Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study

Lee, J H; Kelly, Daniel F.; Oertel, Matthias F.; McArthur, David L.; Glenn, Thomas C.; Vespa, Paul; Boscardin, W. John; Martin, Neil A.

doi:10.3171/jns.2001.95.2.0222

Cited by 105 publications

(79 citation statements)

References 63 publications

(77 reference statements)

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“…Generally, for determination of CO 2 -reactivity methods similar to ours are used [24,25,26], and reactivities are calculated 10 min or 15 min after changing the ventilator settings. Such a time-point may not represent the maximal response in many patients, but rather an arbitrary value that may depend on the rate and extent of induction of hypocapnia.…”

Section: Discussionmentioning

confidence: 99%

Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

et al. 2004

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Objective: In healthy volunteers cerebral blood flow starts to recover towards baseline within a few minutes of continued hyperventilation due to normalisation of perivascular pH. We investigated the timecourse of changes in middle cerebral artery mean flow velocity (FVm) and intracranial pressure (ICP) in head-injured patients during sustained moderate reductions in arterial partial pressure of CO 2 (PaCO 2 ). Design: Observational study. Patients: Twenty-seven sedated, mechanically ventilated patients with severe head injury. Interventions: Measurements were made during and after routine determination of CO 2 -reactivity: an acute 20% increase in respiratory minute volume was followed by a 10-min stabilisation period and 50 min of continued moderate hyperventilation at a constant PaCO 2 (>3.5 kPa). Measurements and results: FVm was monitored with transcranial Doppler, ICP was monitored with intraparenchymal probes. During the 50-min period with stable PaCO 2 FVm increased in 36% of patients. All other patients showed a decline in FVm over the same time period. Overall FVm recovery was 0.03€0.14%·min -1 . The time-course of ICP changes was significantly different from that of FVm, with ICP reaching its lowest value earlier than FVm (23€12 vs 37€20 min; P = 0.001) and returning more rapidly towards baseline than FVm (0.23€0.23 vs 0.

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Section: Discussionmentioning

confidence: 99%

Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

et al. 2004

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“…Pressure autoregulation is impaired in most patients after TBI (Lee et al, 2001), and this impairment can persist for up to 2 weeks post-injury (Sviri et al, 2009). In a study with serial measurements of dynamic autoregulation in 122 TBI patients, the lowest ARI value was seen at 48 h post-injury, when 87% of the patients had a value less than the lower limit of normal (Hlatky et al, 2002).…”

Section: Effects Of Hyperventilation and Hyperoxia On Cerebral Pressumentioning

confidence: 99%

Cerebral Hemodynamic Effects of Acute Hyperoxia and Hyperventilation after Severe Traumatic Brain Injury

Rangel-Castilla

Rivera‐Lara

Gopinath

et al. 2010

Journal of Neurotrauma

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The purpose of this study was to examine the effects of hyperventilation or hyperoxia on cerebral hemodynamic parameters over time in patients with severe traumatic brain injury (TBI). We prospectively studied 186 patients with severe TBI. CO 2 and O 2 reactivity tests were conducted twice a day on days 1-5 and once daily on days 6-10 after injury. During hyperventilation there was a significant decrease in intracranial pressure (ICP), mean arterial pressure (MAP), jugular venous oxygen saturation (Sjvo 2 ), brain tissue Po 2 (Pbto 2 ), and flow velocity (FV). During hyperoxia there was an increase in Sjvo 2 and Pbto 2 , and a small but consistent decrease in ICP, end-tidal carbon dioxide (etco 2 ), partial arterial carbon dioxide pressure (Paco 2 ), and FV. Brain tissue oxygen reactivity during the first 12 h after injury averaged 19.7 AE 3.0%, and slowly decreased over the next 7 days. The autoregulatory index (ARI; normal ¼ 5.3 AE 1.3) averaged 2.2 AE 1.5 on day 1 post-injury, and gradually improved over the 10 days of monitoring. The ARI significantly improved during hyperoxia, by an average of 0.4 AE 1.8 on the left, and by 0.5 AE 1.8 on the right. However, the change in ARI with hyperoxia was much smaller than that observed with hyperventilation. Hyperventilation increased ARI by an average of 1.3 AE 1.9 on the left, and 1.5 AE 2.0 on the right. Pressure autoregulation, as assessed by dynamic testing, was impaired in these head-injured patients. Acute hyperoxia significantly improved pressure autoregulation, although the effect was smaller than that induced by hyperventilation. The very small change in Paco 2 induced by hyperoxia does not appear to explain this finding. Rather, the vasoconstriction induced by acute hyperoxia may allow the cerebral vessels to respond better to transient hypotension. Further studies are needed to define the clinical significance of these observations.

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“…Clinically, continuous methods of autoregulation tests or monitoring rely on the observation of spontaneous responses of CBF to spontaneous fluctuations in MAP or CPP (Zweifel et al, 2008), arterial partial pressure of CO 2 (Puppo et al, 2008) or metabolites (Lee et al, 2001). Study by Lee in 2001 showed that during the first 2 weeks after head injury, CO 2 reactivity remains relatively intact, pressure autoregulation is variably impaired and metabolic suppression reactivity remains severely impaired and they further noted that unlike hypotension, hypoxia or haemorrhagic brain lesions, elevated ICP appears to affect all components of vasoreactivity that were tested (Lee et al, 2001). In similar year, Czosnyka also noted that autoregulation is not only impaired when associated with a high ICP or low arterial blood pressure, but it can also be disturbed by an excessive CPP (Czosnyka et al, 2001).…”

Section: Two Major Parameters To Consider During Multimodality Monitomentioning

confidence: 99%

Neurointensive Care Monitoring for Severe Traumatic Brain Injury

Idris¹,

Mustapha²,

Abdullah³

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study

Cited by 105 publications

References 63 publications

Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

Cerebral Hemodynamic Effects of Acute Hyperoxia and Hyperventilation after Severe Traumatic Brain Injury

Neurointensive Care Monitoring for Severe Traumatic Brain Injury

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