Background: Hyperventilation has been shown to be associated with cerebral vasoconstriction and increased risk of infarction. Our aim was to determine whether spontaneous reduction of end-tidal CO2 (EtCO2) was associated with an increased in brain tissue hypoxia (BTH).
Method: We studied twenty-one 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 mmHg.
Results: Diagnoses included subarachnoid hemorrhage (67%), intracranial hemorrhage (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 mmHg) to 33.9% in patients with EtCO2 < 25 mmHg (p<0.001). The mean tidal volume and minute ventilation of 7 ± 2 ml/kg and 9 ± 2 L/min, respectively. Hypocapnia was associated with higher measured-than-set respiratory rates and maximal minute ventilation values, suggestive of spontaneous hyperventilation. Using a generalized 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: 0.90-0.97; P<0.001) and CPP (OR: 0.98; 95%CI: 0.97-0.99; 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-recognized cause of brain tissue hypoxia after severe brain injury.