EVALUATION OF A NONINVASIVE TRANSCRANIAL DOPPLER AND BLOOD PRESSURE-BASED METHOD FOR THE ASSESSMENT OF CEREBRAL PERFUSION PRESSURE IN PREGNANT WOMEN

2000 ◽  
Vol 19 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Michael A. Belfort ◽  
Cathy Tooke-Miller ◽  
Michael Varner ◽  
George Saade ◽  
Charlotta Grunewald ◽  
...  
2001 ◽  
Vol 20 (1) ◽  
pp. 139-140
Author(s):  
Michael A. Belfort ◽  
Cathy Tooke-Miller ◽  
Michael Varner ◽  
George Saade ◽  
Charlotta Grunewald ◽  
...  

2001 ◽  
Vol 20 (1) ◽  
pp. 139-140
Author(s):  
Michael A. Belfort ◽  
Cathy Tooke-Miller ◽  
Michael Varner ◽  
George Saade ◽  
Charlotta Grunewald ◽  
...  

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.


1999 ◽  
Vol 91 (1) ◽  
pp. 127-130 ◽  
Author(s):  
Pekka Talke ◽  
James E. Caldwell ◽  
Charles A. Richardson

Background The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. Results Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. Conclusions Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245291
Author(s):  
Alexander Ruesch ◽  
Deepshikha Acharya ◽  
Samantha Schmitt ◽  
Jason Yang ◽  
Matthew A. Smith ◽  
...  

The brain’s ability to maintain cerebral blood flow approximately constant despite cerebral perfusion pressure changes is known as cerebral autoregulation (CA) and is governed by vasoconstriction and vasodilation. Cerebral perfusion pressure is defined as the pressure gradient between arterial blood pressure and intracranial pressure. Measuring CA is a challenging task and has created a variety of evaluation methods, which are often categorized as static and dynamic CA assessments. Because CA is quantified as the performance of a regulatory system and no physical ground truth can be measured, conflicting results are reported. The conflict further arises from a lack of healthy volunteer data with respect to cerebral perfusion pressure measurements and the variety of diseases in which CA ability is impaired, including stroke, traumatic brain injury and hydrocephalus. To overcome these differences, we present a healthy non-human primate model in which we can control the ability to autoregulate blood flow through the type of anesthesia (isoflurane vs fentanyl). We show how three different assessment methods can be used to measure CA impairment, and how static and dynamic autoregulation compare under challenges in intracranial pressure and blood pressure. We reconstructed Lassen’s curve for two groups of anesthesia, where only the fentanyl anesthetized group yielded the canonical shape. Cerebral perfusion pressure allowed for the best distinction between the fentanyl and isoflurane anesthetized groups. The autoregulatory response time to induced oscillations in intracranial pressure and blood pressure, measured as the phase lag between intracranial pressure and blood pressure, was able to determine autoregulatory impairment in agreement with static autoregulation. Static and dynamic CA both show impairment in high dose isoflurane anesthesia, while low isoflurane in combination with fentanyl anesthesia maintains CA, offering a repeatable animal model for CA studies.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Minjung K Chae ◽  
Sung Eun Lee ◽  
Sumin Cho ◽  
Taeyoung Kim ◽  
Dukyong Yoon

Introduction: Hypoxic ischemic brain injury (HIBI) is the leading cause of mortality and long-term neurologic disability in survivors of cardiac arrest. Recently, the role of cerebral monitoring is emphasized for individualizing therapy and mitigating secondary brain injury in HIBI patients after return of spontaneous circulation (ROSC). The first step of cerebral monitoring is checking the driving force by cerebral perfusion pressure (CPP). However, as CPP is calculated by mean arterial pressure (MAP) minus intracranial pressure (ICP), the process of obtaining ICP is invasive. Noninvasive CPP can be estimated by parameters obtained from transcranial doppler (TCD). Therefore, we aimed to investigate non-invasively measured CPP from TCD and its association with neurologic outcome in post cardiac arrest patients that underwent targeted temperature management (TTM). Methods: This retrospective single-center study included patients who had been treated with TTM following cardiac arrest and who underwent TCD evaluation between July 2017 and July 2019. We aimed to perform TCD evaluation within 48h of ROSC, but sometimes this could not be achieved due to limited resources. Patients with TCD that was performed after 72 hours were excluded. The MFV was calculated using the peak systolic flow velocity (PSV) and the end-diastolic flow velocity (EDV) as below. Two methods of estimating CPP non-invasively was calculated as below.MFV = PSV+(EDVх2) / 3 eCPP_A= MAP*diastolic FVmca/MFVmca + 14eCPP_B= MFVmca*(MAP-DBP)/FVmean-FVdia Results: Table 1. Baseline characteristics of study population Data are presented as mean (standard deviation), number (%) or median (interquartile range).OHCA, out of hospital cardiac arrest; CPR, cardiopulmonary resuscitation; AED, automated external defibrillator; TCD, transcranial doppler; CPP, cerebral perfusion pressure. Table 2. Cut off values and diagnostic values in predicting poor neurologic outcome with 100% specificityCPP, cerebral perfusion pressure. Conclusion: eCPP cut off values of <50 mmHg and <60mmHg predicted poor neurological outcome with high specificity. This study suggests that eCPP obtained from TCD may be feasible to predict neurologic outcome.


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