Respiratory alkalosis is defined by alveolar hyperventilation and exists when P co2 is less then expected. It is caused by conditions that stimulate respiratory centers, including central nervous system tumors or stroke, infections, pregnancy, hypoxia, and toxins (e.g., salicylates). Anxiety, pain, and overventilation of patients on mechanical ventilators also cause respiratory alkalosis.
Whatever the etiology, the clinical symptoms of acute respiratory alkalosis are predictable from its physiologic effects. Acute reduction in P co2 produces a reduction in hydrogen ion concentration, resulting in an increase in negative charge on anionic buffers. The now relatively negatively charged proteins instead bind calcium, and this reduction in ionized calcium produces carpopedal spasm and paresthesias. 15 Hypocapnia also produces substantial reductions in cerebral blood flow, and results in reduced tissue oxygen delivery because of increased hemoglobin oxygen binding.
The theoretical relationship of hydrogen ion concentration and P co2 predicted by the Kassirer-Bleich equation is that a 1-mmol decrease in [H +] results from each 1-mmHg reduction in Pco2. The actual observed relationship is very close to that predicted by the Kassirer-Bleich equation. 20 Each mmHg reduction in Pco2 results in a 0.75-mmol reduction in [H+] (Eq, 1.O).20
Chronic respiratory alkalosis is unique among the acid-base disorders in that its compensation may be complete. Compensatory events include bicarbonaturia and a reduction in acid excretion, requiring 6 to 72 h to develop fully and at least 1 week to normalize pH. The steady-state relationship between hydrogen ion concentration and Pco2 in chronic respiratory alkalosis observed in normal human subjects at high altitude is shown in Eq,, (1.0.)21
Therapy for acute respiratory alkalosis emphasizes identification and treatment of the underlying cause. The use of paper-bag rebreathing in the treatment of respiratory alkalosis should be avoided. Callaham evaluated paper-bag rebreathing in voluntarily hyperventilating volunteers and found that while the inspired P co2 increased by 20 mmHg in 30 s, it never increased above 40 mmHg. However, inspired oxygen concentration fell by an average of 27 mmHg in 180 s, and in 5 percent of subjects the fall was greater than or equal to 42 mmHg.22 If the cause of hyperventilation is actually cellular hypoxia, such a fall could be catastrophic. 23 Furthermore, there is evidence that expectation of efficacy and suggestion, rather than elevations of inspired CO 2 tension, are responsible for relief of symptoms in hyperventilation.24 An oxygen mask might provide benefits similar to those of paper-bag rebreathing with less risk of hypoxia.
Chronic respiratory alkalosis is seen at high altitudes, particularly among mountaineers climbing over 12,000 ft (where the partial pressure of O 2 is significantly diminished). Acetazolamide is frequently prescribed to counter the physiologic respiratory effects of such ascents.
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