Congestive heart failure is associated with ventricular hypertrophy and dilatation, increased circulating catecholamines, and peripheral vasoconstriction. The extent to which these changes occur, whether they are a favorable "compensatory mechanism" or contribute to cardiocirculatory dysfunction, depends on the cause and severity of the heart failure. The addition of new sarcomeres through ventricular hypertrophy distributes the excess workload of the failing ventricle over more contractile units. In ventricular pressure overload, hypertrophy primarily increases wall thickness and ventricular volume is not usually increased; the converse is true with ventricular volume overload. Hypertrophy can result in enhanced or depressed contractile performance, depending on the stimulus for hypertrophy and method by which contractility is evaluated. The "ventricular function curve," which relates stroke volume to ventricular filling pressure or volume, overestimates the role played by the "Starling principle" as a compensatory mechanism and underestimates how well contractile performance is preserved. The evaluation of end systolic pressure-volume relationships under conditions of variable afterload closely reflects the isometric length-tension relationship and is therefore a more accurate way to quantitate cardiac muscle performance. Pressure overload hypertrophy usually leads to a depression in contractility whereas volume overload may not. An exaggerated sympathoadrenal response is another hallmark of severe heart failure that enhances contractility, helps initiate hypertrophy, and maintains arterial perfusion pressure. A generalized increase in peripheral vascular resistance occurs and is most prominent in those circulations most susceptible to neurohumoral control (renal, splanchnic, cutaneous). This favors perfusion of the cerebral and coronary circulations. Vasoconstriction is further enhanced by the activation of the renin-angiotensin-aldosterone system and secretion of ADH. This results in sodium retention and plasma volume expansion. In early mild heart failure, vasomotor tone may be normal at rest; however, the sympathoadrenal response to exercise may be intense. Moderate alpha receptor stimulation reduces skeletal muscle blood supply and favors the intramuscular redistribution of blood flow from inactive to active muscle fibers, thereby maintaining a normal oxygen consumption. During the later stages of heart failure, increased vascular stiffness due to increased sodium content and excessive norepinephrine appears to restrict nutritional blood flow to exercising muscle at the conductance-vessel level. Vasodilator drugs may reduce aortic impedance and improve cardiac output, may lower ventricular filling pressure, and relieve congestive symptoms, and may result in complex but favorable changes in the distribution of blood flow to the regional circulations.