Respiratory Alkalosis on ABG: Definition and Clinical Significance
Respiratory alkalosis on an arterial blood gas indicates a primary disorder of hyperventilation, characterized by pH >7.45 with PaCO₂ below the normal range of 4.6–6.1 kPa (34–46 mm Hg), reflecting excessive elimination of carbon dioxide relative to tissue production. 1
Key ABG Parameters Defining Respiratory Alkalosis
- pH >7.45 ([H+] <35 nmol/L) confirms the presence of alkalosis 1
- PaCO₂ <4.6 kPa (<34 mm Hg) indicates the respiratory origin, as alveolar ventilation exceeds the rate needed to eliminate CO₂ produced by tissues 1, 2
- Bicarbonate (HCO₃⁻) levels help distinguish acute from chronic respiratory alkalosis:
Pathophysiology and Compensatory Mechanisms
- Hyperventilation drives excessive CO₂ elimination, directly raising pH by reducing carbonic acid formation (CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻) 1
- Initial compensation occurs within minutes through cellular uptake of bicarbonate and intracellular buffering 2
- Chronic compensation develops over hours to days as the kidneys reduce bicarbonate reabsorption, allowing pH to normalize while PaCO₂ remains low 2
Common Clinical Causes
- Pulmonary disorders: Pneumonia, pulmonary embolism, acute respiratory distress syndrome, interstitial lung disease 3, 4
- Extrapulmonary disorders: Sepsis, anxiety/hyperventilation syndrome, pain, fever, pregnancy, liver disease, salicylate toxicity 4
- Central nervous system: Stroke affecting the respiratory center (particularly posterior circulation), meningitis, encephalitis 5
- Iatrogenic: Excessive mechanical ventilation 4
Metabolic Consequences and Organ System Effects
- Electrolyte disturbances: Hypokalemia, hypophosphatemia, hypocalcemia (ionized calcium decreases as alkalosis increases protein binding) 4
- Mild lactic acidosis may develop despite the alkalotic state 4
- Cardiovascular effects: Tachycardia, atrial and ventricular arrhythmias, chest pain (both ischemic and non-ischemic), coronary vasoconstriction 4
- Pulmonary vasodilation occurs in contrast to systemic vasoconstriction 4
- Gastrointestinal changes: Altered perfusion, motility, and electrolyte handling 4
- Neurologic effects: Cerebral vasoconstriction (used therapeutically for elevated intracranial pressure), altered mental status, paresthesias 4, 5
Critical Diagnostic Pitfalls
- Do not confuse with compensated metabolic acidosis: In metabolic acidosis with respiratory compensation, pH remains <7.35 with low PaCO₂ representing appropriate hyperventilation 1
- Mixed acid-base disorders: A patient may have concurrent respiratory alkalosis (low PaCO₂, high pH) and metabolic acidosis (low HCO₃⁻, elevated anion gap), as seen in sepsis or pulmonary embolism 3
- Hyperventilation syndrome is a diagnosis of exclusion after ruling out life-threatening causes such as pulmonary embolism, sepsis, and acute coronary syndrome 3, 4
- Severe respiratory alkalosis (pH >7.70) is rare but can occur with acute ischemic stroke affecting the respiratory center and requires urgent intervention 5
Management Approach
- Identify and treat the underlying cause—correction of respiratory alkalosis is achieved by addressing the primary disorder, not by manipulating ventilation in spontaneously breathing patients 4
- Life-threatening causes require immediate intervention: High-flow oxygen for severe hypoxemia (targeting SpO₂ 94–98%), anticoagulation for pulmonary embolism, antibiotics for sepsis or pneumonia 3
- Calculate anion gap ([Na⁺] - [Cl⁻ + HCO₃⁻]) to detect concurrent metabolic acidosis; anion gap >12 suggests lactic acidosis, ketoacidosis, renal failure, or toxins 3
- In mechanically ventilated patients with iatrogenic respiratory alkalosis: Reduce minute ventilation by decreasing respiratory rate or tidal volume 4
- For severe cases (pH >7.70): Consider mechanical ventilation to control respiratory rate and normalize pH, particularly in stroke patients 5
- Monitor electrolytes closely and correct hypokalemia, hypophosphatemia, and symptomatic hypocalcemia 4