Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased urine acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment.
Published by Elsevier Inc.