作者: Jonathan P Coles , Pawan S Minhas , Tim D Fryer , Peter Smielewski , Franklin Aigbirihio
DOI: 10.1097/00003246-200209000-00002
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摘要: Objective: To investigate the effect of hyperventilation on cerebral blood flow in traumatic brain injury. Design: A prospective interventional study. Setting: specialist neurocritical care unit. Patients: Fourteen healthy volunteers and 33 patients within 7 days closed head injury. Interventions: All subjects underwent positron emission tomography imaging flow. In patients, PaCO2 was reduced from 36 +/- 1 to 29 torr (4.8 0.1 3.9 kPa) measurements repeated. Jugular venous saturation (SjvO2 ) arteriovenous oxygen content differences (AVDO2 were monitored 25 values related variables. Measurements main results: The volumes critically hypoperfused hyperperfused (HypoBV HyperBV, milliliters) calculated based thresholds 10 55 mL.100g(-1).min(-1), respectively. Whereas baseline HypoBV significantly higher ( p 50%) AVDO2 (<9 mL/mL) did not exceed global ischemic thresholds. However, despite these beneficial effects, shifted distribution curve toward range, with a decrease (31 23 mL.100g(-1).min(-1); p<.0001) an increase (22 [1-141] 51 [2-428] mL; p<.0001). Hyperventilation-induced increases apparently nonlinear, threshold value between 34 38 (4.5-5 kPa). Conclusions: Hyperventilation volume severely tissue injured brain, improvements perfusion pressure intracranial pressure. Significant hyperperfusion is uncommon, even at time when conventional clinical management includes role for modest hyperventilation. These reductions regional are associated ischemia, as defined by monitors oxygenation, but may represent regions potentially tissue.