Balancing diuretic therapy in heart failure: loop diuretics, thiazides, and aldosterone antagonists.
In heart failure, sodium is retained by the kidneys despite increases in extracellular volume. There is activation of renin secretion, which culminates in the production of angiotensin II, causing vasoconstriction and aldosterone secretion. These synergistically produce an increase in tubular reabsorption of sodium and water. Diuretics are the mainstay of symptomatic treatment to remove excess extracellular fluid in heart failure. Diuretics that affect the ascending loop of Henle are most commonly used. Thiazide diuretics promote a much greater natriuretic effect when combined with a loop diuretic in patients with refractory edema. Recently, spironolactone, an aldosterone receptor blocking agent, has been recommended to attenuate some of the neurohormonal effects of heart failure. Regardless of the diuretic, patients need to be counseled on the importance of avoiding sodium in their diet
Paul
Sara
S
Heart Failure Clinic, Medical University of South Carolina, Charleston, SC, USA. smcpaul@earthlink.net
D001581:Benzothiadiazines; D004232:Diuretics / Q000627:therapeutic use*; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology; D010953:Plasma Volume / Q000187:drug effects / Q000502:physiology; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use; D016896:Treatment Outcome; D014481:United States; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
D001581:Benzothiadiazines; D004232:Diuretics; D000451:Mineralocorticoid Receptor Antagonists; D049993:Sodium Chloride Symporter Inhibitors