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MD2 Cardio > Basic ECG Interpretation > Flashcards

Basic ECG Interpretation Flashcards

1
Q

Describe a system for ECG interpretation

A

Rhythm and rate Cardiac axis PR interval QRS complexes ST segments and T waves QT interval

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2
Q

Describe 2 methods for calculating rate on ECGs

A

300/no. of large squares between QRS complexes Count QRS complexes over strip (10s) and multiply by 6

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3
Q

What is normal sinus rhythm?

A

1:1 ratio of P waves to QRS complexes

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4
Q

What is respiratory sinus arrhythmia?

A

1:1 ratio of P:QRS but irregularity with respiration (faster with inspiration due to decreased vagal tone)

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5
Q

Distinguish between atrial and ventricular ectopics in terms of their appearance on ECG

A

Atrial: early, narrow complex QRS followed by compensatory pause Ventricular: early, broad complex QRS

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6
Q

Describe the ECG appearance of atrial fibrillation

A

Absence of P waves Irregularly irregular rhythm Always comment on ventricular response rate (>100 is rapid and

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7
Q

Describe the ECG appearance of atrial flutter

What is the ventricular response rate in atrial flutter and why? What does the ventricular response rate of atrial flutter suggest about the underlying cause?

A

“Saw tooth” p waves due to large re-entrant pathway in atrium

Length of the re-entry circuit corresponds to the size of the right atrium and atrial rate is therefore usually a regular 300 bpm (ventricular rate depends on the AV conduction ratio; commonly it is 2:1 resulting in a ventricular rate of 150 bpm)

Higher degree AV blocks can occur with atrial flutter, more commonly where the underlying cause is medications or underlying heart disease

Atrial flutter with 1:1 conduction can occur due to sympathetic stimulation or in the presence of an accessory pathway — especially if AV-nodal blocking agents are administered to a patient with WPW; this is associated with severe haemodynamic instability and progression to ventricular fibrillation

NB. The term “AV block” in the context of atrial flutter is something of a misnomer; AV block is a physiological response to rapid atrial rates and implies a normally functioning AV node

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8
Q

Distinguish between narrow complex and broad complex tachycardias

A

Narrow: QRS 120ms

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9
Q

When might an ECG be abnormal?

A

Cardiac pathology: conduction abnormalities, structural heart disease, ischaemia Systemic pathology: sepsis, PE, intracranial pathology, electrolyte disturbance)

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10
Q

What leads are included in a standard ECG?

A

6 praecordial 6 limb (3 of which are augmented/derived)

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11
Q

List 4 common cardiac presentations where an ECG would be an appropriate 1st line test

A

Chest pain Dyspnoea/HF Palpitations Syncope

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12
Q

What additional leads can be added to a standard 12-lead ECG and what is the clinical scenario in which these may be indicated?

A

Right ventricular leads V4R-V6R (if suspecting right ventricular infarction Posterior leads V7-V9 (if suspecting posterior ischaemia)

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13
Q

P wave

A

Atrial depolarisation

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14
Q

QRS complex

A

Ventricular depolarisation (masks atrial repolarisation)

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15
Q

T wave

A

Ventricular repolarisation

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16
Q

What does the PQ interval represent and what is its normal length?

A

AV conduction time (measured from start of p wave to start of QRS)

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17
Q

Normal equivalent time of a small square (1mm)

A

0.04s

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18
Q

Normal equivalent time of a large square (5mm)

A

0.2s

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19
Q

Normal speed of ECG

A

25 mm/sec (5 big squares = 1 sec)

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20
Q

Normal duration and appearance of QRS complex

A

Usually not >0.1 sec in duration R waves are deflected positively and the Q and S waves are negative

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21
Q

Where are p waves best seen?

A

Leads II, V1

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22
Q

What changes are seen in left axis deviation?

A

Ladies Adore Diamonds (lead i ^, lead II/aVF down)

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23
Q

What changes are seen in right axis deviation?

A

Rover Adores Digging (bone shape: lead I down, lead II/aVF ^)

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24
Q

What does a normal cardiac axis look like?

A

Lead I ^` Lead II/aVF down

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25
Q

List 6 causes of left axis deviation (>-30 degrees)

A

Left anterior hemiblock

IHD

Cardiomyopathy

HTN

WPW syndrome with R sided accessory pathway

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26
Q

List 5 causes of right axis deviation (>+90 degrees)

A

Normal finding in children and tall thin adults

RV volume/pressure overload (RV hypertrophy, ASD, VSD, PE)

Lung pathology (COPD, PE)

Dextrocardia (apex on R side of chest)

WPW syndrome with L sided accessory pathway

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27
Q

List 5 causes of extreme R axis deviation

A

Lead transposition

VT

Emphysema

Hyperkalaemia

Paced rhythm

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28
Q

What is the normal duration of a p wave?

A

Duration

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29
Q

What is p pulmonale and what is it indicative of?

A

Increased p wave voltages Indicative of R atrial dilation

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30
Q

What is p mitrale and what is it indicative of?

A

Bifid p wave Indicative of L atrial dilation (later depolarisation of LA leads to 2 peaks in p wave)

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31
Q

What atrium depolarises first?

A

Right

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32
Q

In what demographic is 1st degree AV block common?

A

Normal individuals, especially young athletic people

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33
Q

What is the difference between 2:1 AV conduction block and complete heart block?

A

2:1 AV conduction block: every 2nd p wave is non-conducted Complete heart block: AV dissociation

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34
Q

What is the “key ECG concept”?

A

QRS complex is predominantly positive if vector of depolarisation moves towards that lead (and vice versa)

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35
Q

List 3 possible abnormalities of the QRS complex

A

Voltages (e.g. increased in LVH, decreased in cardiac amyloidosis) Q waves Conduction (e.g. L or R bundle branch blocks)

36
Q

Identifying LVH on ECG

A

Sum of height of S in V1/V2 and R in V5 or V6 (whichever is larger) ≥35mm/3.5mV (7 large squares)

Or R in aVL ≥11mm

37
Q

What findings can be seen on ECG in R ventricular hypertrophy?

A

Right axis deviation R wave predominant in lead V1 (normally S wave dominant) Inverted T waves in right praecordial leads (V2, V3 in severe cases) Deep S in V6 Peaked P waves may also occur due to right atrial hypertrophy

38
Q

When are Q waves normal?

A

Small septal Q waves in some LV leads may be normal (due to early depolarisation of septum from L to R) Q wave in lead III normal

39
Q

What do pathological Q waves indicate?

A

Marker of electrical silence which implies established full thickness death of myocardium (i.e. scar) ≥25% height of the corresponding R wave (and/or >40ms width and >2mm in depth) Present in >1 contiguous (adjacent) lead

40
Q

Classic morphology for LBBB

A

QRS complex duration >0.12ms (3 small squares) “WilliaM” (W in V1, M in V6) Inverted T waves lateral leads V5-V6, I, aVL No septal Q waves

41
Q

Classic morphology for RBBB

A

QRS complex duration >0.12ms (3 small squares) “MarroW” (M rSR’ in V1, W in V6) Inverted T waves V2-V3 Slurred S wave in V6

42
Q

Inferior leads

A

II, III, aVF

43
Q

Anteroseptal leads

A

V1-V4

44
Q

Lateral leads

A

V5-V6

45
Q

When can ST segment changes NOT be interpreted?

A

If resting pre-existing LBBB

46
Q

4 causes of ST segment changes

A

Myocardial ischaemia/infarction Pericarditis LVH with “strain” pattern Drugs e.g. digoxin toxicity

47
Q

ECG changes in pericarditis

A

Widespread ST segment elevation

48
Q

ECG changes in LVH with “strain” pattern

A

Increased voltages of QRS complexes Strain pattern: ST depression with T wave inversion in lateral leads V5-V6, I, aVL

49
Q

Which coronary artery provides the posterior descending artery?

A

RCA and/or circumflex

50
Q

High lateral leads

A

I, aVL

51
Q

ECG signs of previous infarction

A

Q waves form if full thickness infarction T wave inversion often persists long term

52
Q

Progression of ECG changes in AMI

A

Normal Peaked T wave (timing??) Increasing ST segment elevation (timing??) Q wave formation and loss of R wave T wave inversion

53
Q

What aspects of the ECG are important to assess in a suspected STEMI?

A

Degree of ST elevation (measure number of mm - what is significant??) Assess coronary territory

54
Q

Can ST depression be localised to a territory?

A

No (but elevation can be)

55
Q

What do anteroseptal Q waves suggest? What is the possible significance of these?

A

Full thickness anteroseptal MI May be late presentation STEMI or old infarction with scar formation

56
Q

What kind of ST depression is more concerning?

A

Horizontal or downsloping (suggests significant myocardial ischaemia)

57
Q

ECG changes in digoxin toxicity

A

AF (irregular, no p waves) “Reverse tick” ST depression and T wave inversion in lateral leads

58
Q

In which leads are T waves normally inverted? What does it represent and what is their typical appearance?

A

Leads V1 (sometimes V2), III, aVR Indicates ventricular repolarisation Usually rounded and asymmetrical

59
Q

Causes of T wave abnormalities

A

Same as for ST segment changes (myocardial ischaemia/infarction, LVH with “strain” pattern, digoxin toxicity) Systemic issues (e.g. electrolyte imbalances - K+/Mg2+/Ca2+)

60
Q

What changes to the T wave suggest ischaemic changes? Which are most useful in diagnosing myocardial ischaemia?

A

Tall T wave Biphasic T wave (useful) Inverted T wave (useful) Flat T wave

61
Q

ECG changes in hypokalaemia

A

Flattening of T waves U waves

62
Q

ECG changes in hyperkalaemia

A

Tall, peaked T waves Widening of QRS

63
Q

How is the QT interval measured? What does it represent? In which leads is the T wave optimised? What is its usual length?

A

Measured from start of Q to end of T Represents ventricular depolarisation and repolarisation (Na+ influx and K+ efflux) Leads V3, V4 or II optimise T wave QT interval usually less than half the R-R

64
Q

How is the corrected QT interval calculated?

A

QT(corrected) = QT/(square root of R-R)

65
Q

What is the normal QT(corrected) for women and men?

A

Women:

66
Q

What is the concern with a prolonged QT interval?

A

Predisposes to torsades de pointe

67
Q

List some acquired causes of prolonged QT

A

MED:

MI

Electrolyte imbalance

Drugs

68
Q

What drugs can predispose to prolonged QT?

A

Sotalol Amiodarone Azithromycin Amitriptyline Clozapine

69
Q

What abnormalities are seen with inherited prolonged QT?

A

Defective sodium or potassium channels

70
Q

What is Wolff-Parkinson White?

A

An accessory pathway (macro-reentrant circuit) which bypasses the AV node, leading to earlier (pre-) excitation of the ventricle (“delta wave” with short P-R interval) than would occur with normal conduction May lead to rapid regular tachycardias

71
Q

ECG changes in WPW

A

Short P-R interval “Delta” wave (pre-excitation of ventricle)

72
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Early, narrow QRS followed by compensatory pause

Consistent with atrial ectopics (premature atrial complexes)

73
Q

Causes of narrow complex vs broad complex tachycardia??

A

??

74
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Irregularly irregular rhythm, absence of p waves, rapid ventricular response rate (>100 bpm)

Consistent with AF

75
Q

What is the abnormality? What underlying pathology is this consistent with?

A

“Saw tooth” appearance of p waves due to large re-entrant pathway in atrium, length of the re-entry circuit corresponds to the size of the right atrium and atrial rate is therefore usually a regular 300 bpm (ventricular rate depends on the AV conduction ratio; commonly it is 2:1 resulting in a ventricular rate of 150 bpm)

Consistent with atrial flutter

76
Q

What is the abnormality? What underlying pathology is this consistent with?

A

AF (irregular, no p waves) with “reverse tick” ST segment depression and T wave inversion in lateral leads

Consistent with digoxin toxicity

77
Q

What is the abnormality? What underlying pathology is this consistent with?

A

QRS complex duration >0.12s ,”WilliaM” (W in V1 but not always obvious, and M in V6), inverted T waves in lateral leads V5-V6, I, aVL; no septal Q waves

Consistent with LBBB

78
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Increased voltage of QRS complexes; strain pattern - ST depression with T wave inversion in lateral leads V5-V6, I, aVL

Consistent with LVH with “strain” pattern

79
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Horizontal ST depression

Consistent with myocardial ischaemia

80
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Widespread saddle-shaped ST elevation

Consistent with pericarditis

81
Q

What is the abnormality? What underlying pathology is this consistent with?

A

QRS complex duration >0.12s, “MarroW” (M - rSR’ - pattern in V1 and W in V6), inverted T waves lead V2-V3, slurred S wave in V6

Consistent with RBBB

82
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Right axis deviation; R wave predominant in lead V1 (normally S wave dominant); inverted T waves in right praecordial leads V2, V3 (severe cases); deep S in V6; peaked p waves may also occur due to right atrial hypertrophy

Consistent with RVH

83
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Early, broad complex QRS

Consistent with ventricular ectopics

84
Q

What is the abnormality? What underlying pathology is this consistent with?

A

Short PR interval; delta wave (reflects pre-excitation of the ventricles)

Consistent with Wolff-Parkinson White syndrome

85
Q

Causes of atrial and ventricular ectopics

A

Both are normal electrophysiological phenomenon usually not requiring Ix or treatment (but which may trigger a re-entrant tachydysrhythmia in patients with an underlying predisposition); frequent ectopics may cause palpitations and a sense of the heart “skipping a beat”

Both may be caused by sympathomimetics (anxiety, caffeine, B-agonists), hypokalaemia, hypomagnesaemia, digoxin toxicity, myocardial ischaemia

NB Frequent ventricular ectopics are usually benign EXCEPT in the context of prolonged QT where they may predispose to Torsades de Pointes by causing an “R on T” phenomenon

86
Q

Anatomy of the myocardial conduction system

A

MD2 Cardio (11 decks)

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