Background Hyperventilation has been shown to be associated with cerebral vasoconstriction and increased risk of infarction. Our aim was to determine whether spontaneous reduction in end-tidal CO₂ (EtCO₂) was associated with an increased in brain tissue hypoxia (BTH).

Method We studied 21 consecutive patients (mean age 50±16 years; 15 women) undergoing continuous monitoring for brain tissue oxygenation (PbtO₂), intracranial pressure (ICP), cerebral perfusion pressure (CPP) and EtCO₂; mean values were recorded hourly BTH was defined as brain tissue oxygen tension (PbtO₂) <15 mm Hg.

Results Diagnoses included subarachnoid haemorrhage (67%), intracranial haemorrhage (24%) and traumatic brain injury (10%). Overall, BTH occurred during 22.5% of the study period (490/2179 hourly data). The frequency of BTH increased progressively from 15.7% in patients with normal EtCO₂ (35–44 mm Hg) to 33.9% in patients with EtCO₂<25 mm Hg (p<0.001). The mean tidal volume and minute ventilation were 7±2 ml/kg and 9±2 1/min, respectively. Hypocapnia was associated with higher measured-than-set respiratory rates and maximal minute ventilation values, suggestive of spontaneous hyperventilation. Using a generalised estimated equation (GEE) and after adjustment for GCS, ICP and core temperature, the variables independently associated with BTH events were EtCO₂ (OR: 0.94; 95% CI 0.90 to 0.97; p<0.001) and CPP (OR: 0.98; 95% CI 0.97 to 0.99; p=0.004).

Conclusion The risk of brain tissue hypoxia in critically brain-injured patients increases when EtCO₂ values are reduced. Unintentional spontaneous hyperventilation may be a common and under-recognised cause of brain tissue hypoxia after severe brain injury.