We experienced a patient with VF during the manipulation of a guidewire for bailout carotid stenting during CEA. There were no obvious preoperative risk factors for intraoperative ventricular tachyarrhythmia. No remarkable family or medication history was noted. The results of preoperative blood testing, standard 12-lead ECG, and transthoracic echocardiography were all negative for potential arrhythmia. In particular, the preoperative QT interval was within the normal range. The preoperative QTc was 317 ms, as measured using the tangent method suggested for use in atrial fibrillation [2].
The QT interval is one of the quantitative values associated with the prevalence of ventricular tachyarrhythmia. Reportedly, approximately 80% of patients had a longer QTc after surgery under general anesthesia than those before surgery [3]. In our case, the QTc had increased to 411 ms at the time of anesthesia induction and further increased to 458 ms before the onset of arrhythmia. Each 10-ms increase in QTc contributes approximately a 5% to 7% exponential increase in the risk of TdP in congenital LQTS patients [2]. We concluded that there was significant intraoperative QT prolongation in this case.
It is widely known that different types of cardiomyocytes have different electrophysiological characteristics and are distributed heterogeneously [4]. The spatial heterogeneity of myocardial depolarization results in QT dispersion. Increased QT dispersion seems to be associated with ventricular tachyarrhythmia [5]. At our institution, intraoperative waveform data are stored only for leads II and III. In general, QT dispersion is defined as the difference between the maximum and minimum QT values in a 12-lead ECG [6]. In this study, general QT dispersion was not available, but we were able to measure QTc in leads II and III (Fig. 2). Initially, there was no difference between the two leads, but the QTc difference increased intraoperatively and reached 50 ms just before the onset of ventricular tachyarrhythmia.
We anesthetized the patient with hypercapnia for 4 h. This was to prevent cerebral ischemia. On the other hand, hypercapnia increases both QTc interval and QT dispersion [7]. Permissive hypercapnia may provide an environment for arrhythmogenesis.
Hypomagnesemia is an important risk factor for arrhythmias [8]. Although the mechanism is not clear, magnesium is believed to equalize repolarization. Furthermore, some reports have found a correlation between Mg and QT dispersion [9]. In the present case, hypomagnesemia was observed on postoperative examination.
In this case, there were no circulatory changes before the onset of VF.
Myocardial infarction was denied because cardiac function recovered quickly.
Takotsubo cardiomyopathy is another candidate because it can prolong QT and cause TdP [10]. The suggested mechanism of QT elongation in Takotsubo cardiomyopathy is catecholamine or autonomic effects on the myocardium. However, postoperative echocardiography in the ICU did not reveal any obvious findings suggesting takotsubo cardiomyopathy.
We used phenylephrine up to 0.5 μg-kg-1-min-1 to maintain blood pressure. Some studies have found no QT prolongation or QT dispersion with phenylephrine [11], while other studies on the relationship between afterload and QT dispersion have shown that phenylephrine causes QT dispersion [12].
The possibility of structural changes in the ventricular muscle predisposing ventricular tachyarrhythmia should also be considered. Aging is a well-known risk factor for the development of arrhythmias [13]. In the present study, factors that increase myocardial remodeling could be related to old age, hypertension, diabetes mellitus, and atrial fibrillation. Abnormalities in the myocardial gap junctions and fibrosis of the tissue interstitium seem to lead to the development of heterogeneous repolarization [14].
Finally, the surgical procedure could trigger VF. The ECG trace showed no signs of dysrhythmia before VF onset, and there is no doubt that carotid artery manipulation was the trigger.
There are also reports of TdP developing from carotid dissection [15] and ventricular fibrillation occurring after carotid sinus massage [16]. Moreover, although there are no reports of VF occurring during CEA, we should be aware that carotid manipulation may cause sudden onset of lethal ventricular tachyarrhythmias.
CEA causes the balance of the cardiac autonomic nervous system to be biased toward the sympathetic side [17].
The relative increase in sympathetic modulation after CEA is likely mediated by alterations in the sensitivity of carotid sinus baroreceptors [18].
In conclusion, QT prolongation, QT dispersion, hypercapnia, hypomagnesemia, acute heart disease, use of phenylephrine, advanced age, and carotid artery manipulation were considered as potential causes of intraoperative VF.
