Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury (original) (raw)
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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.
Neurocritical Care, 2023
Background: Critical closing pressure (CrCP) and resistance-area product (RAP) have been conceived as compasses to optimize cerebral perfusion pressure (CPP) and monitor cerebrovascular resistance, respectively. However, for patients with acute brain injury (ABI), the impact of intracranial pressure (ICP) variability on these variables is poorly understood. The present study evaluates the effects of a controlled ICP variation on CrCP and RAP among patients with ABI. Methods: Consecutive neurocritical patients with ICP monitoring were included along with transcranial Doppler and invasive arterial blood pressure monitoring. Internal jugular veins compression was performed for 60 s for the elevation of intracranial blood volume and ICP. Patients were separated in groups according to previous intracranial hypertension severity, with either no skull opening (Sk1), neurosurgical mass lesions evacuation, or decompressive craniectomy (DC) (patients with DC [Sk3]). Results: Among 98 included patients, the correlation between change (Δ) in ICP and the corresponding ΔCrCP was strong (group Sk1 r = 0.643 [p = 0.0007], group with neurosurgical mass lesions evacuation r = 0.732 [p < 0.0001], and group Sk3 r = 0.580 [p = 0.003], respectively). Patients from group Sk3 presented a significantly higher ΔRAP (p = 0.005); however, for this group, a higher response in mean arterial pressure (change in mean arterial pressure p = 0.034) was observed. Exclusively, group Sk1 disclosed reduction in ICP before internal jugular veins compression withholding. This study elucidates that CrCP reliably changes in accordance with ICP, being useful to indicate ideal CPP in neurocritical settings. In the early days after DC, cerebrovascular resistance seems to remain elevated, despite exacerbated arterial blood pressure responses in efforts to maintain CPP stable. Patients with ABI with no need of surgical procedures appear to remain with more effective ICP compensatory mechanisms when compared with those who underwent neurosurgical interventions.
Stroke, 2004
Background and Purpose-Development of a method to continuously assess cerebrovascular autoregulation of patients with traumatic brain injury would facilitate therapeutic intervention and thus reduce secondary complications. Methods-Changes in arterial blood pressure (ABP), intracranial pressure (ICP), cerebral blood flow velocity (CBFV), and pial arteriolar diameter (PAD) induced by acute pressor challenge (norepinephrine; 1 g/[kg ⅐ min]) were evaluated in both uninjured and fluid percussion injured piglets equipped with cranial windows. The linear correlation coefficient and corresponding slope of the regression line of the relationship between highest modal frequency (HMF) of cerebrovascular pressure transmission of ABP to ICP and cerebral perfusion pressure (CPP) were determined for each challenge. Results-For all uninjured piglets, pressor challenge resulted in an inverse relationship between HMF and CPP characterized by significant negative correlation values and negative corresponding regression line slopes with respective group mean values (ϮSD) of Ϫ0.50 (Ϯ0.14) and Ϫ0.6 (Ϯ0.44) Hz/mm Hg, respectively. Consistent with functional autoregulation of the uninjured preparations, pressor challenge resulted in a decrease of PAD, and CBFV remained relatively constant. For all injured piglets, pressor challenge resulted in direct relationship between HMF and CPP, characterized by positive correlation values and corresponding regression line slopes with group mean values of 0.48 (Ϯ0.21) and 1.13 (Ϯ2.08) Hz/mm Hg, respectively. Consistent with impaired autoregulation, PAD and CBFV increased during pressor challenge after brain injury. Conclusions-Evaluation of changes of the HMF of cerebrovascular pressure transmission with respect to CPP changes permits continuous monitoring of cerebral autoregulation.
Critical Care Medicine, 2014
Objectives: The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. Design: Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. Setting: University laboratory. Subjects: Male Sprague-Dawley rats. Interventions: At each cerebral perfusion pressure, dopamineinduced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (∆ intracranial pressure/∆ mean arterial pressure) and induced cerebrovascular reactivity (∆ cerebral blood flow/∆ mean arterial pressure). Measurements and Main Results: At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Conclusions: Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed. (Crit Care Med 2014; XX:00-00) Key Words: blood-brain barrier permeability; cerebral blood flow autoregulation; cerebral perfusion pressure; cortical microvascular shunts; hypoxia; induced cerebrovascular reactivity; induced intracranial pressure reactivity; intracranial pressure C erebrovascular autoregulation is the ability of the brain to maintain cerebral blood flow (CBF) despite changes in cerebral perfusion pressure (CPP), that is, mean
Critical Care Medicine, 2002
Background: Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. Objective: This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. Design: Prospective study. Setting: Neurosurgical intensive care unit Patients: A total of 42 patients with severe head injuries. Interventions: Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. Measurements and Main Results: Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 ؎ 0.32 to 0.71 ؎ 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (>5 mm Hg) in the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. Conclusion: Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.
Cerebral Vascular Changes During Acute Intracranial Pressure Drop
Neurocritical Care, 2018
Objective: This study applied a new external ventricular catheter, which allows intracranial pressure (ICP) monitoring and cerebral spinal fluid (CSF) drainage simultaneously, to study cerebral vascular responses during acute CSF drainage. Methods: Six patients with 34 external ventricular drain (EVD) opening sessions were retrospectively analyzed. A published algorithm was used to extract morphological features of ICP recordings, and a template-matching algorithm was applied to calculate the likelihood of cerebral vasodilation index (VDI) and cerebral vasoconstriction index (VCI) based on the changes of ICP waveforms during CSF drainage. Power change (∆P) of ICP B-waves after EVD opening was also calculated. Cerebral autoregulation (CA) was assessed through phase difference between arterial blood pressure (ABP) and ICP using a previously published wavelet-based algorithm. Results: The result showed that acute CSF drainage reduced mean ICP (P = 0.016) increased VCI (P = 0.02) and reduced ICP B-wave power (P = 0.016) significantly. VCI reacted to ICP changes negatively when ICP was between 10 and 25 mmHg, and VCI remained unchanged when ICP was outside the 10-25 mmHg range. VCI negatively (r = − 0.44) and VDI positively (r = 0.82) correlated with ∆P of ICP B-waves, indicating that stronger vasoconstriction resulted in bigger power drop in ICP B-waves. Better CA prior to EVD opening triggered bigger drop in the power of ICP B-waves (r = − 0.612). Conclusions: This study demonstrates that acute CSF drainage reduces mean ICP, and results in vasoconstriction which can be detected through an index, VCI. Cerebral vessels actively respond to ICP changes or cerebral perfusion pressure (CPP) changes in a certain range; beyond which, the vessels are insensitive to the changes in ICP and CPP.
Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury*
Critical Care Medicine, 2012
S urvival after traumatic brain injury (TBI) is dependent on the control of intracranial hypertension and the provision of hemodynamic support to achieve an "adequate" cerebral perfusion pressure (CPP). However, the idea of a single value (or even a single range) of CPP being adequate for the diverse group of TBI patients is an oversimplification (1-3). Age and premorbid arterial blood pressure (ABP) are examples of factors likely to influence individual CPP targets, with elderly, hypertensive patients requiring a higher CPP compared with young, normotensive patients. Although multimodal brain monitoring, including continuous brain-tissue oxygenation, near infrared spectroscopy, transcranial Doppler ultrasonography, and microdialysis provide valuable information at the bedside regarding the adequacy of CPP, these technologies are costly and restricted to a relatively small number of specialized neurocritical care units. The 2007 Brain Trauma Foundation guidelines advocated randomized controlled trials to verify the feasibility and the impact on outcome of strategies based on individualized CPP management following severe TBI (4). A method for individualization of CPPoriented management based on determination of cerebrovascular reactivity Objectives: We have sought to develop an automated methodology for the continuous updating of optimal cerebral perfusion pressure (CPP opt ) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascular pressure reactivity. We then validated the CPP opt algorithm by determining the association between outcome and the deviation of actual CPP from CPP opt .
2019
Objectives: Cerebrovascular autoregulation can be monitored with a moving linear correlation of blood pressure to cerebral blood flow velocity (mean velocity index, Mx) during cardiopulmonary bypass (CPB). Vascular reactivity can be monitored with a moving linear correlation of blood pressure to cerebral blood volume trended with near-infrared spectroscopy (hemoglobin volume index, HVx). We hypothesized that the lower limits of autoregulation (LLA) and the optimal blood pressure (ABPopt) associated with the most active autoregulation could be determined by HVx in patients undergoing CPB. Methods: Adult patients (n5109) who underwent CPB for cardiac surgery had monitoring of both autoregulation (Mx) and vascular reactivity (HVx). Individual curves of Mx and HVx were constructed by placing each in 5 mmHg bins. The LLA and ABPopt for each subject were then identified by both methods and compared for agreement by correlation analysis and Bland-Altman. Results: The average LLA defined by Mx compared to HVx were comparable (66¡13 and 66¡12 mmHg). Correlation between the LLA defined by Mx and HVx was significant (Pearson r50.2867; P50.0068). The average ABPopt with the most robust autoregulation by Mx was comparable to HVx (75¡11 and 74¡13 mmHg) with significant correlation (Pearson r50.5915; P(0.0001). Discussion: Autoregulation and vascular reactivity monitoring are expected to be distinct, as flow and volume have different phasic relationships to pressure when cerebrovascular autoregulation is active. However, the two metrics have good agreement when identifying the LLA and optimal blood pressure in patients during CPB.
Cerebral pressure autoregulation in traumatic brain injury
Neurosurgical FOCUS, 2008
An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregulation is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with...