Download 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.
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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-
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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.
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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.
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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
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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
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