Anesth Analg 2006;102:233-236
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000184258.64205.9B
CRITICAL CARE AND TRAUMA
Unmasking of Brugada Syndrome by an Antiarrhythmic Drug in a Patient with Septic Shock
Katsuyuki Terajima, MD,
Takesi Yamamoto, MD,
Hidetaka Onodera, MD,
Shinhiro Takeda, MD,
Keiji Tanaka, MD, and
Atsuhiro Sakamoto, MD
Division of Intensive Care and Coronary Care Unit, Nippon Medical School, Tokyo, Japan
Address correspondence and reprint requests to Katsuyuki Terajima, 1–1–5 Sendagi, Bunkyo-ku, Tokyo, 113–8603, Japan. Address e-mail to terajima.katsuyuki{at}nifty.com.
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Abstract
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Asymptomatic Brugada syndrome patients often display concealed Brugada-type electrocardiogram patterns that result in under-diagnosis of this syndrome. These patients include individuals of both genders and a wide range of ages. They are as likely as non-Brugada patients to have normal longevity or to suffer from a critical illness. Here we report a case of septic shock in which Brugada-type electrocardiogram patterns were induced by pilsicainide administration for the treatment of atrial fibrillation. This case report suggests that some drugs used in the treatment of septic shock can unmask the Brugada-type electrocardiogram pattern and induce lethal ventricular tachyarrhythmia.
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Introduction
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Brugada syndrome is thought to be a major cause of sudden death and of syncope and idiopathic ventricular tachyarrhythmia in young people with structurally normal hearts (1). However, this syndrome occurs in both genders and all age groups, including infants (2) and the elderly (3), and shows no correlation with the health of the patient. The syndrome is characterized by a right bundle-branch block with ST elevation in leads V1 to V3, as shown by an electrocardiogram (ECG). The Brugada-type ECG can transiently normalize for a period of time leading to an under-diagnosis of the disease (4). Here we report a case of septic shock with undiagnosed asymptomatic Brugada syndrome that was unexpectedly unmasked by an antiarrhythmic drug for atrial fibrillation (AF).
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Case Report
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An 84-yr-old male patient at the Nippon Medical School, Japan, was suffering from septic shock after aspiration pneumonia. Two months before the incidence of septic shock, a total gastrectomy and partial esophagectomy had been performed to remove the remnants of a previous gastric cancer. A preoperative 12-lead ECG revealed no significant ST-T change (Fig. 1) and an echocardiograph showed no structural abnormalities, with a left ventricular ejection fraction of 65%. The patient had neither a history of syncope nor a family history of sudden death. Before septic shock, the patient had experienced a loss of appetite for 2 days, accompanied by sudden vomiting.
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Figure 1. The preoperative electrocardiogram shows sinus rhythm with no significant ST segment elevation.
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On the morning after he vomited, the patient was febrile, hypotensive, and hypoxemic, with an oxygen saturation of 86%. He was immediately transferred to the intensive care unit (ICU). The patient was tracheally intubated, and the intratracheal fluid contents were suctioned with bronchoscopy. Despite aggressive IV fluid resuscitation, the patient remained hypotensive. Infusion of dopamine at 10 µg · kg–1 · min–1 and norepinephrine at 0.4 µg/kg subsequently commenced. After catecholamine administration, his heart rate was 100 to 120 bpm with sinus rhythm. Blood samples taken from the patient and grown in culture revealed Klebsiella pneumoniae. Hemoperfusion with polymyxin B-immobilized fibers and continuous hemodiafiltration (CHDF) were performed to treat septic shock with acute renal failure; however, catecholamine administration was still required.
On day 2 in the ICU, the patient developed AF (Fig. 2). We subsequently administered 0.6 mg/kg of pilsicainide IV. The AF was converted to sinus rhythm, but the ECG revealed a Brugada-type pattern (Fig. 3). Twelve hours after the administration of pilsicainide, the patient developed ventricular tachycardia (Fig. 4). The serum electrolyte concentrations when the patient showed this ECG pattern and the polymorphic ventricular tachycardia were within normal limits, but the metabolic acidosis was persistent (Table 1). In view of the unmasked characteristic ECG features after administration of pilsicainide IV, the induced ventricular tachyarrhythmia, and the absence of underlying structural heart disease according to echocardiography, the patient was diagnosed with Brugada syndrome. External defibrillation pads were attached to his chest to prevent recurrence of the lethal arrhythmias. The serum creatinine level of the patient was 0.6 to 0.97 mg/dL during his time in the ICU. The 12-lead ECG showed recovery to sinus rhythm after polymorphic ventricular tachycardia, with a Brugada-type pattern (Fig. 5) that persisted 3 days after pilsicainide administration. The creatine kinase isoenzyme MB levels were not increased at 0 and 6 h and the troponin T was not detected (TROPT sensitiveTM, Roche Diagnostics Inc., Basel, Switzerland) at 0, 12, and 18 h after the recovery to sinus rhythm from AF. Asynergy of the left ventricle was not detected by echocardiography 0 and 12 h after the recovery to sinus rhythm. Unfortunately, the patient died on his fifth day in the ICU as a result of sepsis.
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Figure 3. The 12-lead electrocardiogram shows right bundle-branch block and "coved" type ST elevation in leads V1 to V4 (Brugada-type electrocardiogram) after pilsicainide administration.
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Figure 4. The electrocardiogram 12 h after pilsicainide administration shows polymorphic ventricular tachycardia.
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Figure 5. The electrocardiogram after polymorphic ventricular tachycardia shows recovery to sinus rhythm with a Brugada-type pattern.
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Discussion
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A previous study has shown that the incidence of AF increases in critically ill patients who have received significantly more fluids and catecholamines than other patients in an effort to treat septic shock and acute renal failure (5). Therefore, the occurrence of AF in this case was not surprising, as the onset of AF appears to reflect the severity of the critical illness. Moreover, it has been shown that AF occurs in 10% to 39% of all patients with Brugada syndrome (6–8).
Approximately 20%–30% of Brugada patients have mutations in the SCN5A gene on chromosome 3 (9). The SCN5A gene encodes the  subunit of the human cardiac voltage-gated sodium channel. This disorder can be inherited through autosomal dominant transmission, although there is some degree of genetic heterogeneity. Sodium-channel blockers and an autonomic imbalance have previously been thought to help unmask the Brugada-type ECG. Administration of ajmaline, flecainide, or procainamide accentuates ST segment elevation (1) and assists in the diagnosis of Brugada syndrome (10). Pilsicainide, which is a class IC drug, has been found to induce similar ST segment elevation in response to administration of flecainide (11). In patients with severe renal failure, the half-life of elimination for pilsicainide is prolonged to 23.7 hours (12). The elimination and total body clearance of pilsicainide are not always linearly correlated with the creatinine clearance when CHDF is performed. Alpha-adrenergic, but not ß-adrenergic, stimulation has been shown to augment the ST segment elevation in Brugada syndrome (13). The Brugada-type ECG might be preserved by continuous IV administration of norepinephrine and/or insufficient clearance of pilsicainide. Although selective stimulation of muscarinic receptors can augment the ST segment, tachycardia alone cannot prevent a Brugada-type ECG pattern in this situation. The febrile status per se might unmask Brugada syndrome (14). The Brugada-like ECG pattern can also be caused by electrolyte disturbance and ketoacidosis (15), but flecanide drug challenge and electrophysiological studies can exclude an underlying Brugada syndrome. If the Brugada-type ECG shows ST elevation during treatment for sepsis and arrhythmias, Brugada syndrome should be considered. If characteristic Brugada-type ECG patterns are observed in the absence of evidence for ischemia or underlying structural heart disease according to echocardiography, the causes of ST-T elevation should be avoided, defibrillation should be available for lethal ventricular tachyarrhythmias, and methods such as dialysis to remove the causative drugs should be considered.
In summary, the drugs used for treating septic shock, such as norepinephrine and antiarrhythmic drugs, might unmask Brugada syndrome. Asymptomatic patients with concealed Brugada-type ECGs might have an increased risk of developing lethal arrhythmia when treated for septic shock, and this might require external defibrillation. We suggest that on recovery from sepsis, the implantation of an internal defibrillator should be considered for these patients.
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Footnotes
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Accepted for publication July 11, 2005.
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References
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Abstract
Introduction
