The Cerebrovascular CO<sub>2</sub> Reactivity during the Acute Phase of Brain Injury

Ge, Cold; Ft, Jensen; Malmros, R

doi:10.1111/j.1399-6576.1977.tb01213.x

Cited by 36 publications

(17 citation statements)

References 26 publications

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“…Testing versus monitoring Testing of cerebral autoregulation requires the observer to apply a hemodynamic stimulus, such as a pharmacologic increase in arterial pressure [3], increase in arterial partial pressure of CO 2 (PaCO 2 [4]), thigh cuff release [5], application of negative body pressure [6], tilt table declination [7], carotid artery compression [8], etc. In all these methods the observer controls the exact time and grade of stimulation, and synchronously measures a change in CBF to quantify the reactive autoregulatory forces.…”

Section: Factsmentioning

confidence: 99%

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

et al. 2009

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Poor autoregulation and loss of pressure-reactivity are independent predictors of fatal outcome following head injury. Autoregulation is impaired by too low or too high CPP when compared to autoregulation with normal CPP (usually between 60 and 85 mmHg; and these limits are highly individual). Hemispheric asymmetry of the bi-laterally assessed autoregulation has been associated with asymmetry of CT scan findings: autoregulation was found to be worse ipsilateral to contusion or lateralized edema causing midline shift. The pressure-reactivity (PRx index) correlated with a state of low CBF and CMRO2 revealed using PET studies. The PRx is easier to monitor over prolonged periods of time than the TCD-based indices as it does not require fixation of external probes. Continuous monitoring with the PRx can be used to direct CPP-oriented therapy by determining the optimal CPP for pressure-reactivity. Autoregulation indices are able to reflect transient changes of autoregulation, as seen during plateau waves of ICP. However, minute-to-minute assessment of autoregulation has a poor signal-to-noise ratio. Averaging across time (30 min) or by combining with other relevant parameters improves the accuracy. MYTHS: It is debatable whether the TCD-based indices in head injured patients can be calculated using ABP instead of CPP. Thresholds for functional and disturbed autoregulation dramatically depends on arterial tension of CO2--therefore, comparison between patients cannot be performed without comparing their PaCO2. The TCD pulsatility index cannot accurately detect the lower limit of autoregulation. MISSING LINKS: We still do not know whether autoregulation-oriented therapy can be understood as a consensus between CPP-directed protocols and the Lund-concept. What are the links between endothelial function and autoregulation indices? Can autoregulation after head injury be improved with statins or EPO, as in subarachnoid hemorrhage? In conclusion, monitoring cerebral autoregulation can be used in a variety of clinical scenarios and may be helpful in delineating optimal therapeutic strategies.

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Section: Factsmentioning

confidence: 99%

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

et al. 2009

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“…As the cerebrovascular response to hypercapnia helps maintain adequate cerebral blood flow (CBF; Brian, 1998), and as impaired CO 2 reactivity is a common finding in clinical TBI (Cold et al, 1977;Enevoldsen and Jensen, 1978), we tested the cerebrovascular response to hypercapnia. Arterial hypercapnia was induced by ventilating the animal with a gas mixture containing 3% and 5% CO 2 in air.…”

Section: Hypercapniamentioning

confidence: 99%

The Long-Term Microvascular and Behavioral Consequences of Experimental Traumatic Brain Injury after Hypothermic Intervention

Wei

Hamm

Baranova

et al. 2009

Journal of Neurotrauma

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Traumatic brain injury (TBI) has been demonstrated to induce cerebral vascular dysfunction that is reflected in altered responses to various vasodilators. While previous reports have focused primarily on the short-term vascular alterations, few have examined these vascular changes for more than 7 days, or have attempted to correlate these alterations with any persisting behavioral changes or potential therapeutic modulation. Accordingly, we evaluated the long-term microvascular and behavioral consequences of experimental TBI and their therapeutic modulation via hypothermia. In this study, one group was injured with no treatment, another group was injured and 1 h later was treated with 120 min of hypothermia followed by slow rewarming, and a third group was non-injured. Animals equipped with cranial windows for visualization of the pial microvasculature were challenged with various vasodilators, including acetylcholine, hypercapnia, adenosine, pinacidil, and sodium nitroprusside, at either 1 or 3 weeks post-TBI. In addition, all animals were tested for vestibulomotor tasks at 1 week post-TBI, and animals surviving for 3 weeks post-TBI were tested in a Morris water maze (MWM). The results of this investigation demonstrated that TBI resulted in long-term vascular dysfunction in terms of altered vascular reactivity to various vasodilators, which was significantly improved with the use of a delayed 120-min hypothermic treatment. In contrast, data from the MWM task indicated that injured animals revealed persistent deficits in the spatial memory test performance, with hypothermia exerting no protective effects. Collectively, these data illustrate that TBI can evoke long-standing brain vascular and spatial memory dysfunction that manifest different responses to hypothermic intervention. These findings further illustrate the complexity of TBI and highlight the fact that the chosen hypothermic intervention may not necessarily exert a global protective response.

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“…During the early period after TBI, CO 2 vasoreactivity can be transiently impaired, but generally recovers after 4 to 7 days [87,88]. Impaired CO 2 vasoreactivity following TBI may be associated with cerebral hyperemia, cerebral ischemia, or intracranial hypertension [89].…”

Section: Altered Co 2 Vasoreactivitymentioning

confidence: 99%

“…Impaired CO 2 vasoreactivity following TBI may be associated with cerebral hyperemia, cerebral ischemia, or intracranial hypertension [89]. Studies of CO 2 vasoreactivity in adult TBI patients show that CBF changes about 3% for every 1 mmHg change in PaCO 2 but that CO 2 vasoreactivity is less in patients with lower baseline CBF [87]. In one study of 30 infants and young children with severe TBI, CO 2 vasoreactivity changes < 2% were associated with poor outcome [76].…”

Section: Altered Co 2 Vasoreactivitymentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

132

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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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The Cerebrovascular CO₂ Reactivity during the Acute Phase of Brain Injury

Cited by 36 publications

References 26 publications

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

The Long-Term Microvascular and Behavioral Consequences of Experimental Traumatic Brain Injury after Hypothermic Intervention

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

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The Cerebrovascular CO2 Reactivity during the Acute Phase of Brain Injury

Cited by 36 publications

References 26 publications

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

The Long-Term Microvascular and Behavioral Consequences of Experimental Traumatic Brain Injury after Hypothermic Intervention

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

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Product

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The Cerebrovascular CO₂ Reactivity during the Acute Phase of Brain Injury