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Peripheral circulatory adaptations to pump failure of the heart.

Impairment of ventricular performance is the initial step in the development of heart failure, but the symptoms and the reduced exercise capacity cannot solely be explained by left ventricular dysfunction. The degree of ventricular dysfunction in congestive heart failure (CHF) does not correlate with its severity-that is, indices of left ventricular dysfunction do not predict or correlate closely with the functional state of patients with CHF as assessed by exercise tests.' Although right ventricular dysfunction has been linked to the severity of symptoms and exercise intolerance, right ventricular failure seems to be a secondary problem in most cases of clinical systolic heart failure. There is evidence that prognosis is associated with the degree of left ventricular dysfunction, extent of myocardial loss, and cardiac dimensions. Clinical symptoms of heart failure usually emerge with the activation of neurohumoral systems, in particular the sympathetic system and the reninangiotensin system. The study of left ventricular dysfunction (SOLVD) trial confirmed that increases of plasma atrial natriuretic peptide and noradrenalin occur early in the disease and plasma renin activity increases with symptoms.2 Although numerous factors are likely to be involved in the development of symptoms, the decrease in renal perfusion may activate the renin-angiotensin system. Experimental data suggest that this alteration of renal haemodynamics emerges early in the course of heart failure. Sodium retention may also emerge early and compensate for impaired left ventricular dysfunction by increasing the preload. One important clinical symptom in chronic heart failure is early fatigue during physical activity, which has