This was a case of the R-on-T phenomenon caused by undersensing of the pacing wire in a single patient. Notably, the T wave followed the QRS of the PVC. Understanding this phenomenon requires the answers to two questions: First, why were the pacing spikes not inhibited? Second, what caused the PVCs?
The R-on-T pacing in this patient occurred despite lowering the sense threshold to 2 mV, suggesting that simple undersensing is unlikely to explain this phenomenon. Lowering the sense threshold even further than in this case is not a reasonable management in temporary epicardial pacing for patients with prolonged AV delay. Like this patient, severe AV block cases require ventricular pacing to maintain sufficient cardiac output because their ventricular contractions are too rare to do so; therefore excessively low sensing thresholds are not an option. Low threshold sensing numbers cause the pacemaker to sense external factors such as electrical scalpel stimulation or postural change. If pacing is excessively inhibited, patients suffer critical bradycardia and low-output syndrome.
Dispersion of the duration of the action potential and electrical inhomogeneity in the myocardium may explain the undersensing [6]. The electrical voltage waveforms that pacemakers detect are not equal to those identified by surface electrocardiography. Surface electrocardiography reflects electrical activity of the entire heart while the pacemaker electrode contacts the external cardiac muscle directly and senses only the electrical excitation of surrounding cells. Surface electrocardiography is related to space and epicardial wires are related to linear or punctual factors. With peri-lead fibrous or necrotic tissue, pacemakers cannot detect depolarization despite QRS waves appearing on the ECG monitor. Also, the literature provides little information on the best locations for epicardial pacing. In the presented case, the temporary epicardial electrode was placed on the anterior RV, which is the most widely used location for wire implantation because of the easy access. However, one study reported that the anterior RV location provides sub-optimal sensing and stimulation thresholds [7].
In the presented case, the undersensed QRS wave was a wide PVC; therefore, QRS width could be a contributing factor. If the device recognizes the R wave by slew rate, which is the quotient of voltage over time, a wide QRS may impair accurate sensing of R voltage. The duration of the QRS wave would be longer and the slew rate would be smaller despite having the same R wave voltage. Therefore, temporary epicardial pacing devices set at a clinically valid threshold may not detect abnormally wide QRS waves without omission.
We provided anesthetic management to prevent arrhythmias in this patient. We maintained intravascular volume, preload, afterload, heart rate, and contractile force within normal limits by referring to TEE, arterial blood pressure, pulmonary arterial pressure, central venous pressure, cardiac output, and mixed venous blood saturation in oxygen by Swan-Ganz Catheter. We did not use excessive amounts of catecholamines and only 3 mcg/kg/min dopamine was injected. We also maintained the patient’s electrolytes and body temperature at normal levels. The ECG ST slope elevated slowly by the time of sternal closure. TEE performed after the two Vf episodes showed poor contraction of the right coronary artery (RCA) perfusion segments, often caused by RCA ischemia. Intracardiac air was removed carefully and there was little probability that coronary spasm or partial pericardial tamponade occurred. Bleeding in or around the epicardial pacing wires tends to occur in the immediate postoperative period and pericardial hematoma formation around epicardial pacing wires has been reported [8]. Myocardial infarction related to the epicardial pacing wire itself has also been reported [9]. The hypothesis that ischemic RCA perfusion induced frequent PVCs is reasonable.
Following this case, we reviewed our anesthetic records from the past 7 years and found one case of Vf resulting from the R-on-T wave phenomenon; however, we concluded that the cause of the R-on-T in that case was an excessively high sensing threshold. Also, the undersensed QRS wave was one following a P wave.
This case was our first experience of Vf caused by “R on PVC T wave” phenomenon. Some authors suggest that routine use of temporary epicardial pacing wires after valve surgery is only necessary for high risk patients [10, 11]. In addition to the R-on-T pacing, major complications of epicardial wires include infection, myocardial damage, perforation, tamponade, and disruption of coronary anastomoses [4]. Insertion can prolong the operative time and increase the risk of bleeding and patients are also at risk for ventricular arrhythmias during removal of epicardial pacing wires [12]. Therefore, it is important to consider the risks of using temporary epicardial pacing.