ECG criteria
- An additional domed (upwardly convex) deflection immediately following the J point, prior to the ST segment
- Most frequently and clearly visible in the inferior and lateral leads (II, III, aVF, V4–V6), but may be recorded in the majority of leads, particularly in severe hypothermia
- Tolerates further increases in prominence as core body temperature continues to drop, though there is no strict temperature threshold or direct linear correlation between amplitude and temperature
- Accompained by sinus bradycardia, frequently with prolonged PQ, QRS, and QT intervals
- In the presence of shivering, an irregular muscular baseline artifact may occur, which can hinder rhythm assessment; it is non-specific for hypothermia
- Decreases or disappears with rewarming and the restoration of normal body temperature
What it looks like on ECG
The Osborn wave is an additional convex (domed) deformation at the J point that appears as a "hump" at the junction of the QRS complex and the ST segment. Its shape resembles an elevated arch, which is why it is referred to as a "camel hump." The polarity of the wave typically matches the direction of the main QRS deflection in that lead.
The wave is most frequently and clearly seen in the inferior and lateral leads — II, III, aVF, and V4–V6. In severe hypothermia, it may appear in most leads, including the right precordial leads V1–V2 and the limb leads.
The prominence of the Osborn wave generally increases with worsening hypothermia; however, this relationship is not strictly direct or constant. Its amplitude depends on individual patient characteristics and concurrent conditions, meaning the height of the wave cannot reliably be used to gauge exact body temperature. In mild hypothermia (32–35 °C), the wave may be barely noticeable or already distinct; in deeper hypothermia, it is typically larger and more prominent, but without a strict quantitative correlation.
Typical concurrent findings: sinus bradycardia, prolongation of the PQ (PR) interval, widening of the QRS complex, and QT interval prolongation. Shivering may introduce irregular, high-frequency muscular baseline artifacts (tremor artifacts) that can obscure rhythm and segment evaluation; these are non-specific and not obligatory for hypothermia.
| ECG element | Changes in hypothermia |
|---|---|
| Deflection/wave at the J point | Convex Osborn wave |
| Rhythm | Sinus bradycardia |
| PQ interval | Prolonged |
| QRS | May be widened |
| QT | Prolonged |
Mechanism
A drop in myocardial temperature alters the function of cardiomyocyte ion channels. The proposed enhancement of the transient outward potassium current ($I_{to}$) in the epicardium—which is responsible for phase 1 of the action potential—and the resulting increase in the transmural voltage gradient between the epicardium and endocardium at the end of ventricular depolarization is considered the primary mechanism underlying the formation of the Osborn wave. However, this is not universally accepted as the sole explanation, as other temperature-dependent shifts in ion currents likely contribute. The J point on the ECG marks the boundary between the end of the QRS complex and the beginning of the ST segment; the transmural voltage gradient manifests on the surface ECG as an additional domed wave superimposed on this boundary.
Causes
- Accidental systemic hypothermia (e.g., exposure to cold, immersion in water) or induced hypothermia (e.g., therapeutic hypothermia following cardiac arrest)
- Severe hypothyroidism (myxedema) with a moderate decrease in body temperature
- Increased intracranial pressure and certain central nervous system lesions (reported in isolated cases)
- Hypercalcemia: can cause J waves / an Osborn-like pattern even in the absence of hypothermia; if an Osborn wave or similar pattern is detected, serum calcium levels should be checked and the QT interval evaluated, as hypercalcemia is typically associated with QT shortening
- Sepsis accompanied by marked hypothermia
- J waves without hypothermia: encountered in early repolarization syndrome and other J-wave variants; such findings should not be automatically labeled as Osborn waves
Differential diagnosis
- ST-segment elevation in STEMI — the shape of the ST segment in myocardial infarction is variable and does not have to be strictly horizontal or upwardly convex; an Osborn wave may merge with the ST segment and is not always accompanied by its return to the baseline. The diagnostic criterion for STEMI is new ST-segment elevation at the J point in $\ge$2 contiguous leads: generally $\ge$1 mm in all leads other than V2–V3, where thresholds depend on age and sex—$\ge$2.5 mm in men under 40 years, $\ge$2 mm in men aged 40 years and older, and $\ge$1.5 mm in women regardless of age (criteria per the 2009 AHA/ACCF/HRS ECG standardization guidelines; minor variations in threshold definitions exist across sources). Diagnosis always relies not only on these thresholds but also on clinical presentation, serial ECG dynamics, troponin levels, and reciprocal changes—in suspected ACS, ST elevation must not be dismissed as hypothermia without a thorough evaluation.
- Early repolarization syndrome — notching or a wave at the J point without clinical hypothermia and independent of body temperature; differentiation should be based on stable morphology and typical pattern localization, rather than the presence or absence of bradycardia. J waves in early repolarization can themselves become more prominent during bradycardia and attenuate with heart rate acceleration; thus, bradycardia is not a distinguishing feature.
- Brugada type 1 pattern — specific coved ST-segment elevation in the right precordial leads V1–V2; differentiation relies primarily on typical morphology and clinical context. The absence of bradycardia, tremor artifact, or a history of cold exposure aids in differential diagnosis but is not mandatory for exclusion, as the Brugada pattern can be provoked by other triggers (e.g., fever).
- Epsilon wave in arrhythmogenic right ventricular cardiomyopathy — a distinct low-amplitude terminal notch at the end of the QRS complex or the beginning of the ST segment, usually in V1–V3, rather than a domed wave situated directly at the J point; independent of body temperature.
- Motion or tremor artifact — fails to produce a stable, reproducible morphology at the J point across consecutive complexes.
Clinical significance and management
The Osborn wave is not a standalone diagnosis, but rather an electrocardiographic marker frequently seen in hypothermia—especially as it deepens—though it may also appear at higher body temperatures. An ECG alone does not replace the measurement of core body temperature. Its appearance necessitates the immediate measurement and evaluation of core body temperature (rectal or esophageal if severe hypothermia is suspected), assessment of the cardiac rhythm, and screening for associated conduction and repolarization abnormalities.
Severe hypothermia sharply increases myocardial electrical instability: the risk of atrial fibrillation, bradyarrhythmias, and—most dangerously—ventricular fibrillation is markedly elevated, particularly during rough handling of the patient (sudden movements, catheterization, uncautionary intubation). Therefore, patients with hypothermia and an Osborn wave must be managed gently, minimizing mechanical stimuli, while maintaining continuous rhythm monitoring.
Rewarming should be initiated immediately, with the method chosen based on the severity of hypothermia, hemodynamic stability, and the underlying cause: passive or active external rewarming for mild-to-moderate hypothermia with stable hemodynamics, and active internal rewarming (e.g., warm intravenous fluids, warmed humidified air) as indicated. For severe hypothermia with hemodynamic instability or cardiac arrest, extracorporeal rewarming (ECLS/ECMO rewarming) is considered the method of choice when available, as it is the most effective approach. Securing the airway and intubation, when indicated, should not be delayed out of fear of triggering arrhythmias, but should be performed with maximal care. The Osborn wave typically regresses and may completely resolve upon the restoration of normal body temperature, confirming its link to temperature.
Common interpretation errors
- Mistaking an Osborn wave for ST elevation and incorrectly suspecting—or conversely, unjustifiably excluding—STEMI without evaluating the clinical picture, dynamics, troponin levels, and ST-elevation criteria in contiguous leads
- Failing to measure core body temperature when an Osborn wave is newly identified on the ECG
- Confusing muscular tremor artifact with a rhythm disturbance or atrial fibrillation
- Ignoring concurrent QT prolongation, which further increases the risk of ventricular arrhythmias
- Failing to obtain follow-up serial ECGs during rewarming and treatment to assess the evolution of the finding
1. In which leads is the Osborn wave most frequently and clearly detected?
The Osborne wave is most frequently and clearly visible in the inferior and lateral leads — II, III, aVF, and V4–V6.
2. Which ionic mechanism is considered primary in the formation of the Osborne wave?
The putative enhancement of epicardial $I_{to}$ and the resulting increase in transmural voltage gradient is considered the primary mechanism, along with other temperature-induced alterations in ionic currents.
3. Which of the following typically accompanies the Osborne wave in hypothermia?
Hypothermia slows conduction at various levels, causing bradycardia and prolongation of the PQ, QRS, and QT intervals.
Frequently asked questions
At what body temperature does the Osborne wave appear?
The Osborne wave may appear even in mild hypothermia and becomes more pronounced as hypothermia deepens, though there is no strict temperature threshold for its appearance or amplification. The wave amplitude alone cannot reliably indicate the exact core body temperature.
Is the Osborne wave dangerous in itself?
The wave itself is not dangerous, but it signals hypothermia, which is associated with a sharply increased risk of ventricular fibrillation and other life-threatening arrhythmias. The danger stems from the underlying condition, not the ECG finding itself.
How to distinguish the Osborne wave from ST elevation in myocardial infarction?
The Osborne wave is a dome-shaped deflection at the J point, often accompanied by bradycardia and clinical signs of hypothermia; however, its morphology and ST-segment behavior are variable and do not provide a reliable differentiating rule. The diagnosis of STEMI requires a new ST-segment elevation at the J point in $\ge 2$ contiguous leads using threshold values (including specific age- and sex-based thresholds for V2–V3), as well as clinical evaluation, serial ECGs, and troponin levels. When ACS is suspected, STEMI cannot be ruled out solely based on hypothermia or the presence of a J wave, as these findings may coexist.
In which leads is the Osborne wave best visualized?
The wave is most frequently and clearly visible in the inferior and lateral leads — II, III, aVF, and V4–V6. In severe hypothermia, it may be recorded in most leads.
Does the Osborne wave disappear after warming the patient?
Yes, as normal body temperature is restored, the Osborne wave typically diminishes and in many cases disappears, confirming its association with temperature.
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Related terms
More in the section "Pericardium, Lungs, Brain and Others"
Sources
- Goldberger A.L. "Clinical Electrocardiography", current edition
- Surawicz B., Knilans T. «Chou's Electrocardiography in Clinical Practice»
- Orlov, V.N. «Electrocardiography Guide»
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.