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A Comparison of Clinical and Research Practices in Measuring Cerebral Perfusion Pressure: A Literature Review and Practitioner Survey

Kosty, Jennifer A. MD*; LeRoux, Peter D. MD, FACS; Levine, Joshua MD; Park, Soojin MD; Kumar, Monisha A. MD; Frangos, Suzanne RN; Maloney-Wilensky, Eileen CRNP; Kofke, W. Andrew MD, MBA, FCCM§

doi: 10.1213/ANE.0b013e31829cc765
Neuroscience in Anesthesiology and Perioperative Medicine: Brief Report
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BACKGROUND: Our objective was to determine whether there is variability in the foundational literature and across centers in how mean arterial blood pressure is measured to calculate cerebral perfusion pressure.

METHODS: We reviewed foundational literature and sent an e-mail survey to members of the Neurocritical Care Society.

RESULTS: Of 32 articles reporting cerebral perfusion pressure data, the reference point for mean arterial blood pressure was identified in 16: 10 heart and 6 midbrain. The overall survey response rate was 14.3%. Responses from 31 of 34 (91%) United Council for Neurologic Subspecialties fellowship-accredited Neurointensive Care Units indicated the reference point was most often the heart (74%), followed by the midbrain (16%). Conflicting answers were received from 10%.

CONCLUSIONS: There is substantive heterogeneity in both research reports and clinical practice in how mean arterial blood pressure is measured to determine cerebral perfusion pressure.

Published ahead of print August 6, 2013

From the *Perelman School of Medicine; and Departments of Neurosurgery, Neurology, and §Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, Pennsylvania.

Accepted for publication April 27, 2013.

Published ahead of print August 6, 2013

Jennifer A. Kosty, MD, is currently affiliated with the Department of Neurosurgery, University of Cincinnati, Cincinnati, Ohio.

Funding: Institutional support.

Conflict of Interest: See Disclosures at the end of the article.

Reprints will not be available from the authors.

Address correspondence to W. Andrew Kofke, MD, MBA, FCCM, Department of Anesthesiology and Critical Care, University of Pennsylvania, 7 Dulles Bldg., 3400 Spruce St., Philadelphia, PA 19104. Address e-mail to kofkea@uphs.upenn.edu.

In 1959, Lassen1 defined cerebral perfusion pressure (CPP) based on “arterial blood pressure measured at the level of the head,” i.e., the midbrain, using the tragus as an external landmark. However, mean arterial blood pressure (MAP) also is commonly measured at the right atrium (RA). When the head of the bed is elevated 50°, MAP measured at the RA may be higher than that measured at the level of the tragus by up to 18 mm Hg, thereby overestimating actual CPP.2 This MAP difference could be even further exaggerated with higher elevation of the head of the bed or in very tall patients.

The difference in pressure between the RA and tragus may be important when CPP with head elevation is managed near the minimum suggested by the Brain Trauma Foundation (BTF), i.e., 60 mm Hg, with an unspecified reference point.3 Some authors have also suggested that the lower limit of autoregulation in normal humans, previously thought to be near 50 mm Hg,1 may actually be up to 20 mm Hg higher.4 If this is the case, differences in the reference point for calculating MAP may lead to clinically significant differences in cerebral perfusion. We, therefore, sought to ascertain the extent of heterogeneity in foundational research publications and in clinical practice in the calculation of CPP.

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METHODS

The 3rd edition of the BTF’s “Guidelines for the management of severe traumatic brain injury” chapters on (I) Blood Pressure and Oxygenation,5 (VI) Indications for Intracranial Pressure Monitoring,6 (VIII) Intracranial Pressure Thresholds,7 (IX) Cerebral Perfusion Thresholds,8 and (X) Brain Oxygen Monitoring and Thresholds9 were reviewed for cited publications in which CPP was measured. In addition, the Cochrane Library was queried using the search terms “cerebral perfusion pressure,” and “CPP,” and the reference sections of the articles that were returned were examined for additional publications, using the inclusion criterion that CPP was measured as a dependent variable. The methods of all included articles were reviewed to determine whether MAP was referenced to the tragus or RA when calculating CPP. If the reference point was not explicitly described, an effort was made to contact one of the authors.

A nonanonymous survey was also sent by electronic mail to members of the Neurocritical Care Society (NCS) asking whether the MAP measurement used to calculate CPP was taken relative to the tragus or the RA. Informed consent was not required according to IRB standards for this study because participants did not meet criteria as human subjects. The responses to these questions were tallied according to individual member, professional degree, and country. Institution was ascertained in a post hoc manner using the NCS membership directory. This allowed representatives from the U.S.-based United Council for Neurologic Subspecialities (UCNS) fellowship-accredited neurological intensive care unit (neuroICUs) to be identified. We evaluated for trends between reference point and professional degree or country (United States versus non-United States), as well as an interaction between these 2 variables using analysis of variance (SPSS Inc., Chicago, IL).

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RESULTS

Review of Literature

One hundred twenty-seven articles that were eligible for inclusion were identified in the 5 aforementioned chapters of the 3rd edition of BTF “Guidelines.” Two review articles in the Cochrane database were identified.10,11 The reference sections of these articles yielded an additional 47 articles for review. From these 174 articles, 32 met our inclusion criteria. Ultimately, we were able to determine how MAP was measured when calculating CPP in 50% (16 of 32) of these articles: in 38% (6 of 16), MAP was referenced to the tragus12–17 and in 62% (10 of 16), it was referenced to the RA.18–27 These data are summarized in Table 1. Authors from the remaining 16 references could not be contacted or did not recall the CPP measurement method used.28–43

Table 1

Table 1

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Survey

Among the 1680 NCS members who received our survey, 14.3% (241) responded, including representatives from 91% (31 of 34) of UCNS-accredited neuroICUs. The distribution of respondents by professional degree and country of origin are listed in Table 2. Among all respondents, 59% (142 of 241) measured CPP with reference to the RA and 41% (99 of 241) with reference to the tragus. At 74% (23 of 31) of represented UCNS-accredited neuroICUs, MAP was measured at the RA, and, at 16% (5 of 31), it was measured at the tragus. Conflicting responses were received from different members of 10% (3 of 31) of the neuroICUs. Neither were significant trends identified related to response and professional degree or country of origin nor was a significant interaction identified between these 2 variables. Institutional data were not available for all respondents; however, the majority of participants for which this information was available represented academic institutions. No significant trend was seen on this basis in practice.

Table 2

Table 2

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CONCLUSIONS

This survey of the research publications on which clinical practice is based and actual clinical practice indicate significant heterogeneity in clinical practice and in research reports describing or not describing how MAP is measured to determine CPP.

It is notable that some respondents from the same institution gave conflicting responses. This is worrisome because it creates some concern as to whether many physicians in intensive care units, in making CPP-based decisions, really know how CPP is measured in their patients. Alternatively, independent providers may just prefer different methods of measuring CPP.

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CPP Measurement in the Sitting Position

In the sitting position, 50° head-of-bed elevation leads to up to an 18 mm Hg difference in MAP measured at the level of the tragus compared with the level of the RA.2 Failure to appreciate this concept can produce devastating consequences. In neuroanesthesia, it is standard practice during sitting craniotomies to place the blood pressure transducer at the level of the head.44 In the mid-20th century, hypotension to an MAP of 50 mm Hg, the traditionally acknowledged lower limit of cerebrovascular autoregulation, was induced during some neurosurgical procedures, including those in a sitting position. This would likely have produced cerebral hypoperfusion and injury had the blood pressure transducer been placed at the level of the heart, considering that MAP at the midbrain may be 20 mm Hg lower than the heart in the sitting position, and at the superior level of the cortex an additional 10 mm Hg lower still. Such low CPPs may be tolerated by some individuals with adequate cerebrovascular reserve or when surgery is of short duration, but there have been reports of iatrogenic stroke in patients operated on in the seated position when hypotension has been induced with MAP monitored at the arm or leg.45,46 Clinicians treating patients with severe traumatic brain injury (TBI), who are often hypotensive and managed in a head elevated position, should therefore consider this difference in arterial blood pressure measured at the RA versus the tragus.

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The Implications of Our Findings

These unmeasured, but clinically significant, differences in CPP due to the method used for determining MAP may help explain the difficulty multicenter TBI trials have had in demonstrating the benefit of a specific therapy.47 Although a full 90° sitting position is used rarely in the care of patients with severe TBI, a head-of-bed elevation of 30° to 50° is common. Therefore, a reported CPP of 60 mm Hg may vary from a true head-level value of 43 to 60 mm Hg, depending on reference point, head-of-bed elevation, and height of the patient. This added variability might have affected patient outcomes and conceal treatment effects in clinical research trials.

There are several limitations to this study, most notably a 14% overall response rate. Because the survey was sent to the NCS, an international multidisciplinary organization, participants represented various training backgrounds and nationalities, though 74% of responses were from practitioners in the United States, and 73% were medical doctors. We opened the survey to all members to evaluate whether there were differences in practice based on professional degree and country of origin, but found no trends. We do not intend this communication to be a rigorously quantitative evaluation of worldwide practices in CPP measurement. Rather, it is meant to highlight the frequently overlooked principle that CPP experienced at the level of the midbrain often differs, sometimes substantially, from that reported at the level of the heart; that the obviation of this difference by monitoring CPP at the level of the head is a minority practice among respondents; and that this heterogeneity in clinical measurement may affect patient and research outcomes in underappreciated ways.

We suggest that there is a need to standardize CPP measurement practices both in clinical practice and in research publications to avoid potentially deleterious consequences, especially in patients with severe neurologic injuries who may be particularly dependent on appropriate CPP to maintain adequate cerebral blood flow.

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DISCLOSURES

Name: Jennifer A. Kosty, MD.

Contribution: This author participated in design of the study, conducted the study, collected the data, and preparation of the manuscript.

Attestation: Jennifer Kosty approved the final manuscript and attests to the integrity of the original data and the analysis reported in this manuscript. Jennifer Kosty is the archival author.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Peter D. LeRoux, MD, FACS.

Contribution: This author participated in design of the study, interpretation of data analysis, and preparation of the manuscript.

Attestation: Peter LeRoux approved the final manuscript and attests to the analysis reported in this manuscript.

Conflicts of Interest: Dr. LeRoux has been a consultant for Integra, Neurologica, and Codman.

Name: Joshua Levine, MD.

Contribution: Joshua Levine participated in interpretation of the data and preparation of the manuscript.

Attestation: Joshua Levine approved the final manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Soojin Park, MD.

Contribution: Soojin Park participated in interpretation of the data and preparation of the manuscript.

Attestation: Soojin Park approved the final manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Monisha A. Kumar, MD.

Contribution: Monisha Kumar participated in interpretation of the data and preparation of the manuscript.

Attestation: Monisha Kumar approved the final manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Suzanne Frangos, RN.

Contribution: Suzanne Frangos participated in interpretation of the data, IRB communications, and preparation of the manuscript.

Attestation: Suzanne Frangos approved the final manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Eileen Maloney-Wilensky, CRNP.

Contribution: Eileen Maloney-Wilensky participated in preparation of the manuscript.

Attestation: Eileen Maloney-Wilensky approved the final manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: W. Andrew Kofke, MD, MBA, FCCM.

Contribution: W. Andrew Kofke participated in study conception, design of the study, analysis of the data, interpretation of the data, and manuscript preparation.

Attestation: W. Andrew Kofke approved the final manuscript and attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

This manuscript was handled by: Gregory J. Crosby, MD.

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