Causes of Partially Compensated Respiratory Alkalosis
Partially compensated respiratory alkalosis results from sustained hyperventilation that triggers renal bicarbonate excretion, lowering HCO3- while pH remains elevated (>7.45) and PaCO2 remains low (<34 mmHg). 1
Primary Pathophysiological Mechanism
Respiratory alkalosis occurs when alveolar ventilation exceeds the rate needed to eliminate tissue-produced CO2, causing concurrent decreases in PaCO2, increases in pH, and compensatory decreases in blood HCO3- levels. 1 The "partially compensated" state develops when renal compensation has begun but not fully normalized the pH—the kidneys decrease HCO3- reabsorption over hours to days, but arterial pH remains elevated rather than returning to the normal 7.35-7.45 range. 1
Major Clinical Causes
Hypoxemia-Driven Hyperventilation
- Pulmonary disorders including pneumonia, pulmonary embolism, and pulmonary edema stimulate peripheral chemoreceptors, triggering increased ventilation. 2
- Acute pulmonary edema causes patients to hyperventilate to compensate for hypoxemia, producing respiratory alkalosis despite significant respiratory distress. 3
- Pulmonary hypertension induces hyperventilation as a compensatory mechanism to reduce pulmonary vascular resistance—the reduced PaCO2 and increased pH help decrease pulmonary vascular resistance, crucial for maintaining cardiac output. 3
Central Nervous System Stimulation
- CNS lesions including head injury, cerebrovascular accidents, and CNS infections directly stimulate the respiratory center in the medulla, causing hyperventilation. 2
- High altitude exposure triggers hypobaric hypoxia, leading to increased respiratory rate and tidal volume that promotes respiratory alkalosis. 3
Psychiatric and Behavioral Causes
- Anxiety reactions, panic disorders, and hyperventilation syndrome are common causes characterized by abnormal breathing patterns with impressive hyperventilation and increased respiratory frequency. 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. 2
Compensatory Hyperventilation
- Metabolic acidosis compensation occurs when the respiratory system attempts to maintain pH near normal by hyperventilating to blow off CO2. 2
- Heart failure with Cheyne-Stokes breathing creates respiratory alkalosis that may protect the failing heart from decompensation. 2
Iatrogenic Causes
- Mechanical ventilation with excessive settings and inappropriate ventilator management in critical care settings can cause respiratory alkalosis. 2
- Respiratory dyskinesia from antipsychotic medications can lead to respiratory alkalosis, often undiagnosed, including orofacial dyskinesia, dysphonia, and dyspnea. 2
Critical Diagnostic Features
Look for arterial blood gas showing pH >7.45 and PaCO2 <4.6 kPa (34 mmHg) with HCO3- below normal but not fully normalized, indicating partial renal compensation. 4, 1 The bicarbonate will be decreased from baseline but the pH remains alkalotic rather than normalized, distinguishing partial from complete compensation. 1
Important Clinical Pitfalls
Do not disrupt compensatory respiratory alkalosis in patients with underlying metabolic acidosis—if assisted ventilation becomes necessary, target appropriate oxygen saturation (88-92%) to avoid worsening the condition. 2 In patients with chronic respiratory conditions or COPD risk factors, targeting lower SpO2 of 88-92% rather than 94-98% prevents disruption of compensatory mechanisms. 3
Avoid excessive oxygen therapy that could disrupt compensatory mechanisms in patients with chronic respiratory alkalosis. 2 In heart failure with Cheyne-Stokes breathing, respiratory alkalosis should not be aggressively suppressed as it serves a protective compensatory function. 3