Endocrinology of cardiac failure. Pathophysiologic aspects--hemodynamics

The hemodynamic situation in congestive heart failure (CHF) is greatly influenced by compensatory mechanisms within the heart itself as well as released from the central nervous system and from the kidneys. These measures are intended to maintain the cardiac output at a level as beneficial as possible and to distribute the blood flow to regions with the largest metabolic demands. Thus the hemodynamic consequences of CHF are reflected in the central circulation as well as in the periphery. Within the heart the Frank-Starling mechanism, adrenergic stimulation causing increase of heart rate and contractility, and during the chronic course also myocardial hypertrophy are operating. The central nervous and peripheral adaptive measures include increased sympathetic outflow bringing about an increased vasomotor tone with augmentation of pre- and afterload, and activation of the renin-angiotensin-aldosterone system, where angiotensin II further augments vasoconstriction directly and through central nervous stimulation. This vasoconstriction may be counteracted by humoral factors with vasodilatory properties, such as dopamine, bradykinin, acetylcholine and the metabolic products adenosine and lactic acid. The exact role of these and the possible importance of the antidiuretic hormone, arginine vasopressin, the prostaglandin system and the recently discovered atriopeptin remains to be established. As the compensatory mechanisms may maintain a fairly satisfactory hemodynamic situation at rest, investigations should be performed not only at rest but also during exercise to get an over-all impression of the cardiac functional state.(ABSTRACT TRUNCATED AT 250 WORDS)