Anesthesia for cardiac surgery


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Anesthesia for cardiac surgery

  1. 1. Anesthesia for Cardiac Surgery
  2. 2. 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
  3. 3. 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
  4. 4. © 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.
  5. 5. 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
  6. 6. 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- 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
  7. 7. 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
  8. 8. 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 .
  9. 9. 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.
  10. 10. 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.
  11. 11. 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
  12. 12. 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
  13. 13. 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.
  14. 14. 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,
  15. 15. 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
  16. 16. 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.
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. 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 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.
  22. 22. 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 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
  23. 23. 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 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.
  24. 24. 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
  25. 25. 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.