07-ElectroCardEMPrint

the pediatric ecg

retrograde through the accessory pathway, and can appear normal on the ECG but actually
reenters the AV node to start a reentrant type represent an abnormally wide QRS complex
of tachycardia.5,6 Antegrade conduction through tachycardia in an infant. The differential
the AV node followed by retrograde conduction diagnosis of wide complex tachycardia includes
through the accessory pathway produces a sinus/supraventricular tachycardia with bundle-
narrow complex tachycardia (orthodromic branch block or aberrancy, antidromic AV reentry
tachycardia)—the most common form of SVT tachycardia, ventricular tachycardia (VT), and
found in patients with WPW syndrome.5,6 Less coarse ventricular fibrillation.8 ECG findings
commonly, reentry occurs with antegrade that support the presence of VT include AV
conduction through the accessory pathway and dissociation with the ventricular rate exceeding
retrograde conduction through the AV node the atrial rate, a significantly prolonged QRS
(antidromic tachycardia) to produce a wide interval, and the presence of fusion or capture
complex tachycardia.7 Typical ECG findings beats. If there is a right bundle-branch block
of WPW syndrome are a short PR interval, (RBBB), the presence of VT is supported by a
wide QRS, and a positive inflection in the monophasic qR in V1 and a deep S wave in V6. If a
upstroke of the QRS complex, known as a delta left bundle-branch block (LBBB) is present, then
wave. The ECG in patients with SVT will not the presence of VT is supported by a notched
show the delta wave, because tachycardia is S wave and an R-wave duration of more than
mediated through the accessory pathway only 30 msec in V1 and V2 and a Q wave in V6.8
(Figure 18-2). Episodes of SVT in children
with WPW syndrome usually occur early in Conduction Abnormalities
the first year of life.7 These episodes often
resolve during infancy but can recur later in All degrees of AV block can occur in pediatric
life, usually between 6 and 8 years of age.7 patients. It is important to remember that the
normal PR interval in infants is shorter and
Atrial ectopic tachycardia can be differentiated lengthens as cardiac tissue matures with age.
from SVT by the presence of different P-wave Thus, a “normal appearing” PR interval of 200
morphologies. Each P wave is conducted to msec can in fact, represent a pathologic first-
the ventricle, and since the ectopic atrial focus degree AV block in an infant or a young child.
is faster than the SA node, the ectopic focus
determines the ventricular rate (Figure 18-3). Complete heart block is a common cause of
significant bradycardia in pediatric patients and
Although SVTs are more common than can be acquired or congenital (Figure
those of ventricular origin, it is important to 18-4). Causes of congenital heart block include
remember that the normal QRS complex is structural lesions such as transposition of the
shorter in duration in children than in adults. great arteries and maternal connective tissue
As a result, a QRS complex width of 90 msec disorders. Acquired heart block can result

Table 18-4.
Acyanotic congenital heart disease resulting in congestive heart failure: time to presentation and typical ECG
findings

Disorder Week of Life at Presentation ECG Finding
Hypoplastic left heart Within 1st week RVH
Coarctation of the aorta Within 1st week RVH/LVH
Complete AV canal 2–3 weeks BVH or LVH
Patent ductus arteriosus 2–3 weeks LVH
Ventricular septal defect 2–12 weeks LVH

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

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Electrocardiography in Emergency Medicine

from disorders such as Lyme disease, systemic Congenital Heart Disease
lupus erythematosus, muscular dystrophies,
Kawasaki disease, and rheumatic fever.9 Congenital heart disease occurs in 8 of 1,000
live births. Many of the structural congenital
Bundle-branch blocks can be present when heart diseases manifest during the neonatal
there is QRS complex prolongation that is period.10 The signs and symptoms of congenital
abnormal for a given age. RBBB occurs with heart disease can be nonspecific. Infants can
abnormal rightward and anterior terminal present with tachypnea, sudden onset of cyanosis
forces, frequently manifesting on the ECG as an or pallor that can worsen with crying, sweating
rSR' pattern in leads V1 and V2. RBBB is more with feeds, lethargy, or failure to thrive.11
common than LBBB and can be seen after surgical
repair of congenital heart defects, particularly Congenital heart disease lesions that present
ventricular septal defect repairs. Similarly, LBBB in the first 2 to 3 weeks of life are typically
is seen with abnormal leftward and posterior ductal dependent. The ductus arteriosus has
forces, best appreciated in leads V5 and V6. been sustaining blood flow for these infants,
However, because LBBB is rare in children, its and when the ductus closes anatomically at 2 to
presence should raise the possibility of WPW 3 weeks of life, these infants suddenly become
syndrome, which can mimic an LBBB pattern. ill. Depending on the underlying structural
abnormality, these neonates present with either
sudden cyanosis or signs of cardiovascular
collapse. They have been dependent on the

Table 18-5.
Common ECG findings associated with specific congenital heart diseases. Courtesy of Ted Chan, MD,
University of California, San Diego. From: Sharieff GQ, Rao SO. The pediatric ECG. Emerg Med Clin North Am.
2006;24:195-207. Used with permission.

RVH LVH Right atrial Left atrial Right axis Left axis RBBB
+ enlargement enlargement deviation deviation
+ +
Patent ductus (older child) + + + +
arteriosus +
++ (newborn) + +
Atrial septal + + (after
defect ++ + repair)
(newborn) (older child)
Ventricular +
septal defect +
Coarctation of
the aorta
Tetralogy of
Fallot

Transportation + + +
of the great + + +
arteries +
Tricuspid atresia + +
Pulmonary
atresia
Hypoplastic left
heart syndrome
Aortic stenosis

Pulmonary
stenosis

242

the pediatric ecg

ductus arteriosus to supply blood to either the chamber enlargement as a result of the congenital
lungs, as with tetralogy of Fallot and tricuspid defect. Table 18-5 lists the common ECG findings
atresia, or to the systemic circulation as in the associated with specific congenital heart diseases.
case of coarctation of the aorta and hypoplastic
left heart syndrome. The main causes of cyanotic Hypertrophic Cardiomyopathy
congenital heart disease are tetralogy of Fallot,
tricuspid atresia, transposition of the great Most cases of hypertrophic cardiomyopathy
arteries, truncus arteriosus, total anomalous are diagnosed in patients between 30 and 40
pulmonary venous return, and pulmonary years of age, but 2% of cases occur in children
atresia or stenosis. Time of presentation younger than 5 years of age and 7% in children
for cyanotic and acyanotic congenital heart under 10 years of age.17 The clinical presentation
diseases and the common associated ECG varies, with patients experiencing chest pain,
findings are listed in Tables 18-3 and 18-4.12-14 palpitations, shortness of breath, syncopal
or near syncopal episodes, or sudden death.
Left-to-right intracardiac shunts such as Children with hypertrophic cardiomyopathy
ventricular septal or AV canal defects constitute who experience syncope are at significant risk for
the other class of congenital cardiac lesions that sudden death. The hallmark anatomic finding in
present in the first month of life. As the normal these patients is an asymmetric, hypertrophied,
pulmonary vascular resistance falls during the nondilated left ventricle with greater involvement
first month of life, any preexisting left-to-right of the septum than the ventricle itself.
shunt will see a gradual increase in flow across
the shunt, resulting in congestive heart failure. ECG findings include left atrial enlargement
The differential diagnosis of congenital heart and LVH, ST-segment abnormalities, T-wave
diseases that cause congestive heart failure inversions, Q waves, and diminished or absent
includes not only the left-to-right intracardiac R waves in the lateral leads. Premature atrial
shunts but also hypoplastic left heart syndrome, and ventricular contractions, SVT, multifocal
coarctation of the aorta, tricuspid atresia, ventricular dysrhythmias, and new-onset
endocardial cushion defect, patent ductus atrial fibrillation can also be present.
arteriosus, aortic stenosis, interrupted aortic
arch, aortic atresia, and mitral valve atresia.15,16 Myocarditis

An ECG should be obtained in all infants Myocarditis is an inflammatory condition of
suspected of having a congenital heart disease. the myocardium. Although there are numerous
Although the ECG will not make the diagnosis, it causes, including infectious, drug-induced,
can show evidence of conduction abnormalities or endocrine, radiation-induced, and collagen
vascular diseases, the most common etiology in
North America is viral (coxsackie A and B, ECHO

Key Facts

• Right axis deviation is the norm in neonates and young infants; the axis assumes a leftward
direction as the left ventricle enlarges.

• The top-normal QRS duration is 80 msec in children younger than 8 years. Ventricular tachycardia,
therefore, can present in young children with QRS durations as low as 80 to 90 msec.

• Newborns and infants can manifest sinus tachycardia with heart rates as high as 200 to 220
beats/min.

• T-wave inversions in leads V1 through V3 are common and normal from infancy through
adolescence.

• Tachycardia faster than expected for the degree of fever is classic in myocarditis, although
ventricular dysrhythmias, advanced AV blocks, and low-voltage QRS complexes are also common.

243

Electrocardiography in Emergency Medicine

viruses, and influenza viruses).18,19 The clinical 5. Perry JC. Supraventricular tachycardia. In: Garson
presentation varies depending on multiple factors, A Jr, Bricker JT, Fisher DJ, et al, eds. The Science and
including the cause and the age of the patient. Practice of Pediatric Cardiology. 2nd ed. Baltimore,
Neonates and infants can present with symptoms MD: Lippincott Williams & Wilkins; 1998.
such as lethargy, poor feeding, irritability, pallor,
fever, and failure to thrive. Symptoms suggestive 6. O’Laughlin MP. Congestive heart failure in children.
of heart failure (eg, diaphoresis with feeding, Pediatr Clin North Am. 1999;46(2):263-273.
rapid breathing, and respiratory distress) can
also be present. Older children and adolescents 7. Gewitz MH, Vetter VL. Cardiac emergencies. In: Fleisher GR,
can present similarly and might complain of Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 4th ed.
weakness and fatigue, particularly on exertion. Philadelphia, PA: Lippincott Williams & Williams; 2000.
With viral myocarditis, the patient might have
a recent history of a nonspecific viral syndrome 8. Silka M. Emergency management of arrhythmias. In: Deal
type illness. Signs of poor cardiac function, B, Wolff G, Gelband H, eds. Current Concepts in Diagnosis
including signs of congestive heart failure, and Management of Arrhythmias in Infants and Children.
can be present on physical examination. New York, NY: Futura Publishing; 1998:319-322.

Multiple ECG findings can be present. Sinus 9. Fitzmaurice L, Gerardi MJ: Cardiovascular system. In: Gausche-
tachycardia is the most common dysrhythmia. Hill M, Fuchs S, Yamamoto L. The Pediatric Emergency Medicine
A tachycardia faster than expected for the Resource. 4th ed. Sudbury, MA: Jones & Bartlett Publishers; 2004.
degree of fever (10 beats/min for each degree of
temperature elevation) can indicate myocarditis. 10. McCollough M, Sharieff G. Common complaints in the first
Many other dysrhythmias are associated with month of life. Pediatr Emerg Med Clin North Am. 2002;20:27-48.
myocarditis, including junctional tachycardias,
ventricular ectopy, ventricular tachycardias, 11. Savitsky E, Alejos J, Votey S. Emergency department
and even second- and third-degree AV presentations of pediatric congenital heart
blocks. Morphologically, there can be T-wave disease. J Emerg Med. 2003;24:239-245.
flattening or inversion and low QRS complex
voltage less than 5 mm in all limb leads. 12. Woolridge D, Love J. Congenital heart disease in the pediatric
emergency department: pathophysiology and clinical
References characteristics. Pediatr Emerg Med Reports. 2002;7:69-80.

1. Horton L, Mosee S, Brenner J. Use of the 13. Sharieff G, Wylie T. Pediatric cardiac disorders.
electrocardiogram in a pediatric emergency department. J Emerg Med. 2004;26:65-79.
Arch Pediatr Adolesc Med. 1994;148:184-188.
14. Flynn P, Engle M, Ehlers K, et al. Cardiac issues in the pediatric
2. Park MK, Guntheroth WG. How to Read Pediatric ECGs. emergency. Pediatr Clin North Am. 1992;39:955-983.
3rd ed. St Louis, MO: Mosby-Year Book; 1992.
15. DiMaio AM, Singh J. The infant with cyanosis in the
3. Park MK, George R. Pediatric Cardiology for Practitioners. emergency room. Pediatr Clin North Am. 1992;39;987-1006.
4th ed. St Louis, MO: Mosby; 2002:34–51.
16. Wigle ED, Rakowski H, Kimball BP, et al.
4. Robinson B, Anisman P, Eshagh E. A primer on Hypertrophic cardiomyopathy: clinical spectrum
pediatric ECGs. Contemporary Pediatr. 1994;11:69. and treatment. Circulation. 1995;92:1680-1692.

17. Jouriles N. Pericardial and myocardial disease. In:
Marx JA, Hockberger RS, Walls RM, eds. Rosen’s
Emergency Medicine Concepts and Clinical Practice.
5th ed. St Louis, MO: Mosby; 2002:1143-1144.

18. Li MM, Klassen TP, Watters LK. Cardiovascular
disorders. In: Barkin RN, Caputo GL, Jaffe DM, et al,
eds. Pediatric Emergency Medicine Concepts and Clinical
Practice. 2nd ed. St Louis, MO: Mosby; 1997.

19. Kopeck SL, Gersh BJ. Dilated cardiomyopathy and
myocarditis: natural history, etiology, clinical manifestations,
and management. Curr Probl Cardiol. 1987;12:569-647.

Editor’s Note: This chapter has been adapted with permission
from: Sharieff GQ, Rao SO. The Pediatric ECG. Emerg Med Clin
North Am. 2006;24:195-208. Copyright 2006, Elsevier, Inc.

244

the pediatric ecg

Figures

Figure 18-1.
SVT with concomitant RVH. This 4-year-old boy was postoperative from repair of congenital heart disease
(Fontan repair). He was eventually converted to normal sinus rhythm after multiple doses of adenosine. Image
courtesy of Stephanie Doniger, MD, Children’s Hospital San Diego.

Figure 18-2.
WPW syndrome. This child presented in SVT. After his rhythm was converted to sinus rhythm, the delta waves
were apparent. The delta wave is a positive inflection in the upstroke of the QRS complex. Image courtesy of
CDR Jonathan T. Fleenor, MD, Naval Medical Center, San Diego.

245

Electrocardiography in Emergency Medicine

Figures

Figure 18-3.
Atrial flutter. This ECG is from a child who had a Fontan repair for hypoplastic left heart. Image courtesy of
CDR Jonathan T. Fleenor, MD, Naval Medical Center San Diego.

Figure 18-4.
Complete heart block. This ECG is of an infant presenting at birth with complete heart block. Notice
the complete dissociation of P waves from QRS complexes. The child’s mother had systemic lupus
erythematosus, which is commonly associated with complete heart block. Image courtesy of CDR Jonathan T.
Fleenor, MD, Naval Medical Center San Diego.

246

Index

Page references followed by “f” indicate figure and by”t” indicate table.

A acute reperfusion therapy, 3
AAI pacing, 181 acyanotic congenital heart disease, 241f
accessory pathways additional leads, indications for, 98
adenosine
antidromic, 60
in children, 240 AV conduction in response to, 57f, 58f
concealed, 156–157 indications, 52
orthodromic, 60 trial dose, 64
wide complex tachycardia and, 60 advanced emergency medical services, 73
acebutolol, 228 agonal idioventricular rhythms, 29
acute cardiac ischemia, 140f, 151f alcohol intoxication, 230
acute coronary syndrome (ACS), 73–94 altered mental status, 8
differential diagnosis, 1 American College of Cardiology guidelines, 179
ECG changes in, 74–81 American Heart Association guidelines, 63, 107, 179
hospital discharge statistics, 73 aminoglycosides, 229
indications of, 3 amiodarone, 159
mimics of, 119–131, 133–140 andromedotoxin, 223
risk stratification, 3–4 aneurysms
acute myocardial infarction (AMI) anterior wall, 92f
anterior, 3, 77–78 left ventricular, 120, 128f
atrioventricular block in, 31 ventricular, 79
diagnosis of, 79f, 184–185 angina with T-wave inversion, 77
ECG correlates of prognosis, 4 anomalous pulmonary venous return, 243
ECG diagnosis, 183t anterior wall aneurysms, 92f
fibrinolytic therapy, 3 anticonvulsants, 229
inferior, 3 antidromic accessory pathways, 60
isolated posterior, 3 aortic dissection, 206–207, 212
lateral, 103f aortic stenosis, 242t
left bundle-branch block and, 80, 129f apical hypertrophic cardiomyopathy, 123
location of, 78t arrhythmias. see also specific arrhythmias
masked ECG abnormalities in, 9 congenital syndromes, 166t
new ECG technologies, 105–118 in myocarditis, 145
posterior, 78–79 in pericarditis, 143
with right bundle-branch block, 20f arrhythmogenic right ventricular dysplasia (ARVD), 124
in setting of paced rhythm, 94f, 192f characterization, 170
Sgarbossa criteria, 79f diagnosis, 166t, 170–171
ST-segment elevation in, 37f, 150f ECG characterization, 166t, 170–171, 176f
WPW pattern in, 162f genetic factors, 166t, 170
acute myocardial ischemia, 105–118 treatment, 166t, 171

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Electrocardiography in Emergency Medicine

arterial septal defects, 242t use of, 159
Ashman phenomenon, 60 benzothiazepine (diltiazem), 227
atrial ectopic tachycardia, 241 bidirectional ventricular tachycardia, 68f
atrial fibrillation, 55f bisphosphonates, 229
biventricular pacing, 181, 188f
with accessory pathway, 62, 66f, 68f blood supply, myocardial, 88f
with bradycardic ventricular response, 29, 37f body position effects, 115f
capture beats, 69f body surface mapping, 79, 107–110
causes of, 47t
characterization, 48 in acute isolated posterior MI, 118f
clinical significance of, 157 clinical applications of, 109
conduction, 66f color contour maps, 118f
in COPD, 209 data display, 108–109
ECG characteristics, 48t torso contour maps, 108t
fusion beats, 69f bradycardias, 27–29
hyperthyroidism and, 196 above 45 beats/min, 27, 33
rapid ventricular rates in, 190f atrial fibrillation and, 29
slow ventricular rhythm in, 33 definition, 27
in WPW syndrome, 158–159, 163f drug-induced, 230
atrial flutter, 48–49, 49t, 57f, 159 drugs that induce, 229t
atrial tachycardia, 45, 55f ECG manifestations, 27–28
atriofascicular tract, 155 escape pacemakers, 28–29
atrioventricular blocks sinus, 28
2:1, 41f in sodium channel blocker toxicity, 223
atrial tachycardia with, 55f toxic ingestion and, 227
causes of, 30t treatment of, 34
in children, 241–242 types of, 28t
complete, 32, 43f Brechenmacher tract, 155
ECG findings, 29t British Pacing and Electrophysiology Group, 179
first-degree, 12f, 30, 33, 37f broad complex tachycardias. see wide complex
high-grade, 42f
in myocarditis, 145 tachycardias
second-degree, 30–32, 38f, 41f, 42f Brugada algorithm, 63
Brugada pattern, 204, 224, 233f
high-grade, 42f Brugada syndrome, 5
Mobitz type I, 30, 38f
Mobitz type II, 30, 31, 33, 39f age of diagnosis, 166
non-Wenckebach, 39f description, 224
types of, 31t diagnosis, 166t, 167
Wenckebach, 38f ECG characteristics, 124, 166t, 167t, 174f
sinus arrest, 44f genetic factors, 166t
in sodium channel blocker toxicity, 223 sudden cardiac death and, 165–167
third-degree, 29, 33 treatment, 166t, 167
in toxic ingestion, 6 types of, 167, 167t
atrioventricular dissociation, 27, 32, 62–63, 71f bundle-branch blocks. see also left bundle-branch block
atrioventricular heart blocks, 30–31, 31–32, 32
2:1, 31, 41f (LBBB); right bundle-branch block (LBBB)
atrioventricular junctional escape rhythm, 28–29, 36f in children, 242
atrioventricular junctional tachycardias, 62–63 QRS widening, 18
atrioventricular nodal blocking agents, 63, 64 recognition of, 14–16
atrioventricular node conduction, 13 C
atrioventricular node reentrant tachycardia (AVNRT), 45 Cabrera sign, 123
description, 49–50 calcium channel blockers
ECG characteristics, 50t indication, 52
mechanism, 53f toxicity, 34, 227, 235f
termination, 52 use of, 159
atrioventricular reentrant tachycardia (AVRT), 45 capture beats, 62, 69f
antidromic, 158, 163f carbon tetrachloride, 230
clinical significance, 158 cardiac enzymes, diagnostic use of, 74
orthodromic, 158, 163f cardiac glycosides, 226
via an accessory pathway, 50, 50t, 52 cardiac resynchronization, 181, 188f
atropine, 34 cardiac tamponade, 145–147
B cardiorespiratory arrest, 8
β-agonists, 228 cardioversion
β - blockers ECG characteristics, 124
in hypertrophic cardiomyopathy, 169 emergent, 64
indication, 52 use of, 159
toxicity, 34, 227–228 carvedilol, 228
central nervous system events, 209–211, 213
248 cerebrovascular disease, 136–137

chamber sizes, in children, 239–240 index
chest pain
E
anterior wall aneurysm and, 92f early repolarization, 131f
malpractice losses and, 74t
rule-out MI protocols, 2, 3–4 normal variant, 124–125
with ST segment changes, 113f ST-segment elevation in, 112f
chest radiographs, 4–5 T-wave inversion and, 137–138
chloral hydrate, 230 echocardiography, 79, 141, 145
chloroform, 230 electrical alternans, 146–147, 153f, 161f
chloroquine, 228 electrical injuries, 211t, 212–213
cholecystitis, 210t, 211 electrocardiography
chronic obstructive pulmonary disease (COPD), 12-lead

207–208, 208t, 213, 219f in chest pain, 3–4
clinical judgment, need for, 9 in lateral AMI, 103f
clinical presentation normal, 12f
15-lead, 77t, 99
components of, 1–2 15-lead on a 12-lead machine, 99
interpretation of ECGs and, 2 80-lead, 116f, 117f
coarctation of the aorta, 242–243, 242t additional-lead testing
cocaine overdose, 224 indications for, 98t
complete heart block limitations of, 98–99
in myocarditis, 152f additional-lead testing in, 95–104
P waves in, 27 clinical applications of, 2t
concealed accessory pathways, 156–157 clinical scenarios, 2–8
concertina effect, 157, 161f diagnostic limitations, 105–106
conduction abnormalities, intraventricular, 13–25 disposition issues and, 1
congenital arrhythmic syndromes, 166t impact in emergency departments, 1–12, 10f
congenital heart diseases indications for, 10f
ECG findings, 242t interpretation of, 9
incidence of, 242 limitations of, 8–9
continuous ST-segment monitoring new technologies, 105–118
clinical application, 106 pediatric, 237–246
false alarms, 107, 110, 114f prehospital, 73
introduction of, 106 electrolyte imbalances, 193–196, 211
with ST-segment changes, 113f encainide overdose, 224
technology, 106–107 endocardial cushion defects, 243
troubleshooting, 110 endocardial fibroelastosis, 156
underutilization of, 107 epigastric pain, 211
in unstable angina, 114f epinephrine, indications, 34
cor pulmonale, 208 Epstein anomaly, 156
coronary arteries, 88f escape pacemakers
coronary artery infarction, 78t ECG manifestations, 28–29
cyanotic congenital heart disease, 240t rhythms in, 28t
D escape rhythms
DDD pacing, 181, 187f, 190f AV junctional, 28–29, 28t, 36f
decision making idioventricular, 28t, 29, 36f
in the emergency department, 1–12 ethanol intoxication, 230
risk stratification and, 3–4 ethylene glycol, 229
defibrillation in unstable patients, 64 external pacemakers, 34
delta waves, 157, 160f, 162f F
desipramine toxicity, 233f failure to capture, 189f
digitalis effect, 112f, 230 fascicular blocks, 16–18
226-227 ECG criteria, 16t, 17t
digitalis toxicity, 68f, 134–135, 139f left anterior, 16–17, 16t
digoxin, use of, 159 left posterior, 17–18
digoxin effect, 235f fibrinolysis
digoxin toxicity, 52, 226–227, 234f, 235f door-to-needle time, 73
dihydropyridine, 227 indications for, 3
diltiazem (benzothiazepine), 227 Fibrinolytic Therapy Trialists Collaborative Group, 3
diphenhydramine overdose, 224 flecainide overdose, 224
disopyramide, 169 Fleet enema, 229
dissections, thoracic artery, 206–207 focal atrial tachycardia
door-to-ECG time, 73 characterization, 47–48
dopamine, indications, 34 ECG characteristics, 47t
drug overdoses, 223–236 mechanism, 53f
dyspnea, ECGs in, 4–5 fusion beats, 62, 69f
dysrhythmias, types of, 27 G
gastric dilation, 210t, 211

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Electrocardiography in Emergency Medicine

gastrointestinal disorders, 211, 213 ischemia
glucagon, indications for, 34 early stages of, 84f
grayanotoxins, 223 patterns of, 74
H patterns of necrosis, 76–77
halogenated hydrocarbons, 230 prolonged, nonperfused, 85f
heart, blood supply, 88f reperfusion and, 77
heart blocks, 29–34 ST-segment depression in, 112f
subendocardial, 76
acquired, 241–242 symptom onset and, 75t
complete, 241 T waves from, 83f
second degree, 27
sick sinus syndrome, 34 J
types of, 29 James fibers, 155
heart catheterization, 145 junctional tachycardia, 45
heart failure, 181, 188f juvenile T-wave patterns, 137–138, 140f
heart rate, in children, 238, 238t K
“holiday heart,” 230 Kawasaki disease, 242
hydrofluoric acid, 229 Kent bundle, 155, 160f
hyperkalemia Kindwall algorithm, 63
causes of, 228t L
diagnosis of, 8 labetalol, 228
ECG characteristics, 124, 193–195, 198f, 199f, 200f leads, 102f, 104f
presentation, 228–229 left anterior descending coronary artery, 77, 88f, 93f,
ST-segment elevation in, 112f
hyperthyroidism, 156, 196 120
hypertrophic cardiomyopathy (HCM), 167–170 left anterior fascicular blocks, 16–17, 16t, 24f, 25f
in children, 243 left atrial enlargement, 239t
clinical presentation, 167–168 left bundle-branch block (LBBB)
diagnosis, 166t, 168–169
ECG characteristics, 175f acute myocardial infarction with, 129f
ECG characterization, 166t AMI in setting of, 79f
genetic factors, 166t, 167–168 differential diagnosis, 15t
treatment, 166t, 169 ECG characteristics of, 122–123
WPW pattern and, 156 ECG criteria for, 16t
hypocalcemia, 236f incomplete, 16, 23f
drug-induced, 229 ischemia and, 93f
ECG characterization, 195, 201f myocardial infarction with, 80–81
hypokalemia new, 3
causes of, 228t QRS axis deviation, 16
drug-induced, 228–229 slurred R wave, 15, 23f
ECG characteristics, 194–195 ST-segment depression in, 112f, 134, 139f
ECG characterization, 201f ST-segment elevation in, 112f
hypoplastic left heart syndrome, 242–243, 242t left circumflex coronary artery, 88f, 96
hypothermia left posterior fascicular blocks, 17–18, 17t, 24f, 25f
ECG findings in, 195, 203–204, 204t, 212, 216f, 217f left ventricle, posterior infarction, 96
ST-segment elevation in, 125–126 left ventricular aneurysm (LVA), 120, 128f
hypothyroidism, 196–197 left ventricular hypertrophy (LVH)
I ECG characteristics, 105, 123–124, 130f
idioventricular escape rhythms, 28t, 29, 36f ECG correlates of prognosis, 4
infarction with ischemic changes, 130f
area of, 77–78 pediatric ECG criteria, 239, 239t
posterior, 90f ST-segment depression in, 112f, 133–134, 139f
right ventricular, 79 ST-segment elevation in, 112f
size of, 78 lightning strikes, 212–213
inferior wall infarction, 91f lithium overdose, 229–230
intermittent preexcitation, 157, 161f local anesthetic effect. see sodium channel blocker
International Registry of Acute Aortic Dissections, 206
intestinal obstruction, 210t, 211 toxicity
intracardiac shunts, 243 long QT interval
intracranial hemorrhage, 140f
intracranial lesions, 136–137 diagnosis, 166t
intracranial pressure (ICP), 211 ECG characterization, 166t
intraventricular conduction abnormalities, 13–25 genetic factors, 166t
causes of, 13t presentations, 5
features, 13 treatment, 166t
hyperthyroidism and, 196 long QT syndrome
nonspecific, 18–19 characterization, 172
diagnostic criteria, 169t
250 ECG findings, 172, 177f
genetic factors, 172

in hypothyroidism, 196–197 index
nongenetic causes of, 170t
treatment, 172 QRS axis, 238, 238t
low voltage QRS complexes with SVT, 240
ECG findings, 202f nitrate-induced hypotension, 96
in hypothyroidism, 197 non–Q wave myocardial infarction, 74, 76–77
in myocarditis, 146, 152f non-ST-segment elevation MI (NSTEMI), 74, 86f
in pericardial effusion, 153f non-Wenckebach heart block, 27
Lown-Ganong-Levine (LGL) syndrome, 155, 157 nonparoxysmal junctional tachycardia, 49, 49t, 53f
Lyme disease, 145, 241–242 North American Society of Pacing and
M
magnesium, 64, 195–196 Electrophysiology, 179
magnets, in pacemaker assessment, 182t, 183–184, O
orthodromic accessory pathways, 60
191f Osborn wave, 204, 216f
Mahaim fibers, 155 oversensing, 181t, 182, 189f
malpractice losses, 74t oxprenolol, 228
membrane stabilizing effect. see sodium channel P
P waves, 27, 51
blocker toxicity pacemaker dysfunction, 179–192
metabolic abnormalities, 193–202
mitral valve prolapse, 156 approach to, 184
Mobitz type I atrioventricular block, 30 failure to capture, 189f
Mobitz type II atrioventricular block, 31 irregularity of rate, 183
monomorphic ventricular tachycardia, 61, 67f, 72f oversensing, 181t, 189f
multifascicular blocks, 18 pacing failure, 182
multifocal atrial tachycardia, 56f pseudomalfunctions, 183
rapid ventricular rates, 183, 190f
in COPD, 209 undersensing, 181t, 189f
description, 48 pacemakers, 179–192
ECG characteristics, 48 AAI pacing, 181
multifocal ventricular tachycardia, 61 assessment with magnets, 183–184, 191f
muscular dystrophies, 242 biventricular pacing, 188f
myocardial infarction (MI) common modes, 181–182
acute, inferior, 128f components of, 179
acute, isolated posterior, 117f, 118f DDD pacing, 181, 187f
anterior, 83f, 112f dual-chamber function, 186f
assessment protocol, 1 failure to capture, 182–183, 182t
hospital discharge statistics, 73 magnets, uses of, 182t
inferior, 102f, 112f, 162f modes of, 179–180
with left bundle-branch block, 80–81 nomenclature, 179–180, 180t
posterior, 90f, 97, 112f normally paced complexes, 180–181, 184
with right bundle-branch block, 79 output failure, causes of, 182t
transmural, 120 pacing failure, 182–184
ventricular aneurysm and, 79 rate-adaptive, 181–182
myocarditis VVI pacing, 181
acute, 121–122 pancreatitis, 210t, 211
causes of, 144 paroxysmal supraventricular tachycardia, 45, 48, 158
in children, 243–244 partial agonist activity, 228
complete heart block, 152f patent ductus arteriosus, 242, 242t
ECG characteristics, 144–145, 146t, 147 pediatric electrocardiography, 237–246
low voltage in, 146 normal, 237–240
presentation of, 144 penbutolol, 228
right bundle-branch block in, 152f percutaneous coronary interventions, 3
signs and symptoms, 146t pericardial effusion
sinus tachycardia in, 151f, 152f causes of, 146
N ECG characteristics, 145–147, 146t, 152f, 153f
narrow complex tachycardias, 45–58 pericarditis
characteristics, 46t acute, 121–122, 149f
definition, 45 arrhythmias in, 143
diagnosis, 50–52, 51t causes of, 142t
evaluation, 50–52 ECG characteristics, 141–144, 144t, 147, 149f
mechanisms, 46t localized, 150f
sinus rhythm, 54f signs and symptoms, 143t
types of, 46t ST-segment elevation in, 112f
without P waves, 58f stages of, 138, 145t
necrosis, patterns of, 76–77 T-wave inversion and, 138, 140f
negative inotropes, 96, 169 phenylalkylamine (verapamil), 169, 227
neonates pneumothorax, 207, 207t, 213
poisoning. see toxic ingestion

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polymorphic ventricular tachycardia, 61 loss of progression, 85f
posterior myocardial infarction, 96 rate-related bundle-branch block, 60
posterior ventricular infarction, 96–97 rheumatic fever, 242
potassium levels. see hyperkalemia; hypokalemia rheumatic heart disease, 156
potassium rectifier current inhibition, 225–226, 230 right atrial enlargement, 239t
potassium rectifier current inhibitors, 226t right bundle-branch block (RBBB)
PR-interval, pediatric, 238, 238t
PR-interval prolongation, 6 aberrant conduction in, 60
precordial concordance, 62, 70f acute myocardial infarction with, 20f
preexcitation anterolateral STEMI and, 92f
ECG criteria for, 15t
in alternate beats, 161f features of, 14–15
definition, 155 incomplete, 22f, 174f
intermittent, 157 left posterior fascicular blocks plus, 25f
Kent bundle and, 160f myocardial infarction with, 79
preexcitation alternans, 157 in myocarditis, 152f
preexcitation syndromes, 137, 159 notched R-wave variant, 15, 21f
prehospital electrocardiography, 73 qR variant, 14–15, 21f
premature atrial complexes (PACs), 35f QRS complex morphology, 63
premature atrial complexes (PACs), blocked, 33 rSR’ variant, 14, 20f
primary percutaneous interventions (PPCI), 73 ST-segment depression in, 112f
Prinzmetal angina, 119–120 ST/T-wave complex, 14, 20f
procainamide wide complex tachycardia and, 71f
indications, 63 right coronary artery, 88f, 96
overdose, 224 right ventricular dysplasia, 168t
treatment with, 68f right ventricular hypertrophy (RVH)
use of, 159 pediatric ECG criteria, 239, 239t
propoxyphene toxicity, 233f ST-segment depression in, 112f
propranolol, 228 right ventricular infarction, 96
pseudoinfarction patterns, 157, 162f, 211 risk stratification, 3–4
pulmonary atresia, 242t, 243 rule of appropriate discordance, 134
pulmonary emboli (PE) S
differential diagnosis, 4–5 “Salvador Dali” effect, 134
ECG characteristics, 5, 123, 204–206, 204t, 212, San Francisco Syncope Rule, 6
saxitoxin, 223
217f, 218f SCN5A gene mutations, 166
symptoms, 4–5 Sgarbossa criteria, 79f, 80, 81
T-wave inversion and, 136, 140f sick sinus syndrome, 34
pulmonary stenosis, 242t, 243 sinuatrial blocks, 32–34
Q complete, 34
Q waves incomplete, 33
formation of, 76–77, 85f sinuatrial node, 13
pathologic, 76–77, 77t, 89f sinus arrest, 44f
in precordial leads, 76t sinus bradycardia, 35f
QRS axis in neonates, 238, 238t ECG manifestations, 28
QRS complex first-degree AV block and, 37f
axis in neonates, 238 hypothyroidism and, 196
axis in ventricular tachycardia, 63 in toxic ingestion, 6
color coding in body surface mapping, 118f sinus rhythm, 163f
duration in neonates, 238, 238t narrow complex tachycardia, 54f
duration in ventricular tachycardia, 63 normal, 12f, 53f
hybrid in ventricular tachycardia, 62 sinus tachycardia
morphology, 63 characterization, 47
in toxic ingestion, 6 in COPD, 209
QRS complex widening diagnosis, 51
in bundle-branch blocks, 18 in myocarditis, 145, 151f, 152f
in left bundle-branch block, 16, 23f in pericardial effusion, 153f
in right bundle-branch-block, 14 in pericarditis, 143
in toxic ingestion, 6 preexcitation in, 156
QT dispersion, 226 in toxic ingestion, 6
QT-interval prolongation, 6, 225–226. see also long-QT sodium bifluoride, 229
sodium channel blockade. see sodium channel blocker
syndrome
QT interval, in children, 239 toxicity
quinidine-like effect. see sodium channel blocker toxicity sodium channel blocker toxicity, 233f
R
R:S ratios, in bundle-branch block, 14–15 bradyarrhythmias, 225
R waves causes of, 223
ECG findings, 224–225, 230
elevation, 14f

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intraventricular conduction and, 224–225 index
ventricular dysrhythmias in, 225
sodium channel blockers, 224t stroke, T-wave inversion and, 136–137
sodium fluoride, 229 subarachnoid hemorrhage (SAH)
sodium ion channels, 166
sodium phosphate, 229 ECG findings, 208t, 209–211, 219f, 220f, 221f
sodium-potassium ATPase inhibition, 226–227, 230 ST-segment depression in, 112f
sodium-potassium ATPase inhibitors, 226t subendocardial ischemia, 76, 86f
sotalol, 228 sudden cardiac death (SCD)
ST segment inherited syndromes of, 165–177
color coding in body surface mapping, 118f in ischemic heart disease, 165
nonspecific changes, 117f sudden unexplained nocturnal death syndrome. see
progressive changes, 113f
stabilization, 75 Brugada syndrome
ST-segment depression supraventricular tachycardia (SVT)
80-lead ECG, 117f
ACS mimics, 133–135 causes, 60t
ACS prognosis and, 80 in children, 240
area of infarction and, 76, 76t in COPD, 209
body position and, 115f definition, 45
causes of, 112f, 133t, 139f mechanisms of, 53f
digitalis effect, 134–135 in pericarditis, 143
isolated precordial, 95 precordial concordance, 62
in leads V1 to V3, 103f QRS complex morphology, 63
in left bundle-branch block, 134 ventricular tachycardia versus, 61–63
in left ventricular hypertrophy, 133–134 syncope
in posterior infarction, 90f ECG correlates of prognosis, 5–6
right precordial, 3 indications for ECGs, 5–6
subendocardial ischemia and, 76, 86f systemic lupus erythematosus, 241-242
T-wave inversion and, 135–138 T
in toxic ingestion, 6 T-wave inversion, 85t
in UA/NSTEMI, 86f biphasic, 89f
ST-segment elevation causes of, 112f, 135t, 140f
in ACS mimics, 119–131 early repolarization and, 137–138
in acute myocardial infarction, 37f intracranial lesions and, 136–137
in anterior and lateral leads, 85f juvenile T-wave pattern, 137–138
in anterior leads, 84f pericarditis and, 138
causes of, 112f preexcitation syndromes and, 137
differential diagnosis, 119t pulmonary embolism and, 136
isolated inferior, 3 ST-segment depression and, 135–138
in leads V5 to V6, 103f in toxic ingestion, 6
with negative biomarkers T waves
in children, 239
potential for myocardial salvage, 105 color coding in body surface mapping, 118f
normal, 124–125, 131f hyperacute, 74–76, 84f
persistent, 79 from ischemia, 83f
posterior, on 80-lead ECG, 117f pseudo-normalization, 76, 80
on posterior leads, 97 tachyarrhythmias, clinical significance of, 157–159
prognostic features, 75, 75f tachycardias
right ventricular ischemia and, 91f atrial, 45
in toxic ingestion, 6 in children, 240–241
ST-segment elevation acute MI (STEMI) drug-induced, 230
12-lead ECG technique, 74 drugs inducing, 229t
anterior, evolution of, 83f junctional, 45
anterolateral, 87f, 89f, 92f mechanisms, 46–47
definition, 80 narrow complex, 45–58
diagnosis, 3 pacemaker-mediated, 191t
dynamic changes, 106 paroxysmal supraventricular, 45
indications for acute reperfusion therapy, 3 requiring accessory pathways, 158
inferior wall, 87f supraventricular, 45
lateral, 89f wide complex, 59–72
location of, 78f tamponade, 145, 146t, 147
patterns of injury in, 74–76 tetralogy of Fallot, 242, 242t, 243
right ventricular, 79 tetrodotoxin, 223
ST-segment depression in, 80 thoracic aortic dissection, 206–207, 207t, 212
ST-segment morphology, 80 Thrombolysis in Myocardial Infarction category 3, 77
ST/T-wave complex, 20f thyroid disorders, 196–197
Stanford classification, 206 torsade de pointes, 64, 67f
torso contour maps, 108t
toxic ingestion
ECG correlates of prognosis, 6–7

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indications for an ECG, 6–7 W
transesophageal atrial electrodes, 63 Wellens criteria, 63
transesophageal electrocardiography, 63 Wellens syndrome, 77, 80, 88f
transposition of the great arteries, 242t, 243 wide complex tachycardias, 59–72
trichloroethanol, 230
trichloroethylene, 230, 236f algorithms, 64
tricuspid atresia, 156, 242, 242t, 243 approach to, 59–61
tricyclic antidepressant toxicity, 6, 7, 232f capture beats, 69f
U causes, 60t
undersensing, 181t, 182, 189f clinical features, 62
unstable angina (UA) fusion beats, 69f
irregular, 62
continuous ST-segment monitoring, 114f origins of, 63
detection of myocardial infarction in, 106 precordial concordance, 62, 70f
diagnosis, 74 regularity, 62
hospital discharge statistics, 73 with right bundle-branch block, 71f
ST-segment depression in, 86f of supraventricular origin, 60
V therapy, 63–64
vagal maneuvers, 159 torsade de pointes, 67f
vasodilating agents, 96 transesophageal ECG in diagnosis, 63
ventricular aneurysms, 79 ventricular causes, 61, 61f
ventricular conduction, aberrant, 66f wide QRS complex tachycardias. see wide complex
ventricular infarction, 91f
ventricular leads, 95–96, 96–98 tachycardias
ventricular pacing, 112f Wolff-Parkinson-White (WPW) pattern
ventricular preexcitation, 112f
ventricular septal defects, 242t conditions associated with, 156
ventricular tachycardia description, 155
atrioventricular dissociation in, 62–63 ECG characteristics, 160f
bidirectional, 61, 68f gender and, 156
clinical features, 62 incidence, 156
monomorphic, 61, 72f Wolff-Parkinson-White (WPW) syndrome, 5
multifocal, 61 atrial fibrillation in, 163f
polymorphic, 61 capture beats, 69f
precordial concordance, 62 in children, 240
QRS complex morphology, 63 description, 155
regularity of, 62 differential diagnosis, 23f
supraventricular tachycardia versus, 61–63 ECG pattern in, 155
treatment, 64 fusion beats, 69f
verapamil (phenylalkylamine), 169, 227 intermittent preexcitation, 161f
VVI pacing, 181, 192f T-wave inversion in, 137, 140f
type A, 157
type B, 16, 157
Y
Yamaguchi syndrome, 123
Z
ziprasidone toxicity, 234f

254