Anaesthesia For Valvular Heart

Diseases

Made by: Dr. Meenal AggarwalModerator: Dr. Aparna

Introduction

• 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

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

o Note: character, location, intensity, direction of radiation

o Systolic murmurs: AS, PS or MR,TR

o Diastolic murmurs: MS, TS or AR, PR

Dysrhythmias: AF (esp Mitral valve ds.) i.e. with enlarged Lt

atria

• Lab Investigations:

CXR:

o Size & shape of heart & great vessels

o Pulmonary markings

o Enlarged LA (Elevated Lt main bronchus, calcified valve)

ECG:

o Lt or Rt axis deviation (Lt or Rt ventricle hypertrophy)

o P mitrale (Broad notched P wave in Mitral valve ds.)

o Dysrhythmias

o Conduction abnormalities

o Evidence or active ischemia or previous MI

Echo with doppler:

o Evaluating significance of murmurs

o Detection of antomical defects (Hypertrophy, chamber

size, valve area)

o Functional defects (Transvalvular pressure gradient,

magnitude of valvular regurgitation)

Cardiac Catheterisation: Solves discrepancies b/w clinical

and echo findings

o Presence & severity of stenosis or regurgitation

o Intracardiac shunting

o 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:

1. Prosthetic material for cardiac valve repair

2. Previous IE

3. CHD: Unrepaired CHD, Completely repaired with prosthetic

material (during 1st 6 months after procedure), Repaired

defects with residual defect)

4. 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)

MITRAL STENOSIS:

• 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

Pathophysiology of Mitral Stenosis

Mechanical obstruction to LV diastolic filling

Decreased mitral valve orifice

Inc LA volume & pressureDec LV volume

Dec S.V. Inc Pulmn Venous Pressure

Overt Pulmn EdemaRV Hypertrophy & failure

• 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

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

• 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

• 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), neuraxial opioids

May require mechanical ventilation (thoracic surgery)

MITRAL REGURGITATION:

• In RHD, usually assoc with MS

• Other causes: Papillary muscle dysfxn, mitral annular dilatation,

rupture of chordae tendinae, endocarditis, MVP, Congenital

• Pathophysiology:

Dec LV stroke volume

Regurgitation into LA

LA volume overload

LA enlargement & AFPulmn 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

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

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

• 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)

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

• 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)

AORTIC STENOSIS:

• 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

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

AORTIC REGURGITATION:

• 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

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

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

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

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

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)

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

Thank You