Pediatric ECG Interpretation
At birth, the right ventricle is larger and thicker than the left ventricle, reflecting the greater physiological stresses placed upon it in utero (i.e. pumping blood through the relatively high-resistance pulmonary circulation).
This produces an ECG picture reminiscent of right ventricular hypertrophy in the adult: marked rightward axis, dominant R wave in V1 and T-wave inversions in V1-3.
Conduction intervals (PR interval, QRS duration) are shorter than adults due to the smaller cardiac size. Heart rates are much faster in neonates and infants, decreasing as the child grows older.
Common Findings on the Paediatric ECG
The following electrocardiographic features may be normal in children:
- Heart rate >100 beats/min
- Rightward QRS axis > +90°
- T wave inversions in V1-3 (“juvenile T-wave pattern”)
- Dominant R wave in V1
- RSR’ pattern in V1
- Marked sinus arrhythmia
- Short PR interval (< 120ms) and QRS duration (<80ms)
- Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months)
- Slightly long QTc (≤ 490ms in infants ≤ 6 months)
- Q waves in the inferior and left precordial leads.
Normal Paediatric ECG
This ECG of a healthy 2-year old boy displays many of the typical features of the paediatric ECG:
- Heart rate of 110 bpm (normal for age).
- Dominant R waves in V1-3.
- RSR’ pattern (partial RBBB morphology) in V1.
- Juvenile T-wave pattern (T wave inversion in V1-3).
More Normal ECG examples
Normal ECG : 1 Year
Normal ECG : 2 Years
Normal ECG : 5 Years
Normal ECG : 10 Years
A Guide to Paediatric ECG Interpretation
The right ventricular dominance of the neonate and infant is gradually replaced by left ventricular dominance so that by 3-4 years the paediatric ECG resembles that of adults.
- Placement of ECG leads
- Stepwise assessment of the ECG
- Characteristic ECG patterns for particular conditions
- Abnormal rhythms
(1) Placement of ECG leads
In young children, the right ventricle normally extends to the right side of the sternum. To appropriately display right ventricular potentials, ECGs for children in the under five-year age group must include an alternate lead (‘V4R’) on the right side of the chest at a point analogous to the left sided V4.
- V4R: 5th intercostal space, right midclavicular line
- V1: 4th intercostal space, right sternal border
- V2: 4th intercostal space, left sternal border
- V3: use this lead for V4R, must label as such on ECG.
- V4: fifth intercostal space, left midclavicular line.
- V5: anterior axillary line, same horizontal plane as V4
- V6: midaxillary line, same horizontal line as V4.
- Place on top part of arm or leg (less muscle interference).
(2) Stepwise Assessment of the ECG
Sinus: Atrial depolarisation starts from the sinoatrial node. This requires:
- P wave preceding each QRS complex, with a constant PR interval.
- Normal P wave axis (zero to +90 degrees), i.e. P wave is upright in leads I and aVF.
Non-sinus: Some atrial rhythms may have P waves in front of every QRS but with an abnormal P axis (inverted in lead II).
Usual paper speed is 25mm/sec so 1mm (small square) = 0.04 sec, and 5mm (big square) = 0.2 sec. Calculate atrial and ventricular rates separately if different. Many methods to estimate the rate, for example:
- For regular rhythms: 300 / number of large squares in between each consecutive R wave.
- For very fast rates: 1500 / number of small squares in between each consecutive R wave.
- For irregular rhythms: number of complexes on the rhythm strip x 6.
Resting heart rate varies with age:
- Newborn: 110 – 150 bpm
- 2 years: 85 – 125 bpm
- 4 years: 75 – 115 bpm
- 6 years+: 60 – 100 bpm
Ventricular rate is faster at baseline for younger children. The younger the child, the higher the metabolic rate and lower vagal tone. [O’Connor, 2008]
2.3 QRS axis
Calculated using the hexaxial reference system that shows the frontal view of the electrical activity of the heart via the six limb leads.
- Lead 1: the R wave represents the leftward force, the S wave the rightward force.
- aVF: the R wave represents the downward force, the S wave the upward force.
A suggested method of axis calculation
Normal QRS axis varies with age:
- 1 week – 1 month: + 110° (range +30° to +180°)
- 1 month – 3 months: + 70° (range +10° to +125°)
- 3 months – 3 years: + 60° (range +10° to +110°)
- Over 3 years: + 60° (range +20° to +120°)
- Adult: + 50° (range -30° to 105°)
**Initial right ventricular (RV) dominance
In utero, blood is shunted away from the pulmonary vasculature leading to high pulmonary pressures and a relatively thick Right Ventricle (RV)
- Initial Right Axis on ECG is normal and resolves after the first 6 months of life
- An extreme superior Axis (Axis of -90 to -180 degreesis seen with AV canal or osmium primum atrial septal defects.
2.4 ECG intervals
The normal PR interval varies with age and heart rate:
Prolonged PR interval (first degree heart block) may be normal or be seen in:
- Viral or rheumatic myocarditis and other myocardial dysfunctions
- Certain congenital heart disease (Ebsteins, ECD, ASD)
- Digitalis toxicity
Short PR interval occurs in:
- Pre-excitation (eg Wolff-Parkinson-White)
- Glycogen storage disease
Variable PR interval occurs in:
- Wandering atrial pacemaker
- Wenckebach (Mobitz type 1) second degree heart block
QRS duration varies with age:
Prolonged QRS is characteristic of ventricular conduction disturbances:
- Bundle branch blocks
- Pre-excitation conditions (eg WPW)
- Intraventricular block
- Ventricular arrhythmias
QT interval varies with heart rate:
Bazett formula is used to correct the QT for HR:
- QTc = QT measured / (√R–R interval)
- Infants less than 6 months = < 0.49 seconds.
- Older than 6 months = < 0.44 seconds.
QTc is prolonged in:
QTc is short in:
2.5 P wave amplitude and duration
- Normal P-wave amplitude is < 3mm (tall P waves = right atrial enlargement).
- Normal P wave duration is < 0.09 seconds in children and < 0.07 seconds in infants (wide P waves = left atrial enlargement).
- A combination of tall and wide P waves occurs in combined atrial hypertophy.
2.6 QRS amplitude (voltages)
High QRS amplitudes are found in:
- Ventricular hypertrophy
- Ventricular conduction disturbances eg BBB’s, WPW
Low QRS amplitudes are seen in:
Ventricular hypertrophy produces changes in one or more of the following areas: the QRS axis, the QRS voltages, the R/S ratio or the T axis.
R and S wave voltages children
Axis: RAD for the patients age
Voltages: Tall R waves (greater than limits for patient’s age) in right-sided leads V4R and V1. Deep S waves (greater than limits for patient’s age) in left-sided leads V5 and V6.
R/S ratio: Abnormal R/S ratio in favour of RVH.
- Increased R/S ratio (greater than upper limits for child’s age) in V1-2.
- R/S ratio < 1 in V6 (after one month of age).
Abnormal T waves:Upright T waves in V1 and V4R in children 3 days to 6 years (provided that T waves are normal elsewhere, i.e. upright in V6). This is evidence alone of significant RVH.
Abnormal Q waves:qR pattern in V1 (small Q wave, tall R wave) = highly specific for RVH.
Axis: LAD for the patients age (marked LAD is rare with LVH).
- Tall R waves in the left-sided leads V5 and V6 (greater than limits for patient’s age).
- Deep S waves in the right-sided leads V4R and V1 (greater than limits for patient’s age).
- Abnormal R/S ratio in favour of LV
- Decreased R/S ratio in V1-2 (less than upper limits for child’s age)
Abnormal Q waves in V5 and V6
Inverted T waves in I and aVL (LV strain pattern)
- Positive voltage criteria for RVH and LVH (with normal QRS duration).
- Positive voltage criteria for RVH or LVH and relatively large voltages for other ventricle.
- Large equiphasic QRS complexes in two or more limb leads and in mid-precordial leads (V2-5).
Small chest walls exaggerate precordial voltages. Evans et al proposed a practical approach to evaluation:
Abnormal Left Ventricular Large Voltage (“LVH”)
- Use only V6 (the left most precordial lead).
- If R wave of V6 intersects with baseline of V5, this is ABNORMAL
Abnormal Right Ventricular Large Voltage (“RVH”)
Use only V1 (the right most precordial lead)
- Upright T wave in V1: In first week of life is NORMAL. Between week 1 and adolescence this is ABNORMAL
- RSR’ in V1: If R’ is taller than R – this is ABNORMAL.
- Pure R wave in V1: If child > 6 months old – this is ABNORMAL
2.7 Q waves
Normal Q waves:
- Narrow (average 0.02 seconds and less than 0.03 seconds).
- Usually less than 5mm deep in left precordial leads and aVF.
- May be as deep as 8mm in lead III in children younger than 3 years.
Q waves are abnormal if they:
- Appear in the right precordial leads ie V1 (eg severe RVH).
- Are absent in the left precordial leads (e.g. LBBB).
- Are abnormally deep (ventricular hypertrophy of the volume overload type).
- Are abnormally deep and wide (myocardial infarction or fibrosis).
2.8 ST segment
The normal ST is isoelectric. Elevation or depression is judged in relation to the TP segment.
Some ST changes may be normal:
- Limb lead ST depression or elevation of up to 1mm (up to 2mm in the left precordial leads).
- J-point depression: the J point (junction between the QRS and ST segment) is depressed without sustained ST depression, i.e. upsloping ST depression.
- Benign early repolarisation in adolescents: the ST segment is elevated and concave in leads with an upright T wave.
Others are pathological:
- A downward slope of the ST followed by a biphasic inverted T.
- A sustained horizontal ST segment depression 0.08 sec or longer.
Pathological ST segment changes are commonly associated with T wave changes and occur in:
- Myocardial ischaemia or infarction.
- Severe ventricular hypertrophy (ventricular strain pattern).
- Digitalis effect
2.9 T Waves
The precordial T-wave configuration changes over time:
- For the first week of life, T waves are upright throughout the precordial leads.
- After the first week, the T waves become inverted in V1-3 (= the “juvenile T-wave pattern”)
- This T-wave inversion usually remains until ~ age 8; thereafter the T waves become upright in V1-3.
- However, the juvenile T-wave pattern can persist into adolescence and early adulthood (= “persistent juvenile T waves”).
Tall, peaked T waves are seen in:
Flat T waves are seen in:
Large, deeply inverted T waves are seen with:
- Raised intracranial pressure (e.g. intracranial haemorrhage, traumatic brain injury)
2.10 U waves
U Waves are the extra positive deflection at the end of a T wave. Most common causes:
(c) Characteristic ECG patterns for particular conditions
ECG Abnormalities in children:
- Pericarditis (usually viral).
- Myocarditis (viral or rheumatic).
- Myocardial infarction (e.g. in children with anomalous coronary arteries / post-cardiac surgery / thrombophilia).
- Hypocalcaemia / hypercalcaemia.
- Hypokalaemia / hyperkalaemia.
- Wolff-Parkinson-White syndrome (see “Abnormal Rhythms” section below)
Pericardial effusion may produce QRS voltages less than 5 mm in all limb leads. Sub-epicardial myocardial damage causes time dependent change:
- Initial widespread concave ST segment elevation and PR segment depression.
- ST segment returns to normal within 1-3 weeks, along with flattening of the T waves.
- T wave inversion (with isoelectric ST segment) occurs from 2-4 weeks after the onset of pericarditis.
ECG findings of rheumatic or viral myocarditis are relatively non-specific and may include:
- AV conduction disturbances, ranging from PR prolongation to complete AV dissociation.
- Low QRS voltages (5 mm or less in all limb leads)
- Decreased T wave amplitude.
- QT prolongation.
- Tachyarrythmias including SVT and VT.
- ‘Pseudoinfarction’ pattern with deep Q waves and poor R wave progression in precordial leads.
NB. prolonged PR interval is a minor Jones criteria for acute rheumatic fever.
Myocardial infarction / ischaemia
The appearances are normally identical to those seen in adult ischaemia or infarction.
- Infarction: ST elevation in contiguous leads with reciprocal ST depression elsewhere.
- Ischaemia: Horizontal ST depression.
- Hypocalcaemia prolongs the ST segment with resulting prolongation of the QTc.
- Hypercalcaemia shortens the ST segment and the QTc.
The T wave is relatively unaffected in both conditions.
With K+ < 2.5 mmol/L:
- Prominent U waves develop with apparent prolongation of the QTc (prolonged “QU” interval)
- Flat or biphasic T waves
- ST segment depression
As K+ falls further:
- PR interval prolongs.
- Sinoatrial block may occur.
As K + rises (> 6.0 mmol/L):
- Tall peaked T waves, best seen in precordial leads.
- Prolongation of QRS duration.
- Prolongation of PR interval.
- Disappearance of P waves.
- Wide bizarre biphasic QRS complexes (sine waves).
- Eventual asystole.
(e) Abnormal rhythms
Supraventricular Tachycardia (SVT)
Characteristics of SVT
- Rapid regular, usually narrow (< 80 ms) complex tachycardia of 220-320bpm in infants and 150-250 in older children.
- The P wave is usually invisible, or if visible is abnormal in axis and may precede or follow the QRS (“retrograde P waves”).
- 90% of paediatric dysrhythmias are SVT; 90% of SVT are of re-entrant type.
- Half of patients with SVT will have no underlying heart disease.
- Consider fever or drug exposure (particularly sympathomimetics).
- Almost 1⁄4 will have congenital heart disease and 1⁄4 will have WPW.
- SVT may be well tolerated in infants for 12-24 hours. Congestive heart failure later manifests with irritability, poor perfusion, pallor, poor feeding and then rapid deterioration.
- Note that > 95% of wide complex tachycardias in paediatrics are NOT VT, but SVT with aberrancy, SVT with BBB (in pre-existing congenital heart disease) or a type of accessory pathway re-entrant SVT (see below).
- Do NOT use verapamil or beta blockers in infants or children with SVT – may cause profound AV block, negative inotropy and sudden death.
Types of Supraventricular tachycardia (SVT)
Supraventricular tachycardia comprises two main types:
- Re-entrant SVT
- Automatic SVT
- This comprises the majority of SVT (90%).
- HR doses not vary substantially in re-entrant tachycardia.
- Typically begins and ends abruptly.
Requires a bypass pathway between atria and ventricles in addition to the AV node. Bypass pathway can be either an anatomically separate accessory pathway (the Bundle of Kent as in most cases of Wolf-Parkinson-White) or a functionally separate pathway within the AV node (called AV nodal re-entry tachycardia).
For SVT to occur the two pathways must have at least, temporarily, different conduction and recovery rates. A circular rhythm down one path and up the other begins when an atrial or ventricular contraction finds one pathway able to conduct while the other is temporarily refractory.
If the second path is able to conduct by the time the impulse has passed through the AV node, it may conduct the opposite direction; thus setting up a re-entry tachycardia.
The ECG findings will vary according to the type of bypass tract (anatomic or functional) and the direction of the impulse flow through the AV node (atrium to ventricle, or visa versa).
The presence of AV block will interrupt any re-entrant tachycardia that involves the AV node; therefore adenosine (transiently blocks AV conduction) works well for these rhythms. Several atrial rhythms; atrial flutter, atrial fibrillation and sinoatrial node re-entry tachycardia are also considered subgroups of re-entrant SVT. These do not respond to adenosine but the transient slowing of the ventricular rate may unmask the atrial activity and therefore underlying cause of the SVT. A running rhythm strip is therefore imperative.
Example of SVT
Example 1(a) – Narrow-complex tachycardia in a 12-day old boy
- Rapid narrow complex tachycardia at around 300 bpm.
Example 1(b) – Narrow-complex tachycardia in a 12-day old boy — paper speed at 50 mm/sec
- The same patient with the paper at double speed (50 mm/s).
- There are no visible P waves — this is an AV nodal re-entry tachycardia.
Example 1(c) – Normal sinus rhythm in a 12-day old boy
- This is the same patient after reversion to sinus rhythm.
- Slightly peaked P waves, right axis and tall R waves in V1 are all within normal limits for the patients age.
WPW syndrome is characterised by the occurrence of SVT plus specific ECG findings in sinus rhythm. The characteristic pre-excitation is evidenced by a short PR interval and widened QRS with a slurred upstroke or delta wave.
It is caused by earlier ventricular excitation occurring via the accessory pathway than have occurred via the normal AV node alone. With the onset of SVT, conduction reverses (becomes V to A) in the accessory pathway as part of the circular rhythm.
In a small number of patients with WPW, accessory pathway conduction is A to V in SVT (and reversed to become V to A in the AV node). This results in an anomalous ventricular activation sequence and a wide complex QRS (> 120 msec) and followed by retrograde P waves which may be difficult to differentiate from VT.
Examples of WPW
Antidromic AVRT due to WPW in a 5-year old boy.
- Broad complex tachycardia at ~280 bpm.
- This could easily be mistaken for VT; however, remember that >95% of broad complex tachycardias in paediatrics are actually SVT with aberrancy (usually a re-entrant tachycardia).
- This is an antidromic atrioventricular re-entry tachycardia due to WPW.
Example 2(b) – WPW in a 5-year old boy.
This is the resting ECG of the same 5-year boy, shortly after reversion to sinus rhythm. Note:
- Very short PR interval (< 100 ms).
- Slurred upstroke to the QRS complexes = the delta wave.
- In contrast to WPW in adults, the QRS complex is not particularly wide (80-100 ms).
- There is a “pseudoinfarction” Q wave in aVL (simply an inverted delta wave).
- Rightward axis (+90 degrees), RSR’ pattern in V1 and T-wave inversion in V1-2 is normal for age.
See how subtle these changes are compared to WPW in adults.
Antidromic AVRT due to Wolf-Parkinson-White in a 15-year old boy. This case is discussed further in ECG Exigency 004.
Another example of Wolf-Parkinson-White, this time in a 7-year old child, demonstrating:
- Short PR interval.
- Delta waves.
- Mild QRS prolongation.
- Rightward axis (+90 degrees), dominant R wave in V1 and inverted/biphasic T waves in V1-2 are normal for the patients age.
SVT due to abnormal or accelerated normal automaticity (e.g sympathomimetics). Usually accelerate (‘warm up’) and decelerate (‘cool down’) gradually.
- Sinus tachycardia: enhanced automatic rhythm. Rate varies with physiological state.
- Atrial Tachycardia: non-reciprocating or ectopic atrial tachycardia – rapid firing of a single focus in the atria. Slower heart rate (130-160). Rare. Usually constant rather than paroxysmal.
- Junctional Ectopic Tachycardia: difficult to treat, usually occurs in setting of post extensive atrial surgery. Rapid firing of a single focus in the AV node. Slower rhythm – 120-200bpm.
Management of SVT
A 12 lead ECG in SVT and post conversion is essential. Essential to monitor with a rhythm strip during manoeuvres ie in SVT and post conversion – allows later assessment of underlying rhythm in unclear cases.
If reversion to sinus rhythm occurs but is not sustained, there is little to be gained by persisting with that manoeuvre/drug.
1. Acute treatment:
Aim to induce AV nodal slowing
- Infants: ice plus water in bag placed on face for up to 10 seconds – often effective.
- Older children: carotid sinus massage, valsalva manoeuvre (30 –60 seconds), deep inspiration/cough/gag reflex, headstand.
- Half life: <1.5 seconds: transient AV nodal block as well as sinus node block, negative chronotrope, ionotope.
- Side effects: flushing, nausea, dyspnea, bronchospasm are short lived.
- Give 100 mcg/kg rapidly into a large vein. Repeat after 2 minutes with 250 mcg/kg.
- Maximum total dose 12mg
- Be very wary of cardioverting an ‘unstable’ child in a SVT in ED who remains conscious to the point of requiring sedation or anaesthesia.
- Rapid deterioration of the ‘SVT-stressed’ myocardium may occur with anaesthesia.
- If shock is present, synchronous DC shock is indicated 0.5-2 J/kg (monophasic).
2. Chronic treatment
Conducted as an inpatient; either medical or surgical/catheter pathway ablation.
Broad Complex Tachydysrhythmias
VT is extremely rare in children. There is usually a history of structural (congenital) cardiac abnormality.
Occurs in long QT syndrome and with some drugs. Causes syncope if self-terminating or cardiac arrest if prolonged (i.e. degenerates to VF).
Also extremely rare in children and associated with congenital cardiac abnormalities. Treatment is DC shock at 4 joules / kg.
- Paediatric Electrocardiography by Steve Goodacre and Karen McLeod, from the BMJ’s “ABC of Clinical Electrocardiography” series (2002)
- O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram. Part I: Age-related interpretation. Am J Emerg Med. 2008 Feb;26(2):221-8. PMID: 18272106
- Evans WN1, Acherman RJ, Mayman GA, Rollins RC, Kip KT. Simplified pediatric electrocardiogram interpretation. Clin Pediatr (Phila). 2010 Apr;49(4):363-72. PMID: 20118092
LITFL Further Reading
- ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
- ECG A to Z by diagnosis – ECG interpretation in clinical context
- ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
- 100 ECG Quiz – Self-assessment tool for examination practice
- ECG Reference SITES and BOOKS – the best of the rest
- Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric
- Wagner GS. Marriott’s Practical Electrocardiography 12e
- Chan TC. ECG in Emergency Medicine and Acute Care
- Rawshani A. Clinical ECG Interpretation
- Mattu A. ECG’s for the Emergency Physician
- Hampton JR. The ECG In Practice, 6e