Ephedrine‐Triggered Torsades de Pointes in Two Patients Following Desflurane‐Induced QT Prolongation

Abstract

Desflurane‐induced QT prolongation followed by ephedrine‐triggered premature ventricular contractions led to torsades de pointes/ventricular fibrillation in two patients. These cases demonstrate sequential electrocardiographic progression and highlight the importance of careful vasopressor selection during general anesthesia.

QT prolongation is a known risk factor for torsades de pointes (TdP). Volatile anesthetics and vasopressor agents affect ventricular repolarization and cause TdP [1]. We describe two patients who developed TdP triggered by ephedrine following QT prolongation after desflurane administration. In both patients, QT prolongation was observed immediately after desflurane administration (Figure 1). Ephedrine administration triggered premature ventricular contractions (PVCs), leading to the R‐on‐T phenomenon, TdP, and ventricular fibrillation (VF). When QT prolongation is observed following desflurane administration, the risk of ventricular arrhythmias may be increased, and ephedrine should be used with caution.

FIGURE 1.

Intraoperative electrocardiographic changes leading to torsades de pointes (TdP) and ventricular fibrillation (VF). Desflurane‐induced QT prolongation was observed in both cases. Ephedrine triggered premature ventricular contractions (PVCs), resulting in the R‐on‐T phenomenon and subsequent TdP/VF.

1. Case 1

A 21‐year‐old man underwent surgical biopsy for a brain tumor under general anesthesia. Baseline QTc was 424 ms. Immediately after desflurane administration, QT prolongation was observed. Serum potassium, magnesium, and calcium levels were within normal ranges before surgery, and no medications known to prolong the QT interval were used. Ephedrine administration triggered PVCs leading to the R‐on‐T phenomenon, TdP, and VF. The QT interval normalized within 2 days (Figure 2).

FIGURE 2.

Serial electrocardiographic changes and time course of corrected QT (QTc) intervals. (A) Electrocardiographic changes from the preoperative to postoperative periods. (B) Time course of pre‐ and postoperative QTc intervals. Despite the rapid offset of desflurane, QTc normalization required up to two postoperative days.

2. Case 2

A 50‐year‐old woman underwent surgery for endometrial carcinoma. Baseline QTc was 467 ms. After desflurane administration, QT prolongation was observed. Ephedrine administration triggered ventricular bigeminy, leading to TdP and ventricular fibrillation. Serum potassium and calcium levels before surgery were within normal ranges; however, magnesium was not measured immediately before the arrhythmic event. After TdP onset, 20 mEq of magnesium sulfate was administered, and subsequent magnesium levels were above the normal range (2.8 and 3.1 mg/dL), making marked magnesium deficiency at baseline less likely. No medications known to prolong the QT interval were used. Postoperative hypotension was initially managed with phenylephrine, with vasopressin reserved for further decreases in blood pressure; however, vasopressin was not required, and no PVCs were observed. The QT interval improved within 2 days (Figure 2).

Desflurane has been reported to cause greater QT prolongation than sevoflurane, another volatile anesthetic [2]. In contrast, propofol has minimal effects on the QT interval [2]. Desflurane has been consistently reported to prolong QTc and may contribute to delayed ventricular repolarization through increased autonomic tone and enhanced catecholamine responses, particularly during rapid increases in anesthetic concentration [3]. Direct electrophysiological effects on myocardial potassium currents may also contribute to increased arrhythmic susceptibility. QT dispersion, defined as the interlead variability of the QT interval, reflects heterogeneity of ventricular repolarization. Epinephrine, an α‐ and β‐adrenergic agonist, increases QT dispersion and may increase arrhythmic risk [4]. Ephedrine is also an α‐ and β‐adrenergic agonist, similar to epinephrine. In the presence of QT prolongation, β‐adrenergic stimulation may trigger PVCs and cause TdP. In contrast, phenylephrine, a pure α‐adrenergic agonist, has minimal effects on ventricular repolarization and may be a safer option. For the management of hypotension in patients with QT prolongation, vasopressin may be considered when phenylephrine is insufficient. Despite the rapid offset of desflurane, another report has shown that QT interval prolongation may persist for several days after anesthesia [5]. The mechanism underlying this discrepancy remains unclear. Rapid increases in desflurane concentration have been reported to enhance autonomic tone and increase circulating catecholamine and vasopressin concentrations, which may contribute to transient repolarization abnormalities. However, whether direct electrophysiological effects on myocardial potassium currents persist beyond anesthetic elimination remains uncertain. Although electrolyte imbalance cannot be completely excluded, no marked electrolyte abnormality or use of medications known to prolong the QT interval sufficient to explain the arrhythmic events was identified. In Case 1, a relatively elevated heart rate on postoperative day 1 suggested persistent autonomic activation during recovery, and the electrocardiographic findings may not have fully represented a resting condition. Although volatile anesthetic‐induced QT prolongation and catecholamine‐triggered ventricular arrhythmias have been previously reported, to our knowledge, no previous report has clearly demonstrated the sequential electrocardiographic changes from desflurane‐induced QT prolongation to ephedrine‐triggered PVCs and subsequent TdP/VF. Our cases provide clinically recognizable electrocardiographic progression that may help clinicians understand the practical arrhythmogenic sequence occurring during general anesthesia. These findings highlight the importance of careful ECG monitoring and appropriate vasopressor selection in patients with QT prolongation during perioperative period.

Consent

Written informed consent was obtained from both patients for publication of this case report and accompanying images.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.