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Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

ABSTRACT: 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, dopamine-induced 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.

SUBMITTER: Bragin DE

PROVIDER: S-EPMC6395276 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature

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Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

Bragin Denis E DE Statom Gloria L GL Yonas Howard H Dai Xingping X Nemoto Edwin M EM

Critical care medicine 20141201 12

<h4>Objectives</h4>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 incr ...[more]

PMID: 25289933

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Project description:OBJECTIVE:Cerebrovascular reactivity (CR) is a mechanism that maintains stable blood flow supply to the brain. Pressure reactivity index (PRx), the correlation coefficient between slow waves of invasive arterial blood pressure (ABP) and intracranial pressure (ICP) has been validated for CR assessment. However, in clinical ward, not every subarachnoid hemorrhage (SAH) patient has invasive ABP monitoring. Pulse transit time (PTT), the propagation time of a pulse wave travelling from the heart to peripheral arteries, has been suggested as a surrogate measure of ABP. In this study, we proposed to use PTT instead of invasive ABP to monitor CR. APPROACH:Forty-five SAH patients with simultaneous recordings of invasive ABP, ICP, oxygen saturation level (SpO2) and electrocardiograph (ECG) were included. PTT was calculated as the time from the ECG R-wave peak to the onset of SpO2. PTT based pressure reactivity index (tPRx) was calculated as the correlation coefficient between slow waves of PTT and ICP. Wavelet tPRx (wtRx) was calculated as the cosine of wavelet phase shift between PTT and ICP. Meanwhile, PRx and wPRx were also calculated using invasive ABP and ICP as input. MAIN RESULTS:The result showed a negative relationship between PTT and ABP (r??=??-0.58, p???<??0.001). tPRx negatively correlated with PRx (r??=??-0.51, p???=??0.003). Wavelet method correlated well with correlation method demonstrated through positive relationship between wPRx and PRx (r??=??0.82, p???<??0.001) as well as wtPRx and tPRx (r??=??0.84, p???<??0.001). SIGNIFICANCE:PTT demonstrates great potential as a useful tool for CR assessment when invasive ABP is unavailable. Key points • Pulse transit time (PTT), defined as the propagation time of a pulse wave travelling from the heart to the peripheral arteries, has been proposed as a surrogate measure of ABP. The relationship between PTT and ABP in SAH patients remains unknown. • Cerebrovascular reactivity (CR) assessment through PTT has advantages over invasive ABP, as it avoids bleeding and infection risk, and can be used outside of the ICU. • We introduced a new method to assess CR using PTT and ICP through correlation based method and wavelet based method. • We found that beat-to-beat PTT was negatively related with invasive ABP in SAH patients. A significant linear relationship exists between PTT-based CR parameter and a well validated method, PRx. PTT demonstrates great potential as a useful tool for CR assessment when invasive ABP is unavailable in SAH patients.

Project description:Introduction: We investigated the effect of hematoma volume reduction with minimally invasive surgery (MIS) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patients with large spontaneous intracerebral hemorrhage (ICH). Methods: Post-hoc analysis of the Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation (MISTIE III) study, a clinical trial with blinded outcome assessments. The primary outcome was the proportion of ICP readings ≥20 and 30 mmHg, and CPP readings <70 and 60 mm Hg. Secondary outcomes included major disability (modified Rankin scale >3) and mortality at 30 and 365 days. We assessed the relationship between proportion of high ICP and low CPP events and MIS using binomial generalized linear models, and outcomes using multiple logistic regression. Results: Of 499 patients enrolled in MISTIE III, 72 patients had guideline based ICP monitors placed, 34 in the MIS group and 38 in control (no surgery) group. Threshold ICP and CPP events ≥20/ <70 mmHg occurred in 31 (43.1%) and 52 (72.2%) patients respectively. On adjusted analyses, proportion of ICP readings ≥20 and 30 mmHg were significantly lower in the MIS group vs. control group [Odds Ratio (OR) 0.27, 95% Confidence Interval [CI] 0.11-0.63 (p = 0.002); OR = 0.18, 0.04-0.75, p = 0.02], respectively. Proportion of CPP readings <70 and 60 mm Hg were also significantly lower in MIS patients [OR 0.31, 95% CI 0.15-0.63 (p = 0.001); OR 0.30, 95% CI 0.11-0.83 (p = 0.02)], respectively. Higher proportions of CPP readings <70 and 60 mm were significantly associated with short term mortality (p = 0.04), and (p = 0.006), respectively. Long term mortality was significantly associated with higher proportion of time with ICP ≥ 20 (p = 0.04), ICP ≥ 30 (p = 0.04), and CPP <70 mmHg (p = 0.01). Conclusion: Our results are consistent with the hypothesis that surgical reduction of ICH volume decreases proportion of high ICP and low CPP events and that these variables are associated with short- and long-term mortality.

Project description:ObjectivesTargets for treatment of raised intracranial pressure or decreased cerebral perfusion pressure in pediatric neurocritical care are not well defined. Current pediatric guidelines, based on traumatic brain injury, suggest an intracranial pressure target of less than 20 mm Hg and cerebral perfusion pressure minimum of 40-50 mm Hg, with possible age dependence of cerebral perfusion pressure. We sought to define intracranial pressure and cerebral perfusion pressure thresholds associated with inhospital mortality across a large single-center pediatric neurocritical care cohort.DesignRetrospective chart review.SettingPICU, single quaternary-care center.PatientsIndividuals receiving intracranial pressure monitoring from January 2012 to December 2016.InterventionsNone.Measurements and main resultsIntracranial pressure and cerebral perfusion pressure measurements from 262 neurocritical care patients (87 traumatic brain injury and 175 nontraumatic brain injury; 63% male; 8.3 ± 5.8 yr; mortality 11.1%). Mean intracranial pressure and cerebral perfusion pressure had area under the receiver operating characteristic curves of 0.75 and 0.64, respectively, for association of inhospital mortality. Cerebral perfusion pressure cut points increased with age (< 2 yr = 47, 2 to < 8 yr = 58 mm Hg, ≥ 8 yr = 73 mm Hg). In the traumatic brain injury subset, mean intracranial pressure and cerebral perfusion pressure had area under the receiver operating characteristic curves of 0.70 and 0.78, respectively, for association of inhospital mortality. Traumatic brain injury cerebral perfusion pressure cut points increased with age (< 2 yr = 45, 2 to < 8 yr = 57, ≥ 8 yr = 68 mm Hg). Mean intracranial pressure greater than 15 mm Hg, male sex, and traumatic brain injury status were independently associated with inhospital mortality (odds ratio, 14.23 [5.55-36.46], 2.77 [1.04-7.39], and 2.57 [1.03-6.38], respectively; all p < 0.05). Mean cerebral perfusion pressure less than 67 mm Hg and traumatic brain injury status were independently associated with inhospital mortality (odds ratio, 5.16 [2.05-12.98] and 3.71 [1.55-8.91], respectively; both p < 0.01). In the nontraumatic brain injury subset, mean intracranial pressure had an area under the receiver operating characteristic curve 0.77 with an intracranial pressure cut point of 15 mm Hg, whereas mean cerebral perfusion pressure was not predictive of inhospital mortality.ConclusionsWe identified mean intracranial pressure thresholds, utilizing receiver operating characteristic and regression analyses, associated with inhospital mortality that is below current guidelines-based treatment targets in both traumatic brain injury and nontraumatic brain injury patients, and age-dependent cerebral perfusion pressure thresholds associated with inhospital mortality that were above current guidelines-based targets in traumatic brain injury patients. Further study is warranted to identify data-driven intracranial pressure and cerebral perfusion pressure targets in children undergoing intracranial pressure monitoring, whether for traumatic brain injury or other indications.

Project description:BackgroundCerebrovascular reactivity has been identified as a key contributor to secondary injury following traumatic brain injury (TBI). Prevalent intracranial pressure (ICP) based indices of cerebrovascular reactivity are limited by their invasive nature and poor spatial resolution. Fortunately, interest has been building around near infrared spectroscopy (NIRS) based measures of cerebrovascular reactivity that utilize regional cerebral oxygen saturation (rSO2) as a surrogate for pulsatile cerebral blood volume (CBV). In this study, the relationship between ICP- and rSO2-based indices of cerebrovascular reactivity, in a cohort of critically ill TBI patients, is explored using classical machine learning clustering techniques and multivariate time-series analysis.MethodsHigh-resolution physiologic data were collected in a cohort of adult moderate to severe TBI patients at a single quaternary care site. From this data both ICP- and rSO2-based indices of cerebrovascular reactivity were derived. Utilizing agglomerative hierarchical clustering and principal component analysis, the relationship between these indices in higher dimensional physiologic space was examined. Additionally, using vector autoregressive modeling, the response of change in ICP and rSO2 (ΔICP and ΔrSO2, respectively) to an impulse in change in arterial blood pressure (ΔABP) was also examined for similarities.ResultsA total of 83 patients with 428,775 min of unique and complete physiologic data were obtained. Through agglomerative hierarchical clustering and principal component analysis, there was higher order clustering between rSO2- and ICP-based indices, separate from other physiologic parameters. Additionally, modeled responses of ΔICP and ΔrSO2 to impulses in ΔABP were similar, indicating that ΔrSO2 may be a valid surrogate for pulsatile CBV.ConclusionsrSO2- and ICP-based indices of cerebrovascular reactivity relate to one another in higher dimensional physiologic space. ΔICP and ΔrSO2 behave similar in modeled responses to impulses in ΔABP. This work strengthens the body of evidence supporting the similarities between ICP-based and rSO2-based indices of cerebrovascular reactivity and opens the door to cerebrovascular reactivity monitoring in settings where invasive ICP monitoring is not feasible.

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Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

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Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

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