How can low calcium and potassium complicate treatment of a dangerous heart rhythm around surgery?

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This report describes two women with torsade de pointes ventricular tachycardia (TdPVT) around anesthesia and briefly reviews its mechanisms, causes, and treatment. The authors state that its incidence during anesthesia is unknown and its mechanism is not fully understood. This rare but potentially lethal rhythm requires prompt recognition and adequate treatment to prevent hemodynamic compromise and progression to ventricular fibrillation (VF).

Case 1 involved a 68-year-old woman with hypertension and glaucoma admitted for elective cataract extraction. She had undergone thyroidectomy 10 years earlier. Mannitol, 1.5 g/kg/day, was started to lower intraocular pressure. Her preoperative examination and routine blood chemistry were within normal limits. An electrocardiogram (ECG) showed left ventricular hypertrophy and strain, with a normal heart-rate-corrected QT interval (QTc) of 0.32 s. Premedication was oral diazepam 10 mg. After oxygen administration, anesthesia was induced with fentanyl 2 micrograms/kg, thiopental 3 mg/kg, and succinylcholine 1.5 mg/kg; maintenance used N2O/O2 at 60:40, with alcuronium 0.2 mg/kg for paralysis.

Fifteen minutes after induction, multiple premature ventricular beats were followed by a sudden rhythm resembling VF, and blood pressure fell to 70/50 mm Hg. Intravenous lidocaine up to 2 mg/kg followed by bretylium 5 mg/kg had no effect. ECG showed polymorphic ventricular tachycardia with the QRS axis twisting around the baseline at 150/min, suggesting TdPVT. A 200-joule direct-current (DC) shock restored sinus rhythm; the next ECG showed prolonged QTc, 0.53 s. Blood tests showed potassium 3.3 mEq/L (normal 3.5–5), magnesium 1.8 mEq/L (normal 1.5–2.5), total serum calcium 1.6 mEq/L (normal 2.2–2.7), and respiratory alkalosis. The authors attributed the low potassium and calcium to a combination of hyperventilation, mannitol, and previously hidden hypoparathyroidism after total thyroidectomy. Figure 1 depicts sinus rhythm followed by twisting-QRS ventricular tachycardia, with an arrow marking the DC shock that restored sinus rhythm.

Ventricular tachycardia recurred 15 times during anesthesia and subsequently in the intensive coronary care unit. Repeated lidocaine 1 mg/kg, bretylium 5 mg/kg, and electric shocks were fruitless. Replacement was started with potassium chloride 26.4 mEq/h, calcium gluconate 4.4 mEq/h, and magnesium sulphate 4 mEq/h. TdPVT finally subsided when serum calcium reached 2.5 mEq/L and potassium 3.9 mEq/L. Ten days later, cataract extraction proceeded uneventfully using the same anesthetic technique.

Case 2 involved an otherwise healthy 65-year-old woman scheduled for repair of an incarcerated femoral hernia. She had vomited for 6 days and appeared wasted; blood pressure was 120/80 mm Hg and heart rate 120 bpm. Blood chemistry was normal except for mild hypokalemia, 3.4 mEq/L. She received 3000 mL of lactated Ringer's solution. Anesthesia was induced with thiopental 3 mg/kg and succinylcholine 1.5 mg/kg and maintained with fentanyl 5 micrograms/kg, pancuronium 0.08 mg/kg, and isoflurane.

During tracheal extubation, while fully awake, she developed a rhythm resembling ventricular tachycardia. Lidocaine up to 2 mg/kg had no effect. Her trachea was reintubated and she was ventilated with 100% oxygen. ECG revealed TdPVT with QRS waves twisting around the baseline at 160 bpm; blood pressure was 60/40 mm Hg. DC cardioversion at 200 joules restored sinus rhythm. QTc was prolonged to 0.62 s, U waves were present, and blood chemistry showed severe combined metabolic and respiratory alkalosis, hypokalemia, hypocalcemia, and hypochloremia, with normal magnesium. Potassium chloride 26.4 mEq/h, calcium gluconate 44 mEq/h, and magnesium sulphate 4 mEq/h were administered until serum levels normalized. Her trachea was extubated 24 hours after surgery, and she was discharged 3 days later.

The review describes TdPVT, first reported by Dessertenne in 1966, as a pleomorphic or polymorphic ventricular tachycardia. Its French name means “twisting around the (isoelectric) point,” describing the ECG's twisting QRS complexes. Early afterdepolarization—depolarization before a cell has fully repolarized—provides the basis for triggered activity believed to underlie the arrhythmia. Delayed repolarization commonly produces prolonged QTc, although TdPVT can occur without QTc prolongation. Both reported patients had prolonged QTc. QT prolongation can be congenital (CLQTS) or acquired (ALQTS). The supplied text refers to Table 3 for conditions causing QT prolongation and TdPVT and for causes of ALQTS, but does not provide that table's contents.

Diagnostic features described are phasic changes in QRS electrical polarity, frequent spontaneous termination, heart rate greater than 150 bpm with variable RR intervals, frequent initiation by a premature ventricular beat on a prolonged TU wave, and prolonged QTc. CLQTS has a familial pattern, usually involves females, and is sometimes associated with congenital deafness, termed Jervell–Lange-Nielson syndrome in the text. The review describes sudden death as a constant threat and proposes excessive adrenergic responsiveness and an imbalance in sympathetic innervation between the heart's right and left sides as possible causes of arrhythmia. Left stellate ganglionectomy together with beta-blocker therapy has been associated with a significant reduction in cardiac events. Anesthetic techniques reported as used safely include continuous epidural anesthesia with heavy sedation and continuous esmolol infusion. The review advises avoiding excessive adrenergic activity and exogenous catecholamines in CLQTS because of life-threatening arrhythmia risk. It cites intraoperative TdPVT in a child with asymptomatic CLQTS involving local epinephrine infiltration, 1:100,000, for hemostasis during halothane anesthesia.

ALQTS is described as more frequent than CLQTS and often involves two or more causes, such as diuretic-induced hypokalemia combined with quinidine. Unlike in CLQTS, exogenous catecholamines may help in ALQTS by shortening QT. The review describes treatment as addressing electrolyte and metabolic disturbances, correcting iatrogenic factors such as hyperventilation, and withdrawing potentially responsible drugs such as quinidine. Antiarrhythmic choice depends on whether QTc is prolonged. Lidocaine is described as usable with or without prolonged QTc because it shortens QTc, but inconsistently effective; bretylium is described as ineffective and probably proarrhythmic. The text also lists isoproterenol, which induces tachycardia, and drugs it calls Class Ic antiarrhythmics, “mexilene” and tocainide, as options that reduce QTc. Magnesium sulphate has reportedly succeeded as first-line TdPVT therapy even when serum magnesium is normal. DC cardioversion is indicated with hemodynamic compromise, although recurrence is common, as in the first case. Persistent cases may require overdrive atrial or ventricular pacing.

For anesthesia in ALQTS, the review emphasizes correcting electrolyte and acid–base disturbances and considering anesthetic effects on QT. It cites Schmeling and colleagues' finding that halothane, isoflurane, and enflurane prolonged QTc in humans, but no arrhythmias were observed in their patients. Because the second patient received isoflurane, a contribution to her prolonged QTc and TdPVT could not be excluded. Thiopental and propofol have also been reported to prolong QT in normal patients. Although succinylcholine has been implicated in TdPVT, the episodes in these two patients occurred after its effect had evidently worn off.

The authors conclude that the two peri-anesthetic episodes were attributable to combined hypocalcemia and hypokalemia, worsened by hyperventilation-induced alkalosis. They describe TdPVT as not directly related to anesthesia, while noting that perioperative iatrogenic factors could trigger or propagate it: hyperventilation and electrolyte imbalance, with the latter induced by mannitol or intestinal losses. Their concluding message is that prompt diagnosis and treatment matter because TdPVT can degenerate into VF, and antiarrhythmics that lengthen QTc should not be used for it. The authors thank Dr. I. Greenfeld for help preparing the manuscript.