Low output failure
Low cardiac output at rest or during exertion characterizes heart failure caused by common conditions such as congenital, valvular, rheumatic, hypertensive, coronary and cardiomyopathic diseases. Low output failure presents with evidence of systemic vasoconstriction such as cold, paler or cyanotic extremities. Pulse pressure is low.
High cardiac output failure
Conditions that are associated with a very high cardiac output such as anemia, beriberi, paget’s disease of bone and thyrotoxicosis may lead to or precipitate heart failure.
To understand basic pathogenesis of heart failure of each side of the heart is studied separately.
LEFT-SIDED HEART FAILURE
Reduction in the left ventricular output for a given pulmonary venous pressure is called left sided heart failure.
CLINICAL FEATURES
The clinical changes associated with left ventricular failure depend on whether failure is acute or chronic.
Acute left ventricular failure:
- Acute forward failure: An acute severe decrease in cardiac output leads to cardiogenic shock.
- Acute backward failure: Failure of the left ventricle to pump the pulmonary venous return causes increased hydrostatic pressure in pulmonary capillaries with transudation of fluid into the alveolar space, called pulmonary edema. Clinically, pulmonary edema is manifested as dyspnea with cough productive of pink frothy sputum. Edema fluid produces crepitations on auscultation.
Chronic left ventricular failure:
- Chronic forward failure: Decreased cardiac output results in decreased tissue perfusion. Decreased renal blood flow stimulates rennin-angiotensin system and aldosterone formation which causes sodium and water retention from kidney. This sodium and water retention increase blood volume, therefore increasing venous return to already weak heart, resulting in congestion of lungs.
- Chronic backward failure: Inability of heart to pump all the venous return leads to passive venous congestion in the lung which if prolonged induces fibrous thinking of alveolar septa. The thickened alveolar septa intern increases resistance to lung expansion, causing dyspnea.