Because of the complex operation of the mitral valve apparatus is complex abnormal valve function may result from
disease or distortion of the mitral valve leaflets
the valve suspensory or supporting apparatus
or the left ventricle itself
3 Mitral Regurgitation
Two important categories of Etiology
4 Acute MR
Disorders of the mitral annulus
Infective endocarditis (ring abscess)
Trauma (valve surgery)
Paravalvular leaks (prosthetic valves)
Mitral leaflet disorders
Infective endocarditis (vegetations)
Rheumatic heart disease
5 Acute MR
Rupture of chordae tendinea
Myxomatous degeneration (MVP)
Trauma (balloon valvuloplasty blunt chest trauma)
Papillary muscle disorder
Coronary artery disease
Acute global left ventricular dysfunction
Infiltrative disease (amyloidosis etc.)
Trauma (blunt chest trauma)
6 Acute MR
Primary prosthetic mitral valve disorders
Porcine cusp perforation
Porcine cusp degeneration
Immobilization of disk or ball due to thrombus or pannis
7 Chronic MR
Rheumatic heart disease
Healed infective endocarditis
Myxomatous degeneration of leaflets
Sclerosis and mitral calcification of valve and annulus
8 Chronic MR
Ruptured chorade tendineae due to infarct trauma MVP endocarditis
Dilation of mitral valve annulus and LV cavity
Cleft MV or fenestrations
Regurgitant mitral valve functions in parallel with systolic flow across the aortic valve the impedance to ventricular emptying is reduced (which means instead of slowing the process up it increases the process)
Consequently MR enhances left ventricular emptying.
Almost one half of the regurgitant volume is ejected into the left atrium before the aortic valve opens.
The volume of MR depends on the impedance to LV emptying and is increased by hypertension and AS.
Two categories in terms of how the heart is affected
10 Acute MR
Sudden early systolic rise of atrial pressure pulmonary edema and CHF.
Pulmonary congestion and edema is due to increase in pulmonary venous pressure and is more significant in acute MR because the LA does not have time to react to a sudden bolus of blood washing back into it. This is one major hemodynamic difference between acute and chronic MR.
The LA is usually normal in size with an there is little compliance associated with the LA.
11 Acute MR
Depending on the preexisting compliance to the LA will determine the resultant signs and symptoms of the patient
A large volume of regurgitation into a normal noncompliant atrium results in high LA pressures. The LV does not tolerate an acute volume load when compensatory mechanisms of dilation and hypertrophy do not have time to develop LV diastolic and LA pressures increase markedly the patient may suffer from pulmonary edema marked elevation of pulmonary vascular resistance and right heart failure.
12 Chronic MR
There is a longer time interval from mild to end systolic rise
Eventually with the decrease in cardic output there is left ventricular failure because of a volume overload.
The severity can be judged because of left atrial and ventricular enlargement at end diastolic dimensions due t stretching of the annulus and enlargement of the left ventricle during the pushing of large volumes of blood into the left ventricle.
13 Chronic MR
A mild degree of regurgitation produce little derangement in LV function.
Moderate and even severe MR when chronic may be surprisingly well tolerated for years.
In chronic severe MR LV volume overload occurs as the refluxing blood in the LA returns to the LV during diastole. The LV becomes hyperdynamic (contracts more vigorously)
The LA undergo compensatory changes to accommodate the volume overload.
Increases in LV and LA chamber size allow for accommodation of the regurgitant volume at a lower filling pressure that limits pulmonary congestion
14 Chronic MR
LA dilation can be mild to severe and predisposes to atrial fibrillation.
Prolonged LV volume overload results in LV contractile dysfunction and increased LV end-systolic volume.
As this cycle continues MR begets more MR LV dilation continues along with an increase in LV filling pressures
This hemodynamic changes eventually results in decreased cardiac output and pulmonary vascular congestion
15 (No Transcript) 16 Signs and Symptoms
Proxysmal nocturnal dyspnea
Pulmonary edema and shock
17 Signs and Symptoms
Decrease exercise tolerance
Paroxysmal nocturnal dyspnea (occurs late in the course of chronic MR) may be due to low cardiac output
18 Physical Examination
Generally there are no distinguishing features especially in mild MR
But in moderate to severe MR the carotid pulse may be brisk or jerky often with a decreased pulse volume.
Patients with severe MR and PHTN often have functional TR.
In such instances large jugular venous V waves that increase with inspiration will be seen.
Patient with chronic MR frequently have atrial fibrillation. This causes the venous A wave to disappear and the V wave to become more prominent.
19 Heart Sounds
Alterations in the intensity of the first heart sound are common
With severe MR the S1 may be diminished (why)
In severe cases S2 becomes audibly split in expiration and widely split during inspiration. (why)
Patients with severe MR have a shortened LV ejection time because the LV unloads its contents more quickly than normal. This results in early closure of the aortic valve and a widely split S2.
An S3 is common in MR of hemodynamic importance and implies in severe cases in large volume of blood returning to the LV in early diastole and does not necessarily indicate LV failure.
If CHF or LV dysfunction is present the S3 may reflect impaired cardiac function with LV dilation.
Thus detection of an S3 in a subject with MR means one of two things
A large regurgitant volume and good function
Depressed ejection fraction
An S4 of LV origin is never a feature of chronic MV disease. The LA is dilated and complaint and unable to generate an atrial sound.
In acute MR where the atrial is normal in size and has a very high pressure and increased volume an S4 is typical.
Systolic murmur is the most prominent physical finding it is different than the systolic murmur of AS TR VSD
In most cases the murmur commences immediately after the soft S1 and continues beyond and may obscure A2
The holosystolic murmur of chronic MR is usually constant in intensity blowing high-pitched and loudest at the apex with radiation to the axilla and left infrascapular area
When the murmur is confined to late systole the regurgitation is usually mild.
22 Compare and contrast
Chronic Severe and Acute Severe MR
23 Laboratory Examination
LA enlargement and atrial fibrillation in chronic MR
24 Laboratory Examination
Kerley B lines with acute MR
Pulmonary edema with acute MR
25 Cardiac Catheterization
Appearance of contrast material in the left atrium following its injection into the left ventricle indicates the presence of MR.
Estimation of severity can be performed based on the degree of opacification of the LA
26 Cardiac Catheterization
The LA pressure increases and is demonstrated by angiography wit a prominent V wave on the atrial pressure curve.
27 Cardiac Catheterization 28 Treatment
Measure used to treat heart failure
Afterload reduction is particular benefit
By reducing the impedance to ejection into the aorta the volume of blood regurgitating into the left atrium is reduced
Decreasing the left ventricular volume reduces the diameter of the mitral annulus and thereby the regurgitant orifice
Prophylaxis to prevent infective endocarditis
Bioprosthesis (slow and careful consideration before this is done)
Carpentier or Duran Ring
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