ECG Flashcards
Normal electrical axis
Positive in Lead I, II and AvF
Differences in paediatric ECGs vs adults
Faster heart rates
Shorter PR and QRS intervals
RV dominance (apparent RV strain pattern)
i. R axis deviation (> +90°)
ii. T wave inversions in V1-V3
1. Starts in first weeks of life, disappears by school / teenage
iii. Dominant R wave in V1
Q waves in inferior and lateral leads
i. 0-1 month in III up to 4 small squares expected
ii. Abnormal after school age
Potential site of blocks
SAN – internodal tracts – AV node – His – AP fascicles – Purkinje
Sinus p wave characteristics
P wave axis [0° and +75°]
Best seen in leads Il and V1
Upright in leads I and II
Usually biphasic in lead V1 inverted in aVR
Amplitude: < 2.5 small squares (<0.25mV)
Duration: < 3 small squares (< 120ms)
Abnormal p-wave characteristics
- Lack of p-wave
- Retrograde p-wave
Sinoatrial block definition
Delay from SAN to atrial activation - before p wave
First degree SAN block characteristics
can not dx on ECG as this is delay from SAN and P wave
Second degree type I SAN block
with each other beat reduced conduction from SAN to atria, then dropped p-wave, PP interval prolongs across beats
Second degree type II SAN block
regular p-wave, regular QRS, then missed p-wave regularly missed, PP interval regular
Third degree SAN block
full loss of p-waves irregularly
AV block - I degree
PR prolonged
AV block - II degree type I
PR prolongs then drops
Block at the level of the AV node
AV block II degree type II
regular drop
* Block at His – narrow QRS
* Block at Tawara branches – wide QRS
* Block at right and left bundle fascicles – wide QRS
AV block III degree
Complete AV dyssynchrony, ventricular or junctional escape
RBBB characteristics
98th centile or 0.12s
Rightward - anterior terminal vector
V1, V2: rSR’ [R’ > r], downsloping ST segments
V5, V6, I, aVL: broad S waves [duration of S > R]
T wave discordance
ORS axis not be affected
Left axis deviation: concomitant left anterior hemiblock [LAH] or other causes
Right axis deviation: concomitant left posterior hemiblock [LPH] or other causes
LBBB charcteristics
Duration ‚98th centile or 0.12s
Leftward-posterior terminal vector
V1, V2: - broad, deep S [r wave may be absent = QS]
ST elevation, positive T waves
V5, V6, I, aVL: broad (notched) R waves
ST depression, inverted T waves
Left anterior hemiblock [LAH]
QRS prolonged (<98th centile or <0.125]
Terminal vector left-posterior + upward orientation
Left axis deviation (-45° to -90° adults]
II, III, aVF - rS
I, aVL-qR
Left posterior hemiblock [LPH]
QRS prolonged (<9th centile or <0.125]
Terminal vector right-downward orientation
Right axis deviation (+90° to + 180° adults]
II, III, aVF - qR
I, aVL – rS
Always occurs in AVSD
Mechanisms of SVT
Abnormal automaticity
Triggered activity (early and delayed after depolarization)
Re-entry mechanism (abnormal impulse conduction)
Dual AV node pathway (AVNRT) characteristics
Fast (normal) and slow (abnormal) pathway in dual AV node physiology
On usual rhythm, re-entry will compete with forward conduction in slow pathway therefore does not lead to tachycardia
When atrial ectopic happens, this can happen while fest pathway is still refractory, therefore goes down the slow pathway, and then conducts retrograde via fast where it is now no longer refractory (slow-fast)
On ECG key feature will be a retrograde p-wave and short RP interval
When ventricular ectopy, this will lead to an anti-clockwise direction of conduction (up the slow pathway, down the fast pathway) (fast-slow)
On ECG the key feature will be retrograde P but long RP interval
How can P waves help differentiate narrow complex SVTs
Sinus p-waves with long RP interval = sinus tachycardia with atrial ectopy OR sinoatrial node reentrant tachycardia
Abnormal p-waves with one single morphology with long RP interval = ectopic atrial tachycardia
Abnormal p waves with >3 morphologies = multifocal atrial tachycardia
Retrograde p-waves with SHORT RP interval = Typical AVNRT, AVRT or JET
Retrograde p-waves with LONG RP interval = AVRT with slo accessory pathway, atypical AVNRT
Flutter waves = arial flutter
Fibrillatory waves = AF
Retrograde p-waves with LONG RP interval ddx
= AVRT with slo accessory pathway, atypical AVNRT
Retrograde p-waves with SHORT RP interval ddx
= Typical AVNRT, AVRT or JET
Abnormal p waves with >3 morphologies dx
= multifocal atrial tachycardia
SVT, post-adenosine or vagal manouvres NO p-waves seen ddx
JET, atypical AVNRT, AVRT
Wide complex SVT ddx
o SVT with BBB
o Antidromic AVRT (orthodromic – down AV node, back via accessory; antodromic down accessory, back via AV node) NB here you would still see delta wave even within tachycardia
o Aberrant conduction
Differentiating SVT with aberr conduction vs VT
AV dissociation – supports VT
Capture beats
Fusion beats – consistent with VT
Extreme axis deviation (“northwest axis”) - 90° to +180°
Positive or negative concordance in the precordial leads – suggests VT
Absence of RBBB or LBBB morphology – suggests VT
RSR’ in V1 with R>R’ / notched downslope to R wave
QRS complexes > 160ms (adults) suggests VT
Brugada sign – onset of R wave to nadir of S wave >100ms in precordial leads, suggests VT
Josephson sign – notching near the nadir of the S wave, typical of VT
Brugada sign to differentiate SVT aberr cond vs VT
Brugada sign – onset of R wave to nadir of S wave >100ms in precordial leads, suggests VT
Josephson sign to differentiate SVT aberr cond vs VT
Josephson sign – notching near the nadir of the S wave, typical of VT
VT types
Defined as consecutive ventricular beats (100-250bpm), QRS > 98th centile (>0.12s) [if HR >250bpm - ventricular flutter]
Non-sustained (<30 seconds) vs sustained (>30 seconds)
Idiopathic vs secondary to heart disease
Monomorpic VT
(includes RVOT VT and fascicular VT) RVOT = LBBB pattern and inferior axis
Polymorphic VT
(includes torsades de pointe)
Characteristics of RVOT VT
LBBB pattern and inferior axis
Definition of RVH in children
o R/S ratio in V1 > 98th percentile for age
o R/S ratio in V6 < 1 (after one month of age)
o Upright T waves in V1 (first week - early school age when we expect TWI)
o RSR’ in V1 - R’ > R1) [or >15mm (<1year), >10mm (after 1 year)]
Characteristics of non-pathological early repolarization in children
- Lack of clear definition
- J point elevation (> 0.1 mV - excluding V1-V3) in > 2 leads (same territory)
- Onset of QRS slurring or notching above baseline
- Amplitude and slope of the ST-segment not defined (ST elevation modest compared to T wave amplitude, no reciprocal depressions)
Characteristics of normal T waves
- Upslope less steep than downslope
- Concordant with QRS (positive net QRS, positive T-wave)
- Amplitude (adults): Limb leads <5mm, Precordial ieads <10mm men, <8mm women
- aVR- negative
- V1 may be flat or inverted
- !ll, aVL - isolated inversion possible (abnormal if in ≥2 leads from same area)
- aVF - may be flat
- I, I, V5-V6 – positive
- Remember normal TWI in children V1-3 until school/early adolescent
Key points re measuring QTc
U waves should be excluded
Leads II, V5 or lead with longest measurement
Bazzett / Framingham
Narrow complex tachycardia
AV dissociation
Must have RBBB type pattern
(easily mistaken for SVT)
LV fascicular VT (Verapamil sensitive VT)
(re-entrant)
Proportion anterior / posterior fascicular VT
Anterior 95%
Management of LV fascicular VT
Verapamil if stable, DCCV if unstable
Long term oral verapamil +/- ablation (90% success)
Giving IV CCB - setting and precautions
Should be given in PICU
Slow push with cardiac monitoring and BP monitoring
IV calcium to be readily available in case of profound hypotension
in patients with asthma adenosine can precipitate…
bronchospasm
can opt for verapamil instead if recent severe life threatening attack
Greatest risk of verapamil related hypotension in age group…
Neonates and small kids, less so in adolescents
