Haemodynamic Impact of Diuretic Therapy in Chronic Heart Failure

Abstract

An immediate improvement in haemodynamic variables and cardiac performance is achieved in chronic heart failure following diuretic therapy, primarily due to reductions in plasma and extracellular fluid volumes. Humoral markers of these alterations are increased plasma renin, angiotensin and aldosterone levels; these increase maximally over the ñrst week of treatment but attenuate during sustained therapy. There are reciprocal alterations in plasma α-atrial natriuretic peptide levels. These findings suggest that the initial volume contraction is maintained, though somewhat attenuated, during chronic therapy. The neurohumoral consequences of diuretic therapy are of particular interest in heart failure, as they may contribute to diuretic resistance. Activation of the renin-angiotensin system favours the proximal tubular reabsorption of sodium and water, which may result in dilutional hyponatraemia. Diuretics have both direct vascular and non-vascular (volume-dependent) haemodynamic actions. Together these substantially reduce the left heart filling pressure (-29%) with a consequent fall in cardiac output ( 10%). Systemic vascular resistance initially increases but subsequently normalizes, allowing cardiac output to return towards control values. Haemodynamic tolerance to diuretics does not usually occur during sustained oral therapy; additionally, echocardiographic contractility indices and exercise capacity may increase. The vasodilator activity of the diuretics is due to prostaglandin release; the initial pressor action is due to activation of the renin-angiotensin system. Direct pulmonary vasodilatation with improved pulmonary compliance remains an interesting possibility. Over the longer term, substantial reductions in left heart filling pressure during exercise occur at unaltered cardiac output. The impact of diuretic therapy on the underlying myocardial disease process is unknown. There is little direct evidence of ventricular remodelling or of improved intrinsic cardiac performance (as distinct from that due to altered loading conditions). In the absence of such information, it would appear reasonable to combine diuretic therapy with a vasodilator or angiotensin converting enzyme inhibitor, even in patients symptomatically well controlled on diuretic alone.

Effect of short‐term treatment with bumetanide, quinapril and low‐sodium diet on dogs with moderate congestive heart failure

“…Studies of human patients with CHF who were treated with bumetanide showed considerable improvement of clinical signs, both at rest and on exertion, without blood electrolyte changes. 9,10 Similar findings have been partially confirmed in dogs. 11 ACEI have two major functions in CHF: prevention of vasoconstrictive effects of angiotensin II in veins and arteries and reduction of sodium and water retention through inhibition of aldosterone release.…”

Furosemide is associated with acute kidney injury in critically ill patients

“…Some explanations can be proposed for the presence of the deleterious effect of diuretics on renal function in critically ill patients with sepsis/septic shock: a) reduction in preload with renal vasoconstriction, activation of the renin-angiotensin-aldosterone system and sympathetic stimulation (this reduction in preload occurs not only by increased urine output induced by furosemide, but also by a prostaglandin-mediated venodilation) (34,35); b) Dobrowolski et al (36,37) demonstrated a pronounced decrease in medullary blood flow compared to the cortex after administration of furosemide. The differential effect of furosemide on cortical and medullary blood flow may increase the intrarenal risk of medullar ischemia, favoring the development of acute tubular necrosis (36-38).…”

Benefits and Risks of Torasemide in Congestive Heart Failure and Essential Hypertension

“…[20] Loop diuretics given intravenously also have an immediate effect in reducing preload by causing venous dilatation, increasing venous capacitance, and reducing cardiac preloadJ19-21] [20] Loop diuretics given intravenously also have an immediate effect in reducing preload by causing venous dilatation, increasing venous capacitance, and reducing cardiac preloadJ19-21]…”