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Anaesthesia For Valvular Heart Diseases. Made by: Dr. Meenal Aggarwal Moderator: Dr. Aparna. Introduction. Valvular ds : An increased burden on L or R ventricle Could be: Pressure overload ( Stenotic lesions) Volume overload ( Regurgitant lesions)

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anaesthesia for valvular heart diseases

Anaesthesia For Valvular Heart Diseases

Made by: Dr. MeenalAggarwal

Moderator: Dr. Aparna


Valvulards: 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

preoperative assessment
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)

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

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

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

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

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

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

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

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)


  • Most common cause RHD
  • Primarily affects females
  • Diffuse thickening of mitral leaflets & subvalvular apparatus, Calcification
  • Gradual progression (over 20-30 yrs)
  • Other causes: Carcinoid syndrome, LA myxoma, Severe mitral annular calcification, RA, thrombus formation, SLE, congenital

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


    • 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

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


    • Mild MS: Diuretics
    • In AF: Beta blockers, Ca #, Digitalis (H.R. control)
    • Anticoagulants (Warfarin to get INR of 2.5 to 3)
    • Surgical correction:
      • Percutaneousvalvotomy
      • Valve reconstruction
      • Valve replacement, surgical commisurotomy

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+

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)

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), neuraxialopioids
  • May require mechanical ventilation (thoracic surgery)


  • In RHD, usually assoc with MS
  • Other causes: Papillary muscle dysfxn, mitral annular dilatation, rupture of chordaetendinae, endocarditis, MVP, Congenital
  • Pathophysiology:
  • Regurgitation into LA

LA volume overload

Dec LV stroke volume

LA enlargement & AF

  • Pulmn congestion

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)

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


  • 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

Management of Anaesthesia:

  • Prevent events which Dec C.O.
  • Maintain N to slightly higher H.R.
  • Vasodilators to decafterload
  • 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

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)


  • Prolapsed one/ both mitral leaflets into LA during systole
  • M.C. form of valvulards. (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

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


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 81-325mg/d)
  • Pt with AF &/or with atrial thrombi or previous stroke (usually on warfarin)
  • ECG changes (PVC’s, QT prolongation) no implication

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

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)


  • Degeneration & calcification of leaflets (ageing), then stenosis
  • Causes : Elderly, Bicuspid Aortic Valve
  • N valve area: 2.5-3.5 cm2
  • Almost always assoc with some AR

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

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

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


  • Avoid drugs which suppress S.A.node (if occurs give atropine/ glyco/ ephedrine)
  • If persistent tachycardia use esmolol
  • In supravent. tachycardiascardioversion 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, Intraarterialcath, P.A. cath, TEE


  • Causes: IE, RF, Bicuspid aortic valve, ds of root of aorta

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


  • 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

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


  • 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


  • 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

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)


  • M.C.cause: RHD (coexiztant TR, Mitral n aortic valve ds)
  • Inc RA pressure & pressure gradient b/w RA & RV
  • Secondary to Pulmn HT
  • Rarely symptomatic
  • Usually congenital (detected and treated in early childhood)
  • C/F: Syncope, angina, RV Failure
  • Tt: surgical valvotomy