Respiratory alkalosis is always a disorder of hyperventilation, reducing the PCO2 and increasing serum pH (Table 21–16). In pregnancy, progesterone stimulates the respiratory center, producing an average PCO2 of 30 mm Hg and respiratory alkalosis. Salicylates directly stimulate respiration and aspirin toxicity should be suspected when both respiratory alkalosis and an anion gap metabolic acidosis are present, particularly with alkalemia. Symptoms of acute respiratory alkalosis are related to decreased cerebral blood flow induced by the disorder.
++ Table Graphic Jump Location Table 21–16.Causes of respiratory alkalosis. ||Download (.pdf) Table 21–16. Causes of respiratory alkalosis.
Decreased inspired oxygen tension
Cerebrovascular accident (infarction, hemorrhage)
Pharmacologic and hormonal stimulation
Recovery from metabolic acidosis
Interstitial lung disease
Determination of appropriate metabolic compensation may reveal an associated metabolic disorder.
As in respiratory acidosis, the metabolic compensation is greater if the respiratory alkalosis is chronic (see Table 21–11). In acute respiratory alkalosis, HCO3– decreases by 2 mEq/L for every 10 mm Hg decrease in PCO2, whereas in chronic respiratory alkalosis, HCO3– decreases by 4 mEq/L for every 10 mm Hg decrease in PCO2.
A. Symptoms and Signs
In acute cases (hyperventilation), there is light-headedness, anxiety, perioral numbness, and paresthesias. Tetany occurs from a low ionized calcium, since severe alkalosis increases calcium binding to albumin.
B. Laboratory Findings
Arterial blood pH is elevated, and PCO2 is low. Serum bicarbonate is decreased in chronic respiratory alkalosis.
Treatment is directed toward the underlying cause. In acute hyperventilation syndrome from anxiety, the traditional treatment of breathing into a paper bag should be discouraged because it does not correct PCO2 and may decrease PO2. Reassurance may be sufficient for the anxious patient, but sedation may be necessary if the process persists. Hyperventilation is usually self-limited since muscle weakness caused by the respiratory alkalemia will suppress ventilation. Rapid correction of chronic respiratory alkalosis may result in metabolic acidosis as PCO2 is increased with a previous compensatory decrease in HCO3–. The severity of hypocapnia in critically ill patients has been associated with adverse outcomes.