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.