Buy the Book PDA Download

Update Me E-mail alerts The Merck Manual Minute

Print This Topic Email This Topic

(See also Approach to the Patient With Pulmonary Symptoms: Hyperventilation Syndrome.)

Respiratory alkalosis is a primary decrease in Pco₂ with or without compensatory decrease in HCO₃ ⁻; pH may be high or near normal. Cause is an increase in respiratory rate or volume (hyperventilation) or both. Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes light-headedness, confusion, paresthesias, cramps, and syncope. Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and serum electrolyte measurements. Treatment is directed at the cause.

Etiology

Respiratory alkalosis is a primary decrease in Pco₂ (hypocapnia) from an increase in respiratory rate or volume (hyperventilation), or both. Ventilation increase occurs most often as a physiologic response to hypoxia, metabolic acidosis, and increased metabolic demands (eg, fever), and as such is present in many serious conditions. In addition, pain and anxiety and some CNS disorders can increase respirations without a physiologic need.

Pathophysiology

Respiratory alkalosis can be acute or chronic. Distinction is based on the degree of metabolic compensation; excess HCO₃ ⁻ is buffered by extracellular hydrogen ion (H⁺) within minutes, but more significant compensation occurs over 2 to 3 days as the kidneys decrease H⁺ excretion.

Pseudorespiratory alkalosis: Pseudorespiratory alkalosis is low arterial Pco₂ and high pH in mechanically ventilated patients with severe metabolic acidosis from poor systemic perfusion (eg, cardiogenic shock, during CPR). Pseudorespiratory alkalosis occurs when mechanical ventilation (often hyperventilation) eliminates larger-than-normal amounts of alveolar CO₂. Exhalation of large amounts of CO₂ causes respiratory alkalosis in arterial blood (hence on ABG measurements), but poor systemic perfusion and cellular ischemia cause cellular acidosis, leading to acidosis of venous blood. Diagnosis is by demonstration of marked arteriovenous differences in Pco₂ and pH and by elevated lactate levels; treatment is improvement of systemic hemodynamics.

Symptoms and Signs

Symptoms and signs depend on the rate and degree of fall in Pco₂. Acute respiratory alkalosis causes light-headedness, confusion, peripheral and circumoral paresthesias, cramps, and syncope. Mechanism is thought to be change in cerebral blood flow and pH. Tachypnea or hyperpnea is often the only sign; carpopedal spasm may occur in severe cases. Chronic respiratory alkalosis is usually asymptomatic and has no distinctive signs.

Diagnosis

• ABG and serum electrolytes
• If hypoxia present, cause vigorously pursued

Recognition of respiratory alkalosis and appropriate renal compensation discussed in Acid-Base Regulation and Disorders: Diagnosis requires ABG and serum electrolyte measurements. Minor hypophosphatemia and hypokalemia from intracellular shifts and decreased ionized Ca⁺⁺ from an increase in protein binding may be present.

Presence of hypoxia or an increased alveolar-arterial (A-a) O₂ gradient (inspired Po₂ − [arterial Po₂ + ⁵/₄ arterial Pco₂]) requires search for a cause. Other causes are often apparent on history and examination. However, because pulmonary embolism often presents without hypoxia (see Pulmonary Embolism (PE)), embolism must be strongly considered in a hyperventilating patient before ascribing the cause to anxiety.

Treatment

Treatment is directed at the underlying cause. Respiratory alkalosis is not life threatening, so no interventions to lower pH are necessary. Increasing inspired CO₂ through rebreathing (such as from a paper bag) is common practice but may be dangerous in at least some patients with CNS disorders in whom CSF pH may already be below normal.

Last full review/revision July 2008 by James L. Lewis, III, MD

Content last modified July 2008