Menzel M, Doppenberg EM, Zauner A, Soukup J, Reinert MM, Clausen T, Brockenbrough PB, Bullock RCerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure. J Neurosurg Anesthesiol 11:240-251

Department of Anesthesiology and Critical Care, Martin-Luther-University, Halle-Wittenberg, Germany.
Journal of Neurosurgical Anesthesiology (Impact Factor: 2.99). 11/1999; 11(4):240-51. DOI: 10.1097/00008506-199910000-00003
Source: PubMed


Early impaired cerebral blood flow (CBF) after severe head injury (SHI) leads to poor brain tissue oxygen delivery and lactate accumulation. The purpose of this investigation was to elucidate the relationship between CBF, local dialysate lactate (lact(md)) and dialysate glucose (gluc(md)), and brain tissue oxygen levels (PtiO2) under arterial normoxia. The effect of increased brain tissue oxygenation due to high fractions of inspired oxygen (FiO2) on lact(md) and CBF was explored. A total of 47 patients with SHI were enrolled in this studies (Glasgow Coma Score [GCS] < 8). CBF was first assessed in 40 patients at one time point in the first 96 hours (27 +/- 28 hours) after SHI using stable xenon computed tomography (Xe-CT) (30% inspired xenon [FiXe] and 35% FiO2). In a second study, sequential double CBF measurements were performed in 7 patients with 35% FiO2 and 60% FiO2, respectively, with an interval of 30 minutes. In a subsequent study, 14 patients underwent normobaric hyperoxia by increasing FiO2 from 35 +/- 5% to 60% and then 100% over a period of 6 hours. This was done to test the effect of normobaric hyperoxia on lact(md) and brain gluc(md), as measured by local microdialysis. Changes in PtiO2 in response to changes in FiO2 were analyzed by calculating the oxygen reactivity. Oxygen reactivity was then related to the 3-month outcome data. The levels of lact(md) and gluc(md) under hyperoxia were compared with the baseline levels, measured at 35% FiO2. Under normoxic conditions, there was a significant correlation between CBF and PtiO2 (R = 0.7; P < .001). In the sequential double CBF study, however, FiO2 was inversely correlated with CBF (P < .05). In the 14 patients undergoing the 6-hour 100% FiO2 challenge, the mean PtiO2 levels increased to 353 (87% compared with baseline), although the mean lact(md) levels decreased by 38 +/- 16% (P < .05). The PtiO2 response to 100% FiO2 (oxygen reactivity) was inversely correlated with outcome (P < .01). Monitoring PtiO2 after SHI provides valuable information about cerebral oxygenation and substrate delivery. Increasing arterial oxygen tension (PaO2) effectively increased PtiO2, and brain lact(md) was reduced by the same maneuver.

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    • "Thus, as NDs did not present any significant HR variation during SA, this might explain the lack of a significant increase in their CBF. Hypoxia (Fortune et al. 1995, Menzel et al. 1999) and hypercapnia (Ito et al. 2003) are known to increase CBF. As apnoea induces hypoxia and hypercapnia, the main determinant of the CBF increase remains unclear. "

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    • "Expressing the Pbto 2 response as a percentage of the Pao 2 changes observed may help compensate for this problem, but this approach assumes that the Pbto 2 response to changing Pao 2 is linear throughout the range of Pao 2 studied. A study carried out by Menzel and associates (Menzel et al., 1999) suggested that this is the case. Except for the first o 2 r test, the Pao 2 response to 100% oxygen was relatively constant over time for the entire group of patients, suggesting that although the phenomenon may be important in interpreting individual patient responses, this is not the main factor causing Btor to decrease over time for the group. "
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    ABSTRACT: 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. CO₂ and O₂ 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 (Sjvo₂), brain tissue Po₂ (Pbto₂), and flow velocity (FV). During hyperoxia there was an increase in Sjvo₂ and Pbto₂, and a small but consistent decrease in ICP, end-tidal carbon dioxide (etco₂), partial arterial carbon dioxide pressure (Paco₂), and FV. Brain tissue oxygen reactivity during the first 12 h after injury averaged 19.7 ± 3.0%, and slowly decreased over the next 7 days. The autoregulatory index (ARI; normal = 5.3 ± 1.3) averaged 2.2 ± 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 ± 1.8 on the left, and by 0.5 ± 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 ± 1.9 on the left, and 1.5 ± 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 Paco₂ 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.
    Journal of neurotrauma 10/2010; 27(10):1853-63. DOI:10.1089/neu.2010.1339 · 3.71 Impact Factor
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    • "Thus, as NDs did not present any significant HR variation during SA, this might explain the lack of a significant increase in their CBF. Hypoxia (Fortune et al. 1995, Menzel et al. 1999) and hypercapnia (Ito et al. 2003) are known to increase CBF. As apnoea induces hypoxia and hypercapnia, the main determinant of the CBF increase remains unclear. "
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    ABSTRACT: Voluntary apnoea induces several physiological adaptations, including bradycardia, arterial hypertension and redistribution of regional blood flows. Elite breath-hold divers (BHDs) are able to maintain very long apnoea, inducing severe hypoxaemia without brain injury or black-out. It has thus been hypothesized that they develop protection mechanisms against hypoxia, as well as a decrease in overall oxygen uptake. To test this hypothesis, the apnoea response was studied in BHDs and non-divers (NDs) during static and dynamic apnoeas (SA, DA). Heart rate, arterial oxygen saturation (SaO(2)), and popliteal artery blood flow were recorded to investigate the oxygen-conserving effect of apnoea response, and the internal carotid artery blood flow was used to examine the mechanisms of cerebral protection. The bradycardia and peripheral vasoconstriction were accentuated in BHDs compared with NDs (P < 0.01), in association with a smaller SaO(2) decrease (-2.7% vs. -4.9% during SA, P < 0.01 and -6% vs. -11.3% during DA, P < 0.01). Greater increase in carotid artery blood flow was also measured during apnoea in BHDs than in controls. These results confirm that elite divers present a potentiation of the well-known apnoea response in both SA and DA conditions. This response is associated with higher brain perfusion which may partly explain the high levels of world apnoea records.
    Acta Physiologica 03/2009; 197(1):75-82. DOI:10.1111/j.1748-1716.2009.01982.x · 4.38 Impact Factor
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