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Case Reports

Perioperative Torsade de Pointes Ventricular Tachycardia Induced by Hypocalcemia and Hypokalemia

Soroker, David MD; Ezri, Tiberiu MD; Szmuk, Peter MD; Merlis, Polina MD; Epstein, Menashe MD; Caspi, Avi MD

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The incidence of Torsade de Pointes ventricular tachycardia (TdPVT) during anesthesia is not known, and its mechanism is not fully understood. We present two cases of a rare but potentially lethal arrhythmia which occurred during anesthesia. Prompt recognition and adequate therapy are crucial for preventing hemodynamic compromise and degeneration into ventricular fibrillation (VF). The mechanism, causes, and treatment of TdPVT are reviewed briefly.

Case 1

A 68-yr-old hypertensive woman, suffering from glaucoma, was admitted for an elective cataract extraction. She had undergone thyroidectomy 10 yr earlier. Mannitol (1.5 g centered dot kg-1 centered dot day-1) was started to decrease intraocular pressure. Preoperative examination and routine blood biochemistries were within normal limits Table 1. The electrocardiogram (ECG) showed left ventricular hypertrophy, strain, and a normal QT interval corrected to rate (QTc) of 0.32 s. Premedication consisted of diazepam 10 mg orally. After breathing oxygen, anesthesia was induced with fentanyl 2 micro gram/kg, thiopental 3 mg/kg, and succinylcholine 1.5 mg/kg, and maintained with N2 O/O2 60:40 and paralysis was induced by alcuronium 0.2 mg/kg.

Table 1
Table 1:
Biochemical Variables in the Perioperative Period: Case 1

Fifteen minutes after induction of anesthesia, multiple ventricular premature beats followed by a sudden tachyarrhythmia resembling VF, were noticed and blood pressure (BP) decreased to 70/50 mm Hg. Intravenous lidocaine up to 2 mg/kg followed by 5 mg/kg of bretylium had no effect and the arrhythmia persisted.

The ECG trace showed polymorphous ventricular tachycardia (VT) with twisting of the QRS axis around the baseline at a rate of 150/min Figure 1, suggesting a TdPVT. A 200-joule direct current (DC), countershock successfully reversed the VT into sinus rhythm and a second ECG showed sinus rhythm with prolonged QTc interval (0.53 s). Blood biochemistry revealed a potassium of 3.3 mEq/L (normal 3.5-5 mEq/L) and magnesium 1.8 mEq/L (normal 1.5-2.5 mEq/L), total serum calcium 1.6 mEq/L (normal 2.2-2.7 mEq/L), and respiratory alkalosis Table 1. Hypokalemia and hypocalcemia were caused by a combination of hyperventilation, mannitol therapy, and a hidden hypoparathyroidism after total thyroidectomy.

Figure 1
Figure 1:
Sinus rhythm (upper trace), followed suddenly by ventricular tachycardia with twisting of the QRS axis around the baseline--Torsade de Pointes (middle and lower trace). The arrow indicates the point where direct current countershock was applied, reversing Torsade de Pointes ventricular tachycardia into sinus rhythm.

VT recurred 15 times during anesthesia and later in the intensive coronary care unit. Repeated administration of lidocaine (1 mg/kg) bretylium (5 mg/kg), and electric shocks were fruitless. Potassium chloride (26.4 mEq/h) calcium gluconate (4.4 mEq/h), and magnesium sulphate (4 mEq/h) replacement was started. TdPVT finally subsided when the serum levels of calcium and potassium reached 2.5 mEq/L and 3.9 mEq/L, respectively Table 1.

Ten days later, the patient underwent cataract extraction uneventfully under the same anesthetic technique.

Case 2

A 65-yr-old, otherwise healthy woman was scheduled for repair of an incarcerated femoral hernia. She had been vomiting during the last 6 days and looked wasted, with a BP of 120/80 mm Hg and heart rate of 120 bpm. Blood chemistry values were within normal limits, except for a mild hypokalemia (3.4 mEq/L) Table 2.

Table 2
Table 2:
Biochemical Variables in the Perioperative Period: Case 2

Lactated Ringer's solution, 3000 mL, was administered, and anesthesia was induced with thiopental 3 mg/kg and succinylcholine 1.5 mg/kg and maintained with fentanyl 5 micro gram/kg, pancuronium 0.08 mg/kg, and isoflurane. During tracheal extubation, while the patient was fully awake, a tachyarrhythmia resembling VT was noted. Lidocaine up to 2 mg/kg was administered without effect. The trachea was reintubated, and the patient ventilated with 100% oxygen. The ECG trace revealed TdPVT with QRS waves twisting around the baseline at rate of 160 bpm. At the same time, BP was 60/40 mm Hg. DC cardioversion (200 joules) successfully reversed the TdPVT into sinus rhythm. Prolonged QTc interval (0.62 s) and "U" waves were observed, and the blood chemistry showed severe combined metabolic and respiratory alkalosis, hypokalemia, hypocalcemia, and hypochloremia with normal magnesium levels Table 2. Potassium chloride (26.4 mEq/h), calcium gluconate (44 mEq/h), and magnesium sulphate (4 mEq/h), were administered until normal serum levels were obtained Table 2.

Twenty-four hours after surgery, the patient's trachea was extubated and 3 days later she was discharged from the hospital.

Discussion

TdPVT, originally described by Dessertenne in 1966 [1], is related to the group of pleomorphic or polymorphous VT [2]. The name "Torsade de Pointes," meaning, in French, "twisting around the (isoelectric) point," refers to its peculiar ECG pattern of twisting QRS complexes around the baseline [3]. Early after depolarization (depolarization occurring before the cell fully repolarizes), is the basis for triggered activity, which is believed to be the electrophysiologic mechanism for the development of this arrhythmia. Apart from the pleomorphism of the QRS complexes, TdPVT is also characterized by the appearance of prolonged QTc interval, due to delayed repolarization [4-6], although it may occur in the absence of prolong QTc. In our patients, QTc intervals were prolonged.

Prolongation of QT interval may be congenital (CLQTS) or acquired (ALQTS). Conditions known to produce prolonged QT and TdPVT are depicted in Table 3. The diagnosis of TdPVT is based on phasic variation in the electrical polarity of the QRS complex [6], common spontaneous termination [6], heart rate > 150 bpm with varying RR intervals [6], frequent initiation by a premature ventricular beat occurring on a prolonged "TU" wave [6], and prolonged QTc interval [7].

Table 3
Table 3:
Causes of QT Interval Prolongation and Torsade de Pointes Ventricular Tachycardia

CLQTS has a familial pattern [8], is sometimes associated with congenital deafness (Jervell, Lange-Nielson syndrome), and usually involves females. Sudden death is a constant threat, and the possible cause for arrhythmias seems to be an adrenergic over-reactivity and imbalance between the sympathetic innervation of the right and the left sides of the heart. Left stellate ganglionectomy is a useful therapeutic tool and, together with beta-blocker therapy, has been associated with a significant reduction of the cardiac events [16].

Various anesthetic techniques have been used safely in CLQTS, including continuous epidural anesthesia with heavy sedation and continuous infusion of esmolol [17]. Excessive adrenergic activity and the use of exogenous cathecholamines should be avoided due to the risk of life-threatening arrhythmias [8]. Local infiltration with epinephrine (1:100,000) for hemostasis during halothane anesthesia has been involved in the etiology of intraoperative TdPVT in a child with asymptomatic CLQTS [17].

ALQTS occurs more frequently than CLQTS. Its causes are summarized in Table 3. Frequently, two or more underlying causes are involved, such as diuretic-induced hypokalemia and concomitant quinidine therapy. Contrary to CLQTS, exogenous catecholamines may be beneficial in ALQTS by shortening the QT interval. The treatment of ALQTS and TdPVT involves treatment of the underlying causes, such as electrolyte and metabolic disturbances [6], correcting iatrogenic factors (in our case, hyperventilation), and withdrawing any potentially responsible drugs, such as quinidine [6]. Use of antiarrhythmic therapy depends on whether the QTc interval is prolonged. Lidocaine can be used in both cases because it shortens the QTc interval [2], but it is inconsistently effective, whereas bretylium is ineffective and probably proarrhythmic [18]. Isoproterenol, by inducing tachycardia [6] and Class Ic antiarrhythmic drugs (mexilene, tocainide) causing a reduction of QTc interval, may also be used [2]. Magnesium sulphate has been used successfully as a first line therapy of TdPVT, even with normal serum magnesium levels [19]. DC cardioversion is indicated with hemodynamic compromise, although arrhythmia tends to recur [5], as was the case of our first patient. In persistent cases, overdrive atrial or ventricular pacing is indicated [18]. The anesthetic management of patients with ALQTS should take into account the correction of the underlying electrolyte disorders and acid-base imbalance, as well as the effects of the anesthetics on the QT interval.

Schmeling et al. [20] have demonstrated QTc interval prolongation by halothane, isoflurane, and enflurane in humans. Despite this, the authors noted no arrhythmias in their patients. Our second patient received isoflurane; therefore some contribution of this drug in inducing prolonged QTc interval and TdPVT cannot be excluded. Thiopental and propofol have been reported to prolong the QT interval in normal patients [21]. Although succinylcholine has been implicated as a cause of TdPVT [19], in our patients TdPVT occurred when the drug's effect had evidently worn off.

In summary, we present two cases of perianesthetic TdPVT attributed to the combined effect of hypocalcemia and hypokalemia, worsened by alkalosis induced by hyperventilation. Although not directly related to anesthesia, TdPVT might be triggered or propagated by some perioperative iatrogenic factors, such as hyperventilation and electrolyte imbalance, induced in turn by mannitol or intestinal loss. The important implications of prompt diagnosis and treatment of TdPVT are that it may degenerate into VF and should not be treated with antiarrhythmics, which lengthen the QTc interval.

The authors thank Dr. I. Greenfeld for his help in preparing this manuscript.

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        © 1995 International Anesthesia Research Society