Cerebral Autoregulation Testing Research Articles

Effect of Increasing Blood Pressure on Brain Tissue Oxygenation in Adults After Severe Traumatic Brain Injury.

To examine if increasing blood pressure improves brain tissue oxygenation (PbtO2) in adults with severe traumatic brain injury (TBI). Retrospective review of prospectively collected data. Level-I trauma center teaching hospital. Included patients greater than or equal to 18 years of age and with severe (admission Glasgow Coma Scale [GCS] score < 9) TBI who had advanced neuromonitoring (intracranial blood pressure [ICP], PbtO2, and cerebral autoregulation testing). The exposure was mean arterial pressure (MAP) augmentation with a vasopressor, and the primary outcome was a PbtO2 response. Cerebral hypoxia was defined as PbtO2 less than 20 mm Hg (low). MAP challenge test results conducted between ICU admission days 1-3 from 93 patients (median age 31; interquartile range [IQR], 24-44 yr), 69.9% male, White (n = 69, 74.2%), median head abbreviated injury score 5 (IQR 4-5), and median admission GCS 3 (IQR 3-5) were examined. Across all 93 tests, a MAP increase of 25.7% resulted in a 34.2% cerebral perfusion pressure (CPP) increase and 16.3% PbtO2 increase (no MAP or CPP correlation with PbtO2 [both R2 = 0.00]). MAP augmentation increased ICP when cerebral autoregulation was impaired (8.9% vs. 3.8%, p = 0.06). MAP augmentation resulted in four PbtO2 responses (normal and maintained [group 1: 58.5%], normal and deteriorated [group 2: 2.2%; average 45.2% PbtO2 decrease], low and improved [group 3: 12.8%; average 44% PbtO2 increase], and low and not improved [group 4: 25.8%]). The average end-tidal carbon dioxide (ETCO2) increase of 5.9% was associated with group 2 when cerebral autoregulation was impaired (p = 0.02). MAP augmentation after severe TBI resulted in four distinct PbtO2 response patterns, including PbtO2 improvement and cerebral hypoxia. Traditionally considered clinical factors were not significant, but cerebral autoregulation status and ICP responses may have moderated MAP and ETCO2 effects on PbtO2 response. Further study is needed to examine the role of MAP augmentation as a strategy to improve PbtO2 in some patients.

Critical Care Experience With Clinical Cerebral Autoregulation Testing in Adults With Traumatic Brain Injury.

To describe the setting, feasibility, and safety of static cerebral autoregulation testing in critically injured adults with traumatic brain injury (TBI). Methods: We reviewed static autoregulation testing using transcranial Doppler (TCD) ultrasound in patients > 18 years with TBI ICD codes between January 1, 2014, and December 31, 2021. Adverse events during testing were defined as systemic hypertension (systolic blood pressure (SBP>180 mmHg), bradycardia (HR<40 bpm), and high ICP (>30 mmHg). Impaired and absent cerebral autoregulation was defined as an autoregulatory index (ARI) <0.4 and ARI 0, respectively. We characterized prescribed changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targets by autoregulation testing results. Results: A total of 135 patients, median age 31 (interquartile range (IQR) 24, 43) years, 71.9% male, admission Glasgow coma scale (GCS) score 3 (IQR 3, 5.5), and 70.9% with subdural hematoma from severe (GCS 3-8; 133 (98.5%)) and moderate (GCS 9-12; 2 (1.5%)) TBI, underwent 309 attempted testing. All patients were mechanically ventilated and had ICP monitoring; 246 (80%) had brain tissue oxygen monitoring, and 68 (22%) had an external ventricular drain. The median number of autoregulation tests was two (range 1-3) tests/patient, and the median admission to the first test time was two days (IQR 1, 3). Of 55 (17.8%) tests not completed, systemic hypertension (32, 10.4%), intracranial hypertension (10, 3.2%), and bradycardia (3, 0.9%) were transient. Fifty-three (51%) of the first (n=104) autoregulation tests showed impaired/absent cerebral autoregulation. Impaired/absent autoregulation results at the first test were associated with repeat cerebral autoregulation testing (RR 2.25, 95% CI [1.40-3.60], p=0.0007) than intact cerebral autoregulation results. Pre-testing cerebral hemodynamic targets were maintained (n=131; 86.8%) when cerebral autoregulation was impaired (n=151; RR 1.49, 95% CI [1.25-1.77], p<0.0001). However, 15 (9.9%) test results led to higher ICP targets (from 20 mmHg to 25 mmHg), 5 (3.3%) results led to an increase in CPP target (from 60 mmHg to 70 mmHg), and five out of 131 (3.8%) patients underwent decompressive craniectomy and placement of an external ventricular drain. Intact cerebral autoregulation results (n=43/103, 41.7%) were associated with a change in ICP targets from 20 mmHg to 25 mmHg (RR 3.15, 95% CI [1.97-5.03], p<0.0001). Conclusions: Static cerebral autoregulation testing was feasible, safe, and useful in individualizing the care of patients with moderate-severe TBI receiving multimodal neuromonitoring. Testing results guided future testing, cerebral hemodynamic targets, and procedural decisions. Impaired cerebral autoregulation was very common.

Experience with clinical cerebral autoregulation testing in children hospitalized with traumatic brain injury: Translating research to bedside.

To report our institutional experience with implementing a clinical cerebral autoregulation testing order set with protocol in children hospitalized with traumatic brain injury (TBI). After IRB approval, we examined clinical use, patient characteristics, feasibility, and safety of cerebral autoregulation testing in children aged <18 years between 2014 and 2021. A clinical order set with a protocol for cerebral autoregulation testing was introduced in 2018. 25 (24 severe TBI and 1 mild TBI) children, median age 13 years [IQR 4.5; 15] and median admission GCS 3[IQR 3; 3.5]) underwent 61 cerebral autoregulation tests during the first 16 days after admission [IQR1.5; 7; range 0-16]. Testing was more common after implementation of the order set (n = 16, 64% after the order set vs. n = 9, 36% before the order set) and initiated during the first 2 days. During testing, patients were mechanically ventilated (n = 60, 98.4%), had invasive arterial blood pressure monitoring (n = 60, 98.4%), had intracranial pressure monitoring (n = 56, 90.3%), brain-tissue oxygenation monitoring (n = 56, 90.3%), and external ventricular drain (n = 13, 25.5%). Most patients received sedation and analgesia for intracranial pressure control (n = 52; 83.8%) and vasoactive support (n = 55, 90.2%) during testing. Cerebral autoregulation testing was completed in 82% (n = 50 tests); 11 tests were not completed [high intracranial pressure (n = 5), high blood pressure (n = 2), bradycardia (n = 2), low cerebral perfusion pressure (n = 1), or intolerance to blood pressure cuff inflation (n = 1)]. Impaired cerebral autoregulation on first assessment resulted in repeat testing (80% impaired vs. 23% intact, RR 2.93, 95% CI 1.06:8.08, p = 0.03). Seven out of 50 tests (14%) resulted in a change in cerebral hemodynamic targets. Findings from this series of children with TBI indicate that: (1) Availability of clinical order set with protocol facilitated clinical cerebral autoregulation testing, (2) Clinicians ordered cerebral autoregulation tests in children with severe TBI receiving high therapeutic intensity and repeatedly with impaired status on the first test, (3) Clinical cerebral autoregulation testing is feasible and safe, and (4) Testing results led to change in hemodynamic targets in some patients.

Implementation of Multimodality Neurologic Monitoring Reporting in Pediatric Traumatic Brain Injury Management

Background/ObjectiveMultimodality neurologic monitoring (MMM) is an emerging technique for management of traumatic brain injury (TBI). An increasing array of MMM-derived biomarkers now exist that are associated with injury severity and functional outcomes after TBI. A standardized MMM reporting process has not been well described, and a paucity of evidence exists relating MMM reporting in TBI management with functional outcomes or adverse events.MethodsProspective implementation of standardized MMM reporting at a single pediatric intensive care unit (PICU) is described that included monitoring of intracranial pressure (ICP), cerebral oxygenation and electroencephalography (EEG). The incidence of clinical decisions made using MMM reporting is described, including timing of neuroimaging, ICP monitoring discontinuation, use of paralytic, hyperosmolar and pentobarbital therapies, neurosurgical interventions, ventilator and CPP adjustments and neurologic prognostication discussions. Retrospective analysis was performed on the association of MMM reporting with initial Glasgow Coma Scale (GCS) and Pediatric Risk of Mortality III (PRISM III) scores, duration of total hospitalization and PICU hospitalization, duration of mechanical ventilation and invasive ICP monitoring, inpatient complications, time with ICP > 20 mmHg, time with cerebral perfusion pressure (CPP) < 40 mmHg and 12-month Glasgow Outcome Scale—Extended Pediatrics (GOSE-Peds) scores. Association of outcomes with MMM reporting was investigated using the Wilcoxon rank-sum test or Fisher’s exact test, as appropriate.ResultsEighty-five children with TBI underwent MMM over 6 years, among which 18 underwent daily MMM reporting over a 21-month period. Clinical decision-making influenced by MMM reporting included timing of neuroimaging (100.0%), ICP monitoring discontinuation (100.0%), timing of extubation trials of surviving patients (100.0%), body repositioning (11.1%), paralytic therapy (16.7%), hyperosmolar therapy (22.2%), pentobarbital therapy (33.3%), provocative cerebral autoregulation testing (16.7%), adjustments in CPP thresholds (16.7%), adjustments in PaCO2 thresholds (11.1%), neurosurgical interventions (16.7%) and neurologic prognostication discussions (11.1%). The implementation of MMM reporting was associated with a reduction in ICP monitoring duration (p = 0.0017) and mechanical ventilator duration (p = 0.0018). No significant differences were observed in initial GCS or PRISM III scores, total hospitalization length, PICU hospitalization length, total complications, time with ICP > 20 mmHg, time with CPP < 40 mmHg, use of tier 2 therapy, or 12-month GOS-E Peds scores.ConclusionImplementation of MMM reporting in pediatric TBI management is feasible and can be impactful in tailoring clinical decisions. Prospective work is needed to understand the impact of MMM and MMM reporting systems on functional outcomes and clinical care efficacy.Supplementary InformationThe online version contains supplementary material available at 10.1007/s12028-021-01190-8.

Cerebral Autoregulation Is Not Different Between Hot And Thermoneutral Head-Out Water Immersion In Healthy Participants

Recurring hot head-out water immersion (HOWI) enhances peripheral vascular function and cerebral blood velocity during non-immersion conditions (i.e., rest, aerobic exercise, and heat stress). However, it is not known if an acute bout of hot HOWI alters cerebrovascular function (i.e., cerebral autoregulation). PURPOSE: We tested the hypothesis that dynamic cerebral autoregulation is improved during and following an acute bout of hot (HOT) vs. thermoneutral (TN) HOWI. METHODS: Seventeen healthy participants (age: 23±2 y, 5 females) completed two randomized trials which consisted of 30 min of HOT (39°C) or TN (35°C) HOWI. Beat-to-beat blood pressure (MAP), middle cerebral artery blood velocity (MCAv), and end-tidal CO2 tension (PETCO2) were recorded continuously. After 5 min of seated rest, participants breathed through a respiratory impedance device for 5 min while maintaining PETCO2 values to assess cerebral autoregulation using Fourier transformation (n = 11). Cerebral autoregulation testing was completed pre, 30 min into HOWI (during), and immediately post HOWI. Values are reported as a change from baseline (α: mean ± SD). RESULTS: MAP, MCAv, PETCO2, gain, and phase were not different between HOT and TN at pre (P > 0.23 for all). αMAP was lower in HOT vs. TN during (-3±6 vs. 9±5 mmHg; P<0.01) and post (0±5 vs. 10±7 mmHg; P<0.01). αMCAv was lower in HOT vs. TN during (-3±5 vs. 4±4 cm/s; P<0.01) and post (-5±7 vs. 0±5 cm/s; P<0.01). αPETCO2 was lower in HOT vs. TN during (1±2 vs. 2±2 mmHg; P<0.01) and post (-3±2 vs. -1±2 mmHg; P<0.01). αGain was not different between HOT and TN during (HOT: -0.03±0.15 vs. TN: -0.08±0.05 cm/s/mmHg; P=0.18) or post (HOT: 0.04±0.12 vs. TN: -0.03±0.07 cm/s/mmHg; P=0.18). αPhase was not different between HOT and TN during (HOT: 2.9±9.0 vs. TN: 1.0±8.8°; P=0.74) or post (HOT: -1.2±12.8 vs. TN: -2.0±9.7°; P=0.74) CONCLUSION: These data indicate that an acute bout of hot water immersion attenuates cerebral blood velocity vs. thermoneutral water immersion. This response is likely due to the differences in arterial blood pressure and/or arterial carbon dioxide between conditions. However, cerebral autoregulation during and following hot water immersion is not different compared to thermoneutral water immersion in healthy participants. Supported by Office of Naval Research Award N00014-17-1-2665

Prevalence, Evolution, and Extent of Impaired Cerebral Autoregulation in Children Hospitalized With Complex Mild Traumatic Brain Injury.

To examine cerebral autoregulation in children with complex mild traumatic brain injury. Prospective observational convenience sample. PICU at a level I trauma center. Children with complex mild traumatic brain injury (trauma, admission Glasgow Coma Scale score 13-15 with either abnormal head CT, or history of loss of consciousness). Cerebral autoregulation was tested using transcranial Doppler ultrasound between admission day 1 and 8. The primary outcome was prevalence of impaired cerebral autoregulation (autoregulation index < 0.4),determined using transcranial Doppler ultrasonography and tilt testing. Secondary outcomes examined factors associated with and evolution and extent of impairment. Cerebral autoregulation testing occurred in 31 children 10 years (SD, 5.2 yr), mostly male (59%) with isolated traumatic brain injury (91%), median admission Glasgow Coma Scale 15, Injury Severity Scores 14.2 (SD, 7.7), traumatic brain injury due to fall (50%), preadmission loss of consciousness (48%), and abnormal head CT scan (97%). Thirty-one children underwent 56 autoregulation tests. Impaired cerebral autoregulation occurred in 15 children (48.4%) who underwent 19 tests; 68% and 32% of tests demonstrated unilateral and bilateral impairment, respectively. Compared with children on median day 6 of admission after traumatic brain injury, impaired autoregulation was most common in the first 5 days after traumatic brain injury (day 1: relative risk, 3.7; 95% CI, 1.9-7.3 vs day 2: relative risk, 2.7; 95% CI, 1.1-6.5 vs day 5: relative risk, 1.33; 95% CI, 0.7-2.3). Children with impaired autoregulation were older (12.3 yr [SD, 1.3 yr] vs 8.7 yr [SD, 1.1 yr]; p = 0.04) and tended to have subdural hematoma (64% vs 44%), epidural hematoma (29% vs 17%), and subarachnoid hemorrhage (36% vs 28%). Eight children (53%) were discharged home with ongoing impaired cerebral autoregulation. Impaired cerebral autoregulation is common in children with complex mild traumatic brain injury, despite reassuring admission Glasgow Coma Scale 13-15. Children with complex mild traumatic brain injury have abnormal cerebrovascular hemodynamics, mostly during the first 5 days. Impairment commonly extends to the contralateral hemisphere and discharge of children with ongoing impaired cerebral autoregulation is common.

35th international symposium on intensive care and emergency medicine.

35th international symposium on intensive care and emergency medicine.

Transcranial Doppler-based assessment of cerebral autoregulation in critically ill children during diabetic ketoacidosis treatment.

Impaired cerebral autoregulation may be associated with poor outcome in diabetic ketoacidosis. We examined change in cerebral autoregulation during diabetic ketoacidosis treatment. Prospective observational cohort study. Tertiary care children's hospital. Children admitted to the ICU with diabetic ketoacidosis (venous pH < 7.3, glucose > 300 mg/dL, HCO3 < 15 mEq/L, and ketonuria) constituted cases, and children with type I diabetes without diabetic ketoacidosis constituted controls. None. Between 2005 and 2009, 32 cases and 50 controls were enrolled. Transcranial Doppler ultrasonography was used to measure middle cerebral artery flow velocities, and cerebral autoregulation testing was achieved via tilt-table testing. Cases underwent two and controls underwent one cerebral autoregulation test. Cerebral autoregulation was quantified by the autoregulatory index (autoregulatory index < 0.4 = impaired and autoregulatory index 0.4-1.0 = intact autoregulation). The first autoregulation test was obtained early (time 1, 12-24 hr; median [interquartile range], 8 hr [5-18 hr]) during diabetic ketoacidosis treatment, and a second autoregulation test was obtained during recovery (time 2, 36-72 hr; median [ interquartile range], 46 hr [40-59 hr]) from time 0 (defined as time of insulin start). Cases had lower autoregulatory index at time 1 than time 2 (p < 0.001) as well lower autoregulatory index than control subjects (p < 0.001). Cerebral autoregulation was impaired in 40% (n = 13) of cases at time 1 and in 6% (n = 2) of cases at time 2. Five cases (17%) showed persistent impairment of cerebral autoregulation between times 1 and 2 of treatment. All control subjects had intact cerebral autoregulation. Impaired cerebral autoregulation was common early during diabetic ketoacidosis treatment. Although the majority improved during diabetic ketoacidosis treatment, 17% of subjects had impairment between 36 and 72 hours after start of insulin therapy. The observed impaired cerebral autoregulation appears specific to the diabetic ketoacidosis process in patients with type I diabetes.

Young Age as a Risk Factor for Impaired Cerebral Autoregulation after Moderate to Severe Pediatric Traumatic Brain Injury

Little is known about age and cerebral autoregulation in children with traumatic brain injury (TBI). The authors compared cerebral autoregulation between young (aged <4 yr) and older (aged > or =4 yr) children with TBI. After University of Washington's institutional review board approval, a retrospective analysis of prospectively collected data (May 2002 and June 2007) was performed. Eligibility criteria included age 16 yr or younger, moderate to severe (admission Glasgow Coma Scale score <13) TBI, TBI on computed tomography scan, and tracheal intubation. Cerebral autoregulation testing was performed within 72 h after TBI, and autoregulation was quantified using the autoregulatory index. An autoregulatory index less than 0.4 represents impaired cerebral autoregulation. The 12-month Glasgow outcome score was measured. Data are presented as mean +/- SD or range. Thirty-seven children (8.9 +/- 5.1 yr; 0.8-16 yr) were enrolled. Children younger than 4 yr had a higher incidence of impaired cerebral autoregulation (8 of 10 vs. 7 of 27; P = 0.006) and worse 12-month outcome (Glasgow outcome score 3.0 +/- 1.0 vs. 4.0 +/- 1.0; P = 0.02) than older children. Age less than 4 yr (adjusted odds ratio, 12.2; 95% confidence interval, 1.5-98.5) and low Glasgow Coma Scale score (adjusted odds ratio for higher Glasgow Coma Scale, 0.53; 95% confidence interval, 0.30-0.96) were independently associated with impaired cerebral autoregulation. Age less than 4 yr was a risk factor for impaired cerebral autoregulation, independent of TBI severity. Age-related factors may play a role in the mechanisms maintaining or worsening cerebral autoregulation in children after TBI.

Hemispheric Differences in Cerebral Autoregulation in Children with Moderate and Severe Traumatic Brain Injury

To examine hemispheric differences in cerebral autoregulation in children with traumatic brain injury (TBI). After IRB approval and consent, subjects underwent static cerebral autoregulation testing during the first 9 days after PICU admission. Cerebral autoregulation was quantified using the autoregulatory index (ARI). Forty-two (27 M:15 F) children (10 +/- 5 years) with TBI and admission Glasgow coma scale score (5 +/- 2) were enrolled. Seven (54%) of the 13 children with focal TBI and 8 (28%) of 29 children with diffuse TBI had impairment or absence of cerebral autoregulation of at least one hemisphere. In patients with isolated focal TBI, ARI was lower (0.40 +/- 0.40 vs. 0.67 +/- 0.40; P = 0.03) in the side of TBI than in the unaffected hemisphere, but cerebral autoregulation was often impaired on the side without TBI or shift (5/13) on head CT. There was no difference in ARI between hemispheres in children with diffuse TBI, with or without superimposed focal lesions (P = 0.17). Patients with bilateral intact cerebral autoregulation tended to have higher 6 month Glasgow Outcome Score (GOS) than patients with either unilateral or bilateral cerebral autoregulation impairment (GOS 4.0 +/- 0.60 vs. 3.6 +/- 0.80; P = 0.08). Hemispheric differences in cerebral autoregulation were common in children with isolated focal TBI. Absence of TBI on CT was not always associated with intact cerebral autoregulation. Patients with bilaterally intact cerebral autoregulation tended to have better outcomes.

Early Childhood Gender Differences in Anterior and Posterior Cerebral Blood Flow Velocity and Autoregulation

We aimed to describe gender differences in blood flow velocity and autoregulation of the anterior and posterior cerebral circulations in prepubertal children. A prospective observational cohort study was performed at Harborview Medical Center's Cerebrovascular Laboratory after institutional review board approval, consent, and assent procedures. Children underwent measurement of middle cerebral and basilar artery flow velocities and cerebral autoregulation testing of the middle cerebral and basilar arteries. Cerebral autoregulation was quantified using the autoregulatory index, and estimated cerebrovascular resistance was calculated. Autoregulatory index <0.4 reflects impaired cerebral autoregulation. Data are presented as mean +/- SD. Patients were healthy 4- to 8-year-old children. Forty-eight children (24 boys and 24 girls) 4 to 8 years of age (mean: 6 +/- 2 years) were enrolled. Middle cerebral artery flow velocity was higher than basilar artery flow velocity (96 +/- 13 vs 65 +/- 11 cm/s). Girls had higher middle cerebral artery flow velocity (99 +/- 11 vs 91 +/- 13 cm/s) and basilar artery flow velocity (70 +/- 10 vs 61 +/- 9 cm/s) than boys. Cerebral autoregulation was intact in all children. There was no gender difference in autoregulation between the middle cerebral artery (boys: 0.97 +/- 0.07; girls: 0.94 +/- 0.11) or basilar artery (boys: 0.94 +/- 0.13; girls: 0.94 +/- 0.11). Similar to older children and adults, girls between 4 and 8 years of age had higher middle cerebral and basilar artery flow velocity than age-matched boys. This difference may reflect inherent differences in cerebral metabolic rate and/or estimated cerebrovascular resistance between the genders.

Recovery of the blood pressure – cerebral flow relation after carotid stenting in elderly patients

As a sensitive and convenient means for the cerebral hemodynamic monitoring, dynamic cerebral autoregulation testing could be especially useful in medical conditions where less invasive diagnostics and therapies are preferred. This study analysed the effect of carotid stenting on dynamic autoregulation in elderly patients focussing on the relation between blood pressure and cerebral blood flow velocity. We examined 20 patients age 69 +/- 8 years with coexisting cerebrovascular and medical risk factors before and at least six month after stenting of severe carotid stenoses. Data were compared to 24 age-matched healthy controls. Slow spontaneous oscillations were studied in continuous recordings of Transcranial Doppler and beat-to-beat blood pressure. Analysis was based on the "high-pass filter model", which predicts a positive phase relationship between these oscillations. Whereas phase shift angles were diminished (20.4 +/- 14.1 degrees ) before stenting, after stenting these values were significantly increased to normal (48.1 +/- 16.6 degrees ), to the level of controls (46.7 +/- 15.9 degrees ). Medical conditions such as coronary artery disease, arterial hypertension, and dyslipidemia did not diminish this recovery. The level of increase was inversely correlated with the initial autoregulatory deficit (r = -0.68) which was largest with insufficient collateral blood supply and symptomatic carotid stenoses. The study showed that an impaired cerebral autoregulation may recover after stent-guided carotid angioplasty even in the elderly with co-existing medical conditions. In this respect to regain vasomotor capability, patients with cerebrovascular risk factors seemed to benefit particularly.

Cerebral autoregulation in pediatric traumatic brain injury*

The aims of this study were to document the incidence of impaired cerebral autoregulation in children with traumatic brain injury using transcranial Doppler ultrasonography and to examine the relationship between autoregulatory capacity and outcome in children following traumatic brain injury. Prospective cohort study. Harborview Medical Center (level I pediatric trauma center) in Washington state. Thirty-six children <15 yrs old with traumatic brain injury: Glasgow Coma Scale score <9 (n = 12, group 1), Glasgow Coma Scale score 9-12 (n = 12, group 2), and Glasgow Coma Scale score 13-15 (n = 12, group 3). Cerebral autoregulation testing was conducted during extracranial surgery. Mean middle cerebral artery flow velocities were measured using transcranial Doppler as mean arterial pressure was increased to whichever variable was greater: 20% above baseline or a set value (80 mm Hg for <9 yrs and 90 mm Hg for 9-14 yrs). Autoregulatory capacity was quantified by the Autoregulatory Index. Autoregulatory Index <0.4 was considered impaired cerebral autoregulation. Discharge outcome using the Glasgow Outcome Scale score was considered good if the Glasgow Outcome Scale score was > or =4. Twenty-four (67%) of 36 children had an Autoregulatory Index > or =0.4. The incidence of impaired cerebral autoregulation was 42% (five of 12) in group 1, 42% (five of 12) in group 2, and 17% (two of 12) in group 3. Ten (42%) of the 24 children with intact cerebral autoregulation had a good outcome compared with only one of 12 (8%) children with impaired cerebral autoregulation (p =.04). Six of 12 (50%) children with impaired cerebral autoregulation had hyperemia compared with one of 24 (4%) children with intact cerebral autoregulation (p <.01). Hyperemia was associated with poor outcome (p =.01). The incidence of impaired cerebral autoregulation was greatest following moderate to severe traumatic brain injury. Impaired cerebral autoregulation was associated with poor outcome. Hyperemia was associated with impaired cerebral autoregulation and poor outcome.

The lower limit of cerebral autoregulation in children during sevoflurane anesthesia.

In adults, the lower limit of cerebral autoregulation (LLA) is generally considered to be a mean arterial pressure (MAP) of 60 mmHg. The LLA in healthy children has not been identified. The aim of this report is to describe the LLA in anesthetized children and relate it to age. Static cerebral autoregulation testing was performed in children 6 months to 14 years of age during <1 MAC sevoflurane anesthesia. Mean middle cerebral artery flow velocities (Vmca) were continuously measured using transcranial Doppler ultrasonography. MAP was increased with infusion of intravenous phenylephrine incrementally titrated to the greater of either: 1) 20% above baseline MAP or 2) 80 mmHg (<9 years), 90 mmHg (9-14 years). The LLA was defined by the point where the two linear regression lines fitting the Vmca/MAP crossed. The lower limit reserve (LLR) and autoregulatory reserve (ARR%) were defined as follows: LLR=Baseline MAP-LLA; ARR (%)=(LLR/Baseline MAP)x100. There were 13 subjects <2 years of age (group 1), 13 subjects 2 to 5 years of age (group 2), 14 subjects 6 to 9 years of age (group 3), and 13 subjects 10 to 14 years of age (group 4). Older children (groups 3 and 4) had a higher baseline MAP compared with younger children (groups 1 and 2) (82 +/- 10 mmHg vs. 70 +/- 10 mmHg, respectively; P=0.0001). However, there was no difference in LLA (59 +/- 17 mmHg vs. 60 +/- 8 mmHg; P=0.6) between older and younger children. Consequently, the LLR was greater in older children compared with younger children (25 +/- 12 mmHg vs. 12 +/- 10 mmHg, respectively; P=0.0007). Similarly, the ARR was significantly higher in older children compared with younger children (30% +/- 16% vs. 16% +/- 12%; P=0.002). In this study, we found no age-related differences in the LLA. Older children had a greater LLR and ARR compared with young children. The baseline MAP in young children may rest close to the LLA. These findings may have implications for managing hemodynamics in anesthetized children at risk for secondary brain injury.

Cerebral autoregulation in children during sevoflurane anaesthesia

Little is known about cerebral autoregulation in children. The aim of this study was to examine cerebral autoregulation in children. Cerebral autoregulation testing was performed during less than 1 MAC sevoflurane anaesthesia in children (from 6 months to 14 yr) and in adults (18-41 yr). Mean middle cerebral artery flow velocities (V(MCA)) were measured using transcranial Doppler ultrasonography. Mean arterial pressure (MAP) was increased to whichever was greater: 20% above baseline or (i) 80 mm Hg for less than 9 yr, (ii) 90 mm Hg for 9-14 yr, and (iii) 100 mm Hg for adults. Cerebral autoregulation was considered intact if the autoregulatory index was > or =0.4. There were 13 subjects less than 2 yr old (Group 1), 13 subjects 2-5 yr (Group II), 14 subjects 6-9 yr (Group III), 12 subjects 10-14 yr (Group IV), and 12 adults (Group V; control group). All subjects had an autoregulatory index > or =0.4. There was no difference in autoregulatory index between children in Groups I-IV or between children and adults. We found no age-related differences in autoregulatory capacity during low-dose sevoflurane anaesthesia. We report no differences in autoregulatory capacity between children and adults.

Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: the phase relationship between arterial blood pressure and cerebral blood flow velocity.

Impairment of cerebral autoregulation (CA) appears to be an important cause for secondary ischemia after subarachnoid hemorrhage (SAH). It has been shown that graded CA impairment is predictive of outcome. Little is known about whether such impairment is present, what causes CA impairment, whether it precedes vasospasm, and whether it is predictive of outcome in patients with severe aneurysmal SAH. Prospective, controlled study. Neurosurgical intensive care unit. Twelve patients after aneurysmal subarachnoid hemorrhage, 40 controls. Recording of cerebral blood flow velocities and continuous measurement of arterial blood pressure at a controlled ventilatory frequency of six per minute to standardize the influence of intrathoracic pressure changes on blood pressure. We calculated the phase shift angles (deltaphidegrees) between slow (0.1 Hz) arterial blood pressure and cerebral blood flow velocity waves measured by transcranial Doppler ultrasound in the middle cerebral artery during a) posthemorrhage days (PHD) 1-6 (early or prevasospasm phase), and b) during PHD 7-13 (late or vasospasm phase) using a 6/min ventilation protocol, and in 40 controls spontaneously ventilating at the same rate. deltaphi <30 degrees indicated lost CA. Mean flow velocities >100 cm/sec were considered vasospasm. We combined early and late measurements to assess the CA relationship with low cerebral perfusion pressure (CPP) and/or vasospasm. We assessed the Glasgow Outcome Scale (GOS) score at discharge (1 = worst, 5 = best). The admission Hunt and Hess score was 3.6 +/- 0.7. GOS scores were n = 3 (GOS 1), n = 2 (GOS 2), n = 5 (GOS 3), n = 1 (GOS 4), and n = 1 (GOS 5). In the early phase, deltaphi was 40.4 +/- 19.8 degrees (left), and 40.4 +/- 19.2 degrees (right). CPP was 69.4 +/- 10.9, intracranial pressure (ICP) was 6.7 +/- 2.8 mm Hg. In the late phase, deltaphi worsened in six patients and none improved: 32.1 +/- 21 degrees (left), and 26.9 +/- 17.2 degrees (right); CPP was 68.1 +/- 12.1, ICP was 7.5 +/- 3.7 mm Hg. CA was significantly impaired in both phases when compared with normal subjects (deltaphi: 65.7 +/- 24.5 degrees; p < .01 for early, p < .001 for late phase). In the early phase, seven of eight patients in whom autoregulation was intact had a GOS >2 at discharge and disturbed CA on at least one side was predictive of either vegetative condition at discharge or death (p < .01). In the late phase, deltaphi was no longer predictive of outcome. Spasm was present in 8 of 17 vessels (47%) in which CA was lost; no spasm was found in 25 of 28 vessels (89%) in which CA was intact (p < .01). A low CPP was present in 6 of 17 vessels (35%) in which CA was lost; a normal CPP was found in 21 of 27 vessels (78%) in which CA was intact (p > .05, NS). However, 14 of 17 vessels (82%) with lost CA showed spasm and/or low CPP while only 8 of 27 cases (30%) with intact CA had either spasm or low CPP (p < .001). CA can be assessed in a graded fashion in SAH patients. CA impairment precedes vasospasm; ongoing vasospasm worsens CA. CA assessment early after subarachnoid hemorrhage, within PHD 1-6, is predictive of outcome whereas late assessment is not. CA impairment is associated with cerebral vasospasm and low CPP.

Dynamic cerebral autoregulation testing as a diagnostic tool in patients with carotid artery stenosis

Evaluation of dynamic cerebral autoregulation might yield a physiologically more adequate measure of cerebral hemodynamic impairment in carotid artery stenosis than CO2-reactivity. This study re-evaluates and compares the Valsalva maneuver (VM) and phase shift during deep breathing. Nineteen patients with severe carotid artery stenosis and 17 age-matched controls were examined using transcranial Doppler sonography and non-invasive blood pressure recordings (Finapres). Phase shift was determined by crossspectral analysis, responses to VM were graded by the formerly-introduced autoregulation slope index (ASI) and the new Valsalva time index (VTI). Phase shift and autoregulatory indices were significantly reduced on the affected side (p < 0.001). Correlations with CO2-reactivity were significant when pooling values of controls and patients (r from 0.54 to 0.78; p < 0.001). Correlations except for the VTI (r = -0.65; p = 0.002) were not significant considering only the affected side in patients. Correlations of pooled values between phase shift and VM-derived indices were significant (VTI r = -0.62; p < 0.001; ASI r = 0.49; p < 0.001), within patients only when comparing side-to-side differences (VTI r= -0.58; p = 0.009; ASI r = 0.52; p = 0.023). In conclusion, detection of impaired cerebral autoregulation is possible both by deep breathing and VM. The new VTI seems to be more suitable than the conventional ASI. Inter-method agreement concerning the extent of impairment is only acceptable for intra-individual side-to-side differences. Since absolute values of one autoregulation testing method or CO2-reactivity alone might fail, various tests should be combined for comprehensive assessment of cerebral hemodynamic impairment. [Neurol Res 2001; 23: 55-63]

Effect of Pco 2 Changes Induced by Head-Upright Tilt on Transcranial Doppler Recordings

Transcranial Doppler (TCD) monitoring of mean blood flow velocity (mV) during head-upright tilt can allow testing of cerebral autoregulation. Nonetheless, head-upright tilt can induce changes in the ventilation-perfusion relationship and/or respiratory activity that might influence TCD data. Forty-eight healthy volunteers underwent monitoring of mV and end-tidal CO2 in the horizontal position and during head-upright tilt. Both mV and end-tidal CO2 significantly decreased in orthostasis (P < .01). Linear regression analysis showed a significant linkage between end-tidal CO2 and mV changes (r = .83, P < .01). Changes in ventilation-perfusion ratio and in the respiratory pattern induced by head-upright tilt can significantly influence TCD data by determining a PCO2 decrease.

Testing of cerebral autoregulation in head injury by waveform analysis of blood flow velocity and cerebral perfusion pressure.

Thirty five head injured patients were subjected to day-by-day monitoring of intracranial pressure (ICP), arterial blood pressure (ABP) and blood flow velocity (FV) in middle cerebral artery. Parameters describing cerebral autoregulation: flow velocity time average, systolic, diastolic values, pulsatility index (PI), estimate of cerebrovascular resistance (CVR = CPP/FV) etc. were analyzed as functions of CPP (ABP-ICP). The results show that for CPP below 55 mmHg the evidence of exhausted autoregulation can be observed in FV, CVR, PI. The method is helpful in assessment ot the optimal level of CPP in order to reduce the probability of ischaemic brain insults.