Anaesthetic management of mitral valvular heart disease
Presented by :- Dr Sindhu SapruModerator:- Dr Avnish Bharadwaj
Definition:- An acquired or congenital disorder of cardiac valve characterised by stenosis(obstruction) or regurgitation(backward flow) of blood.
Why do we need guidelines for the anaesthetic management of valvular heart disease patients? Still common in the developing world due to the prevalence of Rheumatic Fever. In the past 2 decades, there have been major advances in understanding the natural history and in improving cardiac function in patients with valvular heart disease. Increases survival in this group of patients due to:- Better noninvasive monitors of ventricular function Improved prosthetic heart valves, Better techniques for valve reconstruction Development of guidelines for selecting the proper timing for surgical intervention
Hemodynamic burden on the LV/RV initially tolerated by compensatory mechanisms but eventually leads to cardiac muscle dysfunction, (CHF), or even sudden death. Produce pressure overload (mitral stenosis, aortic stenosis) or volume overload (mitral regurgitation, aortic regurgitation) on the left atrium or left ventricle. Anaesthetic management during the perioperative period is based on the likely effects of drug-induced changes in :- Heart rate and rhythm, Preload, Afterload, Myocardial contractility, Systemic blood pressure, Systemic and pulmonary vascular resistance relative to the pathophysiology of the heart disease.
Includes assessment of (1) the severity of the cardiac disease, (2) the degree of impaired myocardial contractility, and (3) the presence of associated major organ system disease. Recognition of compensatory mechanisms :Increased sympathetic nervous system activity and cardiac hypertrophy Consideration of current drug therapy The presence of a prosthetic heart valve introduces special considerations especially if noncardiac surgery is planned.
History and physical examination Questions designed to define exercise tolerance are necessary to evaluate cardiac reserve in the presence of valvular heart disease and to provide a functional classification according to the criteria established by the NYHA. Dyspnea, orthopnea, and easy fatigability- impaired myocardial contractility. Anxiety, diaphoresis, and resting tachycardia- compensatory increase in sympathetic nervous system activity CHF- frequent in chronic valvular heart disease, Basilar chest rales, jugular venous distention, S3 and dependant edema Typically, elective surgery is deferred until CHF can be treated and myocardial contractility optimized.
History and physical examination Murmur- The character, location, intensity, and direction of radiation of a heart murmur provide clues to the location and severity of the valvular lesion. Cardiac dysrhythmias - seen with all types of valvular heart disease. Atrial fibrillation is common, especially with mitral valve disease associated with left atrial enlargement. Angina pectoris - seen even in the absence of coronary artery disease. It usually reflects increased myocardial oxygen demand due to ventricular hypertrophy.
History and physical examination Valvular heart disease and ischemic heart disease frequently co-exist. Fifty percent of patients with aortic stenosis who are older than 50 years of age have associated ischemic heart disease. The presence of coronary artery disease in patients with mitral or aortic valve disease worsens the long-term prognosis and mitral regurgitation due to ischemic heart disease is associated with an increased mortality
Drug Therapy β-blockers, calcium channel blockers, and digitalis - heart rate control ACE inhibitors and vasodilators -control blood pressure and afterload Diuretics, inotropes and vasodilators- heart failure Antidysrhythmic therapy may also be necessary.
Drug Therapy Aortic and mitral stenosis require a slow heart rate to prolong the duration of diastole and improve left ventricular filling and coronary blood flow. Aortic and mitral regurgitation require afterload reduction and a somewhat faster heart rate to shorten the time for regurgitation. Atrial fibrillation requires a controlled ventricular response so that activation of the sympathetic nervous system, as during tracheal intubation or in response to surgical stimulation, does not cause sufficient tachycardia to significantly decrease diastolic filling time and stroke volume.
Laboratory data ECG- -Broad and notched P waves (P mitrale)- Left atrial enlargement typical of mitral valve disease. -Left and right ventricular hypertrophy -the presence of left or right axis deviation and high voltage. -Others- dysrhythmias, conduction abnormalities, evidence of active ischemia, or previous myocardial infarction. CHEST X RAY- -Cardiomegaly - Valvular calcifications
Laboratory Data DOPPLER ECHO- -Determine significance of cardiac murmurs -Identify hemodynamic abnormalities associated with physical findings -Determine transvalvular pressure gradient -Determine valve area -Determine ventricular ejection fraction -Diagnose valvular regurgitation -Evaluate prosthetic valve function -Determine cardiac anatomy and function, hypertrophy, cavity dimensions, and the magnitude of valvular regurgitation.
Laboratory Data CARDIAC CATHETERISATION -Presence and severity of valvular stenosis and/or regurgitation, coronary artery disease, and intracardiac shunting. -Resolve discrepancies between clinical and echocardiographic findings. -MS/MR: measurement of pulmonary artery pressure and right ventricular filling pressure may provide evidence of pulmonary hypertension and right ventricular failure. - Mitral and aortic stenoses are considered to be severe when transvalvular pressure gradients are more than 10 mm Hg and 50 mm Hg, respectively
Narrowing of the mitral valve orifice causing obstruction to blood flow from left atrium to the left ventricle.
Etiology Commonly encountered disease in the developing world, where the prevalence of rheumatic fever remains high. Most common cause - rheumatic heart disease. Much less common causes include : carcinoid syndrome left atrial myxoma severe mitral annular calcification thrombus formation cor triatriatum rheumatoid arthritis systemic lupus erythematosus, and congenital mitral stenosis. Pure predominant MS- in 40% patients of Rheumatic fever
Diffuse thickening of the mitral leaflets and subvalvular apparatus, commissural fusion, and calcification of the annulus and leaflets . This process occurs slowly, and many patients do not become symptomatic for 20 to 30 years after the initial episode of rheumatic fever. Left ventricular contractility is usually normal. If aortic and/or mitral regurgitation accompany mitral stenosis, there is often evidence of left ventricular dysfunction.
PATHOPHYSIOLOGY Normal mitral valve orifice area - 4 to 6 cm2. Orifice area < 2 cm2 – Blood flow from LA to LV propelled by an elevated left atrioventricular pressure gradient impaired early diastolic filling of LVLV requires the atrial kick to fill with blood. Orifice area < 1 cm2(Severe/Tight MS) – LA pressure of 25 mmHg required to maintain normal cardiac outputtransmitted to the pulmonary circulation pulmonary hypertension. Constant pressure overload of the LA LA dilatation upto 10- 12cm distorts depolarisation pathwayAtrial Fibrillation loss of the atrial kick decrease in cardiac output Congestive Heart failure
PATHOPHYSIOLOGY Tachycardia/AF diastolic filling period of LV decreases elevated LAP pulmonary congestion. Underloaded LV Decrease in LVEDV and LVEDP Reduction in Stroke Volume Cardiac output- Moderate MS: CO normal at rest but rises subnormally during exertion Severe MS ( esp with elevated PVR) : CO subnormal at rest and fails to increase/declines on exertion. Left ventricular systolic function is usually well preserved in patients with mitral stenosis
PATHOPHYSIOLOGY Pulmonary Hypertension in MS results from: (1) Passive backward transmission of LAP (2) Pulmonary arteriolar constriction (3) Interstitial edema in pulmonary vessels (4) Organic obliterative changes in pulmonary vascular bed Patients with long-standing mitral stenosis develop an irreversible component of pulmonary hypertension. Severe Pulmonary Hypertension RV enlargement, secondary TR and PR, and Right Heart Failure. Also leads to decreased pulmonary compliance excacerbation of ventilation perfusion inequalities.
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA functionMitral stenosis
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA function Pulmonary venous pressure Perivascular edema Pulmonary artery pressure Luminal narrowingMitral stenosis
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA function Pulmonary venous pressure Perivascular edema Pulmonary artery pressure Luminal narrowingReversal of pulmonary blood flow Pulmonary compliance Work of breathingMitral stenosis
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA function Pulmonary venous pressure Perivascular edema Pulmonary artery pressure Luminal narrowingReversal of pulmonary blood Cardiac Stable with mild flow output symptoms Severe pulmonary Pulmonary compliance Htn Work of breathing Mitral stenosis
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA function Pulmonary venous pressure Perivascular edema Pulmonary artery pressure Luminal narrowingReversal of pulmonary blood Cardiac Stable with mild flow output symptoms Severe pulmonary Pulmonary compliance Htn Work of breathing Pulmonary vascular resistance Mitral stenosis
Obstruction to LA emptying Difficulty in LV filling LA pressure Change in LA function Pulmonary venous pressure Perivascular edema Pulmonary artery pressure Luminal narrowingReversal of pulmonary blood Cardiac Stable with mild flow output symptoms Severe pulmonary Pulmonary compliance Htn Work of breathing Pulmonary vascular resistance RV overload Mitral stenosis Tricuspid regurgitation
CLINICAL FEATURES Continuous progressive life long disease Latent period of 20-40 yrs from rheumatic fever to onset of symptoms. Onset of symptoms to disability- 10 yrs Progresses slowly (over decades) from the initial signs of mitral stenosis NYHA functional class II symptomsatrial fibrillation NYHA functional class III or IV symptoms accelerated progression and the patients condition deteriorates Symptoms precipitated by sudden changes in heart rate,volume status or CO like fever, anaemia, pregnancy, exercise, thyrotoxicosis etc.
CLINICAL FEATURES Symptoms of mitral stenosis include: Due to decreased CO: Easy fatiguability Syncope Due to increased LAP Pulmonary congestion- Dyspnea, orthopnea Hemoptysis Pulmonary edema Due to LA enlargement Ortners syndrome Atrial Fibrillation (30-40%)- more common in older patients Due to PAH, RV hypertrophy, RVF Chest pain, ascites, edema Causes of death- CHF, systemic embolism, pulmonary embolism, infection
PHYSICAL FINDINGS Inspection- -Mitral facies- Pinkish purple patches on cheeks+ peripheral cyanosis in lips, tip of nose and cheeks. -Malar flush Rarely seen in India -Raised JVP, ascites,pedal edema when RHF develops Palpation- -Pulse – Regular, low volume, all peripheral pulses palpable. -Left parasternal heave when RV hypertrophy develops -Atrial fibrillation- irregular pulse -Hepatomegaly- in RHF -Tapping apex beat not displaced -Diastolic thrill at cardiac apex with patient in lateral recumbent position
PHYSICAL FINDINGS Auscultation -S1 – loud, slightly delayed -S2 – closely split P2 often accentuated -Opening snap –high pitched readily audible in expiration,at or just medial to apex. Follows A2 by 0.05 -0.12s (this time interval varies inversely with severity of MS). Due to forceful opening of mitral valve. As MS progresses mitral valve opens earlier in ventricular diastole. -Murmur – Low pitched, rumbling, diastolic murmur following OS heard best at apex with patient in lateral recumbent postion with bell of stethoscope. Accentuated by mild exercise. Duration correlates with severity of MS. Reappears or louder during atrial systole.
PHYSICAL FINDINGS Auscultation Associated lesions -In severe pulmonary hypertension: pansystolic murmur along left sternal border. Louder during inspiration and diminishes in forced expiration(Carvallo’s sign). -CO markedly reduced – silent MS (murmur not detected) -Graham Steele murmur of PR- high pitched diastolic decrescendo blowing murmur along left sternal border
How to grade severity of mitral stenosis?Severity Area (cm2) PAP Symptoms SignsMild >1.8 Normal Usually absent S2-OS>120ms normal P2Moderate 1.2-1.6 Normal Class II S2-OS 100- 120 ms; normal P2Moderate- 1.0-1.2 Mild Pulmonary Class II-III S2-OS 80-100Severe hypertension ms ; P2 increaseSevere (Tight) <1.0 Mild to severe Class II-IV S2-OS< 80 ms; pulmonary P2 increase RV hypertension lift , Surgery if RHF
DIAGNOSIS ECG P wave -Tall and peaked in lead II and inverted in V1 in severe pulmonary hypertension with RA enlargement. -Wide and notched in LA enlargement ( P Mitrale ). -Absent when Atrial Fibrillation develops. QRS complex- usually normal. Right axis deviation and RV hypertrophy in pulmonary hypertension. CARDIAC CATHETERISATION Valve area, valvular function, CAD Resolves discrepancy between clinical and ECHO findings Assess associated lesions
DIAGNOSIS ECHO- Anatomy of the mitral valve -degree of leaflet thickening, calcification, mobility, extent of involvement of the subvalvular apparatus and anatomic suitability for PBMV. -Also allows evaluation of pulmonary hypertension, ventricular function, associated valvular disease, assess LA for presence or absence of thrombus. -Evaluate patients with changing signs and symptoms MILD MODERATE SEVERE -Follow up Mean valve gradient (mm 6 6–10 >10 Hg) Pressure half time (ms) 100 200 >300 1.6– Mitral valve area (cm2) 1.0–1.5 <1.0 2.0
DIAGNOSIS Chest X Ray -Mitralisation-straightening of the left heart border due to:- Small aortic knuckle- (decreased CO) Increased pulmonary conus Enlarged LA producing convexity LV- no change -Double density of right border- outer and upper border due to enlarged LA -Pulmonary hypertension- Dilated pulmonary arteries with peripheral pruning Dilatation of upper lobe pulmonary veins (Mustache or antler sign) Kerley B lines in lower and mid lung fields -Batwing sign in pulmonary edema- fan shaped opacity from parahilar area to the periphery -Elevation of left mainstem bronchus- (widening of carinal angle) -Mitral valve calcification -Posterior displacement of esophagus (RAO view) -Left lower lobe collapse (compression of left mainstem bronchus) -Miliary shadows of pulmonary henosiderosis
COMPLICATIONS -Atrial dysrhythmias (AF,AFL) -Systemic embolisation (10-25%) – Risk related to age, presence of AF, History of emboli Cerebral-60% -Hemoptysis due to Rupture of bronchial/pulmonary veins Chronic bronchitis Acute pulmonary edema- pink, frothy sputum Pulmonary infarction, anticoagulation, hemosiderosis -Congestive heart failue -Recurrent broncho pulmonary infections -Pulmonary hypertension -Endocarditis
TREATMENT Grade 1 ( Mild MS by echo + dyspnea < Grade III) Diuretics for congestive symptoms Prophylaxis against Rheumatic fever & Infective endocarditis IN presence of AF- anticoagulation, digoxin & drugs for rate control Grade II ( Tight MS + lung congestive symptoms- dyspnea < Grade III) First line treatment as above Severe symptoms not responding to medicines- surgery with commissurotomy, MVR, or balloon valvuloplasty Grade III ( Tight MS + pulmonary hypertension ) Surgical repair Grade IV ( Tight MS + pulmonary hypertension + RHF) Surgery + Treatment of RHF
TREATMENT CHF- restriction of physical activity, salt restricted diet, diuretics and digoxin Atrial fibrillation-Digoxin, β-blockers, calcium channel blockers, or a combination of these medications. Control of the heart rate is critical . Cardioversion for new onset AF. Anticoagulation – in atrial fibrillation because the risk of embolic stroke in such patients is about 7% to 15% per year. Warfarin is administered to a target (INR) of 2.5 to 3.0. Prophylaxis against recurrence of acute rheumatic fever
TREATMENT Percutaneous balloon valvotomy-indicated in Progressive deterioration despite medical treatment MS with complications Asymptomatic patients with a single attack of thromboembolism Mitral valve orifice < 1 cm2 Surgical correction – indicated in MS with MI Active rheumatic carditis MS with left atrial thrombus Extremely tight stenosis Heavy valvular calcification Restenosis Surgical commissurotomy, valve reconstruction, or valve replacement.
ANAESTHETIC MANAGEMENT GOALS Maintain adequate LV diastolic filling Optimise Right heart condition -Maintain slow heart rate ie Avoid tachycardia -Maintain a sinus rhythm if present. Aggressively treat AF -Judicious fluid therapy- Tight control of intravascular volume Overaggressive fluid with elevated LAP- pulmonary edema Less fluids- decreased SV and CO
ANAESTHETIC MANAGEMENT -Maintain adequate SVR with sympathomimetic drugs such as ephedrine and phenylephrine. Avoid vasodilators. -Avoid increases in PVR- Prevent pain, hypoxemia, hypercarbia, acidosis. Patients on pulmonary vasodilators should continue these medications because abrupt withdrawal can exacerbate pulmonary hypertension, particularly with inhaled agents. Right heart function support-inotropes, and maneuvers that may compromise it(eg, overaggressive fluid administration) should be avoided Current ACC/AHA guidelines do not recommend endocarditis prophylaxis for patients with isolated mitral stenosis undergoing surgical procedures. * *http://ether.stanford.edu/Ortho/Anesthetic%20considerations% 20for%20valvular%20patient%20sub%20to%20noncardiac%20surg ery.pdf "
ANAESTHETIC MANAGEMENT Which medications to continue intra operatively?? Diuretics- Evaluate fluid status Check electrolytes on day of surgery Withold on night before surgery if massive fluid shifts expected in surgery Drugs to control AF ( Digoxin, beta blockers, CCB) – Continue in perioperative period Watch serum potassium- in patients receiving digoxin and diuretics Warfarin- switch to heparin perioperative for better control. Titrate to APTT 1.5-2 times normal Continue post op. Management of anticoagulation perioperatively should balance risks of bleeding with the risk of thrombosis and systemic embolization.
ANAESTHETIC MANAGEMENT Preoperative Medication Adequate dose prevents anxiety and tachycardia. Care must be taken to avoid hypotension, which can dramatically decrease left ventricular preload and respiratory depression, which may exacerbate pulmonary hypertension. Morphine 0.1-0.2mg/kg Promethazine 12.5-25mg IM 1-2 hrs before surgery Small dose Benzodiazepenes can be given ( reduce dose of morphine) Anticholinergics- avoided as they increase heart rate
ANAESTHETIC MANAGEMENT Induction Any intravenous induction drug except ketamine, because of its propensity to increase the heart rate. Should be double diluted and given slowly. Etomidate best for hemodynamic stabilty Thiopentone or Midazolam Narcotic( morphine 0.5mg/kg or Fentanyl 5-10 ug/kg) Avoid Propofol- direct and indirect effects on ventricular preload Muscle relaxants that do not induce tachycardia and hypotension from histamine release. Vecuronium + Narcotics- dangerous bradycardia. Hence pancuronium preferred unless basal heart rate is high Rocuronium- vagolytic. Hence slightly increase HR and decrease PAP Benzodiazepenes (midazolam/diazepam) – use cautiously as can cause profound vasodilatation esp with narcotics.
ANAESTHETIC MANAGEMENT Maintainence A nitrous/narcotic anesthetic or a balanced anesthetic that includes low concentrations of a volatile anesthetic Avoid halothane- arrythmogenic Nitrous oxide – Increases PVR . Best avoided in PAH Light anesthesia and surgical stimulation -tachycardia and HTN. Vasodilator therapy ( NTG/ Nitroprusside 0.5-1 ug/kg/min)- desirable in severe PAH Intraoperative fluid replacement must be carefully titrated Reversal- slowly to help ameliorate any drug-induced tachycardia caused by the anticholinergic drug in the mixture.
ANAESTHETIC MANAGEMENT Monitoring ECG, BP, Spo2 Invasive monitoring- depends on the complexity of the surgery and the magnitude of physiologic impairment caused by MS. -Direct arterial pressure -CVP- measure loading conditions and means of transfusing inotropes/dilators -Pulmonary artery catheter- PCWP and CO measurement offer very good estimate of overall ventricular function . Monitor Pulmonary Artery Pressure ( PAP)- useful in PAH Helpful for confirming the adequacy of cardiac function, intravascular fluid volume, ventilation, and oxygenation.
ANAESTHETIC MANAGEMENT Post operative management Risk of pulmonary edema and RHF continues into the postoperative period, so cardiovascular monitoring should continue as well. May require a period of mechanical ventilation: Pain and hypoventilation with respiratory acidosis ,hypercarbia and hypoxemia -increase HR and PVR. Decreased pulmonary compliance and increased work of breathing to avoid hypercarbia . Relief of postoperative pain with neuraxial opioids useful Inotropic support and vasodilator therapy should be continued for prolonged ( 24-48 hrs) in patients with severe PAH.
Abnormal leaking of blood from the leftventricle, through the mitral valve, andinto the left atrium, when the leftventricle contracts, i.e. there is regurgitationof blood back into the left atrium.
Etiology MR due to rheumatic fever is usually associated with mitral stenosis. Acute MR- ischemic heart disease, blunt chest wall trauma, infective endocarditis, rupture of chordae tendineae. Chronic MR: mitral valve prolapse( M/C cause) mitral annular calcification left ventricular hypertrophy, cardiomyopathy, myxomatous degeneration, systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, and carcinoid syndrome congenital lesions such as an endocardial cushion defect,
PATHOPHYSIOLOGY Acute phase Sudden volume overload of both LA and LV. The left ventricle now has to pump out the forward stroke volume plus the regurgitant volume known as the total stroke volume of the left ventricle. Increased ejection fraction initially contractile function deteriorates as disease progressesdysfunctional LV and a decreased EF. Volume and pressure overload of the LA pulmonary congestion Regurgitant fraction >0.6 -severe mitral regurgitation.
PATHOPHYSIOLOGY Chronic phase Compensated Develops slowly over months to years or if the acute phase cannot be managed with medical therapy. Eccentric hypertrophy of the LV plus the increased diastolic volume increase the stroke volume forward CO approaches the normal levels. Volume overload of LADilatation of LA filling pressure decreasesimproves the drainage from the pulmonary veins signs and symptoms of pulmonary congestion decrease. Asymptomatic and have normal exercise tolerances.
PATHOPHYSIOLOGY Chronic phase Decompensated MR for years eventually develop left ventricular dysfunction, the hallmark of this phase. characterized by calcium overload within the cardiac myocytes. The stroke volume of the LV decreases decreased forward CO and an increase in the end systolic volumeincreased filling pressures of the LV and increased pulmonary venous congestionsymptoms of congestive heart failure. LV dilatationdilatation of the mitral valve annulusworsen the degree of MR and an increase in the wall stress of the cardiac chamber as well. EF decreases late in the course of disease.
PATHOPHYSIOLOGY Isolated MR-less dependent on properly timed left atrial contraction for left ventricular filling than patients with co-existing mitral or aortic stenosis. Myocardial ischemia is uncommon because the increased left ventricular wall tension is quickly dissipated as the stroke volume is rapidly ejected into the aorta and left atrium. Acute MR -pulmonary edema and/or cardiogenic shock.
PATHOPHYSIOLOGY The fraction of regurgitant volume depends on (1) the size of the mitral valve orifice; (2) heart rate, which determines the duration of ventricular ejection; (3) pressure gradients across the mitral valve. MR + MS -volume and pressure overload, resulting in a markedly increased left atrial pressure. Atrial fibrillation, pulmonary edema, and pulmonary hypertension develop much earlier in these patients Rheumatic fever–induced MR -marked left atrial enlargement and atrial fibrillation.
Volume overload of LA Volume overload of LV LA dilation Early Normal LA LV filling Fiber size pressures Stroke volume Cardiac output and BP maintainedMitral regurgitation
Volume overload of LA Volume overload of LV LA dilation Normal LA pressuresMitral Regurgitation
Volume overload of LA Volume overload of LV LA dilation Early Normal LA Late LV filling Fiber size pressures Contractility Stroke volume BP and CO Cardiac output and BP maintainedMitral regurgitation
Volume overload of LA Volume overload of LV LA dilation Late Early Normal LA LV filling Fiber size pressures Contractility Stroke volume BP and CO Cardiac output and BP Reflexive arteriolar maintained constriction SVRMitral regurgitation
Volume overload of LA Volume overload of LV LA dilation Early Normal LA Late LV filling Fiber size pressures Contractility Stroke volume BP and CO Cardiac output and BP Reflexive arteriolar maintained constriction SVR RegurgitationMitral regurgitation
Volume overload of LA Volume overload of LV LA dilation Early Normal LA Late LV filling Fiber size pressures Contractility Stroke volume BP and CO Cardiac output and BP Reflexive arteriolar maintained constriction SVR Regurgitation LA pressure PulmonaryMitral regurgitation congestion
Volume overload of LA Volume overload of LV LA dilation Early Late Normal LA LV filling Fiber size pressures Contractility Stroke volume BP and CO Cardiac output and BP Reflexive arteriolar maintained constriction SVR Forward flow Regurgitation LA pressure Pulmonary congestionMitral regurgitation
CLINICAL FEATURES Symptoms Acute MR – -Decompensated CHF(i.e. dyspnea,orthopnea, PND pulmonary edema, -Low cardiac output state (i.e. decreased exercise tolerance). –- -Palpitations (due to LVH or AF) -Cardiovascular collapse with shock- due to papillary muscle rupture or rupture of a chorda tendinea. Chronic compensated MR- -May be asymptomatic, with a normal exercise tolerance and no evidence of heart failure. May be sensitive to small shifts in their intravascular volume status, and are prone to develop CHF. Features of RHF in associated pulmonary hypertension.
PHYSICAL EXAMINATION Depend in the severity and duration of MR. Inspection - Features of CHF ( pt propped up and dyspneic, edema, raised JVP etc) -Precordial bulge Palpation -Pulse- regular, normal pressure usually. May show a sharp upstroke in chronic severe MR narrow pulse pressure in acute severe MR -Systolic thrill at the apex (best in left lateral position at the height of expiration) , hyperdynamic and laterally displaced apex ,palpable rapid filling S3 (chronic severe MR) -Left parasternal heave and epigastric pulsations (RVH) -Palpable P2 I pulmonary area (PAH) - Bipedal pitting edema (CHF)
PHYSICAL EXAMINATION Auscultation -S1 –usually absent,soft or buried in the murmur. -S2-audible. Wide physiological splitting in severe MR (aortic valve closes early) -S3 –low pitched 0.12-0.17s after A2 may be followed by rumbling MDM -S4- in acute severe MR Murmur- High pitched soft blowing holosystolic apical murmur atleast grade III/IV in left lateral position at the height of expiration with radiation to the left axilla and inferior angle of scapula. Intensified by isometric exercise but reduced during Valsalva. Pulmonary area- Ejection systolic murmur with loud P2
PHYSICAL EXAMINATION Acute Chronic P mitrale, AF, Left Ventricular ECG Normal Hypertrophy Cardiomegaly, left atrial Heart size Normal enlargement Heard at the base, radiates Heard at the apex, radiates to Systolic murmur to the neck, the axilla spine, or top of head Apical thrill May be absent Present Jugular venous Present Absent distension
DIAGNOSIS ECG- - LAH (in all cases) -LVH (in 50% cases) -Biventricular hypertrophy -AF Chest X Ray- - Enlarged LA and LV -Signs of pulmonary venous hypertension -Signs of pulmonary edema (acute severe MR) -RVH -Mitral calcification (in co existing MS) Severity of MR evaluated by: -Color-flow and pulsed-wave Doppler -Pulmonary artery occlusion pressure waveform -the size of the V wave correlates with the magnitude of MR -Cardiac catheterisation
DIAGNOSIS ECHO- Confirm diagnosis. Color doppler flow on TEE will reveal a regurgitant jet of blood, a dilated LA and LV and decreased left ventricular function. Also assess mechanism and severity of MR MILD MODERATE SEVERE Area of MR jet (cm2) <3 3.0-6.0 >6 MR jet area as percentage of left atrial 20–30 30–40 >40 area Regurgitant fraction (%) 20–30 30–50 >55.
TREATMENT Drugs- Digoxin, diuretics for CHF Vasodilators ( ACE inhibitors, nitrates) in acute symptomatic MR Warfarin for AF/Thromboembolism Progress insidiously, causing left ventricular damage and remodeling before symptoms have developed. Survival may be prolonged if surgery is performed before the ejection fraction is less than 60% Surgery- -Mitral annuloplasty/valvuloplasty-preferred because restores valve competence, maintains the functional aspects of the mitral valve apparatus, and avoids insertion of a prosthesis. -Mitral valve replacement Patients with an EF <30% or left ventricular end-systolic dimension more than 55 mm do not improve with mitral valve surgery.
ANAESTHETIC MANAGEMENT GOALS Prevention and treatment of events that decrease CO. Improve forward LV Stroke Volume and decrease the regurgitant fraction. Vasodilatation can improve forward flow- NTG/ nitroprusside infusions. Useful in PAH as well but not once RVF sets in. Preload – maintain or slightly increase Maintain or increase HR- Avoid bradycardia Decrease in afterload beneficial- Avoid sudden increase in SVR Minimize drug-induced myocardial depression Avoid hypoxia,hypercarbia and acidosis (all increase PAH)
ANAESTHETIC MANAGEMENT PREMEDICATION + INDUCTION Light premedication preferred Large dose narcotics induction or Opoids + Benzodiazepenes ( Fentanyl + midazolam / sufentanyl+ midazolam) either continuous or intermittent bolus Muscle relaxant Pancuronium preferred as increased HR desirable Vecuronium/ Atracurium- depending on basal HR
ANAESTHETIC MANAGEMENT MAINTAINENCE Volatile anesthetics (Halothane, Isoflurane) Increase in heart rate and minimal negative inotropic effects. Vasodilatation desirable. Nitrous oxide avoided in severe PAH. When myocardial function is severely compromised, use of an opioid-based anesthetic is another option However, potent narcotics can produce significant bradycardia, very deleterious in severe MR. Mechanical ventilation should be adjusted to maintain near-normal acid-base and respiratory parameters. The pattern of ventilation must provide sufficient time between breaths for venous return. Maintenance of intravascular fluid volume is very important for maintaining left ventricular volume and cardiac output in these patients.
ANAESTHETIC MANAGEMENT Monitoring Invasive monitoring- ( CVP, PAC) Not required in Minor surgery with asymptomatic MR Useful in severe MR- detecting the adequacy of CO and the hemodynamic response to anesthetic and vasodilator drugs and facilitating intravenous fluid replacement. Pulmonary artery occlusion pressure – -V waveform to assess severity of MR -May be a poor measure of left ventricular end-diastolic volume in patients with chronic mitral regurgitation. -With acute mitral regurgitation, the left atrium is less compliant, and PAOP does correlate with LA and LV EDP.
Moderate to severe MS/ AS –most significant concern Case reports attest to their safety provided afterload is maintained Epidural- can be used as sole anaesthetic in mild to moderate MS Optimise fluid status and achieve sensory level with titrated doses of Local anaesthetic until adequate for surgery. Basic principles: Afterload support Maintainence of sinus rhythm Careful volume management Avoidance of tachycardia Epidural using opiods- supplement to GA Avoid adrenaline in test dose while inserting catheter.
Left-sided valvular heart lesions present a myriad of potential difficulties during perioperative care for noncardiac surgery. A thorough understanding of the pathophysiology of the presenting lesion along with its implications in the perioperative period is crucial in preventing undesirable outcomes. Patients with left-sided valvular disease require careful preoperative evaluation, optimization and planning,vigilant intraoperative monitoring, and tight hemodynamic control that must be continued into the postoperative period when appropriate. As the population continues to age, we can expect to treat rising numbers of patients with these derangements, making it more crucial than ever to be prepared for these encounters.
Stoeltings Anaesthesia and co existing disease- 5th edition Harrisons Internal medicine- 17th ed Cardiac Anaesthesia- Deepak Tempe Anesthetic Considerations for Patients with Advanced Valvular Heart Disease Undergoing Noncardiac Surgery-Jonathan Frogel, MD*, Dragos Galusca, MD http://ether.stanford.edu/Ortho/Anesthetic%20consideration s%20for%20valvular%20patient%20sub%20to%20noncardiac%2 0surgery.pdf "