Metabolic Alkalosis

Metabolic alkalosis is bicarbonate (HCO₃⁻) accumulation due to

Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO₃⁻ reabsorption, because HCO₃⁻ is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO₃⁻ reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H⁺] excretion) can elevate HCO₃⁻. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis.

The most common causes of metabolic alkalosis are

Among other causes of metabolic alkalosis Causes of Metabolic Alkalosis are disorders that cause

Metabolic alkalosis can be

The 2 forms can coexist, eg, in patients with volume overload made hypokalemic by high-dose diuretics.

Symptoms and signs of mild alkalemia are usually related to the underlying disorder. More severe alkalemia increases protein binding of ionized calcium (Ca⁺⁺), leading to hypocalcemia Hypocalcemia Hypocalcemia is a total serum calcium concentration < 8.8 mg/dL (< 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration < 4... read more and subsequent headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany, and seizures. Alkalemia also lowers threshold for anginal symptoms and arrhythmias. Concomitant hypokalemia Hypokalemia Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common... read more may cause weakness.

Recognition of metabolic alkalosis and appropriate respiratory compensation is discussed in Diagnosis of Acid-Base Disorders Diagnosis Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3⁻) that typically produce abnormal arterial pH values. Acidemia is serum... read more and requires measurement of ABG and serum electrolytes (including Ca and Mg).

Common causes can often be determined by history and physical examination. If history is unrevealing and renal function is normal, urinary Cl⁻ and K⁺ concentrations are measured (values are not diagnostic in renal insufficiency).

Urinary K and the presence or absence of hypertension help differentiate the chloride-unresponsive alkaloses.

Tests in patients with hypertension typically include plasma renin activity and aldosterone and cortisol levels (see Diagnosis of Cushing Syndrome Diagnosis Cushing syndrome is a constellation of clinical abnormalities caused by chronic high blood levels of cortisol or related corticosteroids. Cushing disease is Cushing syndrome that results from... read more and Diagnosis of Primary Aldosteronism Diagnosis ).

Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.

Patients with chloride-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/hour greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L (> 25 mmol/L) and urinary pH normalizes after an initial rise from bicarbonaturia.

Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration alone.

Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent correction of blood pH. Hemofiltration or hemodialysis Hemodialysis In hemodialysis, a patient’s blood is pumped into a dialyzer containing 2 fluid compartments configured as bundles of hollow fiber capillary tubes or as parallel, sandwiched sheets of semipermeable... read more is an option, particularly if volume overload and renal dysfunction are present. Acetazolamide 250 to 375 mg orally or IV once or twice a day increases HCO₃⁻ excretion but may also accelerate urinary losses of K⁺ and phosphate (PO₄⁻); volume-overloaded patients with diuretic-induced metabolic alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.

In patients with severe metabolic alkalosis (pH > 7.6) and kidney failure who otherwise cannot or should not undergo dialysis, hydrochloric acid in a 0.1 to 0.2 normal solution IV is safe and effective but must be given through a central catheter because it is hyperosmotic and scleroses peripheral veins. Dosage is 0.1 to 0.2 mmol/kg/hour. Frequent monitoring of ABGs and electrolytes is needed.