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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
Describe what is seen:
**Complete heart block.** atrial rate is 60bpm ventricular rate is 27bpm slow ventricular escape rhythm
26
Describe what is seen:
2:1 heart block
27
Describe what is seen:
3:1 heart block
28
Describe what is seen:
Mobitz II second degree heart block Intermittent P waves without progressive lengthening of PR interval
29
Describe what is seen:
Mobitz I second degree heart block aka Weckebach phenomenon progressive lengthening of PR interval until a QRS fails to conduct (dropped beat)
30
Describe what is seen:
First degree heart block PR \>0.2s (5 small squares)
31
Describe what is seen:
**R**ight axis deviation leads I and II **r**eaching towards each other
32
Describe what is seen:
**L**eft axis deviation Leads I and II are **l**eaving each other
33
Describe what is seen:
atrial fibrillation irregularly irregular, absent P waves
34
Describe what is seen:
Atrial fibrillation irregularly irregular absent P waves
35
Describe what is seen:
Atrial flutter "saw tooth P waves" at c300bpm
36
Describe what is seen:
atrial tachycardia narrow complex tachycardia at 120bpm each QRS is preceded by an abnormal p wave
37
Describe what is seen:
junctional tachycardia narrow QRS retrograde P waves before, during or after QRS
41
Describe what is seen:
RBBB broad QRS M complex in V1-3 W complex in V6 (slurred S waves)
44
Describe what is seen
LBBB broad QRS dominant S in V1 - W broad R in lateral leads - M
52
Describe what is seen:
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
Describe what is seen
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
Describe the ECG changes seen in right bundle branch block
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
Describe what is seen:
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
Describe what is seen:
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
What is the mechanism in RBBB?
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
What does this V2 lead trace suggest?
posterior MI horizontal ST depression upright T wave dominant R wave (R/S ratio \>1)
60
List causes of RBBB
RVH / cor pulmonale PE IHD rheumatic heart disease myocarditis or cardiomyopathy degenerative disease of conduction system congenital heart disease
62
Describe the ECG changes seen in left bundle branch block
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
List causes of LBBB
aortic stenosis ischaemic heart disease dilated cardiomyopathy anterior MI primary degnerative disease (fibrosis) of the conducting system hyperkalaemia digoxin toxicity
65
Describe the mechanisms in LBBB?
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
Describe what is seen:
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
Describe what is seen:
ST elevation in V1-6 + I and aVL minimal reciprocal depression in III and aVF **anterior STEMI**
68
Describe the ECG changes seen in junctional escape rhythms
no p waves, or p waves completely unrelated to QRS normal QRS, maybe slightly narrow slow HR
69
What is the mechanism of junctional escape rhythms?
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
list causes of junctional escape rhythms
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
Describe the ECG changes seen in a ventricular escape rhythm
ventricular rhythm of 20-40bpm broad QRS complexes, possibly with a LBBB or RBBB morphology
72
Describe what is seen:
ventricular fibrillation
73
what arteries are likely to be blocked in a lateral STEMI
LAD and LCx
74
Describe what is seen:
sinus rhythm broad QRS with slurred upstroke - delta wave dominant R wave in V1 **Wolff-Parkinson-White**
75
Describe the ECG changes seen in a lateral STEMI
ST elevation in the lateral leads (I, aVL, V5-6) reciprocal ST depression in inferior leads (III and aVF)
78
Describe what is seen
**Digoxin effect** "sagging" ST segements hockey stick T waves
79
Describe the ECG changes seen in an inferior MI
ST elevation in II, III and aVF progressive development of Q waves in II, III and aVF reciprocal depression in aVL (±lead I)
80
Describe what is seen:
**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
Which artery most commonly causes an inferior STEMI?
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
Describe the ECG changes seen in posterior MI
In V1-V3: horizontal ST depression tall, broad R waves upright T waves dominant R wave in V2
86
Occlusion of what artery causes an anterior STEMI?
LAD
87
Describe the ECG changes seen in anterior STEMI
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
In what leads would ST elevation be maximal in a septal STEMI?
V1-2
89
In what leads would ST elevation be maximal in an anterior STEMI?
V2-5
90
In what leads would ST elevation be maximal in an anteroseptal STEMI?
V1-4
91
In what leads would ST elevation be maximal in an anterolateral STEMI?
V3-6, I + aVL
94
What is seen in an NSTEMI?
pathological Q waves only
95
Describe the ECG changes that may be seen in a ventricular tachycardia
very broad QRS (\>160ms) no p waves T waves difficult to identify rate \> 200bpm
96
Describe the ECG changes seen in ventricular fibrillation
chaotic irregular deflections of varying amplitude no identifiable P waves, QRS complexes or T waves rate 150-500bpm
97
Causes of VF
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
Describe the ECG changes seen in Wolff-Parkinson-White syndrome
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
what is the mechanism in Wolff-Parkinson-White?
accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)
102
Describe the "digoxin effect"
downsloping ST depression with "sagging" appearance flattened, inverted or biphasic T waves - hockey stick shortened QT
103
What is the mechanism behind the digoxin effect?
shortening of atrial and ventricular refractory periods - producing short QT increased vagal effects at AVN - prolonged PR interval
105
Describe the ECG changes seen in pericarditis
widespread concave ST elevation and PR depression Reciprocal ST depression and PR elevation in aVR
107
What is P Pulmonale?
peaked P waves
108
What is seen in p mitrale?
bifid p waves
109
list causes of p pulmonale
anything that cause right atrial enlargement e.g. tricuspid stenosis, pulomnary hypertension

Medicine (14 decks)

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