Anaesthetic management of mitral valvular heart disease

Presented by :- Dr Sindhu Sapru
Moderator:- Dr Avnish Bharadwaj

 Definition:- An acquired or congenital
disorder of cardiac valve characterised by
stenosis(obstruction) or
regurgitation(backward flow) of blood.

Why do we need guidelines for the anaesthetic management of valvular
heart disease patients?

 Still common in the developing world due to the prevalence of
Rheumatic Fever.

 In the past 2 decades, there have been major advances in
understanding the natural history and in improving cardiac function
in patients with valvular heart disease.

 Increases survival in this group of patients due to:-
Better noninvasive monitors of ventricular function
Improved prosthetic heart valves,
Better techniques for valve reconstruction
Development of guidelines for selecting the proper timing for
surgical intervention

 Hemodynamic burden on the LV/RV initially tolerated by
compensatory mechanisms but eventually leads to cardiac muscle
dysfunction, (CHF), or even sudden death.
 Produce pressure overload (mitral stenosis, aortic stenosis) or
volume overload (mitral regurgitation, aortic regurgitation) on the
left atrium or left ventricle.

 Anaesthetic management during the perioperative period is based
on the likely effects of drug-induced changes in :-
Heart rate and rhythm,
Preload,
Afterload,
Myocardial contractility,
Systemic blood pressure,
Systemic and pulmonary vascular resistance relative
to the pathophysiology of the heart disease.

 Includes assessment of
(1) the severity of the cardiac disease,
(2) the degree of impaired myocardial contractility, and
(3) the presence of associated major organ system disease.

 Recognition of compensatory mechanisms :Increased
sympathetic nervous system activity and cardiac hypertrophy

 Consideration of current drug therapy

 The presence of a prosthetic heart valve introduces special
considerations especially if noncardiac surgery is planned.

 History and physical examination

 Questions designed to define exercise tolerance are necessary to
evaluate cardiac reserve in the presence of valvular heart disease
and to provide a functional classification according to the criteria
established by the NYHA.

 Dyspnea, orthopnea, and easy fatigability- impaired myocardial
contractility.

 Anxiety, diaphoresis, and resting tachycardia- compensatory
increase in sympathetic nervous system activity

 CHF- frequent in chronic valvular heart disease, Basilar chest
rales, jugular venous distention, S3 and dependant edema
Typically, elective surgery is deferred until CHF can be treated
and myocardial contractility optimized.


 Murmur- The character, location, intensity, and direction of
radiation of a heart murmur provide clues to the location and
severity of the valvular lesion.

 Cardiac dysrhythmias - seen with all types of valvular heart
disease. Atrial fibrillation is common, especially with mitral
valve disease associated with left atrial enlargement.

 Angina pectoris - seen even in the absence of coronary
artery disease. It usually reflects increased myocardial oxygen
demand due to ventricular hypertrophy.


 Valvular heart disease and ischemic heart disease frequently
co-exist. Fifty percent of patients with aortic stenosis who are
older than 50 years of age have associated ischemic heart
disease.

 The presence of coronary artery disease in patients with
mitral or aortic valve disease worsens the long-term
prognosis and mitral regurgitation due to ischemic heart
disease is associated with an increased mortality

 Drug Therapy

 β-blockers, calcium channel blockers, and digitalis - heart rate
control

 ACE inhibitors and vasodilators -control blood pressure and
afterload

 Diuretics, inotropes and vasodilators- heart failure

 Antidysrhythmic therapy may also be necessary.

 Drug Therapy

 Aortic and mitral stenosis require a slow heart rate to prolong the
duration of diastole and improve left ventricular filling and coronary
blood flow.

 Aortic and mitral regurgitation require afterload reduction and a
somewhat faster heart rate to shorten the time for regurgitation.


 Atrial fibrillation requires a controlled ventricular response so that
activation of the sympathetic nervous system, as during tracheal
intubation or in response to surgical stimulation, does not cause
sufficient tachycardia to significantly decrease diastolic filling time
and stroke volume.

 Laboratory data

 ECG-
-Broad and notched P waves (P mitrale)- Left atrial enlargement
typical of mitral valve disease.
-Left and right ventricular hypertrophy -the presence of left or right
axis deviation and high voltage.
-Others- dysrhythmias, conduction abnormalities, evidence of active
ischemia, or previous myocardial infarction.

 CHEST X RAY-
-Cardiomegaly
- Valvular calcifications

 Laboratory Data

 DOPPLER ECHO-

-Determine significance of cardiac murmurs
-Identify hemodynamic abnormalities associated with physical
findings
-Determine transvalvular pressure gradient
-Determine valve area
-Determine ventricular ejection fraction
-Diagnose valvular regurgitation
-Evaluate prosthetic valve function
-Determine cardiac anatomy and function, hypertrophy, cavity
dimensions, and the magnitude of valvular regurgitation.

 Laboratory Data

 CARDIAC CATHETERISATION

-Presence and severity of valvular stenosis and/or regurgitation,
coronary artery disease, and intracardiac shunting.

-Resolve discrepancies between clinical and echocardiographic
findings.

-MS/MR: measurement of pulmonary artery pressure and right
ventricular filling pressure may provide evidence of pulmonary
hypertension and right ventricular failure.

- Mitral and aortic stenoses are considered to be severe when
transvalvular pressure gradients are more than 10 mm Hg and 50
mm Hg, respectively

 Etiology
 Pathophysiology
 Clinical features
 Physical findings
 Diagnosis
 Treatment
 Anaesthetic management

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

 Etiology

 Commonly encountered disease in the developing world,
where the prevalence of rheumatic fever remains high.
 Most common cause - rheumatic heart disease.
 Much less common causes include :

carcinoid syndrome
left atrial myxoma
severe mitral annular calcification
thrombus formation
cor triatriatum
rheumatoid arthritis
systemic lupus erythematosus, and
congenital mitral stenosis.

 Pure predominant MS- in 40% patients of Rheumatic fever

 Diffuse thickening of the mitral
leaflets and subvalvular
apparatus, commissural fusion,
and calcification of the annulus
and leaflets .

 This process occurs slowly, and many patients do not become
symptomatic for 20 to 30 years after the initial episode of rheumatic
fever.

 Left ventricular contractility is usually normal.

 If aortic and/or mitral regurgitation accompany mitral stenosis, there is
often evidence of left ventricular dysfunction.

 PATHOPHYSIOLOGY
 Normal mitral valve orifice area - 4 to 6 cm2.

 Orifice area < 2 cm2 – Blood flow from LA to
LV propelled by an elevated left
atrioventricular pressure gradient
impaired early diastolic filling of LVLV requires
the atrial kick to fill with blood.

 Orifice area < 1 cm2(Severe/Tight MS) – LA pressure of 25 mmHg
required to maintain normal cardiac outputtransmitted to the
pulmonary circulation pulmonary hypertension.

 Constant pressure overload of the LA  LA dilatation upto 10-
12cm distorts depolarisation pathwayAtrial Fibrillation
 loss of the atrial kick decrease in cardiac output
Congestive Heart failure

 PATHOPHYSIOLOGY

 Tachycardia/AF  diastolic filling period of LV decreases elevated
LAP  pulmonary congestion.

 Underloaded LV Decrease in LVEDV and LVEDP  Reduction in
Stroke Volume

 Cardiac output-
Moderate MS: CO normal at rest but rises subnormally during
exertion
Severe MS ( esp with elevated PVR) : CO subnormal at rest and fails
to increase/declines on exertion.

 Left ventricular systolic function is usually well preserved in patients
with mitral stenosis

 PATHOPHYSIOLOGY

 Pulmonary Hypertension in MS results from:
(1) Passive backward transmission of LAP
(2) Pulmonary arteriolar constriction
(3) Interstitial edema in pulmonary vessels
(4) Organic obliterative changes in pulmonary vascular bed

 Patients with long-standing mitral stenosis develop an irreversible
component of pulmonary hypertension.

 Severe Pulmonary Hypertension RV enlargement, secondary TR
and PR, and Right Heart Failure. Also leads to decreased pulmonary
compliance  excacerbation of ventilation perfusion inequalities.

Obstruction to LA emptying
Difficulty in LV
filling LA pressure Change in LA
function

Mitral stenosis

Difficulty in LV
function
Pulmonary venous pressure

Perivascular edema Pulmonary artery pressure
Luminal narrowing

Mitral stenosis

Difficulty in LV
function

Luminal narrowing

Reversal of pulmonary blood
flow
Pulmonary compliance
Work of breathing

Mitral stenosis

Difficulty in LV
function

Luminal narrowing

Reversal of pulmonary blood Cardiac Stable with mild
flow output symptoms
Severe pulmonary
Htn
Work of breathing

Mitral stenosis

Difficulty in LV
function

Luminal narrowing

Severe pulmonary
Htn
Work of breathing
Pulmonary vascular resistance

Mitral stenosis

Difficulty in LV
function

Luminal narrowing

Severe pulmonary
Htn
Work of breathing Pulmonary vascular resistance
RV overload
Mitral stenosis Tricuspid regurgitation

 CLINICAL FEATURES
 Continuous progressive life long disease

 Latent period of 20-40 yrs from rheumatic fever to onset of
symptoms.

 Onset of symptoms to disability- 10 yrs

 Progresses slowly (over decades) from the initial signs of mitral
stenosis NYHA functional class II symptomsatrial fibrillation
NYHA functional class III or IV symptoms accelerated progression
and the patient's condition deteriorates

 Symptoms precipitated by sudden changes
in heart rate,volume status or CO like fever,
anaemia, pregnancy, exercise, thyrotoxicosis
etc.


 Symptoms of mitral stenosis include:

 Due to decreased CO:
Easy fatiguability
Syncope
 Due to increased LAP
Pulmonary congestion- Dyspnea, orthopnea
Hemoptysis
Pulmonary edema
 Due to LA enlargement
Ortners syndrome
Atrial Fibrillation (30-40%)- more common in older patients
 Due to PAH, RV hypertrophy, RVF
Chest pain, ascites, edema

 Causes of death- CHF, systemic embolism, pulmonary embolism,
infection

 PHYSICAL FINDINGS

 Inspection-
-Mitral facies- Pinkish purple patches on
cheeks+ peripheral cyanosis in lips, tip of
nose and cheeks.
-Malar flush
Rarely seen in India

-Raised JVP, ascites,pedal edema when
RHF develops

 Palpation-
-Pulse – Regular, low volume, all peripheral pulses palpable.
-Left parasternal heave when RV hypertrophy develops
-Atrial fibrillation- irregular pulse
-Hepatomegaly- in RHF
-Tapping apex beat not displaced
-Diastolic thrill at cardiac apex with patient in lateral recumbent
position


 Auscultation
-S1 – loud, slightly delayed
-S2 – closely split
P2 often accentuated

-Opening snap –high pitched readily audible
in expiration,at or just medial to apex.
Follows A2 by 0.05 -0.12s (this time
interval varies inversely with severity
of MS). Due to forceful opening of mitral
valve. As MS progresses mitral valve opens
earlier in ventricular diastole.

-Murmur – Low pitched, rumbling, diastolic murmur following OS
heard best at apex with patient in lateral recumbent postion with
bell of stethoscope. Accentuated by mild exercise. Duration
correlates with severity of MS. Reappears or louder during atrial
systole.


 Auscultation

Associated lesions

-In severe pulmonary hypertension: pansystolic murmur along left
sternal border. Louder during inspiration and diminishes in forced
expiration(Carvallo’s sign).

-CO markedly reduced – silent MS (murmur not detected)

-Graham Steele murmur of PR- high pitched diastolic decrescendo
blowing murmur along left sternal border

 How to grade severity of mitral stenosis?

Severity Area (cm2) PAP Symptoms Signs
Mild >1.8 Normal Usually absent S2-OS>120ms
normal P2
Moderate 1.2-1.6 Normal Class II S2-OS 100-
120 ms; normal
P2
Moderate- 1.0-1.2 Mild Pulmonary Class II-III S2-OS 80-100
Severe hypertension ms ; P2
increase
Severe (Tight) <1.0 Mild to severe Class II-IV S2-OS< 80 ms;
pulmonary P2 increase RV
hypertension lift , Surgery if
RHF

 DIAGNOSIS

 ECG
P wave
-Tall and peaked in lead II and inverted in V1 in severe pulmonary
hypertension with RA enlargement.
-Wide and notched in LA enlargement ( P Mitrale ).
-Absent when Atrial Fibrillation develops.
QRS complex- usually normal.
Right axis deviation and RV hypertrophy in pulmonary hypertension.

 CARDIAC CATHETERISATION
Valve area, valvular function, CAD
Resolves discrepancy between clinical and ECHO findings
Assess associated lesions

 DIAGNOSIS
 ECHO-
Anatomy of the mitral valve -degree
of leaflet thickening, calcification,
mobility, extent of involvement of the
subvalvular apparatus and
anatomic suitability for PBMV.

-Also allows evaluation of pulmonary
hypertension, ventricular function,
associated valvular disease, assess LA for
presence or absence of thrombus.

-Evaluate patients with changing signs and symptoms
MILD MODERATE SEVERE
-Follow up
Mean valve gradient (mm
6 6–10 >10
Hg)
Pressure half time (ms) 100 200 >300
1.6–
Mitral valve area (cm2) 1.0–1.5 <1.0
2.0

 DIAGNOSIS
 Chest X Ray
-Mitralisation-straightening of the left heart border due to:-
Small aortic knuckle- (decreased CO)
Increased pulmonary conus
Enlarged LA producing convexity
LV- no change
-Double density of right border- outer and upper border due to
enlarged LA
 -Pulmonary hypertension- Dilated pulmonary arteries with peripheral
pruning
Dilatation of upper lobe pulmonary veins (Mustache or antler sign)
Kerley B lines in lower and mid lung fields
-Batwing sign in pulmonary edema- fan shaped opacity from parahilar
area to the periphery
-Elevation of left mainstem bronchus- (widening of carinal angle)
-Mitral valve calcification
-Posterior displacement of esophagus (RAO view)
-Left lower lobe collapse (compression of left mainstem bronchus)
-Miliary shadows of pulmonary henosiderosis

 COMPLICATIONS

-Atrial dysrhythmias (AF,AFL)

-Systemic embolisation (10-25%) –
Risk related to age, presence of AF, History of emboli
Cerebral-60%

-Hemoptysis due to
Rupture of bronchial/pulmonary veins
Chronic bronchitis
Acute pulmonary edema- pink, frothy sputum
Pulmonary infarction, anticoagulation, hemosiderosis

-Congestive heart failue

-Recurrent broncho pulmonary infections

-Pulmonary hypertension

-Endocarditis

 TREATMENT

 Grade 1 ( Mild MS by echo + dyspnea < Grade III)

Diuretics for congestive symptoms
Prophylaxis against Rheumatic fever & Infective endocarditis
IN presence of AF- anticoagulation, digoxin & drugs for rate
control
 Grade II ( Tight MS + lung congestive symptoms- dyspnea < Grade III)
First line treatment as above
Severe symptoms not responding to medicines- surgery with
commissurotomy, MVR, or balloon valvuloplasty

 Grade III ( Tight MS + pulmonary hypertension )
Surgical repair

 Grade IV ( Tight MS + pulmonary hypertension + RHF)
Surgery + Treatment of RHF

 TREATMENT

 CHF- restriction of physical activity, salt restricted diet, diuretics and
digoxin

 Atrial fibrillation-Digoxin, β-blockers, calcium channel blockers, or
a combination of these medications. Control of the heart rate is
critical .
Cardioversion for new onset AF.

 Anticoagulation – in atrial fibrillation because the risk of embolic
stroke in such patients is about 7% to 15% per year. Warfarin is
administered to a target (INR) of 2.5 to 3.0.

 Prophylaxis against recurrence of acute rheumatic fever

 TREATMENT

 Percutaneous balloon valvotomy-indicated in
Progressive deterioration despite medical treatment
MS with complications
Asymptomatic patients with a single attack of thromboembolism
Mitral valve orifice < 1 cm2

 Surgical correction – indicated in
MS with MI Active rheumatic carditis
MS with left atrial thrombus Extremely tight stenosis
Heavy valvular calcification Restenosis

 Surgical commissurotomy, valve reconstruction, or valve
replacement.

 ANAESTHETIC MANAGEMENT

 GOALS Maintain adequate LV diastolic filling

Optimise Right heart condition

-Maintain slow heart rate ie Avoid tachycardia

-Maintain a sinus rhythm if present. Aggressively treat AF

-Judicious fluid therapy- Tight control of intravascular volume
Overaggressive fluid with elevated LAP- pulmonary edema

Less fluids- decreased SV and CO


 -Maintain adequate SVR with sympathomimetic drugs such as ephedrine
and phenylephrine. Avoid vasodilators.

 -Avoid increases in PVR- Prevent pain, hypoxemia, hypercarbia, acidosis.
Patients on pulmonary vasodilators should continue these medications
because abrupt withdrawal can exacerbate pulmonary hypertension,
particularly with inhaled agents.

 Right heart function support-inotropes, and maneuvers that may
compromise it(eg, overaggressive fluid administration) should be
avoided

 Current ACC/AHA guidelines do not recommend endocarditis prophylaxis
for patients with isolated mitral stenosis undergoing surgical procedures. *

*http://ether.stanford.edu/Ortho/Anesthetic%20considerations%
20for%20valvular%20patient%20sub%20to%20noncardiac%20surg
ery.pdf "


 Which medications to continue intra operatively??

 Diuretics- Evaluate fluid status
Check electrolytes on day of surgery
Withold on night before surgery if massive fluid shifts
expected in surgery
 Drugs to control AF ( Digoxin, beta blockers, CCB) –
Continue in perioperative period

 Watch serum potassium- in patients receiving digoxin and diuretics
 Warfarin- switch to heparin perioperative for better control.
Titrate to APTT 1.5-2 times normal
Continue post op.
Management of anticoagulation perioperatively should balance risks
of bleeding with the risk of thrombosis and systemic embolization.


 Preoperative Medication

 Adequate dose prevents anxiety and tachycardia. Care must be
taken to avoid hypotension, which can dramatically decrease left
ventricular preload and respiratory depression, which may
exacerbate pulmonary hypertension.

 Morphine 0.1-0.2mg/kg
Promethazine 12.5-25mg IM 1-2 hrs before surgery
Small dose Benzodiazepenes can be given ( reduce dose of
morphine)
 Anticholinergics- avoided as they increase heart
rate

 Induction

 Any intravenous induction drug except ketamine, because of its
propensity to increase the heart rate.
Should be double diluted and given slowly.
 Etomidate best for hemodynamic stabilty
Thiopentone or Midazolam
Narcotic( morphine 0.5mg/kg or Fentanyl 5-10 ug/kg)
Avoid Propofol- direct and indirect effects on ventricular preload
 Muscle relaxants that do not induce tachycardia and hypotension
from histamine release.
Vecuronium + Narcotics- dangerous bradycardia. Hence
pancuronium preferred unless basal heart rate is high
Rocuronium- vagolytic. Hence slightly increase HR and decrease PAP

 Benzodiazepenes (midazolam/diazepam) – use cautiously as can
cause profound vasodilatation esp with narcotics.

 Maintainence

 A nitrous/narcotic anesthetic or a balanced anesthetic that includes
low concentrations of a volatile anesthetic
Avoid halothane- arrythmogenic
Nitrous oxide – Increases PVR . Best avoided in PAH
 Light anesthesia and surgical stimulation -tachycardia and HTN.
 Vasodilator therapy ( NTG/ Nitroprusside 0.5-1 ug/kg/min)-
desirable in severe PAH
 Intraoperative fluid replacement must be carefully
titrated

 Reversal- slowly to help ameliorate any drug-induced
tachycardia caused by the anticholinergic drug in
the mixture.


 Monitoring

 ECG, BP, Spo2

 Invasive monitoring- depends on the complexity of the surgery and
the magnitude of physiologic impairment caused by MS.
-Direct arterial pressure
-CVP- measure loading conditions and means of transfusing
inotropes/dilators
-Pulmonary artery catheter- PCWP and CO measurement offer
very good estimate of overall ventricular function .
Monitor Pulmonary Artery Pressure ( PAP)- useful in PAH

Helpful for confirming the adequacy of cardiac function,
intravascular fluid volume, ventilation, and oxygenation.

 Post operative management
 Risk of pulmonary edema and RHF continues into the
postoperative period, so cardiovascular monitoring
should continue as well.

 May require a period of mechanical ventilation:
Pain and hypoventilation with respiratory acidosis ,hypercarbia and
hypoxemia -increase HR and PVR.
Decreased pulmonary compliance and increased work of breathing
to avoid hypercarbia .
 Relief of postoperative pain with neuraxial opioids
useful
 Inotropic support and vasodilator therapy should be
continued for prolonged ( 24-48 hrs) in patients
with severe PAH.

Abnormal leaking of blood from the left
ventricle, through the mitral valve, and
into the left atrium, when the left
ventricle contracts, i.e. there is regurgitation
of blood back into the left atrium.

 Etiology

 MR due to rheumatic fever is usually associated with mitral stenosis.

 Acute MR- ischemic heart disease, blunt chest wall trauma, infective
endocarditis, rupture of chordae tendineae.

 Chronic MR:
mitral valve prolapse( M/C cause)
mitral annular calcification
left ventricular hypertrophy,
cardiomyopathy,
myxomatous degeneration,
systemic lupus erythematosus,
rheumatoid arthritis,
ankylosing spondylitis, and
carcinoid syndrome
congenital lesions such as an endocardial cushion defect,

 PATHOPHYSIOLOGY

 Acute phase
 Sudden volume overload of both LA and LV. The left ventricle now
has to pump out the forward stroke volume plus the regurgitant
volume known as the total stroke volume of the left ventricle.
 Increased ejection fraction initially contractile function
deteriorates as disease progressesdysfunctional LV and a
decreased EF.
 Volume and pressure overload of the LA  pulmonary congestion
 Regurgitant fraction >0.6 -severe mitral regurgitation.

 PATHOPHYSIOLOGY

 Chronic phase

 Compensated

 Develops slowly over months to years or if the acute phase cannot
be managed with medical therapy.
 Eccentric hypertrophy of the LV plus the increased diastolic volume
increase the stroke volume forward CO approaches the normal
levels.
 Volume overload of LADilatation of LA  filling pressure
decreasesimproves the drainage from the pulmonary veins signs
and symptoms of pulmonary congestion decrease.
 Asymptomatic and have normal exercise tolerances.

 PATHOPHYSIOLOGY

 Chronic phase

 Decompensated
 MR for years eventually develop left ventricular dysfunction, the
hallmark of this phase. characterized by calcium overload within the
cardiac myocytes.
 The stroke volume of the LV decreases decreased forward CO and
an increase in the end systolic volumeincreased filling pressures of
the LV and increased pulmonary venous congestionsymptoms of
congestive heart failure.
 LV dilatationdilatation of the mitral valve annulusworsen the
degree of MR and an increase in the wall stress of the cardiac
chamber as well.
 EF decreases late in the course of disease.

 PATHOPHYSIOLOGY

 Isolated MR-less dependent on properly timed left atrial contraction
for left ventricular filling than patients with co-existing mitral or
aortic stenosis.

 Myocardial ischemia is uncommon because the increased left
ventricular wall tension is quickly dissipated as the stroke volume is
rapidly ejected into the aorta and left atrium.

 Acute MR -pulmonary edema and/or cardiogenic shock.

 PATHOPHYSIOLOGY

 The fraction of regurgitant volume depends on
(1) the size of the mitral valve orifice;
(2) heart rate, which determines the duration of ventricular ejection;
(3) pressure gradients across the mitral valve.

 MR + MS -volume and pressure overload, resulting in a markedly
increased left atrial pressure. Atrial fibrillation, pulmonary edema,
and pulmonary hypertension develop much earlier in these patients

 Rheumatic fever–induced MR -marked left atrial enlargement and
atrial fibrillation.

Volume overload of LA
Volume overload of LV
LA dilation
Early Normal LA
LV filling Fiber size pressures
Stroke volume
Cardiac output and BP
maintained

Mitral regurgitation

LA dilation
Normal LA
pressures

Mitral Regurgitation

LA dilation
Early
Normal LA Late
LV filling Fiber size pressures Contractility
Stroke volume BP and CO
maintained


LA dilation
Late
Early Normal LA
Reflexive arteriolar
maintained
constriction
SVR


LA dilation
Early Normal LA Late
maintained
constriction
SVR
Regurgitation


LA dilation
Early Normal LA Late
maintained
constriction
SVR

Regurgitation

LA pressure Pulmonary
Mitral regurgitation congestion

LA dilation
Early Late
Normal LA
maintained
constriction
SVR
Forward flow Regurgitation

LA pressure Pulmonary
congestion


 Symptoms
 Acute MR –
-Decompensated CHF(i.e. dyspnea,orthopnea, PND
pulmonary edema,
-Low cardiac output state (i.e. decreased exercise tolerance). –-
 -Palpitations (due to LVH or AF)
-Cardiovascular collapse with shock- due to papillary muscle
rupture or rupture of a chorda tendinea.

 Chronic compensated MR-
-May be asymptomatic, with a normal exercise tolerance and no
evidence of heart failure. May be sensitive to small shifts in their
intravascular volume status, and are prone to develop CHF.
 Features of RHF in associated pulmonary hypertension.

 PHYSICAL EXAMINATION
Depend in the severity and duration of MR.

 Inspection
- Features of CHF ( pt propped up and dyspneic,
edema, raised JVP etc)
-Precordial bulge

 Palpation
-Pulse- regular, normal pressure usually.
May show a sharp upstroke in chronic severe MR
narrow pulse pressure in acute severe MR
-Systolic thrill at the apex (best in left lateral position at the height
of expiration) , hyperdynamic and laterally displaced apex ,palpable
rapid filling S3 (chronic severe MR)
-Left parasternal heave and epigastric pulsations (RVH)
-Palpable P2 I pulmonary area (PAH)
- Bipedal pitting edema (CHF)


 Auscultation
-S1 –usually absent,soft or buried in the
murmur.
-S2-audible. Wide physiological splitting in
severe MR (aortic valve closes early)
-S3 –low pitched 0.12-0.17s after A2 may be
followed by rumbling MDM
-S4- in acute severe MR

 Murmur- High pitched soft blowing holosystolic apical murmur
atleast grade III/IV in left lateral position at the height of expiration
with radiation to the left axilla and inferior angle of scapula.
Intensified by isometric exercise but reduced during Valsalva.
 Pulmonary area- Ejection systolic murmur with loud P2


Acute Chronic

P mitrale, AF, Left Ventricular
ECG Normal
Hypertrophy

Cardiomegaly, left atrial
Heart size Normal
enlargement

Heard at the
base, radiates
Heard at the apex, radiates to
Systolic murmur to the neck,
the axilla
spine, or top of
head
Apical thrill May be absent Present
Jugular venous
Present Absent
distension

 DIAGNOSIS

 ECG-
- LAH (in all cases)
-LVH (in 50% cases)
-Biventricular hypertrophy
-AF

 Chest X Ray-
- Enlarged LA and LV
-Signs of pulmonary venous hypertension
-Signs of pulmonary edema (acute severe MR)
-RVH
-Mitral calcification (in co existing MS)

 Severity of MR evaluated by:
-Color-flow and pulsed-wave Doppler
-Pulmonary artery occlusion pressure waveform -the size of the V
wave correlates with the magnitude of MR
-Cardiac catheterisation

 DIAGNOSIS

 ECHO-
Confirm diagnosis.
Color doppler flow on TEE will reveal a regurgitant jet of blood, a
dilated LA and LV and decreased left ventricular function.
Also assess mechanism and severity of MR

MILD MODERATE SEVERE
Area of MR jet (cm2) <3 3.0-6.0 >6
MR jet area as
percentage of left atrial 20–30 30–40 >40
area
Regurgitant fraction (%) 20–30 30–50 >55

.

 TREATMENT

 Drugs-
Digoxin, diuretics for CHF
Vasodilators ( ACE inhibitors, nitrates) in acute symptomatic MR
Warfarin for AF/Thromboembolism

 Progress insidiously, causing left ventricular damage and remodeling
before symptoms have developed.
Survival may be prolonged if surgery is performed before the
ejection fraction is less than 60%

 Surgery-
-Mitral annuloplasty/valvuloplasty-preferred because restores valve
competence, maintains the functional aspects of the mitral valve
apparatus, and avoids insertion of a prosthesis.
-Mitral valve replacement
 Patients with an EF <30% or left ventricular end-systolic dimension
more than 55 mm do not improve with mitral valve surgery.

 GOALS

 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)


 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 desirable
Vecuronium/ Atracurium- depending on basal HR

 MAINTAINENCE
 Volatile anesthetics (Halothane, Isoflurane)
Increase in heart rate and minimal negative
inotropic effects. Vasodilatation desirable.

 Nitrous oxide avoided in severe PAH.

 When myocardial function is severely compromised, use of an
opioid-based anesthetic is another option However, potent narcotics
can produce significant bradycardia, very deleterious in severe MR.
 Mechanical ventilation should be adjusted to 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)
Not required in Minor surgery with asymptomatic MR
Useful in severe MR- detecting the adequacy of CO and the
hemodynamic response to anesthetic and vasodilator drugs and
facilitating intravenous fluid replacement.

 Pulmonary artery occlusion pressure –
-V waveform to assess severity of MR
-May be a poor measure of left ventricular end-diastolic volume in
patients with chronic mitral regurgitation.
-With acute mitral regurgitation, the left atrium is less compliant,
and PAOP does correlate with LA and LV EDP.

 Moderate to severe MS/ AS –most significant concern
 Case reports attest to their safety provided afterload is
maintained
 Epidural- can be used as sole anaesthetic in mild to moderate
MS
Optimise fluid status and achieve sensory level with titrated
doses of Local anaesthetic until adequate for surgery.

 Basic principles:
Afterload support
Maintainence of sinus rhythm
Careful volume management
Avoidance of tachycardia
 Epidural using opiods- supplement to GA
Avoid adrenaline in test dose while inserting catheter.

 Left-sided valvular heart lesions present a myriad of potential
difficulties during perioperative care for noncardiac surgery.

 A thorough understanding of the pathophysiology of the presenting
lesion along with its implications in the perioperative period is
crucial in preventing undesirable outcomes.

 Patients with left-sided valvular disease require careful preoperative
evaluation, optimization and planning,vigilant intraoperative
monitoring, and tight hemodynamic control that must be continued
into the postoperative period when appropriate.

 As the population continues to age, we can expect to treat rising
numbers of patients with these derangements, making it more
crucial than ever to be prepared for these encounters.

 Stoeltings Anaesthesia and co existing disease- 5th edition
 Harrisons Internal medicine- 17th ed
 Cardiac Anaesthesia- Deepak Tempe
 Anesthetic Considerations for Patients with Advanced Valvular
Heart Disease Undergoing Noncardiac Surgery-Jonathan
Frogel, MD*, Dragos Galusca, MD
http://ether.stanford.edu/Ortho/Anesthetic%20consideration
s%20for%20valvular%20patient%20sub%20to%20noncardiac%2
0surgery.pdf "

Anaesthetic management of mitral valvular heart disease

Anaesthetic management of mitral valvular heart disease

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Anaesthetic management of mitral valvular heart disease

Similar to Anaesthetic management of mitral valvular heart disease (20)

More from Dhritiman Chakrabarti

More from Dhritiman Chakrabarti (20)

Anaesthetic management of mitral valvular heart disease