No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury

Michael N. Diringer, Kent Yundt, Tom O. Videen, Robert E. Adams, Allyson R. Zazulia, Ellen Deibert, Venkatesh Aiyagari, Ralph G. Dacey, Robert L. Grubb, William J. Powers

Research output: Contribution to journalArticle

91 Citations (Scopus)

Abstract

Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6 ± 1.8 and their mean age 27 ± 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59 ± 0.44 ml/100 g/minute [p < 0.01] and 0.31 ± 0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol% (p < 0.02); CMRO2 remained unchanged. Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

Original languageEnglish (US)
Pages (from-to)7-13
Number of pages7
JournalJournal of Neurosurgery
Volume92
Issue number1
StatePublished - Jan 2000

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Cerebrovascular Circulation
Hyperventilation
Oxygen
Intracranial Pressure
Arterial Pressure
Glasgow Coma Scale
Traumatic Brain Injury
Brain Ischemia
Healthy Volunteers
Neck

Keywords

  • Brain injury
  • Cerebral blood flow
  • Cerebral metabolism
  • Hyperventilation
  • Positron emission tomography

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Diringer, M. N., Yundt, K., Videen, T. O., Adams, R. E., Zazulia, A. R., Deibert, E., ... Powers, W. J. (2000). No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury. Journal of Neurosurgery, 92(1), 7-13.

No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury. / Diringer, Michael N.; Yundt, Kent; Videen, Tom O.; Adams, Robert E.; Zazulia, Allyson R.; Deibert, Ellen; Aiyagari, Venkatesh; Dacey, Ralph G.; Grubb, Robert L.; Powers, William J.

In: Journal of Neurosurgery, Vol. 92, No. 1, 01.2000, p. 7-13.

Research output: Contribution to journalArticle

Diringer, MN, Yundt, K, Videen, TO, Adams, RE, Zazulia, AR, Deibert, E, Aiyagari, V, Dacey, RG, Grubb, RL & Powers, WJ 2000, 'No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury', Journal of Neurosurgery, vol. 92, no. 1, pp. 7-13.
Diringer, Michael N. ; Yundt, Kent ; Videen, Tom O. ; Adams, Robert E. ; Zazulia, Allyson R. ; Deibert, Ellen ; Aiyagari, Venkatesh ; Dacey, Ralph G. ; Grubb, Robert L. ; Powers, William J. / No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury. In: Journal of Neurosurgery. 2000 ; Vol. 92, No. 1. pp. 7-13.
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abstract = "Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6 ± 1.8 and their mean age 27 ± 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59 ± 0.44 ml/100 g/minute [p < 0.01] and 0.31 ± 0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol{\%} (p < 0.02); CMRO2 remained unchanged. Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.",
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T1 - No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury

AU - Diringer, Michael N.

AU - Yundt, Kent

AU - Videen, Tom O.

AU - Adams, Robert E.

AU - Zazulia, Allyson R.

AU - Deibert, Ellen

AU - Aiyagari, Venkatesh

AU - Dacey, Ralph G.

AU - Grubb, Robert L.

AU - Powers, William J.

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N2 - Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6 ± 1.8 and their mean age 27 ± 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59 ± 0.44 ml/100 g/minute [p < 0.01] and 0.31 ± 0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol% (p < 0.02); CMRO2 remained unchanged. Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

AB - Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6 ± 1.8 and their mean age 27 ± 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59 ± 0.44 ml/100 g/minute [p < 0.01] and 0.31 ± 0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol% (p < 0.02); CMRO2 remained unchanged. Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

KW - Brain injury

KW - Cerebral blood flow

KW - Cerebral metabolism

KW - Hyperventilation

KW - Positron emission tomography

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