ECGs / dysrhythmias Flashcards
RAD vs LAD
RAD = big P V1 and II (>3mm) (P pulmonale)
LAD = biphasic P in V1, double humped P in II (P mitrale)
RVH vs LVH
RVH = big R V1, big S in V5/V6, V1 T waves up
- qR pattern in V1 (small Q wave, tall R wave) = highly specific for RVH.
LVH = big S V1, big R in V5/V6, V5/V6 T waves down
types of AV block
1st deg- atrial signal delayed but still makes it - PR long
2nd deg
- type 1 = wenckebach = PR interval progressively longer until blocked - and ventricular escape beat happens
- type 2 = randomly dropped beats, sometimes there’s a ratio
3rd deg = complete = ventricular escape beats only
RBBB vs LBBB
William Marrow:
LBBB V1 = W (QRS down), V6 = M … no q waves
RBBB V1 = M (QRS up), V6 = W (aka rSR’, qRs)
with wide QRS
atrial flutter vs atrial fibrillation
flutter = re-entrant rhythm causing flutter saw-tooth f waves with ventricular beats occuring at fixed ratios (due to refractory period)
AFib = irregularyl irregular without P wave
atrial bigeminy
when PAC occurs consistently after every normal cycle
WPW
accessory pathway = bundle of Kent, either type A (left) or B (right)
short PR
delta wave - upsloping
long QRS
NO Q WAVE IN V6!
VT
no p wave, wide QRS
monomorphic e.g. re-entrant/focal
polymorphic - signals from different places e.g. torsades de pointes
Brugada syndrome
type of VF
most common mutation SCN5A - Na channels
ST elevation + RBBB pre-dispose to re-entrant rhythms
QTc - prolonged values
males >440msec
females >460msec
correlate the ECG leads with anatomy
• Lateral = I, aVL, V5, V6
• Inferior = II, III, aVF
• Anterior = V3, V4
• Septal = V1, V2
in infants < 6months:
- comment about QTc
- comment about P waves
• Slightly peaked P waves (< 3mm in height is normal)
• Slightly long QTc (≤ 490ms)
features of a normal neonatal ECG
o RAD
o Dominant R wave in V1
o T wave inversion V1-3
way to calculate axis
I positive, aVF positive = normal axis, 0 to +90
I positive, aVF negative = possible LAD, 0 to -90. if II positive, then normal axis.
I negative, aVF positive = RAD, +90 to 180
I negative, aVF negative = extreme axis, 180 to -90. check lead placement.
what is normal axis degrees wise?
-30 to +90
LAD causes in children (mnemonic)
never LVH in children. HAT SAND:
• HOCM
• AVSD
• Tricuspid atresia
• Single ventricle
• ASD primum
• Noonan’s (especially HCM)
• DORV
superior axis
- what is it
- causes in children (mnemonic)
= S wave > R wave in aVF
NATE is superior:
• Noonan’s
• AVSD
• Tricuspid atresia
• Ebstein anomaly
what is the u wave, and what can cause it
Extra positive deflection at the end of the T wave
o Hypokalaemia
o Normal finding at slower heart rates (sinus bradycardia)
what is the definition of a Q wave that is too deep?
too deep is > 25% R wave amplitude
what would the following suggest, if the q wave was:
1) in the right precordial leads ie V1
2) absent in the left precordial leads
3) abnormally deep and wide
1) in the right precordial leads ie V1 (eg severe RVH)
2) absent in the left precordial leads (e.g. LBBB)
3) abnormally deep and wide (younger = ALCAPA, older = myocardial infarction or fibrosis)
what is the so called juvenile t wave pattern?
T waves become inverted in V1-3 [right precordium], up to V4 permitted
peaked vs flat T waves = what?
Peaked = Hyperkalaemia
Flat = Hypokalaemia / Hypothyroidism
name some causes of a prolonged PR interval
• First degree AV block
• Myocarditis (including rheumatic heart disease)
• Digitalis toxicity
• CHD: AVSD, ASD, Ebstein’s
• Hyperkalaemia
name some causes of prolonged QTc
long QT syndrome
hypoCa
myocarditis
drugs ( COLLAPSE)
incomplete RBBB
• RSR’ in V1 (R waves the same size)
• QRS normal/ mildly prolonged
commonest cause of RBBB vs incomplete RBBB
RBBB = think post-TOF repair
incomplete RBBB = think secundum ASD with RAD
hyperkalaemia vs hypokalaemia
hypokalaemia (flatten)… so T wave flat, with u waves
hyperkalaemia (up)… so peaked T waves > no p waves > wide QRS > sine/ventricular arrhythmias/asystole
hypercalcaemia vs hypocalcaemia
hyperCa = short ST
hypoCa = prolonged ST and QT
myocarditis classic finding
prolonged PR interval (part of jones criteria)
dextrocardia
–ve P wave in I, and +ve in AVF
V5 and V6 no waveform…it’s not going that way!
Ebstein’s - just know it…
RA enlargement
1st degree heart block
RBBB
aortic coarctation ecg
RVH
Not expected as it is a LVOT
However, the RV does all the work in utero pumping blood through the PDA
what is sinus pause vs arrest?
sinus pause - no P wave/QRS for a mo
sinus arrest - lasts longer, then usually have escape beat
causes of sinus pause/arrest
<2s could be normal in infants/adolescents
otherwise, if with syncope = sick sinus syndrome / inc vagal tone / digitalis tox etc
most worrying arrhythmia with sick sinus syndrome
bradytachyarrhythmia (profound brady after tachy) - can cause syncope and death
how to tell difference between PAC vs type II HB
PAC: p premature, PP interval shorter
type II HB: p occurring at right time, PP interval same
atrial ectopic tachycardias
- what
- why do we care
- so how to fix
- ectopic tissue firing willy nilly. tachy and often with HR accelerating
- a/w tachy cardiomyopathy
- cardioversion doesnt work (ectopic still works) - ablation in 90% effective
multifocal atrial tachycardia
- often mistaken for
- age
- how to treat
- SVT
- infants
- adenosine ineffective though - need to use amiodarone (1st line) to slow AV conduction
AF - rhythm vs rate control
rhythm for symptoms, but both same for mortality
rhythm - quinidine / amiodarone
rate - beta blockers / non-DHP
junctional (nodal) rhythm - what is it and associated with what weirdo condition
SA not running the show, AV is
p waves absent
polysplenia
most common symptomatic dysrhythmia in children
SVT
treatment of congenital JET
amiodarone
types of SVT - how to tell they apart
90% re-entrant: after conversion to sinus rhythm, will show WPW pre-excitation
10% automatic from single focus e.g. atrial ectopic, JET
all SVT have narrow QRS and all VT have wide QRS - true or false?
no - most wide QRS in paeds is not VT but SVT with aberrancy, SVT with BBB (in pre-existing congenital heart disease) or a type of accessory pathway re-entrant SVT
what is the only cause of a broad complex tachycardia?
antidromic AVRT
types of SVT - what are they, which more common to produce tchy cardiomyopathy, and age of presentation
where is the p wave?
accessory AV re-entry tachycardia (AVRT) - anatomically separate tract. more incessant, so more likely tachy cardiomyopathy. 1st year of life.
- p after qrs
AV nodal re-entry tachycardia (AVNRT) - functionally separate tracts (at least temporarily) from the AV node to the atrium. Less bad, adolescent.
- p not visible
which conditions are more prone to WPW pre-excitation? (mnemonic)
SHE Cam:
Single ventricle
hamartoma e.g. in TS
Ebstein’s
L-TGA
Cam: Cardiomyopathy (HCM/DCM)
why is a running rhythm strip during SVT treatment important?
some SVTs wont respond to adenosine if the mechanism is from atrial tissue e.g. AF, aflutter, AET. slowing the tachy will however unmask the atrial activity, so need to keep the ECG running
AE of adenosine
flushing, nausea dyspnoea, bronchospasm - beware in asthma
adenosine and WPW - what to consider
can shorten the refractory period and cause it to go into AF –> DC cardioversion
JET vs AET p wave
AET: p wave preceds QRS with abnormal axis
JET: inverted p wave
WPW - avoid what meds and why
digoxin and verapamil
work on AV node
can encourage movement down the accessory (shorter) pathway
what age do we catheter ablate SVT?
> 2yo, as can spotaneously resolve
when does a PVC become a VT?
3 PVCs in a row
PVC vs PAC - age? RR?
PAC more common in infants; RR shorter
PVC more common in older children/adults, RR same
significance of occasional PVCs
none - 50-70% children can have them
what meds to avoid in ventricular arrhythmias needing treatment
Anti-arrythmic agents that prolong the QT interval - amiodarone, sotalol, quinidine
Rx of choice in long QT
propranolol
why do we not use IV verapamil in <1yo
profound hyPOtension
VT with pulse and not shocked - what Rx to use?
amiodarone
VT always equals dysmorphic heart? explain.
No - can have VT in normal heart e.g. RVOT VT / LBBB VT
what is Bazett’s formula
QTc = QT/√RR
*RR is from preceding beat
most long QT syndromes are a result of what biochemical problem?
K channel problem - so K efflux in longer
LQTS 1,2,3
- gene
- t wave
- triggers
LQT1 – KCNQ1, attacks during exercise/ swimming, broad based T waves
LQT2 – KCNH2, response to sudden noise, low amplitude T waves
LQT3 – SCN5A (Na channel!!), attacks during rest/ sleep
most common LQTS phenotype - important doesn’t have what feature of some other LQTS?
Roman-Ward - no deafness (e.g. Jervell and Lange-Nielsen, where less K in endolymph causes SNHL)
big P wave =
= big right atrium
T wave alternans =
beat to beat variation in T wave = long QT
risk factors of SCD with LQTS
Bradycardia for age
An extremely long QTc (>0.55s)
Symptoms at presentation (syncope, seizure, cardiac arrest)
Young at at presentation (<1 month)
Documented Torsades de pointes or VF
T wave alternans
general measures for LQTS besides propranolol
bedside alarm/phone
no competitive sports / no swimming…can prolong QT
COMPLIANCE WITH Rx IS BIGGEST ISSUE
genetic mutation a/w Brugada
SCN5A - Na channel in cardiac myocte
when can you not tell between mobitz I and II?
2:1 (2 p to 1 qrs) block
key feature of mobitz I in children vs adults
sometimes dont get the PR lengthening
Instead the key feature is the pre-block PR is LONGER than the post-block PR
mobitz I vs II - which is worse
II by far - can cause complete HB
common causes of complete heart block in children (and 2 most common)
1) neonatal lupus most common 60-90% (or maternal sjogrens)
2) congenital heart disease (1/3)
3) Cx of cardiac surgery
