- Email: [email protected]
Electrocardiographic manifestations of hypothermia
Electrocardiographic Manifestations of Hypothermia AMAL MATTU, MD*, WILLIAM J. BRADY, MD,† AND ANDREW D. PERRON, MD† Hypothermia is generally defined as a core body temperature less than 35°C (95°F). Hypothermia is one of the most common environmental emergencies encountered by emergency physicians. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. The classic and well-known electrocardiographic (ECG) manifestations of hypothermia include the presence of J (Osborn) waves, interval (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known (ECG) findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. Hypothermia can also blunt the expected ECG findings associated with hyperkalemia. A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia. (Am J Emerg Med 2002;20:314-326. Copyright 2002, Elsevier Science (USA). All rights reserved.)
Hypothermia is generally defined as a core body temperature less than 35°C (95°F). Hypothermia is one of the most common environmental emergencies encountered by emergency physicians. This condition is found in varied geographic regions and during all seasons.1-3 Although cold exposure is likely the most common cause of hypothermia in emergency department (ED) patients, there are many other predisposing factors as well.1 A full review of the evaluation and management of hypothermic patients is beyond the scope of this article. However, emergency physicians should be familiar with the typical electrocardiographic (ECG) manifestations of hypothermia. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. Standard oral thermometers record only as low as 35°C (95°F) accurately.1 Obtaining a rectal temperature with a rectal probe is the most reliable method of diagnosis. Prehospital personnel that perform 12-lead electrocardiography should also be familiar with the ECG signs of hypothermia because thermometers are rarely used in the prehospital evaluation of patients. The classic and well-known ECG manifestations of hypothermia include the presence of J (Osborn) waves, inter-
From the *Division of Emergency Medicine, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, and †Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA. Manuscript received August 28, 2001, accepted August 29, 2001. Reprints are not available. Key Words: Hypothermia, electrocardiogram. Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0011$35.00/0 doi:10.1053/ajem.2002.32633 314
val (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known ECG findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. Hypothermia can also blunt the expected ECG findings associated with hyperkalemia.1 A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia. CASE PRESENTATIONS Case 1 A 75-year-old woman with a history of insulin-dependent diabetes mellitus was brought to the ED by paramedics from her family’s home for evaluation of a decreased level of consciousness. Family members found her in bed unarousable. She had last been seen 10 hours earlier at nighttime, and she appeared normal at that time. The only medications she took, according to family members, were insulin and enalapril. On physical examination, she was lethargic and nonverbal. Her vital signs showed a heart rate of 30 beats per minute (bpm), respiratory rate of 16 breaths/min, blood pressure of 97/43 mm Hg, and rectal temperature of 31.5°C (88.7°F). Fingerstick glucose was 25. The physical examination was otherwise unremarkable. An ECG was obtained (Fig 1) and showed marked sinus bradycardia with a rate of 32 bpm and first-degree atrioventricular (AV) block. The QRS complex was slightly prolonged, and there appeared to be a small terminal deflection at the end of the QRS complexes (J waves), most notable in the lateral precordial leads (V5-V6) and lead II. The patient was treated with intravenous dextrose and active rewarming measures were initiated with warmed intravenous saline and use of a warming blanket. After 2 hours of rewarming, the patient’s temperature was 33.4°C (92.1°F), and the repeat ECG (Fig 2) showed near-complete resolution of the J waves and acceleration of the sinus rate to 58 bpm. After 2 more hours, a final ECG was obtained (Fig 3), showing complete resolution of the J waves as well as normalization of the PR and QRS intervals. The patient was admitted to the intensive care unit, where she fully regained her normal mental status by the time she was normothermic. She reported that she had taken her usual dose of insulin the night before admission, but she had skipped dinner. Her hypothermia was attributed to prolonged hypoglycemia. Case 2 A 71-year-old man with a history of severe multiinfarct dementia was brought to the ED from a nursing home for
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
315
FIGURE 1. Marked sinus bradycardia with a rate of 32 bpm and first-degree AV block. The QRS complex is slightly prolonged with a small terminal deflection at the end of the QRS complexes (J waves), most notable in the lateral precordial leads (V5-V6) and lead II.
evaluation of lethargy. No history was obtainable from the patient. Transfer forms indicated a gradual worsening in his level of consciousness and decreased oral intake over the previous 36 hours. The patient’s medical history was notable for diabetes and hypertension. His only notable medications were insulin and hydrochlorothiazide. During physical examination, the patient appeared lethargic. The
patient’s vital signs showed a heart rate of 45 bpm, respiratory rate of 18 breaths/min, and blood pressure of 86/40 mm Hg. The patient was not cooperative with attempts to obtain an oral temperature so a tympanic temperature was obtained and found to be 35.6°C (96.1°F). An ECG was obtained (Fig 4), showing marked sinus bradycardia with a rate of 46 bpm and a first-degree AV block. The QRS
FIGURE 2. Near-complete resolution of the J waves and acceleration of the sinus rate to 58 bpm.
316
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 3. Complete resolution of the J waves as well as normalization of the PR and QRS intervals.
interval was slightly prolonged. There was voltage criteria for left ventricular hypertrophy (LVH) and ST segment elevation in the precordial leads. The ST segment elevation was presumed to be the result of an acute myocardial infarction but later attributed to J waves after a rectal temperature was obtained and found to be 30.9°C (87.6°F).
FIGURE 4. Marked sinus bradycardia with a rate of 46 bpm and a first-degree AV block. The QRS interval was slightly prolonged. There was voltage criteria for LVH and ST segment elevation in the precordial leads. The ST segment elevation was presumed to be the result of an acute myocardial infarction but later attributed to J waves after a rectal temperature was obtained and found to be 30.9°C.
Active rewarming measures were initiated, including warmed intravenous saline and the use of a warming blanket. Rewarming measures were continued, and after 3 hours the patient’s rectal temperature was 34.4°C (93.9°F). A repeat ECG (Fig 5) showed a markedly increased sinus rate,
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
317
FIGURE 5. Markedly increased sinus rate, normalization of the PR and QRS intervals, and resolution of the J waves as well as the ST segment elevation in the lateral precordial leads. The upright T waves were replaced by inverted T waves in the lateral leads in a strain pattern (LVH with strain).
normalization of the PR and QRS intervals, and resolution of the J waves (and ST segment elevation in the lateral precordial leads). The upright T waves were replaced by inverted T waves in the lateral leads in a “strain” pattern (LVH with strain). During the patient’s hospital course, cardiac enzyme testing and stress testing was performed to evaluate for a possible ischemic cause for the T wave changes. The cardiac workup was normal. Blood and urine cultures grew Escherichia coli. After appropriate antibiotic treatment for urosepsis, the patient was discharged back to the nursing home at his baseline neurologic status. The patient’s discharge ECG showed no further changes. Case 3 A 76-year-old woman was found unresponsive in her apartment by maintenance workers. Neighbors had not seen her for 2 days. The heating unit in her apartment had not been working properly, and the apartment was very cold. Paramedics were called and found her to have absent respirations and no palpable heart rate. They placed her on a cardiac monitor and found her to be in ventricular fibrillation. Paramedics administered 3 electrical defibrillations, which had no effect on the cardiac rhythm. They then administered a 1.5 mg/kg intravenous bolus of lidocaine,
orotracheally intubated her, and transported her to the ED with chest compressions in progress. On arrival to the ED, she continued to have no spontaneous respirations or palpable heart beat. Cardiac monitoring continued to show ventricular fibrillation (Fig 6). Her rectal temperature was 23.5°C (74.3°F). Fingerstick glucose was 30, for which she was given 50 g of intravenous dextrose. Warmed intravenous saline and heated humidified oxygen were administered. Aggressive internal rewarming measures were initiated as well, including heated thoracic lavage (using chest tubes) and heated bladder lavage (using a foley catheter). Chest compressions were continued, but no further antiarrhythmic medications were administered. After approximately 1 hour of resuscitation time, the patient developed a palpable pulse at a rate of 30 bpm. The blood pressure was 60/30 mm Hg. The cardiac rhythm was wide-complex bradycardia (Fig 7), representing either an idioventricular rhythm or a slow junctional rhythm with intraventricular conduction delay. The patient’s temperature was 27.2°C (80.9°F) at this point. Chest compressions were discontinued, but internal rewarming efforts continued using warmed intravenous saline, heated humidified oxygen, and heated bladder lavage. The patient’s heart rate and blood pressure gradually increased with rewarming.
FIGURE 6. brillation.
Ventricular fi-
318
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 7. The cardiac rhythm is a wide-complex bradycardia, representing either an idioventricular rhythm or a slow junctional rhythm with intraventricular conduction delay.
An ECG (Fig 8) was obtained when the patient’s temperature was 29.4°C (84.9°F). It showed a regular rhythm with significant tremor artifact at a rate of 60 beats/min and a normal QRS interval. The distinction between a sinus rhythm versus a junctional rhythm was difficult because of the artifact. (P waves may be present but are obscured by the artifact.) Subtle J waves were present in the lateral precordial leads, and the patient had a prolonged QT interval. The patient’s blood pressure was 90/40 mm Hg. A repeat ECG (Fig 9) was obtained when the patient’s temperature was 33.3°C (91.9°F), showing sinus rhythm with an increased rate. Small J waves are still present, but the QT interval has decreased. A final ECG (Fig 10) was obtained when the patient was normothermic. The J waves were no longer present, and the QRS and QT intervals were now normal. The patient was eventually discharged to a long-term nursing facility with mild cognitive deficits. Case 4 A 52-year-old homeless alcoholic man was brought to the ED by paramedics for evaluation. The patient had been found lying in the fetal position on the sidewalk on a cold winter night. He appeared lethargic but would open his eyes to painful stimuli. He was not responding verbally or following commands. He remained nonverbal in the ED. His vital signs showed a heart rate of 80 bpm, respiratory rate of
FIGURE 8. Regular rhythm with significant tremor artifact at a rate of 60 bpm and a normal QRS interval. The distinction between a sinus rhythm versus a junctional rhythm is difficult because of the artifact (P waves may be present but are obscured by the artifact). Subtle J waves are present in the lateral precordial leads.
17 breaths/min, blood pressure of 104/85 mm Hg, and rectal temperature of 25.6°C (78.1°F). The patient was intubated for airway protection. Heating lamps were applied, and active internal rewarming was initiated with warmed intravenous saline, heated humidified oxygen, and heated bladder lavage. An ECG was obtained shortly after ED arrival (Fig 11), showing large J waves in most leads and a markedly prolonged QT interval. The rhythm was mostly regular, suggesting an accelerated junctional rhythm with a rate of 84 bpm. After 4 hours of active internal warming, the patient’s temperature was 30.7°C (87.3°F), and a repeat ECG (Fig 12) showed atrial fibrillation with a rate of 100 bpm. Subtle J waves remained in the lateral leads, and the QT interval had decreased. The final ECG (Fig 13) was obtained when the patient’s temperature was 35.0°C (95.0°F). It showed sinus tachycardia with complete resolution of the J waves. The QT and QRS intervals were normal. The patient was eventually discharged from the hospital with a full neurologic recovery. Case 5 A 35-year-old homeless woman with a history of injection heroin use and insulin-dependent diabetes mellitus was brought to the ED by paramedics who had found her lying on a sidewalk unresponsive. She did not re-
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
319
FIGURE 9. Sinus rhythm with an increased rate. Small J waves are present with a decreased QT interval.
spond to naloxone administered by the paramedics. On arrival to the ED, the patient remained unconscious. She was unable to offer any history. Her vital signs showed a heart rate of 100 bpm, respiratory rate of 16 breaths/min, blood pressure of 106/66 mm Hg, and rectal temperature of 28.9°C (84.0°F). Her pulse oximetry was 90% on room air. The physical examination was notable for the pres-
ence of pooled secretions at the back of her throat and a depressed gag reflex. An ECG was obtained (Fig 14) and showed atrial fibrillation with a ventricular response of approximately 100 bpm. It also showed prolongation of the QT interval and slight widening of the QRS. There appeared to be small J waves present in the lateral precordial and inferior leads.
FIGURE 10. The J waves are no longer present and the QRS and QT intervals are now normal.
320
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 11. Large J waves are present in most leads and a markedly prolonged QT interval. The rhythm is regular, suggesting an accelerated junctional rhythm with a rate of 84 bpm.
The patient was intubated for purposes of protecting her airway from aspiration. Active rewarming measures were initiated, including administration of warmed intravenous saline, heated humidified oxygen, and heated bladder and gastric lavage. A warming blanket was also applied. The patient was diagnosed and treated for diabetic ketoacidosis, hyperkalemia, and presumed endocar-
FIGURE 12. Atrial fibrillation with a rate of 100 bpm. Subtle J waves are seen in the lateral leads with a decreased QT interval.
ditis (later confirmed by echocardiogram and blood cultures), in addition to hypothermia. Three hours after admission to the intensive care unit, the patient’s repeat rectal temperature was 31.1°C (88.0°F). A repeat ECG was obtained (Fig 15), showing that the rhythm had converted to normal sinus rhythm. There was also normalization of the QRS and QT intervals and resolution
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
321
FIGURE 13. Sinus tachycardia with complete resolution of the J waves. The QT and QRS intervals are normal.
of the J waves in the lateral precordial leads. Small J waves persisted in the inferior leads but resolved by the time the patient was normothermic (Fig 16). Case 6 A 53-year-old homeless alcoholic man was brought to the ED by ambulance from an alley after bystanders witnessed him
stagger and fall to the ground. The ambient outdoor temperature was approximately 4°C (39°F). On arrival to the ED, the patient was somnolent but would wake easily and thrash about the stretcher if attempts were made to examine him. He refused to provide any history, aside from saying that his “lungs are sore” and that he had been drinking vodka all day. He appeared very disheveled; to perform a medical evaluation, the patient
FIGURE 14. Atrial fibrillation with a ventricular response of approximately 100 bpm, prolongation of the QT interval and slight widening of the QRS. Small J waves are present in the lateral precordial and inferior leads.
322
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 15. Normal sinus rhythm. Normalization of the QRS and QT intervals and resolution of the J waves in the lateral precordial leads is also seen. Small J waves are still noted in the inferior leads.
was chemically sedated with intramuscular lorazepam and droperidol. Vital signs were obtained, showing a heart rate of 50 bpm, respiratory rate of 22 breaths/min, blood pressure of 159/66 mmHg, and oral temperature of 34.6°C (94.3°F). Fingerstick glucose was 100. Pulse oximetry was 92% on room air and 99% on 3 L of supplemental oxygen.
FIGURE 16. J waves had resolved by the time the patient was normothermic.
Warmed intravenous fluids supplemented with thiamine and magnesium were initiated. Warm blankets were provided for the patient to treat what was presumed to be mild hypothermia. The chest radiograph was notable for a right lower lobe infiltrate. The ECG (Fig 17) showed a bradycardic rate of 51 bpm. There was significant tremor artifact,
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
323
FIGURE 17. Bradycardic rhythm with a rate of 51 bpm. Significant tremor artifact led to an initial diagnosis of atrial fibrillation; however, the regularity rules against atrial fibrillation and suggests either sinus bradycardia (the artifact may be obscuring the P waves) or a junctional rhythm. J waves are present and prominent in the lateral precordial leads and subtle in the inferior leads.
which led to an initial diagnosis of atrial fibrillation; however, the regularity rules against atrial fibrillation and suggests either sinus bradycardia (the artifact may be obscuring the P waves) or a junctional rhythm. There was also a markedly prolonged QT interval and a prolonged QRS interval. J waves were present, prominent in the lateral precordial leads and subtle in the inferior leads. Flattened T waves were present in the limb leads. After the ECG abnormalities were recognized as suggestive of severe hypothermia, the rectal temperature was obtained and found to be 28.5°C (83.3°F). The patient was treated for hypothermia. After 4 hours of treatment, the patient’s rectal temperature had increased to 31.1°C (88.0°F). A repeat ECG at that time (Fig 18) showed normal sinus rhythm with a rate of 82 bpm. The tremor artifact had improved significantly, and the QRS and QT intervals had normalized. The J waves had resolved as well. However, T wave abnormalities persisted: the T waves remained flat in the inferior leads, but now the patient had developed inverted T waves in V3-V4 and flattened T waves in V5-V6. By the time the patient was normothermic (Fig 19), the T wave abnormalities had resolved. Because of the T wave changes during rewarming, the patient was evaluated for a possible acute coronary syndrome. Cardiac enzyme testing was normal, and a subsequent persantine-thallium test revealed no evidence of coronary ischemia. The patient was treated for pneumonia and discharged several days later. DISCUSSION The 6 cases presented show the well-known as well as some of the less well-known ECG abnormalities associated with hypothermia. A brief discussion of each of these abnormalities follows.
The J Wave The most common and perhaps the most well-known ECG finding in patients with hypothermia is the J wave.4 This finding was first described by Tomasjewski5 in 1938 as a positive deflection in the terminal portion of the QRS complex and elevation of the J point, resembling a domed T wave.6 This QRS abnormality has also been termed the Osborn wave because of Osborn’s7 studies into the mechanism of this change. The exact cause of the J wave is uncertain. Osborn7 originally suggested that the J wave was related to acidosis.8 However, other investigators have been unable to corroborate this theory.9-11 It has also been suggested that a hypothalamic or neurogenic factor is responsible for the J wave,12 but this mechanism has been questioned as well.8,11 Other investigators have suggested that the J wave represents injury current, delayed ventricular depolarization, or early repolarization that occurs in a portion of the ventricle before delayed depolarization is completed in another portion.4,13,14 However, none of these theories has been definitively proven. J waves are most commonly found in the anterior and lateral precordial leads and in lead II,11 although they may be present in only a single lead.15 It was once believed that J waves were pathognomonic for hypothermia. However, J waves have been reported in a patient with subarachnoid hemorrhage without hypothermia,12 in normothermic patients with acute cardiac ischemia,14 and in normal normothermic patients.8 Despite these cases, the presence of J waves is regarded as highly sensitive and specific for hypothermia. They usually occur in patients with core body temperatures less than 32°C (90°F) and often appear larger when the temperature is below 30°C (86°F).8 The size of the J waves usually correlates inversely
324
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 18. Normal sinus rhythm with a rate of 82 bpm. The tremor artifact has improved significantly and the QRS and QT intervals normalized. The J waves have resolved as well. The T wave abnormalities persisted: the T waves remained flat in the inferior leads, but now the patient had developed inverted T waves in V3-V4 and flattened T waves in V5-V6.
with the body temperature;8,16 as the body temperature increases, the J wave gradually becomes smaller, although there are some reports of temporary persistence of the J wave even after achievement of normothermia.11,17,18 The presence of the J wave has no proven prognostic value. Osborn originally proposed that the presence of the J wave
FIGURE 19. By the time the patient was normothermic, the T wave abnormalities have resolved.
was a predictor of ventricular fibrillation and poor prognosis,7 but this has not been confirmed.19-21 Arrhythmia Hypothermia is associated with various atrial and ventricular dysrhythmias. At mild levels of hypothermia
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
325
(⬎32°C, ⬎90°F), sinus rhythm predominates.16 Decreased AV conduction velocity often causes sinus bradycardia. With progressive hypothermia (26°C–32°C, 79°F–90°F), junctional rhythms and atrial reentrant dysrhythmias may occur. Often, the distinction between sinus bradycardia versus junctional rhythms can be difficult; even in the absence of obvious shivering, tremor artifact may be present and obscure the presence of P waves (Fig 8).1,4,16,22 Further confounding the ability to distinguish between sinus and junctional rhythms is a decrease in the amplitude of the P wave with progressive hypothermia.16,23 The artifact may also be mistaken for atrial fibrillation (Fig 17), although the presence of regular QRS complexes weighs against atrial fibrillation and suggests either a sinus or junctional rhythm. True atrial fibrillation, however, is often present at moderate levels of hypothermia.16 More than 50% of patients with moderate hypothermia develop atrial fibrillation4,16,24 with a slow ventricular response. As with sinus and junctional rhythms, the presence of a rapid ventricular rate is usually attributable to another underlying condition (eg, hypovolemia, sepsis, and so on; see case 5). Atrial fibrillation usually converts spontaneously during rewarming or soon after restoration of normothermia.1,16 The occurrence of atrial fibrillation is not associated with an increased mortality rate,16,19 although mesenteric embolization may be a concern.1 Routine anticoagulation for atrial fibrillation has not been studied and is not recommended because of the likelihood of spontaneous conversion and also the risk of an existing coagulopathy because of the hypothermia. As the core temperature falls below 30°C (86°F), there is increased myocardial irritability and ectopic ventricular beats are common.22 Patients are at high risk for the development of ventricular fibrillation at this degree of hypothermia. With further progression of hypothermia (⬍25°C, ⬍77°F), the risk of asystole increases significantly. There are several theories regarding the cause of ventricular fibrillation and asystole in hypothermia, including tissue hypoxia, acid-base disturbances, autonomic dysfunction,1 and iatrogenic factors (insertion of pacing lines, external cardiac message, intravenous epinephrine administration, excessive jostling).19
Figure 4 (case 2) shows J waves in the precordial leads that produced apparent ST segment elevation. The ECG was initially interpreted by the emergency physician as showing an acute injury pattern. Shortly thereafter, however, the rectal temperature was obtained, and the proper diagnosis was made. With warming, this ST segment elevation resolved. Knowledge of this pseudoinfarction pattern is important, especially for prehospital personnel that perform 12-lead electrocardiography in the field, and also for medical command physicians that receive transmitted prehospital ECGs. Prehospital providers are often unable to make a definite diagnosis of hypothermia because they seldom use thermometers. Misdiagnosis of these patients and inappropriate administration of prehospital thrombolytics to these potentially coagulopathic patients could have catastrophic consequences.25
Prolongation of Intervals Increasing levels of hypothermia result in progressive slowing of myocardial conduction, producing prolongation of the cardiac cycle. Delayed AV conduction results in prolongation of the PR interval, and various degrees of AV block may occur.8,22 Prolongation of both the depolarization as well as the repolarization phases of the action potential produce increases in the QRS and QT intervals, respectively, as hypothermia worsens.8
Alteration of Expected ECG Manifestations Associated With Hyperkalemia Hyperkalemia is often associated with metabolic acidosis, rhabdomyolysis, and renal failure,1 any condition of which may be associated with hypothermia. Hypothermia enhances the cardiac toxicity of hyperkalemia and may obscure some of the expected ECG manifestations of hyperkalemia.1 The patients in cases 2 and 5 both presented with moderate levels of hyperkalemia in association with new renal failure. Both patients’ initial ECGs showed very subtle peaked T waves that were initially missed by the treating physicians. The diagnoses of hyperkalemia were made only after the serum potassium levels were obtained from the laboratory, resulting in significant delays in proper treatment. Although impossible to prove, it is possible that the presence of hypothermia resulted in some blunting of the expected ECG manifestations of hyperkalemia in these 2 patients. CONCLUSION Hypothermia is a common condition encountered by emergency physicians, regardless of their geographic location of practice or the season. Although most cases are diagnosed at the time vital signs are checked, there is a clear danger of initial misdiagnosis or delays in the diagnosis. Classic ECG findings include the presence of the J wave, atrial and ventricular dysrhythmias, and prolongation of the PR, QRS, and QT intervals. Hypothermia can also produce pseudoischemia and pseudoinfarction ECG patterns and may blunt the expected ECG findings of hyperkalemia. Thorough knowledge of these ECG manifestations of hypothermia is important to facilitate rapid diagnosis and initiate prompt treatment of this potentially deadly condition.
Pseudoacute Coronary Syndrome Hypothermia can be associated with ECG changes that mimic those of acute coronary syndromes.1 T wave changes can sometimes occur, although no definite pathophysiology for this finding has been determined. Cases 2 and 6 show T wave abnormalities that reverted to baseline with warming. In-hospital workups for cardiac ischemia were negative. The hypothermia J wave can sometimes be mistaken for the ST segment elevation of acute myocardial infarction.25
REFERENCES 1. Danzl DF: Accidental hypothermia, in Rosen P, Barkin R, Danzl DF, et al (eds): Emergency Medicine: Concepts and Clinical Practice. St. Louis, MO, Mosby-Year Book, Inc, 1998, pp 963-986 2. Miller JW, Danzl DF, Thomas DM: Urban accidental hypothermia: 135 cases. Ann Emerg Med 1980;9:456-461 3. White JD: Hypothermia: The Bellevue experience. Ann Emerg Med 1982;11:417-424
326
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
4. Chou T, Knilans TK: Electrocardiography in Clinical Practice: Adult and Pediatric (ed 4). Philadelphia, PA, WB Saunders Company, 1996, pp 547-552 5. Tomasjewski W: Changements electrocardiographiques observes chez un homme mort de froid. Arch Mal Coeur 1938; 31:525-528 6. Drake CE, Flowers NC: ECG changes in hypothermia from sepsis and unrelated to exposure. Chest 1980;77:685-686 7. Osborn JJ: Experimental hypothermia: Respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389-398 8. Gould L, Gopalaswamy C, Kim BS, et al: The Osborn wave in hypothermia. Angiology 1985;36:125-129 9. Emslie-Smith D: The significance of changes in the electrocardiogram in hypothermia. Brit Heart J 1959;21:343-351 10. Thompson R, Rich J, Chmelik F, et al: Evolutionary changes in the electrocardiogram of severe progressive hypothermia. J Electrocardiol 1977;10:62-70 11. Okada M, Nishimura F, Yoshino H, et al: The J wave in accidental hypothermia. J Electrocardiol 1983;16:23-28 12. De Sweit J: Changes simulating hypothermia in the electrocardiogram in subarachnoid hemorrhage. J Electrocardiol 1972;5:193-195 13. Trevino A, Razi B, Beller B: The characteristic electrocardiogram of accidental hypothermia. Arch intern Med 1971;127: 470-473 14. Patel A, Getsos JP, Moussa G, et al: The Osborn wave of hypothermia in normothermic patients. Clin Cardiol 1994;17: 273-276
15. Kernohan RJ: Electrocardiographic and serum-enzyme changes in hypothermia. Ir J Med Sci 1969;8:321-326 16. Okada M: The cardiac rhythm in accidental hypothermia. J Electrocardiol 1984;17:123-128 17. Phillipson EA, Herbert FA: Accidental exposure to freezing: clinical and laboratory observations during convalescence from near-fatal hypothermia. Can Med Assoc J 1967;97:786792 18. Vassallo SU, Delaney KA, Hoffman RS, et al: A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med 1999;6:1121-1126 19. Rankin AC, Rae AP: Cardiac arrhythmias during rewarming of patients with accidental hypothemia. Br Med J (Clin Res Ed) 1984;289:874-877 20. Schwab RH, Lewis DW, Killough JH, et al: Electrocardiographic changes in rapidly induced deep hypothermia. Am J Med Sci 1964;248:290-303 21. Hancock EW: Hypothermia, slow pulse, and an unusual QRS complex. Hosp Pract (Off Ed) 1996;31:25-26 22. Carden D, Doan L, Sweeney PJ, et al: Hypothermia [clinical conference]. Ann Emerg Med 1982;11:497-503 23. Jacob Al, Lichstein E, Vlano SD, et al: A-V block in accidental hypothermia. J Electrocardiol 1978;11:399-402 24. Hicks CE, McCord MC, Blount SG: Electrocardiographic changes during hypothermia and circulatory occlusion. Circulation 1956;13:21-26 25. Glusman A, Hasan K, Roguin N: Contraindication to thrombolytic therapy in accidental hypothermia simulating acute myocardial infarction. Int J Cardiol 1990;28:269-72
Hypothermia is generally defined as a core body temperature less than 35°C (95°F). Hypothermia is one of the most common environmental emergencies encountered by emergency physicians. This condition is found in varied geographic regions and during all seasons.1-3 Although cold exposure is likely the most common cause of hypothermia in emergency department (ED) patients, there are many other predisposing factors as well.1 A full review of the evaluation and management of hypothermic patients is beyond the scope of this article. However, emergency physicians should be familiar with the typical electrocardiographic (ECG) manifestations of hypothermia. Although the diagnosis will usually be evident after an initial check of vital signs, the diagnosis can sometimes be missed because of overreliance on normal or near-normal oral or tympanic thermometer readings. Standard oral thermometers record only as low as 35°C (95°F) accurately.1 Obtaining a rectal temperature with a rectal probe is the most reliable method of diagnosis. Prehospital personnel that perform 12-lead electrocardiography should also be familiar with the ECG signs of hypothermia because thermometers are rarely used in the prehospital evaluation of patients. The classic and well-known ECG manifestations of hypothermia include the presence of J (Osborn) waves, inter-
From the *Division of Emergency Medicine, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, and †Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA. Manuscript received August 28, 2001, accepted August 29, 2001. Reprints are not available. Key Words: Hypothermia, electrocardiogram. Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2004-0011$35.00/0 doi:10.1053/ajem.2002.32633 314
val (PR, QRS, QT) prolongation, and atrial and ventricular dysrhythmias. There are also some less known ECG findings associated with hypothermia. For example, hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction. Hypothermia can also blunt the expected ECG findings associated with hyperkalemia.1 A thorough knowledge of these findings is important for prompt diagnosis and treatment of hypothermia. Six cases are presented that show these important ECG manifestations of hypothermia. CASE PRESENTATIONS Case 1 A 75-year-old woman with a history of insulin-dependent diabetes mellitus was brought to the ED by paramedics from her family’s home for evaluation of a decreased level of consciousness. Family members found her in bed unarousable. She had last been seen 10 hours earlier at nighttime, and she appeared normal at that time. The only medications she took, according to family members, were insulin and enalapril. On physical examination, she was lethargic and nonverbal. Her vital signs showed a heart rate of 30 beats per minute (bpm), respiratory rate of 16 breaths/min, blood pressure of 97/43 mm Hg, and rectal temperature of 31.5°C (88.7°F). Fingerstick glucose was 25. The physical examination was otherwise unremarkable. An ECG was obtained (Fig 1) and showed marked sinus bradycardia with a rate of 32 bpm and first-degree atrioventricular (AV) block. The QRS complex was slightly prolonged, and there appeared to be a small terminal deflection at the end of the QRS complexes (J waves), most notable in the lateral precordial leads (V5-V6) and lead II. The patient was treated with intravenous dextrose and active rewarming measures were initiated with warmed intravenous saline and use of a warming blanket. After 2 hours of rewarming, the patient’s temperature was 33.4°C (92.1°F), and the repeat ECG (Fig 2) showed near-complete resolution of the J waves and acceleration of the sinus rate to 58 bpm. After 2 more hours, a final ECG was obtained (Fig 3), showing complete resolution of the J waves as well as normalization of the PR and QRS intervals. The patient was admitted to the intensive care unit, where she fully regained her normal mental status by the time she was normothermic. She reported that she had taken her usual dose of insulin the night before admission, but she had skipped dinner. Her hypothermia was attributed to prolonged hypoglycemia. Case 2 A 71-year-old man with a history of severe multiinfarct dementia was brought to the ED from a nursing home for
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
315
FIGURE 1. Marked sinus bradycardia with a rate of 32 bpm and first-degree AV block. The QRS complex is slightly prolonged with a small terminal deflection at the end of the QRS complexes (J waves), most notable in the lateral precordial leads (V5-V6) and lead II.
evaluation of lethargy. No history was obtainable from the patient. Transfer forms indicated a gradual worsening in his level of consciousness and decreased oral intake over the previous 36 hours. The patient’s medical history was notable for diabetes and hypertension. His only notable medications were insulin and hydrochlorothiazide. During physical examination, the patient appeared lethargic. The
patient’s vital signs showed a heart rate of 45 bpm, respiratory rate of 18 breaths/min, and blood pressure of 86/40 mm Hg. The patient was not cooperative with attempts to obtain an oral temperature so a tympanic temperature was obtained and found to be 35.6°C (96.1°F). An ECG was obtained (Fig 4), showing marked sinus bradycardia with a rate of 46 bpm and a first-degree AV block. The QRS
FIGURE 2. Near-complete resolution of the J waves and acceleration of the sinus rate to 58 bpm.
316
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 3. Complete resolution of the J waves as well as normalization of the PR and QRS intervals.
interval was slightly prolonged. There was voltage criteria for left ventricular hypertrophy (LVH) and ST segment elevation in the precordial leads. The ST segment elevation was presumed to be the result of an acute myocardial infarction but later attributed to J waves after a rectal temperature was obtained and found to be 30.9°C (87.6°F).
FIGURE 4. Marked sinus bradycardia with a rate of 46 bpm and a first-degree AV block. The QRS interval was slightly prolonged. There was voltage criteria for LVH and ST segment elevation in the precordial leads. The ST segment elevation was presumed to be the result of an acute myocardial infarction but later attributed to J waves after a rectal temperature was obtained and found to be 30.9°C.
Active rewarming measures were initiated, including warmed intravenous saline and the use of a warming blanket. Rewarming measures were continued, and after 3 hours the patient’s rectal temperature was 34.4°C (93.9°F). A repeat ECG (Fig 5) showed a markedly increased sinus rate,
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
317
FIGURE 5. Markedly increased sinus rate, normalization of the PR and QRS intervals, and resolution of the J waves as well as the ST segment elevation in the lateral precordial leads. The upright T waves were replaced by inverted T waves in the lateral leads in a strain pattern (LVH with strain).
normalization of the PR and QRS intervals, and resolution of the J waves (and ST segment elevation in the lateral precordial leads). The upright T waves were replaced by inverted T waves in the lateral leads in a “strain” pattern (LVH with strain). During the patient’s hospital course, cardiac enzyme testing and stress testing was performed to evaluate for a possible ischemic cause for the T wave changes. The cardiac workup was normal. Blood and urine cultures grew Escherichia coli. After appropriate antibiotic treatment for urosepsis, the patient was discharged back to the nursing home at his baseline neurologic status. The patient’s discharge ECG showed no further changes. Case 3 A 76-year-old woman was found unresponsive in her apartment by maintenance workers. Neighbors had not seen her for 2 days. The heating unit in her apartment had not been working properly, and the apartment was very cold. Paramedics were called and found her to have absent respirations and no palpable heart rate. They placed her on a cardiac monitor and found her to be in ventricular fibrillation. Paramedics administered 3 electrical defibrillations, which had no effect on the cardiac rhythm. They then administered a 1.5 mg/kg intravenous bolus of lidocaine,
orotracheally intubated her, and transported her to the ED with chest compressions in progress. On arrival to the ED, she continued to have no spontaneous respirations or palpable heart beat. Cardiac monitoring continued to show ventricular fibrillation (Fig 6). Her rectal temperature was 23.5°C (74.3°F). Fingerstick glucose was 30, for which she was given 50 g of intravenous dextrose. Warmed intravenous saline and heated humidified oxygen were administered. Aggressive internal rewarming measures were initiated as well, including heated thoracic lavage (using chest tubes) and heated bladder lavage (using a foley catheter). Chest compressions were continued, but no further antiarrhythmic medications were administered. After approximately 1 hour of resuscitation time, the patient developed a palpable pulse at a rate of 30 bpm. The blood pressure was 60/30 mm Hg. The cardiac rhythm was wide-complex bradycardia (Fig 7), representing either an idioventricular rhythm or a slow junctional rhythm with intraventricular conduction delay. The patient’s temperature was 27.2°C (80.9°F) at this point. Chest compressions were discontinued, but internal rewarming efforts continued using warmed intravenous saline, heated humidified oxygen, and heated bladder lavage. The patient’s heart rate and blood pressure gradually increased with rewarming.
FIGURE 6. brillation.
Ventricular fi-
318
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 7. The cardiac rhythm is a wide-complex bradycardia, representing either an idioventricular rhythm or a slow junctional rhythm with intraventricular conduction delay.
An ECG (Fig 8) was obtained when the patient’s temperature was 29.4°C (84.9°F). It showed a regular rhythm with significant tremor artifact at a rate of 60 beats/min and a normal QRS interval. The distinction between a sinus rhythm versus a junctional rhythm was difficult because of the artifact. (P waves may be present but are obscured by the artifact.) Subtle J waves were present in the lateral precordial leads, and the patient had a prolonged QT interval. The patient’s blood pressure was 90/40 mm Hg. A repeat ECG (Fig 9) was obtained when the patient’s temperature was 33.3°C (91.9°F), showing sinus rhythm with an increased rate. Small J waves are still present, but the QT interval has decreased. A final ECG (Fig 10) was obtained when the patient was normothermic. The J waves were no longer present, and the QRS and QT intervals were now normal. The patient was eventually discharged to a long-term nursing facility with mild cognitive deficits. Case 4 A 52-year-old homeless alcoholic man was brought to the ED by paramedics for evaluation. The patient had been found lying in the fetal position on the sidewalk on a cold winter night. He appeared lethargic but would open his eyes to painful stimuli. He was not responding verbally or following commands. He remained nonverbal in the ED. His vital signs showed a heart rate of 80 bpm, respiratory rate of
FIGURE 8. Regular rhythm with significant tremor artifact at a rate of 60 bpm and a normal QRS interval. The distinction between a sinus rhythm versus a junctional rhythm is difficult because of the artifact (P waves may be present but are obscured by the artifact). Subtle J waves are present in the lateral precordial leads.
17 breaths/min, blood pressure of 104/85 mm Hg, and rectal temperature of 25.6°C (78.1°F). The patient was intubated for airway protection. Heating lamps were applied, and active internal rewarming was initiated with warmed intravenous saline, heated humidified oxygen, and heated bladder lavage. An ECG was obtained shortly after ED arrival (Fig 11), showing large J waves in most leads and a markedly prolonged QT interval. The rhythm was mostly regular, suggesting an accelerated junctional rhythm with a rate of 84 bpm. After 4 hours of active internal warming, the patient’s temperature was 30.7°C (87.3°F), and a repeat ECG (Fig 12) showed atrial fibrillation with a rate of 100 bpm. Subtle J waves remained in the lateral leads, and the QT interval had decreased. The final ECG (Fig 13) was obtained when the patient’s temperature was 35.0°C (95.0°F). It showed sinus tachycardia with complete resolution of the J waves. The QT and QRS intervals were normal. The patient was eventually discharged from the hospital with a full neurologic recovery. Case 5 A 35-year-old homeless woman with a history of injection heroin use and insulin-dependent diabetes mellitus was brought to the ED by paramedics who had found her lying on a sidewalk unresponsive. She did not re-
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
319
FIGURE 9. Sinus rhythm with an increased rate. Small J waves are present with a decreased QT interval.
spond to naloxone administered by the paramedics. On arrival to the ED, the patient remained unconscious. She was unable to offer any history. Her vital signs showed a heart rate of 100 bpm, respiratory rate of 16 breaths/min, blood pressure of 106/66 mm Hg, and rectal temperature of 28.9°C (84.0°F). Her pulse oximetry was 90% on room air. The physical examination was notable for the pres-
ence of pooled secretions at the back of her throat and a depressed gag reflex. An ECG was obtained (Fig 14) and showed atrial fibrillation with a ventricular response of approximately 100 bpm. It also showed prolongation of the QT interval and slight widening of the QRS. There appeared to be small J waves present in the lateral precordial and inferior leads.
FIGURE 10. The J waves are no longer present and the QRS and QT intervals are now normal.
320
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 11. Large J waves are present in most leads and a markedly prolonged QT interval. The rhythm is regular, suggesting an accelerated junctional rhythm with a rate of 84 bpm.
The patient was intubated for purposes of protecting her airway from aspiration. Active rewarming measures were initiated, including administration of warmed intravenous saline, heated humidified oxygen, and heated bladder and gastric lavage. A warming blanket was also applied. The patient was diagnosed and treated for diabetic ketoacidosis, hyperkalemia, and presumed endocar-
FIGURE 12. Atrial fibrillation with a rate of 100 bpm. Subtle J waves are seen in the lateral leads with a decreased QT interval.
ditis (later confirmed by echocardiogram and blood cultures), in addition to hypothermia. Three hours after admission to the intensive care unit, the patient’s repeat rectal temperature was 31.1°C (88.0°F). A repeat ECG was obtained (Fig 15), showing that the rhythm had converted to normal sinus rhythm. There was also normalization of the QRS and QT intervals and resolution
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
321
FIGURE 13. Sinus tachycardia with complete resolution of the J waves. The QT and QRS intervals are normal.
of the J waves in the lateral precordial leads. Small J waves persisted in the inferior leads but resolved by the time the patient was normothermic (Fig 16). Case 6 A 53-year-old homeless alcoholic man was brought to the ED by ambulance from an alley after bystanders witnessed him
stagger and fall to the ground. The ambient outdoor temperature was approximately 4°C (39°F). On arrival to the ED, the patient was somnolent but would wake easily and thrash about the stretcher if attempts were made to examine him. He refused to provide any history, aside from saying that his “lungs are sore” and that he had been drinking vodka all day. He appeared very disheveled; to perform a medical evaluation, the patient
FIGURE 14. Atrial fibrillation with a ventricular response of approximately 100 bpm, prolongation of the QT interval and slight widening of the QRS. Small J waves are present in the lateral precordial and inferior leads.
322
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 15. Normal sinus rhythm. Normalization of the QRS and QT intervals and resolution of the J waves in the lateral precordial leads is also seen. Small J waves are still noted in the inferior leads.
was chemically sedated with intramuscular lorazepam and droperidol. Vital signs were obtained, showing a heart rate of 50 bpm, respiratory rate of 22 breaths/min, blood pressure of 159/66 mmHg, and oral temperature of 34.6°C (94.3°F). Fingerstick glucose was 100. Pulse oximetry was 92% on room air and 99% on 3 L of supplemental oxygen.
FIGURE 16. J waves had resolved by the time the patient was normothermic.
Warmed intravenous fluids supplemented with thiamine and magnesium were initiated. Warm blankets were provided for the patient to treat what was presumed to be mild hypothermia. The chest radiograph was notable for a right lower lobe infiltrate. The ECG (Fig 17) showed a bradycardic rate of 51 bpm. There was significant tremor artifact,
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
323
FIGURE 17. Bradycardic rhythm with a rate of 51 bpm. Significant tremor artifact led to an initial diagnosis of atrial fibrillation; however, the regularity rules against atrial fibrillation and suggests either sinus bradycardia (the artifact may be obscuring the P waves) or a junctional rhythm. J waves are present and prominent in the lateral precordial leads and subtle in the inferior leads.
which led to an initial diagnosis of atrial fibrillation; however, the regularity rules against atrial fibrillation and suggests either sinus bradycardia (the artifact may be obscuring the P waves) or a junctional rhythm. There was also a markedly prolonged QT interval and a prolonged QRS interval. J waves were present, prominent in the lateral precordial leads and subtle in the inferior leads. Flattened T waves were present in the limb leads. After the ECG abnormalities were recognized as suggestive of severe hypothermia, the rectal temperature was obtained and found to be 28.5°C (83.3°F). The patient was treated for hypothermia. After 4 hours of treatment, the patient’s rectal temperature had increased to 31.1°C (88.0°F). A repeat ECG at that time (Fig 18) showed normal sinus rhythm with a rate of 82 bpm. The tremor artifact had improved significantly, and the QRS and QT intervals had normalized. The J waves had resolved as well. However, T wave abnormalities persisted: the T waves remained flat in the inferior leads, but now the patient had developed inverted T waves in V3-V4 and flattened T waves in V5-V6. By the time the patient was normothermic (Fig 19), the T wave abnormalities had resolved. Because of the T wave changes during rewarming, the patient was evaluated for a possible acute coronary syndrome. Cardiac enzyme testing was normal, and a subsequent persantine-thallium test revealed no evidence of coronary ischemia. The patient was treated for pneumonia and discharged several days later. DISCUSSION The 6 cases presented show the well-known as well as some of the less well-known ECG abnormalities associated with hypothermia. A brief discussion of each of these abnormalities follows.
The J Wave The most common and perhaps the most well-known ECG finding in patients with hypothermia is the J wave.4 This finding was first described by Tomasjewski5 in 1938 as a positive deflection in the terminal portion of the QRS complex and elevation of the J point, resembling a domed T wave.6 This QRS abnormality has also been termed the Osborn wave because of Osborn’s7 studies into the mechanism of this change. The exact cause of the J wave is uncertain. Osborn7 originally suggested that the J wave was related to acidosis.8 However, other investigators have been unable to corroborate this theory.9-11 It has also been suggested that a hypothalamic or neurogenic factor is responsible for the J wave,12 but this mechanism has been questioned as well.8,11 Other investigators have suggested that the J wave represents injury current, delayed ventricular depolarization, or early repolarization that occurs in a portion of the ventricle before delayed depolarization is completed in another portion.4,13,14 However, none of these theories has been definitively proven. J waves are most commonly found in the anterior and lateral precordial leads and in lead II,11 although they may be present in only a single lead.15 It was once believed that J waves were pathognomonic for hypothermia. However, J waves have been reported in a patient with subarachnoid hemorrhage without hypothermia,12 in normothermic patients with acute cardiac ischemia,14 and in normal normothermic patients.8 Despite these cases, the presence of J waves is regarded as highly sensitive and specific for hypothermia. They usually occur in patients with core body temperatures less than 32°C (90°F) and often appear larger when the temperature is below 30°C (86°F).8 The size of the J waves usually correlates inversely
324
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
FIGURE 18. Normal sinus rhythm with a rate of 82 bpm. The tremor artifact has improved significantly and the QRS and QT intervals normalized. The J waves have resolved as well. The T wave abnormalities persisted: the T waves remained flat in the inferior leads, but now the patient had developed inverted T waves in V3-V4 and flattened T waves in V5-V6.
with the body temperature;8,16 as the body temperature increases, the J wave gradually becomes smaller, although there are some reports of temporary persistence of the J wave even after achievement of normothermia.11,17,18 The presence of the J wave has no proven prognostic value. Osborn originally proposed that the presence of the J wave
FIGURE 19. By the time the patient was normothermic, the T wave abnormalities have resolved.
was a predictor of ventricular fibrillation and poor prognosis,7 but this has not been confirmed.19-21 Arrhythmia Hypothermia is associated with various atrial and ventricular dysrhythmias. At mild levels of hypothermia
MATTU, BRADY, AND PERRON ■ HYPOTHERMIA AND THE ECG
325
(⬎32°C, ⬎90°F), sinus rhythm predominates.16 Decreased AV conduction velocity often causes sinus bradycardia. With progressive hypothermia (26°C–32°C, 79°F–90°F), junctional rhythms and atrial reentrant dysrhythmias may occur. Often, the distinction between sinus bradycardia versus junctional rhythms can be difficult; even in the absence of obvious shivering, tremor artifact may be present and obscure the presence of P waves (Fig 8).1,4,16,22 Further confounding the ability to distinguish between sinus and junctional rhythms is a decrease in the amplitude of the P wave with progressive hypothermia.16,23 The artifact may also be mistaken for atrial fibrillation (Fig 17), although the presence of regular QRS complexes weighs against atrial fibrillation and suggests either a sinus or junctional rhythm. True atrial fibrillation, however, is often present at moderate levels of hypothermia.16 More than 50% of patients with moderate hypothermia develop atrial fibrillation4,16,24 with a slow ventricular response. As with sinus and junctional rhythms, the presence of a rapid ventricular rate is usually attributable to another underlying condition (eg, hypovolemia, sepsis, and so on; see case 5). Atrial fibrillation usually converts spontaneously during rewarming or soon after restoration of normothermia.1,16 The occurrence of atrial fibrillation is not associated with an increased mortality rate,16,19 although mesenteric embolization may be a concern.1 Routine anticoagulation for atrial fibrillation has not been studied and is not recommended because of the likelihood of spontaneous conversion and also the risk of an existing coagulopathy because of the hypothermia. As the core temperature falls below 30°C (86°F), there is increased myocardial irritability and ectopic ventricular beats are common.22 Patients are at high risk for the development of ventricular fibrillation at this degree of hypothermia. With further progression of hypothermia (⬍25°C, ⬍77°F), the risk of asystole increases significantly. There are several theories regarding the cause of ventricular fibrillation and asystole in hypothermia, including tissue hypoxia, acid-base disturbances, autonomic dysfunction,1 and iatrogenic factors (insertion of pacing lines, external cardiac message, intravenous epinephrine administration, excessive jostling).19
Figure 4 (case 2) shows J waves in the precordial leads that produced apparent ST segment elevation. The ECG was initially interpreted by the emergency physician as showing an acute injury pattern. Shortly thereafter, however, the rectal temperature was obtained, and the proper diagnosis was made. With warming, this ST segment elevation resolved. Knowledge of this pseudoinfarction pattern is important, especially for prehospital personnel that perform 12-lead electrocardiography in the field, and also for medical command physicians that receive transmitted prehospital ECGs. Prehospital providers are often unable to make a definite diagnosis of hypothermia because they seldom use thermometers. Misdiagnosis of these patients and inappropriate administration of prehospital thrombolytics to these potentially coagulopathic patients could have catastrophic consequences.25
Prolongation of Intervals Increasing levels of hypothermia result in progressive slowing of myocardial conduction, producing prolongation of the cardiac cycle. Delayed AV conduction results in prolongation of the PR interval, and various degrees of AV block may occur.8,22 Prolongation of both the depolarization as well as the repolarization phases of the action potential produce increases in the QRS and QT intervals, respectively, as hypothermia worsens.8
Alteration of Expected ECG Manifestations Associated With Hyperkalemia Hyperkalemia is often associated with metabolic acidosis, rhabdomyolysis, and renal failure,1 any condition of which may be associated with hypothermia. Hypothermia enhances the cardiac toxicity of hyperkalemia and may obscure some of the expected ECG manifestations of hyperkalemia.1 The patients in cases 2 and 5 both presented with moderate levels of hyperkalemia in association with new renal failure. Both patients’ initial ECGs showed very subtle peaked T waves that were initially missed by the treating physicians. The diagnoses of hyperkalemia were made only after the serum potassium levels were obtained from the laboratory, resulting in significant delays in proper treatment. Although impossible to prove, it is possible that the presence of hypothermia resulted in some blunting of the expected ECG manifestations of hyperkalemia in these 2 patients. CONCLUSION Hypothermia is a common condition encountered by emergency physicians, regardless of their geographic location of practice or the season. Although most cases are diagnosed at the time vital signs are checked, there is a clear danger of initial misdiagnosis or delays in the diagnosis. Classic ECG findings include the presence of the J wave, atrial and ventricular dysrhythmias, and prolongation of the PR, QRS, and QT intervals. Hypothermia can also produce pseudoischemia and pseudoinfarction ECG patterns and may blunt the expected ECG findings of hyperkalemia. Thorough knowledge of these ECG manifestations of hypothermia is important to facilitate rapid diagnosis and initiate prompt treatment of this potentially deadly condition.
Pseudoacute Coronary Syndrome Hypothermia can be associated with ECG changes that mimic those of acute coronary syndromes.1 T wave changes can sometimes occur, although no definite pathophysiology for this finding has been determined. Cases 2 and 6 show T wave abnormalities that reverted to baseline with warming. In-hospital workups for cardiac ischemia were negative. The hypothermia J wave can sometimes be mistaken for the ST segment elevation of acute myocardial infarction.25
REFERENCES 1. Danzl DF: Accidental hypothermia, in Rosen P, Barkin R, Danzl DF, et al (eds): Emergency Medicine: Concepts and Clinical Practice. St. Louis, MO, Mosby-Year Book, Inc, 1998, pp 963-986 2. Miller JW, Danzl DF, Thomas DM: Urban accidental hypothermia: 135 cases. Ann Emerg Med 1980;9:456-461 3. White JD: Hypothermia: The Bellevue experience. Ann Emerg Med 1982;11:417-424
326
AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 4 ■ July 2002
4. Chou T, Knilans TK: Electrocardiography in Clinical Practice: Adult and Pediatric (ed 4). Philadelphia, PA, WB Saunders Company, 1996, pp 547-552 5. Tomasjewski W: Changements electrocardiographiques observes chez un homme mort de froid. Arch Mal Coeur 1938; 31:525-528 6. Drake CE, Flowers NC: ECG changes in hypothermia from sepsis and unrelated to exposure. Chest 1980;77:685-686 7. Osborn JJ: Experimental hypothermia: Respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389-398 8. Gould L, Gopalaswamy C, Kim BS, et al: The Osborn wave in hypothermia. Angiology 1985;36:125-129 9. Emslie-Smith D: The significance of changes in the electrocardiogram in hypothermia. Brit Heart J 1959;21:343-351 10. Thompson R, Rich J, Chmelik F, et al: Evolutionary changes in the electrocardiogram of severe progressive hypothermia. J Electrocardiol 1977;10:62-70 11. Okada M, Nishimura F, Yoshino H, et al: The J wave in accidental hypothermia. J Electrocardiol 1983;16:23-28 12. De Sweit J: Changes simulating hypothermia in the electrocardiogram in subarachnoid hemorrhage. J Electrocardiol 1972;5:193-195 13. Trevino A, Razi B, Beller B: The characteristic electrocardiogram of accidental hypothermia. Arch intern Med 1971;127: 470-473 14. Patel A, Getsos JP, Moussa G, et al: The Osborn wave of hypothermia in normothermic patients. Clin Cardiol 1994;17: 273-276
15. Kernohan RJ: Electrocardiographic and serum-enzyme changes in hypothermia. Ir J Med Sci 1969;8:321-326 16. Okada M: The cardiac rhythm in accidental hypothermia. J Electrocardiol 1984;17:123-128 17. Phillipson EA, Herbert FA: Accidental exposure to freezing: clinical and laboratory observations during convalescence from near-fatal hypothermia. Can Med Assoc J 1967;97:786792 18. Vassallo SU, Delaney KA, Hoffman RS, et al: A prospective evaluation of the electrocardiographic manifestations of hypothermia. Acad Emerg Med 1999;6:1121-1126 19. Rankin AC, Rae AP: Cardiac arrhythmias during rewarming of patients with accidental hypothemia. Br Med J (Clin Res Ed) 1984;289:874-877 20. Schwab RH, Lewis DW, Killough JH, et al: Electrocardiographic changes in rapidly induced deep hypothermia. Am J Med Sci 1964;248:290-303 21. Hancock EW: Hypothermia, slow pulse, and an unusual QRS complex. Hosp Pract (Off Ed) 1996;31:25-26 22. Carden D, Doan L, Sweeney PJ, et al: Hypothermia [clinical conference]. Ann Emerg Med 1982;11:497-503 23. Jacob Al, Lichstein E, Vlano SD, et al: A-V block in accidental hypothermia. J Electrocardiol 1978;11:399-402 24. Hicks CE, McCord MC, Blount SG: Electrocardiographic changes during hypothermia and circulatory occlusion. Circulation 1956;13:21-26 25. Glusman A, Hasan K, Roguin N: Contraindication to thrombolytic therapy in accidental hypothermia simulating acute myocardial infarction. Int J Cardiol 1990;28:269-72