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Conversion of Hemiblock to Complete Heart Block by Intraoperative Motor-Evoked Potential Monitoring

Bicket, Mark C. MD; Ritzl, Eva K. MD; Tamargo, Rafael J. MD; Mintz, C. David MD, PhD

doi: 10.1213/XAA.0000000000000095
Case Reports: Case Report

Intraoperative monitoring of nervous system pathways, including assessing the integrity of descending motor pathways with motor-evoked potentials, is often performed in intracranial and spine operations to reduce the risk of iatrogenic neurological impairment. We present a case in which intraoperative monitoring with motor-evoked potentials resulted in complete heart block in a patient with a history of hemiblock. Neuromonitoring has been associated with arrhythmias in patients with ostensibly normal conduction systems, and we propose that monitoring personnel, anesthesiologists, and surgeons need to be aware of this risk and exercise caution when monitoring motor-evoked potentials in patients with known conduction deficits.

From the Departments of *Anesthesiology and Critical Care Medicine, Neurology, and Neurological Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Accepted for publication June 12, 2014.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to C. David Mintz, MD, PhD, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, 720 Rutland Ave., Ross Bldg 370, Baltimore, MD 21205. Address e-mail to

Monitoring the integrity of nervous system pathways during neurosurgical procedures with evoked potentials has become an increasingly common practice, and intraoperative motor-evoked potentials (MEPs) provide an additional monitor of a patient’s neurologic status. MEPs performed under anesthesia stem from train stimulation of the brain that causes the spinal cord and peripheral muscle to produce a neuroelectrical response, and they can be used to assess the integrity of descending motor pathways. Since the first report of such monitoring was published,1 concerns regarding the safety of MEP monitoring have focused primarily on movement-related injury (such as tongue laceration), scalp injury, and postoperative headache,2 although reviews conclude that this monitoring technique is generally quite safe.3 Cardiac complications have only rarely been reported; 1 report describes a case of bradycardia caused by MEPs that spontaneously resolved over a period of 2 minutes.4

We describe a patient with a history of left anterior fascicular block in whom the initiation of a train of MEPs coincided with the onset of third-degree (complete) heart block with concomitant severe hypotension. MEPs were discontinued, and the heart block resolved with pharmacological treatment and did not reoccur during subsequent intraoperative or postoperative care.

The patient kindly provided consent to publish this case report during our postoperative follow-up interview.

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A 62-year-old man with progressive myelopathy resulting from a vertebral artery dural arteriovenous fistula at the C5 level presented for clipping of the fistula. The patient’s preoperative cardiac history was unremarkable, but the routine preoperative electrocardiogram showed left anterior fascicular block (Fig. 1). General anesthesia was induced with 100 mg lidocaine, a total of 250 mg propofol given in divided doses, 150 μg fentanyl, and 10 mg vecuronium. After uncomplicated IV catheter insertion, tracheal intubation, and intra-arterial catheter insertion, the patient was equipped with MEP and sensory-evoked potential neuromonitoring devices and positioned prone. A safety timeout was performed, followed by administration of antibiotic prophylaxis (cefazolin 2 g) and steroids (dexamethasone 10 mg). At this point, which was approximately an hour and a half after induction, neuromonitoring personnel announced the initiation of MEP monitoring. MEPs were elicited by anodic voltage stimulation (400 V), using square pulse trains (duration 500 microseconds, frequency 400 Hz) from electrodes placed in the C3 and C4 positions on the scalp. Third-degree heart block was noted twice to follow MEP artifact on leads II and V5 of the electrocardiogram, and subsequent examination of the electrocardiogram showed a brief return of normal sinus rhythm after a pause in stimulation (Fig. 2). The longest episode of atrioventricular block lasted 12 seconds. Precipitous hypotension (in which mean arterial blood pressure decreased from 88 mm Hg to 42 mm Hg) and the disappearance of arterial pulsations were noted on the arterial blood pressure tracing.

Figure 1

Figure 1

Figure 2

Figure 2

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.

Figure 3

Figure 3

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.

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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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