3. Electrocardiogram
• It is a recording - of time versus voltage – of the
electrical activity of the heart using electrodes placed
on the skin.
• 1887 – Augustus D Waller defined the term and
demonstrated the first ‘electrocardiogram‘, a tracing from
the intact human heart recorded using a mercury
capillary electrometer
• 1895 – Einthoven derived a correction formula that
compensated for the inertia and friction
• Einthoven awarded the Nobel Prize in Physiology or
Medicine 1924 for his ‘discovery of the mechanism of
the electrocardiogram‘.
6. INTERPRETATION OF AN ECG
• Standardization
• Heart rate
• Rhythm
• The QRS axis
• Intervals: PR, QRS, and QT
• The P-wave amplitude and duration
• The QRS wave
• ST-segment and T-wave abnormalities
7. Standardization
• The standard paper speed of ECG is
25mm/sec
• 1mm (small square) = 0.04 sec
(40ms)
• 5mm ( large square) = 0.20 sec
(200ms)
• 2 large squares(10 mm)=1mV
(full standardization)
8. Heart rate
HR= 1500/No of small squares btn
two consecutive RR waves
=300/No of large squares btn
two consecutive RR waves
=50 x No.of QRS within six large
boxes (1.2 ms)
9. RHYTHM
• Sinus rhythm:
i. P wave is positive in leads II
and aVF but negative in aVR
ii. a P wave always precedes each
QRS complex.
iii. PR interval must be constant
• Sinus arrhythmia-heart rate rises
and falls with inspiration and
expiration
11. AXIS
• Normal Axis = QRS axis
between -30 and +100 degrees.
• Left Axis Deviation = QRS axis
less than -30 degrees.
• Right Axis Deviation = QRS axis
greater than +100 degrees.
• Extreme Axis Deviation = QRS
axis between -90 and 180
degrees
12. P WAVE-atrial depolarization
• P wave is the first positive
deflection on the ECG
• Duration-< 0.08 s in infants or
<0.1 s in older children
• Morphology- Monophasic in
lead II, Biphasic in V1
• Axis- between 0° and +75°
• P waves should be upright in
leads I and II, inverted in aVR
13. P WAVE
• Tall (>2.5 mm), narrow, and spiked P
waves are indicative of right atrial
enlargement
• Broad, bifid and sometimes biphasic , are
indicative of left atrial enlargement
• Absent P waves- sinus arrest, AF
• P wave inversion-ectopic atrial and
junctional rhythms
• Presence of ≥ 3 different P wave
morphologies- multifocal atrial rhythm
15. PR INTERVAL
• START OF P WAVE TO START OF QRS COMPLEX
• Duration- 0.12-0.20 seconds
• PR interval > 200 ms - Heart block
• PR interval < 120 ms suggests pre-excitation or AV nodal (junctional)
rhythm.
16. Prolonged PR Interval
First degree AV block
Second degree heart block, Mobitz type I (Wenckebach phenomenon).
17. Short PR interval (<120ms)
1. Preexcitation syndromes
• Wolff-Parkinson-White syndrome
are a short PR interval (<120ms),
broad QRS and a slurred upstroke to
the QRS complex, the delta wave.
2. AV nodal (junctional) rhythm
• Narrow complex, regular rhythms
arising from the AV node.
• P waves are either absent or
abnormal
18. QRS Interval
• Normal QRS width is 70-100 ms
• Narrow complexes (QRS < 100
ms)- supraventricular in origin.
• Broad complexes (QRS > 100 ms)
- Ventricular in origin or due to
aberrant conduction of
supraventricular complexes
19. Narrow Complex Rhythms- supraventricular
• Sinus rhythm: Each narrow
complex is preceded by a normal
P wave.
• Junctional tachycardia: Narrow
QRS complexes with no visible P
waves.
• Atrial flutter: Narrow QRS
complexes with regular flutter
waves.
20. Broad QRS Complexes
RBBB
1. QRS duration > 120ms
2. RSR’ pattern in V1-3 (“M-shaped” QRS
complex)
3. Wide, slurred S wave in lateral leads (I,
aVL, V5-6)
LBBB
1. QRS duration > 120ms
2. Dominant S wave in V1
3. Broad monophasic R wave in lateral leads
(I, aVL, V5-6)
4. Absence of Q waves in lateral leads
5. Prolonged R wave peak time > 60ms in
leads V5-6
21. QT Interval
• Time from the start of the Q
wave to the end of the T wave
• Qt interval varies with age
• Bazett formula: QTc= QT / √ RR
• QTc > 500 is associated with an
increased risk of Ventricular
arrythmias.
• QTc is abnormally short if
< 350ms
Causes of a short QTc (<350ms)
Hypercalcaemia
Congenital short QT syndrome
Digoxin effect
Causes of a prolonged QTc (>440ms)
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Hypothermia
Myocardial ischemia
ROSC Post-cardiac arrest
Raised intracranial pressure
Congenital long QT syndrome
22. T WAVE- Ventricular repolarisation
• The T wave is the positive deflection after each QRS complex. It
represents ventricular repolarisation.
• Upright in all leads except aVR and V1
• Amplitude < 5mm in limb leads, < 10mm in precordial leads
• Inverted T-waves in the right precordial leads (V1-3)
23. • Right bundle branch block
produces T-wave inversion in the
right precordial leads V1-3
• Left bundle branch block
produces T-wave inversion in the
lateral leads I, aVL and V5-6
25. LVH
• Left axis deviation
• Markedly increased LV voltages: huge
precordial R and S waves that overlap
with the adjacent leads (SV1 + RV6 > 35
mm).
• R-wave peak time > 50 ms in V5-6 with
associated QRS broadening.
• LV strain pattern with ST depression and
T-wave inversions in I, aVL and V5-6.
• ST elevation in V1-3.
• Prominent U waves in V1-3.
26. RVH
• Right axis deviation
• Dominant R wave in V1 (> 7
mm tall; R/S ratio > 1)
• Dominant S wave in V6 (> 7
mm deep; R/S ratio < 1).
• Right ventricular strain
pattern with ST depression
and T-wave inversion in V1-
4.
• Voltage criteria for RVH – R
WAVE IN V 1 > 7mm
27. Pediatric vs adult ECG
• Heart rate > 100 beats/min
• Apparent right ventricular strain pattern:
• T wave inversions in V1-3 (“juvenile T-wave pattern”)
• Right axis deviation
• 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 prolonged QTc (≤ 490ms in infants ≤ 6 months)
• Q waves in the inferior and left precordial leads
28. References
• Evans, William & Acherman,
Ruben & Mayman, Gary &
Rollins, Robert & Kip, Kaan.
(2010). Simplified Pediatric
Electrocardiogram
Interpretation. Clinical
pediatrics. 49. 363-72.
10.1177/0009922809336206.
• https://litfl.com/
Editor's Notes
Sum of vectors generated by individual cardiac myocytes
(the presence of an accessory pathway between the atria and ventricles)
Lown–Ganong–Levine syndrome (LGL): Proposed pre-excitation syndrome. Accessory pathway composed of James fibres. Characteristic ECG findings of short PR interval (<120ms); normal P wave axis; normal/narrow QRS morphology in the presence of paroxysmal tachyarrhythmia.
Q wave represents the normal left-to-right depolarisation of the interventricular septum
R wave is the first upward deflection after the P wave
R wave represents early ventricular depolarisation
Familial arrhythmogenic disease associated with paroxysmal atrial and ventricular fibrillation, syncope, and sudden cardiac death
Left axis deviation
Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm).
R-wave peak time > 50 ms in V5-6 with associated QRS broadening.
LV strain pattern with ST depression and T-wave inversions in I, aVL and V5-6.
ST elevation in V1-3.
Prominent U waves in V1-3.
Right axis deviation (+150 degrees).
Dominant R wave in V1 (> 7 mm tall; R/S ratio > 1)
Dominant S wave in V6 (> 7 mm deep; R/S ratio < 1).
Right ventricular strain pattern with ST depression and T-wave inversion in V1-4.