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cardiology > ECGs / dysrhythmias > Flashcards

ECGs / dysrhythmias Flashcards

1
Q

RAD vs LAD

A

RAD = big P V1 and II (>3mm) (P pulmonale)
LAD = biphasic P in V1, double humped P in II (P mitrale)

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2
Q

RVH vs LVH

A

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

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3
Q

types of AV block

A

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

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4
Q

RBBB vs LBBB

A

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

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5
Q

atrial flutter vs atrial fibrillation

A

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

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6
Q

atrial bigeminy

A

when PAC occurs consistently after every normal cycle

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7
Q

WPW

A

accessory pathway = bundle of Kent, either type A (left) or B (right)
short PR
delta wave - upsloping
long QRS
NO Q WAVE IN V6!

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8
Q

VT

A

no p wave, wide QRS
monomorphic e.g. re-entrant/focal
polymorphic - signals from different places e.g. torsades de pointes

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9
Q

Brugada syndrome

A

type of VF
most common mutation SCN5A - Na channels
ST elevation + RBBB pre-dispose to re-entrant rhythms

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10
Q

QTc - prolonged values

A

males >440msec
females >460msec

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11
Q

correlate the ECG leads with anatomy

A

• Lateral = I, aVL, V5, V6
• Inferior = II, III, aVF
• Anterior = V3, V4
• Septal = V1, V2

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12
Q

in infants < 6months:
- comment about QTc
- comment about P waves

A

• Slightly peaked P waves (< 3mm in height is normal)
• Slightly long QTc (≤ 490ms)

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13
Q

features of a normal neonatal ECG

A

o RAD
o Dominant R wave in V1
o T wave inversion V1-3

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14
Q

way to calculate axis

A

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.

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15
Q

what is normal axis degrees wise?

A

-30 to +90

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16
Q

LAD causes in children (mnemonic)

A

never LVH in children. HAT SAND:

• HOCM
• AVSD
• Tricuspid atresia
• Single ventricle
• ASD primum
• Noonan’s (especially HCM)
• DORV

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17
Q

superior axis
- what is it
- causes in children (mnemonic)

A

= S wave > R wave in aVF

NATE is superior:
• Noonan’s
• AVSD
• Tricuspid atresia
• Ebstein anomaly

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18
Q

what is the u wave, and what can cause it

A

Extra positive deflection at the end of the T wave

o Hypokalaemia
o Normal finding at slower heart rates (sinus bradycardia)

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19
Q

what is the definition of a Q wave that is too deep?

A

too deep is > 25% R wave amplitude

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20
Q

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

A

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)

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21
Q

what is the so called juvenile t wave pattern?

A

T waves become inverted in V1-3 [right precordium], up to V4 permitted

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22
Q

peaked vs flat T waves = what?

A

Peaked = Hyperkalaemia
Flat = Hypokalaemia / Hypothyroidism

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23
Q

name some causes of a prolonged PR interval

A

• First degree AV block
• Myocarditis (including rheumatic heart disease)
• Digitalis toxicity
• CHD: AVSD, ASD, Ebstein’s
• Hyperkalaemia

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24
Q

name some causes of prolonged QTc

A

long QT syndrome
hypoCa
myocarditis
drugs ( COLLAPSE)

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25
Q

incomplete RBBB

A

• RSR’ in V1 (R waves the same size)
• QRS normal/ mildly prolonged

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26
Q

commonest cause of RBBB vs incomplete RBBB

A

RBBB = think post-TOF repair
incomplete RBBB = think secundum ASD with RAD

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27
Q

hyperkalaemia vs hypokalaemia

A

hypokalaemia (flatten)… so T wave flat, with u waves
hyperkalaemia (up)… so peaked T waves > no p waves > wide QRS > sine/ventricular arrhythmias/asystole

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28
Q

hypercalcaemia vs hypocalcaemia

A

hyperCa = short ST
hypoCa = prolonged ST and QT

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29
Q

myocarditis classic finding

A

prolonged PR interval (part of jones criteria)

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30
Q

dextrocardia

A

–ve P wave in I, and +ve in AVF
V5 and V6 no waveform…it’s not going that way!

31
Q

Ebstein’s - just know it…

A

RA enlargement
1st degree heart block
RBBB

32
Q

aortic coarctation ecg

A

RVH
Not expected as it is a LVOT
However, the RV does all the work in utero pumping blood through the PDA

33
Q

what is sinus pause vs arrest?

A

sinus pause - no P wave/QRS for a mo
sinus arrest - lasts longer, then usually have escape beat

34
Q

causes of sinus pause/arrest

A

<2s could be normal in infants/adolescents
otherwise, if with syncope = sick sinus syndrome / inc vagal tone / digitalis tox etc

35
Q

most worrying arrhythmia with sick sinus syndrome

A

bradytachyarrhythmia (profound brady after tachy) - can cause syncope and death

36
Q

how to tell difference between PAC vs type II HB

A

PAC: p premature, PP interval shorter
type II HB: p occurring at right time, PP interval same

37
Q

atrial ectopic tachycardias
- what
- why do we care
- so how to fix

A
  • 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
38
Q

multifocal atrial tachycardia
- often mistaken for
- age
- how to treat

A
  • SVT
  • infants
  • adenosine ineffective though - need to use amiodarone (1st line) to slow AV conduction
39
Q

AF - rhythm vs rate control

A

rhythm for symptoms, but both same for mortality
rhythm - quinidine / amiodarone
rate - beta blockers / non-DHP

40
Q

junctional (nodal) rhythm - what is it and associated with what weirdo condition

A

SA not running the show, AV is
p waves absent
polysplenia

41
Q

most common symptomatic dysrhythmia in children

A

SVT

42
Q

treatment of congenital JET

A

amiodarone

43
Q

types of SVT - how to tell they apart

A

90% re-entrant: after conversion to sinus rhythm, will show WPW pre-excitation
10% automatic from single focus e.g. atrial ectopic, JET

44
Q

all SVT have narrow QRS and all VT have wide QRS - true or false?

A

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

45
Q

what is the only cause of a broad complex tachycardia?

A

antidromic AVRT

46
Q

types of SVT - what are they, which more common to produce tchy cardiomyopathy, and age of presentation

where is the p wave?

A

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

47
Q

which conditions are more prone to WPW pre-excitation? (mnemonic)

A

SHE Cam:

Single ventricle
hamartoma e.g. in TS
Ebstein’s
L-TGA
Cam: Cardiomyopathy (HCM/DCM)

48
Q

why is a running rhythm strip during SVT treatment important?

A

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

49
Q

AE of adenosine

A

flushing, nausea dyspnoea, bronchospasm - beware in asthma

50
Q

adenosine and WPW - what to consider

A

can shorten the refractory period and cause it to go into AF –> DC cardioversion

51
Q

JET vs AET p wave

A

AET: p wave preceds QRS with abnormal axis
JET: inverted p wave

52
Q

WPW - avoid what meds and why

A

digoxin and verapamil
work on AV node
can encourage movement down the accessory (shorter) pathway

53
Q

what age do we catheter ablate SVT?

A

> 2yo, as can spotaneously resolve

54
Q

when does a PVC become a VT?

A

3 PVCs in a row

55
Q

PVC vs PAC - age? RR?

A

PAC more common in infants; RR shorter
PVC more common in older children/adults, RR same

56
Q

significance of occasional PVCs

A

none - 50-70% children can have them

57
Q

what meds to avoid in ventricular arrhythmias needing treatment

A

Anti-arrythmic agents that prolong the QT interval - amiodarone, sotalol, quinidine

58
Q

Rx of choice in long QT

A

propranolol

59
Q

why do we not use IV verapamil in <1yo

A

profound hyPOtension

60
Q

VT with pulse and not shocked - what Rx to use?

A

amiodarone

61
Q

VT always equals dysmorphic heart? explain.

A

No - can have VT in normal heart e.g. RVOT VT / LBBB VT

62
Q

what is Bazett’s formula

A

QTc = QT/√RR
*RR is from preceding beat

63
Q

most long QT syndromes are a result of what biochemical problem?

A

K channel problem - so K efflux in longer

64
Q

LQTS 1,2,3
- gene
- t wave
- triggers

A

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

65
Q

most common LQTS phenotype - important doesn’t have what feature of some other LQTS?

A

Roman-Ward - no deafness (e.g. Jervell and Lange-Nielsen, where less K in endolymph causes SNHL)

66
Q

big P wave =

A

= big right atrium

67
Q

T wave alternans =

A

beat to beat variation in T wave = long QT

68
Q

risk factors of SCD with LQTS

A

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

69
Q

general measures for LQTS besides propranolol

A

bedside alarm/phone
no competitive sports / no swimming…can prolong QT
COMPLIANCE WITH Rx IS BIGGEST ISSUE

70
Q

genetic mutation a/w Brugada

A

SCN5A - Na channel in cardiac myocte

71
Q

when can you not tell between mobitz I and II?

A

2:1 (2 p to 1 qrs) block

72
Q

key feature of mobitz I in children vs adults

A

sometimes dont get the PR lengthening
Instead the key feature is the pre-block PR is LONGER than the post-block PR

73
Q

mobitz I vs II - which is worse

A

II by far - can cause complete HB

74
Q

common causes of complete heart block in children (and 2 most common)

A

1) neonatal lupus most common 60-90% (or maternal sjogrens)
2) congenital heart disease (1/3)
3) Cx of cardiac surgery

cardiology (6 decks)

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