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Management of Cerebral Perfusion in Patients under General Anesthesia

This study investigates the effect of phenylephrine on cerebral perfusion in adult patients under anesthesia. The findings suggest that phenylephrine decreases cerebral oxygen saturation and may have a paradoxical effect on cerebral perfusion. Clinical pearls and limitations of the study are discussed.

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Management of Cerebral Perfusion in Patients under General Anesthesia

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  1. Management of Cerebral Perfusion in Patients under General Anesthesia Sandra Larson PhD, CRNA, APN, FNAP

  2. I have no financial relationship with any commercial interest related to the content of this activity. Conflict of Interest Disclosure Statement

  3. Joanna Briggs Approved Systematic Review Protocol

  4. Objective To synthesize best available evidence on the effect of phenylephrine on cerebral perfusion when used to treat anesthesia induced hypotension (AIH)

  5. PICO Question What is the effect of phenylephrine on cerebral perfusion in adult patients under anesthesia? P = Adult patients, + anesthesia I = Phenylephrine C = Not phenylephrine O = MCAv, COS, EEG

  6. Search Strategy • JBI method: • initial search and analysis of keywords and subject headings found in results, • a second, more thorough search using the identified terms, • a final search of references found in identified studies (pearl-growing). • Databases searched: • MEDLINE, EMBASE, CINAHL, Trip Database, PsycINFO (published literature). • Google Scholar, Mednar, Grey Literature Report, and ProQuest (grey/unpublished literature). Search terms: “Phenylephrine,”“Vasoconstrictor agents,”“Cerebral oxygen saturation,”“Cerebral perfusion,”“Cerebral blood flow,”“Cerebral circulation,”“Cerebrovascular circulation,”“Cerebral autoregulation,”“Cerebral desaturation event,”“Cerebral ischemia,”“Beach chair position,”“Sitting position,” and “patient positioning.” Results: 14 articles met inclusion criteria of which 8 involved anesthetized patients and 6 involved awake subjects.

  7. How familiar are you with cerebral oximetry technology? • Very familiar, use it routinely • Familiar, use it occasionally • Familiar, but it is not available • No clue 

  8. In your routine anesthesia practice, which drug do you prefer for treating AIH? • Phenylephrine • Ephedrine

  9. What percent of the time do you use phenylephrine to treat AIH? • 0-25% • 26-50% • 51-75% • 76-100%

  10. Purpose: To investigate the effect of phenylephrine and ephedrine on frontal lobe cerebral oxygen saturation (COS) when used to correct AIH.

  11. Findings Phenylephrine (PE) Ephedrine (EPH) EPH increased MAP (p < 0.001) EPH preserved a normal COS (p > 0.05) EPH restored CO to baseline (p < 0.001) • PE increased MAP (p < 0.001) • PE decreased COS by 14% (p < 0.05). • PE maintained the decreased CO (p > 0.05) There was a slight increase in COS, in both groups, following induction despite AIH (1.0 FIO2 & decreased CMR). Nissen, P., et al. Neurocrit Care, 2010, 12:17-23

  12. Clinical Pearls: • EPH outpaced PE in its ability to increase SV & CO • EPH outpaced PE in its ability to preserve normal COS values. • Based solely on this study, could we argue EPH is the preferred vasoactive agent for treating AIH? • Based solely on this study, could we argue healthy subjects easily tolerate a MAP of 50 mmHg under GET in the supine position breathing 70% oxygen? • Nissen, P., et al. Neurocrit Care, 2010, 12:17-23

  13. Limitations • TIVA, female, PS I-II • Accuracy of CO measurement (Finometer) • Timing of the COS measurement • Pooled vs. individual patient data Nissen, P., et al. Neurocrit Care, 2010, 12:17-23

  14. (1997). Anesthesiology, 86(6) 1431-1433 • Average LLA in humans is closer to 70 mmHg • The AR curve, with its plateau between 50-150 and sharp inflection points, represents statistical averaging. • Enormous individual to individual variability

  15. Purpose • To investigate the effect of PE & EPH on COS in anesthetized patients • To identify the physiological variables that are responsible for the change in COS.

  16. Findings (1st Treatment) Phenylephrine (PE) Ephedrine (EPH) EPH preserved CO (p > 0.05) EPH preserved COS (p > 0.05) • PE decreased CO (-32%; p< 0.001) • PE decreased COS (-7.1%; p < 0.01) • Changes in COS correlated with changes in CO (R2 = .74; p < 0.001) • Changes in COS did not correlate with changes in MAP (p > 0.05) Meng, L. et al, BJA 107(2):209-17 (2011)

  17. PHENYLEPHRINE EPHEDRINE

  18. PHENYLEPHRINE EPHEDRINE

  19. Clinical Pearls: • EPH outpaced PE in preserving tissue perfusion. • Autoregulation is more complex than classic thinking. • A cause-effect relationship between global hemodynamics and cerebral hemodynamics may play a significant role in cerebral perfusion (cardiac output matters). • In general, PE is very likely to exert a paradoxical effect from anticipated. Meng, L. et al, BJA 107(2):209-17 (2011)

  20. Limitations: • TIVA only, 29 patients (20 male), protocol (10 minutes) • Is there a problem with our interpretation of COS data when PE is involved? • Is there a problem with our understanding of cerebral autoregulation? • Is there a problem with our understanding of the effect of alpha agonists on cerebral vessels? Meng, L. et al, BJA 107(2):209-17 (2011)

  21. Purpose To evaluate the effect of PE on COS & MCAv in the upright position.

  22. Findings: Supine • PE decreased COS by 10% (p = 0.02) • Saline maintained a normal COS • PE increased MCAv by 20% (p = 0.04) • Saline had no effect on MCAv Soeding, P.F., et al., BJA 111(2): 229-34 (2013)

  23. Findings: Upright • Both showed an 11% -12% decrease in COS from their respective post infusion values (p < 0.001) • CI decreased in the saline & PE groups by 11% & 24% respectively (p = 0.27), but for different reasons. • In the saline group, end-diastolic volume was reduced (p < 0.03); • In the PE group, EDV was maintained but bradycardia ensued (p < 0.01). Soeding, P.F., et al., BJA 111(2): 229-34 (2013)

  24. Clinical Pearls: • In patients under general anesthesia, the upright position uniquely causes a decline in cardiac output and COS • Saline outpaced PE in preserving tissue perfusion and COS. • An increase in CBFv does not equal an increase in CBF • PE is very likely to exert a paradoxical effect in both TIVA & inhalation anesthesia that could compromise cerebral perfusion in select patients. Soeding, P.F., et al., BJA 111(2): 229-34 (2013)

  25. Limitations: • Pooled vs. individual data • Degree of bradycardia is atypical • Uncertainty regarding interpretation of COS data when PE is involved • Problem with our understanding of cerebral autoregulation? • Problem with our understanding of the effect of alpha agonists on cerebral vessels? Soeding, P.F., et al., BJA 111(2): 229-34 (2013)

  26. Purpose • To evaluate the effect of PE on COS and CBV during hypocarbia, normocarbia, and hypercarbia

  27. Findings • PE caused a decline in COS in all three groups (p < 0.01) • Decline in COS was greatest in the hypcapnic group & lowest in the hypercarbic group. • PE caused a decrease in CO in all three groups (p < 0.001). • PE caused a significant decrease in CBV during hypocapnia (p < 0.01). • The correlation between COS and CBV was significant (p < 0.05), but quite weak (R2 = .15) Meng, A.W. BJA, 108 (5): 815-22 (2012)

  28. Meng, A.W. BJA, 108 (5): 815-22 (2012)

  29. Clinical Pearls: • PE declines in COS are intensified by hypocapnia & blunted by hypercapnia. • Hypocapnia should be corrected prior to administering PE for hypotension. • Regulation of cerebral perfusion involves a wide spectrum of overlapping/integrated mechanisms Meng, A.W. BJA, 108 (5): 815-22 (2012) Willie, C.K. (2014). Integrative regulation of human brain. J Physiol592 (5) 841-859

  30. Limitations: • TIVA only; 14 (11 male, 3 female) • Method for assessing CBV may need validating

  31. Moerman, A.T., Anesthesiology 123 (2), August 2015, p.327-335 Purpose: To determine if paradoxical changes between COS and MAP represent normal cerebral autoregulation.

  32. Paradoxical Response: Possible MOA • Vasoconstriction precipitates a decreased ratio of A:V CBV leading to a decline in COS • Vasodilation precipitates an increased ratio of A:V CBV leading to an increase in COS. Moerman, A.T., Anesthesiology 123 (2), August 2015, p.327-335

  33. Findings: Four response patterns were found. • Pressure passive (35%); impaired autoregulation • Classic (18%); consistent with current beliefs • Paradoxical (29%); opposite of current beliefs • Divergent (18%); decrease with both SNP & PE Moerman, A.T., Anesthesiology 123 (2), August 2015, p.327-335

  34. Clinical Pearls: • The classic AR curve does not accurately characterize autoregulation for the majority of individuals • Autoregulation is more complex than previously understood

  35. Limitations: • Assessed autoregulation: • Under hypothermic conditions (30 degrees C) • During non-pulsatile flow • Did not maintain equal temperatures among the patients • Did not maintain equal PaCO2 among the patients

  36. These are the Highlights of the Remaining Three Studies.

  37. Best Available Evidence • PE bolus causes a decrease in CO & COS. • Hypocarbia exaggerates a PE induced decline in COS. • PE bolus causes an increase in MCAv. • PE bolus most likely causes MCA vasoconstriction. • PE induced MCA vasoconstriction is most likely direct or indirect alpha stimulation of cerebral vessels. • PE decline in COS may reflect a decreased A:V ratio caused by arterial vasoconstriction, and possibly increased venous tone. • There is tremendous variability in individual autoregulation. • CO may be more associated with cerebral perfusion than MAP. • Maintenance of MAP with PE is no guarantee of adequate cerebral perfusion.

  38. Thank you! sandra.larson@rosalindfranklin.edu

  39. Purpose: To discover if SNP induced dilation of the MCA resulted in increased cerebral blood flow while PE induced constriction resulted in decreased cerebral blood flow in the frontal cortex.

  40. Findings • PE decreases COS despite increased MAP • This occurs because PE decreases arterial inflow through constriction of the MCA. • PE also increases venous tone and increases venous outflow. • The net effect is a reduction in CBF and CBV. Stewart, J. M. et al.. Am J Physiol Heart Circ Physiol 304 H1576-H1583 (2013)

  41. Stewart, J. M. et al.. Am J Physiol Heart Circ Physiol 304 H1576-H1583 (2013)

  42. Clinical Pearls: • The decline in COS caused by PE may represent a real decline in arterial oxygen delivery to the brain • EPH not PE is the preferred treatment for AIH because it consistently maintains CO and COS

  43. Limitations: • Patients were not under general anesthesia • Use of conservation of mass equation should be validated by other researchers • Pooled vs. individual patient data

  44. Purpose To determine if PE exerts an alpha adrenergic-mediated cerebral vasoconstriction

  45. Findings • PE decreased COS despite increased MAP (p < 0.001) • PE increased MCAv (p = 0.038) • PE increased IJV flow (p = 0.023) • PE increased IJV diameter (p < 0.001) • PE caused no change in IJVv • PE caused no change on ICAv or ICA diameter Ogoh,S., et al.. ClinFunct Imaging (2011) 31, pp 445-451

  46. Ogoh,S., et al.. Clin Funct Imaging (2011) 31, pp445-451

  47. Hypothesis: • The PE induced decrease in COS may reflect a decrease in A : V contribution of blood in the frontal lobe. • MCA vasoconstricted (increased MCAv) • IJV outflow increased • Limitation: • Patients were not under general anesthesia • RIJ outflow may not reflect LIJ outflow

  48. Alpha Agonists & Cerebral Vessels • Indirect stimulation via sympathetic cervical ganglion • Direct stimulation

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