Search

High-dose firosemide is considered effective in primary renal sodium retention but is not generally recommended in congestive heart failure. In order to evaluate efficacy and safety of high-dose furosemide (greater than 500 mg/day), the authors studied 20 patients (pts) resistant to therapy (including furosemide less than 500 mg/day) selected from 161 pts admitted for chronic heart failure. All refractory pts (15 men and 5 women, mean age sixty +/- 12 years) were in NYHA class IV and showed hyponatremia (130 +/- 5 mEq/L) and impaired renal function (BUN 31 +/- 14 mg/dL, serum creatinine 1.3 +/- 0.3 mg/dL and BUN/creatinine ratio 23 +/- 7). In addition to digitalis, dopamine, angiotensin-converting enzyme inhibitors, or vasodilators, IV high-dose furosemide (775 +/- 419 mg/day, 500-2000) was given for ten +/- five days under daily clinical and laboratory monitoring. Three pts died of low-output syndrome while 16 pts were upgraded to NYHA class III and 1 pt to class II; a mean weight reduction of 7.3 +/- 2.9 kg in ten + five days (0.80 +/- 0.4 kg/day) and a mean diuresis increase of 88 +/- 57% occurred. The maximal dose of furosemide did not correlate with serum creatinine but did correlate with BUN/creatinine ratio (r = 0.78, p less than .001). Pts were discharged on with chronic heart failure, and 43% in the subgroup in NYHA class IV with hyponatremia. High dose furosemide was effective for rapid removal of excess water and salt in "furosemide-resistant" congestive heart failure. The relationship between renal impairment and maximal furosemide doses seems to confirm the role of renal pharmacokinetics in the appearance of furosemide resistance.

In order to evaluate the incidence and the prognostic value of hyponatremia (hypoNa) in patients (pts) with severe chronic heart failure (SCHF), the authors studied 161 consecutive pts (113M, 48F ages sixty-seven +/- ten) with SCHF in NYHA class III-IV. The cause of SCHF was ischemic in 64 pts, hypertensive in 39, valvular in 14, alcohol-related in 3, and idiopathic in 41. Pretreatment hypoNa (less than 135 mmol/L) was found in 64/161 pts (40%) (Group I); Na+ was less than 125 in 10 pts, 125-130 in 19, and 131-135 mmol/L in 35; 42/64 pts (66%) of Group I were in NYHA class IV at admission. In the pts with pretreatment Na+ less than 125 mmol/L, hypoNa was persistent and refractory to high-dose furosemide (less than 500 mg/day) and water restriction. Cardiovascular mortality of Group I pts was 69% within twenty-four months (34 pts died of low-output syndrom and 10 suddenly). All pts with Na+ less than 130 mmol/L died within six months. The 20 pts who normalized Na+ are alive, and in NYHA class II-III (follow-up: twenty-six +/- fifteen, six to sixty months). Pts without hypoNa were 97/161 (Group II), and 58/97 (60%) are alive (follow-up: thirty +/- eighteen, five to fifty-eight months), whereas 39 pts died (27 suddenly, 9 of low-output syndrome, and 3 of extracardiac disease) within twenty-four months. The mortality rate of Group II was significantly lower (40% vs 69%, p less than 0.001) compared with Group I. The two groups were similar for age, sex, and cause and duration of SCHF.(ABSTRACT TRUNCATED AT 250 WORDS)