What are the causes of respiratory alkalosis?

Causes of Respiratory Alkalosis

Respiratory alkalosis results from alveolar hyperventilation that eliminates CO2 faster than tissues produce it, and the causes can be systematically categorized into pulmonary, central nervous system, psychiatric, metabolic compensation, iatrogenic, and physiological states.

Pulmonary Causes

The lungs themselves can drive hyperventilation through several mechanisms:

• Hypoxemia from any cause stimulates peripheral chemoreceptors, triggering compensatory hyperventilation that leads to respiratory alkalosis 1, 2.
• Pneumonia, pulmonary embolism, and pulmonary edema directly stimulate increased ventilation through chemoreceptor activation 1, 2.
• Acute pulmonary edema causes patients to hyperventilate to compensate for hypoxemia, producing respiratory alkalosis despite significant respiratory distress 1.
• Pulmonary hypertension induces hyperventilation as a compensatory mechanism to reduce pulmonary vascular resistance and maintain cardiac output 1.

Central Nervous System Causes

Direct stimulation of the medullary respiratory center produces hyperventilation:

• Head injury, cerebrovascular accidents (stroke), and CNS infections directly stimulate the respiratory center in the medulla, causing pathological hyperventilation 1, 2.
• Any CNS lesion affecting the respiratory control centers can override normal ventilatory feedback mechanisms 2.

Psychiatric and Behavioral Causes

These are among the most common causes in emergency settings:

• Anxiety reactions, panic disorders, and hyperventilation syndrome are characterized by abnormal breathing patterns with impressive hyperventilation and increased respiratory frequency 1, 2.
• Panic disorder commonly presents with clustering of suffocating, smothering, and air hunger sensations, occurring even without reduced ventilatory capacity due to excessive ventilatory drive or increased CO2 sensitivity 1, 2.
• Hyperventilation syndrome is a diagnosis of exclusion in the emergency department setting 3.
• The symptoms can persist even when hypocapnia is not present, as psychological mechanisms maintain the breathing pattern 4.

Compensatory Respiratory Alkalosis

The respiratory system may appropriately hyperventilate to compensate for other disorders:

• Metabolic acidosis triggers compensatory hyperventilation as the respiratory system attempts to maintain pH near normal by blowing off CO2 1, 2.
• Heart failure with Cheyne-Stokes breathing creates respiratory alkalosis that may protect the failing heart from decompensation 1, 2.
• Do not disrupt this compensatory respiratory alkalosis in patients with underlying metabolic acidosis, and if assisted ventilation is necessary, target appropriate oxygen saturation (88-92%) to avoid worsening the condition 1, 2.

Iatrogenic Causes

Medical interventions can inadvertently cause respiratory alkalosis:

• Mechanical ventilation with excessive settings and inappropriate ventilator management in critical care settings commonly causes respiratory alkalosis 1, 2.
• Respiratory dyskinesia from antipsychotic medications can lead to respiratory alkalosis, often undiagnosed, including orofacial dyskinesia, dysphonia, and dyspnea 1, 2.
• Therapeutic hyperventilation is intentionally used for treatment of elevated intracranial pressure 3.

Physiological States

Normal physiological adaptations can produce respiratory alkalosis:

• Pregnancy produces mild respiratory alkalosis with increased ventilation beginning in the first trimester, reaching 20-40% above baseline by term, mediated by elevated serum progesterone levels, resulting in PaCO2 of 28-32 mmHg and plasma bicarbonate of 18-21 mEq/L 5.
• High altitude exposure triggers hypobaric hypoxia, leading to increased respiratory rate and tidal volume that promotes respiratory alkalosis 1.

Critical Diagnostic Pitfalls

• Avoid excessive oxygen therapy that could disrupt compensatory mechanisms in patients with chronic respiratory alkalosis 1, 2.
• In heart failure with Cheyne-Stokes breathing, respiratory alkalosis should not be aggressively suppressed as it serves a protective compensatory function 1.
• Severe respiratory alkalosis can be life-threatening, inducing hypocalcemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction 6.
• Respiratory alkalosis produces multiple metabolic abnormalities including changes in potassium (typically hyperkalemia acutely with hypokalemic overshoot during recovery), phosphate, calcium, and mild lactic acidosis 3, 7.