MITRAL STENOSIS

MITRAL VALVE

MVA 2 sq cm -significant

BICUSPID

MILD MS -- 1.5 TO 2.0

CHORDAE

MOD. MS -- 1.0 TO
1.5

SEVERE MS -- < 1.0

CRITICAL -- < 0.6

LEFT

MVA

SIDED

TENDINAE

- 4 TO 6 sq cm

ETIOLOGY

MOSTLY RHEUMATIC . UNLESS PROVED

OTHERWISE !

Rare causes are

CONGENITAL
CALCIFIC as age advances
COR TRIATRIATUM,CARCINOID SYNDROME
SLE, RHUMATOID ARTHRITIS
INFECTIVE ENDOCARDITIS , LA MYXOMA

 DIFFUSE

THICKENING OF THE
MITRAL LEAFLETS AND
SUBVALVULAR APPARATUS,

COMMISSURAL FUSION,

CALCIFICATION

AND LEAFLETS

OF THE ANNULUS

PATHOPHYSIOLOGY

an abnormally elevated left

atrioventricular pressure gradient
. the
hemodynamic hallmark of MS.

PRESSURE GRADIANT ACROSS MV

LEFT ATRIAL VOLUME OVERLOAD
BOTH VOLUME AND PRESSURE OVERLOAD
PROGRESSIVELY INCREASED LEFT ATRIAL
PRESSURE
LEFT ATRIAL ENLARGEMENT AND
HYPERTROPHY
DISTORTION OF LA CONDUCTION
PATHWAYS ATRIAL FIBRILLATION

Changes in the pulmonary

vasculature

LA PRESSURE IS TRANSMITTED TO PULMONARY VEINSINCREASED PULMONARY VENOUS PRESSURE

PULMONARY VENOUS CONGESTION-DUE TO
TRANSUDATION OF FLUID INTO INTERSTITIAL SPACE
PULMONARY CONGESTION.DECREASED PULMONARY
COMPLIANCE - INCREASED WORK OF BREATHING
PULMONARY OEDEMA-WHEN PULMONARY VENOUS
PRESSURE EXCEED PLASMA ONCOTIC PRESSURE
REACTIVE CHANGES IN THE PULMONARY VASCULAR
BED
PULMONARY ARTERIAL HYPERTENSION

RIGHT VENTRICULAR
CHANGES

.. PULMONARY ARTERIAL HYPERTENSION

RIGHT VENTRICULAR PRESSURE RISES
R V HYPERTROPHY
RV DILATATION
RV FAILURE
TRICUSPID REGURGITATION ,PULMONARY
REGURGITATION.

LEFT VENTRICULAR
CHANGES

DECREASED FILLING

LV FUNCTION USUALY PRESERVED

DECREASED VOLUME

DECREASED PRESSURE

THINNING OF LV WALL

SYMPTOMS

Initial attack of rheumatic carditis

2 decades

Symptoms of mitral stenosis

disability in 4th decade of life
2-5 years
death

Dyspnea

Large mitral orifices

normal flow

mild elevations in LA pressure

Cough

Marked increase in LA
pressure

dysnoea

Precipitated by sudden changes in

Heart rate
Volume status
Cardiac output

As mitral stenosis progresses

Lesser stress

dysnoea

Patients daily activities limited

Orthopnoea

and nocturnal dysnoea

MECHANISM
Pulmonary venous pressure increases
Fluid driven out
Decreases compliance
Increased work of breathing
dysnoea

ACUTE PULMONARY EDEMA

Pulmonary capillary pressures exceed

oncotic pressure

Lymphatic unable to decompress this fluid

Usually preceded by orthopnoea and PND

Can occur suddenly in patients with non

critical mitral stenosis

Pregnancy

One of the most common precipitants

Increased mitral valve flow due to

Increased cardiac output
Increased heart rate
Central blood volume

Maximal at 25 to 27 weeks

Haemoptysis

Rupture of pulmonary bronchial venous

connections

Elevated LA pressures without markedly

elevated pulmonary vascular resistances

Almost never fatal

Recurrent pulmonary emboli

Pulmonary infections
Bronchitis , bronchopneumonia and lobar
pneumonia complicate untreated MS
esp. in winter

Thrombi and emboli

Left atrial appendage

Systemic embolization more in

Atrial fibrillation
Older patients
Reduced cardiac output

DUE TO DECREASED CARDIAC

OUTPUT
LOW EFFORT TOLERANCE
EASY FATIGUABILITY
SYNCOPE
MITRAL FACIES
DUE TO LEFT ATRIAL ENLARGEMENT
ORTNERS SYNDROME
ANGINA DUE TO RV ISCHEMIA IN
SEVERE PULMONARY HTN.

Signs

Mitral facies (pink-purple patches on

cheeks).

JVP prominent a wave

Apex tapping apex ( S1)

Right parasternal heave

Diastolic thrill at the cardiac apex

Auscultation

S1

S2 OS

S1

First heart sound (S1) is accentuated

and snapping
Opening snap (OS) after aortic valve
closureS2-OS GAP LESS THAN 0.08 S
SEVERE D/S
Low pitch diastolic rumble at the apex
Pre-systolic accentuation (esp. if in sinus

Hepatomegaly

Ascities

Ankle odema

Pleural effusion ( right sided)

INVESTIGATIONS

Electrocardiogram
LEFT ATRIAL HYPERTROPHY CAUSES P MITRALE-BIFID APPEARANE OF P WAVE IN
LEAD 2,3 AVF
SECOND HALF OF THE P WAVE IS NEGATIVE IN V1.
ATRIAL FIBRILLATION
RIGHT VENTRICULAR HYPERTROPHY-DOMINANT R
WAVE IN V1 V2.
RIGHT AXIS DEVIATION.
PATIENT ON DIGOXIN-DIGITALIS EFFECTS (ST
DEPRESSION WITH A SAGGING,DECREASED T WAVE
AMPLITUDE,SHORTENED QT,PROMINENT U WAVE)

Echocardiogram
Trans thoracic 2 dimensional echocardiogram with flow doppler
(TTE)
Trans esophageal echocardiogram (TEE)
USED TO ASSESS ANATOMY OF MITRAL VALVE,DEGREE OF
LEAFLET THICKENING,CALCIFICATION,CHANGES IN MOBILITY
AND EXTENT OF INVOLVEMENT OF SUBVALVULAR
APPARATUS,EVALUATION OF CARDIAC CHAMBER
DIMENSIONS,LEFT AND RIGHT VENTRICULAR FUNCTION,OTHER
VALVULAR D/S AND EXMNTN OF LEFT ATRIAL APPENDAGE FOR
PRESENCE OR ABSENCE OF THROMBUS.
SEVERITY OF MITRAL STENOSIS IS ASSSSED BY
CALCULATION OF MITRAL VALVE AREA AND MEASUREMENT OF
TRANSVALVULAR PRESSURE GRADIENT,MITRAL TRANSVALVULAR
PRESSURE GRADIENT HIGHER THAN 10 INDICATES SEVERE D/S.

GRADES OF MS
SEVERITY

MVA(CM2)

EDP
PAP
GRADIENT(
mmhg)

SYMPTOM
S

MILD

>1.5

<5

<30

USUALLY
ABSENT

MODERATE

1-1.5

5-10

30-50

NYHA CLASS
2

SEVERE

<1

>10

>50

NYHA CLASS
3-4

Chest X-Ray

USUALLY NORMAL OR SLIGHTLY ENLARGED CARDIOTHORACIC RATIO

Straightening of left heart border(DUE TO ENLARGED LA APPENDAGE)
Small aortic knuckle due to decreased cardiac output
Elevation of left main stem bronchus due to enlarged left atrium.

Prominence of main pulmonary arteries due to pulmonary hypertension.

Dilation of upper lobe veins moustache or antler sign

Kerly B lines
Double density in mid portion of cardiac silhoutte due to LA enlargement.
Left lower lobe collapse due to compression of left lower lobe bronchus.
Miliary shadows of pul. haemosiderosis. Due to pul.hge
Calcification of mitral valve.
Indentation of esophagus on lateral xray. Due to enlarged LA

Cardiac cathetherization

Discrepancy between clinical and TTE not

resolved with TEE and Cardiac Magnetic
Resonance

Associated lesions assessment

Coronary arteriography

Previous manipulations

Management

Medical treatment :
1. Patients with a Rheumatic MV should be considered
for Penicillin prophylaxis.

2. If in Atrial Fibrillation , should receive long term

anticoagulation (WARFARIN to maintain INR b/w
2.5-3)

Management
3. Digoxin , Beta blockers or Calcium
channel blockers to reduce heart rate of
patients with Atrial Fibrillation.
4. Symptomatic patients would benefit from
Diuretics such as frusemide to reduce left
atrial pressure and reduce Dyspnea.

Management

Patients with moderate to severe MS and

symptoms should have either :
1. Percutaneous balloon Mitral Valvotomy
2. Surgical Valvotomy
- Open
- Closed
3. Mitral valve replacement
- Mechanical prosthesis
- Bioprosthesis

Mitral Stenosis
Management Guidelines
Indications for PMBV (class I and IIa)
Suitable anatomy, no LA clot, mild MR
Symptomatic pts (NYHA class II-IV) with MVA
<1.5 cm2
Asymptomatic pts with MVA <1.5 cm2 and
PASP 50 mmHg at rest, 60 with exercise

PMBV

Pliable leaflets without calcium

Subvalvular structures

No left atrial thrombus

Open valvotomy

PMBV not possible

PMBV unsuccessful

Re stenosis

Open valve commisures

Loosen sub valvular fusion

Remove large deposits of calcium

Remove atrial thrombi

Pregnancy
PMBV with TEE with no or minimal X ray
exposure

Mitral valve replacement

MS with associated significant mitral

regurgitation

Valve severely distorted

Preservation of chordal attachments

Peri operative mortality vary with age , LV

function, presence of CAD and associated
co morbidities

Severe MS , MVA less than 1 cm , NYHA III

ANAESTHETIC
MANAGEMENT

Intraoperative event which

causes significant impact on MS
SINUS TACHYACARDIA OR A RAPID VENTRICULAR
RESPONSE DURING AF.
2. MARKED INCREASE IN CENTRAL BLOOD VOLUME
AS ASSOCIATED WITH OVERTRANSFUSION OR
HEAD DOWN POSITION.
3. DRUG INDUCED DECREASE IN SYSTEMIC
VASCULAR RESISTANCE
4. HYPOXEMIA AND HYPERCARBIA THAT MAY
EXACERBATE PUL.HTN AND EVOKE RIGHT
VENTRICULAR FAILURE.
So management of anesthesia include prevention of
these events.
1.

Atrial fibrillation
Causes rapid ventricular response which significantly decreases
cardiac output and produces pul.edema.
Treatment includes
cardioversion if patient is hemodynamically unstable ,
iv amiodarone (150 mg iv bolus over 15 min followd by 60 mg
per hour for 6 hours then 30 mg per hour with repeat boluses of
150 mg iv as needed upto maximum of 2 g per day)
Metoprolol (5 mgbolus and repeat if needed)
Esmolol (500 microgm per kg iv over 1 minute bolus ,may be
repeated in 5 min)
Diltiazem (10-15 mg iv over 2 min may be repeated in 15 min)
Digoxin (0.25-0. 5mg iv,then 0.25 mg iv every 4-6 hrs to
maximum of 1 mg)

Avoid excessive perioperative fluid

administration ,placement in trendelenberg
position increase central blood volume and
can precipitate chf ,so if necessary systemic
bp and systemic vascular resistance can be
maintained with vasoconstrictor drugs such
as phenylephrine or vasopressin

Avoid hypercarbia,hypoxemia ,lung

hyperinflation and increase in lung water
which causes pul htn and rv failure.
Rv failure may require support with
inotropic and pul.vasodilating drugs

Preoperative medications

Used to decrease anxiety and its associated tachycardia

Preop administration of anticholinergic not recommended (due to
tachycardia)
Drug used for heart rate control continued
Diuretic induced hypokalemia should be detected and treated.
Orhostatic hypotension due to diuretic induced hypovolemia
should be noted and treated.
Anticoagulant therapy,minor surgery contd ,major surgery
discontinued.
Neuraxial anesthesia can be used in absence of anticoagulation .
(its use requires measures to avoid hypotension,maintain
adequate preload,and avoid tachycardia.
Compared with SA,epidural anesthesia may allow better control of
the level of sympathectomy and reduction in bp.
Peripheral nerveblocks may also be used safely.

monitoring
Asymptomatic patient same as monitoring of
patient without valvular heart d/s
TEE,useful in patient with symptomatic mitral
stenosis undergoing major surgery
Major surgery-invasive monitoring like intrarterial
pressure should be considered
Pul artery pressure and LA pressure monitoring
confirm the adequacy of cardiac
function,intravascular fluid volume,ventilation and
oxygenation.
PA Catheter has greater risk of pul.artery rupture in
patients with significant pul.htn.

Induction of anesthesia
Iv induction drug with exception of
ketamine can be used
Tracheal intubation and muscle relaxation
accomplished by nm blocker that do not
induce either tachycardia or hypotension
from histamine rls
Short acting beta blockers to treat episode
of tachycardia during induction.
New onset af with hemodynamic instability
cardioversion given.

Maintenance of anesthesia
Accomplished by drugs with minimal effect on heart
rate,myocardial contractility,systemic and pul vascular
resistance.
Achieved by nitrous/narcotic anesthetic.or by low concentration
of a volatile anesthetic
Nitrous oxide can evoke some pulmonary vasoconstriction and
increase pul vascular resistance if pul htn present.
Reversal of the effect 0f muscle rlxnt should be accomplished
slowly to ameliorate any drug induced tachycardia caused by
anticholinergic in the mixture.
Light anaesthesia avoided as it cause sympathetic stimulation.
Pulmonary vasodilator therapy if pulmonary hypertension is
severe
Intraoperative fluid replacement titrated to prevent volume
overload and development of pulmonary odema

POST OP MX
CARDIOVASCULAR MONITORING CONTINUED
POSTOP-due to risk of pulmonary odema and rt
heart failure
Pain,hyoventilation,respiratory acidosis,hypoxemia
avoided as they cause increase HR and pulmonary
vascular resistance.
Decreased pulmonary compliance and increased
work of breathing need mechanical ventilation after
major thoracic and abdominal surgeries
Neuraxial opoid to relieve post op pain can be used
Anticoagulation therapy restarted as soon as periop
bleeding diminished.

Perioperative Goals

Maintain sinus
rhythm when
possible

Control ventricular
rate in atrial
fibrillation

Maintain heart rate

of 70 90 / min.

Maintain PCWP high enough to ensure as

large a LVEDV as possible without
pulmonary oedema.
Avoid markedly increased central blood
volume ( over transfusion & head down
position).
Maintain a normal LV afterload.

MITRAL REGURGITATION.
AETIOLOGY
1)Rheumatic
2)Associated with IHD leading to papilary
muscle dysfunction,mitral annular dilation,or
rupture of chordae tendinae.
3)Endocarditis,MVP,trauma,trauma,LVH,cardi
omyopathy,myxomatous
degeneration,SLE,RA,Ankylosing
spondylitis,carcinoid syndrome.

PATHOPHYSIOLOGY

Basic change seen is decrease in left ventricular stroke

volume and cardiac output.
Stroke volume portion is regurgitated to LA causing left
atrial volume overload and pulmonary congestion.
Patient with regurgitant fraction >.6 has severe MR
Rheumatic induced MR patient has marked LA
enlargement and AF
Myocardial ischemia uncommen in MR
LV hypertophy and increased LA compliance permit
accomodation of regurgitant volume without increase in
LA pressure so patients are asymptomatic for long years
A/c MR presents as pulmonary odema and cardiogenic
shock.

diagnosis
Symptomsorthopnea,dypnoea,PND,fatigue,recurent
respiratory infections,palpitation,oedema of
feet due to ccf can occur
Signs holosystolic apical murmur with
radiation to axilla,cardiomegaly
seen,hyperdynamic apex beat
Severe MR-presence of apical middiastolic
flow murmur,left ventricular s3,degree of
LVH,presence of systolic thrill with a loud
murmur in apical area.

INVESTIGATIONS

CHEST XRAY-LVH,LAH,SIGNS OF PULMONARY HTN IN A/C MR,RVH.

ECG-LAH,LVH,AF.
ECHO-confirm presence,severity,and cause of MR.Also LA
pressure and size,left ventricular wall thickness,cavitary
dimensions,ventricular function,PA pressure measured,also look
for LA Appendage thrombus
COLOUR FLOW AND PuLSED WAVE DOPPLER ECHO-to calculate
regurgitant volume and regurgitant fraction and measure the
area of regurgitant jet-to asses severity.
PULMONARY ARTERY OCCLUSION WAVE FORM V WAVE reflect
regurgitant flow through mitral valve and size of V correlate
magnitude of MR.
CARDIAC CATHETERISATION ANDCORONARY ANGIOGRAPHY if
severity doutful or valve surgery planned

TREATMENT

Symptomatic patient surgery done even EF is

normal.
Mitral valve repair preferred to mitral valve
replacement.
Early surgery done to prevent LV muscle
dysfunction to progress.
Survival prolonged if surgery performed before EF
<60% or before left ventricular end systolic
dimension of 45mm.
Surgery is not use if EF<30% and LV systolic
dimension >55mm.
Vasodilators used in asymptomatic paient.
Symptomatic patient ACE inhibitors B
BLOCKERS(carvedilol)and biventricular pacing
used to decrease functional MR and improve

ANAESTHESIA
MANAGEMENT
COSIDERATIONS
1)PREVENT BRADYCARDIA.
2)PREVENT INCREASE IN SYSTEMIC
VASCULAR RESISTANCE
3)MINIMISE DRUG INDUCED MYOCARDIAL
DEPRESSION.
4)MONITOR MAGNITUDE OF REGURGITANT
FLOW WITH A PA CATHETER OR ECHO.

So anaesthetic goal is to prevent and treat condition

which decrease cardiac output.
Goal is to improve forward LV stoke volume and
decrese regurgitant fraction.
HR MAINTAINED normal or slightly high as bradycardia
cause severe LV overload.
Increase in SVR also decompensate LV.
Afterload reduction with vasodilator like nitroprusside
with or without ionotropic suuport improve LV function.
Regional anaesthesia which decrease SVR beneficial in
some.
Perop sedation and anticholinergics better tolerated.

INDUCTION
BY IV inducing agent-dosing adjusted to
prevent increase in SVR or decrease in HR.
Pancuronium can be used as muscle
relaxant as it produce increase HR which
cause forward left ventricular stroke
volume.

MAINTENANCE
VOLATILE ANAESTHETIC-iso sevo des used as they decrease
SVR,increase HR,Minimal negative ionotropic effects make them
ideal choice.
Myocardial function severley compromised opoid based
anaesthetic can be used as they cause minimal myocardial
depression.
Potent narcotic avoided as they may cause bradycardia.
Mechanical ventilation adjusted to maintain normal acid base
balance and respiratory parameters.
Sufficient time given between breath for adequatevenous return.
Intravascular volume maintenance for maintaining LV volume
and CO.

MONITORING
ASYMTOMATIC-no need of invasive
monitoring.
SEVERE MR-invasive monitoring used for
detecting adequacy of cardiac output and
hemodynamic response to anaesthetic and
vasodilating drugs.
TEE for major surgeries.
Pulmonary artery occlusion wave form study
.