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Metabolic alkalosis is primary increase in bicarbonate (HCO3−) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3− excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with ABG and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated.
Metabolic alkalosis is bicarbonate HCO3− accumulation due to
Intracellular shift of hydrogen ion (H+—as occurs in hypokalemia)
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 H+ excretion) can elevate HCO3−. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. Causes are listed; the most common are volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) and diuretic use (see Table: Causes of Metabolic Alkalosis).
Causes of Metabolic Alkalosis
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 and subsequent headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany, and seizures. Alkalemia also lowers threshold for anginal symptoms and arrhythmias. Concomitant hypokalemia may cause weakness.
Recognition of metabolic alkalosis and appropriate respiratory compensation is discussed in Acid-Base Disorders : Diagnosis and requires ABG and measurement of 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 indicates significant renal Cl− reabsorption and hence a Cl-responsive cause (see Table: Causes of Metabolic Alkalosis). Urinary Cl > 20 mEq/L suggests a Cl-unresponsive form.
Urinary K and presence or absence of hypertension help differentiate Cl-unresponsive alkaloses. Urinary K < 30 mEq/day signifies hypokalemia or laxative misuse. Urinary K > 30 mEq/day without hypertension suggests diuretic abuse or Bartter or Gitelman syndrome. Urinary K > 30 mEq/day with hypertension requires evaluation for hyperaldosteronism, mineralocorticoid excess, and renovascular disease. Tests typically include plasma renin activity and aldosterone and cortisol levels (see Cushing Syndrome : Diagnosis and see Diagnosis).
Underlying conditions are treated, with particular attention paid to correction of hypovolemia and hypokalemia.
Patients with Cl-responsive metabolic alkalosis are given 0.9% saline solution IV; infusion rate is typically 50 to 100 mL/h greater than urinary and other sensible and insensible fluid losses until urinary Cl rises to > 25 mEq/L and urinary pH normalizes after an initial rise from bicarbonaturia. Patients with Cl-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 is an option, particularly if volume overload and renal dysfunction are present. Acetazolamide 250 to 375 mg po or IV once/day or bid 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/h. Frequent monitoring of ABG and electrolytes is needed.
Metabolic alkalosis is HCO3− accumulation due to acid loss, alkali administration, intracellular shift of hydrogen ion, or HCO3− retention.
The most common causes are volume depletion (particularly when involving loss of gastric acid and Cl from recurrent vomiting or nasogastric suction) and diuretic use.
Metabolic alkalosis involving loss or excess secretion of Cl is termed Cl-responsive
Treat the cause and give patients with Cl-responsive metabolic alkalosis 0.9% saline IV.
Cl-resistant metabolic alkalosis is due to increased aldosterone effect.
Treatment of Cl-resistant metabolic alkalosis involves correction of hyperaldosteronism.
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