Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?
Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). CO2-reactivity and CBF was estimated using AVDO2 (arteriojugular differences of oxygen content). Global cerebral ischemia and increased anaerobic metabolism were considered according to AVDO2 and AVDL respectively. Thirty-three patients with severe and moderate head injury and increased ICP were included. Within 72 hours after accident, patients were hyperventilated for a period of 4 hours. During this time jugular oxygen saturation (SjO2), arterial oxygen saturation (SaO2), ICP, mean arterial blood pressure (MABP), AVDO2 and AVDL were recorded. In our study, most patients preserved CO2-reactivity (88.2%). In these cases HV was very effective in lowering ICP. Our findings showed that this reduction was due to a CBF decrease. According to basal AVDO2 twenty-five patients (75.7%) were considered as hyperemic and eight (24.2%) as not hyperemic. Global ischemia and increased anaerobic metabolism were detected in one case in the non-hyperemic group. According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.
Ausina
A
A
Department of Intensive Care Unit, Vall d'Hebron University Hospitals, Barcelona, Spain.
Báguena
M
M
Nadal
M
M
Manrique
S
S
Ferrer
A
A
Sahuquillo
J
J
Garnacho
A
A
D000293:Adolescent; D000328:Adult; D001921:Brain / Q000098:blood supply*; D001930:Brain Injuries / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000502:physiology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D010102:Oxygen Inhalation Therapy; D011446:Prospective Studies; D014655:Vascular Resistance / Q000502:physiology
D002245:Carbon Dioxide; D019344:Lactic Acid