Abstract
Case Summary
Accidental hypothermia is associated with distinctive electrocardiographic abnormalities that may precede malignant arrhythmias. We report the case of a 31-year-old homeless man admitted for severe hypothermia whose admission electrocardiogram (ECG) showed sinus bradycardia, prominent Osborn (J) waves in inferolateral leads, and marked QT prolongation. No metabolic, toxic, or structural cardiac abnormalities were identified. With active rewarming and supportive care, a progressive and complete normalization of the ECG occurred within 48 hours. This case highlights the diagnostic value, pathophysiology, and reversibility of hypothermia-related ECG findings.
Take-Home Messages
Accidental hypothermia can produce characteristic ECG changes, including prominent Osborn waves and marked QT prolongation. These abnormalities may completely resolve after rewarming in the absence of electrolyte, toxic, or structural cardiac disease.
Key words: electrocardiography, hypothermia, J wave, Osborn wave, QT prolongation
Graphical Abstract
Case Summary
A 31-year-old homeless man was found unconscious outdoors during winter and was admitted to the emergency department for accidental hypothermia. On arrival, he was unresponsive and profoundly cold to touch, requiring immediate admission to the intensive care unit for supportive management and continuous monitoring.
Take-Home Messages
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Accidental hypothermia can produce characteristic ECG changes, including prominent Osborn waves and marked QT prolongation.
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These abnormalities may completely resolve after rewarming in the absence of electrolyte, toxic, or structural cardiac disease.
The admission 12-lead electrocardiogram (ECG) demonstrated sinus bradycardia and prominent positive deflections immediately following the QRS complex, consistent with Osborn (J) waves, most evident in the inferolateral leads (II, III, aVF, V3-V6). In addition, a markedly prolonged QT interval was observed, with a corrected QT of up to 644 ms (Figure 1A). No ventricular arrhythmias were documented during the initial evaluation.
Figure 1.
Serial ECG Changes During Rewarming
(A) Twelve-lead electrocardiogram (ECG) shows sinus bradycardia at 55 beats/min with a normal frontal electrical axis. Atrioventricular and intraventricular conduction are within normal limits. Prominent positive deflections consistent with Osborn (J) waves are evident in precordial leads V2 to V6 and in inferior leads II, III, and aVF. Marked QT interval prolongation is present, with a measured QTc interval of 640 ms using the Framingham formula. (B) Twelve-lead ECG obtained 24 hours after initiation of warming and supportive therapy shows persistent sinus bradycardia at 50 beats/min, accompanied by a reduction in the amplitude of Osborn (J) waves, T-wave inversions, and significant shortening of the corrected QTc interval (440 ms). (C) Twelve-lead ECG recorded 48 hours after admission demonstrates normalization of the previously described abnormalities, with an increase in heart rate to 105 beats/min, complete disappearance of J waves, and restoration of a normal QTc interval (430 ms) recorded during patient awakening in the intensive care unit.
Laboratory testing revealed no electrolyte abnormalities, including normal potassium, calcium, and magnesium levels. Toxicologic screening was negative. Transthoracic echocardiography showed normal cardiac chamber dimensions, preserved biventricular systolic function, and no structural heart disease.
The patient was managed with active and passive rewarming, including warmed intravenous fluids, forced-air warming blankets, and supportive intensive care. No antiarrhythmic therapy was required. Over the subsequent hours, heart rate progressively increased, and the amplitude of the Osborn waves gradually diminished. Serial ECGs demonstrated progressive QT shortening, the emergence of T-wave inversions, and improvement of depolarization abnormalities within 24 hours (Figure 1B). A repeat ECG obtained 48 hours after admission showed complete normalization, with disappearance of J waves and restoration of a normal QT interval (Figure 1C).
Accidental hypothermia induces characteristic electrocardiographic changes through temperature-dependent alterations in myocardial depolarization and repolarization.1 Osborn waves reflect a transmural voltage gradient between epicardial and endocardial myocardium, driven by hypothermia-related impairment of adenosine triphosphate–dependent ionic pumps and modulation of calcium-sensitive transient outward currents, which are more prominent in epicardial cells.2,3 In addition, heterogeneous modulation of epicardial vs endocardial action potentials—partly mediated by calcium-sensitive currents such as Ito—may further accentuate transmural voltage gradients, resulting in secondary T-wave inversion rather than ischemia.2 Notably, as observed in this case, T-wave inversion may manifest during the rewarming phase, likely reflecting a dissociation between recovery of depolarization and repolarization, with the latter recovering more slowly and heterogeneously, leading to increased dispersion of repolarization. Hypothermia also delays ventricular repolarization through slowed calcium channel inactivation, accounting for marked QT prolongation.2 Importantly, these abnormalities are typically fully reversible with rewarming, as illustrated by this case.2,3
The patient regained full consciousness, was discharged after 1 week in stable condition, and was referred to social services. At 1-month follow-up, he remained asymptomatic with a normal ECG.
Funding Support and Author Disclosures
The article fees were supported through an unrestricted educational grant provided by EMCD SRLS, coordinated by Dr Grimaldi. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Acknowledgments
The authors thank Dr Francesco Monti, Director of the Department of Cardiology, and Dr Francesco Rotolo, Head of the Interventional Cardiology Service, both at San Pietro Fatebenefratelli Hospital, for their valuable support.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
References
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