07-ElectroCardEMPrint

pacemakers and pacemaker dysfunction

Figures

Figure 14-9.
Rapid paced ventricular rate caused by pacemaker tachycardia. Tracing from leads V2 and V3 of a patient with
a DDD pacer and pacemaker-mediated tachycardia at the upper rate limit of 100 beats/min. The pacer spikes
from the bipolar leads are barely seen in lead V3 (arrow). The retrograde p wave (p) that is perpetuating the
tachycardia is seen buried in the ventricular complex. The patient’s pacemaker was reprogrammed to prevent
this problem. Image courtesy of Nora Goldschlager, MD.

Figure 14-10.
Magnet application. A: A magnet. B: Lead V1 reveals a normal sinus rhythm with right bundle-branch block.
Placement of a magnet over the pacemaker reveals atrioventricular sequential pacing with 100% capture at
100 beats/min.

AB

191

Electrocardiography in Emergency Medicine

Figures

Figure 14-11.
Acute myocardial infarction in a patient with a single-chamber pacemaker programmed to VVI mode.
A: Normal paced ventricular complexes with left bundle-branch block morphology. The ST segments
are discordant to (in the opposite direction of) the overall direction of the QRS complex. In leads with a
primarily negative QRS deflection, such as II, III, and aVF, there is ST-segment elevation related to expected
repolarization changes. In leads with a primarily positive QRS deflection, such as I, aVL, and V6, there is
expected ST-segment depression. B: New concordant ST-segment elevation in lead V6 and new concordant
ST-segment depression in leads V2, V3, and V4, both diagnostic of acute myocardial infarction. From: Brandt
RR, Hammill SC, Higano ST. Images in cardiovascular medicine: electrocardiographic diagnosis of acute
myocardial infarction during ventricular pacing. Circulation. 1998;97:2274-2275. Used with permission.

A

B

192

C h apter f i ftee n

Metabolic Abnormalities: Effects of
Electrolyte Imbalances and Thyroid
Disorders on the ECG

Fredrick M. Abrahamian, DO, and Malkeet Gupta, MD, MS

Electrolyte Imbalances amplitude of more than 6 mm in the limb
leads and more than 10 mm in the precordial
Hyperkalemia leads.3 A peaked T wave is not absolutely
diagnostic for hyperkalemia—this pattern
The ECG can provide clues to the presence can also be seen in healthy individuals.
of hyperkalemia, especially if the hyperkalemia
is severe. Hyperkalemia is defined as a serum Early AMI can also exhibit tall, peaked
potassium (K+) level of more than 5.1 T waves. However, the T waves associated
mEq/L. It is commonly classified as mild with AMI often have a broad base with
(K+ = 5.5–6.5 mEq/L), moderate (K+ = 6.5–8 a long QT interval. Additionally, the T-
mEq/L), and severe (K+ >8 mEq/L). The wave changes are confined to those leads
likelihood of an abnormal ECG becomes higher overlying the area of infarction, whereas in
as the serum level exceeds 6.7 mEq/L.1 hyperkalemia the changes are more diffuse.

Because hyperkalemia shortens repolarization, Other causes of tall, peaked T waves include
the earliest clue to a high serum potassium hypermagnesemia, left ventricular hypertrophy
level is a change in the T wave. The T waves (LVH), left bundle-branch block (LBBB), and
become symmetrically tall and peaked, with intracranial hemorrhage.3,4 Other ECG findings
pointed tips. The base of the T wave narrows, associated with intracranial bleeding include deep
shortening the QT interval. This is usually inverted T waves, usually seen in precordial leads
best seen in the precordial leads (Figure 15-1). (not common with isolated hyperkalemia unless
Tall, peaked T waves are not apparent until the associated with an ischemic process), prolonged
serum potassium level exceeds 5.5 mEq/L.1,2 QT interval (opposite to hyperkalemia, which
is associated with shortened QT interval), and
A normal T wave is not symmetric, as it prominent U waves (seen with hypokalemia).3
has an initial slow ascent followed by a steep
descent. The T-wave amplitude is usually less The T waves can also change direction and
than 6 mm in the limb leads and 10 mm or less become inverted. In the setting of LVH, the
in the precordial leads. The T wave associated normally inverted lateral T waves can become
with hyperkalemia is symmetric and has an upright (“pseudonormalized”). In the absence

193

Electrocardiography in Emergency Medicine

of underlying cardiac conditions (eg, ischemia), delta wave) and the PR interval duration.11
the T waves commonly revert to their normal The relationship between serum potassium
position with treatment of the hyperkalemia.2,5
levels and ECG changes can vary among
As serum potassium levels continue to patients and can depend on whether the
increase, subsequent ECG changes can electrolyte abnormalities are acute or chronic.2
consist of widening of the QRS complex (seen Hyperkalemic patients who have underlying renal
with K+ >6.5 mEq/L), ST-segment elevation insufficiency, especially those with end-stage
or depression, and P-wave changes (seen renal disease undergoing hemodialysis, with
with K+ >7 mEq/L) (Figures 15-1 and 15-2). even profoundly elevated potassium levels, might
Changes in the P wave can include a decrease not demonstrate significant ECG changes.12,13
in its amplitude (ie, a “flat” appearance),
an increase in the duration (resulting in PR Hypokalemia
interval prolongation), or complete loss of
the P wave, which is frequently seen with a As with hyperkalemia, the ECG can also
serum potassium level above 8 mEq/L.1 provide helpful clues to the presence of
hypokalemia. Hypokalemia is defined as a serum
ST-segment elevation related to hyperkalemia, potassium level of less than 3.5 mEq/L. The
although uncommon, can be diffuse or more likelihood of an abnormal ECG becomes higher
localized, resembling that associated with when the serum potassium level is less than 2.7
AMI.6,7 Unlike the typical plateau or upsloping mEq/L.1 Hypokalemia prolongs repolarization; as
ST segment associated with AMI, the ST- a result, the earliest clues to hypokalemia include
segment elevation in hyperkalemia often changes in the ST segment, T wave, and U wave.
displays a downsloping appearance. The ST
segment returns to baseline with treatment.1,8 ECG changes associated with hypokalemia
occur in no particular order and can include
As the QRS complex widens, it gradually ST-segment depression, a decrease in T-wave
merges with the T wave, resulting in the amplitude (flattening), and prominent U
classic sine wave pattern (Figure 15-3). There waves (best seen in leads V2 to V4) (Figure
is a proportional correlation between the 15-4). In hypokalemia, the U-wave amplitude
duration of the QRS complex and the plasma exceeds the T-wave amplitude in several leads.
potassium concentration.1 Arrhythmias The T and U waves are often separated by
and conduction disturbances seen with a notch and resemble a “camel’s hump.” In
hyperkalemia can include any type of block advanced stages of hypokalemia, the T and U
(eg, LBBB), ventricular tachycardia, ventricular waves fuse, making it impossible to obtain an
fibrillation, idioventricular rhythm, and accurate measurement of the QT interval.1,3,4
asystole. The QRS axis can also shift as a result
of an intraventricular conduction delay.9 Other ECG changes seen in advanced
hypokalemia include T-wave inversion, increased
Although the ECG changes of hyperkalemia amplitude and duration of the P wave (ie, a
are often cited in the order described above, prominent P wave) and QRS complex, and slight
it is important to note that this order might or moderate prolongation of the PR interval.
not happen at all times or it might occur Arrhythmias and conduction disturbances
very fast. Hence, any ECG change resulting associated with hypokalemia can include any
from hyperkalemia mandates immediate type of block, premature atrial or ventricular
clinical attention. Simultaneous alkalosis, complexes, ventricular tachycardia, torsade
hypernatremia, hypercalcemia, or hypothermia de pointes, and ventricular fibrillation.1,3,4
could delay or diminish the characteristic ECG
findings of hyperkalemia.1,10 Hyperkalemia The U-wave amplitude generally varies
can also blunt the ECG findings associated directly with the T-wave amplitude. Normally,
with Wolff-Parkinson-White syndrome by it has an amplitude of less than 2 mm and, on
normalizing the QRS complex (ie, loss of average, is 11% of the T-wave amplitude. It is
often best seen (ie, is larger) in leads V2 and
194

Metabolic Abnormalities

V3. A U wave is considered prominent when demonstrated that hypercalcemia can cause
it has an amplitude of 2 mm or more. The U Osborne “J” waves (similar to those seen in
wave follows the vector of the T wave, but in patients with hypothermia) as well as ST-
contrast to a normal T wave, it has an initial segment elevation that mimics an AMI.18,19
fast ascent followed by a slow descent.1,3
Hypocalcemia
Conditions other than hypokalemia
associated with a prominent U wave can Hypocalcemia is defined as a total ionized
include hypomagnesemia, hypercalcemia, calcium level below 4.5 mEq/L. Hypocalcemia
bradyarrhythmias, hypothermia, LVH, drugs (eg, primarily prolongs the length of the ST segment
digitalis, quinidine, amiodarone, isoproterenol), (ie, prolongs the duration of phase 2) without
organic heart disease, and intracranial pathology affecting the duration of the T wave (Figure
(eg, hemorrhage or cerebrovascular accident). In 15-5). Hypothermia is the only other condition
these conditions, unlike with hypokalemia, the that can have this effect on the ECG.1,3,20
T/U-wave amplitude ratio is usually not altered.1,3,4
The duration of the ST segment is
Hypercalcemia inversely associated with the plasma calcium
concentration. As a result of ST-segment
ECG abnormalities associated with prolongation, the QTc interval is also prolonged,
hypercalcemia are caused by elevations in but rarely more than 140% of normal. A
the concentration of ionized, not protein- prolonged QTc is the most common and earliest
bound, calcium.1,4 Hypercalcemia is defined finding of hypocalcemia.3 If the QTc interval
as a total ionized calcium level of more exceeds 140% of normal, this suggests that
than 5.3 mEq/L. Calcium primarily affects the U wave has been integrated into the T
the plateau section (phase 2) of the cardiac wave and the QU segment is being measured.1
muscle action potential curve, which Prolongation of the QTc interval can result in
corresponds to the ST segment of the ECG. torsade de pointes, but this is less commonly
observed than is the association of torsade de
Hypercalcemia shortens the ST segment (ie, pointes with hypokalemia or hypomagnesemia.
shortens the duration of phase 2) and therefore
shortens the overall duration of the QTc interval. The T-wave morphology is usually not affected,
In addition, because the ST segment becomes because calcium has no effect on phase 3 of the
shortened, the end of the QRS interval often action potential. However, occasionally, flat,
becomes indistinguishable from the beginning low, or sharply inverted T waves can be seen
of the T wave. Although the QTc is inversely in leads with upright QRS complexes. This is
proportional to the degree of hypercalcemia, likely secondary to an alteration in the sequence
this relationship is not a specific one. Many of repolarization. The P-wave morphology,
other factors also affect the length of the QTc PR interval, and QRS complex are usually
interval, including age, sex, and medications.14 not affected by hypocalcemia.1 ST-segment
elevation mimicking myocardial infarction
Severe hypercalcemia can lengthen the T- has also been reported with hypocalcemia.21
wave duration; as a result, the overall QTc
interval can appear normal even though the Magnesium
ST segment is shortened.15 Hypercalcemia
usually has no effect on the morphology of the In the setting of normal potassium and
P wave and T wave. It might cause an increase calcium concentrations, alterations in
in the amplitude of the U wave and slight magnesium levels do not result in any specific
prolongation of the QRS interval duration.1 ECG abnormalities.1 Hypermagnesemia is
defined as a serum magnesium level above 2.5
Hypercalcemia does not commonly result mEq/L. ECG clues to hypermagnesemia are
in cardiac arrhythmias, although sinus similar to those for hyperkalemia and include
bradycardia and ventricular fibrillation have tall, peaked T waves and widening of the QRS
been reported.16,17 A few case reports have
195

Electrocardiography in Emergency Medicine

complex. Hypomagnesemia is defined as a uncommon in patients with hyperthyroidism.
serum magnesium level of less than 1.5 mEq/L. A variety of other less commonly observed
The ECG clues to hypomagnesemia are similar
to the ECG changes seen with hypokalemia: ECG abnormalities have also been reported with
prominent U waves and T-wave flattening.4 hyperthyroidism. In one study, intraventricular
conduction delays occurred in 13% of 466
Thyroid Disorders patients with hyperthyroidism but without
associated heart conditions or other causes
Hyperthyroidism of the conduction delay. The most common
intraventricular conduction abnormalities
The cardiovascular system is exquisitely were incomplete right bundle-branch block
sensitive to circulating thyroid hormones. These and left anterior fascicular block.26 First-degree
hormones act by multiple direct and indirect atrioventricular (AV) block is more common than
mechanisms to alter hemodynamics, causing second- or third-degree AV block in patients with
a variety of ECG changes. Hyperthyroidism is hyperthyroidism. Occasionally, PR prolongation
considered a state of adrenergic hyperactivity; precedes atrial fibrillation. Additional nonspecific
as a consequence, sinus tachycardia is the ST-segment and T-wave changes are seen in
most commonly observed ECG abnormality, up to 25% of patients with hyperthyroidism.27
occurring in nearly half of patients with These nonspecific ST/T-wave changes vary
hyperthyroidism.1 In a study of 880 patients, daily and, unlike the changes of pericarditis or
resting tachycardia was second only to myocarditis, are short lived and transient.1
goiter as the most common symptom of
hyperthyroidism,22 although the frequency of Hypothyroidism
tachycardia decreases with advancing age.1
Hypothyroidism leads to a slowing of
Atrial fibrillation is the second most the metabolic rate and contractility of the
common rhythm observed in patients myocardium; hence, sinus bradycardia
with hyperthyroidism.23,24 The risk of atrial is common in patients with untreated
fibrillation increases after age 55 years.1 hypothyroidism. Additional ECG changes
Despite the relatively common association of associated with hypothyroidism include low-
hyperthyroidism with atrial fibrillation, the voltage QRS complexes, T-wave changes (eg,
converse is not common. In a large study of low-amplitude “flattened” T waves or deeply
patients with atrial fibrillation of new onset, inverted T waves), low P-wave amplitude,
less than 1% were ultimately determined to and a prolonged QT interval.1,3 Because of low
have hyperthyroidism as their inciting event.25 T-wave amplitude, the QT interval is often
Atrial flutter, paroxysmal supraventricular hard to measure accurately. A prolonged QT
tachycardia, and ventricular dysrhythmias are all interval can predispose patients to ventricular

Key Facts

• An ECG is not a reliable diagnostic test for mild to moderate hyperkalemia.
• Alkalosis, hypernatremia, hypercalcemia, and hypothermia can delay or diminish the ECG findings

associated with hyperkalemia.
• In hypokalemia, the U-wave amplitude exceeds the T-wave amplitude in several leads.
• A prominent U wave can also be seen with bradyarrhythmias.
• Severe hypercalcemia can lengthen the T-wave duration and “normalize” the overall QTc interval.
• Hypocalcemia and hypothermia are the only known conditions that can cause ST-segment

prolongation without changing the duration of the T wave.
• A low-voltage QRS complex is a weak predictor of pericardial effusion.

196

Metabolic Abnormalities

dysrhythmias such as torsade de pointes.28,29 10. Mattu A, Brady WJ, Perron AD. Electrocardiographic
manifestations of hypothermia. Am J
Compared with the general population, patients Emerg Med. 2002;20:314-326.

with hypothyroidism have a higher incidence 11. Sridharan MR, Flowers NC. Hyperkalemia
and Wolff-Parkinson-White type preexcitation
of AV block (eg, first-degree AV block) and syndrome. J Electrocardiol. 1986;19:183-187.

intraventricular conduction disturbances.27 12. Aslam S, Friedman EA, Ifudu O. Electrocardiography
is unreliable in detecting potentially lethal
Low-voltage QRS complexes are defined hyperkalemia in hemodialysis patients. Nephrol
Dial Transplant. 2002;17:1639-1642.
as an entire QRS complex (R+S) amplitude of
13. Szerlip HM, Weiss J, Singer I. Profound hyperkalemia
less than 5 mm in each of the limb leads and without electrocardiographic manifestations.
Am J Kidney Dis. 1986;7:461-465.
of less than 10 mm in each of the precordial
14. Wald DA. ECG manifestations of selected metabolic and
leads (Figures 15-5 and 15-6).1,3 The prevalence endocrine disorders. Emerg Med Clin North Am. 2006;24:145-157.

of pericardial effusions in hypothyroidism 15. Lind L, Ljunghall S. Serum calcium and the ECG in patients with
primary hyperparathyroidism. J Electrocardiol. 1994;27:99-103.
is variable, ranging from 3% in subclinical
16. Ziegler R. Hypercalcemic crisis. J Am Soc
hypothyroidism to 80% in myxedematous Nephrol. 2001;12(suppl 17):S3-S9.

states.30 Nonetheless, hypothyroidism rarely 17. Kiewiet RM, Ponssen HH, Janssens EN, et al. Ventricular
fibrillation in hypercalcemic crisis due to primary
accounts for large pericardial effusions. In one hyperparathyroidism. Neth J Med. 2004;62:94-96.

study of patients with large pericardial effusions, 18. Otero J, Lenihan DJ. The “normothermic” Osborn wave induced
by severe hypercalcemia. Tex Heart Inst J. 2000;27:316-317.
only 1.5% of the effusions were attributed to
19. Turhan S, Kilickap M, Kilinc S. ST-segment
hypothyroidism.31 Low-voltage QRS complex, elevation mimicking acute myocardial infarction
in hypercalcemia. Heart. 2005;91:999.
although suggestive, is not diagnostic for and
20. Diercks DB, Shumaik GM, Harrigan RA, et al.
is a weak predictor of pericardial effusion.32–34 Electrocardiographic manifestations: electrolyte
abnormalities. J Emerg Med. 2004;27:153-160.
In addition to hypothyroidism, other
21. Lehmann G, Deisenhofer I, Ndrepepa G, et al. ECG
conditions that can result in low-voltage changes in a 25-year-old woman with hypocalcemia due
to hypoparathyroidism: hypocalcemia mimicking acute
QRS complexes include pericardial effusion, myocardial infarction. Chest. 2000;118:260-262.

chronic constrictive pericarditis, diffuse 22. Nordyke RA, Gilbert FI, Harada AS. Graves’ disease: influence
of age on clinical findings. Arch Intern Med. 1988;148:626-631.
myocardial disease (eg, amyloidosis,
23. Fadel BM, Ellahham S, Ringel MD, et al. Hyperthyroid
scleroderma, cardiac neoplasm), myocardial heart disease. Clin Cardiol. 2000;23:402-408.

fibrosis from chronic ischemic heart disease, 24. Osman F, Gammage MD, Sheppard MC, et al. Clinical review
142: cardiac dysrhythmias and thyroid dysfunction: the
pleural effusion, chronic lung disease (eg, hidden menace? J Clin Endocrinol Metab. 2002;87:963-967.

emphysema), pneumothorax, and obesity.1,3 25. Krahn AD, Klein GJ, Kerr CR, et al. How useful is thyroid
function testing in patients with recent-onset atrial
References fibrillation? The Canadian Registry of Atrial Fibrillation
Investigators. Arch Intern Med. 1996;156:2221-2224.
1. Surawicz B, Knilans TK. Chou’s Electrocardiography
in Clinical Practice. 5th ed. Philadelphia, PA: W B 26. Staffurth JS, Gibberd MC, Hilton PJ. Atrial
Saunders; 2001:23-24;239,268-271,516-539. fibrillation in thyrotoxicosis treated with
radioiodine. Postgrad Med J. 1965;41:663-671.
2. Mattu A, Brady WJ, Robinson DA.
Electrocardiographic manifestations of hyperkalemia. 27. Surawicz B, Mangiardi ML. Electrocardiogram in endocrine
Am J Emerg Med. 2000;18:721-729. and metabolic disorders. Cardiovasc Clin. 1977;8:243-266.

3. O’Keefe JH, Hammill SC, Freed M. The Complete Guide to 28. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular
ECGs. Birmingham, MI: Physician’s Press; 1997:145-185. system. N Engl J Med. 2001;344:501-509.

4. Lipman BC, Cascio T. ECG Assessment and Interpretation. 29. Kumar A, Bhandari AK, Rahimtoola SH. Torsade de
Philadelphia, PA: F A Davis; 1994:252-265. pointes and marked QT prolongation in association with
hypothyroidism. Ann Intern Med. 1987;106:712-713.
5. Dittrich KL, Walls RM. Hyperkalemia: ECG manifestations
and clinical considerations. J Emerg Med. 1986;4:449-455. 30. Chou SL, Chern CH, How CK, et al. A rare case
of massive pericardial effusion secondary to
6. Chawla KK, Cruz J, Kramer NE, et al. Electrocardiographic hypothyroidism. J Emerg Med. 2005;28:293-296.
changes simulating acute myocardial infarction caused
by hyperkalemia: report of a patient with normal 31. Sagrista-Sauleda J, Merce J, Permanyer-Miralda G,
coronary arteriograms. Am Heart J. 1978;95:637-640. et al. Clinical clues to the causes of large pericardial
effusions. Am J Med. 2000;109:95-101.
7. Simon BC. Pseudomyocardial infarction and hyperkalemia: a
case report and subject review. J Emerg Med. 1988;6:511-515. 32. Casale PN, Devereux RB, Kligfield P, et al. Pericardial
effusion: relation of clinical echocardiographic and
8. Wang K, Asinger RW, Marriott HJ. ST-segment electrocardiographic findings. J Electrocardiol. 1984;17:115-121.
elevation in conditions other than acute myocardial
infarction. N Engl J Med. 2003;349:2128-2135. 33. Habashy AG, Mittal A, Ravichandran N, et al. The
electrocardiogram in large pericardial effusion: the
9. Ewy GA, Karliner J, Bedynek JL. Electrocardiographic forgotten “P” wave and the influence of tamponade,
QRS axis shift as a manifestation of size, etiology, and pericardial thickness on QRS
hyperkalemia. JAMA. 1971;215:429-432. voltage. Angiology. 2004;55:303-307.

34. Eisenberg MJ, de Romeral LM, Heidenreich PA, et al. The
diagnosis of pericardial effusion and cardiac tamponade by 12-
lead ECG: a technology assessment. Chest. 1996;110:318-324.
197

Electrocardiography in Emergency Medicine

Figures

Figure 15-1.
A: Hyperkalemia (serum K+ = 8.1 mEq/L). Note the diffuse, tall, peaked, narrow-based T waves. In addition,
there are associated ST-segment depressions in leads V2 through V5 and widened QRS complexes. B: Repeat
ECG after treatment of hyperkalemia. Note the normalization of QRS complexes and ST segments in the
precordial leads. The T waves are not as peaked and tall. They are more asymmetric and have an initial slow
ascent followed by a steep descent.

A

B

198

Metabolic Abnormalities

Figures

Figure 15-2.
Hyperkalemia (serum K+ = 8.4 mEq/L). A closer look at the ECG, especially leads II, V2, and V3, and the rhythm
strip reveals diminished and flattened P waves, which are frequently seen with a serum potassium level of
more than 8 mEq/L. Note the ST-segment depression and T-wave inversion in leads V5 and V6. These ECG
changes reverted to normal with the treatment of hyperkalemia.

199

Electrocardiography in Emergency Medicine

Figures

Figure 15-3.
A: Hyperkalemia (serum K+ = 8.7 mEq/L). The ECG depicts the classic sine wave associated with severe
hyperkalemia, in which the QRS complex widens and merges with the T wave. The interpretation is made
more complicated by the presence of both atrial and ventricular pacing. Although ventricular pacing is
expected to widen the QRS complex, the observed widening is not typical of pacemaker-induced QRS
widening. B: Repeat ECG after aggressive treatment of hyperkalemia. The observed wide QRS complexes are
more typical of those associated with ventricular pacing.

A

B

200

Metabolic Abnormalities

Figures

Figure 15-4.
Hypokalemia (serum K+ = 2.1 mEq/L). Note the ST-segment depression, decrease in T-wave amplitude, and
prominent U waves (best seen in leads II and aVF). In hypokalemia, the U-wave amplitude exceeds the T-wave
amplitude. Because of the close proximity of the T and U waves, the QT interval cannot be measure accurately.
Premature ventricular complexes are most likely caused by advanced hypokalemia. Image courtesy of Amal
Mattu, MD.

Figure 15-5.
Hypocalcemia (ionized serum calcium = 3.3 mEq/L). The QT interval is prolonged, with QT/QTc of 430/530
msec, respectively. Note the prolonged ST segment with a normal T-wave duration. Most other causes of QT
prolongation cause prolongation of the T wave rather than the ST segment. Hypothermia is the only other
exception. Image courtesy of Amal Mattu, MD.

201

Electrocardiography in Emergency Medicine

Figures

Figure 15-6.
Low-voltage QRS. A low-voltage QRS is defined as the entire QRS complex (R+S) amplitude of less than 5
mm in each of the limb leads and less than 10 mm in each of the precordial leads. Low-voltage QRS complex,
although suggestive, is not diagnostic for and is a weak predictor of pericardial effusion. This patient
underwent diagnostic testing, including echocardiography, chest radiography, and blood tests. All test results
were within normal limits. The low voltage was attributed to obesity.

202

C h apter s i x tee n

The ECG in Selected Noncardiac
Conditions

Tarlan Hedayati, MD, and Stuart P. Swadron, MD, FRCPC

Although the ECG changes associated with around 35°C (95°F), the first nonartifact
noncardiac conditions are usually neither ECG abnormalities are progressive sinus
sensitive nor specific, emergency physicians must bradycardia and decreased T-wave voltage.2 Atrial
know how to recognize them and assess their life- fibrillation with a slow ventricular response
threatening potential. Failure to appreciate that a is the most common dysrhythmia associated
single ECG appearance can represent two or more with hypothermia, occurring in 50% to 60%
very different diagnoses can lead to inappropriate of patients. Other ectopic rhythms such as
and dangerous management decisions. This atrial flutter, atrioventricular (AV) junctional
chapter outlines ECG findings associated with rhythm, premature ventricular contractions
several life-threatening noncardiac conditions. (PVCs), ventricular tachycardia, and ventricular
Emphasis is placed on the differential diagnosis fibrillation are also seen but with far less
of certain ECG patterns and the role of the frequency. With progressive hypothermia, there
ECG in emergency decision making. is a prolongation of all the intervals, including
R-R, PR, QRS, and QT. When temperatures
Hypothermia fall below 29.4°C (85°F), the progressive
QRS widening can degenerate to ventricular
Hypothermia, defined as a core body fibrillation and, with further hypothermia,
temperature below 35°C (95°F), has been asystole.2 The vast majority of arrhythmias
linked to both benign and fatal pacemaker associated with hypothermia are reversible with
abnormalities, conduction delays, and cardiac rewarming, although several days to months can
dysrhythmias. The common ECG findings in be required for normal sinus rhythm to return.3,4
hypothermia are summarized in Table 16-1.
The Osborn wave was first described by
The initial finding is a tremor artifact Grosse-Brockhoff and Schoedel in 1943 and
of the baseline caused by shivering. Below later named by Dr. John Osborn in 1953, based
32°C (89.6°F), the body is no longer able to on ECGs obtained from hypothermic dogs. He
generate heat by shivering, so the baseline described the finding as a convex deflection
returns to normal, a finding associated with between the QRS complex and the beginning of
poorer outcome.1 At a body temperature
203

Electrocardiography in Emergency Medicine

the ST segment, so close to the QRS complex that Figure 16-1 shows an ECG typical of a
it produces a “hump” in the terminal portion of patient with hypothermia, demonstrating
the QRS. This reversible finding is detectable in several of the features described above. Figure
80% of patients with a core temperature below 16-2 demonstrates a magnified view of the
30°C (86°F).5 The J wave increases in amplitude Osborn wave, and Figure 16-3 demonstrates
as the temperature falls, eventually leading to resolution of hypothermia-induced abnormalities
T-wave inversion in the same leads. Although it in the same patient after rewarming.
is highly sensitive and specific for hypothermia,
it is not entirely pathognomonic; Osborn waves Pulmonary Embolism
are sometimes seen in the settings of intracranial
hemorrhage, cardiac ischemia, and hypercalcemia Pulmonary embolism (PE) continues to be
and as a normal variant.4,6 The Osborn wave is one of the most underdiagnosed fatal diseases
also referred to as a J wave, camel-hump wave, in emergency medicine. Unfortunately, the ECG
late delta wave, or hypothermic wave and is best abnormalities associated with PE can be subtle
seen in the inferior and lateral precordial leads. and nonspecific. Because many patients with
As the J wave increases in amplitude, the terminal PE present to an emergency department with
portion of the QRS complex rises and can be complaints of chest pain or dyspnea, an ECG is
mistaken for a bundle-branch block, ST-segment usually obtained on arrival. The principal role
elevation pattern, or Brugada syndrome.5,7 of this initial ECG is to identify other cardiac
abnormalities such as acute infarction, ischemia,
The Brugada pattern is defined as ST- pericarditis, and life-threatening dysrhythmias.
segment elevation in leads V1 through V3 and Several ECG findings associated with PE (Table
a right bundle-branch block (RBBB) without 16-2) generally correlate with the severity of
the usual terminal S waves laterally; it has the obstruction of the pulmonary circulation.
been linked to sudden cardiac death in young
patients. Severely hypothermic patients have Multiple investigations focused on the
exhibited this phenomenon.7,8 The best ways emergency department population have
to differentiate a true Brugada syndrome demonstrated that the most common ECG
from a hypothermic mimic are to note the rhythm in patients with acute submassive PE (ie,
presence of Osborn waves and to watch for PE without circulatory collapse) is normal sinus
the reversibility of findings with rewarming. rhythm. Sinus tachycardia, frequently thought to
be near universal in cases of PE, is less common.
Atrial fibrillation and flutter can also be seen.9–11

Morphologic changes associated with PE

Table 16-1.
ECG findings in hypothermia

Artifact Shivering artifact Table 16-2.
Rhythm Sinus bradycardia ECG findings associated with pulmonary embolism
PR, QRS, QT, and R-R interval
prolongation Rhythm Normal sinus rhythm
Atrial fibrillation with slow ventricular Sinus tachycardia
response Morphology ST-segment depression
Junctional rhythms T-wave inversions (V1 through V4 most
Ventricular premature complexes commonly, less often in III and aVF)
Ventricular tachycardia Complete or incomplete RBBB
Ventricular fibrillation S1Q3T3
Asystole Slurred S in V1 or V2
Morphology Decreased T-wave voltage Late R wave in aVR
Osborn J wave PR-segment displacement
Brugada syndrome–like morphology P pulmonale (P-wave amplitude >2.5
mm in lead II)

204

The ecg in selected noncardiac conditions

include a slurred S wave in V1 or V2, decreased with negative diagnostic studies for PE.17
QRS voltage, complete or incomplete RBBB, PR- Petruzzelli et al9 found that, although ST-
segment displacement, and late R in aVR.9 The
findings of prominent S waves in lead I and Q segment depression was common in patients both
waves in lead III, each of amplitude exceeding with and without a final diagnosis of PE, the
1.5 mm, with T-wave inversions present in ST-segment depression resolved in the patients
lead III (the so-called S1Q3T3 pattern) were first ultimately diagnosed with PE as they recovered.9
reported by McGinn and White in the 1930s in a ST-segment depression in the setting of PE is also
series of seven patients with acute cor pulmonale associated with elevated right ventricular end-
caused by PE. These patients had severe embolic diastolic pressure.12 Further, the presence of an
obstruction and massive PE.12,13 Since then, this inverted T wave in leads V1 and V2 correlates with
finding has become closely linked with PE in the severity of the PE.9,12,18 In patients who receive
the minds of most clinicians. However, recent fibrinolytic therapy for treatment of massive PE,
studies have called this association into question. normalization of the T wave was accelerated
The incidence of the S1Q3T3 pattern ranges compared with nonfibrinolyzed patients.18 Thus,
widely in different series (from 10% to 60%) several patterns, including RBBB, ST-segment
and depends on the nature of patient selection depression, and anterior T-wave inversion, in
in each study. Moreover, some data suggest that patients with PE could all be a reflection of
the S1Q3T3 pattern might be equally prevalent in reversible right heart strain. T-wave inversions
certain populations of patients without PE.11,14,15 can occur simultaneously in the anterior leads
as well as in the inferior leads, especially leads
Large PEs can elevate pulmonary artery, right III and aVF. T-wave inversions and ST changes
ventricular, and right atrial pressures, leading to can be easily mistaken for cardiac ischemia,
right ventricular strain and ischemic patterns on leading to an incorrect work-up and disposition.
the ECG (Figures 16-4 and 16-5). P pulmonale
and peaked P waves in leads II, III, and/or aVF Although various ECG abnormalities have
are signs of increased right atrial pressure or been linked to the presence and size of PE,
right atrial enlargement. Because this finding the ECG, by itself, cannot provide a definitive
has been reported equally in patients with diagnosis. Knowledge of the ECG abnormalities
both massive and submassive PE, it has little associated with PE, however, could prompt
value in predicting the size of the embolus.12,16 the emergency physician to initiate further
investigations to pursue this diagnosis. In certain
Incomplete or complete RBBB has been circumstances, it can also lead to initiation of
reported in the setting of PE associated with empiric therapy that might otherwise be withheld
right ventricular strain. The reported incidence until more definitive studies are available.
of RBBB varies widely, from 6% to 67%.14
Dynamic monitoring in an intensive care Thoracic Aortic Dissection
setting has shown that in PE patients with both
S1Q3T3 pattern and a RBBB, the S1Q3T3 pattern Thoracic aortic dissections are classified based
often temporally precedes development of on anatomic location and time from onset. The
the RBBB.11 The presence of incomplete RBBB Stanford classification divides dissections based
has also been associated with elevated mean on the location of the intimal tear. Dissections
pulmonary artery pressure and right ventricular in the ascending aorta are Stanford type A and
end-diastolic pressure.12 The strength of the represent approximately 62% of all dissections;
apparent correlation between RBBB and PE those occurring distal to the left subclavian artery
should not, however, be overstated. In one large are classified as Stanford type B and make up the
study that prospectively followed 212 patients remaining 38%. Within 14 days after the onset of
receiving diagnostic imaging for suspected dissection, morbidity and mortality are high. For
PE, incomplete RBBB and sinus tachycardia this reason, dissection is considered acute within
were significantly more frequent in the group this time period. Patients who survive the initial
2 weeks carry a diagnosis of chronic dissection.19

205

Electrocardiography in Emergency Medicine

Ninety-five percent of patients diagnosed with four of these patients were found to have type A
acute thoracic dissection present with chest dissections; one was treated with fibrinolytics,
pain.20 The most critical diagnosis to differentiate resulting in death secondary to cardiac
from aortic dissection is acute myocardial tamponade. With respect to dysrhythmias, atrial
infarction (MI), specifically ST-segment and ventricular premature beats as well as AV
elevation MI (STEMI), because fibrinolytic or blocks were recorded, but in only a few patients.21
anticoagulation therapy can be cataclysmic for
the patient with dissection. However, these The International Registry of Acute Aortic
conditions can exist contemporaneously; a Dissections is a repository of data about
dissection can progress proximally to involve patients with aortic dissections from 12 referral
the coronary ostia, causing acute occlusion centers in 6 countries. The registry has been
in the proximal coronary artery by an enrolling patients since 1996 and accumulated
intimal flap or hematoma.21 Dissections can data on 464 patients within its first 2 years of
also extend into the atrial septum and AV establishment. Sixty-nine percent of the 464
conduction system, resulting in heart block.22 patients with thoracic dissections followed in
the registry demonstrated some abnormality
A 12-year study of 89 patients diagnosed with on ECG. The most common abnormality
acute aortic dissection in Japan demonstrated was nonspecific ST/T-wave changes (41%),
that 40% of all patients with dissection had an followed by LVH (26%), ischemic patterns
acute ECG abnormality on presentation, defined (15%), and infarction patterns (11%).20
as a new shift in the ST segment larger than
0.1 mm in any lead or a change in the polarity Emergency physicians must consider aortic
or morphology of the T wave. Left ventricular dissection in the differential diagnosis of any
hypertrophy (LVH), bundle-branch blocks, and patient presenting to the emergency department
abnormal Q waves were considered chronic with acute chest pain. Fortunately, the
changes and were seen in 30% of all patients, predominant ECG findings of aortic dissection
most commonly in type B dissections. Acute rarely mimic those of STEMI, lessening the
changes occurred in 55% of patients with type likelihood of unintended administration of
A dissection but only 22% with type B. These fibrinolytic therapy (Table 16-3). Nevertheless,
changes consisted most often of 0.1-mm ST- because most patients with dissection present
segment depression. Type A dissection patients with either nonspecific or frankly ischemic ECG
with acute ECG changes had a higher incidence changes, differentiation of dissection from the
of shock, cardiac tamponade, and hypotension. more common acute coronary syndromes remains
Four of the 89 patients demonstrated ST-segment difficult on the basis of the ECG alone. Therefore,
elevation on ECG: three in the inferior leads imaging studies must be considered, especially
and one in the high lateral leads (I and aVL). All

Table 16-4.
ECG findings associated with pneumothorax

Table 16-3. Left-sided Sinus tachycardia
ECG findings associated with thoracic aortic Decreased QRS voltage
dissection Poor R-wave progression
T-wave inversion in precordial leads
Rhythm Sinus tachycardia Electrical alternans
Atrial and ventricular premature beats Right-sided Sinus tachycardia
AV block S wave in V1
Morphology Nonspecific ST-segment changes S1Q3T3 pattern
Left ventricular hypertrophy Decreased QRS voltage
Ischemic or infarction patterns Anterior or posterior MI pattern (rare)
ST-segment elevation (uncommon)

206

The ecg in selected noncardiac conditions

when elements of the history and physical pneumothorax. Reports of patients with changes
examination suggest the possibility of dissection mimicking both posterior MI (prominent R-
or when anticoagulation is being considered. wave voltage with associated loss of S-wave
voltage in lead V2) as well as anterior wall MI
Pneumothorax (ST-segment elevation and T-wave inversion
in leads V1 through V )3 28,29 underscore the
Pneumothorax is defined as the presence of air importance of the initial radiograph. Moreover,
in the pleural space, resulting in partial or total if the patient’s clinical presentation is more
collapse of the affected lung. Data from intensive suggestive of a pneumothorax than MI, more
care units have shown that ECG changes definitive imaging, including emergent CT of
often precede clinical signs and symptoms of the chest, could be appropriate before specific
pneumothorax.23 Like the signs and symptoms therapy for MI is initiated. After lung re-
of pneumothorax itself, the associated ECG expansion, the ECG should revert to normal.29
changes depend on the size of the collapse, the
presence or absence of tension, and whether the ECG changes in association with left-sided
pneumothorax is right- or left-sided. Because pneumothorax have been widely reported.
most of these patients present with chest pain and All patients with left-sided pneumothorax
dyspnea, an ECG is typically part of the initial in one series demonstrated a decreased QRS
evaluation. The ECG findings associated with amplitude, and approximately half had right axis
pneumothorax are summarized in Table 16-4. deviation.28 Other common findings associated
with left-sided pneumothorax include poor R-
The mechanisms proposed for induction of wave progression and T-wave inversion.24,25 One
ECG abnormalities in pneumothorax include case report described phasic voltage variations
cardiac rotation or displacement, air within the in the ECG that depended on respiration, a
thoracic cavity, acute right ventricular dilation or finding common in pericardial effusions and
overload, and interposition of air or lung tissue tamponade. These variations disappeared after
between the electrodes and cardiac muscle.24,25 tube thoracostomy.30 Another case report detailed
the uncommon findings of PR-segment elevation
One of the largest series looking at patients in the inferior leads (II, III, and aVF) and PR-
with right-sided pneumothoraces comes from segment depression in lead aVR in a patient
a tuberculosis treatment study performed prior with 100% left tension pneumothorax.31 These
to the availability of effective antimicrobial changes also resolved after chest tube placement.
therapy. In that era, creation of an artificial
pneumothorax was an important therapeutic Although pneumothorax is not a diagnosis
modality in tuberculosis. A meta-analysis made by ECG, its ability to cause certain ECG
examining 82 patients with such iatrogenic right changes and mimic other life-threatening
pneumothoraces found that more than one third processes is significant. If emergent
of them had an S wave in lead I and right axis decompression becomes necessary, a repeat
deviation.26 In addition, case reports of the S1Q3T3 ECG is essential to ensure that the signs that
pattern typically associated with pulmonary could indicate other conditions have resolved.
embolism have described the same pattern
in patients with pneumothoraces, even very Chronic Obstructive
small (10%) ones.26,27 Thus, careful examination Pulmonary Disease
of the chest radiograph from a patient with
right axis deviation on the ECG can obviate Chronic obstructive pulmonary disease
the need for further diagnostic evaluation if a (COPD) is characterized by progressive
pneumothorax is found. Diagnostic certainty is inflammation and obstruction of the airways.
enhanced with resolution of the axis changes Because of the ensuing hyperinflation, the
following reexpansion of the affected lung.26,27 diaphragm occupies a lower, stiffer position and
the heart is forced into a more vertical position,
ECG abnormalities consistent with acute MI with a clockwise rotation along its longitudinal
are rarely present in patients with right-sided
207

Electrocardiography in Emergency Medicine

axis. This results in a rightward shift of the severe to severe disease (Figure 16-6).34
P and QRS axes in the frontal plane and a P-wave abnormalities can be dynamic and
posterior displacement of the QRS vector in the
horizontal plane. It also produces a larger P-wave reversible during an acute COPD exacerbation.
amplitude in the inferior leads and a smaller QRS Asad et al35 compared the initial emergency
amplitude in the limb leads. The hyperinflated department ECGs of 50 patients with acute
lungs also add to the relatively low QRS voltage COPD exacerbations with subsequent
seen in COPD patients. As the disease advances, posttreatment ECGs from the inpatient unit.
chronic hypoxia leads to pulmonary arterial Ninety-six percent of patients who initially
vasoconstriction, increased pulmonary artery had a P-wave amplitude greater than 1.5 mm
pressure, and right heart strain. This right heart in leads II and aVF demonstrated a significant
strain eventually results in right ventricular decrease in P-wave amplitude 24 hours after
hypertrophy, dilation, and failure, known as initiation of treatment. One patient whose P-
cor pulmonale. The ECG findings associated wave amplitude had decreased with treatment in
with COPD are summarized in Table 16-5. the emergency department developed a second
COPD exacerbation on the ward; the repeat ECG
In 1959, Spodick32 described verticalization of demonstrated an increase in P-wave amplitude
the frontal P-wave axis in patients with diffuse in association with the repeat exacerbation. This
lung disease. Normally, this axis varies between lability in the P-wave amplitude can provide
+45° and +64°. A rightward shift in the P axis a fast, noninvasive method of evaluating the
to +70° to +90°, most easily recognized as a presence, degree, and resolution of acute right
negative P wave in lead aVL, was found in 83% heart strain in the setting of COPD exacerbations.
of the 79 consecutive patients in Spodick’s series.
P-axis verticalization has a sensitivity of 89% ECG findings associated with COPD also
and specificity of 96% in COPD.33 Subsequent have prognostic value. In one study, COPD
studies demonstrated a relationship between patients who demonstrated either a P-wave axis
increasing verticality of the P axis and the degree greater than 90° or an S1S2S3 pattern (seen in
of airway obstruction. P pulmonale, defined as up to 25% of patients) had a 3-year survival
tall and peaked P waves greater than 2.5 mm rate of 44%. If both signs were present, the
in the inferior leads, is typically associated 3-year survival rate dropped to 14%.36 Another
with right heart strain or enlargement. This
finding has been reported in up to 25% of Table 16-6.
COPD patients, typically those with moderately ECG findings associated with subarachnoid
hemorrhage

Table 16-5. Rhythm Sinus tachycardia
ECG findings associated with chronic obstructive Sinus bradycardia
pulmonary disease Paroxysmal supraventricular
tachycardia
Rhythm Sinus tachycardia Atrial fibrillation
Multifocal atrial tachycardia AV block
Atrial fibrillation Ventricular premature complexes
Morphology P wave axis >90° Ventricular tachycardia
Decreased QRS amplitude Ventricular fibrillation
QRS axis >90° (right axis deviation) Morphology T-wave inversion
Poor R-wave progression Prominent U waves
Q waves anterolaterally ST-segment depression
P pulmonale (P-wave amplitude >2.5 ST-segment elevation
mm in leads II, III, aVF) QT prolongation
S1S2S3 pattern Pathologic Q waves

208

The ecg in selected noncardiac conditions

study found that COPD patients demonstrating dysrhythmias. These must also be considered.
a P-wave amplitude of more than 2 mm had
a 4-year survival rate of 42%.37 This seems Central Nervous System
logical in that more ECG findings of right Events
heart strain mean the disease process is more
severe and thus the mortality rate is higher. Many reports have documented ECG changes
associated with acute neurologic events.
QRS abnormalities in association with ECG abnormalities have been consistently
COPD have also been reported. In addition to described for a wide variety of neurologic
a decreased QRS amplitude, indeterminate or conditions, including stroke,40–44 increased
right axis deviation of more than 60° in the intracranial pressure,45 and epilepsy.46–51
frontal plane has been described in about 60%
of patients.38 The 4-year survival rate for COPD From the emergency physician’s point of
patients with QRS axis deviation between +90° view, it is important to understand the acute
and +180° was 37% in one study.37 Poor R-wave changes that occur with central nervous system
progression with Q waves from lead V1 to the events because they must be differentiated
lateral leads occurs in almost 10% of COPD from those that can reflect a primary cardiac
patients. Partial or complete normalization process. This is especially true when the clinical
of this finding can sometimes be achieved by picture is ambiguous. For example, a stroke
simply shifting the chest leads one interspace could be secondary to an aortic dissection,
inferiorly on the chest wall, mimicking the diminished cardiac output during an acute
new position of the heart caused by the coronary syndrome, or an embolism from
diaphragmatic changes described above. a mural thrombus complicating myocardial
infarction. Therapy directed at a primary cardiac
The most common dysrhythmias associated process (eg, heparin for myocardial ischemia)
with COPD are supraventricular in origin: can be dangerous in a patient in whom ECG
sinus tachycardia, multifocal atrial tachycardia, changes were merely a reflection of a stroke.
and atrial fibrillation. These dysrhythmias In some cases, this critical distinction can
tend to be transient, occur in association with be made only with the assistance of further
acute exacerbations, and typically resolve testing, typically imaging with computed
with treatment. Although there have been tomography or magnetic resonance.
reports of PVCs and nonsustained ventricular
tachycardia in patients with COPD and A relationship between stroke and the ECG
respiratory failure, these are uncommon.39 tracing has been recognized for many decades.
Because large numbers of patients who suffer
Although the abnormalities and dysrhythmias stroke have co-existing disease that affects
described above are typical in patients with their baseline ECG, it has been very difficult to
COPD, these patients often present with co- study this relationship. However, in the case of
morbid conditions, acute and chronic, that also subarachnoid hemorrhage (SAH), in which ECG
influence the ECG. In particular, manifestations changes are often dramatic, the relationship is
of ischemic heart disease can be superimposed much more clearly understood, in part, because
on or obscured by these changes. For emergency the younger population affected by SAH is less
physicians, the presence of underlying ischemia likely to have underlying cardiac disease.
is a constant consideration, and changes
consistent with both ischemia and pulmonary The ECG changes associated with SAH
disease should be treated as being of cardiac (Table 16-6) likely result from increased activity
origin, especially if they do not resolve with along the neurohumoral axis, specifically a
appropriate treatment aimed at the pulmonary surge in sympathetic output and circulating
disease. In addition, medications used for catecholamines. This results in a number of
treatment such as -adrenergic agents and cardiovascular effects, including increased
theophylline result in specific ECG changes and myocardial oxygen demand, increased afterload,
and possibly coronary vasospasm. Several

209

Electrocardiography in Emergency Medicine

studies have documented specific evidence of cardiac troponin I. These findings underscore
myocardial dysfunction such as wall motion the importance of distinguishing patients
abnormalities on echocardiography. In a with primary cardiac events from those in
minority of cases, increases in serum biomarkers whom the ECG changes are secondary to SAH.
demonstrate actual myocardial necrosis.40 Moreover, even when a primary central nervous
Therefore, the ECG changes in SAH often system event has been confirmed by imaging
mimic those of primary cardiac processes such or analysis of the cerebrospinal fluid, the
as coronary ischemia and can cause dilemmas possibility exists of cardiac infarction occurring
in emergency department management. simultaneously. The presence of both entities
can influence management significantly.
The most prominent ECG finding associated
with SAH is the appearance of inverted, peaked Significant, but reversible, ST-segment
T waves (Figure 16-7). These were first described depression is shown in Figure 16-9. The
by Byer in 1947 and subsequently by many abnormality resolved after treatment for SAH.
other authors.40 In the largest series reported,
involving 406 patients with SAH, 32% had Q waves have also been reported in SAH
abnormalities of the T wave.44 It was inverted (3% in the largest series), which can further
and large (>5 mm) in 2.5% of patients, negative complicate its differentiation from ACS. The
with a more modest amplitude in another 15%, ST-segment and Q-wave changes that can mimic
and notched in another 8%. Other abnormalities ACS can persist for weeks, but they do eventually
of repolarization are even more common such resolve.54 Because the published data in case
as the presence of U waves and prolongation series on cardiac biomarkers are not necessarily
of the QT interval (Figure 16-8). In a study by paired with ECG changes, it is difficult to
Rudehill et al,44 47% of all patients presented with conclude how many of these patients actually
U waves larger than 1 mm, and 24% presented suffer myocardial damage as a secondary process
with a QTc of more than 440 msec. These to SAH. In one study, ST-segment deviation
patients are at risk of torsade de pointes.52,53 in patients with SAH did not correlate with
elevation of the cardiac troponin I concentration.41
Although abnormalities of the ST segment are
less common in SAH, they can create an even Although normal sinus rhythm is the
greater dilemma in the management of patients in most common rhythm seen in patients
whom a primary cardiac event appears possible. with SAH, a variety of bradyarrhythmias
Fortunately, in SAH, ST-segment depression and tachyarrhythmias has been described,
is more common than ST-segment elevation,
so therapies most perilous to intracranial Table 16-7.
hemorrhage, such as fibrinolytic agents, are less ECG findings associated with selected
likely to be entertained. Nonetheless, the use of gastrointestinal disorders
antiplatelet and anticoagulant agents commonly
employed in the management of non-ST–segment Pancreatitis
elevation ACS could be equally devastating to a
patient with SAH. Rudehill et al44 found that ST- Rhythm Sinus tachycardia
segment depression occurred in 15% of patients
with SAH but there was no case of ST-segment Morphology ST-segment elevation
elevation. In another series involving 100 patients
with SAH, only 3% had ST-segment depression. T-wave inversion
No patients had ST-segment elevation when
measured from the J point; however, 9% had Intraventricular conduction delays and
ST-segment elevation when it was measured at bundle-branch blocks
60 msec from the J point, and 21% of patients
in this series had an elevated concentration of Gastric dilation and intestinal obstruction

210 Morphology ST-segment elevation

T-wave inversion

Cholecystitis

Rhythm Sinus tachycardia

Morphology ST-segment elevation

Brugada-type pattern

The ecg in selected noncardiac conditions

dating back to the observations of Harvey sudden unexpected death in epilepsy, which
Cushing at the turn of the last century. The is many times higher than the death rate in
more commonly reported dysrhythmias are the general population.46–51 Although many of
supraventricular tachycardia, sinus bradycardia the dysrhythmias described during seizures
(likely caused by increased intracranial are likely related to respiratory compromise,
pressure), AV blocks, and premature beats, neurohumoral influences and antiepileptic drugs
both atrial and ventricular.40,41,43,44,55 also influence the ECG and are partly responsible
for QT-interval and ST-segment changes.
Only in the minority of cases is a normal
ECG obtained from a patient with SAH, even Selected Gastrointestinal
when patients with a history of cardiovascular Disorders
disease are excluded.44 The literature is
subject to spectrum bias toward patients with Gastrointestinal disorders often present
more severe cases of SAH, ie, those who are with symptoms typical of ACS such as
diagnosed on presentation and admitted. In chest pain and epigastric pain. Multiple
recent years, the literature on SAH has focused case reports and studies have described the
on “sentinel leaks,” small warning bleeds various ECG findings associated with these
that frequently precede a more catastrophic disease processes (Table 16-7). Clinically,
SAH. It is not known whether the incidence the ECG is not helpful in the diagnosis of
of ECG changes is different in this patient these disorders, but the ECG abnormalities
population, but it is likely to be much lower. associated with them can create uncertainty
and result in further cardiac investigations.
Increased intracranial pressure is
associated with sinus bradycardia. It is part Patients with pancreatitis (inflammation of
of the reflex described by Cushing, which the pancreas and surrounding tissues) typically
also includes an increase in systolic blood present with upper abdominal pain that can
pressure. Other ECG abnormalities described radiate to the mid-back. They generally appear in
in association with increased intracranial distress and can present with tachycardia because
pressure include many of those described of pain, fever, or shock. Electrolyte abnormalities
with SAH. Because only limited data are such as hypocalcemia, hypomagnesemia,
available, it can be difficult to discriminate hyperkalemia, and hypokalemia are common
the changes that are specific to each.45 in pancreatitis and, if they are severe enough,
lead to ECG abnormalities. Several case reports
Several clinicians have also investigated have described ST-elevation “pseudo-infarction”
the ECG changes related to epilepsy—during patterns, T-wave inversions, intraventricular
seizures themselves and during the post- conduction delays, and bundle-branch blocks
ictal period. Much of this research is aimed in these patients.56–58 Unfortunately, there
at uncovering the underlying mechanism of have been no large studies investigating ECG
abnormalities in patients with pancreatitis and
Table 16-8. normal electrolyte levels. Investigators have also
ECG findings associated with electrical injuries been unable to link serum pancreatic amylase
or lipase levels with the prevalence of ECG
Rhythm Sick sinus syndrome abnormalities in patients with pancreatitis.59
Supraventricular dysrhythmias
Ventricular extrasystole Case reports have described gastric dilation
Ventricular tachycardia and intestinal obstruction causing ST-segment
Morphology ST-segment elevation elevation in the inferior or anterior leads and
QT prolongation T-wave inversions in lateral leads. In all cases,
Bundle-branch blocks prompt resolution of the abnormalities was
Nonspecific ST/T changes achieved with nasogastric decompression.60–62

Finally, acute cholecystitis, or inflammation

211

Electrocardiography in Emergency Medicine

of the gallbladder, has also been associated exposure. Cardiac injury is caused by passage
with ECG abnormalities, including ST-segment of the exogenous electrical current across the
elevation patterns63 and Brugada-type pattern.64 heart, disrupting normal cardiac electrical
The obvious risk to patients with acute pathways. The thermal and ischemic injuries
cholecystitis and with these patterns on the ECG produced by electrical current also contribute
is a delay in definitive surgical treatment while to dysrhythmias and ECG abnormalities
a cardiology work-up and clearance are pursued. following electrical injuries (Table 16-8).
However, although emergency physicians should
be aware of these pseudo-infarction patterns, The immediate lethal effect of electrical
pursuit of a life-threatening cardiovascular injuries is a result of asystole or ventricular
cause of such ECG abnormalities is essential. fibrillation and represents the most common
cause of death. Lethal domestic AC injury
Electrical Injuries typically results in ventricular fibrillation,
whereas lightning strikes produce asystolic
Electrical injuries are categorized as arrests.65 As many as half of all victims of
alternating current (AC) or direct current electrical injuries have some ECG abnormality.
(DC) and as high-voltage (>1,000 V) or low- ECG findings following lightning injuries appear
voltage exposure. Residential AC emits 120 to to be related to the type of strike. A direct cloud-
220 volts, and high-tension power lines can to-victim strike can result in life-threatening
generate well over 100,000 volts of AC. Lightning pericardial effusions and QTc prolongation; a
injuries represent very brief, high-voltage DC “side-splash” (lightning that hits an object and

Key Facts

Hypothermia
• Shivering artifact can be seen on ECG in hypothermic patients at temperatures above 32°C

(89.6°F).
• The most common rhythm in hypothermia is atrial fibrillation with a slow ventricular response.
• Specific morphologies such as the Osborn wave and Brugada pattern are common in severely

hypothermic patients.
Pulmonary Embolism
• Patients with PE frequently present with normal sinus rhythm; tachycardia could be the exception

rather than the rule.
• The S1Q3T3 pattern traditionally associated with PE is an unreliable finding that can neither confirm

nor exclude the presence of PE.
• Several morphologic patterns seen in PE, including right axis deviation, right bundle-branch block,

ST-segment depression, and anterior T-wave inversion, could be ECG reflections of reversible right
heart strain, but their absence is not sufficient to rule out the diagnosis.
• PE frequently simulates cardiac ischemia with T-wave inversions and ST-segment changes.
Thoracic Aortic Dissection
• Chest pain is almost always a feature of the presentation of patients with thoracic aortic dissection.
• LVH and Q waves are frequent, but typically chronic, findings.
• Many patients with dissection have acute ST/T-wave changes, but these are most commonly
nonspecific.
• Rarely, dissection presents with ST-segment elevation. In these cases, further tests must be
done to clarify the pathology. ST-segment elevation could represent primary MI or dissection
with secondary involvement of the coronary ostia. Proper treatment depends on making this
determination correctly.

212

The ecg in selected noncardiac conditions

then the victim secondarily) results in sinus voltage, or a history of cardiac disease should
tachycardia and nonspecific ST/T-wave changes. also be admitted for cardiac monitoring.
A third type of lightning strike is a current that
enters the ground and then spreads to the victim; References
these patients typically have sinus tachycardia or
nonspecific ST/T-wave changes as well.66 Other 1. Graham CA, McNaughton GW, Wyatt JP. The electrocardiogram
abnormalities and dysrhythmias described after in hypothermia. Wilderness Environ Med. 2001;12(4):232-235.
electrical injuries include ST-segment elevation,
bundle-branch blocks, sick sinus syndrome, 2. Mustafa S, Shaikh N, Gowda RM, et al. Electrocardiographic
supraventricular dysrhythmias, ventricular features of hypothermia. Cardiology. 2005;103(3):118-119.
extrasystole, and ventricular tachycardia.67–69
3. Vassallo SU, Delaney KA, Hoffman RS, et al. A prospective
Patients with documented dysrhythmias in evaluation of the electrocardiographic manifestations of
the field or an abnormal ECG on emergency hypothermia. Acad Emerg Med. 1999;6(11):1121-1126.
department presentation should be admitted
to a monitored setting. Patients with chest 4. Aslam AF, Aslam AK, Vasavada BC, et al. Hypothermia:
pain, loss of consciousness, exposure to high evaluation, electrocardiographic manifestations, and
management. Am J Med. 2006;119(4):297-301.

5. Nolan J, Soar J. Images in resuscitation: the ECG in
hypothermia. Resuscitation. 2005;64(2):133-134.

6. Mattu A, Brady WJ, Perron AD. Electrocardiographic
manifestations of hypothermia. Am J
Emerg Med. 2002;20(4):314-326.

7. Noda T, Shimizu W, Tanaka K, et al. Prominent
J wave and ST segment elevation: serial
electrocardiographic changes in accidental hypothermia.
J Cardiovasc Electrophysiol. 2003;14(2):223.

Key Facts

Pneumothorax
• Pneumothorax induces ECG findings and thus can mimic other life-threatening conditions such as

PE and MI.
• These changes are transient, resolving with treatment of the pneumothorax.
Chronic Obstructive Pulmonary Disease
• COPD can cause a variety of chronic changes on the ECG, mostly related to a shift of the position

of the heart within hyperinflated lungs and to elevated right-sided heart pressures.
• Some abnormalities such as an increase in the P-wave amplitude can be transient during acute

exacerbations and can resolve with treatment.
• Tachyarrhythmias are common in COPD patients. They can be related to the underlying disease, to

cardiac ischemia, or to the effects of medications.
• ECG findings suggestive of ischemia in patients with COPD should prompt further evaluation, as

the two conditions frequently co-exist.
Central Nervous System Events
• The relationship between central nervous system events and the ECG is best studied in the setting

of SAH.
• QT-interval prolongation and abnormalities of the ST segment and T wave can mimic those

associated with ACS. In some cases, this may create sufficient clinical uncertainty to warrant
further and more definitive investigation to rule out a simultaneous cardiac process.
Gastrointestinal Disorders
• ECG findings are not helpful in the diagnosis of acute gastrointestinal processes, but ECG
abnormalities associated with gastrointestinal disorders have been described.
• Any changes suggestive of acute ischemia should be investigated concurrently with management
of the underlying gastrointestinal disorder.
Electrical Injuries
• Patients with ECG abnormalities following exposure to an electrical current that has crossed
through the heart should receive continuous monitoring.

213

Electrocardiography in Emergency Medicine

8. Ansari E, Cook JR. Profound hypothermia mimicking a 32. Spodick DH. Electrocardiographic studies in pulmonary
Brugada type ECG. J Electrocardiol. 2003;36(3):257-260. disease. I. Electrocardiographic abnormalities in diffuse
lung disease. Circulation. 1959;20:1067-1072.
9. Petruzzelli S, Palla A, Pieraccini F, et al. Routine
electrocardiography in screening for pulmonary 33. Baljepally R, Spodick DH. Electrocardiographic
embolism. Respiration. 1986;50(4):233-243. screening for emphysema: the frontal plane P
axis. Clin Cardiol. 1999;22(3):226-228.
10. Richman PB, Loutfi H, Lester SJ, et al. Electrocardiographic
findings in emergency department patients with pulmonary 34. Ikeda K, Kubota I, Takahashi K, et al. P-wave
embolism. J Emerg Med. 2004;27(2):121-126. changes in obstructive and restrictive lung diseases.
J Electrocardiol. 1985;18(3):233-238.
11. Petrov DB. Appearance of right bundle-branch block
in electrocardiograms of patients with pulmonary 35. Asad N, Johnson VM, Spodick DH. Acute right atrial
embolism as a marker for obstruction of the main strain: regression in normal as well as abnormal P-
pulmonary trunk. J Electrocardiol. 2001;34(3):185-188. wave amplitudes with treatment of obstructive
pulmonary disease. Chest. 2003;124(2):560-564.
12. Stein PD, Dalen JE, McIntyre KM, et al. The
electrocardiogram in acute pulmonary embolism. 36. Incalzi RA, Fuso L, De Rosa M, et al. Electrocardiographic
Prog Cardiovasc Dis. 1975;17(4):247-257. signs of chronic cor pulmonale: a negative prognostic
finding in chronic obstructive pulmonary disease.
13. McIntyre KM, Sasahara AA, Littmann D. Relation of Circulation. 1999;99(12):1600-1605.
the electrocardiogram to hemodynamic alterations in
pulmonary embolism. Am J Cardiol. 1972;30(3):205-210. 37. Kok-Jensen A. Simple electrocardiographic features of
importance for prognosis in severe chronic bronchial
14. Chan TC, Vilke GM, Pollack M, et al. obstruction. Scand J Respir Dis. 1975;56(5):273-284.
Electrocardiographic manifestations: pulmonary
embolism. J Emerg Med. 2001;21(3):263-270. 38. Kilcoyne MM, Davis AL, Ferrer MI. A dynamic
electrocardiographic concept useful in the diagnosis of cor
15. Ahonen A. Electrocardiographic changes in massive pulmonale: result of a survey of 200 patients with chronic
pulmonary embolism. I. Analysis of the changes in P wave obstructive pulmonary disease. Circulation. 1970;42(5):903-924.
and QRS complex. Acta Med Scand. 1977;201(6):539-542.
39. Incalzi RA, Pistelli R, Fuso L, et al. Cardiac arrhythmias and
16. Ahonen A. Electrocardiographic changes in massive left ventricular function in respiratory failure from chronic
pulmonary embolism. II. Analysis of the changes in ST obstructive pulmonary disease. Chest. 1990;97(5):1092-1097.
segment and T wave. Acta Med Scand. 1977;201(6):543-545.
40. Davis TP, Alexander J, Lesch M. Electrocardiographic
17. Rodger M, Makropoulos D, Turek M, et al. Diagnostic changes associated with acute cerebrovascular disease: a
value of the electrocardiogram in suspected pulmonary clinical review. Prog Cardiovasc Dis. 1993;36(3):245-260.
embolism. Am J Cardiol. 2000;86(7):807-809,A810.
41. Sommargren CE, Zaroff JG, Banki N, et al. Electrocardiographic
18. Ferrari E, Imbert A, Chevalier T, et al. The ECG in pulmonary repolarization abnormalities in subarachnoid hemorrhage.
embolism. Predictive value of negative T waves in precordial J Electrocardiol. 2002;35(suppl):257-262.
leads—80 case reports. Chest. 1997;111(3):537-543.
42. Oppenheimer SM. Neurogenic cardiac effects of
19. Khan IA, Nair CK. Clinical, diagnostic, and management cerebrovascular disease. Curr Opin Neurol. 1994;7(1):20-24.
perspectives of aortic dissection. Chest. 2002;122(1):311-328.
43. Andreoli A, di Pasquale G, Pinelli G, et al. Subarachnoid
20. Hagan PG, Nienaber CA, Isselbacher EM, et al. The hemorrhage: frequency and severity of cardiac
International Registry of Acute Aortic Dissection (IRAD): new arrhythmias: a survey of 70 cases studied in the
insights into an old disease. JAMA. 2000;283(7):897-903. acute phase. Stroke. 1987;18(3):558-564.

21. Hirata K, Kyushima M, Asato H. Electrocardiographic 44. Rudehill A, Olsson GL, Sundqvist K, et al. ECG abnormalities
abnormalities in patients with acute aortic dissection. in patients with subarachnoid haemorrhage and intracranial
Am J Cardiol. 1995;76(16):1207-1212. tumours. J Neurol Neurosurg Psychiatry. 1987;50(10):1375-1381.

22. Jessen ME, Horn VP, Weaver DE, et al. Successful surgical 45. Jachuck SJ, Ramani PS, Clark F, et al. Electrocardiographic
repair of aortic dissection presenting with complete heart abnormalities associated with raised intracranial
block [abstract]. Ann Thorac Surg. 1996;62(4):1202-1203. pressure. Br Med J. 1975;1(5952):242-244.

23. Ti LK, Lee TL. The electrocardiogram complements a 46. Opherk C, Coromilas J, Hirsch LJ. Heart rate and
chest radiograph for the early detection of pneumothorax EKG changes in 102 seizures: analysis of influencing
in post-coronary artery bypass grafting patients. J factors. Epilepsy Res. 2002;52(2):117-127.
Cardiothorac Vasc Anesth. 1998;12(6):679-683.
47. Oppenheimer SM, Cechetto DF, Hachinski VC. Cerebrogenic
24. Raev D. A case of spontaneous left-sided pneumothorax cardiac arrhythmias. Cerebral electrocardiographic influences
with ECG changes resembling acute myocardial and their role in sudden death. Arch Neurol. 1990;47(5):513-519.
infarction. Int J Cardiol. 1996;56(2):197-199.
48. Kandler L, Fiedler A, Scheer K, et al. Early post-
25. Ortega-Carnicer J, Ruiz-Lorenzo F, Zarca MA, convulsive prolongation of QT time in children.
et al. Electrocardiographic changes in occult Acta Paediatr. 2005;94(9):1243-1247.
pneumothorax. Resuscitation. 2002;52(3):306-307.
49. Zijlmans M, Flanagan D, Gotman J. Heart rate changes and ECG
26. Goddard R, Scofield RH. Right pneumothorax with the abnormalities during epileptic seizures: prevalence and definition
S1Q3T3 electrocardiogram pattern usually associated with of an objective clinical sign. Epilepsia. 2002;43(8):847-854.
pulmonary embolus. Am J Emerg Med. 1997;15(3):310-312.
50. Tigaran S, Molgaard H, Dam M. Atrio-ventricular block:
27. Summers RS. The electrocardiogram as a diagnostic a possible explanation of sudden unexpected death in
aid in pneumothorax. Chest. 1973;63(1):127-128. epilepsy. Acta Neurol Scand. 2002;106(4):229-233.

28. Alikhan M, Biddison JH. Electrocardiographic changes with 51. Tigaran S. Cardiac abnormalities in patients with refractory
right-sided pneumothorax. South Med J. 1998;91(7):677-680. epilepsy. Acta Neurol Scand. 2002;177(suppl):9-32.

29. Maheshwari M, Mittal SR. Right-sided pneumothorax simulating 52. Di Pasquale G, Andreoli A, Lusa AM, et al. Cardiologic
anterior wall myocardial infarction. Indian Heart J. 2004;56(1):73. complications of subarachnoid hemorrhage. J
Neurosurg Sci. 1998;42(1 suppl 1):33-36.
30. Kozelj M, Rakovec P, Sok M. Unusual ECG variations in left-
sided pneumothorax. J Electrocardiol. 1997;30(2):109-111. 53. Di Pasquale G, Pinelli G, Andreoli A, et al. Torsade de pointes
and ventricular flutter-fibrillation following spontaneous cerebral
31. Strizik B, Forman R. New ECG changes associated with a tension subarachnoid hemorrhage. Int J Cardiol. 1988;18(2):163-172.
pneumothorax: a case report. Chest. 1999;115(6):1742-1744.

214

The ecg in selected noncardiac conditions

54. Brouwers PJ, Wijdicks EF, Hasan D, et al. Serial 62. Mixon TA, Houck PD. Intestinal obstruction mimicking acute
electrocardiographic recording in aneurysmal subarachnoid myocardial infarction. Tex Heart Inst J. 2003;30(2):155-157.
hemorrhage. Stroke. 1989;20(9):1162-1167.
63. Ryan ET, Pak PH, DeSanctis RW. Myocardial infarction mimicked
55. Weidler DJ. Myocardial damage and cardiac by acute cholecystitis. Ann Intern Med. 1992;116(3):218-220.
arrhythmias after intracranial hemorrhage. A
critical review. Stroke. 1974;5(6):759-764. 64. Furuhashi M, Uno K, Satoh S, et al. Right bundle branch
block and coved-type ST-segment elevation mimicked
56. Albrecht CA, Laws FA. ST segment elevation pattern by acute cholecystitis. Circ J. 2003;67(9):802-804.
of acute myocardial infarction induced by acute
pancreatitis. Cardiol Rev. 2003;11(3):147-151. 65. Carleton SC. Cardiac problems associated with
electrical injury. Cardiol Clin. 1995;13(2):263-266.
57. Hung SC, Chiang CE, Chen JD, et al. Images in
cardiovascular medicine: pseudo-myocardial 66. Lichtenberg R, Dries D, Ward K, et al. Cardiovascular effects
infarction. Circulation. 2000;101(25):2989-2990. of lightning strikes. J Am Coll Cardiol. 1993;21(2):531-536.

58. Pezzilli R, Barakat B, Billi P, et al. Electrocardiographic 67. Blackwell N, Hayllar J. A three year prospective audit
abnormalities in acute pancreatitis. Eur of 212 presentations to the emergency department
J Emerg Med. 1999;6(1):27-29. after electrical injury with a management protocol.
Postgrad Med J. 2002;78(919):283-285.
59. Rubio-Tapia A, Garcia-Leiva J, Asensio-Lafuente E, et al.
Electrocardiographic abnormalities in patients with acute 68. Kose S, Iyisoy A, Kursaklioglu H, et al. Electrical
pancreatitis. J Clin Gastroenterol. 2005;39(9):815-818. injury as a possible cause of sick sinus syndrome.
J Korean Med Sci. 2003;18(1):114-115.
60. Frais MA, Rodgers K. Dramatic electrocardiographic
T-wave changes associated with gastric 69. Varol E, Ozaydin M, Altinbas A, et al. Low-tension
dilatation. Chest. 1990;98(2):489-490. electrical injury as a cause of atrial fibrillation: a case
report. Tex Heart Inst J. 2004;31(2):186-187.
61. Asada S, Kawasaki T, Taniguchi T, et al. A case of ST-
segment elevation provoked by distended stomach
conduit. Int J Cardiol. 2006;109(3):411-413.

215

Electrocardiography in Emergency Medicine

Figures

Figure 16-1.
Hypothermia. This is the initial ECG of a 34-year-old patient with a history of schizophrenia, seizure
disorder, and crack cocaine abuse, who was “found down.” His rectal temperature when he reached the
emergency department was 28.3°C (83°F). Although shivering in hypothermia is not typically seen at such
low temperatures, shivering artifact is seen. The regularity of the ventricular response (QRS complexes)
helps to differentiate this baseline pattern from atrial fibrillation, which is also common in hypothermia. The
ventricular rate of 97 is uncharacteristically rapid for severe hypothermia, and might be influenced by other
elements of presentation, such as a seizure or medication effect. Osborn J waves can be seen in the terminal
QRS.

Figure 16-2.
Hypothermia. Osborn J wave, magnified.

216

The ecg in selected noncardiac conditions

Figures

Figure 16-3.
Hypothermia. This is a subsequent ECG of the patient from Figure 16-1 after rewarming. Note the resolution of
both the shivering artifact and Osborn J waves.

Figure 16-4.
Pulmonary embolism. This is the ECG of a 36-year-old patient with recurrent deep vein thrombosis and PE
who presented to the emergency department with increasing dyspnea for 3 weeks. The ECG demonstrates
several described features associated with PE, including sinus tachycardia (rate 109), the S1Q3T3 pattern, P
pulmonale (large peaked P waves, seen prominently in leads II and V2), as well as T-wave inversions in leads V1
through V3.

217

Electrocardiography in Emergency Medicine

Figures

Figure 16-5.
Pulmonary embolism. This series of ECGs was obtained from a 55-year-old patient who presented to the
emergency department with multiple long bone and pelvic fractures following a motor vehicle accident.
A: The patient’s baseline ECG on admission. B: Five days later, the patient developed acute dyspnea and an
ECG obtained at that time revealed sinus tachycardia with new deep T-wave inversions in leads V1 through
V4, a finding correlated with larger pulmonary emboli and acute right heart strain. CT pulmonary angiogram
confirmed presence of a large right pulmonary artery embolus with extension into the right lower lobe branch.
C: The ECG findings resolved 12 hours after initiation of heparin.

A

B

C

218

The ecg in selected noncardiac conditions

Figures

Figure 16-6.
Chronic obstructive pulmonary disease. This is the ECG of a 42-year-old patient with a history of COPD,
admitted for an acute exacerbation. The tracing demonstrates both P pulmonale (see also in Figure 16-4), as
well as verticalization of the P-wave axis, which can be identified by the inverted p wave in lead aVL. Both
findings have been associated with moderate to severe COPD.

Figure 16-7.
Subarachnoid hemorrhage. Deep inverted T waves are often the most dramatic ECG finding in patients with
SAH. This 31-year-old patient presented to the emergency department with acute onset headache and seizure.
Initial ECG showed sinus tachycardia. This subsequent ECG obtained during emergent ventriculostomy
placement shows marked T-wave inversions anterolaterally. Image courtesy of Amal Mattu, MD.

219

Electrocardiography in Emergency Medicine

Figures

Figure 16-8.
Subarachnoid hemorrhage. The ECG demonstrates marked QT prolongation and U waves in a 36-year-old
patient with SAH. The U waves here are most prominent in lead V2 and buried in the T wave of lead V3, giving
it a notched appearance.

220

The ecg in selected noncardiac conditions

Figures

Figure 16-9.
Subarachnoid hemorrhage. A: This ECG in a 75-year-old patient with SAH demonstrates significant ST-
segment depression in leads V1 to V3. The rhythm in the tracing degenerates to polymorphic ventricular
tachycardia. B: In a subsequent postoperative ECG, the ST-segment changes resolve.

A

B

221

Electrocardiography in Emergency Medicine
222

C h apter Seve n tee n

ECG Manifestations of Drug Overdose

Suzanne Doyon, MD

Emergency physicians routinely evaluate the pharmacologic effect of the drug; therefore,
ECGs from poisoned patients. Drugs the toxicity represents an extension of the
from widely different pharmacologic pharmacologic effect of the medication (eg,
classes can behave similarly in overdose procainamide, flecainide). In other instances,
and have similar effects on the ECG. the sodium channel–blocking properties are
secondary to the pharmacologic effect of the
For the purpose of this chapter, drugs drug (eg, cyclic antidepressants, chloroquine).
have been divided into five main groups The sodium channel blocker group is therefore
based on the five main ECG manifestations: diverse (Table 17-1). Regardless of the agent, the
sodium channel blockers, potassium rectifier effect of blocking myocardial sodium channels
current (IKr) inhibitors, sodium-potassium results in one or more of the following ECG
ATPase inhibitors, calcium channel blockers, findings: intraventricular conduction defects,
and -adrenergic blockers (-blockers). It ventricular dysrhythmias, and bradyarrhythmias.
is important to keep in mind that one agent
can belong to more than one group. A number of naturally occurring toxins
possess sodium channel blocking properties.
Sodium Channel Blocker Grayanotoxins, mainly andromedotoxin, found
Toxicity in the leaves and flowers of rhododendron
species, can inhibit sodium channels and cause
The following terms are used bradycardia and atrioventricular (AV) block.1 In
interchangeably in the medical literature: contrast, two other naturally occurring sodium
“sodium channel blockade,” “local anesthetic channel blockers, saxitoxin and tetrodotoxin,
effect,” “membrane stabilizing effect,” and produce a plethora of gastrointestinal and
“quinidine-like effect.” In this discussion, neurologic effects, including respiratory
the preferred and more descriptive term arrest, but little or no cardiac effect.
“sodium channel blocker effect” is used.
223
Poisoning by medications with sodium
channel–blocking properties is common. In
many instances, these properties are essential to

Electrocardiography in Emergency Medicine

Intraventricular Conduction predictive values of these ECG findings are 66%
Sodium channel blockers will slow phase 0 of and 100%, respectively.2 When 79 patients with
cyclic antidepressant overdose were prospectively
the action potential, decrease propagation of the evaluated and scrutinized, the amplitude of the
action potential, and thus slow intraventricular terminal R wave and the R:S ratio in lead aVR
conduction. Clinically, this is manifested as were statistically significantly greater in patients
prolongation of the QRS complex to 100 msec with severe cyclic antidepressant poisoning
or more and the appearance of morphologic compared with post-treatment patients and
changes in the QRS complex in aVR. patients with other poisonings.3 The presence
of a QRS interval prolongation or the Brugada
A rightward axis deviation of the terminal pattern or of an R wave in aVR less than 3 mm in
40 msec of the frontal plane QRS axis in aVR amplitude is superior to a urine toxicology screen
is associated with the presence of a tricyclic at detecting the presence of a sodium channel
antidepressant.2 (The terminal 40-msec axis is not blocker, including all cyclic antidepressants,
easily measured in the absence of sophisticated and should supplant the need for routine urine
computer-assisted technology and therefore is not toxicology screening for cyclic antidepressants
readily accessible in emergency departments.) in overdose patients.4 Occasionally a right
An abnormal rightward axis deviation can be bundle-branch block (RBBB) pattern is detected
estimated by observing the QRS pattern in leads along with the ECG findings described above.
I and aVR. A negative deflection of the S wave (of
the QRS) in lead I and a positive deflection of the The Brugada syndrome (described in
R wave (of the QRS) in aVR signifies a rightward greater detail in Chapter 13) is a cardiac
axis deviation (Figure 17-1). In the general disorder associated with a genetic defect in
overdose population, the positive and negative the α subunit of the sodium channel, causing
sodium channel dysfunction. The myocardium
Table 17-1. remains structurally normal.5 The syndrome is
Sodium channel blockers characterized by RBBB and unusual ST-segment
elevation in V1 through V3. Sodium channel
Antidepressants blockers can unmask the Brugada ECG pattern
amitriptyline, nortriptyline, desipramine, imipramine, and are often administered to confirm the
diagnosis of Brugada syndrome. The Brugada
doxepin, maprotiline, amoxapine, paroxetine, syndrome is associated with an increased
citalopram, venlafaxine incidence of sudden death. Sodium channel
Amantadine blocker overdoses can mimic the Brugada
Anesthetics pattern in the absence of any abnormality of
bupivacaine the sodium channel. In a large case series, 17%
-Blockers of overdoses with cyclic antidepressants met
propranolol, acebutolol, betaxolol, oxprenolol the criteria for Brugada pattern on ECG.6 In
Carbamazepine another case series,7 the incidence was 15%. In
Chloroquine and hydroxychloroquine cyclic antidepressant overdoses, the mortality
Class IA antiarrhythmics rate was 6.7% among patients presenting with
procainamide, quinidine, disopyramide the Brugada pattern and 2.4% if the Brugada
Class IC antiarrhythmics pattern was absent. The Brugada pattern has
encainide, flecainide, propafenone been detected following overdoses with other
Calcium channel blockers sodium channel blockers, ie, diphenhydramine,
diltiazem, verapamil cocaine, procainamide, flecainide, and
Diphenhydramine encainide.7–10 In intoxicated patients in whom
Orphenadrine the substance is unknown, early recognition of
Antipsychotics Brugada conduction abnormalities is important
mesoridazine, thioridazine, loxapine, quetiapine
Propoxyphene
Quinine

224

ecg manifestations of drug overdose

and suggests the presence of sodium channel is unclear but may be related to depression of
blocking medications (Figures 17-2 and 17-3). the slope of phase 4 of the action potential.

In some cases, the sodium channel blocker The presence of a wide QRS complex
toxicity is so profound that both the right and and bradycardia is an ominous sign,
left bundles are progressively more and more indicating a profound degree of sodium
affected, resulting in a dangerously lengthened channel blockade (Figure 17-4).
QRS complex in which supraventricular and
ventricular rhythms become indistinguishable Potassium Rectifier Current
from each other.11 The development of Inhibition
a sine wave is usually preterminal.
Poisoning by IKr inhibitors is also common. It is
The prolongation of the QRS complex and its estimated that 3% of all noncardiac medications
morphology are important prognostic indicators. are associated with IKr inhibition.15 Similar to the
In one study on tricyclic antidepressant sodium channel blockers, genetic predisposition
overdoses, a QRS complex larger than 120 msec can play a role in determining susceptibility
was associated with a 33% incidence of seizures, to IKr inhibitors. The IKr inhibitor group of
and a QRS complex of more than 160 msec, a substances is just as large and diverse as the
50% incidence of ventricular dysrhythmias.12 sodium channel blocker group and includes class
Other studies have confirmed that QRS IA antiarrhythmics (procainamide, quinidine,
prolongation (>100 msec) is associated with an and disopyramide), class III antiarrhythmics
increased risk of coma, seizures, and ventricular (sotalol, amiodarone), antibiotics (erythromycin,
dysrhythmias. Furthermore, a terminal R wave clarithromycin), antifungals (ketoconazole,
in aVR of 3 mm or more and an R:S ratio of 0.7 or itraconazole), antimalarials (chloroquine,
more is associated with an increased incidence quinidine), neuroleptics (haloperidol,
of seizures and dysrhythmias.3,13 Conversely, droperidol, ziprasidone), antidepressants (cyclic
absence of QRS prolongation or absence of antidepressants, venlafaxine), gastrointestinal
an R wave in aVR after 6 hours’ observation motility agents (cisapride), chemotherapeutic
is associated with absence of seizures and agents (arsenic), and tacrolimus (Table 17-2).15–19
arrhythmias and with a good outcome.12,14
Blockade of the (outward) IKr prolongs the
Ventricular Dysrhythmias cardiac cycle and lengthens the QT interval.
It also delays repolarization and decreases the
Sodium channel blockers can prolong difference in potential across the myocardial
intraventricular conduction to the extent membrane. This less-than-expected difference in
that unidirectional blocks and reentrant potential can result in activation of the inward
circuits develop, resulting in ventricular current (early after-depolarization), which can
tachycardia. The ventricular tachycardia can trigger another action potential. The triggered
deteriorate into ventricular fibrillation. action potential can deteriorate into reentrant
circuitry and result in polymorphic ventricular
Bradyarrhythmias tachycardia (torsade de pointes). IKr inhibition is
therefore associated with QT prolongation and
Many sodium channel blockers possess torsade de pointes (Figure 17-5). QT interval
anticholinergic or intrinsic sympathomimetic prolongation occurs when the QTc interval
properties and are associated with tachycardia. is larger than 0.44 msec in men and more
Bradycardias and bradyarrhythmias are than 0.46 msec in women. However, there is
rare. However, sodium channel blockers no direct relationship between degree of QTc
can depress automaticity and cause sinus interval prolongation and torsadogenicity. In a
bradycardia, escape junctional rhythms, small case series of six sotalol overdoses,20 QT
ventricular rhythms, and even asystole in prolongation was usually present in the first 4
large overdoses. The mechanism by which hours after ingestion and progressed until 15
sodium channel blockers inhibit automaticity
225

Electrocardiography in Emergency Medicine

hours after ingestion. QT prolongation averaged example, disopyramide is a racemic mixture of
172% of normal. Ventricular dysrhythmias two enantiomers. The first enantiomer shortens
occurred in five of the six patients and included the QT interval and the second lengthens it.18
multifocal ventricular extrasystoles, ventricular
tachycardia, and ventricular fibrillation. The Some authors suggest that “QT dispersion”
risk of ventricular dysrhythmias was greatest is a better predictor of torsade de pointes
between 4 and 20 hours after ingestion. than QT prolongation. QT dispersion refers
One patient had persistent ventricular to the difference between the shortest and
dysrhythmias for 48 hours after ingestion. the longest QT interval on the 12-lead ECG.
The risk of torsade de pointes is greatest if
Drug stereoisomers can differ from each the QT dispersion exceeds 100 msec.21
other and from the racemic mixture of the
two. Identification and characterization of Sodium-Potassium ATPase
individual isomers of a drug is helpful. For Inhibition

Table 17-2. Inhibitors of the sodium-potassium ATPase
Potassium rectifier current inhibitors pump are a much smaller group of substances.
Digoxin is the best known of these agents, but
Antidepressants a number of naturally occurring toxins figure
amitriptyline, nortriptyline, imipramine, desipramine, prominently in this group (Table 17-3). This group
will be referred to generally as cardiac glycosides.
doxepin, amoxapine, maprotiline, venlafaxine
Antihistamines Cardiac glycosides inhibit the outward
loratadine, diphenhydramine movement of sodium and inward movement
Antipsychotics of potassium, resulting in an increase in
chlorpromazine, droperidol, haloperidol, extracellular potassium and an increase
in intracellular sodium. The increase in
mesoridazine, thioridazine, pimozide, quetiapine, intracellular sodium activates the sodium-
risperidone, ziprasidone calcium exchange pump and results in an
Arsenic trioxide increase in intracellular calcium, which, in
Bepridil turn, stimulates myosin activity and exerts a
Chloroquine positive inotropic effect. Cardiac glycosides also
Cisapride depress AV nodal conduction. Therapeutically,
Citalopram cardiac glycosides are used to increase
Class IA antiarrrhythmics inotropy and slow AV nodal conduction.
quinidine, procainamide, disopyramide
Class IC antiarrhythmics Digitalis Effect
encainide, flecainide, moricizine, propafenone Cardiac glycosides have been associated with
Class III antiarrhythmics
amiodarone, dofetilide, ibutilide, sotalol several ECG changes, including the “digitalis
Fluoroquinolones effect,” ie, abnormally inverted or flattened T
ciprofloxacin, gatifloxacin, levofloxacin, moxifloxacin, waves coupled with sagging or scooping ST-
sparfloxacin
Halofantrine Table 17-3.
Hydroxychloroquine Sodium-potassium ATPase inhibitors
Lithium
Macrolides Bufadienolides
clarithromycin, erythromycin Digoxin and digitoxin
Opioids Foxglove
methadone, levo-alpha ethyl methadol (LAAM) Lily-of-the-valley
Pentamidine Oleander
Quinine Red squill
Tacrolimus

226

ecg manifestations of drug overdose

segment depression (Figures 17-6 and Calcium Channel Blockers
17-7). These findings are particularly evident in
precordial leads with very tall R waves and can The incidence of calcium channel blocker
be confused with diffuse ischemic disease, left toxicity increased during the past decade.
ventricular strain, combined anterior-inferior Cardioactive calcium channel blockers inhibit
infarction, subendocardial infarction, and the high-voltage L-type calcium channels
hypokalemia. Other ECG changes associated found in myocardium and smooth muscle.
with cardiac glycosides include QT shortening Inhibition of these types of calcium channels
resulting from rapid ventricular repolarization prevents the inward movement of calcium
and PR interval prolongation resulting from into cells. Depletion of intracellular calcium
increased vagal tone. Importantly, all of these slows conduction and decreases contractility.
changes can occur at therapeutic drug levels Calcium channel blockers therefore decrease
and do not necessarily indicate toxicity. chronotropy and inotropy of the myocardium
and cause peripheral vasodilation.
Cardiac glycoside toxicity is associated with
a wide array of ECG manifestations. These The dihydropyridine subclass of calcium
changes result from the cardiac-glycoside– channel blockers (nifedipine, amlodipine,
induced increase in intracellular calcium, nicardipine) has an increased affinity for
causing increased automaticity, and a cardiac- peripheral smooth muscle receptors. Overdoses
glycoside–induced increase in vagal tone, causing with these agents often result in hypotension
slowed automaticity. The result is a mixture of with an accompanying reflex tachycardia.
tachyarrhythmias and bradyarrhythmias. Atrial, The phenylalkylamine (verapamil) and
junctional, and ventricular premature beats and benzothiazepine (diltiazem) subclasses of
tachycardia, sinus bradycardia, bundle-branch calcium channel blockers possess a strong
blocks, and varying degrees of AV nodal blocks affinity for the myocardium calcium channels,
can occur separately or together (Figure 17-6). resulting in hypotension and bradycardia, which
The most common dysrhythmia is frequent can result in myocardial ischemia. Interestingly,
premature ventricular beats. Paroxysmal verapamil has exhibited some sodium channel
atrial tachycardia with variable block is highly blockade effects both in vitro and in vivo.22
indicative of cardiac glycoside toxicity, as
are accelerated junctional rhythms (Figure The most common ECG manifestation of
17-7). Bidirectional ventricular tachycardia dihydropyridine calcium channel blocker
has been described almost exclusively in toxicity is reflex tachycardia. More profound
the context of cardiac glycoside toxicity.21 dihydropyridine toxicity is associated with
bradycardia and AV nodal block and junctional
Acute poisoning of the sodium-potassium and ventricular bradyarrhythmias.
ATPase pump by cardiac glycosides can raise
the serum potassium concentration acutely, The most common ECG finding in verapamil
and the added effects of hyperkalemia on the and diltiazem overdoses is bradycardia. Severe
ECG can be detected. Hyperkalemia causes overdoses are associated with AV nodal block
spiked T waves, lengthening of the PR interval, and junctional and ventricular bradyarrhythmias
and widening of the QRS complex. Conversely, (Figure 17-8). A widening of the QRS complex
chronic inhibition of the sodium-potassium can be present, although the significance of
ATPase pump causes a much more gradual, time- this finding is unknown. In life-threatening
dependent increase in serum potassium, which is overdoses, asystole will occur. ECG changes
eliminated systematically by the renal system and indicative of myocardial ischemia can be present.
is therefore not associated with hyperkalemia.
-Blockers

-Blocker toxicity, like calcium channel
blocker toxicity, is seen with increasing
frequency. -Blockers competitively inhibit
1- and 2-adrenergic receptors in varying

227

Electrocardiography in Emergency Medicine

degrees and with varying effects. Inhibition of duration and lengthens the QT interval. These
1-receptors results in a decrease in the force and effects predispose the individual to torsade
rate of myocardial contraction and a decrease in de pointes and ventricular dysrhythmias.
AV nodal conduction. Inhibition of 2-receptors
relaxes smooth muscle in the vasculature of Special Cases
the bronchi and the gastrointestinal tract.
Potassium
-Blockers do not necessarily have a shared Drug-induced hypokalemia can occur
“class effect.” For example, propranolol
nonselectively inhibits 1- and 2-receptors. following overdoses of -agonists (albuterol),
Metoprolol selectively inhibits 1-receptors. methylxanthines (caffeine, theophylline), and
In addition to their effects on -adrenergic chloroquine (Table 17-4). It is manifested by
channels, -blockers have several properties muscle weakness, areflexic paralysis, and
that modify their effects and their ECG respiratory failure. ECG changes are common and
manifestations. Labetalol and carvedilol, include sagging of the ST segment, decreased T-
for example, inhibit α-receptors. When wave amplitude, and increased U-wave amplitude.
labetalol is administered intravenously,
the ratio of :α inhibition is 7:1; with oral Drug-induced hyperkalemia can occur
administration, the ratio is 5:1. Therefore, following overdoses of cardiac glycosides
labetalol behaves largely like a -blocker. (digoxin) and -blockers (Table 17-4).
Hyperkalemia presents with nausea and
Acebutolol, oxprenolol, penbutolol, and
pindolol have intrinsic sympathomimetic Table 17-4.
activity, also termed partial agonist activity. In Compounds capable of causing hypokalemia and
theory, these agents appear less toxic in overdose hyperkalemia
situations. Pindolol has been associated with
hypertension and tachycardia in overdose, but Hypokalemia
the data are insufficient to state that pindolol -adrenergic agonists
is safer. Propranolol, betaxolol, oxprenolol, and bicarbonate
acebutolol cause sodium channel blockade. carbonic anhydrase inhibitors
Propranolol possesses the most sodium channel chloroquine, hydroxychloroquine, quinine
blocking properties of this group. Sotalol, and diuretics
possibly acebutolol, inhibit IKr. Propranolol insulin
causes hypoglycemia in overdose situations. licorice
methylxanthines (caffeine, theophylline)
The most common ECG manifestation of oral hypoglycemics
-blocker toxicity is AV block followed by sympathomimetics
bradycardia. In one small case series,23 first- toluene
degree AV block (PR interval prolongation
of 216 msec) was the most common ECG Hyperkalemia
finding. Bradycardia was infrequent in this case amiloride
series, but its absence could be the result of angiotensin-converting enzyme inhibitors
confounding variables such as administration of -blockers
sympathomimetic agents. QRS prolongation (>100 cardiac glycosides
msec) was found in 8 of the 13 symptomatic fluoride
overdose victims and was most pronounced with heparin
overdoses of acebutolol, raising the question nonsteroidal anti-inflammatory drugs
of whether propranolol truly possesses more penicillin (potassium)
sodium channel blockade effects than acebutolol. potassium supplements
succinylcholine
Sotalol is unique among -blockers because triamterene
it inhibits IKr and prolongs the action potential trimethoprim

228

ecg manifestations of drug overdose

vomiting, muscle weakness, ascending diuretic therapy. Ingestion of cholecalciferol,
paralysis, and respiratory failure. ECG a rodenticide, can increase calcium enough to
changes include the presence of tall peaked make the patient symptomatic. Symptoms of
T waves, QRS prolongation, loss of amplitude hypercalcemia include lethargy, constipation,
of the P wave, and prolongation of the PR nausea, and mental status changes. A shortened
interval. As the hyperkalemia progresses, QT interval is the classic ECG abnormality
a sine wave configuration emerges. found in cases of severe hypercalcemia.

Calcium Lithium
Drug-induced hypocalcemia occurs with Lithium overdose is fairly common. Lithium

therapeutic uses of anticonvulsants and can cause shifts in and depletion of intracellular
aminoglycosides. It can occur following potassium and also affects intracellular pools
severe life-threatening overdoses of ethylene of calcium, causing ECG changes. It can cause
glycol, sodium fluoride, sodium bifluoride,
hydrofluoric acid, bisphosphonates, and sodium Table 17-6.
phosphate (Fleet enema) and after exposure Compounds capable of inducing tachycardia
to the output of a phosphate-containing fire
extinguisher. Symptoms of hypocalcemia Amphetamines
include paresthesia, carpopedal spasms, ephedrine, pseudoephedrine, epinephrine,
tetany, and seizures. ECG changes associated
with hypocalcemia include prolongation of methylphenidate, methamphetamine
the QT interval and occasional prolongation Anticholinergics
of the QRS interval as well (Figure 17-9).24,25 atropine, scopolamine, benztropine, cyclobenzaprine,

Drug-induced hypercalcemia occurs rarely others
but can result from (usually chronic) overdose Antihistamines
of antacids or vitamin D or from thiazide diphenhydramine, chlorpheniramine, meclizine,

Table 17-5. others
Compounds capable of inducing bradycardia Antipsychotic agents
haloperidol, risperidone, olanzapine, others
Antiarrhythmics Arsenic (acute)
procainamide, disopyramide, quinidine, sotalol Carbamates
α-Adrenergic agonists aldicarb, benfuracarb, carbaryl, carbofuran,
clonidine, tizanidine, guanfacine
-Blockers methomyl, oxamyl
propranolol, metoprolol, atenolol, others Carbon monoxide
Calcium channel blockers Cocaine
verapamil, diltiazem Cyclic antidepressants
Carbamates amitriptyline, nortriptyline, imipramine, desipramine
Sevin Disulfiram-ethanol
Ciguatera Iron
Digitalis glycosides Methylxanthines
digoxin theophylline, caffeine
Opioids Monoamine oxidase inhibitors
Organophosphates phenelzine, isocarboxazid, moclobemide, selegiline,
malathion
Sedative-hypnotics rasagiline, tranylcypromine, procarbazine
benzodiazepines, barbiturates, baclofen, zolpidem, Phencyclidine
Organophosphates
others chlorpyrifos, diazinon, dichlorvos, malathion,

parathion
Sedative-hypnotics
benzodiazepines, barbiturates, glutethimide, zolpidem

and others, ethchlorvynol
Thyroxine

229

Electrocardiography in Emergency Medicine

diffuse T-wave inversion, QTc prolongation, usually resistant to standard antiarrhythmic
ventricular dysrhythmias, AV nodal conduction agents but respond to the administration
defects, sinuatrial nodal dysfunction, and of -blockers such as propranolol.28
even myocarditis. In one small case series,26
55% of patients with supratherapeutic lithium Ethanol
levels had QTc greater than 440 msec. The
combination of T-wave inversion in lateral Acute ethanol intoxication has been associated
precordial leads together with a QTc prolongation with several cardiac arrhythmias. The basic
of 440 msec or more yielded a sensitivity of electrophysiologic effects of ethanol on the heart
64% and a specificity of 97% in predicting are not well described, but hyperadrenergic
supratherapeutic lithium levels. These changes states, electrolyte abnormalities, impaired vagal
are reversible and correct themselves as lithium tone, and repolarization abnormalities occur
levels decrease into the therapeutic range. following ethanol consumption. The term
“holiday heart” generally refers to de novo atrial
Halogenated Hydrocarbons fibrillation following a period of heavy ethanol
consumption. Ventricular tachyarrhythmias
Halogenated hydrocarbons include are also associated with heavy ethanol intake.
chloroform, chloral hydrate, carbon tetrachloride, Heavy ethanol consumption by healthy human
trichloroethanol, and trichloroethylene. volunteers has been associated with increased
Halogenated hydrocarbon overdoses are QT dispersion, the interlead difference in
associated with varied ECG manifestations the QT interval. It is a marker for ventricular
stemming from the fact that they sensitize inhomogeneity and electrical instability.29
the myocardium to catecholamines. Sinus
tachycardia, ventricular ectopy, ventricular Conclusion
tachycardia, ventricular fibrillation, and
sudden death have been reported (Figure Overdose patients can present with a wide
17-10).27,28 The mechanism of dysrhythmias array of ECG changes. In many instances, a
appears to be related to endogenous common mechanism affecting a particular
catecholamine release causing extrasystoles component of the cardiac action potential
in the setting of altered repolarization, accounts for the ECG manifestations. Knowledge
usually prolonged QTc interval. In one case and understanding of these mechanisms
series,27 11 of 12 chloral hydrate overdose are helpful in the management of overdose
patients admitted to an ICU had ventricular victims. Sodium channel blocker overdoses are
ectopic activity. Halogenated-hydrocarbon– quite common and usually manifest by QRS
induced ventricular tachyarrhythmias are prolongation, tall R waves in aVR, or the Brugada
pattern. Potassium channel blocker overdoses

Key Facts

• Drug toxicities should be considered in the differential diagnosis for patients presenting with
tachycardias and bradycardias (Tables 17-5 and 17-6).

• Sodium channel blocker overdoses are associated with prolongation of the QRS complex,
prominent R waves in aVR, and occasionally a Brugada pattern on the ECG.

• Sodium channel blocker overdoses with QRS prolongation greater than 120 msec are more likely to
lead to seizures, coma, malignant tachyarrhythmias, and death.

• IKr inhibitor overdoses are associated with QTc prolongation.
• Sodium-potassium ATPase inhibitor overdoses can present with either bradyarrhythmias or

tachyarrhythmias.
• Digitalis effect is not synonymous with digitalis toxicity, although they often coexist.

230

ecg manifestations of drug overdose

are manifest by prolongation of the QTc. Cardiac 13. Liebelt EL, Ulrich A, Francis PD, et al. Serial
electrocardiogram changes in acute tricyclic antidepressant
glycosides cause a wide assortment of ECG overdoses. Crit Care Med. 1997;25:1721-1726.

abnormalities, including bradycardia, AV nodal 14. Shannon M. Duration of QRS disturbances after
severe tricyclic antidepressant intoxication. J
block, and bidirectional ventricular tachycardia. Toxicol Clin Toxicol. 1992;30:377-386.

Multiple medications cause electrolyte changes. 15. De Ponti F, Poluzzi E, Montanaro N, et al. QTc and
psychotropic drugs. Lancet. 2000;356:75-76.
Lithium causes reversible nonspecific T-
16. Drolet B, Khalifa M, Daleau P, et al. Block of the rapid
wave changes and QTc prolongation. Finally, component of the delayed rectifier potassium current by
the prokinetic agent cisapride underlies the drug-related
halogenated hydrocarbons, like chloral hydrate, lengthening of the QT interval. Circulation. 1998;97:204-210.

can cause resistant ventricular ectopy in overdose 17. Mancuso EM, Brady WJ, Harrigan RA, et al.
Electrocardiographic manifestation: long QT
situations. In all instances, defining the cause syndrome. J Emerg Med. 2004; 27:385-393.

of the ECG abnormality will guide therapy. 18. Mehvar R, Brock DR, Vakily M. Impact of stereoselectivity
on the pharmacokinetics and pharmacodynamics of
References antiarrhythmic drugs. Clin Pharmacokinet. 2002;41:533-558.

1. Ozhan H, Akdemir R, Yazici M, et al. Cardiac 19. Kolecki PF, Curry SC. Poisoning by sodium channel
emergencies caused by honey ingestion: a single centre blocking agents. Crit Care Clin. 1997;13:830-848.
experience. Emerg Med J. 2004;21(6):742-744.
20. Neuvonen PJ, Elonen E, Vuorenmae T. Prolonged Q-T
2. Neimann JT, Bessen HA, Rothstein RJ, et al. interval and severe tachyarrhythmias, common features of
Electrocardiographic criteria for tricyclic antidepressant sotalol intoxication. Eur J Clin Pharmacol. 1981;20:85-89.
cardiotoxicity. Am J Cardiol. 1986;57:1154-1159.
21. Valent S, Kelly P. Digoxin-induced bidirectional
3. Liebelt EL, Francis PD, Woolf AD. ECG lead aVR versus QRS ventricular tachycardia. N Engl J Med. 1997;336:550.
interval in predicting seizures and arrhythmias in acute tricyclic
antidepressant toxicity. Ann Emerg Med. 1995;26:195-201. 22. Holstege CP, Elderidge DL, Rowden AK. ECG manifestations: the
poisoned patient. Emerg Med Clin North Am. 2006;24:159-177.
4. Wolfe TR, Caravati EM, Rollins DE, et al. Terminal 40-
ms frontal plane QRS axis as a marker for tricyclic 23. Love JN, Enlow B, Howell JM, et al. Electrocardiographic
antidepressant overdose. Ann Emerg Med. 1989;18:348-351. changes associated with -blocker toxicity.
Ann Emerg Med. 2002;40:603-610.
5. Brugada P, Brugada J, Mont L, et al. A new approach to
the differential diagnosis of a regular tachycardia with a 24. Holstege CP, Baer A, Brady WJ. The electrocardiographic
wide QRS complex. Circulation. 1991;83:1649-1659. toxidrome: the ECG presentation of hydrofluoric acid
ingestion. Am J Emerg Med. 2005;23:171-176.
6. Monteban-Kooistra WE, van de Berg MP, Tulleken JE, et
al. Brugada electrocardiographic pattern elicited by cyclic 25. Doyon S, McGrath JM. Hyperphosphatemia and
antidepressant overdose. Intensive Care Med. 2006;32:281-285. cardiac arrest after insufflation of dry chemical fire
extinguisher [abstract]. Clin Toxicol. 2003;41:38.
7. Goldgran-Toledano D, Sideris G, Kevorkian JP, et al.
Overdose of cyclic antidepressant and the Brugada 26. Chih-Hsin Hsu, Ping-Yen Liu, Jyh-Hong Chen, et al.
syndrome. N Engl J Med. 2002;346:1591-1592. Electrocardiographic abnormalities as predictors of over-
the-range lithium levels. Cardiology. 2005;103:101-106.
8. Lopez-Barbeito B, Lluis M, Delgado V, et al.
Diphenhydramine overdose and the Brugada sign. 27. Graham SR, Day RO, Lee R. Overdose with
Pacing Clin Electrophysiol. 2005;27:730-732. chloral hydrate: a pharmacologic and therapeutic
review. Med J Aust. 1988;149:686-688.
9. Littmann L, Monroe MH, Kerns II WP, et al. Brugada
syndrome and “Brugada sign”: clinical spectrum with a 28. Zahedi A, Grant MH, Wong DT. Successful
guide for the clinician. Am J Heart. 2003;145:768-778. treatment of chloral hydrate cardiac toxicity with
propranolol. Am J Emerg Med. 1999;17:490-491.
10. Banta TA, St Jean A. The effect of phenothiazines on the
electrocardiogram. Can Med Assoc J. 1964;91:537. 29. Huseyin U, Cagdas O, Ahmet Murat G, et al.
Acute alcohol intake and QT dispersion in healthy
11. Nattel S, Keable H, Sasyniuk BI. Experimental amitriptyline subjects. J Stud Alcohol. 2005;66:555-558.
intoxication: electrophysiologic manifestations and
management. J Cardiovasc Pharmacol. 1984;6:83-89.

12. Boehnert M, Lovejoy FH. Value of the QRS duration
versus the serum drug level in predicting seizures and
ventricular arrhythmias after acute overdose of tricyclic
antidepressants. N Engl J Med. 1985;313:474-479.

231

Electrocardiography in Emergency Medicine

Figures

Figure 17-1.
Close-up of lead aVR from a patient with overdose of a tricyclic antidepressant, demonstrating a positive
deflection of the R wave, consistent with a rightward axis.

Figure 17-2.
Cyclic antidepressant toxicity. The ECG demonstrates the four classic ECG features: tachycardia, widening
of the QRS complexes, rightward axis, and tall R wave in lead aVR. Lead V1 also demonstrates Brugada
syndrome–type morphology.

232

ecg manifestations of drug overdose

Figures

Figure 17-3.
Propoxyphene toxicity. The ECG demonstrates Brugada syndrome–type morphology in lead V1.

Figure 17-4.
Desipramine toxicity. The presence of combined wide QRS complex and bradycardia (nearly a sine-wave
pattern) signifies a profound degree of sodium channel dysfunction.

233

Electrocardiography in Emergency Medicine

Figures

Figure 17-5.
Ziprasidone toxicity. The ECG demonstrates a markedly prolonged QT interval.

Figure 17-6.
Digoxin toxicity. The ECG demonstrates sinus tachycardia with Wenckebach conduction. The lateral precordial
leads nicely demonstrate the classic “digoxin effect”: sagging, scooping ST-segment depression immediately
following the QRS complex. This finding is commonly found in patients taking digoxin, although its presence
alone is not specific for digoxin toxicity.

234

ecg manifestations of drug overdose

Figures

Figure 17-7.
Digoxin toxicity. The ECG demonstrates an accelerated junctional rhythm with pronounced “digoxin effect” in
the inferior leads.

Figure 17-8.
Calcium channel blocker toxicity. The ECG demonstrates a junctional rhythm with occasional aberrantly
conducted beats, causing some of the QRS complexes to appear wider than others.

235

Electrocardiography in Emergency Medicine

Figures

Figure 17-9.
Severe hypocalcemia caused by phosphate exposure. The ECG demonstrates a markedly prolonged QT-
interval, causing virtual loss of the T-P segment.

Figure 17-10.
Trichloroethylene toxicity. The rhythm strip demonstrates frequent ventricular ectopy due to ventricular
irritability, caused by endogenous catecholamine release.

236

C h apter e i g h tee n

The Pediatric ECG

Ghazala Q. Sharieff, MD

A recent review of pediatric emergency recording period. The settings of the ECG must
department utilization revealed that the most be full standard, defined as 10 mm/mV with
common reasons for obtaining ECGs in children a standard paper speed of 25 mm/sec. These
are chest pain, suspected dysrhythmias, settings can be changed to elucidate certain
seizures, syncope, drug exposure, electrical features; however, a standard ECG is the only
burns, electrolyte abnormalities, and abnormal one that should be referenced to normal values.
physical examination findings.1 Of the 71 Frequently, additional right ventricular and
pediatric ECGs reviewed over a 15-month posterior left ventricular precordial leads (V3R,
period, 14 (20%) had clinical significance V4R, and V7) are included with pediatric ECGs
such as prolonged QT syndrome, ventricular to provide additional information on cardiac
hypertrophy, or premature ventricular beats.1 physiology in patients with complex congenital
A systematic approach to interpretation, with abnormalities. These leads can be ignored
special attention to rate, rhythm, axis, ventricular when evaluating most pediatric patients.
and atrial hypertrophy, and the presence of
ischemia or repolarization abnormalities, Many subtleties in the pediatric ECG are age
is helpful when reading pediatric ECGs. related. For example, fetal circulation relies
heavily on the right side of the heart; therefore,
The Normal Pediatric ECG at birth, the right ventricle is larger than the
left ventricle. Rapid changes occur over the first
There are many systematic techniques for year of life as a result of the dramatic changes
interpreting ECGs, and no one method is in circulation and cardiac physiology. During
particularly better than another. Note that the infancy, increased physiologic stress and work
electronic interpretation provided by many of the left ventricle lead to its enlargement.
ECG machines is likely to be inaccurate in By 6 months of age, the left ventricle is
children, because the machines are calibrated approximately double the thickness of the
with adult values. The interpretations are, right ventricle. After infancy, changes are more
however, reasonably accurate in calculating gradual until late adolescence and adulthood.
intervals, which are averaged over the entire
Normal ECG values in the newborn, infant,

237

Electrocardiography in Emergency Medicine

child, and adolescent are listed in Table 18-1.2-4 R wave (increased R:S ratio) in leads V1 and V2
Normal ranges for these values are categorized and a small-amplitude R wave (decreased
by age for heart rate, QRS axis, PR and QRS R:S ratio) in leads V5 and V6. As the cardiac and
intervals, and R- and S-wave amplitudes. circulatory physiology matures, the left ventricle
becomes increasingly dominant. Over time, the
Heart Rate QRS axis shifts from rightward to a more normal
In children, cardiac output is determined position, and the R-wave amplitude decreases
in V1 and V2 and increases in V5 and V6.
primarily by heart rate as opposed to stroke
volume. With age, the heart rate decreases QRS Duration
as the ventricles mature and stroke volume The QRS complex duration varies with
plays a larger role in cardiac output. Hence,
heart rates appropriate for age and activity age. In children, the QRS complex duration
must be recognized. The average resting is shorter, possibly because of their smaller
heart rate varies with age: in newborns it muscle mass, and gradually increases with
can range from 90 to 160 beats/min and in age. In neonates it measures 30 to 80 msec
adolescents from 50 to 120 beats/min. and in adolescents from 50 to 100 msec. A
QRS duration exceeding 80 msec in children
Axis younger than 8 years of age or exceeding 100
In utero, blood is shunted away from the msec in older children can be pathologic.

lungs by the patent ductus arteriosus, and the PR Interval
right ventricle provides most of the systemic The PR interval (measured as the time from
blood flow. As a result, in the newborn, the right
ventricle is the dominant chamber. In the neonate the onset of the P wave to the onset of the
and young infant (up to 2 months), the ECG QRS complex) also varies with age, gradually
shows right ventricular dominance and right axis increasing with cardiac maturity and muscle
deviation. Most of the QRS complex is composed mass. In neonates, it ranges from 80 to 150 msec
of right ventricular mass. Across the precordium, and in adolescents from 120 to 200 msec.2
the QRS complex demonstrates a large-amplitude

Table 18-1.
Pediatric electrocardiography: normal intervals. Courtesy of Ra’id Abdullah, MD, University of Chicago,
Chicago, Illinois. From: Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am. 2006;24:195-208.
Used with permission.

Age Heart rate QRS axis PR QRS R in V1 S in V1 R in V6 S in V6
(beats/min) (degrees) interval interval (mm) (mm) (mm) (mm)
1st week
1–3 weeks 9 0 –160 60 –180 (sec) (sec) 5–26 0–23 0 –12 0 –10
1–2 months 10 0 –18 0 45 –16 0 0.0 8 – 0.15 0.03–0.08 3–21 0 –16 2–16 0 –10
3–5 months 120 –18 0 30 –135 0.0 8 – 0.15 0.03–0.08 3–18 0 –15 5 –21 0 –10
6–11 months 105 –185 0 –135 0.0 8 – 0.15 0.03–0.08 3–20 0 –15 6–22 0 –10
1–2 years 110 –170 0 –135 0.0 8 – 0.15 0.03–0.08 2–20 0.5–20 6–23 0 –7
3–4 years 9 0 –165 0 –110 0.07– 0.16 0.03–0.08 2–18 0.5 –21 6–23 0 –7
5–7 years 70 –14 0 0 –110 0.0 8 – 0.16 0.03–0.08 1–18 0.5 –21 4–24 0–5
8–11 years 65 –14 0 0 –110 0.0 9 – 0.17 0.04–0.08 0.5 –14 0.5 –24 4–26 0–4
12–15 years 60 –130 -15 –110 0.0 9 – 0.17 0.04–0.08 0 –14 0.5–25 4–25 0–4
>16 years 65 –130 -15 –110 0.0 9 – 0.17 0.04–0.09 0 –14 0.5 –21 4–25 0–4
50 –120 -15 –110 0.0 9 – 0.18 0.04–0.09 0 –14 0.5–23 4–21 0–4
0.12– 0.20 0.05 – 0.10

238

the pediatric ecg

QT Interval adolescence. Upright T waves in V1 after 3 days of
age can be a sign of right ventricular hypertrophy.
Because the QT interval (measured as the
time from the beginning of the QRS complex Chamber Size
to the end of the T wave) varies greatly with
heart rate, it is usually corrected (QTc), An assessment of chamber size is important
most commonly using Bazett’s formula: when analyzing the pediatric ECG for underlying
clues to congenital heart abnormalities. P waves
QTc = QT / √R-R interval greater than 2 mm in infants and greater than
During the first 6 months of life, the 3 mm in adolescents can indicate right atrial
normal upper limit of the QTc interval is enlargement. Because the right atrium depolarizes
490 msec. Beyond this period, the normal before the left atrium, P-wave duration greater
upper limit of the QTc interval decreases than 80 msec in infants and 120 msec in
to between 440 and 460 msec, the range adolescents indicates left atrial enlargement.
normally found in older children and adults.
Right ventricular hypertrophy (RVH) is best
T Waves seen in leads V1 and V2 with an rSR', QR (no S),
or a pure R (no Q or S). RVH is also suggested by
In pediatric patients, T-wave changes on the presence of a large S wave in lead V6, upright
the ECG tend to be nonspecific and are often T waves in leads V1 through V3 after the first
a source of controversy. What is agreed on is week of life, or persistence of the right ventricular
that flat or inverted T waves are normal in the dominance pattern of the neonate. Similarly, left
newborn. In fact, the T waves in leads V1 through ventricular hypertrophy (LVH) is suggested by
V3 are usually inverted after the first week of the presence of tall R waves in lead V6, large S
life through the age of 8 years (the “juvenile” T- wave in lead V1, left ventricular “strain” pattern in
wave pattern). This pattern can persist into early leads V5 and V6, and a mature precordial R-wave

Table 18-2.
ECG criteria for ventricular and atrial hypertrophy. From: Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med
Clin North Am. 2006;24:195-208. Used with permission.

The presence of any of the following is suspicious for hypertrophy. It is not necessary for all criteria to be met.
Right ventricular hypertrophy

R wave >98th percentile in lead V1 (see Table 18-1)*
S wave >98th percentile in either lead I or lead V6 (see Table 18-1 for upper limits)
RSR' pattern in leads V1, with the R' height being >15 mm in infants <1 year of age or >10 mm in children >1 year of

age
Q wave in V1
Left ventricular hypertrophy
R-wave amplitude >98th percentile in lead V5 or V6 (see Table 18-1)
R wave <5th percentile in lead V1 or V2 (see Table 18-1)
S-wave amplitude >98th percentile in lead V1 (see Table 18-1)
Q wave >4 mm in lead V5 or V6
Inverted T wave in V6
Right atrial enlargement
Peaked P wave in leads II and V1 that is >3 mm in infants <6 months of age and >2.5 mm in infants <6 months of

age
Left atrial enlargement

P-wave duration is >0.08 seconds in a child <12 months of age or >0.10 seconds in children ≥1 year of age
Terminal or deeply inverted P wave in V1 or V3R

*qR wave pattern in V1 is seen in 10% of normal newborns.

239

Electrocardiography in Emergency Medicine

progression in the newborn period. Evidence sign of sinus node dysfunction. However, it is
of enlargement of both ventricles on the ECG important to keep in mind that the normal range
indicates biventricular hypertrophy (Table 18-2). for heart rate is higher in children (Table 18-1).

The Abnormal Pediatric ECG Supraventricular tachycardia (SVT) is the most
common symptomatic dysrhythmia in infants
Tachycardias and children. Infants with SVT typically present
with nonspecific complaints such as “fussiness,”
Tachycardias can be classified broadly poor feeding, pallor, and lethargy. Older children
into those that originate from loci above the might complain of chest pain, “pounding” in
atrioventricular (AV) node (ie, supraventricular), their chest, dizziness, or shortness of breath
those that originate from the AV node (AV and have an altered level of consciousness. The
node reentrant tachycardias), and those that diagnosis often begins in triage with the nurse
are ventricular in origin. AV node reentrant reporting that “the heart rate is too fast to count.”
tachycardias are more common in the adult
population; the vast majority of tachycardias In newborns and infants with SVT, the heart
in children are supraventricular in origin. It is rate is faster than 220 beats/min and can be as
important to record continuous ECG or rhythm fast as 280 beats/min,5 whereas in older children,
strips under specific conditions: when the child SVT is defined as a heart rate of more than 180
is in tachycardia, while medication is being beats/min. On the ECG, SVT is evidenced by
pushed, and after conversion to sinus rhythm. a narrow QRS complex tachycardia without
On recognition of a tachycardia, item-by-item discernible p waves or beat-to-beat variability
review can help clarify the ECG tracing. Is (Figure 18-1). However, the initial ECG can
it regular or irregular? Is the QRS narrow or be normal, so a 24-hour rhythm recording
wide? Does every P result in a single QRS? (Holter monitor) or an event monitor can
be necessary to document the dysrhythmia
Sinus tachycardia can be differentiated from if the patient is experiencing intermittent
other tachycardias by a narrow QRS complex and episodes. In children younger than 12 years
a P wave preceding every QRS complex. Sinus of age, the most common cause of SVT is an
tachycardia is a normal rhythm with activity accessory AV pathway; in adolescents, AV node
and exercise and can be a normal physiologic reentry tachycardia becomes more evident.4
response to stresses such as fever, dehydration,
volume loss, anxiety, and pain. A practical tip SVT can be associated with Wolff-Parkinson-
is to count the heart rate using a stethoscope White (WPW) syndrome. In patients with
rather than trying to palpate a very rapid pulse. this syndrome, SVT is generally initiated by
Sinus tachycardia that occurs at rest can be a premature atrial depolarization that travels to
the ventricles via the normal AV pathway, moves

Table 18-3.
Cyanotic congenital heart disease: time to presentation and typical ECG findings

Disorder Week of Life at Presentation ECG Finding
Transposition of the great vessels Birth–1 week RVH
Total anomalous pulmonary venous 1 week RVH
return
Tricuspid atresia 1–4 weeks LVH
Severe pulmonic stenosis 1–4 weeks RVH
Tetralogy of Fallot 1–12 weeks RVH
Truncus arteriosus Anytime in infancy BVH

LVH, left ventricular hypertrophy; RVH, right ventricular hypertrophy; BVH, biventricular hypertrophy

240