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Left-Sided Heart Failure

Heart failure can affect predominantly the left or the right

side of the heart or may involve both sides. The most

common causes of left-sided cardiac failure are ischemic

heart disease (IHD), systemic hypertension, mitral or aortic

valve disease, and primary diseases of the myocardium

(e.g., amyloidosis). The morphologic and clinical effects of

left-sided CHF stem from diminished systemic perfusion

and the elevated back-pressures within the pulmonary


Clinical Features

Dyspnea (shortness of breath) on exertion is usually the

earliest and most signifiant symptom of left-sided heart

failure; cough also is common as a consequence of flid

transudation into air spaces. As failure progresses, patients

experience dyspnea when recumbent (orthopnea); this

occurs because the supine position increases venous return

from the lower extremities and also elevates the diaphragm.

Orthopnea typically is relieved by sitting or standing, so

patients usually sleep in a semiseated position. Paroxysmal

nocturnal dyspnea is a particularly dramatic form of breathlessness, awakening patients from sleep with extreme

dyspnea bordering on feelings of suffocation.

Other manifestations of left ventricular failure include

an enlarged heart (cardiomegaly), tachycardia, a third

heart sound (S3), and fie rales at the lung bases, caused by

the opening of edematous pulmonary alveoli. With progressive ventricular dilation, the papillary muscles are

displaced outwards, causing mitral regurgitation and a

systolic murmur. Subsequent chronic dilation of the left

atrium can cause atrial firillation, manifested by an “irregularly irregular” heartbeat. Such uncoordinated, chaotic

atrial contractions reduce the ventricular stroke volume

and also can cause stasis. The stagnant blood is prone to

form thrombi (particularly in the atrial appendage) that

can shed emboli and cause strokes and manifestations of

infarction in other organs.

Systemically, diminished cardiac output leads to

decreased renal perfusion that in turn triggers the reninangiotension-aldosterone axis, increasing intravascular

volume and pressures . Unfortunately, these

compensatory effects exacerbate the pulmonary edema.

With further reduction in renal perfusion, prerenal azotemia

may supervene, with impaired excretion of nitrogenous

wastes and increasing metabolic derangement. In severe

CHF, diminished cerebral perfusion can manifest as hypoxic

encephalopathy with irritability, diminished cognition, and

restlessness that can progress to stupor and coma.

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