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From the Department of Anesthesia, BC Women’s Hospital, Vancouver, British Columbia, Canada.
Address correspondence to: Dr. Vit Gunka, Department of Anesthesia, BC Women’s Hospital, 4500 Oak Street, Vancouver, BC V6H 3N1, Canada. Phone: 604-875-2158; Fax: 604-875-2733; E-mail: vgunka{at}cw.bc.ca
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Clinical features: A 31-yr-old woman, gravida 2 para 1 known to have LQTS and an AICD, presented in labour at 35 weeks gestation, three weeks before her scheduled CS. Her previous delivery by CS under spinal anesthesia at our institution was uneventful. On this occasion, we elected to administer spinal anesthesia because she was asymptomatic (no arrhythmia or cardiac arrest) for the last few years, was hemodynamically stable, and had received uneventful spinal anesthesia before.
Conclusion: Spinal anesthesia was used safely for CS in this parturient with LQTS.
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Because LQTS patients are at a high risk of developing ventricular arrhythmia and cardiac arrest, the anesthetic technique used for these patients must avoid anything that will induce an arrhythmia such as tachycardia, hypotension or increased catecholamine release by pain or stress. Although spinal anesthesia may cause hypotension that can result in arrhythmia and cardiac arrest, it has several other advantages like dense, reliable block, fast onset, low risk of local anesthetic toxicity, and reduction of catecholamine release.
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The pertinent information about her current AICD is as follows: Medtronic GEM 7227 CX (pacer/defibrillator) implanted in March 13/2000; Lead (ventricular) Medtronic 6936; AICD pacemaker mode VVI.
The device was last interrogated one week before the operation. It was functioning well and no episodes of tachycardia or defibrillations were recorded. The pacing threshold was (amplitude) 2.0 volts, (pulse width) 0.10 msec and sensing at 10 mV. The battery status was excellent and the lead impedance was good.
Her first pregnancy was complicated by preterm labour. She had an emergency CS due to decreased fetal movement. Spinal anesthesia was administered in the sitting position using a 25-gauge (G) Whitacre needle at the L3 to L4 interspace with 10.5 mg of hyperbaric bupivacaine 0.75%, fentanyl 15 µg and preservative free morphine 200 µg.
Unfortunately, the anesthetic record did not provide details regarding the application and removal of a magnet over the AICD. Her intra- and postoperative courses were uneventful.
During her second pregnancy her obstetrician scheduled a repeat CS at 38 weeks gestation. She was seen in the anesthesia consultation clinic early in her pregnancy and her previous history was reviewed. She had no allergies. Her medications consisted of unfractionated heparin 7500 units subcutaneously BID, aspirin 81 mg po OD (for antiphospholipid antibody syndrome) and oxprenolol 80 mg po OD.
The physical examination revealed a fit looking woman with normal airway and spine. Her complete blood count, electrolytes (sodium, potassium, magnesium), and coagulation profile were within normal limits. Her electrocardiogram (ECG) showed normal sinus rhythm, heart rate 75 beats•min–1, inverted T-waves in lead III, and a corrected QT interval (QTc) of 406 msec (normal < 440 msec). Discussion was held regarding options for anesthetic management for a repeat CS. As she had received an uneventful spinal anesthetic for her first delivery the decision was made that spinal anesthesia would be used providing there were no new complicating factors.
The cardiologist was contacted for information about the AICD. The information obtained was that the defibrillation function of this AICD is deactivated when the magnet is applied to it and, as soon as the magnet is removed, the defibrillation function is reactivated and the program of the AICD will not be affected.
When she presented in the operating room (OR), the ECG, automatic blood pressure cuff and oxygen saturation monitor were applied. The "crash cart" with defibrillator was located in the OR. The magnet was then placed over the AICD to deactivate defibrillation. The patient remained in normal sinus rhythm and no change was noted. Following prehydration with 1 L of normal saline (iv bolus), spinal anesthesia was induced in the sitting position using a 25-G Whitacre needle at the L2 to L3 interspace with 10.5 mg of hyperbaric bupivacaine 0.75%, fentanyl 15 µg and preservative free morphine 200 µg.
After the induction of anesthesia, the blood pressure dropped from 120/70 mmHg to 90/60 mmHg. Two doses of phenylephrine 100 µg were given and the blood pressure rose to 110/65 mmHg. Ephedrine was not administered in order to avoid tachycardia and increased release of catecholamines. The pulse remained between 70 to 90 beats•min–1. The patient did not require any additional vasopressors. A T4-sensory block to ice was achieved before surgery. Bipolar cautery was used during the surgery. The intraoperative course was uneventful. The patient delivered a male child weighing 2.810 kg with Apgar scores of 9 and 9 at one minute and five minutes, respectively.
Postoperatively, removing the magnet reactivated the defibrillation function of the AICD. This did not affect her heart rate or rhythm and she was transferred to the recovery room for continuous ECG monitoring for 24 hr. The patient remained in normal sinus rhythm for 24 hr postoperatively and no arrhythmia was noted.
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Discussion |
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Long QT interval syndrome is symptomatic in approximately 60% of patients.2 The symptoms of LQTS are syncope (26–30%), seizure (10%) and cardiac arrest (9%), usually secondary to adrenergic arousal. Forty percent of patients are asymptomatic and, in these, the diagnosis is made by family history of LQTS or by routine ECG.
The diagnosis of LQTS is based on ECG, clinical history, and family history.3,4 The ECG criteria include prolonged QTc interval > 440 msec (using the formula of Bazette QTc = QT measured in seconds/
RR interval in seconds),1 Torsades de pointes, T wave alternans, and a notched T wave in any three leads. The clinical history may include syncope (especially if associated with stress), or congenital deafness, and the family history includes a family member with LQTS or sudden cardiac death in an immediate family member before the age of 30 yr.
The treatment of LQTS is directed at preventing fatal dysrhythmias (especially Torsades de Pointes) and sudden death.1 The estimated mortality rate in untreated symptomatic LQTS patients exceeds 20% in the first year after diagnosis. In 1993, Garson and associates reported that effective treatment reduced the ten-year mortality risk from 50% to 3–4%.5
Treatment options may include beta-blockers, pacemaker, AICD, and/or left cervicothoracic sympathectomy.3 Beta-blockers are the first line of treatment. In 1985, Schwartz reported a decrease in mortality from 71% in untreated patients to 6% in those who were treated. However, beta-blockers were ineffective in approximately 25% of cases.3 Antibradycardia pacing involves a permanent pacemaker that aims to prevent bradycardia and pauses, which could trigger an arrhythmia. Patients with this type of pacemaker must continue to take beta-blockers.6
AICD is indicated in patients with persistent symptoms (e.g., syncope) or a documented arrhythmia despite beta-blockers, or when the initial presentation is a cardiac arrest.1 Insertion of an AICD reduces the incidence of sudden death when the episode of Torsades de Pointes is prolonged or proceeds to ventricular fibrillation.7 Even after AICD implantation, these patients should continue to take beta-blockers.
Left cervicothoracic sympathectomy is reserved for patients who are refractory to other types of treatment. Genotype-directed therapy is still under investigation as a treatment option for the future.
The anesthetic management of a patient with LQTS starts with assessment, focusing on the patient’s history, medication use and any other pertinent details, such as pacemaker or AICD. The goal is to optimize the patient’s status preoperatively and discuss their anesthetic management. If the patient is symptomatic, a cardiology consultation is advisable and the patient should be advised to continue medication such as beta-blockers, including on the day of surgery. Hypokalemia, hypomagnesemia, and hypocalcemia should be corrected preoperatively and drugs that prolong the QT interval like antiarrhythmic agents class Ia (e.g., quinidine), class Ic (e.g., sotalol), and class III (e.g., amiodarone) should be avoided in the preoperative period. To avoid catecholamine release and triggering of cardiac dysrhythmia the patient should be calm and aware of the anesthetic plan preoperatively.
If the patient has an AICD or pacemaker, a full history about the device must be documented including the indication for insertion (if other than LQTS), the type of device, the information and the date of last interrogation, the date of the last battery change, any symptoms that indicate malfunction and the response to a magnet. The manufacturer or the cardiologist who implanted it must be contacted to obtain details about the management of the device intraoperatively.8,9
Intraoperatively, the goal is to prevent and treat any dysrhythmia that can result from prolonged QT interval. Prolonged QT interval can be precipitated by drugs (thiopentone, succinylcholine, epinephrine, and norepinephrine),10 electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), hypothermia,10 and any cause of sympathetic stimulation. An external pacemaker and defibrillator must be available in the OR before induction of anesthesia. Any episode of Torsades de Pointes should be treated by cardioversion/defibrillation and magnesium sulphate 30 mg•kg–1 iv over two to three minutes followed by an infusion of 2 to 4 mg•min–1. In patients with a pacemaker or AICD, the usual intraoperative precautions should be taken to avoid disruption of function. This includes using bipolar electrocautery, instead of monopolar, and placing the current return pad as far as possible from the device. Mangar reported a pacemaker failure intraoperatively when a magnet was placed on the pacemaker with the use of monopolar electrocautery.11
Each anesthetic technique has advantages and disadvantages. General anesthesia for CS in a parturient with LQTS has been reported.12 The anesthesiologist should be cautious during induction of general anesthesia. The risk of dysrhythmia is increased due to sympathetic stimulation and increased catecholamine release during intubation and skin incision. Although halothane, enflurane, isoflurane, and sevoflurane have been used as a component of uneventful anesthesia in known LQTS patients who were beta-blocked1 these drugs prolong the QT interval in normal people when used as the sole induction or maintenance agent.13,14 In particular, halothane is known to sensitize the myocardium to catecholamines, resulting in dysrhythmia in normal people. Regional anesthesia in the form of epidural anesthesia15 has been used for CS in a patient with LQTS. Spinal anesthesia has been reported in a non-pregnant patient.16 The major advantage of regional anesthesia is the reduction in catecholamine levels during surgery. The disadvantages are parasympathetic override, potentially causing bradycardia, PR prolongation, and hypotension, which could result in dysrhythmia.
The postoperative course should include recovery in a monitored setting for 24 hr. If the patient has an AICD or a pacemaker, the device must be interrogated by the cardiologist to recheck the program once surgery is finished.
In summary, we report the safe use of spinal anesthesia in a parturient with LQTS presenting for CS.
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Accepted for publication March 1, 2004. Revision accepted August 2, 2004.
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2 Ackerman MJ. The long QT syndrome: ion channel diseases of the heart. Mayo Clin Proc 1998; 73: 250–69.[Medline]
3 Schwartz PJ. Idiopathic long QT syndrome: progress and questions. Am Heart J 1985; 109: 399–411.[Medline]
4 Schwartz PJ, Moss AJ, Vincent GM, Crampton RS. Diagnostic criteria for the long QT syndrome: an update. Circulation 1993; 88: 782–4.
5 Garson A Jr, Dick M II, Fournier A, et al. The long QT syndrome in children: an international study of 287 patients. Circulation 1993; 87: 1866–72.
6 Eldar M, Griffin JC, Van Hare GF, et al. Combined use of beta-adrenergic blocking agents and long-term cardiac pacing for patients with the long QT syndrome. J Am Coll Cardiol 1992; 20: 830–7.[Abstract]
7 Wilde AA. Is there a role for implantable cardioverter defibrillators in long QT syndrome? J Cardiovasc Electrophysiol 2002; 13: S110–3.[Medline]
8 Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery – executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 2002; 94: 1052–64.
9 Trankina MF. Perioperative pacemaker - ICD management. ASA Newsletter May 2002; volume 66. Available from URL; http://www.asahq.org/Newsletters/2002/5_02/whatsnew_502.htm.
10 Swenerton JE, Huckell VF. Disorders of cardiac conduction. In: Gambling DR, Douglas MJ (Eds). Obstetric Anesthesia and Uncommon Disorders, 1st ed. Philadelphia: W.B. Saunders Company; 1998: 39–49.
11 Mangar D, Atlas GM, Kane PB. Electrocautery-induced pacemaker malfunction during surgery. Can J Anaesth 1991; 38: 616–8.
12 Freshwater JV. Anaesthesia for caesarean section and the Jervell, Lange-Nielson syndrome (prolonged Q-T interval syndrome). Br J Anaesth 1984; 56: 655–7.
13 Kuenszberg E, Loeckinger A, Kleinsasser A, Lindner KH, Puehringer F, Hoermann C. Sevoflurane progressively prolongs the QT interval in unpremedicated female adults. Eur J Anaesthesiol 2000; 17: 662–4.[Medline]
14 Schmeling WT, Warltier DC, McDonald DJ, Madsen KE, Atlee JL, Kampine JP. Prolongation of the QT interval by enflurane, isoflurane, and halothane in humans. Anesth Analg 1991; 72: 137–44.[Medline]
15 Ryan H. Anaesthesia for caesarean section in a patient with Jervell, Lange-Nielson syndrome. Can J Anaesth 1988; 35: 422–4.
16 Palkar NV, Crawford MW. Spinal anaesthesia in prolonged Q-T interval syndrome. Br J Anaesth 1986; 58: 575–6.
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