Heart failure is a state of avid renal salt and water retention. These responses initially help to restore cardiac output, but eventually become maladaptive when cardiac output is not augmented by volume expansion and when edema formation develops. In the kidney, this antinatriuretic/antidiuretic milieu is established by neurohumoral activation, namely, the sympathetic nerves, renin-angiotensin-aldosterone axis, and vasopressin. Diuretics, particularly loop diuretics, are important therapeutic tools in the management of heart failure; however, altered drug pharmacokinetics and pharmacodynamics may result in reduced efficacy. Management strategies that have been shown to be effective in overcoming diuretic resistance in heart failure are (1) sodium restriction, (2) increased dosing frequency, (3) intravenous route of administration, (4) high-dose loop diuretic administration, (5) continuous intravenous infusion of loop diuretics, and (6) combination of loop diuretics with distal-acting diuretics. In addition to their natriuretic effect, loop diuretics possess immediate and direct cardiovascular actions which are particularly important in the setting of decompensated heart failure.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Jan 1 1994|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine