Respiratory Acidosis

Respiratory acidosis occurs when alveolar ventilation is inadequate to eliminate CO₂, causing PaCO₂ to rise above 45 mmHg and pH to fall below 7.35. The core problem is always hypoventilation — anything that depresses the respiratory drive, obstructs airways, or impairs gas exchange at the alveolar level. Acute causes include opioid overdose, anesthesia recovery, pneumothorax, and severe asthma exacerbation. Chronic causes include COPD, obesity hypoventilation syndrome, and neuromuscular diseases like myasthenia gravis or ALS. In acute respiratory acidosis, pH drops sharply because the kidneys haven't had time to compensate; expect HCO₃⁻ to rise only ~1 mEq/L per 10 mmHg rise in PaCO₂ (e.g., pH 7.28, PaCO₂ 58, HCO₃⁻ 26). In chronic respiratory acidosis, renal compensation begins within hours but reaches full effect over 3–5 days, with HCO₃⁻ rising ~3.5 mEq/L per 10 mmHg PaCO₂ increase, bringing pH near-normal despite persistently elevated PaCO₂ (e.g., pH 7.35, PaCO₂ 58, HCO₃⁻ 32). Nursing assessment priorities include monitoring respiratory rate, depth, and pattern; oxygen saturation; and level of consciousness. Rising CO₂ causes CO₂ narcosis — progressive somnolence, confusion, and eventually coma. For the client with COPD, high-flow oxygen can worsen CO₂ retention through suppression of hypoxic ventilatory drive and V/Q mismatch changes; titrate to SpO₂ 88–92% using low-flow oxygen. Interventions focus on restoring ventilation: repositioning, incentive spirometry, bronchodilators, suctioning, naloxone for opioid-induced hypoventilation, or mechanical ventilation when conservative measures fail.