Causes of Respiratory Acidosis
Respiratory acidosis results from any condition that causes carbon dioxide production to exceed pulmonary elimination, fundamentally due to inadequate alveolar ventilation. 1
Pathophysiologic Mechanism
Respiratory acidosis develops when CO₂ accumulates because ventilation cannot match metabolic CO₂ production, leading to CO₂ combining with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions, thereby lowering blood pH below 7.35 with PaCO₂ exceeding 46 mm Hg. 1
Primary Categories of Causes
Central Nervous System Impairment
- Brain injuries, strokes, or tumors affecting the medullary respiratory centers impair central respiratory drive, preventing adequate ventilatory response. 1
- Drug overdose (particularly opioids, sedatives, or anesthetics) suppresses the central respiratory drive, leading to acute hypoventilation. 2
Respiratory Muscle and Chest Wall Dysfunction
- Neuromuscular disorders (including spinal cord injury, myasthenia gravis, Guillain-Barré syndrome, or muscular dystrophy) prevent effective respiratory muscle contraction. 2
- Chest wall abnormalities (such as severe kyphoscoliosis, flail chest, or obesity hypoventilation syndrome) mechanically restrict ventilation. 2
- A rapid, shallow breathing pattern with increased respiratory rate but small tidal volumes signals respiratory-muscle pump failure and inadequate alveolar ventilation. 1
Airways and Parenchymal Disease
- Chronic obstructive pulmonary disease (COPD) is the most common cause of chronic respiratory acidosis, with stable severe COPD frequently exhibiting chronic compensated respiratory acidosis. 1, 3
- Acute COPD exacerbations produce acute-on-chronic respiratory acidosis because patients with already-elevated baseline bicarbonate cannot buffer additional CO₂ rises during decompensation. 1
- Significant ventilation/perfusion mismatching with increased physiological dead space leads to hypercapnia, largely resulting from a shift to rapid shallow breathing that increases the dead space/tidal volume ratio. 3
- Severe asthma exacerbations can cause acute respiratory failure with CO₂ retention when airway obstruction becomes critical. 2
- Pulmonary edema (cardiogenic or non-cardiogenic) impairs gas exchange at the alveolar level. 2
Increased Dead Space
- Pulmonary embolism or other conditions that increase physiological dead space reduce effective alveolar ventilation relative to total minute ventilation. 2
- Pleural disease (including large effusions, pneumothorax, or hemothorax) compresses lung tissue and reduces effective ventilation. 2
Increased CO₂ Production
- High glucose loads during peritoneal dialysis can produce excess CO₂ that overwhelms limited ventilatory capacity in patients with respiratory compromise, resulting in acute respiratory acidosis. 4
- Fever, sepsis, or increased metabolic demand raises CO₂ production beyond the capacity of impaired ventilatory systems. 2
Clinical Distinction: Acute vs. Chronic
- Acute respiratory acidosis shows pH < 7.35 with elevated PaCO₂ but only minimal bicarbonate elevation (typically < 28 mmol/L) because metabolic compensation is limited to immediate intracellular buffering. 1
- Chronic respiratory acidosis demonstrates sustained PaCO₂ elevation with renal compensation raising serum bicarbonate often > 28 mmol/L; pH may normalize after 3–5 days as the kidneys increase bicarbonate reabsorption and enhance hydrogen ion excretion. 1, 5
Common Clinical Pitfall
Administering high-concentration oxygen to COPD patients with chronic CO₂ retention can worsen ventilation/perfusion mismatching and induce hypoventilation, leading to severe acidosis. 3 Controlled oxygen therapy targeting SpO₂ 88–92% is essential in this population to maintain adequate oxygenation without suppressing hypoxic respiratory drive.