(See also Acid-Base Regulation Acid-Base Regulation Metabolic processes continually produce acid and, to a lesser degree, base. Hydrogen ion (H+) is especially reactive; it can attach to negatively charged proteins and, in high concentrations... read more and Acid-Base Disorders Acid-Base Disorders 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 .)
Etiology
Metabolic alkalosis is bicarbonate (HCO3−) accumulation due to
Acid loss
Alkali administration
Renal HCO3− retention
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
Diuretic use
Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction)
Among other causes of metabolic alkalosis Causes of Metabolic Alkalosis 
are disorders that cause
Bicarbonate excess
Renal acid loss
Metabolic alkalosis can be
Chloride (Cl)-responsive: Involves loss or excess secretion of Cl; it typically corrects with IV administration of NaCl-containing fluid.
Chloride-unresponsive: Does not correct with NaCl-containing fluids, and typically involves severe magnesium (Mg) and/or potassium (K) deficiency or mineralocorticoid excess.
The 2 forms can coexist, eg, in patients with volume overload made hypokalemic by high-dose diuretics.
Symptoms and Signs
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 4.7 mg/dL ( 1.17... 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 cause is... read more may cause weakness.
Diagnosis
Arterial blood gas (ABG) and serum electrolyte measurements
Diagnosis of cause (usually clinical)
Sometimes measurement of urinary Cl− and K+
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 Cl < 20 mEq/L (< 20 mmol/L) indicates significant renal Cl− reabsorption and hence a Cl-responsive cause (see table Causes of Metabolic Alkalosis Causes of Metabolic Alkalosis
)Urinary Cl > 20 mEq/L (> 20 mmol/L) suggests a chloride-unresponsive form.
Urinary K and the presence or absence of hypertension help differentiate the chloride-unresponsive alkaloses.
Urinary K < 30 mEq/day (< 30 mmol/day) signifies hypokalemia or laxative misuse.
Urinary K > 30 mEq/day (> 30 mmol/day) in a patient without hypertension suggests diuretic abuse or Bartter syndrome Bartter Syndrome and Gitelman Syndrome Bartter syndrome and Gitelman syndrome are autosomal recessive renal disorders characterized by fluid, electrolyte, urinary, and hormonal abnormalities, including renal potassium, sodium, chloride... read more or Gitelman syndrome Bartter Syndrome and Gitelman Syndrome Bartter syndrome and Gitelman syndrome are autosomal recessive renal disorders characterized by fluid, electrolyte, urinary, and hormonal abnormalities, including renal potassium, sodium, chloride... read more .
Urinary K > 30 mEq/day (> 30 mmol/day) in a patient with hypertension requires evaluation for hyperaldosteronism, mineralocorticoid excess, and renovascular disease.
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 ).
Treatment
Cause treated
IV 0.9% saline solution for chloride-responsive metabolic alkalosis
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.
Key Points
Metabolic alkalosis is bicarbonate (HCO3−) accumulation due to acid loss, alkali administration, intracellular shift of hydrogen ion, or renal HCO3− retention.
The most common causes are volume depletion (particularly when involving loss of gastric acid and chloride (Cl) due to recurrent vomiting or nasogastric suction) and diuretic use.
Metabolic alkalosis involving loss or excess secretion of Cl is termed chloride-responsive.
Treat the cause and give patients with chloride-responsive metabolic alkalosis 0.9% saline IV.
Chloride-resistant metabolic alkalosis is due to increased aldosterone effect.
Treatment of chloride-resistant metabolic alkalosis involves correction of hyperaldosteronism.
