Paediatric ECG Interpretation

Background

  • 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.

Example of a 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).

 

A Guide to Paediatric ECG Interpretation

The following comprehensive guide to paediatric ECG interpretation was produced by Paediatric Emergency Specialists Dr Gary Geelhoed and Dr Barbara King from the Princess Margaret Hospital for Children in Perth, Western Australia. It is so good that I have reproduced it almost verbatim (with a few extra ECGs from the LITFL archives). Enjoy!

“The ECG in Paediatric ED”

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.

Contents

(a) Placement of ECG leads
(b) Stepwise assessment of the ECG
(c) Normal ECGs for various ages
(d) Characteristic ECG patterns for particular conditions
(e) Abnormal rhythms

 

(a) 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 extra lead (‘V4R’) on the right side of the chest at a point analogous to the left sided V4.

Precordial leads:

  • 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, right midclavicular line
  • V5: anterior axillary line, same horizontal plane as V4
  • V6: midaxillary line, same horizontal line as V4.

Limb leads: Place on top part of arm or leg (less muscle interference).

 

(b) Stepwise Assessment of the ECG

1. Rhythm

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).

 

2. Rate

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.

[Or just use the computer reading!]

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

 

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.

  • In lead 1, the R wave represents the leftward force, the S wave the rightward force.
  • In aVF, the R wave represents the downward force, the S wave the upward force.

A suggested method of axis calculation: the successive approximation method.

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°)

 

4. ECG intervals

The intervals of the ECG are illustrated below.

waves of the ecg

 

PR Interval

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
  • Hyperkalaemia

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

Read more about the PR interval here

 

QRS Duration

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

Read more about QRS duration here.

 

QT Interval

QT interval varies with heart rate.

Bazett’s formula is used to correct the QT for HR:

QTc = QT measured / (√R–R interval)

Normal QTc

  • Infants less than 6 months = < 0.49 seconds.
  • Older than 6 months = < 0.44 seconds.

QTc is prolonged in:

QTc is short in:

Read more about QT abnormalities here.

 

5. P wave amplitude and duration

Read about the normal adult P wave here.

 

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.

 

Right ventricular hypertrophy

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.

Compare this with the criteria for RVH in adults.

 

Left ventricular hypertrophy

Axis: LAD for the patients age (marked LAD is rare with LVH).

Voltages:

  • 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).

R/S ratio: 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)

Compare this with the criteria for LVH in adults

 

Biventricular hypertrophy

  • 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).


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).

 

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.
  • Early repolarisation in adolescents: the ST segment is elevated and concave in leads with an upright T wave. Read more about benign early repolarisation here.

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.

  • A = upsloping ST depression / J-point depression (normal variant)
  • B = downsloping ST depression (usually abnormal)
  • C = horizontal ST depression (usually abnormal)

Pathological ST segment changes are commonly associated with T wave changes and occur in:

  • Pericarditis.
  • Myocardial ischaemia or infarction.
  • Severe ventricular hypertrophy (ventricular strain pattern).
  • Digitalis effect.

 

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:

 

10. U waves

A U Wave is an extra positive deflection at the end of a T wave. Most common causes:

Normal U wave in an adolescent

Read more about the U wave here.

 

(c) Normal ECGs at various ages

 

(d) Characteristic ECG patterns for particular conditions

ECG Abnormalitites in children:

  • Pericarditis (usually viral).
  • Myocarditis (viral or rheumatic).
  • Myocardial infarction (e.g. in children with anomalous coronary arteries / post-cardiac surgery / thrombophilia).
  • Hypo/hypercalcaemia.
  • Hypo/hyperkalaemia.
  • Wolff-Parkinson-White syndrome (see “Abnormal Rhythms” section below)

 

Pericarditis

Pericardial effusion may produce QRS voltages less than 5 mm in all limb leads.

Sub-epicardial myocardial damage causes time dependant 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.

Read more about pericarditis here.

 

Myocarditis

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.

Calcium abnormalities

The T wave is relatively unaffected in both conditions.

 

Potassium abnormalitites

Hypokalaemia

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.

Hyperkalaemia

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 Tachycardias

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.

SVT at ~250 bpm (the RSR' pattern in V1 is a normal finding in children)

 Types of SVT

Supraventricular tachycardia comprises two main types:

  1. Re-entrant SVT
  2. Automatic SVT

Re-entrant SVT

  • This comprises the majority of SVT (90%)
  • HR doses not vary substantially in re-entrant tachycardia.
  • Typically begins and ends abruptly.

Mechanisms

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.

Different types of re-entry loops: Functional loop within the AV node (left); anatomical loop involving an accessory pathway = the Bundle of Kent (right)

 

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.

 

Wolff-Parkinson-White Syndrome

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

Example 2(a) – 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.

 

Example 3 – Antidromic AVRT due to WPW in a 15-year old boy

  • Another example of antidromic AVRT due to WPW — this patient was discussed in ECG Exigency 004.

 

Example 4 – WPW in a 7-year old girl

Another example of WPW, 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.

Automatic SVT

SVT due to abnormal or accelerated normal automaticity (e.g sympathomimetics). Usually accelerate (‘warm up’) and decelerate (‘cool down’) gradually.

Includes:

  • 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: aims to induce AV nodal slowing

Vagal manoeuvres

  • 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.

Adenosine

  • 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

Cardioversion

  • 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

• VT is extremely rare in children. There is usually a history of structural (congenital) cardiac abnormality.

Polymorphic VT / Torsades de Pointes

• Occurs in long QT syndrome and with some drugs. Causes syncope if self-terminating or cardiac arrest if prolonged (i.e. degenerates to VF).

VF

  • Also extremely rare in children and associated with congenital cardiac abnormalities. Treatment is DC shock at 4 joules / kg.

Useful Links

Check out these other great resources on paediatric ECG interpretation:

  • Paediatric Electrocardiography by Steve Goodacre and Karen McLeod, from the BMJ’s “ABC of Clinical Electrocardiography” series (2002).
  • The Paediatric ECG by Ghazala Sharieff and Sri Rao from the Emergency Medicine Clinics of North America (2006).
  • Paediatric ECG of the Week by Marion Tipple – an online selection of paediatric ECGs to test your skills. Dr Tipple (a paediatric cardiologist) also has a cool i-phone app called “Paed ECG” with more of the same.

Further Reading

Author Credits

  • Words – Ed Burns (Introduction, ECG interpretations); Gary Geelhoed & Barbara King (Guide to Paediatric ECG Interpretation)
  • Pictures – Ed Burns (ECGs), Gary Geelhoed & Barbara King (diagrams)
  • Web Editing – Ed Burns

References

  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
  • Hampton JR. The ECG Made Easy. 7th edition. London: Churchill Livingstone 2008.
  • Park MK. Pediatric Cardiology for Practitioners. 5th edition. St Louis: Mosby 2007.
  • Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th Edition. Saunders Elsevier 2008.
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