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Medicine > ECGs > Flashcards

ECGs Flashcards

1
Q

What HR is considered sinus tachycardia?

A

>100bpm

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2
Q

Name some causes of sinus tachycardia

A

Anxiety, dehydration, recent exercise, sepsis, pneumonia etc etc

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3
Q

What lead(s) would you look in to assess sinus bradycardia/tachycardia?

A

any - rhythm strip is best

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4
Q

What HR is considered sinus bradycardia?

A

<60bpm

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5
Q

List some causes of left axis deviation

A

left anterior hemiblock

WPW syndrome

inferior MI

ventricular tachycardia

LVH

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6
Q

What is the most likely cause of right axis deviation? List any alternative causes

A

RVH is most likely

normal variant - tall thin people

lateral MI

WPW syndrome

dextrocardia or R/L arm lead switch

left posterior fascicular block

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7
Q

How would you detect left axis deviation?

A

Look for lead I and II “Leaving” each other - small lead I, negative lead II and III

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8
Q

What is a more likely cause of left axis deviation, conduction issues or LVH?

A

conduction issues

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9
Q

What is the mechanism of atrial flutter?

A

a re-entry circuit within right atrium

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10
Q

List some causes of AF

A

ischaemic heart disease

thyrotoxicosis (hyperthyroidosis)

sepsis

valvular heart disease

alcohol excess

PE

hypokalaemia/hpomagnesaemia

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11
Q

What is the mechanism of atrial tachycardia?

A

A single ectopic focus, outside the SAN that’s triggering rapid depolarisation of the atria

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12
Q

List causes of atrial tachycardia

A

digoxin toxicity

atrial scarring

catecholamine excess

congenital abnormatlities

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13
Q

What is the mechanism of junctional tachycardia?

A

AV junctional pacemaker rhythm exceeds that of SAN. There is increased automaticity in AVN coupled with decreased automaticity in SAN.

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14
Q

List causes of first degree heart block

A

increased vagal tone

athletic training

inferior MI

mitral valve surgery

Myocarditis (Lyme disease)

electrolyte disturbances (e.g. hyperkalaemia)

AV nodal blocking drugs:

beta blockers

CCBs

digoxin

amiodarone

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15
Q

Describe the ECG trace in Mobitz type I 2nd degree heart block (Wenckebach phenomenon)

A

progressive lengthening of PR interval, followed by absent QRS (a non-conducted P wave), then cycle repeats

PR interval is longest just before dropped beat, and shortest just after

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16
Q

What is the mechanism of Mobitz I 2nd degree heart block?

A

usually due to reversible conduction block at AVN - malfunctioning AVN cells progressively fatigue until they fail to conduct an impulse (dropped beat)

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17
Q

List causes of Mobitz I 2nd degree heart block

A

Drugs: beta blockers CCBs digoxin amiodarone

Increased vagal tone (e.g. athletes)

inferior MI

myocarditis

cardiac surgery

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18
Q

Describe the ECG trace in Mobitz type II 2nd degree heart block

A

intermittent non-conducted P waves without progressive prolongation of PR interval

P waves ‘march through’ at constant rate

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19
Q

What is the mechanism of Mobitz II 2nd degree heartblock?

A

usually due to failure of conduction at His-Purkinje system

generally due to structural damage to conducting system “all-or-nothing”

  • no progressive fatigue like in Mobitz I, instead His-Purkinje cells suddenly and unexpectedly fail to conduct
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20
Q

List causes of Mobitz II 2nd degree heart block

A

Anterior MI (septal infarction wiht necrosis of bundle branches)

Idiopathic fibrosis of conducting system

cardiac surgery

inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)

autoimmune (SLE, systemic sclerosis)

infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)

hyperkalaemia

Drugs: beta blockers CCBs digoxin amiodarone

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21
Q

List causes of complete heart block

A

inferior MI

AVN blocking drugs - CCBs, beta blockers, digoxin

Idiopathic degeneration of conducting system

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22
Q

In what lead(s) is complete heart block best seen?

A

II and V1

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23
Q

What is the mechanism of complete heart block?

A

there is complete absence of AV conduction - end point of second degree heart block.

Either progressive fatigue of AVN cells (mobitz I) or due to sudden onset of complete conduction throughout His-Purkinje system (mobitz II)

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24
Q

What is the clinical significance of complete heart block? How would it be treated?

A

high risk of sudden cardiac death - urgent admission for cardiac monitoring, backup temporary pacing followed by permanent pacemaker insertion

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25
Q

Describe what is seen:

A

Complete heart block.

atrial rate is 60bpm

ventricular rate is 27bpm

slow ventricular escape rhythm

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26
Q

Describe what is seen:

A

2:1 heart block

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27
Q

Describe what is seen:

A

3:1 heart block

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28
Q

Describe what is seen:

A

Mobitz II second degree heart block

Intermittent P waves without progressive lengthening of PR interval

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29
Q

Describe what is seen:

A

Mobitz I second degree heart block

aka Weckebach phenomenon

progressive lengthening of PR interval until a QRS fails to conduct (dropped beat)

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30
Q

Describe what is seen:

A

First degree heart block

PR >0.2s (5 small squares)

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31
Q

Describe what is seen:

A

Right axis deviation

leads I and II reaching towards each other

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32
Q

Describe what is seen:

A

Left axis deviation

Leads I and II are leaving each other

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33
Q

Describe what is seen:

A

atrial fibrillation

irregularly irregular, absent P waves

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34
Q

Describe what is seen:

A

Atrial fibrillation

irregularly irregular

absent P waves

35
Q

Describe what is seen:

A

Atrial flutter

“saw tooth P waves” at c300bpm

36
Q

Describe what is seen:

A

atrial tachycardia

narrow complex tachycardia at 120bpm

each QRS is preceded by an abnormal p wave

37
Q

Describe what is seen:

A

junctional tachycardia

narrow QRS

retrograde P waves before, during or after QRS

41
Q

Describe what is seen:

A

RBBB

broad QRS

M complex in V1-3

W complex in V6 (slurred S waves)

44
Q

Describe what is seen

A

LBBB

broad QRS

dominant S in V1 - W

broad R in lateral leads - M

52
Q

Describe what is seen:

A

ST elevation in I and aVL (high lateral leads)

reciprocal ST depression in III and aVF (inferior leads)

acute MI localised to superior part of lateral wall -

high lateral STEMI

occluded first branch of LAD

53
Q

Describe what is seen

A

ST elevation in inferior (II, III, aVF) leads and lateral (I, V5-V6) leads

ST depression in V1-V3 suggests associated posterior infarction

acute anterolateral STEMI with posterior extension

occlusion of proximal circumflex

55
Q

Describe the ECG changes seen in right bundle branch block

A

broad QRS >120ms

RSR pattern in V1-3 (‘m’ shaped complex)

wide, slurred S waves in lateral leads (I, aVL, V5-6) giving a ‘W’ shaped complex in V6

(MarroW - M in V1, W in V6, rr = right)

possible ST depression in precordial leads (V1-3)

56
Q

Describe what is seen:

A

ST elevation in leads II, III and aVF

Q-wave formation in III and aVF

reciprocal ST depression and T wave inversion in aVL

inferior STEMI

circumflex occlusion - ST elevation in lead II = lead III

57
Q

Describe what is seen:

A

marked ST elevation in leads II, III and aVF

reciprocal changes in aVL

inferior STEMI

RCA occlusion as ST elevation in lead III> lead II

58
Q

What is the mechanism in RBBB?

A

activation of R ventricle is delayed as depolarisation has to spread across septum from left ventricle due to blockage of R bundle of Purkinje fibres

left ventricle is activated normally, so early part of QRS is unchanged, but delayed R ventricle activation produces a secondary R wave in V1-3 and a slurred S wave in lateral leads

59
Q

What does this V2 lead trace suggest?

A

posterior MI

horizontal ST depression

upright T wave

dominant R wave (R/S ratio >1)

60
Q

List causes of RBBB

A

RVH / cor pulmonale

PE

IHD

rheumatic heart disease

myocarditis or cardiomyopathy

degenerative disease of conduction system

congenital heart disease

62
Q

Describe the ECG changes seen in left bundle branch block

A

broad QRS >120ms

dominant S wave in V1 - W

broad, notched R wave in V6 - M

(WilliaM - W in V1, M in V6, ll = left)

no Q waves in lateral leads (I, V5-6, small Q waves in aVL)

prolonged R wave peak time >60ms in V5-6

63
Q

List causes of LBBB

A

aortic stenosis

ischaemic heart disease

dilated cardiomyopathy

anterior MI

primary degnerative disease (fibrosis) of the conducting system

hyperkalaemia

digoxin toxicity

65
Q

Describe the mechanisms in LBBB?

A

septum is activated R to L instead of L to R

spreads via right bundle branch, and then via septum to left bundle branch

this extends the QRS duration and removes Q waves in lateral leads

as the venrticles are activated sequentially, broad R waves are produced

66
Q

Describe what is seen:

A

ST elevation is maximal in anteroseptal leads (v1-V4)

Q waves present in septal leads (V1-2)

hyperacute (peaked) T waves in (V2-4)

hyperactute anteroseptal STEMI

67
Q

Describe what is seen:

A

ST elevation in V1-6 + I and aVL

minimal reciprocal depression in III and aVF

anterior STEMI

68
Q

Describe the ECG changes seen in junctional escape rhythms

A

no p waves, or p waves completely unrelated to QRS

normal QRS, maybe slightly narrow

slow HR

69
Q

What is the mechanism of junctional escape rhythms?

A

there are pacemaker cells at various points in the conduction system

junctional escape rhythm occurs when the rate of AV node depolarisation is less than the intrinsic rate of an ectopic pacemaker

70
Q

list causes of junctional escape rhythms

A

severe sinus bradycardia

sinus arrest

sino-atrial exit block

high-grade second degree heart block (4:1, 5:1 etc)

complete heart block

hyperkalaemia

drugs:

beta blockers

CCBs

digoxin poisoning

71
Q

Describe the ECG changes seen in a ventricular escape rhythm

A

ventricular rhythm of 20-40bpm

broad QRS complexes, possibly with a LBBB or RBBB morphology

72
Q

Describe what is seen:

A

ventricular fibrillation

73
Q

what arteries are likely to be blocked in a lateral STEMI

A

LAD and LCx

74
Q

Describe what is seen:

A

sinus rhythm

broad QRS with slurred upstroke - delta wave

dominant R wave in V1

Wolff-Parkinson-White

75
Q

Describe the ECG changes seen in a lateral STEMI

A

ST elevation in the lateral leads

(I, aVL, V5-6)

reciprocal ST depression in inferior leads (III and aVF)

78
Q

Describe what is seen

A

Digoxin effect

“sagging” ST segements

hockey stick T waves

79
Q

Describe the ECG changes seen in an inferior MI

A

ST elevation in II, III and aVF

progressive development of Q waves in II, III and aVF

reciprocal depression in aVL (±lead I)

80
Q

Describe what is seen:

A

pericarditis

widespread concave ST elevation and PR depression throughout V2-V6 and I, II, aVL, aVF

reciprocal ST depression and PR elevation in aVR

81
Q

Which artery most commonly causes an inferior STEMI?

A

right coronary artery

(more ST elevation in lead III than II)

LCx can cause it less commonly

(ST elevation in lead II = lead III)

84
Q

Describe the ECG changes seen in posterior MI

A

In V1-V3:

horizontal ST depression

tall, broad R waves

upright T waves

dominant R wave in V2

86
Q

Occlusion of what artery causes an anterior STEMI?

A

LAD

87
Q

Describe the ECG changes seen in anterior STEMI

A

ST elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)

reciprocal ST depression in the inferior leads (mainly III and aVF)

88
Q

In what leads would ST elevation be maximal in a septal STEMI?

A

V1-2

89
Q

In what leads would ST elevation be maximal in an anterior STEMI?

A

V2-5

90
Q

In what leads would ST elevation be maximal in an anteroseptal STEMI?

A

V1-4

91
Q

In what leads would ST elevation be maximal in an anterolateral STEMI?

A

V3-6, I + aVL

94
Q

What is seen in an NSTEMI?

A

pathological Q waves only

95
Q

Describe the ECG changes that may be seen in a ventricular tachycardia

A

very broad QRS (>160ms)

no p waves

T waves difficult to identify

rate > 200bpm

96
Q

Describe the ECG changes seen in ventricular fibrillation

A

chaotic irregular deflections of varying amplitude

no identifiable P waves, QRS complexes or T waves

rate 150-500bpm

97
Q

Causes of VF

A

myocardial iscahemia/infarction

electrolyte abnormalities

cardiomyopathy (dilated, hypertrophic, restrictive)

Long QT

Brugada syndrome

Drugs

environmental - electrical shock, drowing, hypothermia

PE

cardiac tampnoade

blunt trauma

99
Q

Describe the ECG changes seen in Wolff-Parkinson-White syndrome

A

sinus rhythm

right axis deviation

short PR interval

sluured upstroke of the QRS complex, best seen in V3 and V4 - wide QRS due to this delta wave

dominant R wave in V1

101
Q

what is the mechanism in Wolff-Parkinson-White?

A

accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)

102
Q

Describe the “digoxin effect”

A

downsloping ST depression with “sagging” appearance

flattened, inverted or biphasic T waves - hockey stick

shortened QT

103
Q

What is the mechanism behind the digoxin effect?

A

shortening of atrial and ventricular refractory periods - producing short QT

increased vagal effects at AVN - prolonged PR interval

105
Q

Describe the ECG changes seen in pericarditis

A

widespread concave ST elevation and PR depression

Reciprocal ST depression and PR elevation in aVR

107
Q

What is P Pulmonale?

A

peaked P waves

108
Q

What is seen in p mitrale?

A

bifid p waves

109
Q

list causes of p pulmonale

A

anything that cause right atrial enlargement

e.g. tricuspid stenosis, pulomnary hypertension

Medicine (14 decks)

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