Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 962-964 |
| Number of pages | 3 |
| Journal | New England Journal of Medicine |
| Volume | 282 |
| Issue number | 17 |
| DOIs | |
| State | Published - Apr 23 1970 |
All Science Journal Classification (ASJC) codes
- General Medicine
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