Hyperventilation following head injury: Effect on ischemic burden and cerebral oxidative metabolism*

@article{Coles2007HyperventilationFH,
  title={Hyperventilation following head injury: Effect on ischemic burden and cerebral oxidative metabolism*},
  author={Jonathan P. Coles and Tim D. Fryer and Martin R. Coleman and Peter Smielewski and Arun Kumar Gupta and Pawan Singh Minhas and Franklin I. Aigbirhio and D. A. Chatfield and Guy B. Williams and S. J. Boniface and T Adrian Carpenter and John C. Clark and John D. Pickard and David K. Menon},
  journal={Critical Care Medicine},
  year={2007},
  volume={35},
  pages={568-578}
}
Objective:To determine whether hyperventilation exacerbates cerebral ischemia and compromises oxygen metabolism (CMRO2) following closed head injury. Design:A prospective interventional study. Setting:A specialist neurocritical care unit. Patients:Ten healthy volunteers and 30 patients within 10 days of closed head injury. Interventions:Subjects underwent oxygen-15 positron emission tomography imaging of cerebral blood flow, cerebral blood volume, CMRO2, and oxygen extraction fraction. In… 
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Early Derangements in Oxygen and Glucose Metabolism Following Head Injury: The Ischemic Penumbra and Pathophysiological Heterogeneity
TLDR
The low CBF and maintained CMRO2 in the high OEF ROIs is consistent with classical cerebral ischemia and the presence of an ‘ischemic penumbra’ following early head injury, while the metabolic heterogeneity that was observed suggests significant pathophysiological complexity.
Cerebral metabolism is not affected by moderate hyperventilation in patients with traumatic brain injury
TLDR
Moderate short-term hyperventilation has a potent effect on the cerebral blood flow, as shown by TCCD, with a concomitant ICP reduction.
Mild hyperventilation in traumatic brain injury - relation to cerebral energy metabolism, pressure autoregulation and clinical outcome.
Moderate hypocapnia for intracranial pressure control after traumatic brain injury: a common practice requiring further investigations
TLDR
A large, prospective, observational cohort, the Center-TBI initiative, and a very interesting window of the current practices regarding PaCO2 management in the first week after severe TBI in Europe is offered.
Acute hypoxia increases the cerebral metabolic rate – a magnetic resonance imaging study
  • M. Vestergaard, U. Lindberg, +6 authors H. Larsson
  • Medicine, Biology
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2016
TLDR
It is concluded that marked changes in brain homeostasis occur in the healthy human brain during exposure to acute hypoxia, which could represent an increase in neuronal activity.
Pathophysiologic Mechanisms of Cerebral Ischemia and Diffusion Hypoxia in Traumatic Brain Injury.
TLDR
Tissue hypoxia after TBI is not confined to regions with structural abnormality and can occur in the absence of conventional macrovascular ischemia and is a target for novel neuroprotective strategies.
Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury
TLDR
Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen, cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury.
Spontaneous hyperventilation and brain tissue hypoxia in patients with severe brain injury
TLDR
The risk of brain tissue hypoxia in critically brain-injured patients increases when EtCO2 values are reduced, and unintentional spontaneous hyperventilation may be a common and under-recognised cause ofbrain tissue hyp oxia after severe brain injury.
Hyperventilation in neurological patients: from physiology to outcome evidence
TLDR
Although hyperventilation is commonly applied in patients with TBI or intracranial hemorrhage or in those undergoing craniotomy, its effects on patient outcomes have not been proven by quality research.
The use of hyperventilation therapy after traumatic brain injury in Europe: an analysis of the BrainIT database
TLDR
While overall adherence to current BTF-G seems to be the rule, its recommendations on early prophylactichyperventilation as well as the use of additional cerebral oxygenation monitoring during forced hyperventilation are not followed in this sample of European TBI centers.
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References

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TLDR
Hyperventilation increases the volume of severely hypoperfused tissue within the injured brain, despite improvements in cerebral perfusion pressure and intracranial pressure.
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TLDR
The clear relationship between the frequency of cerebral ischemia and hypocarbia, combined with the rarity of hyperemia, suggests that hyperventilation should be used with caution and monitored carefully in children with severe head injuries.
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TLDR
This study sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/ min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2).
Incidence and Mechanisms of Cerebral Ischemia in Early Clinical Head Injury
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  • Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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TLDR
The results suggest significant ischemia within the first day after head injury and the ischemic burden represented by this “traumatic penumbra” is poorly detected by bedside clinical monitors and has significant associations with outcome.
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TLDR
This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma.
No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury.
TLDR
It is concluded 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.
Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension.
TLDR
Hyperemia was found at all age levels (15 to 85 years), and there was a highly significant association between hyperemia and the occurrence of intracranial hypertension, defined as an intrusion above 20 mm Hg.
Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia.
TLDR
The results support the hypothesis that early ischemia after traumatic brain injury may be an important factor determining neurological outcome, and suggest that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.
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TLDR
It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4-5 and that the course of ICP was most stable in the HV + THAM group, although mean ICP could be kept well below 25 mm Hg in all three groups.
Hyperventilation-induced cerebral ischemia in patients with acute brain lesions: demonstration by xenon-enhanced CT.
TLDR
These findings document hyperventilation-induced ischemia in acute brain lesions, and demonstrate that this phenomenon affects both injured and apparently intact areas of the brain.
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