The problem of defining heart failure.
A succession of theories arising from last century has attempted to explain why patients with damaged hearts develop peripheral edema. Opposed to the original simple concepts of backward failure, a number of theories of forward failure have been proposed, the cardiac output being considered inadequate for capillary permeability, renal function, or the metabolic needs of the body. Any theory needs to take account of the neuroendocrine stimulation now known to occur under these conditions. This article presents evidence for the belief that the condition arises when the cardiac output becomes insufficient to maintain the arterial blood pressure without the support of excessive neuroendocrine activity. This explains why the edematous state may be evoked in patients who have a severe reduction in peripheral resistance as well as in those with a reduced cardiac output. While the clinical concept of cardiac failure arose from the consideration of the formation of edema in patients with cardiac disease, the term has also come to be used by laboratory investigators studying the immediate effects of reducing the strength of ventricular contraction. The application of the same name to two different conditions has led to confusion, and this review stresses the importance of definition of terms.
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D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D002199:Capillary Permeability / Q000502:physiology; D004487:Edema / Q000209:etiology*; D006333:Heart Failure / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D009203:Myocardial Infarction / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D009435:Synaptic Transmission / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology