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714 PA R T I V / Pathophysiology and Management of Heart Disease
Pathophysiology low and pulse pressure may be narrowed secondary to decreased
stroke volume. Jugular venous pressure can be normal or elevated
Mitral regurgitation occurs as the result of inadequate closure of in the patient with right-sided heart failure. Breath sounds can
the mitral valve, allowing regurgitant flow back into the left range from basilar crackles to dullness secondary to pleural effu-
atrium during each left ventricular systole. Its severity depends sion. In addition, hepatosplenomegaly, hepatojugular reflux, pe-
on the volume of regurgitant flow. Regurgitant flow also increases ripheral edema, and ascites may be present in the patient with
left atrial pressure, causing left atrial dilation and pulmonary con- right-sided heart failure.
gestion. During diastole, the regurgitant volume returns to the
left ventricle and increases its volume load. In chronic mitral re-
gurgitation, persistent volume overload results in progressive ven- Diagnostic Tests
tricular dilation and mild hypertrophy. Over time, chronic vol- TTE can identify the structural cause of the mitral regurgitation
ume overload will result in systolic heart failure. In acute mitral as well as gauge left atrial size, left ventricular dimensions and
regurgitation, neither the left atrium nor the ventricle has had performance, pulmonary artery pressures, and right heart func-
sufficient time to adjust to the increased volume load. Left atrial tion. Color flow Doppler allows for the assessment of severity of
pressure rises quickly, resulting in pulmonary congestion and regurgitation. TEE is better than TTE for defining mitral valve
edema. anatomy and discriminating prosthetic valves and paravalvular
leaks.
Clinical Manifestations Cardiac catheterization is used to identify coexisting coronary
artery disease and to grade the severity of mitral regurgitation.
Patients with acute versus chronic mitral regurgitation vary in Left ventriculography can assess left ventricular function and dis-
clinical presentation and physical examination findings. In acute tinguish any wall motion abnormalities. Right heart catheteriza-
mitral regurgitation, symptoms progress rapidly. Symptoms are tion quantifies pulmonary artery pressures and allows for evalua-
typically those of left ventricular failure. The patient is usually tion of the large V waves in the pulmonary artery wedge tracing.
tachycardiac to compensate for the reduced forward stroke vol- Electrocardiography in chronic mitral regurgitation may
ume. Patients are dyspneic secondary to pulmonary congestion demonstrate left ventricular hypertrophy and left atrial enlarge-
and edema; they are often orthopneic and have paroxysmal noc- ment or P mitrale (characterized by M-shaped P waves). Atrial fib-
turnal dyspnea and poor exercise tolerance. Patients may also have rillation may occur with acute and chronic mitral regurgitation.
signs of biventricular failure because right-sided failure may occur Patients with ischemic papillary muscle dysfunction may demon-
secondary to pulmonary hypertension. Patients with acute mitral strate ischemic changes, and patients with papillary muscle rup-
regurgitation often present to the emergency department with re- ture can show acute inferior, posterior, or anterior myocardial in-
ports of sudden inability to breathe. New-onset atrial fibrillation farction.
can occur. Patients with ischemic mitral insufficiency or papillary Chest radiography in chronic mitral regurgitation shows left
muscle rupture may also report chest pain. ventricular hypertrophy and left atrial enlargement. Calcification
During the compensatory phase of chronic mitral regurgita- of the mitral valve annulus and apparatus may also be seen. In
tion, patients may be relatively asymptomatic for years. Initial acute or decompensated chronic mitral regurgitation, pulmonary
signs of mitral regurgitation include exertional dyspnea, orthop- vascular redistribution and pulmonary edema can be observed. If
nea, paroxysmal nocturnal dyspnea, cough, palpitations, new the heart is of normal size, the degree of mitral regurgitation is so
atrial fibrillation, and lower extremity edema. Symptoms may oc- mild or so acute that eccentric left ventricular hypertrophy has not
cur so gradually that patients may present subacutely to the clinic had time to develop.
with symptoms as vague as fatigue and inability to sleep.
Medical Management
Physical Assessment
Medical therapy for mitral regurgitation is geared toward afterload
On examination, the most easily noted characteristic of either reduction to promote forward flow and minimize regurgitation into
chronic or acute mitral regurgitation is the holosystolic murmur, the left atrium and pulmonary vasculature. In patients with acute or
which is heard best at the apex and radiates to the axilla (see Table decompensated chronic mitral regurgitation, intravenous vasodila-
29-3). The murmur of mitral regurgitation may vary somewhat tors such as nitroprusside can reduce filling pressures and ventricu-
depending on the underlying cause. Patients may have an S 3 gal- lar cavity size and promote forward flow with afterload reduction.
lop in moderate-to-severe regurgitation caused by high diastolic Intravenous diuretics are used to reduce volume overload. In acutely
flow into the ventricle. An S 4 gallop is uncommon in chronic mi- ill patients refractory to medications, intra-aortic balloon counter-
pulsation can be used further to reduce afterload while maintaining
tral regurgitation. However, in acute mitral regurgitation, an S 4
gallop is common because the left atrium and ventricle are non- coronary perfusion with diastolic augmentation.
compliant. The patient with rheumatic heart disease may also In patients with chronic mitral regurgitation or those in acute
have a diastolic murmur related to coexisting mitral stenosis. heart failure who are being weaned from intravenous inotropes
Because of left ventricular dilation, patients with chronic mi- and vasodilators, other afterload-reducing agents, such as an-
tral regurgitation have an easily palpated, left laterally displaced giotensin-converting enzyme inhibitors, nitrates, or hydralazine,
point of maximal impulse. Patients with a markedly enlarged left may be used. Diuretics can treat chronic and acute volume over-
atrium may have a left parasternal lift because of anterior dis- load. Some practitioners continue to advocate the use of digoxin,
placement of the apex. Patients with acute or decompensated especially for patients in atrial fibrillation. In the patient with
chronic mitral regurgitation may be anxious and diaphoretic be- chronic but compensated mitral valve regurgitation, mitral sur-
cause of left ventricular failure. Blood pressure may be normal to gery can be safely deferred or avoided. The patient should be care-

