Anaesthetic management of Valvular Heart Disease

Presented by :- Dr Ravi shankar sharma Sanjay gandhi memorial hospital,Rewa

Patient details

• Name: Mrs. Savitha ,staff nurse• Age: 42 years • Sex: female

• Chief Complaints :-Large pelvic mass(suspected to be ovarian

cyst),scheduled for excision of mass. -Palpitations since 6 weeks -Breathlessness since 4 weeks -Fatigue since 2 weeks

History of Presenting Illness

• Palpitation –Intermittent, Associated with exertion Relieved on rest 6 weeks duration• Breathlessness- Gradual in onset,she can climb

2 flights of stairs without difficulty but feels breathlessness beyond this point

-Progressive in nature (NYHA II) -4 weeks duration

• Fatigue – - Feeling of weakness - 2 weeks duration h/o rheumatic heart disease since 12 yrs of age,

took T/t in form of penicillin injections every 21 days for 8 years till age 20 and then discontinued

h/o normal previous pregnancy 15 year agoH/o Ballon mitral valvotomy -13 yr ago.No h/o hypertension, Diabetes mellitus,

tuberculosis ,bronchial asthma or epilepsy

• Family history:-no h/o similar complaints in the family was

noted• Personal history:-VegetarianReduced appetiteNormal bladder and bowel movementDisturbed sleepNo addiction

General physical examination• An elderly female patient , moderately built and

nourished• No pallor/icterus/cyanosis/oedema/clubbing• weight-55kgs, • Height-160cm,• Pulse-90/min,• B.P.-110/70 mm of hg • Respiratory rate-16/min• JVP:-not raised

• Respiratory system:-B/L equal air entryNormal vesicular breath soundNo added sounds

• Central nervous system:-Conscious Well oriented to time place and personNo neurological deficits

• Per abdominal examionation:- Distended in the pelvic regionNo free fluidNo dilated veins• Cardiovascular system:-Inspection: No deformity, smallscar mark

present over the precordium, no engorged superficial veins , no visible pulsations

Palpation: Apex beat felt in 5th IC space medial to left mid clavicular line , abesence of parasternal heave

• Auscultation:-S1 S2 heard,(S1 is short,shrp,accentuated)Opening snap heard near the apex(after s-2)Low pitched mid diastolic murmur at apex(no

radiation)

Investigations:-

• Hb-12.4 gm%• TLC-7400 cells/cumm(P-76,L-17,M-4,E-3,B-0)• Platelet-2.3lac.• Blood group-B+ve• BT:-3min.• CT:-4 min.• RBS:-94 mg/dl• Urea:-38 mg/dl• Creatinine:-1.3mg/dl

• Na+:-135 meq/l• K+:-4.5meq/l• Cl-: 104meq/l• HIV 1&2-non reactive• HbsAg-Non reactive• ECG:-sinus Rhytm ,H.R.-75/min, Right axis

deviation• ECHO:-normal left ventricular systolic functionNo regional wall motion abnormalitiesEjection fraction-50%• CXR:-cardiomegaly, prominent Bronchovascular

marking

Substantiation

disturbed sleep

Absent Parasternal heave – mild disease

Edema & Hepatomegaly absent – mild disease

Opening snap +murmur at apex

Childhood history

Female Patient

Rheumatic Heart Disease

Edema & hepatomegaly

absent

Palpitations Dyspnea

Absent parasternal heave – mild disease

Opening Snap + low pitched mid diastolic

murmur

2D – Echo – Mitral Valve 2.0 cms2,(theory), Transvalvular pressure 8 mm of Hg

Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.

MITRAL STENOSIS

Narrowing of the mitral valve orifice causing obstruction to blood flow from left atrium to the left ventricle.

Etiology of Mitral Stenosis

1. Rheumatic Heart Disease-M.C. cause2. Congenital – Parachute Mitral Valve3. Hunter’s Syndrome4. Hurler’s Syndrome5. Drugs – Methysergide6. Carcinoid syndrome7. Amyloidosis8. Mitral annular Calcification9. Rheumatoid Arthritis10. Systemic Lupus Erythematosis11. Infective endocarditis with large vegetations. 12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral

Stenosis (MS) rheumatic origin

Pathophysiology

Decreased LV filling

Increased left atrial pressure and volume

Pulmonary vein pressure

Transudation of fluid into pulmonary interstitial space

Pulmonary compliance

Work of breathing

Progressive Dyspnea

Adaptation Atrial Kick

Adaptation

Lymphatic drainage and thickening of basement membrane

Pulmonary hypertension

Palpitations

Breathlessness Haemoptysis

Pathophysiology

Almost all chambers are shown here , except…

Left Ventricle

So, are we to assume that Left Ventricle

remains unaffected..?

Pathophysiology

The answer is NO. Left Ventricle is affected

Decreased filling ultimately manifests as

1. muscle atrophy

2. Inflammatory myocardial fibrosis

3. Scarring of sub valvular apparatus

4. Abnormal pattern of left ventricle contraction

5. Decreased left ventricular compliance with diastolic dysfunction

6. Right to left shift due to pulmonary hypertension

Common symptoms

1. Dyspnoea

2. Orthopnea

3. Paroxysmal Nocturnal Dyspnea

4. Palpitation

5. Fatiguability

6. Haemoptysis

7. Recurrent Bronchitis

8. Cough

9. Chest pain

10. Right hypochondrial Pain (hepatomegaly)

Mitral Stenosis: Physical Examination

S1 S2 OS S1

• First heart sound (S1) is loud and snapping

• Opening snap (OS)

• Low pitch diastolic rumble at the apex

• Pre-systolic accentuation (esp. if in sinus rhythm)

GRADING :-

Normal Orifice: 4 – 6 Cms2

4-6 cms2

< 2.5 cms2

1.5- 2.5 cms2

1.0 – 1.5 cms2

< 1.0 cms2

Mild MS – 1.5 – 2.5 Cms2

(Dyspnea on severe exertion)

Moderate MS – 1.0 – 1.5 Cms2

(PND ± pulmonary oedema)

Severe/ Critical- < 1.0 Cms2

(Orthopnea – Class IV)

Symptoms start < 2.5 Cms2

Anatomy

Mitral Valve area is calculated using Gorlin’s Equation:

Area = Cardiac Output/ (DFP or SEP) (HR) 44.3 C √ΔP

DFP = Diastolic Filling Pressure

C = Empirical Constant

SEP = Systolic Ejection Period

ΔP = Pressure Gradient

HR = Heart Rate

Cormier’s grading of Mitral valve anatomy

Echocardiographic group Mitral valve anatomy

Group 1 Pliable non calcified anterior mitral leaflet and mild subvalvular disease(ie thin chordae>/=10mm long)

Group 2 Pliable non calcified anterior mitral leaflet and severe subvalvular disease(thickened chordae<10mmlong)

Group 3 Calcification of mitral valve of any extent as assesed by fuoroscopy ,whatever the state of subvalvular apparatus

DiagnosisOne needs to assess anatomy of Mitral Valve Leaflet in terms of

1. Thickening

2. Calcification

3. Mobility

4. Extent of involvement and subvalvular apparatus

One also needs to assess extent of stenosis

5. Mitral Valve area

6. Transvalvular pressure gradient Also to be assessed are

7. Cardiac chamber dimension 2. Pulmonary hypertension

3. Ventricular function 4. Associated valvular disease

5. Examination of Left Atrial Thrombus

Diagnosis

Assess extent of calcification

1. Disappearance of Opening snap especially if calcification is more.

Assessment of X-Ray (P-A View)

2. Left Atrial Enlargement – Mitralisation of heart

3. Straightening of Left Heart Border

4. Elevation of Left mainstem Bronchus

5. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary

Vascular Congestion.

6. Kerley’s B lines

Assessment of X-Ray (RAO view)

1. Oesophagus is pushed or curved backward by enlarged left atrium.

DiagnosisAssessment of ECG

1. Broad notched “P” Waves signifying atrial enlargement.

2. Atrial Fibrillation (f- waves replacing p-waves)

3. Right Ventricular Enlargement

2D – Echocardiography Doppler study

4. Chamber Enlargement 1. To know the speed and direction of blood

flow.

5. Valve pathology

6. Valve movement

7. Mitral Orifice

Blood Examination

1. TC and DC 2. ESR

3. ASO Titre

Treatment1. Mild Mitral stenosis – Diuretics

Restriction of physical activity

Salt-restricted diet

2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet)

β- Blockers

Calcium Channel Blockers

Control of heart rate is paramount, because tachycardia impairs left ventricular

filling and further increases left atrial pressure.

3. Anticoagulation – Warfarin to normalise INR 2.5 to 3.0

Treatment

4. Surgery if Pulmonary hypertension develops

Percutaneous balloon valvotomy

Surgical commisurotomy

Valve reconstruction

5. Valve replacement

Starr-Edwards ball valve

Bjork-Shiley disc valve

Porcine bio-prosthesis

6. Prophylaxis against recurrence of rheumatic fever

Inj. Benzathine Penicillin 1.2 million units.

Anaesthetic Management

Anaesthetic ManagementPrinciple involved:

Cardiac Output

Decrease in cardiac output

Hypotension

Tachycardia

Reduced ventricular filling

Vicious cycle

Increased ventricular filling

Trendelenburg's position, Autotransfusion due to uterine contraction

Precipitation of CHF 1

2

3

Anaesthetic ManagementPrinciple involved:

1. Prevent decrease in cardiac output, as hypotension because of this causes

reflex tachycardia, which in turn reduces ventricular filling further

compromising cardiac output.

2. Avoid hypotension for the same reason listed above. If hypotension ensues,

treat with Ephedrine or Phenylephrine.

3. Avoid precipitating Congestive Heart Failure due to factors such as Trendelenburg’s position Autotransfusion due to uterine contraction leading to increased central blood volume. 4. Avoid precipitation of Right Ventricular Failure Hypercarbia Hypoxemia Lung Hyperinflation Increase in lung waterIf Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.

Anaesthetic ManagementPreoperative Medication

1. Decrease anxiety (decreases tachycardia),also avoide anti- cholinergics.

2. Drugs used to control heart rate to be continued till day of surgery

3. Hypokalemia if present secondary to diuretic therapy to be addressed

4. If intended surgery is a minor surgery, continue anticoagulant therapy

5. If intended surgery is a major surgery, discontinue anticoagulant therapy. Induction of Anaesthesia

6. Avoid Ketamine – Increases heart rate, Avoide Propofol(fall in blood pressure)

(ETOMIDATE/THIOPENTONE)-Better choice

7. Avoid Atracurium – Increased histamine release causes hypotension which

manifests as tachycardia.(vecuronium-preffered)

Anaesthetic ManagementMaintenance of Anaesthesia

1. Drugs should have minimal effects on hemodynamic pattern

2. Balanced anaesthesia with Narcotic/ N2O /Volatile anaesthetic(avoide

halothane)

3. N2O causes insignificant pulmonary vasoconstriction. It is significant only if

pulmonary hypertension exists. So, one needs to treat pulmonary

hypertension preoperatively.

4. Cardiac stable muscle relaxants are to be used. (preferably avoid Pancuronium)

5. Avoid lighter planes of anaesthesia (To avoid tachycardia)

6. Fluid Management:

Avoid Hypervolemia - -> Worsens pulmonary edema

Avoid Hypovolemia - -> Sacrifices already decreased left ventricular filling,

which further decreases Cardiac output. Hypovolemia secondary to

blood loss and vasodilatory effects of anaesthesia ought to be avoided.

Anaesthetic ManagementMonitoring

1. Transesophageal Echocardiography

2. Intra-arterial pressure

3. Pulmonary artery pressure to be monitored

4. Left atrial pressure Principle:

5. Ensure adequacy of cardiac function

intravascular fluid volume

ventilation

oxygenation A word of caution regarding Pulmonary artery pressure monitoring: -When measured too frequently, the risk of pulmonary artery rupture is far too high.

Anaesthetic ManagementPost Operative

1. Assess postoperative risk of pulmonary oedema and right heart failure and

manage accordingly.

2. Avoid pain as pain begets hypoventilation which leads to respiratory acidosis,

hypoxemia which manifests as raised heart rate and pulmonary vascular

resistance.

3. After Major thoracic or abdominal surgery, the decreased pulmonary

compliance and increased work of breathing requires mechanical ventilation.

Role of regional anaesthesia in MS:-

Regional anaesthesia (Sub Arachnoid Block, Epidural, peripheral nerve blocks)

Sub Arachnoid Block:-can be used in mild cases of MS only-sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia should be avoided

Epidural Block: compared with spinal anaesthesia epidural anaesthesia allow better control of level of sympathectomy and reduction in blood pressure-can be used as a sole anaesthesia technique in patients with mild to moderate MS

Peripheral nerve blocks : can be used safely-ASRA guidelines on regional anaesthesia in patient receiving anticoagulation or thrombolytic theory should be followed

The New York Heart Association (NYHA) Grading of functional capacity of the heart:

CLASS INo functional limitation of activity

Symptoms with extra ordinary physical work.

CLASS II Mild limitation of physical activity.

Symptoms with ordinary physical work

CLASS IIIMarked limitation of physical activity Symptoms with less than

ordinary physical work

CLASS IV Severe limitation of physical activity Symptoms at rest

Management of pregnancy with MS

Prognosis depends on the functional status

v NYHA classes I and II lesions usually do well during pregnancy and have a favorable prognosis (mortality rate of <1%). v NYHA classes III and IV -mortality rate of 5% to 15%. -These patients should be advised against becoming pregnant.

Why does pregnancy aggravate the symptoms of Mitral stenosis

I. ↑ in blood volume by 30-50%→↑ in pulmonary capillary hydrostatic

pressure→ ↑ risk of pulmonary oedemaII. ↓in systemic vascular resistanceIII. ↑ in HR by 10-20 beats /min→ ↓diastolic filling time of LVIV. C.O. ↑ by 30-50% after 5th month &returns to normal within 3 days

of deliveryV. Because TPG ↑by square of CO,TPG ↑ significantly →LA pressure

→symptomsVI. During labour &delivery →sympathetic stimulation →tachycardia →

↑COVII. ↑in venous return to heart d/t autotransfuson and IVC compression

→decompensationVIII. Enlarged atrial dimension predispose to atrial arrythmias including

atrial fibrillationIX. Also induces changes in haemostasis which contribute to increased

coagulability and thromboembolic stroke

Anaesthetic Options

VAGINAL DELIVERY : Recommended whenever possible if the haemodynamic condition is

stable at the end of pregnancy

• Epidural anaesthesia is recommended

• Tachycardia, secondary to labour pain, increases flow across the mitral valve, producing sudden rises in left atrial pressure, leading to acute pulmonary oedema. This tachycardia is averted by epidural analgesia without significantly altering the patient haemodynamics.

• LA can be used to provide Perineal anaesthesia

• Caesarean section is indicated for OBSTETRIC REASONS ONLY.

When to give Infective Endocarditis Prophylaxis..?

Aortic Stenosis• Aortic stenosis (AS) is narrowing of the aortic

valve resulting in obstruction of blood flow from the left ventricle to the ascending aorta during systole.

-Normal aortic valve area is 2.5 to 3.5 cm²

Etiology

• congenital bicuspid aortic valve (2%).

• Rheumatic heart disease.

• Valve Calcification.

Pathophysiology:-

AS severity

Severity Mean gradient,mm Hg

Aortic valvearea, cm2

Mild <25 >1.5

Moderate 25-40 1.0-1.5

Severe >40 <1.0

Critical >80 <0.7

Normal aortic valve area is 2.5 to 3.5 cm²

Aortic Stenosis: Physical Findings

S1 S2 S1 S2

Mild-Moderate Severe

An early peaking murmur is typical for mild to moderate ASLate peaking murmur is consistent with severe AS. Delayed A2Pulsus Tardus-pulse ie slowly rising to peak and then has a low down slope

Medical Treatment• Antibiotic prophylaxis is NOT recommended in all pts with AS for

prevention of infective endocarditis.

• Caution with diuretics and vasodilators (reduce preload)

• HTN should be treated cautiously with appropriate antihypertensives (preload dependence)

• Statins have been studied to see if they cause regression or delayed progression of leaflet calcification (need more data)

Effective treatments for severe AS:-1.Surgical replacement of the aortic valve 2.Transcatheter aortic valve replacement (TAVR)

Anesthesia concerns:– Maintain normal sinus rhythm – Avoide bradycardia or tachycardia– Watch out for vasodilation(hypotension)Rx-

phenylephrine– Optimize i/vascular fluid volume to maintain venous

return and left ventricular filling– Mild to moderate AS may tolerate spinal or epidural

(epidural preferred)– Spinal and epidural contraindicated in severe AS– High risk of myocardial ischaemia

Pregnancy considerations

Caesarean section: -General anaesthesia with the aid of invasive haemodynamic

monitoring. Aggressive maintenance of systemic blood pressure with vasopressors (e.g. phenylephrine).

- Spinal anaesthesia is generally contraindicated. - vaginal delivery under carefully introduced and limited epidural analgesia in mild cases

Mitral Regurgitation A portion of the LV volume is ejected back into

LA during systole because of an incompetent valve.

EtiologyACUTE– Myocardial ischemia

or infarctions– Infective

Endocarditis– Chest trauma

CHRONIC Rheumatic fever Incompetent valve Destruction of mitral valve

annulus

Chronic MR: PathophysiologyVol load imposed on LA & LV (usually it gradually ↑ over time)

Large total SV (supra normal EF) and normal forward SV

MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR

↑ Preload, LV hypertrophy, & reduced or normal afterload (low resistance LA provides unloading of LV)

↑ LVEDP &↑ LAP

Compensatory dilatation of LA & LV to accommodate vol load at lower pressure; this helps relieve pul congestion

LV hypertrophy (eccentric) stimulated by LV dilatation (↑ wall stress- Laplace Law)

Chronic MR: Pathophysiology..continue

Reduced forward SV/CO

MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR

Pul congestion & pHTN

Contractile dysfunction

↓ EF, ↑ end-systolic volume ↑ LVEDP/ vol, ↑ LAP

Regurgitant fraction >0.6 -severe mitral regurgitation.

Symptoms and signs

Acute phaseC/f of decompensated

congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea),

- decreased exercise tolerance -Palpitations.- cardiogenic shock

Chronic phase

• may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure.

• individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).

MOHAMMAD ALADAM

The symptoms associated with mitral regurgitation are dependent on which phase of the disease.

MITRAL REGURGITATION

Acute Chronic

ECG Normal P mitrale, AF, Left Ventricular Hypertrophy

Heart size Normal Cardiomegaly, left atrial enlargement

Systolic murmurHeard at the base, radiates to the neck, spine, or top of head

Heard at the apex, radiates to the axilla

Apical thrill May be absent Present

Jugular venous distension Present Absent

Chest X Ray- - Enlarged LA and LV,

-Signs of pulmonary venous hypertension-RVH-Mitral calcification (in co existing MS)

Severity of MR evaluated by:-Color-flow and pulsed-wave Doppler-Pulmonary artery occlusion pressure waveform -Cardiac catheterisation-ECHO-confirms diagnosis ,Also assess mechanism and severity of MR

DIAGNOSIS:-

MILD MODERATE SEVERE

Area of MR jet (cm2) <3 3.0-6.0 >6MR jet area as percentage of left atrial area 20–30 30–40 >40

Regurgitant fraction (%) 20–30 30–50 >55

• TREATMENT

• Drugs- Digoxin, diuretics for CHFVasodilators ( ACE inhibitors, nitrates) in acute symptomatic MRWarfarin for AF/Thromboembolism

• Surgery--Mitral annuloplasty/valvuloplasty-Mitral valve repair> replacement

• Patients with an EF <30% or left ventricular end-systolic dimension more than 55 mm do not improve with mitral valve surgery.

• 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 goals

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 desirableVecuronium/ Atracurium- depending on basal HR

• MAINTAINENCE• Volatile anesthetics ( Isoflurane ,sevo, des)

Increase in heart rate and minimal negative inotropic effects. Vasodilatation desirable.(afterload reduction)

• Nitrous oxide avoided in severe PAH.• myocardial function is severely compromised--- opioid-based anesthetic potent narcotics → bradycardia, deleterious in severe MR.

MAINTAINENCE cont......• Mechanical ventilation → 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.

• Monitoring • Invasive monitoring- ( CVP, PAC)

Useful in severe MR- detecting the adequacy of CO and the hemodynamic response to anesthetic and vasodilator drugs

• facilitating intravenous fluid replacement.

• Pulmonary artery occlusion pressure –-V waveform to assess severity of MR

Aortic regurgitation (AR)Aortic regurgitation (AR) is a diastolic reflux of blood from the aorta into the left ventricle owing to failure of coaptation of the valve leaflets during diastole- d/t aortic valve disease/aortic root dilatation or combination of both

Etiology

Acute AR

• Infective endocarditis

• Prosthetic valve dysfunction

• Aortic dissection

• Trauma

• Systemic hypertension

Chornic AR

• Bicuspid Aortic Valve• Rheumatic and SLE• Degenerative

andHypertension• Anorectic drugs • Aortitis• Giant cell arteritis• Ankylosing spodylitis• Connective tissue disorders

Symptoms:-

Asymptomatic: 10-15 Years

PALPITATION -( early symptom), head pounding - on exertion, exertional dyspnoea , orthopnoea , paroxysmal nocturnal dyspnoea ,excessive diaphoresis , angina ,ccf - late

Corrigan pulse or Water hammer pulse or Collapsing pulse ie Rapid rise and rapid fall ,Bisferiens’s pulse -two peaks in systole

Widened pulse pressure along with dec. diastolic blood pressure

Early diastolic murmur, Austin flint murmur( Soft, low pitched rumbling mid diastolic murmur)

Peripheral Signs of AR• Lighthouse sign ( blanching of forehead)• Landolfi’s sign ( alternate dilatation and contraction of iris)• Becker’s sign (prominent retinal artery pulsations)• De Musset’s Sign (head bobs with heart beat)• Corrigan’s sign ( Dancing carotids )• Muller’s sign (systolic pulsation of uvula)• Corrigan’s pulse (water hammer pulse)• Quninckey’s sign (pulsatile nailbed)• Palfrey’s sign ( pistol shot sounds in radial artery )• Rosenbach’s sign (pulsations in liver)• Gerhart’s sign ( pulsations in spleen )• Traube’s sign (Pistol shot sounds in femoral artery)• Duroziez murmur (murmur heard over femoral artery) systolic on

proximal compression , diastolic on distal compression • Hill sign (popliteal systolic pressure – Brachial 20-40 – mild, 40-60 –

mod > 60 mm Hg severe AR)

• ECG- shows Lt axis deviation• CXR- Cardiomegaly ,Hypertrophy and dilatation of LV• Echo• Doppler examination-to identify the presence and severity • AR quantification by Based on– Color flow Doppler (Jet width and jet area measurement)– Continuity equation &Regurgitant jet velocity assessment

Treatment:-Vasodilators , inotropes(improves LV stroke volume

&↓reguirgitant volume chronic aortic regurgitation (requires surgery) Long term Rx with nifedipine/hydralazine –delays the need

of surgey

Diagnosis:-

Anesthetic considerations

– Maintain normal heart rate (avoide bradycardia)– Keep SVR low– Avoid myocardial depression– GA is usual choice for patient with AR– Spinal/Epidural well tolerated.

Pregnancy considerations-During labour, epidural analgesia improves forward flow, and is therefore the anaesthetic of choice in patient’s requiring an operative delivery.