Every patient was admitted to the cardiac intensive care unit for a postoperative period of at least 36 h; no patient presented worsening in ST segment elevation. The patient who had hemoperitoneum had sinus tachycardia without changes in the ST segment.
The prevalence of Brugada syndrome has not been accurately estimated but, according to previous studies, the disease is not uncommon. The incidence may be even more frequent in the younger population and it is the most common cause of sudden death in individuals younger than 50 years without underlying cardiac disease in the Japanese population (5) and in South Asia (6). Roberts and Brugada (7) report an estimated incidence of this form of sudden death between 26 and 38 per 100,000 people per year. Anesthesiologists should be aware of Brugada syndrome because it is not a rare disease; from 20% to 60% of idiopathic ventricular fibrillation could be associated with this syndrome.
Risk stratification in these patients is important for defining treatment: e.g., the choice of cardioverter-defibrillator implantation (4). Current studies only propose risk stratification for nonsurgical patients; the few reports available did not demonstrate any heart rate instability, electrical storm or other adverse events during surgery, therefore more data are necessary for a better risk evaluation in surgical patients. We can only extrapolate this information from the studies conducted in nonsurgical patients. Priori et al. (4) showed, in a prospective evaluation, that asymptomatic subjects are at less risk for sudden death and that management strategies should be based on risk stratification algorithms. Brugada et al. (8) proposed a risk stratification scheme based on screening with programmed electrical stimulation of asymptomatic patients, but this test is not reproducible and it is useless for risk stratification (4,9,11). Other authors proposed different criteria for risk stratification but they all need to be confirmed: Priori et al. (9) proposed S wave width ≥0.08 s in V1 and ST elevation ≥0.18 mV in V2; Atarashi and Ogawa (10) proposed ST elevation >0.15 mV at baseline with pilsicainide-induced additional ST elevation >0.1 mV, and Morita et al. (11) proposed the simultaneous presence of syncopes and ST segment elevation at ECG baseline.
All our patients presented an ECG pattern of Brugada syndrome at rest, incomplete right bundle branch block, and different width of ST elevation from V1 to V3. Applying the criteria reported above, three of our patients were in a high risk or intermediate risk subgroup for malignant dysrhythmias.
During general anesthesia, many factors could precipitate ventricular fibrillation in these patients. This is only the fifth report about general anesthesia administration in patients with Brugada Syndrome. In a study from Japan (12) concerning a patient without obvious heart disease, and in a study by Brugada et al. (3), it has been suggested that bradycardia could precipitate arrhythmia and that the degree of ST elevation increases with the heart rate. Polymorphic ventricular fibrillation is also inducible with one or two ventricular premature beats during ventricular pacing. For this reason we monitored the ECG trace and used an automated ECG ST segment trending monitor (Datex, Helsinki; Finland) (13) to detect any change. During anesthetic induction with propofol all of our patients had a decrease in heart rate without changes in the ST segment. During anesthesia their heart rates were stable and never <60 bpm.
Many drugs can have a proarrhythmic effect. In patients with Brugada syndrome, Class I antiarrhythmic drugs (14) sodium channel blockers (specifically procainamide and ajmaline) can induce ST segment elevation because they interact directly with the receptors affected by the syndrome. The muscarinic and α-adrenergic receptor agonists cause an increase in ST segment elevation (12) in the general population and in many cases of Brugada syndrome (4). Psychotropic (15) drugs also have electrophysiologic effects: amitriptyline induces cardiac sodium channel blockade but also causes the reduction in the inward sodium current and a prominent outward current (several mutations on the SCN5A gene produce the same effects); phenotiazines modify the action potential of cardiac myocytes, an effect similar to that reported for quinidine; fluoxetine depresses sodium and calcium channel activation producing a shortening in action potential duration. The final effect of all these drugs is a reduction in action potential duration. Recently it has been reported that epidural bupivacaine administration could induce the ECG characteristic pattern of Brugada syndrome; bupivacaine binds to the sodium channel and produces a depression of the rapid phase of depolarization in Purkinje fibers (16); the patient in this report had a resting ECG showing a right bundle branch block. The authors discussed the potential risk of serious arrhythmias with bupivacaine use. Volatile anesthetics can also interfere with QT interval in patients without Brugada syndrome: a prospective double-blind randomized study (17) found a significant increasing QT interval during induction with isoflurane, no changes with sevoflurane, and significant shortening with halothane. We used sevoflurane in every patient and there were no changes in QT interval.
The ion channel abnormality of Brugada syndrome should be temperature sensitive (18); we therefore monitored esophageal temperature in every patient.
Cardiac arrhythmias, even in the general population, are most likely to occur in the postoperative period (19); therefore it was necessary, during recovery in the intensive care unit, to detect and treat them. Hence, we decided to monitor our patients for 36 postoperative hours.
Brugada syndrome is an increasingly recognized disorder. The ECG pattern should alert the clinician to suspect possible Brugada syndrome. If this finding is confirmed further investigation is justified. However, there is a degree of genetic heterogeneity, and some patients affected by the syndrome do not show the typical ECG pattern. Follow-up data indicate that the risk of ventricular tachyarrhythmia is minimal in the absence of a resting ECG abnormality and the absence of adverse events reported during anesthesia should be reassuring. For these patients many situations that could precipitate ventricular fibrillation happen during anesthesia. Even if the few reports (12,20,21) did not detect any arrhythmic problem, it is difficult to draw a firm conclusion, especially because of the heterogeneous nature of the mutation leading to Brugada syndrome. Risk stratification criteria currently do not allow identification of patients who run the risk of malignant arrhythmias, and surgical patients probably need different criteria for this stratification. It is our opinion that with an adequate anesthetic plan the risk during major or minor procedures should be the same; during major procedures the risk may be increased for the longer procedure time.
Even if there were no reported problems during surgery, general, regional, or local anesthesia should be carefully managed and should include, at least, monitoring ST segment on ECG, measuring invasive arterial blood pressure and body temperature, keeping an external defibrillator ready in the operating room and, if possible, avoiding drugs that could trigger arrhythmias. We used the necessary intraarterial blood pressure monitoring to readily detect the hemodynamic effects of any dysrhythmia or any drug or other trigger mechanism. Anesthesiologists should consider the risk/benefit ratio of arterial cannulation, especially for short surgery procedures or for regional and local anesthesia.
1. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992;20:1391–6.
2. Chen Q, Kirsh GE, Zhang D et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998;392:293–6.
3. Brugada J, Brugada R, Brugada P. The syndrome of right bundle branch block, ST elevation in V1–V3 and sudden death: The Brugada syndrome. Eurace 1999;1:156–66.
4. Priori SG, Napolitano C, Gasparini M et al. Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome. Circulation 2000;102:2509–15.
5. Furuhashi M, Uno K, Tsuchihashi K, et al. Prevalence of asymptomatic ST segment elevation in right precordial leads with right bundle branch block (Brugada-type ST shift) among the general Japanese population. Heart 2001;86:161–6.
6. Nademanee K, Veerakul G, Nimmanit S, et al. Arrhytmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation 1997;96:2595–600.
7. Roberts R, Brugada R. Genetics and Arrhythmias. Annu Rev Med 2003;54:257–67.
8. Brugada P, Geelen P, Brugada R, et al. Prognostic value of electrophysiologic investigations in Brugada syndrome. J Cardiovasc Electrophysiol 2001;12:1004–7.
9. Priori SG, Napolitano C, Gasparini M, et al. Natural history of Brugada Syndrome. Circulation 2002;105:1342–52.
10. Atarashi H, Ogawa S. New ECG criteria for high-risk Brugada syndrome. Circ J 2003;67:8–10.
11. Morita H, Takenaka-Morita S, Fukushima-Kusano K, et al. Risk stratification for asymptomatic patients with Brugada syndrome: Prediction of induction of ventricular fibrillation by noninvasive methods. Circ J 2003;67:312–6.
12. Kasanuki H, Ohnishi S, Ohtuka M, et al. Idiopathic ventricular fibrillation induced with vagal activity in patients without obvious heart disease. Circulation 1997;95:2277–85.
13. Leung JM, Voskanian A, Bellows WH, et al. Automated electrocardiographic ST segment trending monitors: Accuracy in detecting myocardial ischemia. Anesth Analg 1998;87:4–10.
14. Brugada J, Brugada R, Brugada P. Pharmacological and device approach to therapy of inherited cardiac diseases associated with cardiac arrhythmias and sudden death. J Electrocardiol 2000;33:41–7.
15. Rouleau F, Asfar P, Boulet S, et al. Transient ST segment elevation in right precordial leads induced by psychotropic drugs: Relationship to the Brugada syndrome. J Cardiovasc Electrophysiol 2001;12:61–5.
16. Phillips N, Priestley M, Denniss AR, Uther JB. Brugada-type electrocardiographic pattern induced by epidural bupivacaine. Anesth Analg 2003;97:264–7.
17. Niyazi G, Ismail K, Cengiz BD, et al. The effects of volatile anesthetics on the Q-Tc interval. J Cardio Vasc Anesth 2001;15:188–91.
18. Dumaine R, Towbin J, Brugada P et al. Ionic mechanism responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res 1999;85:803–9.
19. O’Kelly B, Brower WS, Massie B, et al. Ventricular arrhythmias in patients undergoing noncardiac surgery: The study of perioperative ischemia research group. JAMA 1992;268:217–21.
20. Edge CJ, Blackman DJ, Gupta K, Sainsbury M. General anesthesia in a patient with Brugada syndrome. Br J Anaesth 2002;89:788–91.
© 2005 International Anesthesia Research Society
21. Lafuente M, Pascual B, Abengochea B, et al. Brugada syndrome and anesthesia: A case report. Rev Esp Anestesiol Reanim 1998;45:301–2.