Does intravenous furosemide improve hemodynamics and survival in patients with left ventricular dysfunction associated with acute myocardial infarction?
Fifteen patients with acute myocardial infarction and an elevated pulmonary capillary wedge pressure were given 40 mg furosemide intravenously within 24 hr of diagnosis of infarction. We divided the patients into two groups on the basis of the diuretic response to furosemide: nine who responded with a diuresis of greater than 400 ml in two hours, and six with a lower diuresis. The nine patients who responded well had a 35% fall in pulmonary capillary wedge pressure, from 21 to 12 mm Hg ( P < 0.01), accompanied by a small but significant decrease in arterial pressure at the end of two hours. There was no apparent increase in left ventricular function in these patients as shown by the relationship of left ventricular filling pressure and stroke work index, but all survived. The nonresponders failed to show significant hemodynamic changes, were significantly older, had a higher serum urea nitrogen (SUN) than the responders and had higher pulmonary capillary wedge pressures. Despite further therapy with much higher doses of furosemide and digitalis, five of the six nonresponders (83%) died. Furosemide is of value in relieving pulmonary congestion in patients with moderate congestive heart failure associated with myocardial infarction. It should be given cautiously, as an initial dose of 40 mg intravenously may cause a large fall in cardiac output and systemic pressure in occasional patients. Furosemide cannot, however, be recommended as the primary therapeutic agent in patients with severe left ventricular dysfunction complicating acute myocardial infarction.
KIELY et al. (Sat,) studied this question.