COLLEGE OF NURSING

BSN 2-3

Metabolic Alkalosis
Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-)
concentration. This occurs as a consequence of a loss of H+ from the body or a gain
in HCO3-. In its pure form, it manifests as alkalemia (pH >7.40). As a compensatory
mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in
arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that
would otherwise occur. Normally, arterial PaCO2 increases by 0. 5-0

Etiology
Metabolic alkalosis is bicarbonate (HCO3-) accumulation due to:
 Acid loss
 Alkali administration
 Intracellular shift of hydrogen ion (H+—as occurs in hypokalemia)
 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.
 Signs and Symptoms
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.

Intervention and 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 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.