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Hemodynamic effects of intravenous digoxin in patients with severe heart failure initially treated with diuretics and
Insights
Intravenous digoxin improved cardiac function in patients with severe heart failure, increasing cardiac index and ejection fraction. This study demonstrates digoxin
Area of Science:
- Cardiology
- Pharmacology
Background:
- Severe heart failure (New York Heart Association class IV) presents significant challenges in patient management.
- Initial treatment often involves diuretics and vasodilators, aiming for clinical compensation.
- The role of digoxin in decompensated heart failure, particularly in treatment-naïve patients, requires further elucidation.
Purpose of the Study:
- To evaluate the acute hemodynamic effects of intravenous digoxin in patients with advanced heart failure.
- To assess digoxin's impact on cardiac index, left ventricular stroke work index, ejection fraction, and pulmonary capillary wedge pressure.
Main Methods:
- Eleven male patients with idiopathic or ischemic cardiomyopathy and New York Heart Association class IV heart failure were studied.
- Patients were initially treated with intravenous furosemide and vasodilators until clinical compensation.
- Hemodynamic parameters were measured before and for 6 hours after administering intravenous digoxin (1 mg total dose).
Main Results:
- Digoxin administration significantly increased cardiac index (2.6 to 3.3 L/min/m²), left ventricular stroke work index (27 to 43 g·m/m²), and ejection fraction (21% to 29%).
- Mean pulmonary capillary wedge pressure decreased significantly (24 to 17 mm Hg).
- These improvements occurred in patients previously treated with diuretics and vasodilators.
Conclusions:
- Intravenous digoxin effectively improves acute hemodynamics in patients with severe heart failure.
- Digoxin enhances contractility and reduces filling pressures in this patient population.
- These findings support the use of digoxin as an adjunctive therapy in managing decompensated heart failure.
Abstract:
The purpose of this study was to assess the hemodynamic effects of intravenous digoxin in patients with New York Heart Association class IV heart failure, who had never previously been treated with digitalis drugs, and who were initially treated only with diuretics and systemic vasodilators to clinical end points of compensation. Eleven male patients, 5 with idiopathic and 6 with ischemic cardiomyopathy, had sinus rhythm and were hospitalized with congestive heart failure not precipitated by an acute ischemic event. All 11 patients were treated with intravenous furosemide and various vasodilators without invasive hemodynamic monitoring for a mean period of 4.3 +/- 2.1 days. This therapy resulted in subjective and objective improvement in all patients as reflected by a significant decrease in heart failure score from 9.5 +/- 2.2 to 2.7 +/- 2.3 (p less than 0.001). When compensation was achieved by clinical criteria, the patients were instrumented and hemodynamics obtained before and serially thereafter for 6 hours after the intravenous administration of digoxin given in two 0.5 mg doses 2 hours apart. In response to digoxin, cardiac index increased from 2.6 +/- 0.7 liters/min per m2 to a peak of 3.3 +/- 0.6 liters/min per m2 (p less than 0.005); left ventricular stroke work index (g X m/m2) increased from 27 +/- 16 to 43 +/- 23 (p less than 0.005) and the ejection fraction (eight patients) increased from 21 +/- 13% to 29 +/- 11% (p less than 0.04). Mean pulmonary capillary wedge pressure decreased from 24 +/- 7 to a minimum of 17 +/- 4 mm Hg (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)