Effects of ethanol on respiratory function in traumatic brain injury

It has been observed that traumatic brain injury (TBI) increases the susceptibility of the brain to subsequent hypoxia, and prolonged apnea occurs in ethanol (EtOH)-treated animals following brain injury. This investigation tests the hypothesis that EtOH suppresses ventilation and hypercapnic respiratory drive following TBI. Immature pigs were anesthetized with halothane and received a 2 to 3 atm fluid-percussion brain injury. Respiratory parameters, including tidal volume, frequency, ventilation (VE), and arterial blood gases were measured on 100% O2 and on 5% to 6% inspired CO2 in O2 prior to and at 10, 60, 120, and 180 minutes after TBI. Hypercapnic response sensitivity (S) was measured as the change in VE per mm Hg increase in PaCO2. Intracranial pressure, mean arterial blood pressure, heart rate, brain temperature, glucose, and EtOH levels were also monitored. Three groups were studied: the first group of six received EtOH (3.5 gm/kg, intragastrically) without brain injury; the second group of six received TBI without EtOH; the third group of eight received EtOH and TBI. Ethanol levels were 121 +/- 13 (standard error of the mean) mg/dl in the EtOH/TBI group (136 +/- 25 in the EtOH group) at the time of injury, and 175 +/- 12 mg/dl in the EtOH/TBI group (200 +/- 20 mg/dl in the EtOH group) at 120 minutes after injury. The EtOH/TBI animals had significantly lower VE and S, and higher PaCO2 following brain injury (p < 0.05, repeated-measures analysis of variance). No significant differences were identified between groups for pH, PaCO2, intracranial pressure, heart rate, brain temperature, or glucose levels. Ethanol intoxication leads to significant impairment of respiratory control following traumatic brain injury and may contribute to brain injury in intoxicated trauma victims.