scholarly journals Comparison of Frequency and Time Domain Methods of Assessment of Cerebral Autoregulation in Traumatic Brain Injury

2014 ◽  
Vol 35 (2) ◽  
pp. 248-256 ◽  
Author(s):  
Xiuyun Liu ◽  
Marek Czosnyka ◽  
Joseph Donnelly ◽  
Karol P Budohoski ◽  
Georgios V Varsos ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Transfer Function ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Flow Index ◽  
Mean Flow ◽  
Arterial Blood ◽  
Welch Method ◽  
Autoregulation Index

The impulse response (IR)-based autoregulation index (ARI) allows for continuous monitoring of cerebral autoregulation using spontaneous fluctuations of arterial blood pressure (ABP) and cerebral flow velocity (FV). We compared three methods of autoregulation assessment in 288 traumatic brain injury (TBI) patients managed in the Neurocritical Care Unit: (1) IR-based ARI; (2) transfer function (TF) phase, gain, and coherence; and (3) mean flow index (Mx). Autoregulation index was calculated using the TF estimation (Welch method) and classified according to the original Tiecks’ model. Mx was calculated as a correlation coefficient between 10-second averages of ABP and FV using a moving 300-second data window. Transfer function phase, gain, and coherence were extracted in the very low frequency (VLF, 0 to 0.05 Hz) and low frequency (LF, 0.05 to 0.15 Hz) bandwidths. We studied the relationship between these parameters and also compared them with patients’ Glasgow outcome score. The calculations were performed using both cerebral perfusion pressure (CPP; suffix ‘c’) as input and ABP (suffix ‘a’). The result showed a significant relationship between ARI and Mx when using either ABP ( r=−0.38, P<0.001) or CPP ( r=−0.404, P<0.001) as input. Transfer function phase and coherence_a were significantly correlated with ARI_a and ARI_c ( P<0.05). Only ARI_a, ARI_c, Mx_a, Mx_c, and phase_c were significantly correlated with patients’ outcome, with Mx_c showing the strongest association.

Dynamic modulation of cerebrovascular resistance as an index of autoregulation under tilt and controlled Pet CO2

2002 ◽  
Vol 283 (3) ◽  
pp. R653-R662 ◽  
Author(s):  
Michael R. Edwards ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson
Keyword(s):  
Transfer Function ◽  
Function Analysis ◽  
Low Frequency ◽  
Mean Flow ◽  
Low Frequencies ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Frequency Changes

Transfer function analysis of the arterial blood pressure (BP)-mean flow velocity (MFV) relationship describes an aspect of cerebrovascular autoregulation. We hypothesized that the transfer function relating BP to cerebrovascular resistance (CVRi) would be sensitive to low-frequency changes in autoregulation induced by head-up tilt (HUT) and altered arterial Pco 2. Nine subjects were studied in supine and HUT positions with end-tidal Pco 2(Pet CO2 ) kept constant at normal levels: +5 and −5 mmHg. The BP-MFV relationship had low coherence at low frequencies, and there were significant effects of HUT on gain only at high frequencies and of Pco 2 on phase only at low frequencies. BP → CVRi had coherence >0.5 from very low to low frequencies. There was a significant reduction of gain with increased Pco 2 in the very low and low frequencies and with HUT at the low frequency. Phase was affected by Pco 2 in the very low frequencies. Transfer function analysis of BP → CVRi provides direct evidence of altered cerebrovascular autoregulation under HUT and higher levels of Pco 2.

scholarly journals Lack of correlation between cerebral vasomotor reactivity and dynamic cerebral autoregulation during stepwise increases in inspired CO2 concentration

2016 ◽  
Vol 120 (12) ◽  
pp. 1434-1441 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Seon-Ok Kim ◽  
Darren S. DeLorey ◽  
Tony G. Babb ◽  
Benjamin D. Levine ◽  
...  
Keyword(s):  
Transfer Function ◽  
Cerebral Autoregulation ◽  
Function Analysis ◽  
Low Frequency ◽  
Frequency Range ◽  
Vasomotor Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Cerebral Vasomotor Reactivity ◽  
Dynamic Cerebral Autoregulation

Cerebral vasomotor reactivity (CVMR) and dynamic cerebral autoregulation (CA) are measured extensively in clinical and research studies. However, the relationship between these measurements of cerebrovascular function is not well understood. In this study, we measured changes in cerebral blood flow velocity (CBFV) and arterial blood pressure (BP) in response to stepwise increases in inspired CO2 concentrations of 3 and 6% to assess CVMR and dynamic CA in 13 healthy young adults [2 women, 32 ± 9 (SD) yr]. CVMR was assessed as percentage changes in CBFV (CVMRCBFV) or cerebrovascular conductance index (CVCi, CVMRCVCi) in response to hypercapnia. Dynamic CA was estimated by performing transfer function analysis between spontaneous oscillations in BP and CBFV. Steady-state CBFV and CVCi both increased exponentially during hypercapnia; CVMRCBFV and CVMRCVCi were greater at 6% (3.85 ± 0.90 and 2.45 ± 0.79%/mmHg) than at 3% CO2 (2.09 ± 1.47 and 0.21 ± 1.56%/mmHg, P = 0.009 and 0.005, respectively). Furthermore, CVMRCBFV was greater than CVMRCVCi during either 3 or 6% CO2 ( P = 0.017 and P < 0.001, respectively). Transfer function gain and coherence increased in the very low frequency range (0.02-0.07 Hz), and phase decreased in the low-frequency range (0.07–0.20 Hz) when breathing 6%, but not 3% CO2. There were no correlations between the measurements of CVMR and dynamic CA. These findings demonstrated influences of inspired CO2 concentrations on assessment of CVMR and dynamic CA. The lack of correlation between CVMR and dynamic CA suggests that cerebrovascular responses to changes in arterial CO2 and BP are mediated by distinct regulatory mechanisms.

Development of a low-frequency autoregulation index for calculation of optimal CPP in severe traumatic brain injury

2013 ◽  
Vol 28 (1) ◽  
pp. e8 ◽  
Author(s):  
Fabian Guiza ◽  
Bart Depreitere ◽  
Martin Schuhmann ◽  
Greet Van Den Berghe ◽  
Geert Meyfroidt
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Low Frequency ◽  
Autoregulation Index

scholarly journals Novel index for predicting mortality during the first 24 hours after traumatic brain injury

2019 ◽  
Vol 131 (6) ◽  
pp. 1887-1895
Author(s):  
Hakseung Kim ◽  
Hack-Jin Lee ◽  
Young-Tak Kim ◽  
Yunsik Son ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Autoregulation ◽  
Area Under The Curve ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Reactivity Index ◽  
Predictive Capacity ◽  
Arterial Blood ◽  
Prediction Of Mortality

OBJECTIVEFailure of cerebral autoregulation and subsequent hypoperfusion is common during the acute phase of traumatic brain injury (TBI). The cerebrovascular pressure-reactivity index (PRx) indirectly reflects cerebral autoregulation and has been used to derive optimal cerebral perfusion pressure (CPP). This study provides a method for the use of a combination of PRx, CPP, and intracranial pressure (ICP) to better evaluate the extent of cerebral hypoperfusion during the first 24 hours after TBI, allowing for a more accurate prediction of mortality risk.METHODSContinuous ICP and arterial blood pressure (ABP) signals acquired from 295 TBI patients during the first 24 hours after admission were retrospectively analyzed. The CPP at the lowest PRx was determined as the optimal CPP (CPPopt). The duration of a severe hypoperfusion event (dHP) was defined as the cumulative time that the PRx was > 0.2 and the CPP was < 70 mm Hg with the addition of intracranial hypertension (ICP > 20 or > 22 mm Hg). The outcome was determined as 6-month mortality.RESULTSThe cumulative duration of PRx > 0.2 and CPP < 70 mm Hg exhibited a significant association with mortality (p < 0.001). When utilized with basic clinical information available during the first 24 hours after admission (i.e., Glasgow Coma Scale score, age, and mean ICP), a dHP > 25 minutes yielded a significant predictive capacity for mortality (p < 0.05, area under the curve [AUC] = 0.75). The parameter was particularly predictive of mortality for patients with a mean ICP > 20 or > 22 mm Hg (AUC = 0.81 and 0.87, respectively).CONCLUSIONSA short duration (25 minutes) of severe hypoperfusion, evaluated as lowered CPP during worsened cerebrovascular reactivity during the 1st day after TBI, is highly indicative of mortality.

scholarly journals Cerebral pressure autoregulation in traumatic brain injury

2008 ◽  
Vol 25 (4) ◽  
pp. E7 ◽  
Author(s):  
Leonardo Rangel-Castilla ◽  
Jaime Gasco ◽  
Haring J. W. Nauta ◽  
DaviD O. Okonkwo ◽  
Claudia S. Robertson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gold Standard ◽  
Cerebral Autoregulation ◽  
Secondary Injury ◽  
Neurointensive Care Unit ◽  
Arterial Blood ◽  
Severe Tbi ◽  
Pressure Autoregulation ◽  
Over Time

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 dynamic autoregulation methods. Hyperventilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

2020 ◽  
Vol 132 (6) ◽  
pp. 1952-1960 ◽  
Author(s):  
Seung-Bo Lee ◽  
Hakseung Kim ◽  
Young-Tak Kim ◽  
Frederick A. Zeiler ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Status ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Clinical Parameters ◽  
Artifact Removal ◽  
Clinical Events ◽  
Arterial Blood ◽  
Before And After

OBJECTIVEMonitoring intracranial and arterial blood pressure (ICP and ABP, respectively) provides crucial information regarding the neurological status of patients with traumatic brain injury (TBI). However, these signals are often heavily affected by artifacts, which may significantly reduce the reliability of the clinical determinations derived from the signals. The goal of this work was to eliminate signal artifacts from continuous ICP and ABP monitoring via deep learning techniques and to assess the changes in the prognostic capacities of clinical parameters after artifact elimination.METHODSThe first 24 hours of monitoring ICP and ABP in a total of 309 patients with TBI was retrospectively analyzed. An artifact elimination model for ICP and ABP was constructed via a stacked convolutional autoencoder (SCAE) and convolutional neural network (CNN) with 10-fold cross-validation tests. The prevalence and prognostic capacity of ICP- and ABP-related clinical events were compared before and after artifact elimination.RESULTSThe proposed SCAE-CNN model exhibited reliable accuracy in eliminating ABP and ICP artifacts (net prediction rates of 97% and 94%, respectively). The prevalence of ICP- and ABP-related clinical events (i.e., systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and poor cerebrovascular reactivity) all decreased significantly after artifact removal.CONCLUSIONSThe SCAE-CNN model can be reliably used to eliminate artifacts, which significantly improves the reliability and efficacy of ICP- and ABP-derived clinical parameters for prognostic determinations after TBI.

scholarly journals 217 The end-tidal and arterial carbon dioxide gradient in serious traumatic brain injury after pre-hospital emergency anaesthesia: a retrospective observational study

2020 ◽  
Vol 37 (12) ◽  
pp. 847.1-847
Author(s):  
James Price ◽  
Daniel Sandbach ◽  
Ari Ercole ◽  
Alastair Wilson ◽  
Ed Barnard
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Thoracic Injury ◽  
Secondary Brain Injury ◽  
Hospital Emergency ◽  
Hospital Arrival ◽  
Arterial Blood ◽  
End Tidal ◽  
Emergency Anaesthesia

Aims/Objectives/BackgroundIn the United Kingdom (UK), 20% of patients with severe traumatic brain injury (TBI) receive pre-hospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5kPa to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5kPa ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. Our primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival.Methods/DesignA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a pre-hospital critical care team in the East of England between 1st April 2015 to 31st December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% confidence intervals (95%CI). ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results/Conclusions107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 minutes of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol.The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa, with only moderate correlation of ETCO2 and PaCO2 at hospital arrival (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95%CI 1.4–2.0) kPa with upper and lower limits of agreement of 3.6 (95%CI 3.0–4.1) kPa and -0.2 (95%CI -0.8–0.3) kPa respectively. There was no significant gradient correlation in patients with a co-existing serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa, p=0.01. Patients who underwent pre-hospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa.Lower ETCO2 targets than previously recommended may be safe and appropriate. The use of pre-hospital PaCO2 measurement is advocated.

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