HEMODYNAMIC IMPACT OF DIURETIC THERAPY IN CHRONIC HEART-FAILURE

An immediate improvement in haemodynamic variables and cardiac perform ance 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, angi otensin and aldosterone levels; these increase maximally over the firs t week of treatment but attenuate during sustained therapy. There are reciprocal alterations in plasma a-atrial natriuretic peptide levels. These findings suggest that the initial volume contraction is maintain ed, though somewhat attenuated, during chronic therapy. The neurohumor al consequences of diuretic therapy are of particular interest in hear t failure, as they may contribute to diuretic resistance. Activation o f the renin-angiotensin system favours the proximal tubular reabsorpti on of sodium and water, which may result in dilutional hyponatraemia. Diuretics have both direct vascular and non-vascular (volume-dependent ) haemnodynamic 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 subseque ntly normalizes, allowing cardiac output to return towards control val ues. 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 presser action is due to activation of the renin-angiotensin system. Direct pu lmonary vasodilatation with improved pulmonary compliance remains an i nteresting possibility. Over the longer term, substantial reductions i n left heart filling pressure during exercise occur at unaltered cardi ac output. The impact of diuretic therapy on the underlying myocardial disease process is unknown. There is little direct evidence of ventri cular remodelling or of improved intrinsic cardiac performance (as dis tinct from that due to altered loading conditions). In the absence of such information, it would appear reasonable to combine diuretic thera py with a vasodilator or angiotensin converting enzyme inhibitor, even in patients symptomatically well controlled on diuretic alone.