Clinical features of Kawasaki Disease

Clinical features of Kawasaki Disease

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Kawasaki disease (KD), formerly known as mucocutaneous lymph node syndrome and infantile polyarteritis nodosa, is an acute febrile vasculitis of childhood.

Kawasaki disease is the leading cause of acquired heart disease in children in the United States and Japan.

Fever is characteristically high (104°F or higher), remittent, and unresponsive to antibiotics. The duration of fever without treatment is generally 1–2 wk, but it may persist for 3–4 wk. Prolonged fever is prognostic for the development of coronary artery disease.

In addition to fever, the five characteristic features of Kawasaki disease are: bilateral bulbar conjunctival injection, usually without exudate; erythema of the oral and pharyngeal mucosa with strawberry tongue and dry, cracked lips, and without ulceration; edema and erythema of the hands and feet; rash of various forms (maculopapular, erythema multiforme, or scarlatiniform) with accentuation in the groin area; and nonsuppurative cervical lymphadenopathy, usually unilateral, with node size of ?1.5 cm.

Perineal desquamation is common in the acute phase. Periungual desquamation of the fingers and toes begins 1–3 wk after the onset of illness and may progress to involve the entire hand and foot.

Other features include extreme irritability that is especially prominent in infants, aseptic meningitis, diarrhea, mild hepatitis, hydrops of the gallbladder, urethritis and meatitis with sterile pyuria, otitis media, and arthritis. Arthritis may occur early in the illness or may develop in the 2nd–3rd week, generally affecting hands, knees, ankles, or hips. It is self-limited but may persist for several weeks.

Cardiac involvement is the most important manifestation of Kawasaki disease. Myocarditis, manifested as tachycardia out of proportion to fever occurs in at least 50% of patients; decreased ventricular function occurs in a smaller number of patients. Pericarditis with a small pericardial effusion is common during the acute illness. Coronary artery aneurysms develop in up to 25% of untreated patients in the 2nd–3rd wk of illness and are best detected by two-dimensional echocardiography. Giant coronary artery aneurysms (?8 mm internal diameter) pose the greatest risk for rupture, thrombosis or stenosis, and myocardial infarction . Significant valvular regurgitation and systemic artery aneurysms may occur but are uncommon. Axillary, popliteal, or other arteries may also be involved and manifest as a localized pulsating mass.

Clinical Phases of Disease:

Kawasaki disease is generally divided into three clinical phases.

The acute febrile phase, which usually lasts 1–2 wk, is characterized by fever and the other acute signs of illness. The dominant cardiac manifestation is myocarditis. In addition, a macrophage activation syndrome may rarely be evident .

The subacute phase begins when fever and other acute signs have abated, but irritability, anorexia, and conjunctival injection may persist. The subacute phase is associated with desquamation, thrombocytosis, the development of coronary aneurysms, and the highest risk of sudden death in those who have developed aneurysms. This phase generally lasts until about the 4th wk.

The convalescent phase begins when all clinical signs of illness have disappeared and continues until the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) return to normal, ?6–8 wk after the onset of illness.

Certain clinical and laboratory findings may predict a more severe outcome. These include male gender, age <1 yr, prolonged fever, recrudescence of fever after an afebrile period, and the following laboratory values at presentation: low hemoglobin or platelet levels, high neutrophil and band counts, hyponatremia, and low albumin and age-adjusted serum IgG levels. Scoring systems based on these factors, however, have not proven sufficiently sensitive for selective treatment of patients based on risk.

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Atrial Flutter in Children

Atrial Flutter in Children

The following article covers a topic that has recently moved to center stage--at least it seems that way. If you've been thinking you need to know more about it, here's your opportunity.
Once you begin to move beyond basic background information, you begin to realize that there's more to Atrial,Flutter,Children,tachycardia,,AV block than you may have first thought. 
Introduction
Atrial flutter is an electrocardiographic descriptor used both specifically and nonspecifically to describe various atrial tachycardias. The term was originally applied to adults with regular atrial depolarizations at a rate of 260-340 beats per minute (bpm). Historically, the diagnosis of atrial flutter was restricted to those patients whose surface electrocardiogram (ECG) revealed the classic appearance of "flutter waves." This sharp demarcation is used less frequently in the current era.

In the fetus, atrial flutter is defined as a rapid regular atrial rate of 300-600 bpm accompanied by variable degrees of atrioventricular (AV) conduction block, resulting in slower ventricular rates.

When the atrial rate is so rapid, normal AV nodes usually have a physiologic second-degree block, with a resultant 2:1 conduction ratio. In individuals with AV nodal disease or increased vagal tone, or when certain drugs are used, higher degrees of AV block may develop. In individuals with accessory AV nodal pathways, a 1:1 conduction ratio may occur, with resultant ventricular rates of 260-340 bpm, which can cause sudden death. A 1:1 conduction ratio may also occur when the atrial rate is relatively slow (eg, < 340 bpm) during atrial flutter or when physiologic processes facilitate AV nodal conduction such that a rapid ventricular response can still result in sudden death.

Atrial flutter is infrequent in children without congenital heart disease. Patients who have undergone Mustard, Senning, or Fontan procedures are more prone to develop this arrhythmia because of atrial scars from surgery and right atrial enlargement, such as is found after the classic Fontan operation.

Similarly, patients who have undergone surgical repair of atrial septal defect, total anomalous pulmonary venous connection, and tetralogy of Fallot may later develop atrial flutter. Individuals with muscular dystrophies such as Emery-Dreifuss and myotonic dystrophy may also develop atrial flutter, as well as those with dilated, restrictive, and hypertrophic cardiomyopathies.

Treatment of children with atrial flutter may involve medication, pacing, cardioversion, radiofrequency catheter ablation, or surgical procedures (see Treatment). Drug therapy of atrial flutter in children can be classified under the 3 broad headings of ventricular rate control, acute conversion, and chronic suppression (see Medication).

Pathophysiology
Atrial flutter is a reentrant arrhythmia circuit confined to the atrial chambers. As a rule, atrial flutter originates in the right atrium, whereas atrial fibrillation, which is more frequent in adults, originates in the left atrium.

A flutter circuit typically surrounds an anatomical or functional barrier and includes a zone of slow conduction (or conduction over an extended circuit) and an area of unidirectional block, as required for reentry of all types. Frequently, a premature beat blocks one limb of the circuit and is sufficiently delayed in the other limb (while traversing around the anatomical or functional barrier) to allow for recovery from refractoriness in the first limb.

The reentrant circuits that occur in children with atrial flutter after congenital heart disease surgery are believed to involve abnormal atrial tissue that has been subject to chronic cyanosis, inflammation secondary to surgery, scarring, and increased wall stress in cases of enlarged atria. Such circuits may encircle anatomical barriers such as atriotomy scars or surgical anastomoses, and they may use areas of slow conduction along baffle limbs and other sites of injury in addition to the tricuspid valve–coronary sinus isthmus.

Sinus node dysfunction with bradycardia is generally present in many of these patients years after surgery. This is a contributing factor for development and maintenance of atrial flutter.

Atrial flutter circuits in children with congenital heart disease are typically more variable than those in adults. For the most part, atrial flutter circuits in adults are confined to the tricuspid valve–coronary sinus isthmus (or isthmus-dependent flutter).

In the fetus, atrial flutter occurs mainly during the third trimester. The atrium is believed to reach a critical mass to support an intra-atrial macroreentry circuit at about 27-30 weeks’ gestation.
Etiology
Most fetuses and neonates with atrial flutter have structurally normal hearts. However, when atrial flutter is detected in a fetus, structural cardiac anomalies such as Ebstein anomaly of the tricuspid valve and AV septal defects should be ruled out because of a higher incidence of such defects in these cases.

Some newborns and young children have associated conditions or anomalies that may predispose them to atrial flutter. Atrial septal aneurysms appear to be associated with sustained atrial arrhythmias in newborns. Restrictive cardiomyopathies are also associated with refractory atrial flutter. In Costello syndrome, the dysmorphic appearance is also associated with a dysrhythmia characterized as chaotic atrial tachycardia, and this dysrhythmia may include long episodes of atrial flutter.

Atrial flutter is not uncommon in the immediate postoperative period after congenital heart surgery. Surgery-induced inflammation of the pericardium, scarring, and volume overload may trigger atrial flutter.

Case reports have linked atrial flutter to ingestion of herbal medicines and certain foods. These episodes did not recur after avoidance of the triggers.

Atrial flutter and atrial fibrillation have been related to obesity, alcohol consumption, and hyperthyroidism.[1, 2, 3] One study reported that in adults, diabetes mellitus is a strong independent risk factor for development of atrial flutter and atrial fibrillation.[4]
Epidemiology

According to one United States study, 57% of patients with double-inlet left ventricle who undergo the Fontan operation may be expected to present with atrial flutter or fibrillation by 20 years after surgery.[5] The mean annual incidence of new dysrhythmias (predominantly atrial flutter) after the Fontan operation is 5%.

In one international review, atrial flutter accounted for 26.2% of all cases of fetal tachyarrhythmias, and supraventricular tachycardia (SVT) accounted for 73.2%.[6] In an earlier population study of 3383 English newborns by Southall and colleagues, only 1 newborn had atrial flutter.[7] This likely underestimated the incidence of atrial flutter in utero because spontaneous conversion often occurs during birth and subsequent recurrence is uncommon.

A long-term follow-up study into adulthood of patients undergoing the Mustard or Senning procedure for correction of D-transposition of the great vessels demonstrated SVT in 48%, of which atrial flutter was the most common type (73%). Arrhythmias accounted for 12.7% of pediatric cardiology consultations in a major pediatric academic medical center, of which atrial flutter was the second most common type.
Sexual and age-related differences in incidence

Following atrial septal defect repair, the prevalence of atrial flutter is higher in females (70.7%) than in males. Patients with Fontan repairs present with flutter either as children or as adults. Patients with repaired tetralogy of Fallot tend to present with atrial flutter as young adults. Because the Mustard and Senning procedures are now rarely performed, the cohort of patients with this substrate typically consists of older adolescents and adults.

One study reported that the recurrence rate of atrial flutter and fibrillation in women with preexisting cardiac rhythm disorders during pregnancy was the highest of all the studied arrhythmias, reaching 52%.

Prognosis
Neonatal atrial flutter is usually a self-limiting illness, requiring only conversion of the rhythm with esophageal atrial pacing or cardioversion. Incisional reentrant atrial tachycardia following complex atrial surgery in the repair of congenital heart disease may occur early in the postoperative period; this event is predictive of the occurrence of late postoperative flutter. The prevalence of atrial flutter in several classes of postoperative patients increases with the duration of follow-up care.

Morbidity and mortality in patients with atrial flutter largely depend on the following factors:

    Age at presentation
    Cardiac anatomy (normal anatomy vs congenital heart disease)
    Integrity and anatomy of the myocardial conduction system (normal sinus node vs sinus node dysfunction; AV block vs normal AV node, with or without accessory pathways)
    Ventricular function
    Prompt recognition of the arrhythmia and initiation of adequate therapy

The fetus with atrial flutter may have significant morbidity and be at risk for mortality. According to one review, hydrops fetalis developed in as many as 40% of fetuses with atrial flutter. The mortality rate in these fetuses was 8%.[6]

Mortality in newborns with atrial flutter is uncommon. Most patients remain in sinus rhythm following their initial conversion, and the need for antiarrhythmic prophylaxis in these patients during infancy is debated.

In patients with postoperative atrial flutter that develops late following repair of congenital heart disease, the severity of presentation depends on the atrial flutter rate, conduction ratio, and presence of ventricular dysfunction. In patients who have undergone the Mustard procedure, Holter recordings incidentally capturing episodes of sudden fatality confirm that rapidly conducted atrial flutter is the dysrhythmia most frequently responsible for these fatalities.

In contrast, patients who have undergone the Fontan procedure rarely die suddenly but frequently present with symptomatic atrial flutter. This may be caused by a relatively slower atrial flutter rate, a higher degree of AV conduction block, or both.

Prolonged episodes of atrial flutter in asymptomatic or mildly symptomatic patients may be associated with development of atrial thrombi and although rarely in the congenital heart disease population, the possibility of thromboembolic events.

When women with heart disease and arrhythmias reach childbearing age, arrhythmias can recur during pregnancy. These arrhythmias significantly increase the risk for the mother and fetus
 
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Interpretation of Electrocardiogram in Children

Electrocardiogram Interpretation in Children

This interesting article addresses some of the key issues regarding ECG,Electrocardiogram,children,QRS.Rhythm. A careful reading of this material could make a big difference in how you think about ECG,Electrocardiogram,children,QRS.Rhythm.

Sometimes the most important aspects of a subject are not immediately obvious. Keep reading to get the complete picture.

    Electrocardiography is critical in the diagnosis of electrical disorders of the heart. It may serve as a useful screening tool in the evaluation of patients of suspected structural defects or abnormalities of the myocardium.
    Newborns have a large variability in electrocardiogram (ECG) voltages and intervals due in large part to hemodynamic and myocardial adaptations that are needed once the placenta is no longer part of the circulatory system.
    Changes continue, albeit at a slower pace, from infancy through adolescence.
    Algorithms used to interpret ECGs in adults cannot be used in children. This section is a basic, although incomplete, guide to the pediatric ECG.
Rate
    The usual recording speed is 25 mm/sec; each little box (1 mm) is 0.04 seconds and each big box (5 mm) is 0.2 seconds.
    With a fast heart rate, count the R-R cycles in 6 large boxes (1.2 seconds) and multiply by 50.
    With a slow heart rate, count the number of large boxes between R waves and divide into 300 (1 box = 300, 2 boxes = 150, 3 boxes = 100, 4 boxes = 75).
    Table below lists normal heart rates.
Rhythm

    Are the QRS deflections regular? Variation in the rate up and down in concert with respirations is normal (sinus arrhythmia) and can be pronounced in young healthy hearts.
    Irregular QRS pattern suggests the possibility of an atrial arrhythmia. With pauses and narrow QRS, look for evidence of atrial premature contractions with P waves of different of appearance and/or axis as compared with sinus beats. The early P wave may not conduct, leading to longer pauses (blocked atrial premature contractions).
    The QRS may be prolonged if conduction down the atrioventricular (AV) node is delayed (aberrant conduction). Wide QRS complexes with pauses may represent premature contractions from a ventricular focus, especially if the T-wave morphology is also altered with the opposite axis.
    Look for a P wave before each QRS at an expected interval, usually between 100 and 150 milliseconds. The P wave should be upright in I and aVF for the typical location of sinus node. The sinus P wave is up in leads I, II, aVF, pure negative in aVR, and usually biphasic in lead V1—first positive, then negative.
        Inverted P waves associated with slower heart rates, along with a low atrial rhythm, are a normal finding.
        Inverted P waves associated with tachycardias are abnormal and may be ectopic atrial tachycardia or other forms of supraventricular tachycardia (SVT).
PR Interval

    The PR interval represents atrial depolarization.
QRS Axis and Duration

    The QRS axis shows the direction of ventricular depolarization.
        Left axis deviation can suggest left ventricular hypertrophy or left bundle branch block (LBBB).
        Right axis deviation can suggest right ventricular hypertrophy or right bundle branch block (RBBB)
    The QRS duration represents ventricular depolarization. Normal times for depolarization depend on age. A prolonged QRS may indicate bundle branch block, hypertrophy, or arrhythmia.
    Normal Heart Rates in Children*
    Age     Heart rate (beats/ min)
    0–1 mo     145 (90–180)
    6 mo     145 (105–185)
    1 yr     132 (105–170)
    2 yr     120 (90–150)
    4 yr     108 (72–135)
    6 yr     100 (65–135)
    10 yr     90 (65–130)
    14 yr     85 (60–120)

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The abnormal pediatric ECG -2

Conduction abnormalities

All degrees of AV block may occur in pediatric patients. It is important
to remember that the normal PR interval in infants is shorter and lengthens
as cardiac tissue matures with age. A normal appearing PR interval of 0.20
sec may thus in fact represent a pathologic first-degree AV block in an infant
or young child.
Complete heart block is a common cause of significant bradycardia in
pediatric patients and may be acquired or congenital (Fig. 6). Causes of congenital
heart block include structural lesions like L-transposition of the
great arteries, or maternal connective tissue disorders. Acquired heart block
may result from disorders such as Lyme disease, systemic lupus erythematosus,
muscular dystrophies, Kawasaki disease, or rheumatic fever [11].
Bundle branch blocks (BBB) may be present when there is QRS complex
prolongation abnormal for a given age. Right BBB occurs with abnormal
rightward and anterior terminal forces, frequently manifesting on ECG as
an rSR# pattern in leads V1 and V2. Right BBB is more common than left
BBB and can be seen after surgical repair of congenital heart defects, particularly
ventricular septal defect repairs. Similarly, left BBB is seen with abnormal
leftward and posterior forces, best appreciated in leads V5 and V6. Left
BBB is rare in children, however, and the possibility of WPW should be considered,
because this syndrome can mimic a left BBB pattern.
Congenital heart
With an incidence of 8/1000 live births, many of the structural congenital
heart diseases present in the neonatal period [12]. The signs and symptoms
of congenital heart disease may be nonspecific, however. Infants may present
with tachypnea, sudden onset of cyanosis or pallor that may worsen with
crying, sweating with feeds, lethargy, or failure to thrive [13].
Congenital heart disease lesions that present in the first 2–3 weeks of life
are typically the ductal-dependent cardiac lesions. During this period the
ductus arteriosus had been sustaining blood flow for these infants. When
the ductus closes anatomically at 2–3 weeks of life, these infants suddenly


become ill. Depending on the underlying structural abnormality, these neonates
present with sudden cyanosis or signs of cardiovascular collapse.
These newborns have depended on the ductus arteriosus to supply blood
to the lungsdas with tetralogy of Fallot (ToF) or tricuspid atresia (TA)d
or to the systemic circulationdas in the case of coarctation of the aorta
(CoA) or hypoplastic left heart syndrome (HLHS). The main causes of
cyanotic congenital heart disease are ToF, TA, transposition of the great
arteries (TGA), truncus arteriosus, total anomalous pulmonary venous
return (TAPVR), and pulmonary atresia or stenosis. Time of onset and
the common associated ECG findings are listed in Table 3 [14–16].
The other class of congenital cardiac lesions that present in the first
month of life are the left-to-right intracardiac shunts, such as ventricular
septal or atrioventricular canal defects. As the normal pulmonary vascular
resistance falls over the first month of life, any pre-existing left-to-right
shunt sees a gradual increase in flow across the shunt, resulting in congestive
heart failure. The differential diagnosis of congenital heart diseases that
cause congestive heart failure include not only the left-to-right intracardiac
shunts, but also HLHS, CoA, TA, endocardial cushion defect, patent ductus
arteriosus (PDA), aortic stenosis, interrupted aortic arch, aortic atresia, and
mitral valve atresia [17,18].
An ECG should be obtained in all infants suspected of having congenital
heart disease. Although the ECG does not make the diagnosis, it can show
evidence of conduction abnormalities or chamber enlargement as a result of
the congenital defect. In addition, the ECG provides a means of assessing
the degree of cardiac flow obstruction, chamber hypertrophy, and the development
of dysrhythmias as a result of the congenital heart disease.
Several ECG findings can be associated with specific congenital heart diseases
(Table 3). The ECG can seem normal or age-appropriate for some
congenital heart diseases. These include cases of PDA, mild-moderate pulmonary
stenosis, TGA, ASD, VSD, and CoA, though the presence of abnormalities
on the ECG is generally the rule.
RVH is the most common abnormality seen with congenital heart disease
and can be seen with pulmonary stenosis, ToF, TGA, and VSD with pulmonary
stenosis or pulmonary hypertension, CoA (newborn), pulmonary valve
atresia, HLHS, and ASD. RVH may be difficult to distinguish during the
early neonatal period because of the normal right ventricular predominance
on the ECG at this age. The abnormality becomes clear, however, with later
infancy and early childhood.
LVH is seen in lesions with small right ventricles, such as tricuspid atresia,
pulmonary atresia with intact ventricular septum, and lesions with left
ventricular outflow track obstruction (AS, CoA, hypertrophic cardiomyopathy
[HCM]). LVH also can be seen in older children with PDA and larger
VSD or AV canal defects (Fig. 7).
In conjunction with ventricular changes, atrial abnormalities can be detected
on the ECG with congenital heart disease. RAE occurs with large
left-to-right shunts, causing RA volume overload, and can be seen with ASD,
atrioventricular canal defects, tricuspid atresia, Ebstein anomaly, and severe
pulmonary stenosis. LAE can be seen with mitral stenosis or insufficiency, left
heart obstruction, and complete AV canal defects.
Abnormal QRS axis deviations are seen commonly with congenital heart
defects. Right axis deviation can occur with ASD, ToF, CoA, TGA, and
pulmonary stenosis. Left axis deviation can be seen with large VSD, tricuspid
atresia, TGA, and complete AV canal defects (Fig. 7). Right BBB can be
seen with ASD, complete AV defects, small VSD, and after repair of ToF. It
is important to keep in mind, however, that incomplete right BBB can be
a normal part of the involution of right ventricular forces during infancy
and early childhood (Fig. 8).
Hypertrophic cardiomyopathy
Although most cases of HCM are diagnosed at 30–40 years of age, 2% of
cases occur in children younger than 5 years of age and 7% occur in children
younger than 10 years of age [19]. Clinical presentation varies, with patients
experiencing chest pain, palpitations, shortness of breath, syncopal or near
syncopal episodes, or sudden death. The hallmark anatomic finding in patients
who have HCM is an asymmetric, hypertrophied, nondilated left ventricle
with greater involvement of the septum than the ventricular free wall.
ECG findings include LAE and LVH, ST-segment abnormalities, T-wave
inversions, Q waves, and diminished or absent R waves in the lateral leads.
Premature atrial and ventricular contractions, supraventricular tachycardia,
multifocal ventricular dysrhythmias, or new onset atrial fibrillation also may
be present.


Myocarditis
An inflammatory condition of the myocardium, this disease has numerous
causes; the most common etiology in North America is viral (Coxsackie A
and B, ECHO viruses, and influenza viruses) [20,21]. The clinical presentation
varies depending on multiple factors, including etiology and patient age. Neonates
and infants may present with symptoms such as lethargy, poor feeding,
irritability, pallor, fever, and failure to thrive. Symptoms suggestive of heart
failure like diaphoresis with feeding, rapid breathing, tachycardia, or respiratory
distress also may be present. Older children may complain of weakness
and fatigue, particularly on exertion. Signs of poor cardiac function, including
signs of congestive heart failure, may be present on examination.
Multiple ECG findings may be present. Sinus tachycardia is the most
common dysrhythmia. A tachycardia faster than expected for the degree
of fever (10 bpm for each degree of temperature elevation) may indicate
myocarditis. Many other dysrhythmias may be associated with myocarditis,
including junctional tachycardias, ventricular ectopy, ventricular tachycardias,
and even second- and third-degree AV blocks. Morphologically there
may be T-wave flattening or inversion and low QRS complex voltage, less
than 5 mm in all limb leads.


source:
Pediatric ECG
Ghazala Q. Sharieff, MDa,b,*, Sri O. Rao, MDc
aChildren’s Hospital and Health Center/University of California–San Diego,
3020 Children’s Way, San Diego, CA 92123
bPediatric Emergency Medicine, Palomar-Pomerado Hospitals/California
Emergency Physicians, 555 East Valley Parkway, Escondido, CA 92025, USA
cDivision of Pediatric Cardiology, Children’s Hospital and Health Center,
3020 Children’s Way, San Diego, CA 92123, USA

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The abnormal pediatric ECG -1

Tachydysrhythmias

The tachydysrhythmias can be classified broadly into those that originate
from loci above the AV node (supraventricular), those that originate from
the AV node (AV node re-entrant tachycardias), and those that are ventricular in origin. Although AV node re-entrant tachycardias are more
common in adults, the vast majority of tachycardias in children are supraventricular
in origin. It is important to record continuous ECG or rhythm
strips with the child in tachycardia, while medication is being pushed, and
when converted to sinus rhythm. On recognition of a tachycardia, stepwise
questioning can help clarify the ECG tracing. Is it regular or irregular? Is
the QRS complex narrow or wide? Does every P wave result in a single
QRS complex?


Sinus tachycardia can be differentiated from other tachycardias by a narrow
QRS complex and a P wave that precedes every QRS complex. Sinus
tachycardia is a normal rhythm with activity and exercise and can be a normal
physiologic response to stresses, such as fever, dehydration, volume
loss, anxiety, or pain. Sinus tachycardia that occurs at rest may be a sign
of sinus node dysfunction. It is important to keep in mind, however, that
the normal range for heart rate is higher in children (see Table 1).
Supraventricular tachycardia (SVT) is the most common symptomatic
dysrhythmia in infants and children, with a frequency of 1 in 250–1000 patients
[6]. The peak incidence of SVT is during the first 2 months of life.
Infants with SVT typically present with nonspecific complaints, such as fussiness,
poor feeding, pallor, or lethargy. Older children may complain of chest
pain, pounding in their chest, dizziness, shortness of breath, or may demonstrate
an altered level of consciousness. The diagnosis often begins in triage
with the nurse reporting that ‘‘The heart rate is too fast to count.’’
In newborns and infants with SVT, the heart rate is greater than 220 bpm
and can be as fast as 280 bpm, whereas in older children, SVT is defined as
a heart rate of more than 180 bpm [7]. On the ECG, supraventricular tachycardia
is evidenced by a narrow QRS complex tachycardia without discernible
P waves or beat-to-beat variability (Fig. 3). The initial ECG may be
normal, however, and a 24-hour rhythm recording (eg, Holter monitor) or
an event monitor may be necessary to document the dysrhythmia in cases
of intermittent episodes. In children younger than 12 years of age, the
most common cause of supraventricular tachycardia is an accessory atrioventricular
pathway, whereas in adolescents, AV node re-entry tachycardia
becomes more evident
SVT can be associated with Wolff Parkinson White (WPW) syndrome.
SVT in WPW syndrome generally is initiated by a premature atrial depolarization
that travels to the ventricles by way of the normal atrioventricular
pathway, travels retrograde through the accessory pathway, and re-enters
the AV node to start a re-entrant type of tachycardia [7,8]. Antegrade conduction
through the AV node followed by retrograde conduction through
the accessory pathway produces a narrow complex tachycardia (orthodromic
tachycardia) and is the most common form of SVT found inWPWsyndrome
 Less commonly re-entry occurs with antegrade conduction through the
accessory pathway and retrograde conduction through the AV node (antidromic
tachycardia) to produce a wide complex tachycardia [9]. Typical


ECG findings of WPW are a short PR interval, wide QRS complex, and
a positive slurring in the upstroke of the QRS complex, known as a delta
wave (Fig. 4). The ECG in most WPW SVT does not show the delta wave,
because tachycardia is not conducted down through the accessory pathway.
Episodes of SVT in children who have WPW usually occur early in the first
year of life [9]. Episodes of SVT often resolve during infancy but may recur
later in life, usually from 6–8 years of age [9].
Atrial ectopic tachycardia may be differentiated from SVT by the presence
of different P-wave morphologies. Each P wave is conducted to the
This ECG was done shortly after adenosine was administered and the rhythm converted
to sinus. Note the abnormally short PR interval for age and the presence of a delta wave
(arrows) at the beginning of the QRS complex. The delta wave is not uniformly apparent in
all leads.


ventricle, and because the ectopic atrial focus is faster than the SA node, the
ectopic determines the ventricular rate (Fig. 5).
Although supraventricular tachycardias are more common than those of
ventricular origin, it is important to remember that the normal QRS complex
is shorter in duration in children than adults. As a result, a QRS complex
width of 0.09 sec may seem normal on the ECG but actually represents
an abnormal wide QRS complex tachycardia in an infant. The differential
diagnosis of wide complex tachycardia includes sinus/supraventricular
tachycardia with bundle branch block or aberrancy, antidromic AV re-entry
tachycardia, ventricular tachycardia (VT), or coarse ventricular fibrillation. ECG findings that support the presence of VT include AV dissociation
with the ventricular rate exceeding the atrial rate, significantly prolonged
QRS complex intervals, and the presence of fusion or capture beats. If there
is a right bundle branch block, the presence of VT is supported by a qR
complex in V1 and a deep S wave in V6. If there is a left bundle branch block
present, then the presence of VT is supported by a notched S wave and an
R-wave duration of O0.03 sec in V1 and V2 and a Q wave in V.
source:

Pediatric ECG
Ghazala Q. Sharieff, MDa,b,*, Sri O. Rao, MDc
aChildren’s Hospital and Health Center/University of California–San Diego,
3020 Children’s Way, San Diego, CA 92123
bPediatric Emergency Medicine, Palomar-Pomerado Hospitals/California
Emergency Physicians, 555 East Valley Parkway, Escondido, CA 92025, USA
cDivision of Pediatric Cardiology, Children’s Hospital and Health Center,
3020 Children’s Way, San Diego, CA 92123, USA

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Normal Electrocardiogram (ECG) Interpretation in Children

 The normal pediatric ECG

There are many systematic techniques for interpreting ECGs and no one
method is particularly better than another. A caveat to the electronic interpretation
that many ECG machines conduct is that they are manufactured
and calibrated with adult values in the software package; hence, the machine
interpretation is frequently inaccurate with children. On the other hand,
they are reasonably accurate in calculating intervals that are averaged
over the entire recording period. The settings of the ECG, however, must
be full standard, defined as 10 mm/mV with a standard paper speed of 25
mm/sec. These settings can be changed on the machine to elucidate certain
features, but a standard ECG is the only one that should be referenced to
normal values. Frequently, additional right ventricular and posterior left
ventricular precordial leads (V3R, V4R, and V7) are included with pediatric
ECGs to provide additional information on patients who have complex congenital
abnormalities. In most pediatric patients, these leads can be ignored.
Table 1 lists the normal pediatric ECG values seen in the newborn,
infant, child, and adolescent [3–5]. This table lists normal ranges for heart
rate, QRS axis, PR and QRS complex intervals, and R- and S-wave amplitudes,
all of which significantly change with age. Rapid changes occur over
the first year of life as a result of the dramatic changes in circulation and
cardiac physiology. After infancy, subsequent changes are more gradual
until late adolescence and adulthood.
Heart rate
In children, cardiac output is determined primarily by heart rate as
opposed to stroke volume. With age, the heart rate decreases as the ventricles
mature and stroke volume plays a larger role in cardiac output.
Age and activity-appropriate heart rates thus must be recognized. Average
resting heart rate varies with age; newborns can range from 90–160 beats per
minute (bpm) and adolescents from 50–120 bpm. The average heart rate
peaks about the second month of life and thereafter gradually decreases until
adolescence (Fig. 1). Heart rates grossly outside the normal range for age
should be scrutinized closely for dysrhythmias
QRS axis
In utero, blood is shunted away from the lungs by the patent ductus
arteriosus, and the right ventricle provides most of the systemic blood
flow. As a result, the right ventricle is the dominant chamber in the newborn
infant. In the neonate and young infant (up to 2 months), the ECG shows
right ventricular dominance and right QRS axis deviation (Fig. 1). Most
of the QRS complex is reflective of right ventricular mass. Across the precordium,
the QRS complex demonstrates a large amplitude R wave (increased
R-/S-wave ratio) in leads V1 and V2, and small amplitude R wave
(decreased R-/S-wave ratio) in leads V5 and V6. As the cardiac and circulatory
physiology matures, the left ventricle becomes increasingly dominant.
Over time, the QRS axis shifts from rightward to a more normal position,
and the R-wave amplitude decreases in leads V1 and V2 and increases in
leads V5 and V6
PR interval
Similarly, the PR interval also varies with age, gradually increasing with
cardiac maturity and increased muscle mass. In neonates, it ranges from
0.08–0.15 sec and in adolescents from 0.120–0.20 sec [3]. The normal shorter
PR interval in children must be taken into account when considering the
diagnosis of conduction and atrioventricular (AV) block.
QRS complex duration
The QRS complex duration varies with age. In children, the QRS complex
duration is shorter, possibly because of decreased muscle mass, and
gradually increases with age. In neonates it measures 0.030–0.08 sec and
in adolescents 0.05–0.10 sec. A QRS complex duration exceeding 0.08 sec
in young children (younger than 8 years of age) or exceeding 0.10 sec in
older children may be pathologic. As a result, slight prolongation of what
may appear as a normal QRS complex can indicate a conduction abnormality
or bundle branch block in children.
QT interval
Because the QT interval varies greatly with heart rate, it is usually corrected
(QTc), most commonly using Bazett’s formula: QTc ¼ QT/ORR interval.
During the first half of infancy, the normal QTc is longer than in
older children and adults. In the first 6 months of life, the QTc is considered
normal at less than 0.49 sec. After infancy, this cutoff is generally 0.44 sec.
T waves
In pediatric patients, T-wave changes on the ECG tend to be nonspecific
and are often a source of controversy. What is agreed on is that flat or inverted
T waves are normal in the newborn. In fact, the T waves in leads V1
through V3 usually are inverted after the first week of life through the age of
8 years as the so-called ‘‘juvenile’’ T-wave pattern (see Fig. 1). In addition,
this pattern can persist into early adolescence (Fig. 2). Upright T waves in
V1 after 3 days of age can be a sign of right ventricular hypertrophy (RVH).
Chamber size
An assessment of chamber size is important when analyzing the pediatric
ECG for underlying clues to congenital heart abnormalities. P waves greater
than 2 mV (2 small boxes) in infants and greater than 3 mV (3 small boxes)
in adolescents may indicate right atrial enlargement (RAE). Because the
right atrium depolarizes before the left atrium, P-wave duration greater
than 0.08 sec (2 small boxes) in infants and 0.12 sec (3 small boxes) in adolescents
indicates left atrial enlargement (LAE).
RVH is best seen in leads V1 and V2 with an rSR#, QR (no S), or a pure R
(no Q or S) wave. RVH also may be suggested by the presence of a large S
wave in lead V6, upright T waves in leads V1–V3 after the first week of life,
or persistence of the right ventricular dominance pattern of the neonate.
Similarly, left ventricular hypertrophy (LVH) is suggested with the presence
of tall R waves in lead V6, large S wave in lead V1, left ventricular ‘‘strain’’
pattern in leads V5 and V6, and a mature precordial R-wave progression in
the newborn period. Biventricular hypertrophy is seen when ECG criteria
for enlargement of both ventricles is seen
source:
Pediatric ECG
Ghazala Q. Sharieff, MDa,b,*, Sri O. Rao, MDc
aChildren’s Hospital and Health Center/University of California–San Diego,
3020 Children’s Way, San Diego, CA 92123
bPediatric Emergency Medicine, Palomar-Pomerado Hospitals/California
Emergency Physicians, 555 East Valley Parkway, Escondido, CA 92025, USA
cDivision of Pediatric Cardiology, Children’s Hospital and Health Center,
3020 Children’s Way, San Diego, CA 92123, USA

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