Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.[1][4] This condition is one of the four primary disturbance of acid–base homeostasis.[5]
The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction:
This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis).[10][11]
The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual.[1]
The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentrations (and blood pH) after a respiratory or metabolic acid-base disturbance[12]
Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur.[3] If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels.[16]
InThe Andromeda Strain, one of the characters is exposed to contamination, but saves himself by increasing his respiratory rate to induce alkalosis.[17]
Unwin, R.; Stidwell, R.; Taylor, S.; Capasso, G. (1997-11-01). "The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo". American Journal of Physiology. Renal Physiology. 273 (5): F698–F705. doi:10.1152/ajprenal.1997.273.5.F698. ISSN1931-857X. PMID9374832.
