Electrocardiogram Changes Associated With Hypothermia

Hypothermia is defined as a rectal temperature of less than 35 °C or less than 95 °F.1,2 Hypothermia has been subdivided into mild (32 °C-35 °C), moderate (28 °C-32 °C) and severe (< 28 °C).3 Body temperature at these ranges has been shown to contribute to the development of characteristic electrocardiographic (ECG) changes.1,2 A common cause of accidental hypothermia in the past has been overexposure to excessive cold in the outside environment. The Centers for Disease Control and Prevention reported an average of 1301 hypothermia-related deaths per year from 1991 to 2011.4 Sixty-seven percent of these deaths were males.4 In recent years, hypothermia has been associated with increased mortality in trauma patients as well as those with severe sepsis.3 Additionally, therapeutic hypothermia has become a common intervention in some patients following cardiac arrest who may be on extracorporeal mechanical support.5 Hypothermia has been identified as having serious consequences on the cardiovascular system, as it can lead to ventricular fibrillation.3 The purpose of this column is to review the effects of hypothermia on the ECG. A case study of accidental hypothermia is presented.Hypothermia contributes to several changes on the ECG related to lengthening of the action potential, slowing of conduction through the myocardium, and prolonging depolarization of the tissue.1 The classic ECG sign in hypothermia is the presence of Osborn waves.The Osborn wave is a deflection that appears at the J point of the QRS complex, the point where the QRS complex joins the ST segment. The J point represents the end of depolarization and beginning of repolarization. The additional wave, called interchangeably the Osborn wave or the J wave, is in the same direction as the QRS complex.6 Figure 1 is an example of the “J point” in 2 leads from a normal ECG (A and B) and the Osborn wave (C) in someone with hypothermia. The size or amplitude of the Osborn wave increases as the body temperature falls.1 However, not all patients with hypothermia will exhibit an Osborn wave. Studies on patients with accidental hypothermia have demonstrated a variable incidence (50%-80% of cases) on the development of an Osborn wave.7 Another study noted that the Osborn wave was present in 100% of cases with severe hypothermia, 75% of cases with moderate hypothermia, and 10.7% of cases with mild hypothermia.8 Interestingly, Osborn waves have appeared in the setting of acidosis.9 Additionally, Osborn waves have been found to be associated with many conditions, including Brugada syndrome, hypercalcemia, myocardial ischemia, and sub-arachnoid hemorrhage.10Clinical implications of Osborn waves are nonspecific at this time. As stated previously, they tend to appear at lower levels of hypothermia. Some have noted that the appearance of Osborn waves may be a precursor to ventricular fibrillation and/or sudden cardiac death.1 Of interest are reports about patients with head trauma who are not on any sedation and are hypothermic. They develop Osborn waves associated with their hypothermia but are not shivering. This may be a clue for suspecting brain death.11 Researchers believe more research needs to be done to fully understand the incidence of the Osborn wave due to the variability described above.3Other effects of hypothermia on the ECG include prolongation of the PR, QRS, and QT intervals, a decrease in the amplitude of the P wave, and conduction abnormalities. If there is a rapid onset of hypothermia, sympathoadrenal activation occurs, increasing circulating norepinephrine levels in the blood. This increase contributes the development of sinus tachycardia as well as atrial and ventricular arrhythmias.1 The occurrence of atrial fibrillation is common in the setting of moderate and severe hypothermia.Bradyarrhythmias are also common in hypothermia, with sinus bradycardia being the most common. The lower the temperature, the slower the heart rate. Other bradyarrhythmias that may occur are junctional and idioventricular rhythms, as well as atrioventrical (AV) blocks, which are due to the blocking effect hypothermia has on the AV node.3 A note of caution is necessary when analyzing the ECG complex and rhythms in patients with hypothermia. P waves may be missed if the amplitude is markedly decreased. The patient may be shivering, producing artifacts distorting the baseline as well as waveforms.Hypothermia also impairs myocardial diastolic function, thereby impairing ventricular filling. It is believed that the bradycardia that develops helps to offset the impact of the diastolic dysfunction. Guidelines indicate that external pacing or the administration of chronotropic medications are not recommended to increase cardiac output.12A 71-year-old woman was found by a neighbor unconscious and lying in her front yard early one morning in January. During the night, the outside temperature was 16 °F. It appeared she had gone outside to check on something in her yard, fallen, hit her head, and become unconscious. She did not respond to any stimuli. Emergency services were called. Upon arrival, personnel completed their assessment and transported her to the nearest hospital in the community. In the emergency department, she was placed on a monitor and a full physical examination was conducted. She was shivering, with a regular sinus bradycardia in the 50s, respiratory rate 6/min and irregular, rectal temperature of 86 °F (30 °C), indicating moderate hypothermia. Her skin was cyanotic and cold. She was intubated and placed on ventilatory support. An ECG was obtained (Figure 2). Note the Osborn waves in leads II, III, aVF, and V3 through V6. She was admitted to the intensive care unit, where active and passive rewarming was initiated using a forced-air warming system along with warmed normal saline infusions. The following morning (day 2), her temperature was 95.8 °F (35.4 °C) rectally. She remained intubated and was responding to painful stimuli. Her ECG (Figure 3) reveals a sinus rhythm with a rate of 100/min. The Osborn waves were absent. By day 5, she was awake and alert, extubated, and transferred to the medicine unit.The management of hypothermia starts with rewarming the patient. The common practice for rewarming has been to apply heating pads and water bottles to the chest, groin, and axilla. The use of forced-air warming systems or external temperature control systems are effective. Warmed saline infusions may be used as well. In recent years, the use of venoarterial extracorporeal membrane oxygenation has been found to provide an effective rewarming process with complete cardiopulmonary support in patients who have experienced cardiac arrest.4 While some consider extracorporeal membrane oxygenation to be the criterion standard for treating severe hypothermia, others point out that much more research needs to be done.5,13Severe accidental hypothermia represents a high risk for morbidity and mortality. In the past 10 to 15 years, interest in hypothermia has increased because of interest in its effects as part of targeted temperature management in patients who have experienced cardiac arrest. Experts agree that the ECG changes that occur with accidental hypothermia may assist with timely diagnosis and interventions for hypothermia. Caution is required in interpreting ECGs, as mentioned previously, if the patient is shivering, because it contributes to distortion of the ECG waveforms.

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AACN Advanced Critical Care
Published
2025-12-09
DOI
https://doi.org/10.4037/aacnacc2025895
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Cardiac Arrest and Resuscitation
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article

Electrocardiogram Changes Associated With Hypothermia

Barbara Leeper
AACN Advanced Critical Care
Cardiac Arrest and Resuscitation
article

Electrocardiogram Changes Associated With Hypothermia

Barbara Leeper
article en

Abstract

Hypothermia is defined as a rectal temperature of less than 35 °C or less than 95 °F.1,2 Hypothermia has been subdivided into mild (32 °C-35 °C), moderate (28 °C-32 °C) and severe (< 28 °C).3 Body temperature at these ranges has been shown to contribute to the development of characteristic electrocardiographic (ECG) changes.1,2 A common cause of accidental hypothermia in the past has been overexposure to excessive cold in the outside environment. The Centers for Disease Control and Prevention reported an average of 1301 hypothermia-related deaths per year from 1991 to 2011.4 Sixty-seven percent of these deaths were males.4 In recent years, hypothermia has been associated with increased mortality in trauma patients as well as those with severe sepsis.3 Additionally, therapeutic hypothermia has become a common intervention in some patients following cardiac arrest who may be on extracorporeal mechanical support.5 Hypothermia has been identified as having serious consequences on the cardiovascular system, as it can lead to ventricular fibrillation.3 The purpose of this column is to review the effects of hypothermia on the ECG. A case study of accidental hypothermia is presented.Hypothermia contributes to several changes on the ECG related to lengthening of the action potential, slowing of conduction through the myocardium, and prolonging depolarization of the tissue.1 The classic ECG sign in hypothermia is the presence of Osborn waves.The Osborn wave is a deflection that appears at the J point of the QRS complex, the point where the QRS complex joins the ST segment. The J point represents the end of depolarization and beginning of repolarization. The additional wave, called interchangeably the Osborn wave or the J wave, is in the same direction as the QRS complex.6 Figure 1 is an example of the “J point” in 2 leads from a normal ECG (A and B) and the Osborn wave (C) in someone with hypothermia. The size or amplitude of the Osborn wave increases as the body temperature falls.1 However, not all patients with hypothermia will exhibit an Osborn wave. Studies on patients with accidental hypothermia have demonstrated a variable incidence (50%-80% of cases) on the development of an Osborn wave.7 Another study noted that the Osborn wave was present in 100% of cases with severe hypothermia, 75% of cases with moderate hypothermia, and 10.7% of cases with mild hypothermia.8 Interestingly, Osborn waves have appeared in the setting of acidosis.9 Additionally, Osborn waves have been found to be associated with many conditions, including Brugada syndrome, hypercalcemia, myocardial ischemia, and sub-arachnoid hemorrhage.10Clinical implications of Osborn waves are nonspecific at this time. As stated previously, they tend to appear at lower levels of hypothermia. Some have noted that the appearance of Osborn waves may be a precursor to ventricular fibrillation and/or sudden cardiac death.1 Of interest are reports about patients with head trauma who are not on any sedation and are hypothermic. They develop Osborn waves associated with their hypothermia but are not shivering. This may be a clue for suspecting brain death.11 Researchers believe more research needs to be done to fully understand the incidence of the Osborn wave due to the variability described above.3Other effects of hypothermia on the ECG include prolongation of the PR, QRS, and QT intervals, a decrease in the amplitude of the P wave, and conduction abnormalities. If there is a rapid onset of hypothermia, sympathoadrenal activation occurs, increasing circulating norepinephrine levels in the blood. This increase contributes the development of sinus tachycardia as well as atrial and ventricular arrhythmias.1 The occurrence of atrial fibrillation is common in the setting of moderate and severe hypothermia.Bradyarrhythmias are also common in hypothermia, with sinus bradycardia being the most common. The lower the temperature, the slower the heart rate. Other bradyarrhythmias that may occur are junctional and idioventricular rhythms, as well as atrioventrical (AV) blocks, which are due to the blocking effect hypothermia has on the AV node.3 A note of caution is necessary when analyzing the ECG complex and rhythms in patients with hypothermia. P waves may be missed if the amplitude is markedly decreased. The patient may be shivering, producing artifacts distorting the baseline as well as waveforms.Hypothermia also impairs myocardial diastolic function, thereby impairing ventricular filling. It is believed that the bradycardia that develops helps to offset the impact of the diastolic dysfunction. Guidelines indicate that external pacing or the administration of chronotropic medications are not recommended to increase cardiac output.12A 71-year-old woman was found by a neighbor unconscious and lying in her front yard early one morning in January. During the night, the outside temperature was 16 °F. It appeared she had gone outside to check on something in her yard, fallen, hit her head, and become unconscious. She did not respond to any stimuli. Emergency services were called. Upon arrival, personnel completed their assessment and transported her to the nearest hospital in the community. In the emergency department, she was placed on a monitor and a full physical examination was conducted. She was shivering, with a regular sinus bradycardia in the 50s, respiratory rate 6/min and irregular, rectal temperature of 86 °F (30 °C), indicating moderate hypothermia. Her skin was cyanotic and cold. She was intubated and placed on ventilatory support. An ECG was obtained (Figure 2). Note the Osborn waves in leads II, III, aVF, and V3 through V6. She was admitted to the intensive care unit, where active and passive rewarming was initiated using a forced-air warming system along with warmed normal saline infusions. The following morning (day 2), her temperature was 95.8 °F (35.4 °C) rectally. She remained intubated and was responding to painful stimuli. Her ECG (Figure 3) reveals a sinus rhythm with a rate of 100/min. The Osborn waves were absent. By day 5, she was awake and alert, extubated, and transferred to the medicine unit.The management of hypothermia starts with rewarming the patient. The common practice for rewarming has been to apply heating pads and water bottles to the chest, groin, and axilla. The use of forced-air warming systems or external temperature control systems are effective. Warmed saline infusions may be used as well. In recent years, the use of venoarterial extracorporeal membrane oxygenation has been found to provide an effective rewarming process with complete cardiopulmonary support in patients who have experienced cardiac arrest.4 While some consider extracorporeal membrane oxygenation to be the criterion standard for treating severe hypothermia, others point out that much more research needs to be done.5,13Severe accidental hypothermia represents a high risk for morbidity and mortality. In the past 10 to 15 years, interest in hypothermia has increased because of interest in its effects as part of targeted temperature management in patients who have experienced cardiac arrest. Experts agree that the ECG changes that occur with accidental hypothermia may assist with timely diagnosis and interventions for hypothermia. Caution is required in interpreting ECGs, as mentioned previously, if the patient is shivering, because it contributes to distortion of the ECG waveforms.

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