At this point, the patient was returned to the supine position in anticipation of a possible need for resuscitation, and vasopressors were administered (ephedrine 40 mg and epinephrine 20 μg). Heart rate and arterial blood pressure returned to their normal values, and sinus rhythm was restored. In discussion with the surgical and neuromonitoring teams, the correlation between MEPs and this event was noted, and MEPs were not used subsequently. The sequence of events is depicted in Figure 3, which is a screen capture of the electronic anesthesia record. No further episodes of third-degree heart block or hypotension occurred, and no additional vasopressors were given for the remainder of the case.
During uneventful surgery and recovery in the neurocritical care unit for 1 day, the patient exhibited no additional cardiac symptoms (e.g., palpitations, angina, arrhythmia, or ischemic events). The patient was discharged home on postoperative day 5.
Third-degree heart block, or complete heart block, results when conduction through the atrioventricular node fails, resulting in dissociation between the activity of the atria and the ventricles. The etiology of intraoperative complete heart block includes hypoxia, hyperkalemia, antiarrhythmic medications, and iatrogenic causes involving electrical or mechanical stimulation of the atrioventricular node, which may result from cardiac surgery5 or catheters interfering with a fascicle.6 Left anterior fascicular block is a very common finding in male patients at and beyond middle age, and a progression to third-degree heart block is very unusual and typically occurs in conjunction with right bundle branch block in the setting of sclerotic diseases that affect the conduction system such as Lev disease and Lenègre disease.7 While a rare association of neuromonitoring with cardiac arrhythmias has been discussed in the literature,8 MEPs have not been implicated as a cause of disrupted atrioventricular node conduction.
While we cannot exclude the possibility of coincidence, the temporal relationship of the MEP monitoring with the episodes of complete heart block and sudden hypotension suggests that the stimulation from the MEPs was the most likely cause of the patient’s hemodynamic compromise. No antiarrhythmic medication was administered to the patient before or during the surgery. Additional doses of antibiotic and steroid were given at the conclusion of the case without evidence of adverse hemodynamic effects.
On the basis of the current literature, we hypothesize 4 possible mechanisms by which MEPs could have caused complete heart block in our patient: First, a cardiac arrhythmia may result from direct electrical stimulation of the anteromedial hypothalamus, which regulates parasympathetic outflow via the vagal nerve.9 This potential problem can be minimized by placing the stimulation electrodes closer together in an attempt to avoid deep stimulation. In our case, the stimulation needles were placed relatively far apart in an attempt to improve the quality of MEP signals, which were poor in this patient. Second, the cardiac conduction system itself could have been disrupted by a stray current path through the heart that completed a circuit between the motor and sensory electrodes.8 This is unlikely because the motor and sensory electrode headboxes are on different circuits in our equipment, and our intraoperative monitoring systems are regularly checked for proper grounding. Third, it is possible that complete heart block occurred as a manifestation of a seizure induced by neuromonitoring, which is rare but has been reported.2 In our case, there was no clinical evidence of seizure activity, and the limited electroencephalogram monitoring which we performed as an adjunct to MEP monitoring did not show any electrical seizure activity. Fourth, direct stimulation of the vagus nerve could have produced a complete heart block.10 While the heart block may have been due to vagal mediation, it is unlikely that direct vagal nerve stimulation occurred our stimulation electrodes were located on the patient’s scalp. Patients such as ours with an underlying conduction defect are at a higher risk for progression of those defects when parasympathetic output is increased by any mechanism.
In conclusion, MEP monitoring is one form of intraoperative neurologic monitoring of patients that may be linked to sudden changes in hemodynamic status, as evidenced in this case of complete heart block. Patients who have a baseline defect in cardiac conduction pathways may be at a greater risk for cardiac arrhythmias. In this setting, we recommend conducting a test of intraoperative neurologic monitoring under controlled conditions. During this test, good communication between the anesthesia and monitoring teams is important. The anesthetic team should be prepared to resuscitate the patient, and the test should occur before incision while the patient is still supine, and thus easily accessed if necessary for pacing or other resuscitative measures.
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© 2014 International Anesthesia Research Society
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