What are the causes of respiratory alkalosis?

Causes of Respiratory Alkalosis

Respiratory alkalosis results from alveolar hyperventilation that exceeds the body's CO2 production, and the causes can be systematically categorized into psychological, pulmonary, central nervous system, cardiac, iatrogenic, and compensatory mechanisms. 1

Psychological and Anxiety-Related Causes

• Anxiety reactions, panic disorders, and hyperventilation syndrome are among the most common causes encountered in emergency settings, characterized by abnormal breathing patterns with impressive hyperventilation, increased respiratory frequency, and decreased PaCO2. 1
• Hyperventilation syndrome is a diagnosis of exclusion after ruling out organic causes, where patients eliminate more carbon dioxide than produced, resulting in respiratory alkalosis and elevated blood pH. 2
• Severe cases of psychogenic hyperventilation can produce life-threatening respiratory alkalosis (pH >7.6) with associated hypocalcemia, extreme adrenergic sensitivity, and cerebral/myocardial vasoconstriction. 3

Pulmonary Causes

• Hypoxemia stimulates peripheral chemoreceptors leading to increased ventilation, and specific pulmonary disorders that trigger this response include:
  • Pneumonia 1
  • Pulmonary embolism 1
  • Pulmonary edema 1
• In acute pulmonary edema, patients hyperventilate to compensate for hypoxemia despite significant respiratory distress, creating the paradox of respiratory alkalosis concurrent with respiratory distress. 4
• Pulmonary hypertension causes respiratory alkalosis as a compensatory mechanism to reduce pulmonary vascular resistance through hyperventilation-induced reduction in PaCO2. 4
• High altitude-induced hypobaric hypoxia leads to increased respiratory rate and tidal volume, promoting respiratory alkalosis while potentially causing pulmonary edema. 4

Central Nervous System Causes

• Direct stimulation of the respiratory center in the medulla causes hyperventilation, with common CNS causes including:
  • Head injury 1
  • Cerebrovascular accidents (stroke) 1
  • Central nervous system infections 1
• Therapeutic hyperventilation is deliberately used for treatment of elevated intracranial pressure. 5

Cardiac Causes

• Heart failure with Cheyne-Stokes breathing creates physiological hyperventilation as a compensatory mechanism, producing respiratory alkalosis that may protect the failing heart from decompensation. 1
• Myocardial infarction and cardiac ischemia can trigger hyperventilation and respiratory alkalosis. 5

Iatrogenic Causes

• Mechanical ventilation with excessive settings and inappropriate ventilator management in critical care settings is a common iatrogenic cause of respiratory alkalosis. 1
• Excessive oxygen therapy can disrupt compensatory mechanisms in patients with chronic respiratory conditions. 1

Compensatory Respiratory Alkalosis

• Compensatory hyperventilation occurs as a physiological response to metabolic acidosis to maintain pH near normal, representing an appropriate rather than pathological response. 1
• In these cases, the respiratory alkalosis should not be disrupted, as it is a necessary compensatory mechanism. 6

Important Clinical Pitfalls

• Never attempt to correct compensatory respiratory alkalosis in patients with metabolic acidosis, as this disrupts essential physiological compensation. 6
• If assisted ventilation is necessary in patients with compensatory mechanisms, target SpO2 of 88-92% rather than higher levels to avoid worsening the condition. 1
• In patients with COPD or risk factors for hypercapnic respiratory failure, maintain lower oxygen saturation targets (88-92%) rather than the standard 94-98%. 4
• Avoid aggressive suppression of respiratory alkalosis in heart failure patients with Cheyne-Stokes breathing, as this may be protective. 4

Systemic Effects to Monitor

• Respiratory alkalosis produces multiple metabolic abnormalities including changes in potassium (initial hyperkalemia followed by hypokalemic overshoot), phosphate, calcium, and development of mild lactic acidosis. 5, 7
• Cardiac effects include tachycardia, ventricular and atrial arrhythmias, and both ischemic and non-ischemic chest pain. 5
• The hyperkalemic response during acute respiratory alkalosis is mediated by enhanced alpha-adrenergic activity and counterregulated by beta-adrenergic stimulation. 7