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Authors: Sarah W. Alander, MD, Instructor of Pediatrics, Division of Emergency Medicine, Children’s Mercy Hospital; James Edward Hulse, III, MD, Associate Professor of Pediatrics, Department of Cardiology, Children’s Mercy Hospital; Jane F. Knapp, MD, Professor of Pediatrics, Division of Emergency Medicine, Children’s Mercy Hospital, Kansas City, MO.
Peer Reviewer: James C. Perry, MD, Director of Cardiology, Electrophysiology, Children’s Hospital San Diego, CA.
The electrocardiogram (ECG) is an important study in the evaluation of many pediatric disease processes. Critical decisions in the care of the child in the emergency department (ED) depend on accurate and timely analysis, yet, reading pediatric ECGs presents a number of challenges to emergency physicians because of the differences between children and adults, variants of normal ECGs, and changes that occur with age. The resulting confusion can delay diagnosis and lead to inappropriate or unnecessary care. This article reviews basic pediatric ECG interpretation and focuses on the accurate identification of rhythm disturbances. The majority of the discussion is organized by presenting symptoms recognizing the problem-focused nature of an ED visit. Extensive tables summarize the important aspects of ECG interpretation, and an ECG supplement provides sample tracings to further enhance the clinical skills of the emergency physician. —The Editor
Common reasons for obtaining an ECG on a child include: chest pain, irregular or rapid heart beats, seizure, syncope, cyanosis, drug exposure, electrolyte disturbances, and an abnormal cardiac examination.1
These indications foster an approach to pediatric ECG interpretation that emphasizes recognition of abnormal findings and identification of disease processes that require a cardiac evaluation. A wide variety of chief complaints will be used to illustrate common and uncommon pediatric ECG abnormalities and rhythm disturbances in addition to emphasizing the relevant differences between children and adults. The major drawback for this model is that there are rhythm disturbances that occur with more than one chief complaint. To eliminate repetition, each major category includes a comprehensive differential and the most important or representative examples for each situation.
A systematic approach is essential to ECG interpretation. This includes an analysis of rate, rhythm, axis, forces, and repolarization. Textbooks, handbooks, and short reference articles provide excellent and concise reviews of the basics and contain the necessary tables listing normal, age-related values.2-4 A favorite pediatric ECG text is an essential reference for the ED.
The child’s ECG changes over time with the normal growth of the heart. Changes in pulmonary and systemic blood pressures produce corresponding changes in the ECG, such that the characteristics of normal change every few years.5
Interpretation begins by establishing the heart rate and determining whether it is normal or abnormal for the age of the patient. Heart rates requiring rapid cardiopulmonary assessment are listed by age in Table 1.
|Table 1. Heart Rates Requiring Rapid Cardiopulmonary Assessment|
< 80 bpm or > 200 bpm
< 80 bpm or > 180 bpm
< 80 bpm or > 180 bpm
> 8 years
< 60 bpm or > 160 bpm
|Adapted from Pediatric Advanced Life Support Manual. Dallas: American Heart Association; 1997.|
|Table 2. Causes of ST Changes in Children|
|Hyper- or hypokalemia||Emetine intoxication|
|Duchenne's muscular dystrophy||Myotonic dystrophy|
|Early ventricular repolarization||Normal atrial repolarization|
|Table 3. Criteria for Ventricular Hypertrophy|
|Right ventricular hypertrophy|
|Primary Criteria(at least one)|
|• R in V1 above the 98th percentile for age|
|• S in V6 above 98th percentile for age|
|• Upright T in V1 after three days of age until adolescence|
|Secondary Criteria(support the diagnosis in the presence of primary criteria)|
|• R/S ratio in V1 above the 98th percentile for age|
|• R/S ratio in V6 < 1 after one month of age|
|• A qR pattern in V1|
|• Normal duration RSR' in V3R or V1 with R' > 15 mm if , < 1 year, > 10 mm thereafter|
|Left ventricular hypertrophy|
|| • R in V6 above 98th percentile for age|| • S in V1 above 98th percentile for age|| • Inverted T waves in V6||Secondary Criteria|| • R/S ratio in V1 below 2nd percentile for age|| • Q wave > 4 mm in V5 or V6||Adapted from Harriet Lane Handbook. 14th ed. St. Louis: Mosby; 1996.|
Prolonged QT interval. Historically, a QTc greater than 0.44 sec is considered to be abnormal.27 Recent studies show that the QT interval is influenced by gender and age as discussed in "The Basics of the Pediatric ECG" section in this issue. A prolonged QTc (see Figure 8 in enclosed supplement) represents abnormal electrical recovery of the ventricle, leaving the myocardium vulnerable to develop ventricular tachyarrhythmias, particularly when provoked by sympathetic stimuli. Patients with syncope as a result of a prolonged QTc will often give a history of pain, physical exertion, or emotional stress provoking the event.26 Patients with a QTc greater than 0.50 sec appear to be most at risk for sudden cardiac death. Most concerning is the potential for these patients to develop torsade de pointes, a polymorphous form of ventricular tachycardia that is difficult to treat successfully.25 (See Figure 9 in enclosed supplement.)
Prolonged QTc can be congenital or acquired. The congenital forms are inherited in a dominant mode of transmission. Acquired prolongation of the QTc is associated with metabolic derangements such as hypocalcemia, hypomagnesemia, hypokalemia, and hypothermia. Numerous drugs, such as antiarrhythmics, cisapride, antifungals, and erythromycin, also prolong the QTc .28
Heart block. A wide range of congenital or acquired etiologies can cause atrioventricular (AV) conduction abnormalities in children. Congenital heart disease (either pre- or postoperative), cardiomyopathy, myocarditis, Lyme carditis, and certain drug ingestions are a few representative examples that may result in a variety of AV blocks.29 Children without pre-existing risk factors and structurally normal hearts can also have heart block. In the patient presenting with syncope, both Mobitz type II second degree AV block and complete heart block (third-degree block) should be included in the differential diagnosis.23,26
Mobitz type II second degree AV block is defined as intermittent loss of AV conduction without a preceding lengthening of the PR interval for at least two consecutive beats.29 While not very common in children, it causes concern when identified because of its association with Stokes-Adams attacks and sudden cardiac death.29
Complete heart block may be congenital, with an incidence of 1 in 22,000 live births. With current monitoring standards during pregnancy and delivery, most cases of congenital heart block are identified early; it would be unusual for this condition to first present in the ED. However, some patients may not be symptomatic until later in childhood, at which time syncope may be the presenting symptom. Heart block may also occur in the setting of structural heart disease, particularly in patients with L-transposition of the great vessels. Surgical repair of a VSD, AV canal, transposition of the great vessels, or the Fontan procedure for single ventricle, may place the child at risk for complete heart block due to anatomical involvement or proximity of the surgical site to the AV node.29 With complete heart block, the atria and ventricles beat independently of each other. Therefore, the atrial rhythm is regular, as noted by a normal PP interval, and the ventricular rate is also regular as noted by a regular, but much slower RR interval.2 (See Figure 10 in enclosed supplement.)
Aortic stenosis. Aortic stenosis is a general term used to describe several lesions of the left ventricular outflow tract. Accounting for 3-8% of all patients with congenital heart disease, these lesions are further categorized anatomically as valvar, fibromuscular subvalvar, and supravalvar aortic stenosis. Clinically, pediatric patients can be divided into in two groups: those who develop critical symptoms of congestive heart failure in infancy (10-15%) and those who develop symptoms in adolescence and young adulthood.
Of particular concern for the emergency physician is the teenager with aortic stenosis. A previously healthy patient may present with exercise-induced syncope or anginal chest pain and be at risk for sudden cardiac death. This patient’s ECG will show left ventricular hypertrophy: R is of greater than normal amplitude in leads V5 and V6, and S is greater than normal in V1 and V2. The patient may also show the "strain" pattern: flat or inverted T waves or ST depression in the left precordial leads. (See Figure 11 in enclosed supplement.)
Sinus arrhythmia. Sinus arrhythmia is most frequently a variation of normal. Sinus arrhythmia is sometimes referred to as respiratory sinus arrhythmia because it represents a cyclic variation of the sinus rhythm with respiration. The rate increases toward end inspiration and decreases toward end expiration. The ECG shows progressive shortening of the PP intervals followed by prolongation of the PP intervals. Sinus arrhythmia is more pronounced with a slow heart rate and tends to disappear with increased heart rate. It is found in virtually all normal school age children during 24-hour electrocardiograms.30,31 Sinus arrhythmia, though most commonly seen in normal children, occurs in the diseased heart as well.
Sinus pauses averaging more than one second in duration also have been reported in healthy children on 24-hour ECG monitoring.32
Second degree AV block. An irregular ventricular rhythm occurs with second degree AV block. Mobitz type I and Mobitz type II second degree AV blocks are distinguished by ECG findings. Mobitz type I second degree AV block, also known as Wenkebach, is characterized by progressive lengthening of the PR interval terminating in a blocked P wave. The consequence is a missed QRS complex or dropped beat. The grade of the second degree block is quantified by the ratio of all P waves to conducted P waves. There are at least three P waves in a Wenkebach sequence, two of which are conducted, producing a 3:2 block. Another ECG feature is that the RR interval becomes progressively shorter before the blocked P wave. In most cases, Mobitz type I second degree AV block is a benign, nonprogressive phenomenon in children with otherwise normal hearts.33
Extrasystoles. Extrasystoles are premature beats and can be either atrial, AV junctional, or ventricular in origin. Most extrasystoles have a uniform shape on the ECG. When more than one pattern is observed, they are termed multiform. Atrial extrasystoles are defined by early P waves. The early P wave frequently looks different than other normally conducted P waves. It may be followed by a normal appearing QRS complex, one of a different shape, or by no QRS. When the abnormal P wave is superimposed on a T wave and the QRS morphology of the extrasystolic beat is a different shape, it can be difficult to differentiate between an atrial and a ventricular extrasystole.
Ventricular extrasystoles are identified by a QRS complex with a different shape from the prevailing rhythm that is not preceded by a P wave. Ventricular extrasystoles may be found on the routine ECG in 1-2% of normal children.34 Most of them are uniform and infrequent. Multiform ventricular extrasystoles are rare in children and raise the concern of heart disease. The differential for ventricular extrasystoles includes: congenital heart disease, especially after cardiac surgery; undiagnosed myocardial disease; mitral valve prolapse; Marfan’s syndrome; long QT syndrome; drug ingestions; hypoxia; and acidosis. In particular, a healthy patient presenting with ventricular extrasystoles should be carefully screened for prolonged QT syndrome.
Cardiac involvement must be considered in the child who has sustained a serious or focal blunt or penetrating injury to the torso. Although the ECG is frequently abnormal after chest trauma, it is not sufficiently sensitive or specific to confirm the diagnosis of myocardial contusion.
Myocardial contusion. Most children will experience symptoms of myocardial contusion soon after injury.35 The child with myocardial contusion who is conscious and verbal commonly complains of precordial chest pain. The most common ECG finding is a sinus tachycardia, which is excessive for age and unexplained by other factors. The most common rhythm disturbance is frequent, premature ventricular complexes. Signs of myocardial injury similar to an infarction pattern with ST-segment elevation, T wave changes, or presence of abnormal Q waves may be present. (See Figure 12 in enclosed supplement.)
Other chest injury. A penetrating wound to the heart can produce atrioventricular conduction defects at the level of the injury. Ventricular rhythm disturbances can also occur.
Acute pericarditis and cardiac tamponade can occur with either blunt or penetrating injury to the chest. ECG changes may be seen with the accumulation of fluid under pressure in the pericardium. As previously noted, the QRS complex can be normal or low-voltage. Electrical alternans is an alteration of electrical amplitude of the T wave and QRS complex with each cycle that occurs with large effusions.
Air is a poor conductor of electrical activity. Therefore, in patients with a pneumomediastinum or pneumothorax when air is between the heart and the recording electrode, the amplitudes of the P, QRS, and T waves may be decreased, depending on the location of the air. ST segment changes can also occur.
Head injury. Sinus bradycardia occurs as part of Cushing’s triad in response to increased intracranial pressure accompanying serious head injury. Patients with head injury may also exhibit ST segment changes and prolongation of the QT interval.
A wide range of drugs and other substances ingested by children produce cardiac effects. In the previously healthy child who presents with a rhythm disturbances, the ECG can be helpful to formulate a differential diagnosis and to guide management.
Rhythm disturbances from drug effects can be caused by direct or indirect sympathomimetic effects, anticholinergic effects, the effects of altered central nervous system regulation of the peripheral autonomic system, and direct effects on the myocardial membranes.36-40 Some drugs produce toxicities by more than one of these mechanisms. Clinical management should be based on countering the mechanism of drug action; access to detailed pharmacologic information is essential in the ED. (See Table 7.)