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Anaesthesia For Valvular Heart Diseases
Made by: Dr. Meenal Aggarwal Moderator: Dr. Aparna
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Introduction
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Valvular ds: An increased burden on L or R ventricle
Could be: Pressure overload (Stenotic lesions) Volume overload (Regurgitant lesions) Initially tolerated d/t compensatory mechanisms Eventually cardiac muscle dysfunction CHF ; even sudden death
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Preoperative Assessment
Aim: to know Severity of Disease Degree of impaired myocardial contractility Presence of assoc. organ system diseases O/H: Symptoms: Dyspnea, orthopnea, easy fatiguability (Impaired myocardial contractility) Anxiety, diaphoresis, resting tachycardia (Compensatory increase in sympathetic activity) Angina (d/t assoc CAD, or inc. myocardial O2 demand)
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Drug therapy: Beta Blockers Digitalis ACE inhibitors Vasodilators Diuretics Ionotropes Antiarrhythmic drugs Control HR (AS & MS: Allows diastolic filling) Control BP and so dec. afterload (AR, MR) Control of CHF
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O/E: Signs: Inspection: Raised JVP Auscultation: Basilar chest rales, S3, Murmurs Murmurs: D/t turbulent flow across the defective valve Note: character, location, intensity, direction of radiation Systolic murmurs: AS, PS or MR,TR Diastolic murmurs: MS, TS or AR, PR Dysrhythmias: AF (esp Mitral valve ds.) i.e. with enlarged Lt atria
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Lab Investigations: CXR: Size & shape of heart & great vessels Pulmonary markings Enlarged LA (Elevated Lt main bronchus, calcified valve) ECG: Lt or Rt axis deviation (Lt or Rt ventricle hypertrophy) P mitrale (Broad notched P wave in Mitral valve ds.) Dysrhythmias Conduction abnormalities Evidence or active ischemia or previous MI
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Echo with doppler: Evaluating significance of murmurs Detection of antomical defects (Hypertrophy, chamber size, valve area) Functional defects (Transvalvular pressure gradient, magnitude of valvular regurgitation) Cardiac Catheterisation: Solves discrepancies b/w clinical and echo findings Presence & severity of stenosis or regurgitation Intracardiac shunting CAD
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Transvalvular pressure gradient (TVPG) (Severe MS when > 10mmHg, Severe AS when > 50 mm Hg)
Pulmonary artery pressures (Pulmn HT) Assessment of Prosthetic Valve function: Dysfunction (Change in intensity/ quality of clicks, new or change in characteristics of murmurs) Tranthoracic Echo: To assess ring stability and leaflet motion Transesophageal Echo: Better resolution MRI: For prosthetic valve regurg, paravalvular leak Cardiac Catheterisation: For TVPG, Effective valve area
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Complications of prosthetic valves:
Risk of thromboembolism (Anticoagulation) Subclinical intravascular hemolysis Risk of endocarditis (AB) Management of anti coagulation: Can be continued in minor surgery with min blood loss For major surgery (Stop warfarin 3-5 days preop, UF heparin or LMWH started & continued upto day/ day before of surgery, restarted post op) Avoid elective surgery with in 1 month after an acute thromboembolic episode
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In pregnancy (TE prophylaxis to continue, S/C LMWH given + low dose aspirin)
Prophylaxis of Bacterial endocarditis: Infection likely from frequent exposure to bacteremia Weigh Risk to benefit ratio (AB resistance) Prophylaxis given to following pts: Prosthetic material for cardiac valve repair Previous IE CHD: Unrepaired CHD, Completely repaired with prosthetic material (during 1st 6 months after procedure), Repaired defects with residual defect) Cardiac transplant pt who develop valvulopathy
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AB prophylaxis not required for GU or GIT procedure
Required for skin incision/ Biopsy or Resp tract invasive procedure For dental procedures (manipulation of gingiva, Mucosa)
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MITRAL STENOSIS: Most common cause RHD Primarily affects females
Diffuse thickening of mitral leaflets & subvalvular apparatus, Calcification Gradual progression (over yrs) Other causes: Carcinoid syndrome, LA myxoma, Severe mitral annular calcification, RA, thrombus formation, SLE, congenital
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Pathophysiology of Mitral Stenosis
Decreased mitral valve orifice Mechanical obstruction to LV diastolic filling Dec LV volume Inc LA volume & pressure Dec S.V. Inc Pulmn Venous Pressure RV Hypertrophy & failure Overt Pulmn Edema Pathophysiology of Mitral Stenosis
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Diagnosis: Clinical signs: opening snap (in early diastole), rumbling diastolic heart murmur Venous thrombosis (stasis, decreased activity) CXR: -LA enlargement (straightening of left heart border, elevation of left main stem bronchus, double density of LA) -Mitral calcification -Evidence of pulmn congestion ECG: Broad notched P wave (P mitrale), AF
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Echo: (Anatomical details: Leaflet thickening, calcification, changes in mobility, chamber dimension, thrombus) Severity assessed by: - Mitral valve area, TVPG Also for Pulmn HT, Ventricular function
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Treatment: Mild MS: Diuretics In AF: Beta blockers, Ca #, Digitalis (H.R. control) Anticoagulants (Warfarin to get INR of 2.5 to 3) Surgical correction: Percutaneous valvotomy Valve reconstruction Valve replacement, surgical commisurotomy
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Management of Anaesthesia:
Avoid tachycardia (prevents filling) Avoid decrease in SVR (use vasopressors which avoid Tachycardia) Do no permit volume overload (can ppt CHF) Prevent hypercarbia & hypoxemia, lung hyperinflation (Worsen Pulmn HT) If RVF : Requires ionotropic support & pulmonary vasodilators Premedication: decrease anxiety (watch for resp depression), Continue drugs for HR control, Treat diuretic induced hypoK+
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Anticoagulant therapy (acc to minor or major procedure), coagulation tests for regional anaesthesia
Induction: I/V agents (except ketamine), MR (which doesn’t Inc HR or Dec BP d/t histamine release) Maintenance: Min effect on HR, SVR & PVR, contractility (N2O+ opioid+ Low conc Volatile agents) Reversal achieved slowly (to avoid tachycardia d/t glyco/atropine) Prevent light plane of anaesthesia (symp stimulation) Pulmonary vasodilator may be required Careful fluid replacement intraop (risk of Pulmn edema)
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Monitoring: In asymptomatic (routine)
Symptomatic/ major surgery (Intraarterial pressure monitoring, Pulmonary artery pressure, LA pressure: at higher risk of rupture of pulmn A so done carefully and less frquently, TEE) Post operative management: Prevent fluid overload Manage pain (to prevent tachycardia, hypoventilation so hypoxia), neuraxial opioids May require mechanical ventilation (thoracic surgery)
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MITRAL REGURGITATION:
In RHD, usually assoc with MS Other causes: Papillary muscle dysfxn, mitral annular dilatation, rupture of chordae tendinae, endocarditis, MVP, Congenital Pathophysiology: Regurgitation into LA LA volume overload Dec LV stroke volume LA enlargement & AF Pulmn congestion
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Regurgitant fraction depends on:
Size of valve orifice Heart rate Pressure gradient across MV (SVR) When MR develops gradually: LV becomes more compliant When acute MR: No compensation, sudden sever Dec in S.V. l/t cardiogenic shock, with pulmn congestion When MR+ MS : both volume and pressure overload Diagnosis: O/E: holosystolic apical murmur, radiation to axilla CXR: Cardiomegaly (LA & LV hypertrophy)
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Diagnosis cont… ECG: Lt axis deviation Echo: Confirms MR, Anatomy (LA size, LV wall thickness, cavity dimension), S.V., LA appendage for thrombus Doppler: Severity assessment (Calculation of regurgitant volume and fraction), area of regurgitant jet Pulmn A. Occ. Pressure: Shows a ‘V’ wave in the waveform signifies regurgitation Cardiac catheterisation: If surgery planned or severity doubtful Coronary angiography: In elderly patients
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Treatment: Surgical: Mitral valve repair (preferred as apparatus preserved) Mitral valve replacement Survival increased by surgery of performed before LVEF < 60%, or before End systolic LV dimension >= 45mm Patients who do not improve with surgery: * LVEF < 30% * LV end systolic dimension > 55mm Medical : Vasodilators (Acute MR) Beta #, ACE inhibitors Biventricular pacing
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Management of Anaesthesia:
Prevent events which Dec C.O. Maintain N to slightly higher H.R. Vasodilators to dec afterload Ionotropes to improve LV contraction Induction: I/V agent used MR (pancuronium beneficial- raises HR) Maintainence: Inhalational agents (Dec rise in BP & SVR caused by surgical stimulation) iso, des, sevo
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Opioids (when severely compromised myocardial function)
Mechanical ventilation (allow venous return) Maintain I/V volume Monitoring: Asymptomatic / minor surgery (no invasive monitoring) Severe MR (Pulmn A. Catherisation V wave)
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MITRAL VALVE PROLAPSE:
Prolapsed one/ both mitral leaflets into LA during systole M.C. form of valvular ds. (young women) With or Without MR Causes: Marfan’s, RHD, Myocarditis, thyrotoxicosis, SLE Diagnosis: Usually benign, but can l/t IE, cerebral embolisation, Severe MR, Severe dysrrhythmias, sudden death C/F: Palpitation, anxiety, orthostatic symptoms, dysnea, fatigue, atypical chest pain
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Echo: valve prolapse of 2mm or more above mitral annulus
With/ without leaflet thickening (elderly/connective ts. ds) Functional form (mild bowing) Management of Anaesthesia: Influenced by degree of MR Basis: Larger LV will have lesser prolapse Inc sympathetic activity Dec SVR Upright posture hypovolemia Increase MR
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Inc LV vol will Dec MVP (HTN/ Vasoconst, drug induced myocardial depression, volume resuscitation)
Preoperative Evaluation: Differentiate functional MVP from significant MR Usually< 45 y, female Beta blocker for arrhythmias (continued) If H/O Transient neurological event with sinus rhythm, no atrial thrombi (pt usually on aspirin mg/d) Pt with AF &/or with atrial thrombi or previous stroke (usually on warfarin) ECG changes (PVC’s, QT prolongation) no implication
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Pt may have systolic clicks, murmur even without symptoms (no need of cardio consultation)
In older men (MVP can present with CHF) pt on diuretics, ACE inh Anaesthesia technique: When LV function normal, tolerates both GA & regional Induction: I/V agent (assess need to avoid dec in SVR) Etomidate (min Myocardial depression) Ketamine not to be used (Enhances LV emptying so inc MR) Maintenance: Minimize sympathetic nervous system activity d/t surgical stimuli
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Volatile anaesthetics with N2O +/- Opioids
Low dose: 0.5 MAC (iso, des, sevo) in significant MR Any MR (keep in mind vagolytic/ histamine induced effects) Unexpected ventricular arrhythmias can occur intra op (Beta blocker or lignocaine) Proper fluid balance Vasopressors may be required Avoid controlled hypertension technique (increases MVP) Monitoring: Routine Significant MR/ LV dysfunction (Pulmn A. catheter)
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AORTIC STENOSIS: Degeneration & calcification of leaflets (ageing), then stenosis Causes : Elderly, Bicuspid Aortic Valve N valve area: cm2 Almost always assoc with some AR
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Angina may occur despite absence of CAD (Inc myocardial demand, dec supply)
Syncope (fall in SVR can’t be compensated by inc C.O.) Diagnosis: C/F: angina, syncope, dyspnea on exertion O/E: Systolic murmur best heard in aortic area (be careful as mostly patients undiagnosed) CXR: Prominent ascending aorta ECG: LV hypertrophy Echo with doppler: Bileaflet aortic valve, thickening/ calcification of aortic valve, decreased mobility, LV hypertrophy
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Echo cont… Valve area, TVPG Cardiac Catheterisation Coronary Angiography Exercise stress testing for Asymptomatic patients Treatment: Asymptomatic: Continue medical therapy (delay Surgery untill s/s appear) Aortic Valve replacement Coronary revascularisation (if co-existant CAD) Percutaneous aortic balloon valvuloplasty
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Management of Anaesthesia:
Maintain N sinus rhythm Avoid bradycardia/ tachycardia Avoid hypotension (if occurs aggressive Tt required) Optimise I/V fluid volume CPR is generally ineffective in AS (Not enough CO generated) Induction: GA preferred (regional causes Hypotension) I/V agents used (ones which do not dec SVR) If LV function compromised opioid induction
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Maintenance: Avoid drugs which suppress S.A.node (if occurs give atropine/ glyco/ ephedrine) If persistent tachycardia use esmolol In supravent. tachycardias cardioversion to be done Chanced of VT present (Lidocaine & defib) If LV dyfxn (avoid drugs depressing myocardial contractility) NM blocker with min hemodynamic effects I/V fluid vol to be maintained Monitoring: ECG, Intraarterial cath, P.A. cath, TEE
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AORTIC REGURGITATION:
Causes: IE, RF, Bicuspid aortic valve, ds of root of aorta
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Magnitude of regurgitation depends on:
Time available for regurgitation (H.R. dependent) Pressure gradient across the valve (SVR dependent) Diagnosis: C/F: Dysnea, orthopnea, fatigue, coronary ischemia O/E: Diastolic murmur (Lt sternal border), bounding pulses, wide pulse pressure, Austin Flint murmur (low pitched diastolic murmur) CXR & ECG: LV enlargement & hypertrophy Echo: LVEF & ESV, Severity of regurgitation (on doppler) Cardiac cath & MRI
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Treatment: Surgical: Replacement (even in asymptomatic) Immediate surgery in acute AR (as l/t sudden heart failure) Ross procedure (Pulmonic valve autograft) Valve reconstruction Medical: Vasodilators (Nitroprusside) Ionotropes (Dobutamine) Long term Nifedipine/ Hydralazine
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Management of Anaesthesia:
Avoid bradycardia (HR above 80/min), use atropine Avoid inc in SVR Minimize myocardial depression If LV failure (vasodilators and ionotropes) GA chosen Induction: I/V agent which doesn’t inc SVR or dec HR Maintenance: N2O + volatile agent &/or opioid Iso, Des, Sevo good (inc HR, dec SVR, min myo depression) If severe LV dysfunction high dose opioid (caution: bradycardia) NM blocker: Pancuronium useful, modest tachycardia
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Monitoring: Minor surgery with asymptomatic ds. (routine) Severe AR: Pulmonary A catheter TEE Useful for guiding I/V volume replacement, detecting myocardial depression, measuring response to vasodilators
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TRICUSPID REGURGITATION:
Usually functional (d/t RV enlargement or Pulmn HT) IE, Carcinoid, RHD, Ebstein anomaly Mild TR in highly trained athletes Pathophysiology: Regurgitation through TV RA vol Overload (but minimal rise in RA pressure) O/E: Raised JVP, Hepatomegaly, ascites, edema Tt: Tt the cause (improve lung fxn, relieve LV failure, dec PHT) Surgery (rarely for TR alone), Tricuspid annuloplasty/ valvuloplasty/ replacement
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Management of Anaesthesia:
Keep CVP to high Normal IPPV may decrease venous return Avoid hypoxemia & hypercarbia (to prevent inc Pulmn A. pressure) N2O: weak Pulmn A. vasoconst (may inc TR) Intra op measurement of RA pressure to guide fluid therapy Very high LA pressure can l/t R L shunt (patent foramen ovale)
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PULMONARY REGURGITATION:
TRICUSPID STENOSIS: M.C.cause: RHD (coexiztant TR, Mitral n aortic valve ds) Inc RA pressure & pressure gradient b/w RA & RV PULMONARY REGURGITATION: Secondary to Pulmn HT Rarely symptomatic PULMONARY STENOSIS: Usually congenital (detected and treated in early childhood) C/F: Syncope, angina, RV Failure Tt: surgical valvotomy
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Thank You
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