Key result
Dual-acting vasodilators relieve pulmonary congestion and boost cardiac output in heart failure unless filling pressures fall.
Why the study?
The effects and tolerability of venous and arteriolar vasodilatation in reducing load on the failing heart and improving its performance are not fully understood.
Venous dilators appear tolerated despite preload reduction in HF; leaves open compensatory mechanisms and applicability.
1 To reduce load on the failing heart would seem likely to improve its performance, but it is remarkable that apparently adverse effects such as reduced filling pressure and arterial vasodilatation are so well tolerated. 2 The reduction in filling pressure (preload) produced by venous vasodilators must lead to a fall in cardiac output unless compensated in some other way. Not all parts of the venous system behave in the same way and the venous capacitance increased by venous dilators such as nitrates seems to be analogous to the mean systemic pressure of Guyton (1963). 3 Arteriolar vasodilatation (afterload) can lead to an increase in cardiac output best expressed on the Sarnoff model as a higher ventricular function curve. The larger stroke volume may prevent any fall in blood pressure so that coronary flow is maintained and there is no reflex tachycardia. A combination of preload and afterload reduction has the advantage of reducing filling pressure to clear pulmonary congestion and increasing cardiac output in persisting failure, but it may produce an adverse net fall in output if the filling pressure is initially low.
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John Hamer (1981) conducted a review in Congestive heart failure. Vasodilators was evaluated. Combined preload and afterload reduction with vasodilators clears pulmonary congestion and increases cardiac output in persisting heart failure, but may reduce output if filling pressure is low.
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