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For further information, see CMDT Part 23-21: Respiratory Alkalosis
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Elevated arterial blood pH, low PCO2
Always a disorder of hyperventilation, which reduces the PCO2 and increases the serum pH
Causes (Table 23–16)
In pregnancy, progesterone stimulates the respiratory center, producing an average PCO2 of 30 mm Hg
Salicylates
Directly stimulate respiration
Suspect aspirin toxicity when both respiratory alkalosis and an anion gap metabolic acidosis are present, particularly with alkalemia
Symptoms are related to decreased cerebral blood flow
The severity of hypocapnia in critically ill patients has been associated with adverse outcomes
Determination of appropriate metabolic compensation may reveal an associated metabolic disorder
Metabolic compensation is greater if the respiratory alkalosis is chronic
In acute respiratory alkalosis, HCO3– decreases by 2 mEq/L for every 10 mm Hg decrease in PCO2
In chronic respiratory alkalosis, HCO3– decreases by 4 mEq/L for every 10 mm Hg decrease in PCO2
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Arterial blood pH is elevated, and PCO2 is low
Serum bicarbonate is decreased in chronic respiratory alkalosis
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Treatment is directed toward the underlying cause
In acute hyperventilation syndrome from anxiety, 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–