The Influence of Vasopressor-Induced Arterial Blood Pressure Elevation on Muscle-Recorded Motor Evoked Potentials

Transcranial electrical stimulation muscle-recorded motor evoked potentials (Tc-mMEPs) are used to monitor the spinal cord motor tracts during spinal surgery. There is considerable intra- and interindividual variability in the signals recorded, causing a high incidence of false positive warnings. Inadequate blood pressure is commonly blamed for false positive warnings and is usually managed with fluid and vasopressor therapy. The aim of the study was to systematically investigate the effects of norepinephrine and ephedrine-induced arterial blood pressure elevation on Tc-mMEPs.

Twenty-five patients undergoing spinal surgery were included in this prospective observational study. After anesthetic induction and positioning, but before incision, a norepinephrine infusion was used to increase the mean arterial pressure (MAP) from approximately 60 to 100 mm Hg. Tc-mMEP amplitudes and area under the curves (AUC) were recorded from the abductor hallucis (AH), tibialis anterior (TA), and hand muscles every 2 minutes. Voltage thresholds of the AH, TA, and hand muscles were determined at MAP values of 60, 80, and 100 mm Hg. The primary objective was to determine the effects of increasing the MAP with a vasopressor infusion on Tc-mMEP amplitude, AUC, and threshold. For the secondary objective, the outcomes were adjusted for depth of anesthesia and propofol concentrations. Post hoc analyses included adjusting for confounders, noradrenaline infusion rate, and use of ephedrine, investigating the effects of cardiac index on Tc-mMEP characteristics, investigating the influence of increasing MAP on the excitability of the peripheral nervous system, and investigating the effects of MAP on BIS.

In the AH, TA, and hand muscles, Tc-mMEP amplitudes and AUC were significantly associated with MAP ( P < .02). A 10 mm Hg increase of the MAP was associated with a 11.0% to 17.7% increase in the amplitude and a 10.5% to 16.8% increase in the AUC. When adjusting for BIS, propofol concentrations, and use of ephedrine, MAP remained only significantly associated with the Tc-mMEP amplitude ( P = .002) and AUC ( P = .003) of the AH muscles. The influence of cardiac index on Tc-mMEP amplitude and AUC provided similar results when compared to the influence of MAP on Tc-mMEP amplitude and AUC. No influence of increasing MAP on the excitability of the peripheral nervous system was found. Increasing MAP significantly increased BIS values, even when corrected for propofol concentrations.

Elevation of MAP is associated with significantly higher Tc-mMEP amplitudes, AUCs, and lower voltage threshold. When corrected for BIS, propofol concentration, and use of ephedrine, the associations between increasing MAP and Tc-mMEP characteristics were largely attenuated. BIS values significantly increased by increasing MAP, when corrected for propofol concentration. Thereby, our results imply that increasing MAP increases the cortical excitability.