio 80designed to improve perioperative outcome andreduce costs by reducing hospital stay for patients 60undergoing coronary revascularization. Early extu-bation (<8 hours) is the hallmark of this program. 40A number of anesthetic techniques allow early extu- 20bation without increasing the risk of adverse car-diac and noncardiac outcomes. Generally, patients 0selected for inclusion in the protocol are low-risk 0 1 2 3 4 Hourscoronary revascularization patients, but more cen- Postoperative recoveryters are including all cardiac surgical patients. Risk Variable Rocuronium Pancuronium P valuefactors contributing to prolonged postoperative ven- Duration of ventilatory weaning (min) 90 (40–315) 180 (50–180) <0.05 ICU arrival until extubation (min) 335 (185–1290) 460 (225–1350) <0.05tilation in coronary revascularization patients are TOF ratio at initiation of ventilatory weaning 0.99 (0.87–1.21) 0.14 (0.00–1.11) <0.05 Data are median (range).female sex, advanced age, congestive heart fail- ICU, intensive care unit; TOF, train-of-four.ure (CHF) requiring preoperative diuretic therapy, Fig. 4.13 The use of pancuronium (0.08–0.10 mg/kg) orand unstable angina. Both the anesthetic tech- rocuronium (0.6–0.8 mg/kg) was evaluated in 82 patientsnique and the maintenance of normothermia are undergoing coronary artery bypass grafting surgery. Theimportant with this technique; however; the most bar graph shows the train-of-four ratios were measuredimportant element for success in a hospital sys- upon arrival to the intensive care unit and then eachtem is the adoption of a “fast-track extubation hour for the next 4 hours. Significant differences wereprotocol.” Using such a protocol identifies appro- noted between groups at all time intervals (P < 0.05). The postoperative recovery profiles are shown below inpriate patients, alerts the care team of the clini- the figure. Data are median (range). ICU, intensive carecal pathway, and facilitates a scheduled weaning unit; TOF, train-of-four. (From Murphy GS, Szokol JW,process. Marymont JH et al. Recovery of neuromuscular function The following is an example of a fast-track pro- after cardiac surgery: pancuronium versus rocuronium.tocol. There are many approaches, however, and Anesth Analg 2003;96:1301–7, with permission.)
    • 114 Chapter 4• Post-CPB, the isoflurane is maintained and 1.00 P = 0.48no additional narcotic is administered. Either 0.98propofol, 20–50 µg/kg/min or dexmedetomidine 0.96 Event-free survival0.1–0.7 mg/kg/min is started prior to transport tothe ICU. 0.94 On pump (90.6%) 0.92Off-pump coronary artery bypassgrafting 0.90Off-pump coronary artery bypass (OPCAB) graft 0.88surgery offers an alternate technique to traditional Off pump (88.0%)on-pump CABG. Advantages of this technique 0.86include potentially decreased postoperative morbid- 0 0 60 120 180 240 300 360ity in some patients and reduced resource utilization Days since randomizationand total cost. CPB is avoided in this technique, and No. at risktherefore, so are all of the potential problems with On pump 139 130 128 127 127 127 126myocardial preservation. Various investigators have Off pump 142 132 131 128 127 126 125demonstrated better myocardial energy preserva- Fig. 4.14 Kaplan–Meier estimates of survival free fromtion, less oxidative stress, and minimal myocar- stroke, myocardial infarction, and repeated coronarydial damage with this technique. New advances in revascularization. P = 0.48 by log-rank test. Results frommyocardial stabilizing devices allow a still opera- a multicenter, randomized evaluating off pump coronary artery bypass grafting to traditional on-pump coronarytive field and excellent surgical conditions (the main artery bypass grafting. In this investigation, 139 patientsadvantage of CABG with cardioplegia and a flac- with single or double vessel coronary disease werecid heart). There are several reports in the literature randomly assigned to on-pump surgery and 142 patientscomparing outcome between on-pump CABG and to off-pump surgery. At 1 year, the rate of freedom fromOPCAB. As expected, the results vary; however, it death, stroke, myocardial infarction and coronaryappears that there is no difference in outcome in low reintervention was 90.6% after on-pump surgery andrisk patients with either technique (Fig. 4.14). There 88.0% after off-pump surgery (absolute difference, 2.6%; 95% confidence interval, −4.6 − 9.8). The graft patencyis a consistent cost savings with OPCAB. The anes- was similar between groups. On-pump surgery wasthetic management of these patients is strikingly associated with $1839 in additional direct costs perdifferent from traditional on-pump CABG. These patient compared to off-pump surgery. (Fromdifferences are reviewed below. Nathoe HM, van Dijk D, Jansen EW et al. A comparison In contrast to on-pump CABG, brief periods of of on-pump and off-pump coronary bypass surgery inischemia are necessary during the operative pro- low risk patients. N Engl J Med 2003;348:394–402, withcedure. These ischemic periods may be reduced permission.)in some patients with the placement of a tempo-rary coronary stent, however, there remains some significant ischemia is essential. During the occlu-time of interrupted blood flow. The ischemic bur- sion and anastomoses, the anesthesiologist shouldden is usually of such short duration, that there is monitor the appropriate ECG leads highlighting thelittle risk of significant long-term damage; however, target area, the TEE for new RWMA, continuousthere may be some element of stunning and imme- CO, and mixed venous oxygen saturation. It isdiate myocardial dysfunction. In addition, there important to note that OPCAB procedures requiremay be a cumulative global dysfunction after several extensive positioning of the heart, and this posi-sequential occlusions in multiple graft procedures. tioning changes the observed monitoring (especiallyIn fact, it is common for a patient to tolerate TEE windows); nonetheless, following trends willa one-or-two vessel OPCAB bypass, but a three- allow the clinician opportunity to intervene whenor-four-vessel procedure often results in signifi- appropriate in these complex procedures.cant support required to complete the procedure. OPCAB procedures are associated with hemo-Because ischemia is anticipated, monitoring for dynamic instability. These hemodynamic changes
    • Anesthesia for Myocardial Revascularization 115may be secondary to the ischemic episodes as effort, with cellular death ensuing after approxi-well as the positioning requirements of the heart mately 15 minutes. If the ischemic episode is pre-and resultant preload alterations. In general, main- ceded by one or more sub-lethal ischemic episodes,taining systemic BP (and, hence, CPP) is essen- the myocardium is altered in such a way as to limittial. Techniques to maintain BP include adequate tissue injury and prolong the interval of ischemicvolume loading prior to ischemia, Trendelenburg tolerance. In experimental models, infarct size isposition, norepinephrine or phenylephrine infu- measured with and without ischemic precondition-sions, and atrial pacing if bradycardia occurs. ing. With ischemic preconditioning, the infarct sizePlacement of a coronary stent allows blood flow is approximately 25% smaller. This protective ben-during much of the anastomoses and is helpful in efit is seen immediately after the preconditioningreducing ischemic time. Occasionally, the patient event, and again at 24 hours (a “second window”may require inotropic support during the OPCAB of protection). There are several proposed mecha-procedure. In some patients, ischemic mitral regur- nisms for both acute and late preconditioning. In thegitation develops of worsens with heart manipula- acute phase, the preconditioning involves an alter-tion, positioning and ischemia. In addition to the ation of the Katp channel. Late protection involvessteps outlined above to support the systemic BP, heat shock protein synthesis.milrinone may be effective in this circumstance. Several pharmacologic agents can induce ischemicObviously, the quicker the operative procedure and preconditioning like effects. Recent work sug-the less time the heart is ischemic, the better the gests that some anesthetic agents may possesspatient will tolerate the procedure. One last cau- pharmacologic ischemic preconditioning properties.tion involves the occurrence of sudden, significant Anesthetic preconditioning (APC) is defined as thedysrhythmias during OPCAB. Occasionally, upon administration of a volatile anesthetic before thereperfusion, the heart may respond with multi- period of myocardial ischemia. In animal studies,focal premature contractions, ventricular tachy- contractility is preserved and infarct size is reducedcardia, or even ventricular fibrillation. Awareness approximately 40%. The mechanism of the APCof this potential and prompt intervention for fib- effect is likely multifactorial and includes preser-rillation is essential. In most cases, the ventricular vation of adenosine triphosphate (ATP) and highdysrhythmias are self-limiting. energy phosphates, decreased polymorphonuclear There are many potential methods to reduce neutrophil (PMN) adhesion during reperfusion,the impact of the obligate ischemic insult. Main- reduced calcium loading and alteration of the Katptaining a normal acid-base balance and electrolyte channel (Fig. 4.15).profile are important. In addition, pharmacologic There are compelling animal data in multipleinterventions may include nitroglycerin infusion, studies affirming the anesthetic preconditioningmagnesium supplementation, use of calcium antag- effects of the volatile anesthetics. In clinical prac-onists (with the anticipated ischemic-reperfusion tice, the data remains indirect and there is currentlyinjury and possible calcium overload), tight glu- no clear translated therapeutic approach utiliz-cose control, and choice of anesthetic and ischemic ing APC. Anesthetic preconditioning is difficultpreconditioning. to demonstrate clinically because of the compli- cated patient scenario, the hemodynamic alter-Ischemic preconditioning and ations during surgery, and the uncontrolled mix ofanesthetic preconditioning anesthetic, analgesics and vasoactive medicationsIschemic preconditioning is process whereby short, used during surgery. In vitro, isoflurane, sevoflu-transient periods of tissue ischemia render the tissue rane, and desflurane all enhance muscle recov-resistant to subsequent usually lethal periods of ery in atrial tissue after an ischemic-reperfusionischemia. This process exists in many organ systems event. Isoflurane immediately before aortic cross-in the body including the heart, kidneys, lungs, clamping in patients undergoing CABG decreasesbrain and spinal cord. In the myocardium, ischemia the troponin I and creatine kinase-MB releaseresults in an immediate reduction in contractile postoperatively. There is reduced ST segment
    • 116 Chapter 4 Volatile anesthetics G-protein-coupled receptors Extracellular G K+ PKC ROS K+ Volatile anestheticsFig. 4.15 Multiple endogenous signaling pathways intracellular kinases, or have direct effects onmediate volatile anesthetic-induced myocardial mitochondria to generate reactive oxygen species (ROS)protection. A trigger initiates a cascade of signal that ultimately enhance KATP channel activity. Volatiletransduction events, resulting in the activation of an anesthetics may also directly facilitate KATP channelend-effector that promotes resistance against ischemic opening. Dashed arrows delineate the intracellular targetsinjury. Mitochondrial adenosine triphosphate-sensitive that may be regulated by volatile anesthetics; solid arrowspotassium (KATP ) channels have been implicated as the represent potential signaling cascades. (From Tanaka K,end-effector in this protective scheme, but sarcolemmal Ludwig LM, Kersten JR et al. Mechanisms ofKATP channels may also play a role. Volatile anesthetics cardioprotection by volatile anesthetics. Anesthesiologysignal through adenosine and opioid receptors, modulate 2004;100:707–21, with permission.)G proteins, stimulate protein kinase C (PKC) and otherchanges and preservation of cardiac index com- in advanced techniques of pain control includingpared to inpatients who did not receive pre- intrathecal and epidural analgesia. In the acutetreatment with a volatile anesthetic. In off-pump setting, pain is largely surgical in origin; persistentCABG, patients randomized to sevoflurane had less pain may be due to tissue destruction, intercostaltroponin I release compared to those randomized to nerve trauma, rib fractures, wound infection, thepropofol. sternal wires, or nonunion of the sternum. The In summary, ischemic preconditioning and anes- techniques for postoperative analgesia are manythetic preconditioning are new and exciting areas of including local anesthetic infiltration, nerve blocks,investigation. The full clinical impact of these phys- opioids, nonsteroidal anti-inflammatory agents,iologic and pharmacologic mechanisms remains to α-adrenergic drugs, and intrathecal and epiduralbe determined. techniques. Each technique has unique advantages and disadvantages.Intrathecal and epidural anesthesia and Intrathecal analgesia has been widely investigatedanalgesia for cardiac surgery since the 1980s. Intrathecal opioids (morphine, fen-Pain after cardiac surgery may be severe and limit tanyl, sufentanil) reliably extend the duration ofpatient recovery. Traditionally, pain treatment is analgesia without significant impact on extubationwith IV opioids; however, there is recent interest times. The addition of clonidine to the opioid further
    • Anesthesia for Myocardial Revascularization 117enhances the opioid effect. Some authors have Glucose management duringadministered hyperbaric bupivacaine (20–30 mg), coronary artery bypass surgeryhyperbaric lidocaine (150 mg), or both with mor- Recent data suggest that tight perioperative controlphine to induce a “total spinal” and complete of blood glucose in diabetic patients improvesthoracic cardiac sympathectomy. This technique outcome after cardiac surgery (Fig. 4.16). Hyper-reduces β-receptor dysfunction and lowers the stress glycemia has several adverse effects on the heartresponse (as measured by circulating epinephrine, after an ischemic-reperfusion injury. In animalnorepinephrine and cortisol levels) during CABG models, blood glucose correlates with infarct sizesurgery. As predicted, the fall in HR and BP in and the beneficial effects of ischemic precondi-the majority of these patients required pharmaco- tioning are abolished with hyperglycemia. Further,logic intervention. The role of total spinal anesthesia hyperglycemia reduces coronary collateral bloodfor CABG is controversial and remains undefined flow through a nitric-oxide-mediated mechanism.at this time. In summary, although safe, intra- Effective treatment with insulin during the peri-thecal administration of analgesics reliably produces operative period is enhanced with a continuousanalgesia, however, there is no additional clinical infusion of insulin as compared to intermittentbenefit. bolus insulin. Most agree that maintaining a glucose The same is true of epidural analgesia. Multiple level < 200 mg/dL is appropriate. Some evidenceclinical reports demonstrate that thoracic epidural suggests that insulin therapy should be initiatedanalgesia is associated with good pain control, but when the glucose level is > 110–150 mg/dL.there is limited benefit beyond this single measure.For both intrathecal and epidural techniques, there Emergency coronary arteryis no evidence of improved outcome in mortality bypass surgeryor MI. Anesthesia for emergency coronary artery bypass Both techniques carry risk. Hypotension is com- surgery provides some unique challenges. Thesemon and can be significant. Administration of patients typically are those suffering from complica-local anesthetics always carries the risk of IV tions of cardiac catheterization or of catheter-basedabsorption and myocardial depression. Dense anal- interventional techniques to treat coronary stenosis.gesia may mask postoperative myocardial ischemia. Patients presenting with failed coronary angioplastyNeuroaxial opioids are associated with pruritus, procedures fall into three categories:nausea and vomiting, urinary retention, and res- 1 Hemodynamically stable, nonischemic patients.piratory depression. Finally, and perhaps most Some of these patients will have sustained noconcerning, is the risk of spinal hematoma for- endothelial damage and can be managed as electivemation. The incidence of hematoma formation is coronary revascularization patients. Some patientsapproximately 1:220 000 for intrathecal instrumen- will have sustained endothelial damage and are attation and 1:150 000 for epidural instrumentation. risk for subsequent thrombus formation and vesselThis risk increases in the cardiac surgical patient closure. These patients may require surgical revas-because of the systemic heparinization; however, cularization but can afford to wait several hours.it is difficult to quantify this risk. This is time enough to complete a comprehensive In summary, intrathecal and epidural techniques anesthetic evaluation and to allow further gastricare practiced in some hospitals with good results. emptying if necessary.The data affirm reliable analgesia, but there is no 2 Hemodynamically stable, ischemic patients. Theseimprovement in mortality or MI. Other parame- patients require urgent revascularization. Theters, such as dysrhythmias, respiratory failure and ischemic interval should be limited to < 3 hoursearly extubation may be improved with regional to avoid infarction. An intra-aortic balloon pumptechniques (Table 4.3). There remains significant may be in place to temporize this condition. Anes-controversy regarding the role of these techniques thetic evaluation should be concise and focused.in adult cardiac surgical practice. Communication with the cardiologist is essential to
    • 118 Chapter 4 Table 4.3 Outcomes for thoracic epidural analgesia (TEA) and intrathecal analgesia (IT) versus general anesthesia (GA) for cardiac surgery. A meta-analysis of 15 trials enrolling 1178 patients having neuroaxial analgesia after cardiac surgery demonstrates no differences in the rates of mortality or myocardial infarction after coronary artery bypass grafting with central neuroaxial analgesia. There were associated improvements in faster time until tracheal extubation, decreased pulmonary complications and cardiac dysrhythmias in reduced pain scores. The majority of these benefits, however, may be reduced or eliminated with changing cardiac practice using fast track techniques, use of beta-blocking agents, amiodarone, or nonsteroidal anti-inflammatory drugs for postoperative analgesia. (From Liu SS, Block BM, Wu CL. Effects of perioperative central neuraxial analgesia on outcome after coronary artery bypass surgery. Anesthesiology 2004;101:155–61.) Outcome No. TEA GA OR or WMD P-value (95% confidence interval) Death 1178 0.7% 0.3% 1.56 (0.35–6.91) 0.56 Myocardial infarction 1026 2.3% 3.4% 0.74 (0.34–1.59) 0.44 Dysryhthmias 913 17.8% 30% 0.52 (0.29–0.93) 0.03 Pulmonary complications 644 17.2% 30.3% 0.41 (0.27–0.60) <0.00001 Time to tracheal extubation (h) 905 6.9∗ 10.4∗ −4.5 (−7 to −2) 0.0005 VAS pain score at rest (mm) 392 12.4∗ 19.6∗ −7.8 (−15 to −0.6) 0.03 VAS pain score with activity (mm) 222 14∗ 27.6∗ −11.6 (−19.7 to −3.5) 0.005 Death 668 0.3% 0.6% 0.88 (0.13–5.72) 0.89 Myocardial infarction 290 3.9% 5.7% 0.75 (0.24–2.31) 0.61 Dysryhthmias 204 24.8% 29.1% 0.81 (0.42–1.53) 0.51 Time to tracheal extubation (h) 588 10.4∗ 10.9∗ −0.85 (−1.83 to 0.12) 0.09 Time to tracheal extubation for 189 7.1∗ 9.3∗ −1.2 (−1.8 to −0.7) <0.0001 small-dose IT (h) Morphine use per day (mg) 816 14∗ 22∗ −11 (−15 to −7) <0.00001 VAS pain score (mm) 315 13.4∗ 23.4∗ −16 (−27 to −4.9) 0.005 Pruritus 506 10.1% 2.5% 2.9 (1.2–6.7) 0.01 Nausea/vomiting 490 31.3% 28.5% 1.27 (0.81–2.0) 0.3 Random effects model used for all analyses. ∗ Weighted by number of subjects. GA, general anesthesia; IT, intrathecal analgesia; OR, odds ratio; TEA, thoracic epidural analgesia; VAS, visual analog scale; WMD, weighted mean difference (inverse variance method).determine the extent of jeopardized myocardium, high risk for aspiration, a nonparticulate antacid andcurrent vasoactive agents, anticoagulation methods metoclopramide 10–20 mg IV can be administered.(heparin, streptokinase, tissue plasminogen activa- A rapid sequence induction can be accomplishedtor (tPA), clopidogrel, and abciximab), NPO status, with etomidate 0.15–0.30 mg/kg and succinyl-current laboratory values, and vascular access. The choline 1.0–1.5 mg/kg, in conjunction with fen-arterial access used for the catheterization proce- tanyl (10 µg/kg) or sufentanil (1 µg/kg). Etomidatedure (femoral artery) should be left in place and produces minimal cardiovascular effects at thisused for monitoring in the operating room. Femoral dosage when administered in conjunction withvein sheaths can be used for venous access. A PAC narcotics. Alternatively, sufentanil 5 µg/kg and suc-is commonly placed via the femoral vein and can be cinylcholine 1.0–1.5 mg/kg can be used in a rapid-used as well. Induction can be accomplished eas- sequence technique. Hypotension and ischemiaily and safely using the high-dose narcotic tech- must be aggressively treated. After induction, place-nique described previously. For patients deemed at ment of additional intravascular catheters can be
    • Anesthesia for Myocardial Revascularization 119 70 The femoral vein PAC often is not in a sterile 60 ∗ Poor intraoperative glycemic control sheath and is distant from the head of the bed. If % of patients with morbidity Tight intraoperative glycemic control peripheral venous access is poor, a large-bore dou- 50 ∗ ble lumen (16- or 14-gauge) central venous line 40 can be placed at the same time as the PAC. Because 30 these patients usually are anticoagulated with at ∗ least heparin, placement of these catheters using 20 ∗ ultrasonic guidance should be considered. ∗ ∗ 10 3 Hemodynamically unstable, ischemic patients. These patients require emergent revascularization. 0 Total CV Resp. Inf. Renal Neuro. Others Evaluation must often be performed in the hallwayFig. 4.16 Incidence of severe in-hospital morbidity on the way to the operating room. Communicationbetween patients in whom intraoperative glycemic with the cardiac catheterization team is essential.control was poor or tight. Two hundred consecutive Some of these patients are mildly hypotensive,diabetic patients undergoing on-pump heart surgery requiring minimal cardiovascular pharmacologicwere enrolled. A standard insulin protocol based on support; whereas, others may be intubated andsubcutaneous intermediary insulin was given the receiving cardiopulmonary resuscitation (CPR). Themorning of the surgery. Intravenous insulin therapy wasinitiated intraoperatively from blood glucose goal is to establish CPB as expeditiously as possible.concentrations of 180 mg/dL or greater and titrated Vascular access for monitoring and volume infusionaccording to a predefined protocol. Poor intraoperative can be obtained on the surgical field if necessary.glycemic control was defined as four consecutive blood All existing intravascular access should be used.glucose concentrations >200 mg/dL without any decrease For more stable patients, the induction techniquesin despite insulin therapy. Postoperative blood glucose described above are applicable. For patients receiv-concentrations were maintained below 140 mg/dL by ing CPR, scopolamine 0.005 mg/kg or midazolamusing aggressive insulin therapy. The main endpointswere severe cardiovascular, respiratory, infectious, 0.05–0.1 mg/kg in conjunction with a nondepolar-neurologic, and renal in-hospital morbidity. Insulin izing muscle relaxant may be all that is necessary.therapy was required intraoperatively in 36% of patients, Although the in-hospital mortality is high (approxi-and poor intraoperative glycemic control was observed in mately 50%), there are good data demonstrating a18% of patients. Poor intraoperative glycemic control benefit to emergency surgical intervention (surgerywas significantly more frequent in patients with severe or angioplasty) versus initial medical stabilization inpostoperative morbidity (37 vs. 10%; P < 0.001). The patients presenting in cardiogenic shock after a MIadjusted odds ratio for severe postoperative morbidityamong patients with a poor intraoperative glycemic (Fig. 4.17).control as compared with patients without was 7.2(95% confidence interval, 2.7–19.0). CV, cardiovascular Post-CPB managementmorbidity; Inf., infectious morbidity; Neuro., neurologic The assumption that coronary revascularization willmorbidity; Resp., respiratory morbidity (see text for produce a patient with normal myocardial func-definitions of different morbidities). ∗ P < 0.05 vs. tight tion after CPB is erroneous. Immediate improve-control. (From Ouattara A, Lecomte P, Le Manach Y et al. ments in LV systolic and diastolic function mayPoor intraoperative blood glucose control is associatedwith a worsened hospital outcome after cardiac surgery occur within the first 10 minutes after terminationin diabetic patients. Anesthesiology 2005;103:677–94, of CPB; however, many patients require inotropicwith permission.) and vasoactive support. There may be depression of both RV and LV systolic function (reduced EF, LVaccomplished in parallel with the surgical prepara- stroke work index (SWI), cardiac index (CI)) withtion. In particular, a PAC can be placed via the right the nadir occurring approximately 4 hours afterinternal jugular vein. This substantially improves termination of CPB.the ability to manipulate and position the PAC Coronary revascularization may be less thanand to infuse vasoactive agents at a proximal site. complete for technical reasons, such as occurs with
    • 120 Chapter 4 100 saphenous vein grafts. In humans, infusion of epinephrine to increase systemic BP during the 80 post-CPB period increases IMA graft flow, nore- Percentage 60 pinephrine infusion does not change IMA graft flow, and phenylephrine infusion reduces IMA 40 graft flow. Some animal models suggest that such 20 changes are due to the effects of vasoactive sub- stances on IMA vascular tone, whereas others impli- 0 cate changes in systemic BP. In humans, vasopressor IMS ERV IMS ERV IMS ERV 2 weeks 6 months 1 year associated increases in systemic BP are accompa- post-discharge post-MI post-MI nied by increases in saphenous vein graft flows.Fig. 4.17 Outcome of 126 SHOCK trial hospital Additional work is required to determine moresurvivors with at least one interview, 69 assigned to the precisely how changes in graft vascular resistance,emergency revascularization (ERV) group and 57 systemic BP, and myocardial oxygen consumptionassigned to the initial medical stabilization (IMS) group.There were significant differences between treatment contribute to these flow variations. Nonetheless, itgroups at 6 months (P = 0.035) and 1 year (P = 0.014). should be kept in mind that the choice of vasopres-White bars = New York Heart Association (NYHA) sor may affect flow through engrafted arteries andfunctional class I/II; ruled bars = NYHA functional class veins.III/IV; black bars = deceased. MI, myocardial infarction. Inadequate myocardial protection during the(From Sleeper LA, Ramanathan K, Picard MH et al. procedure will adversely affect LV systolic function.Functional status and quality of life after emergency This is particularly likely if the patient has sufferedrevascularization for cardiogenic shock complicatingacute myocardial infarction. J Am Coll Cardiol a preoperative ischemic event or has poor preop-2005;46:266–73, with permission.) erative ventricular function. In these patients, opti- mization of preload and HR are necessary first stepssmall distal vessels. Communication with the sur- in obtaining hemodynamic stability. Patients withgeon is necessary to determine the success of the compromised systolic function are often dependentoperative procedure. The sense of security that on HR for increases in CO. In addition, patients withaccompanies a “successful” operative procedure reduced ventricular compliance and distensibilitymust be tempered with the knowledge that a signifi- will be dependent on atrial systole to provide an ade-cant number of patients (35–50%) continue to have quate LVEDV without a high mean PCWP. For theseevidence of myocardial ischemia in the post-bypass reasons, pacing of the atrium (with intrinsic con-period after apparently successful revascularization. duction via the atrioventricular (AV node) or of theMost episodes occur in the immediate (0–8 hours) atrium and ventricle (when AV nodal dysfunctionpostoperative period. The development of post- exists) may be necessary.CPB RWMA and the development of ECG-detected Attention to the metabolic condition of theischemia in the immediate postoperative period are patient is required in the postoperative period.both associated with adverse clinical outcome. These patients often require electrolyte supplemen- There may be alterations in the vascular tone tation (potassium and magnesium), as well as strictof the native coronary circulation during the post- ventilatory management to control acid-base bal-CPB period. Coronary vasospasm may occur distal ance in the immediate hours after CABG. Thereto bypass grafts or in segments of artery that have are significant issues regarding continued ther-not been bypassed. This usually is heralded by the mal regulation, coagulation and glycemic control.presence of elevated ST segments in the absence There is a growing body of research in the areaof a precipitating hemodynamic event. Spasm is of strict glycemic control. Several authors haveeffectively treated with IV nitroglycerin. published data suggesting that tight control of glu- Vasoactive substances used during the post-CPB cose (110–150 mg/dL) is associated with superiorperiod may affect flow through the IMA and outcome in both critically ill patients and those
    • Anesthesia for Myocardial Revascularization 121after CABG. A regular insulin infusion (2–8 units/h) The most commonly used inotropic agents areis indicated when the glucose is >150 mg/dL. described below. Use of inotropic agents post-CPB Optimization of preload after termination of CPB should be used with the knowledge that both adultsrequires careful attention and is facilitated by use and children exhibit uncoupling of β-adrenoceptorsof TEE and the PCWP and CVP. Preload reserve from the Gs -protein-adenylate cyclase complex(preload recruitable stroke work) can be assessed after CPB. This desensitization may contribute to aby infusion of blood from the CPB circuit in incre- relative catecholamine resistance in the post-CPBments of 10–15 mL/kg (“give a hundred”). One period.of three distinct hemodynamic responses will beobserved: Dopamine• Intact preload reserve. Infusion of volume produces Dopamine possesses β1 -adrenergic, α1 -adrenergic,an increase in MAP with little or no change in and dopaminergic activities. Some of the α activ-PCWP or CVP. TEE demonstrates normal LV and ity is due to release of endogenous norepinephrine.RV chamber volume. CO increases. For this subset At doses of 2–3 µg/kg/min, the dopaminergic activ-of patients, further infusion of volume to improve ity is maximal, resulting in preferential dilationhemodynamics is warranted. of renal, mesenteric, and coronary vasculature.• Optimized preload. Infusion of volume produces lit- Alpha-agonists do not antagonize this dopaminer-tle or no change in MAP with no change or a small gic activity. This makes dopamine a useful agentincrease in PCWP or CVP. TEE demonstrates a LV for preservation of renal blood flow in the pres-or RV at the upper limits of size for the particular ence of α-agonists. β1 -Induced enhanced inotropypatient. Obviously, pre-CPB assessment of LV and occurs at doses between 1 and 10 µg/kg/min; how-RV dimensions is necessary to take full advantage of ever, at doses above 4–6 µg/kg/min dopamine’sthis modality. CO may increase slightly or remain α-adrenergic activity increases such that SVR, PVR,unchanged. For this subset of patients, no further and PCWP increase with little concomitant increaseinfusion of volume to improve hemodynamics is in CO. This combination of increased ventricularwarranted. wall radius and afterload may cause detrimen-• Exhausted preload reserve. Infusion of volume will tal increases in myocardial oxygen consumption.produce no change or a fall in MAP with a substan- At doses >10 µg/kg/min, the α-adrenergic effectstial increase in PCWP or CVP. TEE will demonstrate of dopamine predominate, producing vasoconstric-a distended LV or RV. CO may decrease slightly tion. Dopamine’s chronotropic and dysrhythmicor should remain unchanged. For this subset of effects increase as the dose increases.patients, no further infusion of volume to improvehemodynamics is warranted. Initiation of inotropic Dobutaminesupport will improve hemodynamics and reduce Dobutamine possesses β1 -, β2 -, and α1 -adrenergicventricular dimensions. activities. The predominant effect is enhanced Several risk factors are associated with an inotropy through βl stimulation. The β2 and α1increased incidence of inotropic agent use after activities are balanced such that mild vasodi-CPB. Factors related to inotrope use include low lation occurs at the commonly used dosesEF <55%, older age, cardiac enlargement, female from 5–20 µg/kg/min. Dobutamine decreases PVR,sex, and higher baseline and post-contrast LVEDP. blunts hypoxic pulmonary vasoconstriction, andFor patients with an EF >55%, the presence of increases coronary blood flow. Dobutamine maypreoperative wall motion abnormalities and an actually reduce myocardial oxygen consumption inincrease of >10 mmHg in LVEDP with contrast the failing heart. Although dobutamine increasesinjection is associated with the need for inotropes. contractility, it reduces LV radius and end-diastolicIn addition, for patients with an EF > 45%, pro- pressure while increasing arterial pressure andlonged duration of CPB is associated with the need maintaining HR. Dobutamine is less likely to causefor inotropes. tachycardia than dopamine.
    • 122 Chapter 4Epinephrine (cAMP). In addition, milrinone possesses vasodila-Epinephrine possesses β1 -, β2 -, and α1 -adrenergic tor activity by virtue of PDE III inhibition in vascularactivities. At doses of 1–3 µg/min, epinephrine has smooth musc1e. Milrinone increases cardiac index,a potent inotropic effect mediated through β1 stim- reduces LVEDP and LVEDV, reduces systolic BP,ulation, with little effect on vasomotor tone due to and has little effect on HR. Like dobutamine in thethe balance of β2 and α1 stimulation. As the failing heart, this increase in cardiac index may bedose increases above 3 µg/min, progressively more associated with a decrease in myocardial oxygenα1 activity occurs, with resultant mixed inotropic consumption due to the concomitant reduction inand vasoconstrictive effects. Doses above 3 µg/min wall stress. Milrinone reduces PVR.also cause progressive decreases in renal blood flow. Milrinone does not act via βl -receptors, and isAbove 10 µg/min, epinephrine is primarily a vaso- synergistic with βl -agents in augmenting inotropy.constrictor. Epinephrine’s vasoconstrictive effects Evidence demonstrates that PDE III inhibitors arealso reduce venous capacitance. Although coronary at least as effective as epinephrine in improvingblood flow is maintained, epinephrine may not be post-CPB function and that the combination of thefavorable to myocardial oxygen balance, because in two agents produces effects at least as large as theaddition to increasing contractility, it increases sys- sum of the two agents individually. The benefit oftolic BP, increases LVEDV and pressure, and reduces the two agents together is particularly marked fordiastolic BP while increasing HR. the RV. Epinephrine is often the agent of choice to ter- Milrinone requires a 50 µg/kg loading dose fol-minate CPB. The potent inotropic and balanced lowed by an infusion of 0.375–0.500 µg/kg/min.peripheral vascular effects allow prompt, reliable Loading milrinone while on CPB just beforetermination of CPB while avoiding the ventricular termination attenuates the effects of the acutedistension and systemic hypotension that compro- vasodilation.mise subendocardial perfusion. Critics point outthat the potent inotropic effects of epinephrine Levosimendanmay not be necessary in every instance, and thus, The catecholamines and PDE III inhibiting drugsepinephrine’s potentially deleterious effects on the act through different pathways to increase inotropymyocardial and renal blood flow can be avoided if by ultimately increasing intracellular calcium con-another agent is selected. centration (Fig. 4.18). Levosimendan is a new inotropic agent that acts without increasing intra-Norepinephrine cellular calcium concentration. There is increasedNorepinephrine possesses βl - and α1 -adrenergic inotropy without impairment of diastolic function.activity. The α1 effects of norepinephrine are man- Levosimendan is a myofilament calcium sensitizerifest at low doses (1–2 µg/min) and predominate as that increases myocardial contractility by stabiliz-the dose increases. Norepinephrine reduces renal ing the calcium bound conformation of troponin C.blood flow, elevates both systolic and diastolic The systolic interaction of actin and myosin is pro-BP, reduces venous capacitance, and generally longed. The enhanced calcium binding is dependentcauses a reflex decrease in HR. Although coro- on the intracellular calcium concentration, withnary blood flow is maintained, norepinephrine may augmentation occurring in the presence of highernot be favorable to myocardial oxygen consump- systolic calcium concentrations; however, the aug-tion, because there is increased contractility and mentation is unaffected by the lower calcium con-afterload. centrations during diastole. This selective action preserves diastolic relaxation and diastolic function.Milrinone In addition to the inotropic effects, levosimendanMilrinone is a potent inotropic agent that acts by inhibits PDE III in higher concentrations. The druginhibiting phosphodiesterase III (PDE III) to increase causes vasodilation and an increase in HR. Finally,intracellular cyclic adenosine monophosphate levosimendan stimulates ATP-sensitive potassium
    • Anesthesia for Myocardial Revascularization 123 Ca2+ β-AR voltage-gated Na+ Ca2+ Catecholamines L-type Ca2+-channel ATP Gs A PDE III-inhibitors P Digoxin C K+ Na+ PDE III Ca2+ ATP cAMP Calcium-induced Ca2+ release PKA SR P Tnl RyR2 Actin Ca2+ Ca2+ TnC Myosin P PL Levosimendan Ca2+ ATP Ca2+ SERCA2Fig. 4.18 Schematic illustration mechanism of action of troponin C (TnC) and initiates contraction (inotropicpositive inotropic drugs. β-adrenergic stimulation effect). Phosphorylation of PL enhances relaxation by(catecholamines) and phosphodiesterase (PDE) III increased reuptake of Ca2+ back into the SR by the SRinhibition increase cyclic adenosine monophosphate Ca2+ adenosine triphosphatase isoform 2 (SERCA2)(cAMP), which acts via protein kinase A (PKA) to (lusitropic effect). Phosphorylation of TnI enhances thephosphorylate calcium channel protein, phospholamban rate of relaxation by decreasing the sensitivity of(PL), and troponin I (TnI). Phosphorylation (P) of myofilaments to Ca2+ . Levosimendan binds to TnCcalcium channel protein enhances sarcolemmal inward during systole and thereby increases the sensitivity ofmovement of Ca2+ , which subsequently increases Ca2+ myofilaments to Ca2+ without alteration of Ca2+ levels.movement from the sarcoplasmic reticulum (SR) AC, adenylate cyclase; ATP, adenosine triphosphate;through the calcium release channel (ryanodine receptor β-AR, β-adrenoceptor; Gs , stimulatory guaninetype 2, RyR2) to the cytosol (calcium-induced Ca2+ nucleotide binding proteins. (From Toller WG, Stranz C.release). Digoxin increases cytosolic Ca2+ by inhibition Levosimendan, a new inotropic and vasodilator agent.of sarcolemmal Na+ –K+ –adenosine triphosphatase and Anesthesiology 2006;104:556–69, with permission.)Na+ –Ca2+ exchange. Cytosolic Ca2+ binds tochannels, which improves coronary blood flow, shock, and use in the perioperative period in cardiacreduces preload and afterload, and may have rel- surgical patients. Currently the drug is approvedevant anti-ischemic actions. for 24-hour administration due to its metabolism At the time of this writing, levosimendan is yielding biologically active metabolites (OR-1896, aapproved for use in over 30 countries world-wide, weak calcium sensitizing agent and PDE III inhibitorand there are ongoing trials in the United States and with an elimination half life of 96 hours). InEurope. Indications for the drug include treatment placebo-controlled trials of cardiac surgical patients,for the acute decompensation of CHF, inotropic levosimendan effectively increased HR, MAP, andsupport during myocardial ischemia, cardiogenic CO. There were decreases in SVR, SV, and PVR.
    • 124 Chapter 4Levosimendan was administered in either an 18 or a small dose (0.5–1.0 µg/min) of norepinephrine36 µg/kg bolus and 0.2–0.3 µg/kg/h infusion. to normalize SVR. As the doses of epinephrine and dopamine are increased, SVR may increase,Calcium and the addition of nitroprusside to the inotropicCalcium chloride 5–10 mg/kg is a commonly may be necessary to reduce afterload and improveused adjuvant during termination of CPB. Recent systolic performance. Epinephrine in combina-evidence, however, suggests that calcium admin- tion with nitroprusside is a reliable approach toistration may be no better than placebo in aug- severe ventricular failure. Elevations of PCWPmenting LV function, RV function, and CI after above 15–18 mmHg should be treated with nitro-emergence from CPB. Calcium administration does glycerin to prevent ventricular dilatation and pul-increase MAP, however. monary congestion and to improve subendocardial The higher doses of calcium (10 mg/kg) can blood flow.attenuate the effects of inotropic agents that are The addition of milrinone is useful when theseβ-adrenergic receptor agonists, such as dobutamine measures fail to produce acceptable hemodynam-and epinephrine. No such effects are seen with mil- ics (CI > 2 L/min/m2 , PCWP < 18 mmHg, CVP <rinone. A recent investigation suggests that entry 15 mmHg, systolic BP > 90 mmHg, or MAP >of calcium ions through calcium channels atten- 50 mmHg). More specific guidelines for treatmentuates adenylyl cyclase, which may explain the of RV dysfunction are addressed in Chapter 7.observation. Continued LV and RV dysfunction in the setting of Ionized calcium levels decrease during CPB but aggressive inotropic and vasodilator support is anapproach normal before separation from CPB. indication for placement of a mechanical circulatoryHypocalcemia is rarely present as an indication for assist device, as discussed in Chapter 11.calcium administration, except perhaps in neonatesand infants, who are more prone to hypocalcemia. Long-term outcome after CABGIn addition, because loss of calcium homeostasis is More than 800 000 patients undergo CABG surgeryone of the hallmarks of ischemia, the administration each year around the world. The patient populationof calcium in the vulnerable reperfusion interval is changing (older patients with more significantafter aortic cross-clamp removal may exacerbate cell morbidities), and the pharmacologic and surgicalinjury and death. interventions are ever evolving. Nonetheless, CABG For routine termination of CPB in which remains a mainstay therapy. The long-term adverseSVR is in the normal range and inotropic sup- events after CABG are many and reflect the mor-port is needed, epinephrine, 0.015–0.05 µg/kg/min, bidities and insult seen in this population. In adopamine, 1–5 µg/kg/min, or dobutamine, recent review of 176 studies (205 717 patients)5–10 µg/kg/min, are reasonable choices because the in-hospital adverse events were death (1.7%);they provide inotropic support with little concomi- nonfatal MI (2.4%); nonfatal stroke (1.3%); gastro-tant vasoconstriction and afterload increase. For intestinal bleeding (1.5%); and renal failure (0.8%).situations in which cardiac index is low and SVR is The 30-day mortality was 2.1%. Meta-analyseselevated, therapy with a vasodilator such as nitro- show that age greater than 70 years, female sex, lowprusside may be all that is necessary to relieve EF, history of stroke, MI, or heart surgery, and theafterload mismatch. If an inotrope is necessary in presence of diabetes or hypertension are all asso-this situation, dobutamine is a good choice because ciated with increased 30-day mortality after CABGit possesses some vasodilatory activity. (Table 4.4). When the CI remains low (<2.0 L/min/m2 ), it is Longer-term outcome is also a subject of greatappropriate to increase the inotrope dose or add interest. Recent work in patients with multivessela second agent. Dobutamine may be increased disease demonstrates that there is no difference into 15–20 µg/kg/min; however, the progressive mortality between stenting and surgery (Fig. 4.19).decrease in SVR may require the addition of There is no difference in stroke or MI between these
    • Table 4.4 Post-coronary artery bypass graft surgery (CABG) adverse event incidence and mortality in 205 717 patients. In-hospital adverse event incidence MI Non-fatal MI Stroke Non-fatal GI bleeding Renal Mortality 30-day stroke failure mortalityAll CABG Mean % (SE) 3.89 (0.66) 2.44 (0.28) 2.24 (0.27) 1.32 (0.15) 1.46 (0.29) 0.79 (0.15) 1.65 (0.14) 2.06 (0.16) Median % 2.94 2.44 1.8 1.29 1.23 0.67 1.54 1.99 n (k) 69 487 (52) 11 973 (52) 26 750 (21) 31 132 (52) 12 897 (8) 22 798 (23) 75 933 (105) 81 136 (70)North America Mean % (SE) 3.56 (0.59) 2.82 (0.58) 2.29 (0.39) 1.25 (0.19) 1.11 (0.14) 0.88 (0.16) 1.96 (0.20) 2.00 (0.19) Median % 3.30 2.83 1.71 1.06 1.01 0.86 2.00 1.98 n (k) 49 969 (32) 2454 (18) 13 777 (12) 25 555 (28) 7332 (3) 21 410 (14) 59 014 (49) 47 158 (39)Europe Mean % (SE) 2.59 (0.33) 2.55 (0.36) 2.42 (1.18) 1.30 (0.27) 1.33 (0.91) 0.99 (0.74) 1.30 (0.22) 2.21 (0.40) Median % 2.53 2.52 1.66 0.67 1.66 0.49 1.00 2.08 n (k) 13 418 (15) 8389 (24) 6515 (4) 4256 (13) 220 (2) 625 (5) 12 893 (33) 21 156 (21)Multinational/other Mean % (SE) 9.81 (5.54) 1.94 (0.51) 2.43 (0.22) 1.27 (0.31) 1.93 (0.62) 0.06 (0.16) 1.38 (0.33) 1.72 (0.38) Median % 3.92 1.66 2.18 1.96 1.32 0.00 1.52 1.61 n (k) 6100 (5) 1130 (10) 6458 (5) 1321 (11) 5345 (3) 763 (4) 4026 (23) 13 240 (10)Elective CABG Mean % (SE) 2.84 (0.81) 2.32 (0.40) 2.35 (0.60) 1.01 (0.21) 1.18 (0.48) 0.45 (0.18) 1.48 (0.19)∗ 1.50 (0.29)∗ Median % 2.17 2.00 1.59 0.64 1.23 0.22 1.00 1.23 n (k) 3313 (17) 3371 (32) 1680 (7) 9170 (24) 510 (2) 1333 (6) 7912 (47) 7764 (21)Mixed CABG Mean % (SE) 4.32 (0.89) 2.64 (0.36) 2.21 (0.31) 1.51 (0.20) 1.50 (0.35) 0.89 (0.18) 1.81 (0.18)∗ 2.23 (0.19)∗ Median % 3.22 2.59 1.86 1.56 1.24 0.89 1.89 2.07 n (k) 66 174 (35) 8602 (20) 25 070 (14) 21 962 (28) 12 387 (6) 21 465 (17) 68 021 (58) 73 372 (49)RCTs Mean % (SE) 6.26 (1.66)∗ 2.64 (0.42) 2.73 (0.98) 1.00 (0.16)∗∗ 1.23 (0.41) 0.39 (0.23)∗ 1.51 (0.21)∗ 1.57 (0.28) Median % 4.21 2.94 1.86 1.78 1.23 0.05 0.98 1.69 n (k) 3449 (22) 2604 (34) 1111 (5) 3790 (19) 730 (4) 2189 (10) 4949 (48) 4 913 (23)Cohort studies Mean % (SE) 2.70 (0.22)∗ 2.21 (0.38) 2.15 (0.27) 1.52 (0.18)∗∗ 1.53 (0.40) 0.98 (0.14)∗ 1.80 (0.18)∗ 2.21 (0.19) Median % 2.51 1.75 1.67 0.61 1.24 0.89 1.83 2.03 n (k) 66 038 (30) 9369 (18) 25 639 (16) 27 342 (33) 12 167 (4) 20 609 (13) 70 984 (57) 76 223 (47) Anesthesia for Myocardial Revascularization Continued p. 126 125
    • 126Table 4.4 (Continued). In-hospital adverse event incidence MI Non-fatal MI Stroke Non-fatal GI bleeding Renal Mortality 30-day stroke failure mortality Chapter 4 Single centre Mean % (SE) 2.77 (0.26)∗∗ 2.34 (0.28) 2.17 (0.37) 1.29 (0.16) 1.06 (0.23) 0.97 (0.19) 1.47 (0.15)∗ 1.87 (0.16)∗ Median % 2.55 2.37 1.60 1.40 1.16 0.84 1.30 1.83 n (k) 48 655 (40) 11 742 (49) 11 728 (16) 26 977 (47) 1977 (4) 6472 (15) 45 572 (93) 54 218 (54) Multicentre Mean % (SE) 7.87 (2.66)∗∗ 6.10 (3.50) 2.43 (0.30) 1.43 (0.41) 1.60 (0.40) 0.62 (0.22) 2.52 (0.26)∗ 2.68 (0.38)∗ Median % 4.04 6.45 2.59 1.18 1.31 0.51 2.63 2.65 n (k) 20 832 (12) 231 (3) 15 022 (5) 4155 (5) 10 920 (4) 16 326 (8) 30 361(12) 26 918 (16) Mean EF < 50% Mean % (SE) 2.79 (0.92) 1.82 (0.58) 3.81 (3.02) 0.82 (0.48) 1.47 (0.29) 1.09 (0.41) 1.45 (0.38) 1.56 (0.42) Median % 2.20 1.82 4.03 0.00 1.42 0.89 2.00 1.92 n (k) 4722 (8) 698 (5) 256 (2) 2824 (7) 1697 (1) 2758 (5) 7622 (15) 5 338 (9) Mean EF > 50% Mean % (SE) 5.99 (1.85) 2.37 (0.46) 1.69 (0.26) 1.21 (0.24) 1.02 (0.24) 0.48 (0.17) 1.68 (0.25) 1.61 (0.35) Median % 3.07 2.41 1.67 1.18 1.16 0.49 1.51 1.23 n (k) 22 213 (18) 8100 (18) 10 186 (9) 7973 (15) 1757 (2) 6567 (7) 29 121 (40) 8 535 (17) Mean age ≤ 60 yrs Mean % (SE) 3.19 (0.94) 2.49 (0.54) 2.75 (0.82) 1.41 (0.42) N/A 0.00 (2.80) 1.21 (0.27) 1.15 (0.44)∗∗ Median % 2.37 2.68 2.33 0.80 N/A 0.00 1.00 0.78 n (k) 4303 (12) 2540 (13) 1613 (5) 1273 (6) N/A 25 (1) 5885 (25) 3 260 (12) Mean age > 60 yrs Mean % (SE) 4.14 (0.84) 2.44 (0.36) 1.94 (0.23) 1.28 (0.16) 1.46 (0.29) 0.75 (0.16) 1.77 (0.16) 2.26 (0.17)∗∗ Median % 3.18 2.51 1.67 1.45 1.23 0.6 1.59 2.07 n (k) 63 035 (39) 9219 (37) 24 681 (15) 26 524 (44) 12 897 (8) 13 926 (20) 45 921 (76) 74 288 (54) No prior CABG Mean % (SE) 2.73 (0.72) 1.99 (0.46) 1.82 (0.40) 0.99 (0.31) 2.63 (1.84) 1.23 (1.10) 1.18 (0.28) 1.66 (0.35) Median % 3.33 1.83 1.27 0.66 2.63 1.00 1.00 1.81 n (k) 2606 (11) 2115 (18) 1097 (4) 3240 (10) 76 (1) 270 (4) 27 625 (25) 8 390 (14) Some patients with prior CABG Mean % (SE) 6.47 (1.83) 2.57 (0.88) 2.19 (0.34) 1.80 (0.15) 1.53 (0.40) 0.86 (0.22) 1.92 (0.25) 2.27 (0.23) Median % 3.32 1.86 1.8 1.74 1.24 0.9 2.01 2.52 n (k) 45 306 (18) 6986 (6) 19 252 (12) 17 619 (15) 12 167 (4) 16 263 (9) 32 177 (30) 48 599 (28)∗P < 0.05. ∗∗ P < 0.01.CABG, coronary artery bypass graft surgery; EF, ejection fraction; GI, gastrointestinal; MI, myocardial infarction; N/A, not available; RCT, randomized controlled trial; SE, standard error.(From Nalysnyk L, Fahrbach K, Reynolds MW et al. Adverse events in coronary artery bypass graft (CABG) trials: a systematic review and analysis. Heart 2003;89:767–72.)
    • Anesthesia for Myocardial Revascularization 127(a) (b) 100% 100% 90% 80% Event free survivalSurvlval for death 90% 70% 60% 80% 50% Bypass surgery Bypass surgery 40% p(log-rank)=0.810 p(log-rank)=0.810 Stented angioplasty Stented angioplasty 0% 0% 0 150 300 450 600 750 900 1050120013501500165018001950 0 150 300 450 600 750 900 1050120013501500165018001950 Days since randomization Days since randomization Pat. At risk 1 year 2 years 3 years 4 years 5 years Pat. At risk 1 year 2 years 3 years 4 years 5 years CABG 588 583 577 568 559 CABG 553 544 535 523 515 Stent 585 582 576 567 552 Stent 543 536 521 507 491(c) (d) 100% 100% 90% 90% Event free survivalEvent free survival 80% 80% 70% 70% 60% 60% 50% 50% Bypass surgery Bypass surgery 40% 40% Stented angioplasty p(log-rank) = 0.0001 Stented angioplasty 0% 0% 0 150 300 450 600 750 900 1050120013501500165018001950 0 150 300 450 600 750 900 1050120013501500165018001950 Days since randomization Days since randomization Pat. At risk 1 year 2 years 3 years 4 years 5 years Pat. At risk 1 year 2 years 3 years 4 years 5 years CABG 532 515 502 483 473 CABG 566 552 541 523 511 Stent 441 417 393 375 350 Stent 464 441 422 408 382Fig. 4.19 (a) Kaplan–Meier curves showing freedom patients, mortality was 13.4% in the stent group andfrom death. (b) Kaplan–Meier curves showing freedom 8.3% in the CABG group (P = 0.27; RR, 1.61; 95% CI,from death/cerebrovascular accident/myocardial 0.71–3.63). Overall freedom from death, stroke, orinfarction or revascularization. (c) Kaplan–Meier curves myocardial infarction was not significantly differentshowing freedom from death/cerebrovascular between groups (18.2% in the stent group vs. 14.9% inaccident/myocardial infarction or revascularization. the surgical group; P = 0.14; RR, 1.22; 95% CI,(d) Kaplan–Meier curves showing freedom from 0.95–1.58). The incidence of repeat revascularization wasrevascularization. A total of 1205 patients with the significantly higher in the stent group (30.3%) than inpotential for equivalent revascularization were randomly the CABG group (8.8%; P < 0.001; RR, 3.46; 95% CI,assigned to coronary artery bypass graft (CABG) surgery 2.61–4.60). The composite event-free survival rate was(n = 605) or stent implantation (n = 600). The primary 58.3% in the stent group and 78.2% in the CABG groupclinical end point was freedom from major adverse (P < 0.0001; RR, 1.91; 95% CI, 1.60–2.28). (Fromcardiac and cerebrovascular events (MACCE) at 1 year; Serruys PW, Ong AT, van Herwerden LA et al. Five-yearMACCE at 5-year follow-up constituted the final outcomes after coronary stenting versus bypass surgerysecondary end point. At 5 years, there were 48 and 46 for the treatment of multivessel disease: the final analysisdeaths in the stent and CABG groups, respectively (8.0 of the Arterial Revascularization Therapies Study (ARTS)vs. 7.6%; P = 0.83; relative risk (RR), 1.05; 95% randomized trial. J Am Coll Cardiol 2005;46:575–81, withconfidence interval (CI), 0.71–1.55). Among 208 diabetic permission.)
    • 128 Chapter 4two groups. The stenting group had a significantly Lan Kwak Y. Reduction of ischemia during off-pump coro-higher incidence of repeat revascularization. nary artery bypass graft surgery. J Cardiothorac Vasc Anesth 2005;19:667–77.Suggested reading Nalysnyk L, Fahrbach K, Reynolds MW et al. Adverse events in coronary artery bypass graft (CABG) trials:Chaney MA. Intrathecal and epidural anesthesia and a systematic review and analysis. Heart 2003;89:767–72. analgesia for cardiac surgery. Anesth Analg 2006;102: Tanaka K, Ludwig LM, Kersten JR et al. Mechanisms of 45–64. cardioprotection by volatile anesthetics. AnesthesiologyEagle KA, Guyton RA, Davidoff R et al. ACC/AHA 2004 2004;100:707–21. Guideline update for coronary artery bypass graft Van Mastrigt GA, Maessen JG, Heijmans J et al. Does fast surgery: summary article. Circulation 2004;110:1–9. track treatment lead to a decrease of intensive care unitGroban L, Dolinski SY. Transesophageal echocardio- and hospital length of stay in coronary artery bypass graphic evaluation of diastolic function. Chest 2005;128: patients? A meta-regression of randomized clinical 3652–63. trials. Crit Care Med 2006;34:1624–34.
    • CHAPTER 5Anesthesia for Valvular Heart DiseaseWhile the number of cardiac procedures for other procedures during this repair (i.e. carotidcoronary artery bypass grafting (CABG) is falling in endarterectomy, CABG, septal myomectomy,the USA, the number operations for heart valve dis- a Maze procedure (a series of surgical incisionsease is increasing. Over 5 million persons have mod- in the atrium intended to interrupt the circularerate to severe valvular regurgitation in the USA pattern of electrical activity associated with atrialalone. The aging population, expanding indications fibrillation), or other intervention)? What is thefor surgery, improvements in valve construction, clinical condition of the patient? Is the patient inand improvements in patient morbidity and mortal- a compensated or uncompensated state? With ASity after surgical intervention all suggest that valve the timing of surgery will have a great impactsurgery is likely to increase in coming years. This on outcome depending on the patient’s condition.chapter will review anesthesia for patients with a For example, a patient in the early to mid-stagesvariety of valvular heart conditions. There will be of AS will have a hyperdynamic, hypertrophiedspecial emphasis on the more common lesions of heart that will likely perform well after cardiopul-the aortic and mitral valves. monary bypass (CPB). In contrast, a patient in the late stages of AS will be in congestive heart fail- ure (CHF), have a reduced ejection fraction (EF),General considerations and will likely require extensive inotropic supportPreoperative evaluation after CPB.In valvular heart disease, there are a number of his- Review of imaging and laboratory studies istory and physical findings that directly influence essential prior to moving the patient to the oper-anesthetic management. Posting a case as “aortic ating room. Imaging of the heart will give thevalve replacement” or “mitral valve replacement” diagnosis and degree of the structural abnormality.provides no information on whether this is for aor- Preoperative echocardiography will establish thetic stenosis (AS), aortic regurgitation (AR), or both; type of lesion (stenotic versus regurgitant), the heartmitral stenosis (MS), mitral regurgitation (MR), or function, and the valve gradients. The valve area isboth. The anesthesiologist must dig further and find of critical importance in assessing any stenosis. Inout the specific valvular pathology. This knowledge patients with normal left ventricular (LV) function,is essential in preparing hemodynamic goals for the aortic valve gradients in severely stenotic lesionsinduction, maintenance, and postoperative care of may be very high (Fig. 5.1). In patients with poorthese patients. ventricular performance, there may be anatomically Additional information is required unrelated to critical lesions (aortic valve area <0.7 cm2 ) and athe valve pathology. For example, will there be low gradient. These patients are especially prone to 129
    • 130 Chapter 5 of Anesthesiologists (ASA) standard monitors, a uri- nary Foley catheter, and arterial and central lines are essential. Many institutions routinely use pul- monary artery catheters to monitor cardiac out- put (CO), mixed venous oxygenation, pulmonary artery pressures, and pulmonary capillary wedge pressures (PCWPs). Although this is standard prac- tice by many clinicians, outcome data supporting pulmonary artery catheterization are lacking. Intraoperative transesophageal echocardiogra- phy (TEE) is rapidly becoming an essential compo- nent of anesthesia for all heart valve procedures. Extensive preoperative evaluation by TEE oftenFig. 5.1 Deep transgastric long-axis transesophageal reveals previously unknown structural or func-echocardiographic image in a patient with severe aortic tional defects. In addition, TEE can provide instantstenosis. The velocity of flow is very high at 5 m/s with assessment of the status of a valve repair proce-a peak gradient of 101 mmHg and a mean gradient of dure. TEE may also diagnose perivalvular leaks67 mmHg. This is clearly severe aortic stenosis. after valvular replacement requiring prompt inter- vention. The assessment of air in the left side ofintraoperative instability with the induction of gen- the heart is important after an open-heart proce-eral anesthesia and may require significant inotropic dure. TEE may assist in locating the air therebysupport post-CPB. Other important imaging studies facilitating direct venting procedures. TEE is help-include coronary angiography to rule out concur- ful in guiding post-CPB hemodynamic interventionrent coronary artery disease, a chest radiograph, and and treatment. In recognition of this tool’s util-perhaps, thoracic computed tomography (CT) or ity in cardiac surgical procedures, the Americanmagnetic resonance imaging (MRI) to evaluate tho- Society of Echocardiography and the Americanracic anatomy. A chest X-ray is essential in “redo” Heart Association provide a class 1 recommendationoperations involving the heart and mediastinum. for TEE use in all heart valve surgical proceduresThe heart may be adhered to the posterior margin of (Table 5.1).the sternum rendering sternotomy quite hazardous. Other special monitoring devices in heart valveAll precautions including adequate venous access, surgery may include processed electroencephalo-immediate availability of blood products, and intra- gram (EEG) monitoring for either patient awarenessoperative awareness and vigilance are required in or for EEG activity during procedures in which it isthese situations. desirable that all electrical activity stop (i.e. deep Atrial natriuretic peptides are useful markers hypothermic circulatory arrest). Cerebral oximetrywhen following patients with heart failure due has no special application in surgery for heart valveto valvular pathology. In severe AS, natriuretic disease.peptides increase with increasing New York HeartAssociation (NYHA) functional classes and decreas- Premedicationing LV EF. Natriuretic peptide levels fall after Great caution is advised when prescribing pre-successful aortic valve surgery. medication in patients with valvular heart disease. In patients with preserved LV function, morphine sulfate 0.1 mg/kg intramuscularly (IM) and oralMonitoring lorazepam 1.5 hours before scheduled incision timeMonitoring during valvular surgery varies little are appropriate. Supplemental oxygen should befrom monitoring required during other types of instituted at the time of premedication. Reducingheart surgery. In addition to the American Society dosing, or no premedication at all, is indicated for
    • Anesthesia for Valvular Heart Disease 131Table 5.1 Recommendations for intraoperative echocardiography. (Reprinted from Cheitlin MD, Armstrong WF,Aurigemma GP et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography–summaryarticle: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines(ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). J Am CollCardiol 2003;42:954–70.)Class I1 Evaluation of acute, persistent, and life-threatening hemodynamic disturbances in which ventricular function and itsdeterminants are uncertain and have not responded to treatment2 Surgical repair of valvular lesions, hypertrophic obstructive cardiomyopathy, and aortic dissection with possible aorticvalve involvement3 Evaluation of complex valve replacements requiring homografts or coronary re-implantation, such as the Ross procedure4 Surgical repair of most congenital heart lesions that require cardiopulmonary bypass5 Surgical intervention for endocarditis when preoperative testing was inadequate or extension to perivalvular tissue issuspected6 Placement of intracardiac devices and monitoring of their position during port-access and other cardiac surgicalinterventions7 Evaluation of pericardial window procedures in patients with posterior or loculated pericardial effusionsClass IIa1 Surgical procedures in patients at increased risk of myocardial ischemia, myocardial infarction, or hemodynamicdisturbances2 Evaluation of valve replacement, aortic atheromatous disease, the Maze procedure, cardiac aneurysm repair, removal ofcardiac tumors, intracardiac thrombectomy, and pulmonary embolectomy3 Detection of air emboli during cardiotomy, heart-transplant operations, and upright neurosurgical proceduresClass IIb1 Evaluation of suspected cardiac trauma, repair of acute thoracic aortic dissection without valvular involvement, andanastomotic sites during heart and/or lung transplantation2 Evaluation of regional myocardial function during and after off-pump coronary artery bypass graft procedures3 Evaluation of pericardiectomy, pericardial effusions, and pericardial surgery4 Evaluation of myocardial perfusion, coronary anatomy, or graft patency5 Dobutamine stress testing to detect inducible demand ischemia or to predict functional changes after myocardialrevascularization6 Assessment of residual duct flow after interruption of patent ductus arteriosusClass III1 Surgical repair of uncomplicated secundum atrial septal defectelderly or debilitated patients, patients with poor prior to surgery. These medications are associatedventricular function, or patients with poor pul- with significant hypotension during and after CPBmonary function. Most prudently, premedication in some patients. Data on the harmful effects ofcan wait until the patient arrives in the preopera- withholding ACE-I medications are undetermined.tive holding area. At this time, the anesthesiologist Consultation with the cardiologist and surgeon ismay administer intravenous (IV) midazolam and/or required before stopping any antiplatelet agentsfentanyl while directly observing and monitoring prior to surgery. In many centers, patients withthe patient. stable symptoms will wait 3–5 days after stopping All cardiac medications may be continued until clopidogrel. It is common for patients with valvularthe time of surgery. There is debate on holding heart disease to present with atrial fibrillation or aangiotensin converting enzyme inhibitors (ACE-I) mechanical valve, and thus require anticoagulation.
    • 132 Chapter 5Coordination regarding the administration of these after surgery. There are case reports of aortic valvemedications during the perioperative period is replacement in conscious patients under regionalessential. anesthesia without intubation. Given the signifi- cant issues with anticoagulation, it is unlikely thatInduction and maintenance of regional anesthesia will replace traditional generalanesthesia anesthesia for valvular surgery.No specific agents or techniques are indicated foreither induction or maintenance of anesthesia in Weaning from bypass andany specific valvular condition. Rather, adherence the post-bypass periodto preset hemodynamic goals will provide appro- Repairing or replacing the valve may fundamentallypriate guidance when choosing anesthetic agents. change the hemodynamic goals of the patient fromThere are a number of ways to achieve these the pre-bypass period. A normal valvular profilegoals safely in the patient presenting for valve may be observed immediately after CPB (Fig. 5.2).surgery. The anticipation is that the heart will now per- Patient awareness during cardiac surgical proce- form normally; however, that does not necessarilydures requires special attention. Awareness occurs follow. The heart suffers an acute insult with thein approximately 0.13% of surgical patients. Multi- surgical intervention, aortic cross-clamping, and thevariate logistic regression identified increasing ASA myocardial depressant effects of the various anes-status, and type of procedure as risk factors for thetic agents. As with any cardiac surgical proce-recall. For cardiac surgical procedures, the odds ratio dure, there may be evidence of new regional wallfor recall is 3.58 with a 95% confidence interval motion abnormalities, global cardiac dysfunction,of 0.72–17.9. As with any procedure, attention to and peripheral vascular dysfunction. In valvularhemodynamic signs, depth of anesthesia, the use of heart surgery, the heart requires time to remodelbenzodiazepines, and inhalational agents will likely before significant improvement is observed.reduce the risk of operative recall. In some patients, however, hemodynamics may There are good data to support the concept of be greatly improved post-bypass. In simple, com-“fast-track” or early extubation protocols in the pensated AS, the patient may be hyperdynamiccare of patients presenting for CABG surgery. Thesebenefits include reduced hospital stay, intensivecare unit stay, and reduced cost of care. Data onearly extubation protocols in valve surgery are lesscommon, although one might expect similar ben-efit as observed in CABG surgery. One should beaware, however, that many valvular procedures arecomplex in nature, requiring extended CPB time,potential deep hypothermic circulatory arrest, andincreased requirements for blood and blood prod-uct transfusion. All of these factors may limit theopportunity for early extubation. There are limited reports of regional anesthesiafor valvular heart surgery. Mos