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Respiratory alkalosis
Last reviewed: 12.07.2025
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Respiratory alkalosis is a primary decrease in PCO2 with or without a compensatory decrease in HCO3; pH may be high or close to normal. The cause is an increase in respiratory rate and/or tidal volume (hyperventilation). Respiratory alkalosis may be acute or chronic. The chronic form is asymptomatic, but the acute form causes dizziness, impaired consciousness, paresthesia, spasms, and fainting. Signs include hyperpnea or tachypnea, carpopedal spasm.
[ Causes respiratory alkalosis
Respiratory alkalosis is characterized by a primary decrease in PCO2 (hypocapnia) due to an increase in respiratory rate and/or tidal volume (hyperventilation). Increased ventilation is often observed as a physiological response to hypoxia, metabolic acidosis, increased metabolic demands (e.g., fever), and is often observed in many severe conditions. Also, pain, anxiety, and some CNS disorders can increase respiration without a physiological need.
Respiratory alkalosis may be acute or chronic. The difference is based on the degree of metabolic compensation; within minutes, excess HCO3 is bound by extracellular H, but more significant compensation is observed after 2-3 days, when the kidneys reduce H excretion.
Pseudo-respiratory alkalosis is characterized by low arterial and high pH in patients with severe metabolic acidosis due to poor systemic circulation (eg, cardiogenic shock, during cardiopulmonary resuscitation). Pseudo-respiratory alkalosis occurs when mechanical ventilation (often hyperventilation) removes larger than normal amounts of alveolar CO2. Large amounts of alveolar CO2 cause overt respiratory alkalosis on arterial blood gas measurements, but poor systemic perfusion and cellular ischemia result in cellular acidosis, which leads to venous acidosis. Diagnosis is based on demonstrating a significant arteriovenous difference in pH and elevated lactate; treatment involves improving systemic hemodynamics.
Symptoms respiratory alkalosis
The symptoms of respiratory alkalosis depend on the rate and extent of the fall in PCO2. Acute respiratory alkalosis causes dizziness, altered consciousness, peripheral and perioral paresthesias, spasms, and syncope; the mechanism is thought to involve changes in cerebral blood flow and pH. Often the only sign is tachypnea or hyperpnea; in severe cases, carpopedal spasm may be present. Chronic respiratory alkalosis is usually asymptomatic and has no distinguishing features.
Diagnostics respiratory alkalosis
Arterial blood gas and plasma electrolyte levels should be measured. Minor hypophosphatemia and hypokalemia may be observed due to intracellular movement and decreased ionized Ca++ levels with increased protein binding capacity.
The presence of hypoxia or an elevated alveolar-arterial gradient [inspiratory PO2 - (arterial PO2 + 5/4 arterial PCO2)] requires a search for a cause. Other causes are usually obvious from the history and examination. However, because pulmonary embolism often occurs without hypoxia, embolism must first be excluded in hyperventilating patients before attributing the cause to anxiety.
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Treatment respiratory alkalosis
Treatment of respiratory alkalosis is directed at the underlying cause; respiratory alkalosis is not a life-threatening condition, so pH-altering measures are not necessary. Increasing the inspired CO2 content during rebreathing (e.g., using a paper bag) is used quite often, but may be dangerous in patients with CNS disorders, in whom the CSF pH may be below normal.