Spontaneous hyperventilation and brain tissue hypoxia in patients with severe brain injury.

Abstract

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 CO(2) (EtCO(2)) was associated with an increased in brain tissue hypoxia (BTH). We studied 21 consecutive patients (mean age 50+/-16 years; 15 women) undergoing continuous monitoring for brain tissue oxygenation (PbtO(2)), intracranial pressure (ICP), cerebral perfusion pressure (CPP) and EtCO(2); mean values were recorded hourly BTH was defined as brain tissue oxygen tension (PbtO(2)) <15 mm Hg. 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 EtCO(2) (35-44 mm Hg) to 33.9% in patients with EtCO(2)<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 EtCO(2) (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). The risk of brain tissue hypoxia in critically brain-injured patients increases when EtCO(2) values are reduced. Unintentional spontaneous hyperventilation may be a common and under-recognised cause of brain tissue hypoxia after severe brain injury.