Key result
Patients with congestive heart failure utilize central and peripheral circulatory mechanisms, including the Frank-Starling principle and myocardial hypertrophy, to compensate for diminished cardiac output.
Reviews the central and peripheral compensatory mechanisms, particularly the role of peripheral resistance vessels, in congestive heart failure.
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No immediate practice change; leaves open targeted modulation of compensatory mechanisms for future trials.
ONE of the principal characteristics of patients with congestive heart failure is the diminished response of cardiac output with physiologic stress.1 There are a number of circulatory mechanisms, both central and peripheral, by which the patient with heart failure compensates for this inability to augment cardiac output adequately. The central compensatory mechanisms include the use of the Frank-Starling principle, development of myocardial hypertrophy and increased sympathetic drive to the heart.2 Thus, the increased blood volume resulting from the renal retention of sodium and secondary aldosteronism leads to an increased ventricular filling pressure and the operation of the ventricle higher on . . .
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Zelis et al. (1970) conducted a review in Congestive Heart Failure. Patients with congestive heart failure utilize central and peripheral circulatory mechanisms, including the Frank-Starling principle and myocardial hypertrophy, to compensate for diminished cardiac output.
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