Using the relationship between brain tissue regional saturation of oxygen and mean arterial pressure to determine the optimal mean arterial pressure in patients following cardiac arrest: A pilot study
CCCF ePoster library. Bhate T. Oct 27, 2015; 117345; P59 Disclosure(s): Dr. Griesdale is supported by a VGH & UBC Hospital Best of Health Fund
Dr. Tahara Bhate
Dr. Tahara Bhate
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P59


Topic: Retrospective or Prospective Cohort Study


Using the relationship between brain tissue regional saturation of oxygen and mean arterial pressure to determine the optimal mean arterial pressure in patients following cardiac arrest: A pilot study



Tahara Bhate, M. Sekhon, P. Smielewski, P. Brasher, D. Foster, D. Menon, A. Gupta, M. Czosnky, K. Gin, G. Wong, D. Griesdale

Division of Critical Care, Dept of Medicine, Vancouver General Hospital, University of British Columbia, Vancouver, Canada | Division of Critical Care Medicine, Dept of Medicine, Vancouver General Hospital, University of British Columbia, Vancouver, Canada | Neurocritical Care Unit, Addenbrooke's Hospital, Cambridge University Hospitals Trust, Cambridge University, Cambridge, United Kingdom (Great Britain) | Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Insitute, Vancouver, Canada | Division of Critical Care Medicine, Dept of Medicine, Vancouver General Hospital, University of British Columbia, Vancouver, Canada | Neurocritical Care Unit, Addenbrooke's Hospital, Cambridge University Hospitals Trust, Cambridge University, Cambridge, United Kingdom (Great Britain) | Neurocritical Care Unit, Addenbrooke's Hospital, Cambridge University Hospitals Trust, Cambridge University, Cambridge, United Kingdom (Great Britain) | Neurocritical Care Unit, Addenbrooke's Hospital, Cambridge University Hospitals Trust, Cambridge University, Cambridge, United Kingdom (Great Britain) | Division of Cardiology, Dept of

Introduction: Hypoxic Ischemic Brain Injury (HIBI) is a major cause of morbidity and mortality following cardiac arrest1,2. HIBI is characterized by specific pathophysiology which includes elevated intracranial pressure (ICP), cerebral edema, and dysfunctional cerebral autoregulation3. Impaired cerebral autoregulation causes the autoregulatory zone to become narrowed and right shifted4, with important implications for mean arterial pressure (MAP) thresholds in post-arrest patients. Specifically, patients sustained at MAPs outside the autoregulatory range are at risk of secondary brain injury due to hypo or hyperperfusion. Similar impaired cerebral autoregulation is seen in traumatic brain injury (TBI) patients5. Invasive assessment of cerebral autoregulation in the TBI population has been used to determine patient specific optimal MAPs (MAPOPT), which are often greater than 80 or 90 mmHg6,7. Goal-directed hemodynamic targeting of these patient specific thresholds is associated with improved outcomes in TBI patients6, and offers alternative to the current American Heart Association (AHA) recommended uniform target MAP of >65mmHg in all post-arrest patients8.

Objectives: To assess the use of cerebral oximetry as a non-invasive measurement of cerebral autoregulation and MAPOPT in post-cardiac arrest patients, based on dynamic, real time fluctuations in regional brain oxygen saturation (rSO2) and MAP.

Methods: Prospective observational study in 20 patients admitted post-cardiac arrest. All patients underwent continuous rSO2 monitoring using the INVOS® cerebral oximeter and invasive intra-arterial MAP monitoring. ICM+® brain monitoring software is then used to calculate a real time cerebral oximetry index (COx), a moving Pearson correlation coefficient (value -1 to +1) between 30 consecutive, 10-sec averaged values of MAP and corresponding rSO2 signals. Positive correlation between rSO2 and MAP, where decreasing MAP leads to decreased rSO2, generates a positive COx value, with COx >0.3 considered indicative of dysfunctional autoregulation; negative COx values, generated when rSO2 remains constant with MAP fluctuation, indicate intact autoregulation. COx is plotted against MAP, and a U-shaped curve generated by ICM+®; MAPOPT is the nadir of this curve (see Figure 1).

Results: Patients underwent a median of 33 hours of monitoring (IQR 23-45.5) post-ROSC, with monitoring starting a median of 16.5 hours (IQR 9-19) after ROSC. Dysfunctional autoregulation (COx>0.3) was present 8.5% of the time (56 of 656 hourly measurements) across the cohort, an average of 11 ± 17% per patient. There was no relationship between COx and either MAP or end-tidal carbon dioxide (EtCO2) with iterative polynomial regression (p=0.33 and 0.23, respectively). Increasing COx was associated with increasing temperature on iterative polynomial regression (p<0.001) (See Figure 2). MAPOPT overall was generated for all 20 patients, and for 101 of 118 (85.6 %) 6 hour monitoring intervals. The mean MAP and MAPOPT were 76 ± 11 mmHg and 76 ± 9 mmHg respectively. However, MAP differed from MAPOPT by >5mmHg 47 ± 21% of time, per patient. Figure 3 displays the density of differences between MAP and MAPOPT across the cohort.

Conclusion: We demonstrated the ability to assess cerebral autoregulation and determine patient specific MAPOPT using cerebral oximetry in patients after cardiac arrest. This study justifies further observational work to examine the relationship between cerebral autoregulation and COx, time-within MAPOPT ranges, and neurological outcomes.

References: 1. Lemiale V, Dumas F, Mongardon N, et al. Intensive care unit mortality after cardiac arrest: the relative contribution of shock and brain injury in a large cohort. Intensive Care Med 2013;39(11):1972–80.

2. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med 2004;30(11):2126–8.


3. Nolan JP, Neumar RW, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Coun. Resuscitation 2008;79(3):350–79.


4. Sundgreen C, Larsen FS, Herzog TM, Knudsen GM, Boesgaard S, Aldershvile J. Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest. Stroke 2001;32(1):128–32.


5. Steiner L a, Coles JP, Johnston AJ, et al. Assessment of cerebrovascular autoregulation in head-injured patients: a validation study. Stroke 2003;34(10):2404–9.


6. Aries MJH, Czosnyka M, Budohoski KP, et al. Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit Care Med 2012;40(8):2456–63.


7. Griesdale DEG, Ortenwall V, Norena M, et al. Adherence to guidelines for management of cerebral perfusion pressure and outcome in patients who have severe traumatic brain injury. J Crit Care 2015;30(1):111–5.


8. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 Suppl 3):S768–86.
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