Anesth Analg 2003;97:264-267
© 2003 International Anesthesia Research Society
REGIONAL ANESTHESIA
Brugada-Type Electrocardiographic Pattern Induced by Epidural Bupivacaine
Nicole Phillips, MBBS*,
Mark Priestley, MBBS FANCZA*,
A. Robert Denniss, MD FRACP
, and
John B. Uther, MD AO, MBBS, FRACP
Departments of *Anesthesia and
Cardiology, Westmead Hospital, Westmead, Australia
Address correspondence and reprint requests to Nicole Phillips, Department of Anaesthesia, Level 3, Westmead Hospital, Westmead NSW 2145, Australia. Address e-mail to nicolephillips{at}optusnet.com.au
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Abstract
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IMPLICATIONS: In this case report, we describe the postoperative occurrence of electrocardiogram changes suggestive for the Brugada syndrome in a patient receiving a continuous epidural bupivacaine infusion. After withdrawal of bupivacaine, the electrocardiogram changes were reversible. The patient’s history was unremarkable except for an incomplete right bundle branch block. We conclude that local anesthetics, particularly bupivacaine, have the potential to induce serious arrhythmias in patients with Brugada syndrome.
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Introduction
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The Brugada syndrome causes sudden cardiac death potentially hastened by class I antiarrhythmic drugs. In 1992, Pedro and Joseph Brugada (1) described a series of 8 patients successfully resuscitated from ventricular fibrillation (VF). They all shared the features of apparent right bundle branch block (RBBB) with ST elevation in leads V1–V3, structurally normal hearts, and a propensity to VF/ventricular tachycardia. Mutations in the 
subunit of the sodium channel have been identified as causing an abnormality in the sodium current responsible for rapid depolarization (2). Since the original description, there have been several reports and reviews (3–5), yet little is known about the anesthetic implications of this syndrome. IV sodium channel blockers can unmask Brugada syndrome (6). We present a case in which epidural bupivacaine seems to have produced the typical electrocardiographic (ECG) changes of Brugada syndrome, and postulate that early diagnosis and cessation of the bupivacaine infusion may have prevented a potentially fatal arrhythmia from occurring.
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Case Report
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A 77-yr-old man underwent elective gastrectomy for carcinoma of the stomach. He had reflux esophagitis for which he was prescribed omeprazole, and had no other medical illnesses. He denied symptoms of ischemic heart disease. Blood pressure was recorded in preadmission clinic as 130/60.
An exercise stress test and ECG was normal 10 yr previously. The preoperative ECG showed a partial RBBB (Fig. 1), similar to a tracing obtained 5 yr previously by the patient’s local physician. Routine preoperative blood tests, including serum electrolytes, were normal.
Before the induction of general anesthesia, an epidural catheter was inserted at T9/T10 intervertebral space. The paramedian approach was used, with the patient in the sitting position. Loss of resistance to saline was achieved at 5 cm, and 5 cm of catheter was left in the epidural space. A test dose was not used. Aspiration of the catheter was negative for blood and cerebrospinal fluid. Bupivacaine 10 mL 0.25% was given in 2-mL increments over 5 min to establish a block, and an infusion of 0.125% bupivacaine and 2.5 µg/mL fentanyl commenced at 8 mL/h. Anesthesia was induced with midazolam 2 mg, propofol 150 mg, fentanyl 200 µg, and rocuronium 50 mg. The patient was tracheally intubated with a 7.5 cuffed endotracheal tube. Anesthesia was maintained with sevoflurane. After an uneventful 2-h operation, the patient was extubated and transferred to recovery. A bolus dose of 8 mL of 0.125% bupivacaine and 2.5 µg/mL fentanyl was given on arrival in recovery with good effect. He was admitted to the surgical high-dependency ward, after a 45-min stay in recovery. The acute pain team reviewed the patient 4 h postoperatively and noted he was pain free. His systolic arterial blood pressure at this time was 100 mm Hg and heart rate 75 bpm.
His systolic arterial blood pressure remained 80–100 mm Hg. A total of 1000 mL of IV colloid solution was infused to maintain a systolic blood pressure of 100 mm Hg. He had pain at the top of the surgical incision and received two 5-mL epidural boluses of 0.125% bupivacaine with 2.5 µg/mL fentanyl, 1 3 h postoperatively, and the other at 11 h postoperatively. Both boluses resulted in relief of pain. After the second epidural bolus, his systolic arterial blood pressure decreased to 80 mm Hg. He felt otherwise well, had no chest pain or shortness of breath, and had good analgesia. An ECG was performed (Fig. 2) which showed apparent RBBB, with new coved (convex-curved) ST elevation in V1–V3. Although a provisional diagnosis of acute myocardial infarction was made by the resident staff, a consultant cardiologist was contacted who made a provisional diagnosis of Brugada syndrome, unmasked by the sodium blocking effects of bupivacaine. Bupivacaine was ceased after a total infusion time of 17 h (total of 442.5 mg of bupivacaine). Patient-controlled epidural meperidine was commenced. Serial troponin T and creatine kinase MB index levels remained within normal limits, and the ECG changes subsided over the following 48 h (Fig. 3). The patient made a complete and uneventful recovery and subsequent echocardiography revealed normal coronary arteries, normal myocardial contractility, and normal valves. There was no evidence for hypertrophic cardiomyopathy. Unfortunately, serum bupivacaine levels were not analyzed. The patient’s immediate family was screened but no baseline ECG abnormalities were found. There was no family history of sudden cardiac death or syncope.
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Discussion
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In a review of 163 reported cases of Brugada syndrome (5), 92% were male and 58% were of Asian origin. The syndrome has been seen in all age groups, including infants (7), but it peaks in the fourth decade. The prevalence of the Brugada-type ECG pattern was 0.16% when screening 10,000 healthy working adults (8). Another group screened 12,000 noncardiac hospital patients and found 52 had ECGs typical of the Brugada syndrome (9). The medical history and physical examination of patients are typically unremarkable, but there may be a family history of sudden cardiac death or syncope.
The characteristic ECG pattern is an RBBB with right precordial ST segment elevation (V1–V3). The widened S wave in the left lateral leads of a true RBBB is usually absent. The QT interval is normal and there is absence of reciprocal ST depression as seen in ischemia. The ST elevation may be "coved" or "saddle shaped." The ECG can transiently normalize leading to an under-diagnosis of the disease (4).
The disorder can be inherited with an autosomal dominant mode of transmission; however, a degree of genetic heterogeneity exists. An abnormal SCN5A gene, which encodes for the subunit of the cardiac sodium channel, has been identified in 15% of patients with Brugada syndrome (10). A review of the complex genetic and electrophysiological basis of Brugada has been published (4). Electrical heterogeneity in the right ventricular epicardium leads to a reentrant mechanism, which can result in ventricular tachycardia or VF. This can be exacerbated by the presence of sodium channel blockers. The use of a sodium channel blocker, particularly flecainide, to help induce the typical ECG pattern, is a well documented method to assist in making the diagnosis (6,11). Sodium channel blockers further reduce the fast inward sodium current responsible for depolarization leading to repolarization of the right ventricular epicardium. However, one study found that a pharmacological challenge with sodium channel blockers was unable to unmask most silent gene carriers (10).
The convincing nature of the ECG changes, the exclusion of any plausible alternative diagnosis, and the small sensitivity and potential danger of the test discouraged us from challenging the patient with a sodium channel blocker. Patients with Brugada syndrome who present with syncope or near sudden death have a poor prognosis without intervention. In a series of 63 patients reported by Brugada (12), 30% died or had near sudden death over a 34-month period. Antiarrhythmic drugs are of little use in preventing arrhythmias and the treatment of choice in this group is an implantable cardioverter-defibrillator (5,12).
A second group of patients manifesting a Brugada-like ECG have been described. They have an incidental finding of a Brugada-like ECG, are asymptomatic, and have no family history of sudden death. These patients seem to have a more benign course (10).
This is the first reported case of bupivacaine inducing the characteristic ECG pattern of Brugada syndrome. The only previously documented local anesthetic shown to induce this pattern was cocaine (13), albeit as a recreational drug, rather than as a local anesthetic. Sodium channel blockers have been used to identify concealed Brugada syndrome, but class Ib drugs (specifically lidocaine) did not induce the characteristic ECG changes (14). Bupivacaine, however, causes greater depression of the rapid phase of depolarization in Purkinje fibers and ventricular muscle than lidocaine (15), and remains bound to the sodium channels for a longer period of time. The true clinical significance for anesthesiologists of an interaction between local anesthetics, particularly bupivacaine, and patients with Brugada syndrome is unclear, but we believe this case demonstrates the potential to increase the risk of serious arrhythmias, and anesthesiologists should be aware of such a possibility.
The development of a Brugada-like ECG tracing after the administration of bupivacaine warrants the immediate discontinuation of this medication and immediate cardiological evaluation.
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References
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Accepted for publication March 3, 2003.
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Abstract
Introduction
