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"Effect of Sevoflurane on QT Interval in a Patient with Congenital Long QT Syndrome"
1Gallagher, JD, Weindling, SN, Anderson, G, Fillinger, MP, Effect of Sevoflurane on QT Interval in a Patient with Congenital Long QT Syndrome, Anesthesiology, 1998 December; 89(6) 1569-1573
The authors begin this paper by noting that enflurane, halothane, and isoflurane tend to prolong the QT interval in healthy patients.
The question is what would be the effects of these and related agents in individuals who have idiopathic long QT syndrome.
A number of effects have been reported for individuals with long QT syndrome. Examples:
Cardiac arrest and death during halothane anesthesia
No QT interval change with enflurane
Decreased QT interval with isoflurane.
The authors conclude that it is probably is unreasonable to extrapolate from anesthetic effects on the QT interval in healthy patients to the anesthetic effects on the QT interval in patients with idiopathic long QT syndrome.
Another example is that thiopental will tend to prolong the QT interval in healthy patients but has no effect on the QT interval in patients with long QT syndrome.
The authors present this case report which examines the effect of sevoflurane on the QT interval in the patient with congenital long QT syndrome.
Case report:
This case considers a 17-year-old, 49 kg female, otherwise healthy, patient who presented for impacted wisdom teeth extraction.
Identification of congenital long QT syndrome followed from a preoperative examination in which an irregular pulse was noted.
Secondary to this irregularity, an ECG was ordered. An initial ECG was normal, with the QT interval of 362 msec; which when corrected for heart rate resulted in a QTc of 396 msec.
The recording was, however, continued and and rhythm abnormalities noted shortly thereafter.
These abnormalities consisted of multifocal premature ventricular extrasystoles as well as a 14-beat run of polymorphic ventricular tachycardia (135 beats/min.) which was associated with a prolonged QTc of 526 msec.
The patient was not conscious of the arrhythmia.
Following the identification of prolonged QTc syndrome, surgery was postponed electrophysiological evaluation ordered.
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1Case Report Continues:
No family history of deafness was noted; however, family records indicated that the patient' s maternal great-grandmother died suddenly at age 50 in the absence of known medical problems. The patient's mother's ECG revealed QTc elevation (564 msec) [QT interval, 440 msec; heart rate = 99 beats/minute]. The patient in the case did not exhibit syncope associated with emotion or physical distress. Utilizing the criteria above, to establish the probability of congenital long QT syndrome, it was concluded that the patient probably did have congenital long QT syndrome.
Application of the criteria enumerated in the table above in this context revealed the following:
QTc of 460-470 msec on a subsequent resting ECG (2 points);
T-wave alternans shown on Holter recording (1 point)[4T wave alternans (TA) is a repolarization event that is characterized by a microvolt beat to beat change in the T wave and ST segmental amplitudes. The mechanism responsible for TA is a beat to beat)variation of the repolarization sequence that may be due to either an alternation of action potential duration, frequently associated with the long QT syndrome or an alternation of the time course of repolarization often observed in ischemic disease.]
Low heart rate for age (43 beats/min; 0.5 points)
Torsades-like polymorphic ventricular tachycardia (2 points)
> 4 points using this system of scoring corresponds to a high probability of long QT syndrome
The authors note that although QT-interval prolongation on the resting ECG is the hallmark of long QT syndrome, it need not be present (current patient). Furthermore patients may have symptomatic long QT syndrome such as torsades de pointes and sudden death even with normal QT intervals.
In this patient transthoracic echocardiography showed no abnormality.
Initial Holter monitor analysis yield 337 runs of asymptomatic, polymorphic ventricular tachycardia, sometimes consisting of 11 beats.
Prognostic factors do not allow prediction with respect to which patients will develop fatal arrhythmias; therefore, this patient was treated despite detection of only nonsustained ventricular tachycardia using Holter monitoring.
Subsequently (over a three-month period), intravenous lidocaine was determined to abolish extrasystoles and that nadolol was somewhat helpful. Nadolol, 80 mg, twice-daily, was not only shown to reduce heart rate to 50 beats/min. but also decreased the number of ventricular tachycardic runs 251/day (long as run = 18 beats).
Since arrhythmias persisted, 300 mg oral
labetalol given twice-daily was evaluated. It had been suggested
that in some cases in which beta adrenergic antagonists were not
effective, labetalol which exhibits both 
and 
adrenergic receptor antagonism might be effective. In this case,
labetalol shown to decreased the likelihood of polymorphic
ventricular tachycardia to 37 episode/day (longest run = 5
beats). In this time surgery was rescheduled.
Initially, upon arrival at the same day surgery waiting area, the initial ECG indicated a heart rate of 72 beats/minute with the QT interval of 362 msec yielding a QTc of 396 msec. Midazolam is administered by incremental, IV dosing (total dose = 4 mg). ECG recordings noted below:
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1Heart Rate and QT interval corrected for heart rate using QTc = QTo (
), Bizett's formula is noted below:
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Left axis (diamonds) = QTc interval
Right axis (circles) = heart rate at various times during the case
Sevoflurane (1.2% and 1.8% during the time marked by the arrows.
Data points before the arrow indicate, in sequence:
Midazolam administration
Initiation of lidocaine infusion
Propofol and fentanyl induction
Relaxation using rocuronium
Intubation
Nitrous oxide inhalation
then sevoflurane administration
No extrasystoles were noted during sevoflurane administration.
Blood pressure was stable (100/50 mmHg).
Discontinuation of sevoflurane was associated with a return to shorter QTc intervals.
Analgesia at the tooth extraction site was provided by a total of 6 ml, 0.25% bupivacaine (no epinephrine).
Emergence which included reversal of neuromuscular blockade with neostigmine 2 mg and 0.3 mg iv glycopyrrolate, awakening and extubation occurred with an increase in BP to 130/75 mm Hg but without an increase in QTc.
With awakening, single monoform ventricular extrasystoles were noted (12/min); Following extubation, as noted above (panel D), multiform ventricular extrasystoles appeared. iv labetalol (5 mg) administration resulted in arrhythmia resolution; labetalol mechanism: probably adrenergic receptor blockade.
Heart rate and QTc following labetalol noted by last points in the Fig. above
In PACU, lidocaine infusion was continued, but after 1 hour, multiform ventricular extrasystoles reappeared, necessitating administration of 5 mg iv labetalol, which terminated with arrhythmia. Lidocaine was discontinued and the patient was monitored for several hours and did not exhibit additional arrhythmic episodes.
The patient was discharged with no adverse sequelae.
In the discussion section, the authors point out that long QT syndrome can cause syncope, sudden death from cardiac arrhythmias and seizures.
The arrhythmias associated with long QT syndrome include polymorphic ventricular arrhythmias (torsades) and ventricular fibrillation.
Certain medications such as quinidine and terfenadine can result in QT prolongation. A number of other drugs including some antidepressants (tricyclics), antipsychotics e.g. thioridazine, droperidol, risperidone and certain antimicrobials such as ketoconazole, erythromycin, trimethoprim-sulfamethoxazole as well as the diuretic indapamide. Some of these drugs interact with the rapid component of the delayed rectifier K current (Ikr).
The present paper does not deal with acquired-long QT syndrome but rather an inherited form.
The two types of an inherited forms include an autosomal recessive form (Jervell-Lange-Neilsen) which is associated with congenital deafness and the more common autosomal dominant form (Romano-Ward).
The authors point out that > 35 mutations have been identified in four cardiac ion-channel genes which code for the 3 channel proteins that regulate cardiac cell ion currents.
QT interval may be a prolonged by (a) mutation-induced functional loss of rapid activating delayed rectifier K+ channels (LQT2) or (b) mutation- induced functional loss of slowly activating delayed rectifier K+ channels (LQT1) or (c) interference with inactivation both the inward sodium current (INa) thus prolonging repolarization (LQT3). The relationship responsible for torsades and polymorphic ventricular tachycardia in patients with long QT syndrome remains to be elucidated.
Anesthetic management of patients with long QT syndrome includes continuation of preoperative antiarrhythmic medication and insuring sufficient premedication to reduce anxiety.
Catecholamine release may induce interoperative arrhythmias.
Catecholamine release is associated with increased sympathetic nervous system activity and might be expected during intubation and emergence. To reduce sympathetic outflow increases, ketamine, halothane, and pancuronium administration probably should be avoided.
The authors utilize several contemporary approaches to manage the patient in this case.
For example, local anesthetic solutions which contain epinephrine may induce polymorphic ventricular tachycardia as a result of some systemic catecholamine effect. Accordingly, epinephrine was not added to the local anesthetic preparation used in this case.
Another example is a Jervell-Lange-Nielsen patient did not exhibit a prolongation of the QT intervalrespond following propofol. Acordingly,propofol is included in the anesthetic protocol for this case's patient.
Sevoflurane was chosen because its use would speed emergence and probably reduces action-potential duration.
Preparation: The authors were prepared to take additional action had the patient not responded well to iv labetalol administration, i.e. had the arrythmias not resolved. Preparation included the presence of a transcutaneous pacemaker/defibrillator in the room and conductive pads had been placed on the patient. Therefore, pacing was immediately available had bradycardia developed. Bradycardia is a significant risk factor with respect to malignant arrhythmias in long QT interval patients. If malignant arrhythmias had developed and had not been controllable by other means, iv magnesium and amiodarone therapy had been considered.
1Gallagher, JD, Weindling, SN, Anderson, G, Fillinger, MP, Effect of Sevoflurane on QT Interval in a Patient with Congenital Long QT Syndrome, Anesthesiology, 1998 December; 89(6) 1569-1573
2Drugs and the QTc interval" Australian Prescriber, 25(3), 2001
3Medical Algorithm Project
4Hunt, AC T Wave Alternans in high arrhythmic risk patients: Analysis in time and frequency domains: A pilot study, BMC Cardiovascular Disorders.
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