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Raised arterial pCO₂ after trauma signals alveolar hypoventilation, which occurs when either the neural drive to breathe is depressed (respiratory centre injury) or when the chest wall/diaphragm cannot generate adequate ventilation (respiratory apparatus injury). Both mechanisms are well-recognized causes of hypercapnic (type II) respiratory failure after head, cervical cord, or thoracic trauma, whereas isolated lung contusion more often produces hypoxaemia with near-normal CO₂ levels because CO₂ diffuses much more readily than O₂ [Roussos & Koutsoukou, 2003, PMID 14621112; Slack & Shucart, 1994, PMID 7867288]. Hence injury to either or both sites best explains the elevated PaCO₂.