Respiratory Alkalosis

How to Cite This Chapter: To KC-Y, Franek E, Kokot F. Respiratory Alkalosis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.19.2.4.?utm_source=nieznany&utm_medium=referral&utm_campaign=social-chapter-link Accessed March 28, 2024.
Last Updated: February 14, 2022
Last Reviewed: February 14, 2022
Chapter Information

Definition, Etiology, PathogenesisTop

Respiratory alkalosis is defined as an increase in blood pH to >7.45 due to primary hypocapnia (caused by hyperventilation).

Hypocapnia due to hyperventilation may be caused by stimulation of the respiratory center (eg, due to pain, excitement, cold), hypoxia (causes of hypoxemia and hypoxia: see Respiratory Failure), organic central nervous system changes (cerebrovascular disease in >90% of cases), or psychiatric disorders.

Renal compensation for respiratory alkalosis involves an increase in the urinary excretion of bicarbonate and a decrease in bicarbonate production. Maximal renal compensation of respiratory alkalosis takes several days.

Clinical Features and DiagnosisTop

Clinical manifestations depend on the underlying condition. Hypocapnia is manifested by altered mental status, features of cerebral ischemia, paresthesia, and pyramidal symptoms. Alkalosis may precipitate tetany or its equivalents (see Hypocalcemia).

Diagnostic criteria for respiratory alkalosis include permanent or episodic hyperventilation, pH >7.45, low partial pressure of carbon dioxide in arterial blood (PaCO2), and normal or low bicarbonate concentration [HCO3]. In patients with compensated respiratory alkalosis, pH is (close to) normal, PaCO2 is low, and [HCO3] is decreased.

TreatmentTop

1. Treatment of the underlying condition.

2. Symptomatic treatment (rarely; only in patients without hypoxia):

1) Instruct the patient to breathe into a plastic bag (to increase the respiratory dead space) in case of symptomatic respiratory alkalosis, usually acute.

2) Short-term use of sedatives or drugs that have depressive effects on the respiratory center (benzodiazepines, barbiturates) may play a limited role in anxiety-induced hyperventilation, leading to symptomatic chronic respiratory alkalosis.

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