Atrioventricular (AV) junctional rhythm, another consecutive escaped rhythm, usually has a normal QRS duration without a P wave or with a retrograde P wave. If complicated with a bundle branch block, the QRS duration gets longer. AV junctional rhythm might lack effective atrial contraction and reduce the cardiac output than sinus rhythm, because atrial contraction contributes to approximately 15 to 25 % of the diastolic filling of the ventricle [7]. AIVR originates from the His, the Purkinje system or the working contractile ventricular cells [1]. Ventricular pacing has been shown to result in dyssynchronous left ventricular (LV) electrical activation and mechanical contraction, to worsen LV ejection fraction [8]. AIVR is not artificial ventricular pacing, but its abnormal impulse conducting pathway might cause dyssynchronous LV contraction.
Some anesthetics have been described to be associated with AIVR because of toxicity. Cocaine might induce AIVR either through the production of myocardial ischemia or as a direct result of ion channel alterations [3, 9]. Halothane was reported to be associated with AIVR due to a depressant effect on slow inward calcium current and intracellular calcium accumulation [4]. Desflurane was also reported to induce AIVR because of a sympathetic imbalance [5]. Propofol was publicized to be associated with arrhythmias in humans [10]. In the guinea pig heart, the ionic mechanism underlying the negative chronotropic action of propofol on sinoatrial node (SN) automaticity was associated with propofol-induced bradycardia observed in clinical settings [11]. Similar to propofol, remifentanil also depresses sinus node function and most parameters of atrioventricular (AV) nodal function, causing remifentanil-related severe bradyarrhythmias [12]. In this case, the negative chronotropic action of propofol and remifentanil on sinus and AV nodal function might have induced the ectopic focus more often than usual.
AIVR is also associated with higher vagal tone and lower sympathetic activity [13], and the AIVR related to sympathetic nerve block during spinal anesthesia for cesarean section was reported [14]. Propofol suppresses both sympathetic and parasympathetic tone, but the suppression of sympathetic tone is more than that of parasympathetic tone [15]. Remifentanil also induces higher vagal tone [16]. In this case, superior vagal tone related to propofol and remifentanil might have induced AIVR. However, ventricular rhythm was not detected during the postoperative 24-h period including his sleeping hours, time of the parasympathetic nerve predominance. We did not succeed in clarifying the trigger of the idioventricular rhythm observed in the Holter ECG, but his activity at the time of the record was higher than that at the postoperative 24-h period. Not parasympathetic nerve predominance during sleep but imbalance of the autonomic nerve caused by anesthetics might have induced AIVR more frequently.
Naranjo algorithm is a questionnaire designed by Naranjo et al. for determining the likelihood of whether an adverse drug reaction is actually due to the drug rather than the result of other factors [17]. Probability is assigned via a score termed definite (9–13 points), probable (5–8 points), possible (1–4 points) or doubtful (0 point). On using Naranjo’s scale, we obtained a scale of 5, which makes propofol and remifentanil probable causes for the event. The adverse event appeared after their administration (+2). The adverse event improved when they were discontinued (+1). The reaction was less severe when their doses were decreased (+1), because the surgery 1 year prior had no episode of an AIVR with balanced anesthesia using sevoflurane, remifentanil, and propofol, the doses of which were lower than those at this time. The arrhythmias were objectively recorded on an ECG trace (+1).
Most AIVRs are usually well tolerated and do not need specific treatment. Increasing the sinus rate is the recommended treatment for AIVR, therefore, atropine and atrial pacing rhythm can help to control it [1, 2]. Ephedrine is controversial because it can potentially increase AIVR duration [14].
Benign AIVRs with no structural heart disease and no electrolytic abnormality, such as in this case, usually require no intervention. However, sometimes it can present as a more severe arrhythmia requiring treatment, because AIVR might be induced by reperfusion after acute myocardial infarction, some cardiomyopathies, myocarditis, and in newborn infants with various congenital heart diseases [1, 2].