scholarly journals Optimal Cerebral Perfusion Pressure Guided by Brain Oxygen Pressure Measurement

Author(s):  
Matyas Kovacs ◽  
Lorenzo Peluso ◽  
Hassane Njimi ◽  
Olivier Dewitte ◽  
Elisa Bogossian ◽  
...  

Abstract BackgroundAlthough increasing cerebral perfusion pressure (CPP) is commonly accepted to improve brain tissue oxygen pressure (PbtO2), it remains unclear whether recommended CPP targets (i.e. > 60 mmHg) would result in adequate brain oxygenation in brain injured patients. The aim of this study was to identify the target of CPP associated with normal brain oxygenation. MethodsProspectively collected data including patients suffering from acute brain injury and monitored with PbtO2, in whom daily CPP challenge using vasopressors was performed. Initial CPP targets were >60 mmHg; norepinephrine infusion was modified to have an increase in CPP of at least 10 mmHg at two different steps above the baseline values. Whenever possible, the same CPP challenge was performed for the following days, for a maximum of 5 days. CPP “responders” were patients with a relative increase in PbtO2 from baseline values >20%.ResultsA total of 53 patients were included. On the first day of assessment, CPP was progressively increased from 73 [70-76] to 83 [80-86] and 92 [90-96] mmHg, which resulted into a significant PbtO2 increase (from 20 [17-23] mmHg to 22 [20-24] mmHg and 24 [22-26] mmHg, respectively; p<0.001). Median CPP value corresponding to PbtO2 values > 20 mmHg was 79 [74-87] mmHg, with 2 (4%) patients who never achieved such target. Similar results of CPP targets were observed the following days. A total of 25 (47%) were PbtO2 responders during the CPP challenge on day 1, in particular if low PbtO2 was observed at baseline. ConclusionsPbtO2 monitoring can be an effective way to individualize CPP values to avoid tissue hypoxia. Low PbtO2 values at baseline can identify the responders to the CPP challenge.

2021 ◽  
Vol 12 ◽  
Author(s):  
Matyas Kovacs ◽  
Lorenzo Peluso ◽  
Hassane Njimi ◽  
Olivier De Witte ◽  
Elisa Gouvêa Bogossian ◽  
...  

Background: Although increasing cerebral perfusion pressure (CPP) is commonly accepted to improve brain tissue oxygen pressure (PbtO2), it remains unclear whether recommended CPP targets (i. e., &gt;60 mmHg) would result in adequate brain oxygenation in brain injured patients. The aim of this study was to identify the target of CPP associated with normal brain oxygenation.Methods: Prospectively collected data including patients suffering from acute brain injury and monitored with PbtO2, in whom daily CPP challenge using vasopressors was performed. Initial CPP target was &gt;60 mmHg; norepinephrine infusion was modified to have an increase in CPP of at least 10 mmHg at two different steps above the baseline values. Whenever possible, the same CPP challenge was performed for the following days, for a maximum of 5 days. CPP “responders” were patients with a relative increase in PbtO2 from baseline values &gt; 20%.Results: A total of 53 patients were included. On the first day of assessment, CPP was progressively increased from 73 (70–76) to 83 (80–86), and 92 (90–96) mmHg, which resulted into a significant PbtO2 increase [from 20 (17–23) mmHg to 22 (20–24) mmHg and 24 (22–26) mmHg, respectively; p &lt; 0.001]. Median CPP value corresponding to PbtO2 values &gt; 20 mmHg was 79 (74–87) mmHg, with 2 (4%) patients who never achieved such target. Similar results of CPP targets were observed the following days. A total of 25 (47%) were PbtO2 responders during the CPP challenge on day 1, in particular if low PbtO2 was observed at baseline.Conclusions: PbtO2 monitoring can be an effective way to individualize CPP values to avoid tissue hypoxia. Low PbtO2 values at baseline can identify the responders to the CPP challenge.


2020 ◽  
pp. 3892-3897
Author(s):  
David K. Menon

Normal intracranial pressure is between 5 and 15 mm Hg in supine subjects. Intracranial hypertension (ICP >20 mm Hg) is common in many central nervous system diseases and in fatal cases is often the immediate cause of death. Increases in intracranial volume and hence—given the rigid skull—intracranial pressure may be the consequence of brain oedema, increased cerebral blood volume, hydrocephalus, and space-occupying lesions. Brain perfusion depends on the cerebral perfusion pressure which is mean arterial pressure minus intracranial pressure. The normal brain autoregulates cerebral blood flow down to a lower limit of cerebral perfusion pressure of about 50 mm Hg in healthy subjects, and perhaps 60–70 mm Hg in disease. Cerebral perfusion pressure reduction to below these values results in cerebral ischaemia.


1998 ◽  
Vol 26 (Supplement) ◽  
pp. 83A
Author(s):  
Alan H Tyroch ◽  
Krista L Kaups ◽  
Chester L Morris ◽  
Kenneth L Stewart ◽  
Ronna R Mallios

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