Abstract
Metabolic alkalosis is an increase in blood pH to >7.45 due to a primary increase in serum bicarbonate (HCO3−). Metabolic alkalosis results from alkali accumulation or acid loss, and it is associated with a secondary increase in carbon dioxide arterial pressure (PaCO2). Metabolic alkalosis is a common acid-base disorder, especially in critically ill patients. The pathogenesis of chronic metabolic alkalosis includes two derangements, generation of metabolic alkalosis via gain of alkali or loss of acid and maintenance of metabolic alkalosis by increased tubular HCO3− reabsorption (failure of the kidneys to excrete excess alkali). Metabolic alkalosis is the most common acid-base disorder in hospitalized patients, particularly in the surgical critical care unit. Mortality increases as pH increases.
Highlights
BackgroundThe focus of this review article is the pathophysiology of metabolic alkalosis, as well as its causes, diagnosis, and management
Metabolic alkalosis is an increase in blood pH to >7.45 due to a primary increase in serum bicarbonate (HCO3−)
A high blood pH >7.45, i.e., low arterial blood hydrogen (H+) defines alkalemia, if serum HCO3− is high, the alkalemia is due to metabolic alkalosis, while if carbon dioxide arterial pressure (PaCO2) is low, the alkalemia is due to respiratory alkalosis
Summary
The focus of this review article is the pathophysiology of metabolic alkalosis, as well as its causes, diagnosis, and management. An ABG sample in a patient with severe metabolic alkalosis showed pH 7.55, PaCO2 49 mmHg, HCO3− 38 mmol/l, and a base excess of 14 mmol/l. ABGs are required to ascertain the diagnosis of acidbase disorders because high serum HCO3− can result from metabolic alkalosis or metabolic compensation for respiratory acidosis. Pendred syndrome patients do not have renal abnormalities under basal conditions They are at risk of developing life-threatening metabolic alkalosis in case of volume depletion or treatment with thiazide diuretics [36]. Peritoneal dialysis or hemodialysis (with a low HCO3− in the dialysate {30-32 mmol/l}) are helpful in correcting metabolic alkalosis in patients with advanced chronic kidney disease (CKD) or who are already on dialysis [40]. Forty percent of patients receiving indomethacin discontinued treatment due to gastrointestinal adverse reactions
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