The role of diuretics in the treatment of chronic heart failure

Altered renal function with renal NaCl-retention can be observed early in the course of congestive heart failure. The afferent pathway of this altered regulation involves changes occurring in the high pressure system as a consequence of foreward failure such as an increase in baroreceptor reflex activity. Efferent pathways may include the renin-angiotensin-aldosterone system, the sympathetic nervous system, prostaglandins, dopamine, ANF, and AVP. At present, the relative importance of these systems in mediating renal NaCl-retention in heart failure is still unclear. Expansion of the extracellular fluid volume as a consequence of renal NaCl-retention may, at least acutely, compensate for compromised myocardial function via the Frank-Starling mechanism. As a consequence of volume expansion, chronically increased cardiac preload and possibly afterload may however even aggravate cardiac failure. Diuretics may therefore induce variable effects in patients with congestive heart failure. Acutely, they may ameliorate symptoms of congestion in spite of the possibility of a further decrease in cardiac index. Chronically, they may reduce cardiac pre- and afterload. Through a variety of mechanisms, they may therefore increase cardiac performance in spite of a fall in filling pressures.