title: Effect of hemorrhage and hypotension on transcranial motor-evoked potentials in swine.
abstract: BACKGROUND
  Transcranial motor-evoked potentials (TcMEPs) monitor spinal cord motor tract integrity. Using a swine model, the authors studied the effects of vasodilatory hypotension, hemorrhage, and various resuscitation efforts on TcMEP responses.
  
  
  METHODS
  Twelve pigs were anesthetized with constant infusions of propofol, ketamine, and fentanyl. Animals were incrementally hemorrhaged, until bilateral tibialis anterior TcMEP amplitude decreased to less than 40% of baseline or until 50% of the blood volume was removed. Mean arterial pressure (MAP), cardiac output (CO), and oxygen delivery (DO2) were examined. Resuscitation with phenylephrine, epinephrine, and colloid were evaluated. In seven animals, vasodilatory hypotension was examined. Paired comparisons and multivariate analysis were performed.
  
  
  RESULTS
  Hemorrhage significantly reduced (as a percentage of baseline, mean±SD) TcMEPs (left, 33±29%; right, 26±21%), MAP (60±17%), CO (49±12%), and DO2 (43±13%), P value less than 0.001 for all. Vasodilation reduced MAP comparably, but TcMEPs, CO, and DO2, were not significantly lowered. After hemorrhage, restoration of MAP with phenylephrine did not improve TcMEPs, CO, or DO2, but similar restoration of MAP with epinephrine restored (to percentage of baseline) TcMEPs (59±40%), and significantly increased CO (81±17%) and DO2 (72±19%) compared with both hemorrhage and phenylephrine, P value less than 0.05 for all. Resuscitation with colloid did not improve TcMEPs. Multivariate analysis revealed that changes in TcMEPs were more closely associated with changes in CO and DO2 as compared with MAP.
  
  
  CONCLUSIONS
  Hypotension from hemorrhage, but not vasodilation, is associated with a decrease in TcMEP amplitude. After hemorrhage, restoration of TcMEPs with epinephrine but not phenylephrine indicates that CO and DO2 affect TcMEPs more than MAP. Monitoring CO may be beneficial in major spine surgery when using TcMEP monitoring.
authors.affiliation: * Professor, ‡ Associate Professor, Department of Anesthesiology and Perioperative Care, † Clinical Neurophysiologist, Division of Operating Room Services, University of California, San Francisco, San Francisco, California.
authors.forename: Jeremy A
authors.initials: JA
authors.lastname: Lieberman
authors.forename: John
authors.initials: J
authors.lastname: Feiner
authors.forename: Russ
authors.initials: R
authors.lastname: Lyon
authors.forename: Mark D
authors.initials: MD
authors.lastname: Rollins
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D004558:Electric Stimulation; D019054:Evoked Potentials, Motor / Q000502:physiology*; D005260:Female; D005440:Fluid Therapy; D006439:Hemodynamics / Q000502:physiology; D006470:Hemorrhage / Q000503:physiopathology*; D007022:Hypotension / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012151:Resuscitation; D013552:Swine; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside