Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury (original) (raw)
Related papers
Reactivity of Brain Tissue Oxygen to Change in Cerebral Perfusion Pressure in Head Injured Patients
Neurocritical Care, 2009
Objective It has been reported recently that correlation between brain tissue oxygen (PbtO 2 ) and cerebral perfusion pressure (CPP) may serve as an indicator of cerebral autoregulation after subarachnoid hemorrhage. We aimed to compare similar indices describing interaction between changes in intracranial pressure (ICP), arterial blood pressure (ABP), and brain tissue oxygen to verify their clinical utility in patients after traumatic brain injury. Materials and Methods Retrospective analysis of multimodal monitoring of 32 patients suffering from head injury, admitted in the Neurosciences Critical Care Unit, Addenbrooke's Hospital, Cambridge, UK. Initial 24 h intervals of continuous ABP, ICP, and PbtO 2 recordings were analyzed. Index of tissue oxygen reactivity ORx was evaluated as the correlation coefficient between PbtO 2 and CPP over a period of 60 min and compared to the index of pressure reactivity PRx. ''Optimal CPP'' and a hypothetical ''optimal PbtO 2 '' were defined as the ranges of CPP and PbtO 2 at which PRx or ORx were indicating best cerebrovascular milieu.
Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain injury*
Critical Care Medicine, 2003
To study the relationship between arterial blood pressure, intracranial pressure, directly measured brain tissue oxygenation (PtIO 2), and middle cerebral artery blood flow velocity in severely head-injured patients. Design: Prospective study. Setting: Neurosurgical intensive care unit. Patients: A total of 14 patients with severe head injury. Interventions: Pharmacologic blood pressure manipulations using norepinephrine. Measurements and Main Results: We assessed the magnitude of PtIO 2 related to changes in cerebral perfusion pressure in 12 of the patients. We calculated in all the static rate of regulation, which is an index to describe the change of cerebrovascular resistance, using cerebral artery blood flow velocity in relation to changing cerebral perfusion pressure. Finally, we calculated the rate of change in PtIO 2 , which quantifies the percentage of change in PtIO 2 divided by the percentage of change in cerebral perfusion pressure. It is a new marker for cerebral tissue oxygen regulation based on direct measurement of PtIO 2. There was a plateau phase for the cerebral perfusion pressure-PtIO 2 relation that was similar to the autoregulatory plateau seen in the relationship between cerebral perfusion pressure and cerebral artery blood flow velocity. The rate of change in PtIO 2 demonstrated a significant correlation with the static rate of regulation (R ؍ ؊.61, p < .05). A decrease in intracranial pressure when arterial blood pressure increased from 70 to 90 mm Hg was strongly correlated with static rate of regulation (R ؍ .79, p < .001). Conclusions: Cerebral tissue PO 2 demonstrates a plateau phase similar to what is known about cerebral blood flow velocity, which suggests a close link between cerebral blood flow and oxygenation. Static cerebral autoregulation is significantly correlated with cerebral tissue oxygen reactivity.
Intensive Care Medicine Experimental
Background Brain tissue oxygen tension (PbtO2) and cerebrovascular pressure reactivity monitoring have emerged as potential modalities to individualize care in moderate and severe traumatic brain injury (TBI). The relationship between these modalities has had limited exploration. The aim of this study was to examine the relationship between PbtO2 and cerebral perfusion pressure (CPP) and how this relationship is modified by the state of cerebrovascular pressure reactivity. Methods A retrospective multi-institution cohort study utilizing prospectively collected high-resolution physiologic data from the CAnadian High Resolution-TBI (CAHR-TBI) Research Collaborative database collected between 2011 and 2021 was performed. Included in the study were critically ill TBI patients with intracranial pressure (ICP), arterial blood pressure (ABP), and PbtO2 monitoring treated in any one of three CAHR-TBI affiliated adult intensive care units (ICU). The outcome of interest was how PbtO2 and CPP ...
Neurosurgery, 2012
BACKGROUND: Cerebrovascular pressure reactivity is the principal mechanism of cerebral autoregulation. Assessment of cerebral autoregulation can be performed by using the mean flow index (Mx) based on transcranial Doppler ultrasonography. Cerebrovascular pressure reactivity can be monitored by using the pressure reactivity index (PRx), which is based on intracranial pressure monitoring. From a practical point of view, PRx can be monitored continuously, whereas Mx can only be monitored in short periods when transcranial Doppler probes can be applied. OBJECTIVE: To assess to what degree impairment in pressure reactivity (PRx) is associated with impairment in cerebral autoregulation (Mx). METHODS: A database of 345 patients with traumatic brain injury was screened for data availability including simultaneous Mx and PRx monitoring. Absolute differences, temporal changes, and association with outcome of the 2 indices were analyzed. RESULTS: A total of 486 recording sessions obtained from 201 patients were available for analysis. Overall a moderate correlation between Mx and PRx was found (r = 0.58; P , .001). The area under the receiver operator characteristic curve designed to detect the ability of PRx to predict impaired cerebral autoregulation was 0.700 (95% confidence interval: 0.607-0.880). Discrepancies between Mx and PRx were most pronounced at an intracranial pressure of 30 mm Hg and they were significantly larger for patients who died (P = .026). Both Mx and PRx were significantly lower at day 1 postadmission in patients who survived than in those who died (P , .01). CONCLUSION: There is moderate agreement between Mx and PRx. Discrepancies between Mx and PRx are particularly significant in patients with sustained intracranial hypertension. However, for clinical purposes, there is only limited interchangeability between indices.
Journal of Neurotrauma, 2020
Pressure reactivity index (PRx) and brain tissue oxygen (PbtO 2) are associated with outcome in traumatic brain injury (TBI). This study explores the relationship between PRx and PbtO 2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution intensive care unit (ICU) sub-study cohort, we evaluated those patients with archived high-frequency digital intraparenchymal intracranial pressure (ICP) and PbtO 2 monitoring data of, a minimum of 6 h in duration, and the presence of a 6 month Glasgow Outcome Scale-Extended (GOSE) score. Digital physiological signals were processed for ICP, PbtO 2 , and PRx, with the % time above/below defined thresholds determined. The duration of ICP, PbtO 2 , and PRx derangements was characterized. Associations with dichotomized 6-month GOSE (alive/dead, and favorable/unfavorable outcome; £ 4 = unfavorable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO 2 episodes. However, most of the acute ICU physiological derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO 2 episodes. Low PbtO 2 without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6 months for thresholds of 0 (area under the curve [AUC] 0.734, p = 0.003), > +0.25 (AUC 0.747, p = 0.002) and > +0.35 (AUC 0.745, p = 0.002). Similar relationships were not seen for % time with ICP >20 mm Hg, and PbtO 2 < 20 mm Hg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO 2. However, the majority of the deranged cerebral physiology seen during the acute ICU phase is impairment in cerebrovascular reactivity, with most impairment occurring in the presence of normal PbtO 2 levels. Measures of cerebrovascular reactivity appear to display the most consistent associations with global outcome in TBI, compared with ICP and PbtO 2 .
Brain tissue oxygen response in severe traumatic brain injury
Acta Neurochirurgica, 2003
Objective. To investigate clinical relevance and prognostic value of brain tissue oxygen response (TOR: response of brain tissue pO 2 to changes in arterial pO 2) in traumatic brain injury (TBI). Patients and methods. In a prospective cohort study TOR was investigated in 41 patients with severe TBI (Glasgow Coma Score 8) in whom continuous monitoring of brain tissue oxygen pressure (PbrO 2) was performed. TOR was investigated each day over a five day period for 15 minutes by increasing FiO 2 on the ventilator setting. FiO 2 was increased directly from baseline to 1.0 for a period of 15 minutes under stable conditions (145 tests). In 34 patients the effect of decreasing PaCO 2 was evaluated on TOR by performing the same test after increasing inspiratory minute volume on the ventilator setting to 20% above baseline. Arterial blood gas analysis was performed before and after changing ventilator settings. Multimodality monitoring, including PbrO 2 was performed in all patients. Outcome at six months was evaluated according to the Glasgow Outcome Scale. For statistical analysis the Mann-whitney U-test was used for ordinally distributed variables, and the Chi-square test for categorical variables. Predictive value of TOR was analyzed in a multivariable model. Results. 145 tests were available for analysis. Baseline PbrO 2 varied from 4.0 to 50 mmHg at PaO 2 values of 73-237 mmHg. At FiO 2 settings of 1.0, PbrO 2 varied from 9.1-200 mmHg and PaO 2 from 196-499 mmHg. Three distinct patterns of response were noted: response type A is characterized by a sharp increase in PbrO 2 , reaching a plateau within several minutes; type B by the absence of a plateau, and type C by a short plateau phase followed by a subsequent further increase in PbrO 2. Patterns characterized by a stable plateau (type A), considered indicative of intact regulatory mechanisms, were seen more frequently from 48 hours after injury on. If present within the first 24 hours after injury such a response was related to more favorable outcome (p ¼ 0.06). Mean TOR of all tests was 0.73 AE 0.59 with an median TOR of 0.58. Patients with an unfavourable outcome had a higher TOR (1.03 AE 0.60) during the first 24 hours, compared to patients with a favorable outcome (0.61 AE 0.51; p ¼ 0.02). Multiple logistic regression analysis supported the independent predictive value of tissue oxygen response for unfavorable outcome (odds ratio 4.8). During increased hyperventilation, mean TOR decreased substantially from 0.75 AE 0.54 to 0.65 AE 0.45 (p ¼ 0.06; Wilcoxon test). Within the first 24 hours after injury a decrease in TOR following hyperventilation was significantly related to poorer outcome (p ¼ 0.01). Conclusions. Evaluation of TOR affords insight in (disturbances in) oxygen regulation after traumatic brain injury, is of prognostic value and may aid in identifying patients at (increased) risk for ischemia.
Relationship between brain tissue oxygen (PbrO2) and cerebral perfusion pressure (CPP)
Critical Care, 1997
Background and objectives: The optimal mode of treatment in spontaneous supratentorial intracerebral hemorrhage (SICH) is controversial. We assessed the value of hematoma evacuation in SICH in a case-control study. Methods: One hundred and forty-five patients with SICH without tumor or vascular abnormalities. Indication for surgery were made upon admission in 11 and after clinical deterioration in 13 patients. Assessed were age, sex. Glasgow Coma Scale (GCS), pupillary reaction on admission, localisation, etiology and hematoma volume, presence of ventricular blood, and Glasgow Outcome Scale on discharge. From further analysis patients > 80 years or with hematoma volume < 10 ml were excluded. Statistical analysis included: (i) a multiple regression model to determine prognostic factors; (ii) comparison between medical and surgical patients; (iii) matching the 24 evacuated with 24 medical patients according to those parameters retained from the regression model and additionally to other suspected factors influencing outcome; (iv) comparison between both groups to confirm comparability; and (v) testing for different outcome between the groups. Results: Prognostic factors were GCS, hematoma volume and location. All 24 evacuated patients could be matched to a medically treated patient regarding age, hematoma volume and location. GCS and pupillary reaction. Differences between both groups could not be detected. Outcome was not different between the medical and surgical group. Conclusions: Hematoma evacuation does not improve outcome in supratentorial spontaneous hemorrhages. Since mainly deteriorating patients were evacuated, the only effect of hematoma evacuation may be to stop deterioration rather than to improve overall outcome. P002 Is 'brain swelling' a clinical particular kind of severe brain injury?
Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans
Canadian Journal of Physiology and Pharmacology, 2002
This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s1·mmHg1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s1·mmHg1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min1·mmHg1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min1·mmHg1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the t...