It is the graphical representation or recording of electrical activity of the heart. We can diagnose rhythm and conduction disturbance as well as some congenital heart diseases by seeing the specific pattern. Pediatric ECG,s are different from those of adults. RV dominance is seen in the neonate and young infant as an effect of fetal circulation. It is gradually replaced by LV dominance throughout childhood and early adulthood. Pediatric ECG has some special characteristics:
1. Faster heart rate
2. PR interval. QRS duration and QT interval is shorter than adults.
3. RV dominance in ECG is characterized by

A. Right axis deviation.
B. Large rightward force (Tall R in aVR and right precordial leads and deep S in lead 1 and left precordial leads.)
C. The R/S ratio is large in RPLs.
D. The T wave is inverted in V1 with exception of first 3 days of life when it is upright.

ECG interpretation
  1. Rhythm sinus or not considering P axis.
  2. Heart rate (atrial and ventricular)
  3. The QRS axis
  4. Interval and duration(PR and QT interval and QRS duration)
  5. The P wave amplitude and duration.
  6. The QRS amplitude and R/S ratio, abnormal Q wave.
  7. ST segment and T wave abnormalities.
Normal Hear rate in children ;
  1. Neonate 110 – 150
  2. I month to 2 year 85-125
  3. >2 year to 4 year 75-115
  4. Over 4 year 60 – 100
QRS Axis.
Normal range:

a. 1 week to 1 month + 10 degree
b. 1-3 months + 70 degree
c. 3 months to 3 years + 60 degree
d. 3 years + 60 degree e. Adult +50 degree

Abnormal QRS axis

1. Left axis deviation (LAD) is seen in LVH, LBBB, Endocardial cushion defect, Tricuspid Atresia.
2. Right Axis deviation (RAD) seen in RVH, RBBB.
3. Superior axis is seen in left anterior hemiblock and extreme RAD.

PR interval

It varies with age and heart rate.

a. Prolong PR interval is seen in myocarditis, digitalis and quinidine toxicity, Hyperkalemia, ASD, Ebstein anomaly, myocardial dysfunction etc.
b. Short PR interval is seen in Wolff-Parkinson-White syndrome, Lown-Ganong-Levine syndrome, Duchenne-muscular Dystrophy, Friedreich Ataxia, Pheochromocytoma, Glycogen storage disease and in some normal children.

QT interval

QT interval varies with heart rate. The Herat rate-corrected QT interval is called QTc. It can be calculated by Bazett,s Formula.
QTc= QT/ square root of RR interval. A normal range is 0.40 +/_ 0.014 sec, Long QT interval is a serious precondition for ventricular arrhythmia.

Various components of ECG tracing
Following are some tracing of ECG which are found in some arrhythmias
and CHD.
1. Heart Block:

a). 1st degree heart block:

1st degree heart block

b) 2nd-degree heart block:
Mobitz type I: (Wenckebach Phenomenon).
Description: The PR interval becomes progressively prolonged until one QRS complex is dropped completely.

2nd degree heart block ( Mobitz type I )

Mobitz type II:
Description: The AV conduction is all or none. AV conduction is either normal or completely blocked.

2nd degree heart block ( Mobitz type II)

C. Complete Heart Block:

Complete heart block

2. Arrhythmias
     a. Supraventricular Tachycardia (SVT):


b. Ventricular Fibrillation

Chaotic tracing with no recognizable waves or complexes

c. Ventricular Tachycardia (VT)

Regular or irregular rythms, rate 150-250, no P waves, no PR intervals

d. Pulse less electrical activity (Occational spikes)

Pulseless electrical activity

e. Asystole (No spikes or waves)


3. Chamber Hypertrophy

1. Right Atrial hypertrophy is characterized by tall peaked P wave in Lead I and II. It may be due to right atrial volume or pressure overload secondary to tricuspid stenosis, pulmonary stenosis, pulmonary hypertension etc.

Right atrial Hypertrophy

2. Left atrial hypertrophy is due to volume and pressure overload of left atrium which is secondary to mitral or aortic vavular disease or systemic hypertension. It is characterized by biphasic P wave.

Left atrial hypertrophy
Left atrial abnormality

3. Right Ventricular Hypertrophy is a consequence of right-sided volume and pressure overload. It is characterized by tall R in V1 and deep S in V6. , rsR in V1 and V2 without widening of QRS complex. QR in V1 and V2 or pure r in V1 and V2 with or without ST changes.

Right ventricular hypertrophy

4. Left Ventricular hypertrophy is a consequence of LV volume or pressure overload. It is characterized by tall R in v6, lead 1 and deep S in V5,V6 and lead III.

Left ventricular hypertrophy
4. Congenital Heart Diseases

a. Atrial Spetal Defect (ASD):

B. Ventricular Septal Defect (VSD): Left ventricular/ Biventricular hypertrophy.
C. Patent Ductus Arteriosus (PDA): Normal axis, biventricular hypertrophy
D. Tetralogy of Fallot (TOF): Right axis deviation, Right ventricular hypertrophy
Other Cardiac Condition with ECG Findings
1. Right Bundle Branch Block (MARROW)
2. Left Bundle Branch Block (WILLIAM)

Note: (description of ECG photographs):

*1st deg heart block- Prolonged PR interval, regular rhythm.
*2nd deg heart block (Type 1)-PR interval progressively lengthens until I P wave is not conducted,
irregular rhythm.
*Complete heart block– No relation between P wave & QRS complexes, regular rhythm.
*SVT-Rate-150-250/m, regular rhythm, P wave & PR interval not seen, Narrow QRS.
*ASD-Tall P, Right ventricular hypertrophy (RVH) typically rsR pattern.
*VSD-Left ventricular hypertrophy (LVH)-tall R in V5 & V6.
*TOF-RVH with right axis deviation.
*RBBB– Broad QRS complex, Notched QRS complex and rSR pattern in V1-V2, wide & deep
S in V5-V6 and lead I.
*LBBB– Broad QRS complex, Notched QRS complex in V5-V6 and lead I & aVL, ST elevation,
left axis deviation.

3. Long QT Syndrome:

Long QT syndrome (LQTS) is a disorder of ventricular repolarization characterized by a prolonged QT interval on the ECG and ventricular arrhythmias, usually torsades de pointes, that may result in sudden death. LQTS occurs as the result of a defect in the ion channels, causing a delay in the time it takes for the electrical system to recharge after each heartbeat. It may result in sudden death. It can also cause sudden, uncontrollable, dangerous arrhythmias in response to exercise or stress.

Some acquired causes of QT Prolongation.

1. Drugs
Antibiotics: Erythromycin, clarithromycin,
telithromycin, azithromycin, trimethoprim- sulfamethoxazole.
Antifungal agents: Fluconazole, itraconazole, ketoconazole.
Antiprotozoal agents: Pentamidine isethionate.
Antihistamines: Astemizole, terfenadine (Seldane), (Seldane has been removed from the market for this reason).
Antidepressants: Tricyclics such as imipramine (Tofranil), amitriptyline (Elavil), desipramine (Norpamin), and doxepin (Sinequan).
Antipsychotics: Haloperidol, resperidone, phenothiazines such as thioridazine (Mellaril) and chlorpromazine (Thorazine).
Antiarrhythmic agents:
Class 1A (Sodium channel blockers): quinidine, procainamide, disopyramide. Class III (Prolong depolarization): Amiodarone (Rare), bretylium, dofetillide.
N- acetyl– Procainamide, sotalol
Lipid- lowering agents: Probucol.
Antianginals: Befpridil
Diuretics (Through K loss): Furosemide (Lasix), ethacrynic acid (Edecrine).
Oral hypoglycemic agents: Glibenclamide, glyburide. Organophosphate insecticides.
Promotility agents: Cisapride. Vasodilators: Prenylamine.
2. Electrolyte Distrubances:
Hypokalemia: Diuretics, Hyperventilation. Hypocalcemia. Hypomagnesemia.
3. Underlying Medical Conditions:
Bradycardia: Complete atrioventricular block, severe bradycardia, sick sinus syndrome. Myocardial dysfunction: Antracycidiotoxicity, congestive heart failure, myocarditis, cardiac tumors.
Endocrinopathy: Hyperparathyroidism, hypothyroidism, pheochromocytoma.
Neurologic: Encephalitis, head trauma, stroke, subarachnoid hemorrhage.
Nutritional: Alcoholism, anorexia nervosa, starvation.
Ref: Myung K Park. The Pediatric cardiology
handbook. 4rth edition.MOSBY.

Diagnostic criteria. A presentation with syncope or sudden cardiac death, in combination with a long QT interval on an ECG, typically suggests long QT syndrome (LQTS) and leads to genetic testing to diagnose the disease.

Long QT syndrome
Schwartz diagnostic criteria for long QT syndrome
ECG Findings

(In the absence of medications or disorders known to prolong the QTc interval)

For borderline cases of LQTS Schwartz et al refined diagnostic criteria using the point system.
a. </= , 1 point = low probability of LQTS
b. 2 to 3 point = intermediate probability of
c. >/=4 point = high probability of LQTS
Note: Routinely check serum levels of potassium (and sometimes magnesium) and thyroid function in patients who present with QT prolongation after arrhythmic events, to eliminate secondary reasons for repolarization abnormalities.

Management of congenital long QT syndrome.

1. General measures.

a. Physicians should avoid prescribing medications that prolong the QT interval.
b. No competitive sport is allowed. Swimming is not advised.

2. Treatment of congenital Long QT syndrome

a. B-blockers. B-blockers are the current treatment of choice. They reduce both syncope and sudden cardiac death, but cardiac events continue to occur while on B-blocker therapy. There is a consensus that all symptomatic children with long QT syndrome should be treated with propranolol or other B-blockers. (e,g, atenolol, metoprolol).
b. The ICD appears to be most effective therapy for high-risk patients, defined as those with aborted cardiac arrests or recurrent cardiac events despite conventional therapy (with B-blockers), and those with extremely prolonged QTc intervals (e.g, > 0.60 seconds). Patients with ICD should be kept on B-blockers.
c. Left cardiac sympathetic denervation.
d. Targeted Pharmacologic therapy. Sodium channel blocker mexiletine was used in patients with mutation in the
sodium channel gene SCN5A (LQT3) with significant shortening of the QTc.

3. Treatment of acquired long QT syndrome.
The management of acquired LQTS invoices acute treatment of arrhythmias (with intravenous magnesium), discontinuation of any precipitating drug, and correction of any metabolic abnormalities (such as hypokalemia or hypomagnesemia).

Short QT Syndrome:

Short QT syndrome is characterized by a very short QTc (<300 ms), symptoms of palpitation, dizziness or syncope and family history of sudden death. The cause of death is believed to be ventricular fibrillation. The syndrome is transmitted as an autosomal dominant manner. Treatment plans similar to those described for long QT syndrome should apply.

Brugada Syndrome:

The rare condition is more common among young men in Southeast Asia. Mutations in the sodium channel appear to be the cause of the condition. The patient may present with complaints of blackout or palpitations. The ECG typically shows RBBB with J point elevation and concave ST elevation best seen in V1. There may be a family history of sudden death. Diagnosis is suspected on the basis of the ECG appearance, which may not always be present, however. No antiarrhythmic drug, including B-blockers, appears to reduce the risk of death in these patients. The current standard practice, therefore, is to use an ICD to protect most patients.

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