Therapeutic hypothermia after cardiac arrest - cerebral perfusion and metabolism during upper and lower threshold normocapnia.
During cardiac arrest and after successful resuscitation a continuum of ischaemia-reperfusion injury develops. Mild hypothermia exerts protective effects in the postresuscitation phase but also alters CO₂ production and solubility, which may lead to deleterious effects if overlooked when adjusting the ventilation of the resuscitated patient. Using a multimodality approach, the effects of different carbaemic states on cerebral perfusion and metabolism were evaluated during therapeutic hypothermia. Eight comatose survivors of prehospital cardiac arrest were cooled to 33°C for 24 h and underwent a 60 min phase of interventional lower threshold normocapnia according to temperature non-corrected pCO₂ (4.2 kPa) and higher threshold normocapnia according to corrected pCO₂ (6.0 kPa) in a random order. Prior to, during and after each phase, cerebral perfusion and metabolites via a microdialysis catheter were measured. During upper-threshold pCO₂, an increase in middle cerebral artery mean flow velocity (MFV) and jugular bulb oxygen saturation (jSvO₂) were observed with a concomitant decrease in cerebral lactate concentration. Lower threshold normocapnia was associated with a decrease in MFV in most patients. In all patients jSvO₂ decreased but no change in cerebral lactate was observed. In seven patients jSvO₂ decreased below 55%. These changes were not reflected to intracranial pressure or cerebral oximetry. During induced hypothermia, lower threshold normocapnia was associated with decreased cerebral perfusion/oxygenation but not reflected to interstitial metabolites. Upper threshold pCO₂ increased cerebral perfusion and reduced cerebral lactate. Vigilance over the ventilatory and CO₂ analysis regimen is mandatory during mild hypothermia.