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Hypothermia-induced J waves
International Journal of Cardiology 114 (2007) e116 – e117 www.elsevier.com/locate/ijcard
Letter to the Editor
Hypothermia-induced J waves Fabián J. Arnaldo ⁎, Nikolaos Anatoliotakis University of Florida Jacksonville, Department of Medicine, Jacksonville, FL, USA Received 16 February 2006; accepted 8 July 2006 Available online 17 October 2006
Abstract A 36 years old woman with acquired immunodeficiency syndrome was admitted to the hospital for pulmonary Mycobacterium Avis Complex infection. Seventy-two hours after the admission she became hypothermic and bradycardic. The ECG showed sinus bradycardia, J waves in leads II, III, aVF, aVR, aVL, V5 and V6 along with QT prolongation and T wave abnormalities. After rewarming the J waves and repolarization abnormalities disappeared. The proposed cellular basis of hypothermia-induced J waves is the accentuation of the spike-and-dome morphology of the action potential of M and epicardial cells. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Electrocardiology; Electrophysiology; Hypothermia; Osborn waves
A 36 years old woman with acquired immunodeficiency syndrome was admitted to the hospital for productive cough, fever and pulmonary Mycobacterium Avis Complex infection. Seventy-two hours after the admission she was noticed to be bradycardic and the temperature was 89.3 °F (32 °C). The ECG showed sinus bradycardia, J waves in leads II, III, aVF, V5 and V6, T wave inversion in lead V1, biphasic T waves in leads V2 to V4, and prolonged QT interval (Fig. 1). A small notch in aVR and a pseudo R prime wave in AVL were also indicative of J waves. Serum potassium was 4.0 mEq/l, magnesium 1.6 mg/dl and ionize calcium 1.21 mmol/l. The patient was rewarmed, the body temperature increased to 97.2 °F (36.2 °C) and a repeat ECG showed sinus tachycardia, disappearance of the J waves and normalization of T waves and QT interval (Fig. 2). John J Osborn described the J wave during experimental hypothermia in 1953 [1]. Hypothermia is clinically associated with electrocardiographic abnormalities such as sinus bradycardia, J waves, QT interval prolongation and T wave inversion. J waves are commonly seen in leads II, III, aVF, V5 and V6 and become larger as the body temperature decreases [2]. J waves are not specific of hypothermia and can ⁎ Corresponding author. 655 West 8th St, LCR Building 2nd Floor, Department of Medicine, Jacksonville, FL 32216, United States. Tel.: +1 904 244 8129; fax: +1 904 244 3634. E-mail address: [email protected] (F.J. Arnaldo). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.037
be seen in diverse clinical settings like hypercalcemia, early repolarization and the Brugada syndrome. The proposed cellular basis of hypothermia-induced J waves is the accentuation of the spike-and-dome morphology of the action potential of M and epicardial cells [3]. This epicardial accentuation is mediated by a transient outward current (Ito) that does not occur in the endocardium, originating a transmural voltage gradient responsible for the appearance of a camel-hump wave at the end of the QRS complex. References [1] Osborn John J. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol Nov 1953;175:389–98 [Legacy content]. [2] Vasallo SU, Delaney KA, Hoffman RS, Slater W, Goldfrank L. A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med 1999;6:1121–6. [3] Yan GX, Antzelevich C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372–9.
F.J. Arnaldo, N. Anatoliotakis / International Journal of Cardiology 114 (2007) e116–e117
e117
Fig. 1. A 12-lead ECG obtained during hypothermia showing J waves (marked with arrows) and prolonged QT interval (Corrected QT interval: 570 ms).
Fig. 2. A 12-lead ECG taken after patient rewarming showed disappearance of J waves and normal repolarization. A mild shift in the QRS axis was also observed.
Letter to the Editor
Hypothermia-induced J waves Fabián J. Arnaldo ⁎, Nikolaos Anatoliotakis University of Florida Jacksonville, Department of Medicine, Jacksonville, FL, USA Received 16 February 2006; accepted 8 July 2006 Available online 17 October 2006
Abstract A 36 years old woman with acquired immunodeficiency syndrome was admitted to the hospital for pulmonary Mycobacterium Avis Complex infection. Seventy-two hours after the admission she became hypothermic and bradycardic. The ECG showed sinus bradycardia, J waves in leads II, III, aVF, aVR, aVL, V5 and V6 along with QT prolongation and T wave abnormalities. After rewarming the J waves and repolarization abnormalities disappeared. The proposed cellular basis of hypothermia-induced J waves is the accentuation of the spike-and-dome morphology of the action potential of M and epicardial cells. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Electrocardiology; Electrophysiology; Hypothermia; Osborn waves
A 36 years old woman with acquired immunodeficiency syndrome was admitted to the hospital for productive cough, fever and pulmonary Mycobacterium Avis Complex infection. Seventy-two hours after the admission she was noticed to be bradycardic and the temperature was 89.3 °F (32 °C). The ECG showed sinus bradycardia, J waves in leads II, III, aVF, V5 and V6, T wave inversion in lead V1, biphasic T waves in leads V2 to V4, and prolonged QT interval (Fig. 1). A small notch in aVR and a pseudo R prime wave in AVL were also indicative of J waves. Serum potassium was 4.0 mEq/l, magnesium 1.6 mg/dl and ionize calcium 1.21 mmol/l. The patient was rewarmed, the body temperature increased to 97.2 °F (36.2 °C) and a repeat ECG showed sinus tachycardia, disappearance of the J waves and normalization of T waves and QT interval (Fig. 2). John J Osborn described the J wave during experimental hypothermia in 1953 [1]. Hypothermia is clinically associated with electrocardiographic abnormalities such as sinus bradycardia, J waves, QT interval prolongation and T wave inversion. J waves are commonly seen in leads II, III, aVF, V5 and V6 and become larger as the body temperature decreases [2]. J waves are not specific of hypothermia and can ⁎ Corresponding author. 655 West 8th St, LCR Building 2nd Floor, Department of Medicine, Jacksonville, FL 32216, United States. Tel.: +1 904 244 8129; fax: +1 904 244 3634. E-mail address: [email protected] (F.J. Arnaldo). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.037
be seen in diverse clinical settings like hypercalcemia, early repolarization and the Brugada syndrome. The proposed cellular basis of hypothermia-induced J waves is the accentuation of the spike-and-dome morphology of the action potential of M and epicardial cells [3]. This epicardial accentuation is mediated by a transient outward current (Ito) that does not occur in the endocardium, originating a transmural voltage gradient responsible for the appearance of a camel-hump wave at the end of the QRS complex. References [1] Osborn John J. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol Nov 1953;175:389–98 [Legacy content]. [2] Vasallo SU, Delaney KA, Hoffman RS, Slater W, Goldfrank L. A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med 1999;6:1121–6. [3] Yan GX, Antzelevich C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372–9.
F.J. Arnaldo, N. Anatoliotakis / International Journal of Cardiology 114 (2007) e116–e117
e117
Fig. 1. A 12-lead ECG obtained during hypothermia showing J waves (marked with arrows) and prolonged QT interval (Corrected QT interval: 570 ms).
Fig. 2. A 12-lead ECG taken after patient rewarming showed disappearance of J waves and normal repolarization. A mild shift in the QRS axis was also observed.