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Osborn waves and incessant ventricular fibrillation during therapeutic hypothermia
Resuscitation 81 (2010) 500–501
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Letter to the Editor Osborn waves and incessant ventricular fibrillation during therapeutic hypothermia Sir, A 33-year-old man suddenly collapsed and presented with ventricular fibrillation (VF) when the emergency team arrived. Conversion to sinus rhythm and return of spontanous circulation was achieved with a single shock from a defibrillator. The patient was admitted to hospital comatose, mechanically ventilated but haemodynamically stable. Therapeutic hypothermia was initiated using the Arctic Sun (www.medivance.com) external cooling system. Initial ECG and echocardiography were quite normal. Coronary artery disease was excluded by angiography. Clinical and laboratory examination revealed no pathology. While the patient was hypothermic (33 ◦ C/91.4 ◦ F) progressive ECG changes appeared. The heart rate decreased to 35/min and the QRS complexes became wide with the appearance of a prominent J wave (Osborn wave) at the beginning of the ST segment (Fig. 1). The ST segment became elevated mimicking the saddle-back type Brugada ECG pattern (Fig. 2). Eight hours after initiation of hypothermia, incessant VF started. After each defibrillation attempt only a few sinus beats occurred before VF recurred (Fig. 3). Chest compression was performed with the LUCAS-CPR (www.lucas-cpr.com) system for 60 min. Neither infusion of magnesium nor injection of beta-
blocker, amiodarone or lidocaine was effective in stopping the VF. Injection of a bolus of adrenaline followed by an adrenaline infusion and rewarming the patient to 35 ◦ C/95 ◦ F stopped the electrical storm. Afterwards the patient was stable without any ectopic beats. Electrocardiogram changes disappeared (Fig. 4). The following day, the patient regained consciousness and had no neurological deficit. Because of his family history, with three sudden cardiac deaths, a hereditary ion-channel disease was suggested. However Ajmalin testing was negative and the QT interval was within normal range. Magnetic resonance tomography of the heart found no abnormalities. A cardioverter-defibrillator was successfully implanted. Hypothermia is well known to cause heart rhythm and other ECG abnormalities. Sinus bradycardia occurs when core temperature drops below 35.5 ◦ C/95.9 ◦ F. Common ECG changes below 32 ◦ C/89.6 ◦ F are PR interval prolongation, increased QT interval and widening of the QRS complex, along with J-point elevation (Osborn waves). These changes are rare during mild hypothermia. The hypothermic myocardium is less responsive to antiarrhythmic drugs and more difficult to defibrillate at temperatures below 28 ◦ C/82.4 ◦ F.1 Recent data suggest that mild hypothermia decreases rather than increases the risk for arrhythmias2 and may even provide a better treatment. Nevertheless, severe ECG changes may be associated with malignant arrhythmias. An increase of the transmural voltage gradient is the underlying mechanism for the J-point elevation which also occurs in the Brugada
Figs. 1–4. (1) Shows the osborn waves (prominent J wave at the beginning of the ST segment), (2) the elevated ST segment mimicking saddle-back type of Brugada pattern, (3) shows ventricular fibrillation and (4) the normal ECG the day after stopping cooling. 0300-9572/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2009.12.011
Letter to the Editor / Resuscitation 81 (2010) 500–501
syndrome.3 A linkage between Brugada syndrome and hypothermia has already been reported.4 It has been suggested that the appearance of a Brugada-like ECG pattern during hypothermia may provide evidence for a common underlying cellular arrhythmogenic mechanism of Brugada syndrome and hypothermia-induced changes.5 Our case supports this hypothesis, not only because a corresponding ECG pattern was present when the electrical storm started, but also because catecholamines were effective in stopping the arrhythmia, which is also known for recurrent Vf in congenital Brugada syndrome. The suggested unspecified hereditary cardiac ion channelopathy in our patient might have predisposed to the development of the incessant arrhythmia even during mild hypothermia.
501
4. Nishida K, Fujiki A, Mizumaki K, et al. Canine model of Brugada syndrome using regional epicardial cooling of the right ventricular outflow tract. J Cardiovasc Electrophysiol 2004;15:936–41. 5. Bonnemeier H, Mäuser W, Schunkert H. Brugada-like ECG pattern in severe hypothermia. Circulation 2008;118:977–8.
Elisabeth Lassnig ∗ Edwin Maurer Roland Nömeyer Bernd Eber Department of Internal Medicine, Division of Cardiology and Intensive Care, General Hospital Wels, Austria ∗ Corresponding
Conflict of interest statement None. References 1. Polderman KH, Herold I. Mechanisms of action, physiological effect, and complications of hypothermia. Crit Care Med 2009;37(Suppl.):S186–202. 2. Rhee BJ, Zhang Y, Boddicker KA, et al. Effect of hypothermia on transthoracic defibrillation in a swine model. Resuscitation 2005;65:79–85. 3. Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372–9.
author at: II nd Medical Department, Division of Cardiology and Intensive Care, General Hospital Wels, Grieskirchnerstrasse 42, A-4600 Wels, Austria. Tel.: +43 7242 415 2215; fax: +43 7242 415 3992. E-mail address: [email protected] (E. Lassnig) 12 December 2009 16 December 2009
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Letter to the Editor Osborn waves and incessant ventricular fibrillation during therapeutic hypothermia Sir, A 33-year-old man suddenly collapsed and presented with ventricular fibrillation (VF) when the emergency team arrived. Conversion to sinus rhythm and return of spontanous circulation was achieved with a single shock from a defibrillator. The patient was admitted to hospital comatose, mechanically ventilated but haemodynamically stable. Therapeutic hypothermia was initiated using the Arctic Sun (www.medivance.com) external cooling system. Initial ECG and echocardiography were quite normal. Coronary artery disease was excluded by angiography. Clinical and laboratory examination revealed no pathology. While the patient was hypothermic (33 ◦ C/91.4 ◦ F) progressive ECG changes appeared. The heart rate decreased to 35/min and the QRS complexes became wide with the appearance of a prominent J wave (Osborn wave) at the beginning of the ST segment (Fig. 1). The ST segment became elevated mimicking the saddle-back type Brugada ECG pattern (Fig. 2). Eight hours after initiation of hypothermia, incessant VF started. After each defibrillation attempt only a few sinus beats occurred before VF recurred (Fig. 3). Chest compression was performed with the LUCAS-CPR (www.lucas-cpr.com) system for 60 min. Neither infusion of magnesium nor injection of beta-
blocker, amiodarone or lidocaine was effective in stopping the VF. Injection of a bolus of adrenaline followed by an adrenaline infusion and rewarming the patient to 35 ◦ C/95 ◦ F stopped the electrical storm. Afterwards the patient was stable without any ectopic beats. Electrocardiogram changes disappeared (Fig. 4). The following day, the patient regained consciousness and had no neurological deficit. Because of his family history, with three sudden cardiac deaths, a hereditary ion-channel disease was suggested. However Ajmalin testing was negative and the QT interval was within normal range. Magnetic resonance tomography of the heart found no abnormalities. A cardioverter-defibrillator was successfully implanted. Hypothermia is well known to cause heart rhythm and other ECG abnormalities. Sinus bradycardia occurs when core temperature drops below 35.5 ◦ C/95.9 ◦ F. Common ECG changes below 32 ◦ C/89.6 ◦ F are PR interval prolongation, increased QT interval and widening of the QRS complex, along with J-point elevation (Osborn waves). These changes are rare during mild hypothermia. The hypothermic myocardium is less responsive to antiarrhythmic drugs and more difficult to defibrillate at temperatures below 28 ◦ C/82.4 ◦ F.1 Recent data suggest that mild hypothermia decreases rather than increases the risk for arrhythmias2 and may even provide a better treatment. Nevertheless, severe ECG changes may be associated with malignant arrhythmias. An increase of the transmural voltage gradient is the underlying mechanism for the J-point elevation which also occurs in the Brugada
Figs. 1–4. (1) Shows the osborn waves (prominent J wave at the beginning of the ST segment), (2) the elevated ST segment mimicking saddle-back type of Brugada pattern, (3) shows ventricular fibrillation and (4) the normal ECG the day after stopping cooling. 0300-9572/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2009.12.011
Letter to the Editor / Resuscitation 81 (2010) 500–501
syndrome.3 A linkage between Brugada syndrome and hypothermia has already been reported.4 It has been suggested that the appearance of a Brugada-like ECG pattern during hypothermia may provide evidence for a common underlying cellular arrhythmogenic mechanism of Brugada syndrome and hypothermia-induced changes.5 Our case supports this hypothesis, not only because a corresponding ECG pattern was present when the electrical storm started, but also because catecholamines were effective in stopping the arrhythmia, which is also known for recurrent Vf in congenital Brugada syndrome. The suggested unspecified hereditary cardiac ion channelopathy in our patient might have predisposed to the development of the incessant arrhythmia even during mild hypothermia.
501
4. Nishida K, Fujiki A, Mizumaki K, et al. Canine model of Brugada syndrome using regional epicardial cooling of the right ventricular outflow tract. J Cardiovasc Electrophysiol 2004;15:936–41. 5. Bonnemeier H, Mäuser W, Schunkert H. Brugada-like ECG pattern in severe hypothermia. Circulation 2008;118:977–8.
Elisabeth Lassnig ∗ Edwin Maurer Roland Nömeyer Bernd Eber Department of Internal Medicine, Division of Cardiology and Intensive Care, General Hospital Wels, Austria ∗ Corresponding
Conflict of interest statement None. References 1. Polderman KH, Herold I. Mechanisms of action, physiological effect, and complications of hypothermia. Crit Care Med 2009;37(Suppl.):S186–202. 2. Rhee BJ, Zhang Y, Boddicker KA, et al. Effect of hypothermia on transthoracic defibrillation in a swine model. Resuscitation 2005;65:79–85. 3. Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372–9.
author at: II nd Medical Department, Division of Cardiology and Intensive Care, General Hospital Wels, Grieskirchnerstrasse 42, A-4600 Wels, Austria. Tel.: +43 7242 415 2215; fax: +43 7242 415 3992. E-mail address: [email protected] (E. Lassnig) 12 December 2009 16 December 2009