Which of the following arterial blood gas results would be consistent with metabolic alkalosis?

Topic Resources

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 arterial blood gas 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

• 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)

• 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.

• Arterial blood gas (ABG) and serum electrolyte measurements

• Diagnosis of cause (usually clinical)

• Sometimes measurement of urinary Cl− and K+

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) 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.

• 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.

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.

• 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.

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