Systematic interpretation against age-specific norms, the physiology behind each finding, measurement technique, congenital & arrhythmia signatures, and a presentation-based approach. Illustrated, with an RCH vs Starship comparison.
Read first. An interpretation aid, not a substitute for senior/cardiology review. Interpret every ECG within the clinical picture; a senior clinician reviews all abnormal findings and any child with cardiac red flags is discussed even if the trace is normal. Machine-reported values are a guide only — measure manually. ECG traces here are schematic illustrations, not patient recordings. Drug doses are indicative — confirm against CREDD / local protocol. Follow local Metro South / QLD cardiology pathways (QCH / CATCH 13 22 82).
Interpretation checklistwork top to bottom · tick as you go · tap to collapse
Don't skip step 1. A wrong age or miscalibration makes every value below meaningless. A normal ECG never excludes cardiac disease — escalate on red flags regardless.
1
What the ECG is actually showing you
each deflection = one electrical event
The ECG is a voltage-vs-time recording of myocardial depolarisation and repolarisation. A deflection is positive when the wavefront travels toward a lead, negative when away, and biphasic when perpendicular. Every abnormality — hypertrophy, block, ischaemia, channelopathy — is a distortion of this basic sequence.
P (atrial depolarisation) → PR segment (AV-node delay) → QRS (ventricular depolarisation) → ST → T (ventricular repolarisation) → occasional U wave.
Why the shapes: the QRS is tall & sharp because a large ventricular mass depolarises fast via His–Purkinje; the P is small & rounded (small atrial mass); the flat PR segment is the AV-node delay that lets atrial contraction top up the ventricles before systole; the T is broad because repolarisation is slower and less synchronised than depolarisation.
Physiology — the AV-node delay
The PR segment is isoelectric not because nothing happens but because the impulse is held in the AV node (~100 ms). This synchronises atrial "kick" with ventricular filling. Bypass it (accessory pathway → WPW) and PR shortens with a delta wave; exaggerate it (fibrosis, high vagal tone, ↑K⁺, myocarditis, digoxin) and you get first-degree block.
2
Before you read
calibration decides every number
Standard paper: 25 mm/s, 10 mm/mV.
1 small sq = 0.04 s & 1 mm; 1 large sq = 0.2 s & 5 mm. A calibration pulse should be 10 mm tall.
Four checks before interpreting
Right child + age — age reframes every value below.
Calibration & paper speed — 25 mm/s, 10 mm/mV; note half-standard (5 mm/mV) traces, which halve apparent voltages.
Lead placement & artefact — infant tremor/movement mimics flutter/VT; check all limb leads present.
Compare with old ECGs if available, and read the machine's numbers only after checking them.
3
How to measure — the numbers that get miscalled
axis · rate · QTc technique
QRS axis — quadrant method
Read the net QRS deflection in lead I and aVF, then place the quadrant. Refine by finding the most isoelectric limb lead — the axis lies roughly perpendicular to it.
Lead I
aVF
Axis quadrant
+
+
Normal (0 to +90°)
+
−
Left axis deviation (0 to −90°)
−
+
Right axis deviation (+90 to +180°)
−
−
Extreme / "superior" / NW axis
Interpret against age
RAD is normal in the newborn (up to +180°) and only abnormal once you'd expect the LV to dominate. Conversely a superior/left axis in an infant is a red flag for AVSD or tricuspid atresia — the counter-clockwise depolarisation loop of an endocardial cushion defect. Always compare the measured axis to the §6 age range, not the adult range.
Rate
Regular rhythm
300 ÷ number of large squares between two R waves (300-150-100-75-60-50), or 1500 ÷ small squares for precision.
Irregular rhythm
Count QRS complexes in a 6-second strip × 10 — the only reliable method when R–R varies.
Two rates?
In complete heart block, measure the atrial (P–P) and ventricular (R–R) rates separately.
QT and QTc — where errors happen
Tangent method: end of T = where the steepest downslope tangent meets baseline.
Measure in lead II or V5, over 3–5 beats, take the longest. Exclude the U wave.
Bazett over-corrects at fast rates and under-corrects at slow ones, and is unreliable above ~100 bpm — so a "long" QTc on a crying, tachycardic infant is often spurious: settle the child and repeat. Fridericia (÷ ∛RR) is steadier at rate extremes. A prominent U wave merged into T falsely lengthens QT — measure a lead without it.
4
The systematic read
same order, every time — with differentials
1
Rate
Normal for age (§6)? Tachy: sinus (has a cause) vs SVT vs VT vs flutter/AF. Brady: sinus (vagal/athlete/sleep — but ominous in a hypoxic neonate), junctional, AV block, ↑ICP, hypothyroid, hypothermia, drugs.
2
Rhythm
Sinus = upright P in I/II/aVF preceding every QRS, uniform P morphology, constant PR. Sinus arrhythmia (phasic with respiration) is normal & healthy. Non-sinus P axis → ectopic atrial/junctional. AV dissociation → block or VT.
3
Axis
Quadrant from I/aVF (§3). LAD → LVH, LAFB. Superior/NW axis → AVSD, tricuspid atresia, also WPW, VT. RAD beyond age norm → RVH, RV strain.
4
P wave
Tall >3 mm (P pulmonale) = RAE → Ebstein, tricuspid atresia, severe PS, pulmonary HTN. Wide/bifid >0.10 s (P mitrale) = LAE → MV disease, large L→R shunt, LV failure, HOCM.
5
PR interval
Age-dependent (§6). Long = 1° AV block (vagal/normal, myocarditis, rheumatic, ↑K⁺, digoxin, ASD, Ebstein). Short + delta → WPW. Short without delta → glycogen storage, junctional.
6
QRS duration
>0.12 s pathological (limit lower in the young). Wide → BBB, WPW, ventricular rhythm, hyperkalaemia, Na-channel-blocker toxicity (TCA). ‘WiLLiaM MaRRoW’: V1/V6 — W…M = LBBB, M…W = RBBB.
7
QRS voltage & Q waves
R/S vs age limits (§8) for RVH/LVH. Abnormal Q: in V1 (RVH/single ventricle), deep/wide in I-aVL-V5-6 (HCM, or ALCAPA in an infant with heart failure), absent in V5–6. Low voltages → effusion, myocarditis, hypothyroid.
Inversion V1–V3 is the normal childhood pattern. Upright T in V1 from 4 d–4 yr = RVH. Peaked → ↑K⁺; flat + U → ↓K⁺; deep symmetric TWI in V1–3 beyond childhood → ARVC or RV strain.
10
QT / QTc
Bazett + tangent, lead II/V5 (§3). Thresholds differ by guideline (§7). Long → LQTS, ↓Ca²⁺/↓K⁺/↓Mg²⁺, drugs, ↑ICP. Short → ↑Ca²⁺, short-QT syndrome. Suspect LQTS → cardiology before discharge.
5
Why a child's ECG changes as they grow
the RV hands over to the LV
Almost every paediatric quirk comes from one story: the RV is dominant at birth and the LV takes over through childhood. Track that shift and the age changes in axis, precordial voltages and T waves all follow.
Physiology — fetal RV dominance
In the fetus the lungs are collapsed and pulmonary vascular resistance is high; most RV output is shunted across the ductus into the systemic circulation, so the RV pumps at systemic pressure and is as thick as or thicker than the LV at birth. After birth the lungs open, PVR falls, the ductus closes, and the LV progressively hypertrophies to meet the systemic load while the RV regresses — playing out on the ECG over the first months to years.
V1 — newborn
Dominant R, upright T. RV mass points at V1.
V1 — young child
rS, inverted T (juvenile pattern).
V1 — adolescent
rS, T upright again (V3→V2→V1).
Physiology — axis swings left
QRS axis points toward the heavier ventricle. Newborn RV dominance → right axis (+110 to +180°); as the LV outgrows the RV the vector rotates to the adult +60°, mostly done by 6 months.
Physiology — fast rate, short intervals
Infants have a high metabolic rate, small stroke volume (output maintained by rate), low vagal tone, and a physically small heart → short conduction distances → short PR and QRS. All lengthen as the child grows.
6
Age-related normal values
the reference you reach for
Heart rate (awake)
Age
Mean
Range (bpm)
Newborn
145
120–170
6 months
145
110–170
1 year
132
105–150
2 years
120
95–150
4 years
108
80–150
6 years
100
75–140
10 years
90
60–130
14+ years
85
60–115
QRS axis by age
Age
Mean
Range
1 wk–1 mo
+110°
+30 to +180°
1–3 mo
+70°
+10 to +125°
3 mo–3 yr
+60°
+10 to +110°
>3 yr
+60°
+20 to +120°
Adult
+50°
−30 to +105°
PR interval & QRS duration by age
Age
PR interval (s)
QRS duration (s)
<1 yr (infant)
0.08–0.12
≤0.07
1–3 yr
0.10–0.14
≤0.07
4–5 yr
0.11–0.15
≤0.08
6–8 yr
0.12–0.16
≤0.08
9–11 yr
0.12–0.17
≤0.09
12–16 yr
0.12–0.17
≤0.10
>16 yr (adult)
0.12–0.20
≤0.10
Park/Guntheroth-derived limits. PR & QRS increase with age as the heart grows; QRS >0.12 s is pathological at any age. QTc stays roughly constant across childhood (upper limit ~440–450 ms). Starship/LITFL heart-rate bands are broader but carry the same message.
7
RCH vs Starship — how the two compare
same backbone, one cut-off that matters
Both share the same lineage (Davignon/Park values), stepwise method, calibration and RVH/LVH criteria — more alike than different. The QTc threshold genuinely differs and changes who you flag.
Feature
RCH (Melbourne)
Starship (Auckland)
Approach
Systematic read; heavily worked with pattern examples & escalation advice
Bazett + tangent (notes unreliability at high rates)
QTc normal cut-off
>340 and ≤450 ms — single threshold, all ages
Age-split: <6 mo <490 ms · >6 mo <440 ms
RVH / LVH
Axis, voltages, R/S ratio, T-axis, Q waves
Same + practical "Evans rules" (V1 for RVH, V6 for LVH)
Escalation
Explicit: senior review of all abnormals; cardiology for suspected long QT; red flags even if ECG normal
Interpretation-focused; refer per local pathways
The difference that matters — QTc. A 3-month-old with QTc 460 ms is normal by Starship (<490 for <6 mo) but prolonged by RCH (>450). The Starship age-split reflects the physiologically longer QT of early infancy. Practically: don't over-call a modestly long QTc in an infant, but any borderline/clearly prolonged QTc — in either system — warrants a manual tangent re-measure once the child is calm, then a cardiology conversation.
8
Chamber enlargement & hypertrophy
atria on the P, ventricles on the QRS
Atrial enlargement (the P wave)
RAE — P pulmonale
Tall, peaked P >3 mm (best II, V1). Causes: tricuspid atresia, Ebstein, severe pulmonary stenosis, pulmonary HTN, ToF.
LAE — P mitrale
Wide, notched/bifid P >0.10 s (II), deep negative terminal in V1. Causes: mitral disease, large L→R shunt (VSD/PDA), HOCM, LV failure.
Ventricular hypertrophy — voltage upper limits (mm, 98th centile)
Wave (ULN)
<1 mo
1–6 mo
6–12 mo
1–3 yr
3–8 yr
8–12 yr
12–16 yr
R in V1 (RVH)
24
19
20
18
16
12
10
S in V6 (RVH)
10
9
7
7
5
4
4
R in V6 (LVH)
15
22
23
23
26
26
22
S in V1 (LVH)
18
15
18
21
23
25
22
1 mV = 10 mm. Voltage above the age limit is suggestive, not diagnostic — combine with axis, R/S ratio and T-wave/strain changes.
Physiology — why hypertrophy changes the trace
A thicker ventricle generates a larger depolarisation vector toward itself: taller R over that ventricle, deeper S opposite, axis pulled toward the hypertrophied side. Severe hypertrophy disorders subendocardial repolarisation → the "strain" pattern (RVH: right-precordial ST↓/TWI; LVH: I, aVL, V5–6). Children's thin chest walls exaggerate precordial voltages, so isolated high voltages are a common normal variant — hence the practical Evans rules: RVH → use V1 (upright T after the neonatal window, R′>R, or pure R); LVH → use V6.
RVH V1: tall R + upright T
± RAD, deep S in V6, qR in V1.
LVH V6: tall R + strain
± LAD, deep S in V1, TWI I/aVL/V5–6.
9
Congenital heart disease — ECG signatures
pattern → think of
The ECG rarely makes the diagnosis but often points to it. Combine axis + chamber pattern + specific clues, and always correlate with saturations, murmur and echo.
ECG pattern
Think of
Superior / NW axis (LAD in an infant) + RVH or combined
Post-op ToF/VSD repair (RV incision), secundum ASD
Deep Q + TWI in I/aVL/V5–6 in an infant with heart failure
ALCAPA (anomalous left coronary) — infarct pattern until proven otherwise
Regional ST↑ / new Q / ischaemia in a febrile child
Kawasaki disease with coronary aneurysm/thrombosis
Low QRS voltages ± electrical alternans
Pericardial effusion, myocarditis
Positive QRS in aVR / reversed R-wave progression
Dextrocardia or limb-lead reversal — check before calling pathology
10
Bradyarrhythmias & AV block
look at the P–QRS relationship
Sinus bradycardia
Normal P–QRS, slow rate. Athletes, sleep, high vagal tone; also raised ICP, hypothyroid, hypothermia, drugs, anorexia — and hypoxia (an ominous late sign in the neonate).
1° AV block
Long PR, every P conducts. Usually benign; also myocarditis, rheumatic fever, ↑K⁺, digoxin, Ebstein/ASD.
2° Mobitz I (Wenckebach)
Progressive PR lengthening → dropped QRS, then repeats. Usually nodal & benign (vagal); rarely needs action.
2° Mobitz II
Constant PR, sudden dropped QRS. Infranodal — can progress to complete block. Pathological → cardiology.
3° complete block
AV dissociation: regular P–P and regular (slower) R–R, independent of each other. Congenital CHB → maternal anti-Ro/La (neonatal lupus); also post-cardiac-surgery, myocarditis. May need pacing.
Wenckebach — PR lengthens beat to beat, then a QRS is dropped.
Why: progressive AV-nodal fatigue until a P fails to conduct; the node then recovers and the cycle restarts.
Complete heart block — Ps march through independent of the slow escape QRS.
Why: no atrial impulse reaches the ventricle; a junctional/ventricular escape pacemaker takes over at its own slow intrinsic rate.
11
Tachyarrhythmias
narrow vs broad decides the pathway
Rhythm
Recognise
First-line (per local guideline)
Sinus tachycardia
Normal P axis, rate varies, has a cause (fever, pain, hypovolaemia, anaemia, sepsis). Usually <220 infant / <180 child.
Treat the cause.
SVT (AVRT / AVNRT)
Narrow, very regular, ~220–300, abrupt onset/offset, P absent or abnormal, minimal rate variability. AVRT (accessory pathway) commonest in infants.
Stable: vagal (ice to face in infants, Valsalva) → adenosine 0.1→0.2→0.3 mg/kg rapid push. Unstable: synchronised DCCV 1 J/kg. Avoid verapamil in infants.
Atrial flutter
Sawtooth F waves (II/III/aVF, V1), atrial ~300 with variable AV block.
Neonatal / post-atrial surgery. Cardiology; DCCV or overdrive pacing.
Why: a ventricular focus/circuit depolarises the myocardium slowly cell-to-cell, bypassing His–Purkinje → wide QRS.
Distinguishing SVT from sinus tachycardia
Sinus tachy has visible P waves, beat-to-beat variability and an obvious cause, and rarely exceeds 220 (infant)/180 (child). SVT is strikingly regular, faster, with abrupt onset/offset and no clear P. A broad-complex tachycardia is VT until proven otherwise — do not give AV-nodal blockers blindly (dangerous in pre-excited AF).
12
Electrolytes, metabolic & drug effects
the ECG as a chemistry screen
Hyperkalaemia
Peaked T → flat/absent P + PR long → wide QRS → sine wave → VF/asystole. Why: ↑K⁺ raises resting potential (Na-channel inactivation → slow conduction) & speeds repolarisation (peaked T).
Hypokalaemia
Flat/inverted T, prominent U waves, ST depression, long QU. Arrhythmia risk, especially with digoxin.
Hypocalcaemia
Long QT via a long ST segment (T normal). Common in neonates. Why: low Ca²⁺ prolongs phase-2 plateau.
Hypercalcaemia
Short QT (short/absent ST).
Hypomagnesaemia
Long QT; predisposes to torsades — often coexists with ↓K⁺/↓Ca²⁺.
Effect: sagging "reverse-tick" ST, short QT. Toxicity: almost any arrhythmia — classically atrial tachycardia with block, junctional rhythm, bidirectional VT, AV block.
TCA / Na-channel-blocker overdose
Wide QRS, terminal R wave in aVR, tachycardia, long QT. QRS width predicts seizures/arrhythmia → sodium bicarbonate.
Hypothermia — Osborn (J) wave at the QRS–ST junction.
Hypocalcaemia — long ST stretches the QT; the T stays normal.
13
Long QT syndrome
the one you cannot miss
Prolonged repolarisation predisposes to early afterdepolarisations → torsades de pointes → syncope, seizure, sudden death. Congenital (ion-channel) or acquired. Suspect it in exertional/emotional/startle syncope and in any "atypical seizure".
Any cardiac red flag → discuss with senior even if the ECG is normal
Suspected long QT, WPW, Brugada, VT, complete block or structural disease → cardiology
Haemodynamic instability → resuscitate, treat the rhythm, retrieval
Cardiac red flags
Exertional chest pain or syncope · syncope without prodrome or with palpitations · poor exercise tolerance · family history of early cardiac death, arrhythmia, cardiomyopathy or channelopathy · abnormal cardiac examination. Any of these warrant senior discussion and may need 24-hour/exercise ECG or echocardiogram.
Local paediatric team
First call for red flags, abnormal exam or abnormal ECG.
Paediatric cardiology
Long QT, WPW, Brugada, structural disease, arrhythmia. QCH via CATCH.
CATCH
13 22 82
QCH advice, disposition & transfer (24 h).
RSQ
1300 799 127
Critical-care advice & retrieval of the unstable child.