Key result
Vasodilator therapy is discussed as a treatment for acute and chronic heart failure to address elevated left ventricular filling pressure and systemic vascular resistance.
Discusses the physiological rationale for vasodilator therapy in acute and chronic heart failure.
Supports vasodilator rationale in HF with elevated pressures; leaves open optimal integration with contemporary therapies.
DURING the last few years, there has been a great deal of interest in vasodilator therapy in cases of acute and chronic heart failure. Better understanding of cardiac physiology and development of bedside hemodynamic monitoring techniques using flowdirected catheters have provided impetus to evaluate different physiologic and pharmacologic interventions in acutely ill patients. Most patients with congestive heart failure have elevation of the left ventricular filling pressure (LVFP) and low cardiac output. Elevated LVFP (index of blood volume) is a compensatory phenomenon in the early stage of heart failure to maintain cardiac output. This beneficial effect may later result in excessive myocardial oxygen demand, decreased coronary flow, and symptoms of pulmonary congestion. Similarly, arterial constriction occurring initially in heart failure may be appropriate to maintain circulation to vital organs, but may eventually result in a decrease in cardiac output because of the elevated systemic vascular resistance.1 Experimental evidence shows
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Jawahar L. Mehta (1977) conducted a review in Heart failure. Vasodilator therapy was evaluated. Vasodilator therapy is discussed as a treatment for acute and chronic heart failure to address elevated left ventricular filling pressure and systemic vascular resistance.
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