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

Coles, Jonathan P.; Fryer, Tim D.; Coleman, Martin R.; Smielewski, Peter; Gupta, Arun Kumar; Minhas, Pawan Singh; Aigbirhio, Franklin I.; Chatfield, Doris A.; Williams, Guy B.; Boniface, Simon; Carpenter, T. Adrian; Clark, John C.; Pickard, John D.; Menon, David

doi:10.1097/01.ccm.0000254066.37187.88

Cited by 244 publications

(133 citation statements)

References 52 publications

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“…In one study of 30 infants and young children with severe TBI, CO 2 vasoreactivity changes < 2% were associated with poor outcome [76]. Since CO 2 vasoreactivity is not routinely examined in individual patients, hyperventilation to induce cerebral vasoconstriction and reduce CBF, ICP and cerebral blood volume may unintentionally lead to secondary ischemic damage after TBI [90,91]. Alternatively, hyperventilation may not be effective in TBI if CO 2 vasoreactivity is decreased.…”

Section: Altered Co 2 Vasoreactivitymentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

133

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Traumatic brain injury is a global health concern and is the leading cause of traumatic morbidity and mortality in children. Despite a lower overall mortality than in adult traumatic brain injury, the cost to society from the sequelae of pediatric traumatic brain injury is very high. Predictors of poor outcome after traumatic brain injury include altered systemic and cerebral physiology, including altered cerebral hemodynamics. Cerebral autoregulation is often impaired following traumatic brain injury and may adversely impact poor outcome. Although altered cerebrovascular hemodynamics early after traumatic brain injury may contribute to disability in children, there is a paucity of information regarding changes in cerebral blood flow and cerebral autoregulation after pediatric traumatic brain injury. In this article, we discuss normal pediatric cerebral physiology and cerebrovascular pathophysiology following pediatric traumatic brain injury.

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Section: Altered Co 2 Vasoreactivitymentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

133

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“…All have used surrogate endpoints such as jugular venous oxygen saturation or metabolic imaging of the brain. [10][11][12][13] There is reasonable consistency among these studies that hyperventilation can adversely alter the measured parameters and may increase the areas of potentially ischemic brain. Presumably, this is due to arterial constriction, not only resulting in a reduction of ICP but also producing ischemia at the same time.…”

Section: Hyperventilation For Neurocritical Carementioning

confidence: 86%

“…Toutes ces études ont eu recours à des critères de substitution tels que la saturation en oxygène de la veine jugulaire ou l'imagerie métabolique du cerveau. [10][11][12][13] Une certaine cohérence existe entre ces études, soutenant que l'hyperventilation peut modifier de façon nuisible les paramètres mesurés et pourrait augmenter les zones potentiellement ischémiques du cerveau. Il est possible que cela soit dû à une constriction artérielle, provoquant non seulement une réduction de la PIC mais aussi une ischémie dans le même temps.…”

Section: L'hyperventilation Dans Les Soins Intensifs Neurologiquesunclassified

L’hyperventilation: un vent néfaste qui souffle parfois favorablement

Gelb

Chan

2008

Can J Anesth/J Can Anesth

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H yperventilation has been an integral part of the management of neurosurgical patients for the past 50 years. It has been so emblematic that a blindfolded individual could easily identify a neurosurgical operating room by the sound of the hard working ventilator. However, the routine use of hyperventilation has been re-evaluated with the emergence of evidence that it could be harmful.The first description of the benefits of hyperventilation in neuroanesthesia was published in 1957. 1 In the report, Furness reviewed the outcomes of 72 patients receiving "adequate ventilation" with a fixed ventilatory frequency of 20 breaths·min -1 during craniotomy. Although there was no formal assessment of the operating conditions and no measurement of arterial carbon dioxide tension (PaCO 2 ), "gradually the neurosurgeons were completely convinced" that hyperventilation produced better conditions compared with their previous experience using spontaneous ventilation. The report neglected to distinguish among the roles of hypocapnia, mechanical ventilation vs spontaneous breathing, and the contribution of muscle relaxation. 2,3 These latter were the subject of much debate and some research over the next decade. Neurophysiology of hyperventilationHyperventilation increases cerebral perivascular pH, resulting in cerebral arterial vasoconstriction and the decrease in cerebral blood flow (CBF) and cerebral blood volume (CBV). The CBV response to hyperventilation is blunted when compared to that of CBF. In general, for every mmHg decrease in PaCO 2 , there is a 1% decrease in CBV and a 2-3% decrease in CBF. 4 It is the reduction in CBV associated with hyperventilation that explains the decrease in intracranial pressure (ICP). 4,5 This response gradually normalizes over 12-24 hr. If hyperventilation is extended beyond this period, a restoration to normal PaCO 2 values may result in hyperemia and elevated ICP. Hyperventilation for neurocritical careGiven its favourable effect on ICP in experimental circumstances, aggressive hyperventilation was seen as a cheap, easy, and reversible treatment for patients with intracranial hypertension. Other perceived benefits included a redistribution of CBF to ischemic regions of the brain and the reversal of acidosis in the brain and cerebrospinal fluid (CSF). 4 Despite these claims, good outcome studies demonstrating a clear benefit of hyperventilation in the operating room or the neurocritical care unit were lacking. Indeed, studies using ICP as a surrogate endpoint often reported variable responses after hyperventilation in critically ill patients. 6,7 We believe this may be attributed to the heterogeneity of the human diseases as opposed to the controlled environment in the laboratory.The enthusiasm for hyperventilation therapy came to a sudden halt when almost 17 years ago Muizelaar et al. 8 reported the deleterious effect of prolonged hyperventilation in brain injured patients. A total of 113 patients with severe head injury were randomized to receive hyperventilation (PaCO 2 , 24-28 mmHg), h...

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“…The injuries are limited locally along the nail track [9]. But hyperventilation may cause cerebral hypoperfusion, further causing ischaemia [11]. Adequate perioperative hydration along with the use of vasopressors to maintain a CPP of 60mm Hg maintains CBF and tissue oxygenation.…”

Section: Discussionmentioning

confidence: 99%