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Cardiovascular Medicine > ECG's > Flashcards

ECG's Flashcards

1
Q

Reading an ECG - what to do first

A

Confirm patients name and age, and the ECG date

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2
Q

Reading an ECG - How to calculate rate

A

To calculate, divide 300 by the number of big squares between the two consecutive R waves. A normal rate is 60-100bpm

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3
Q

What is considered a normal rate?

A

60-100bpm

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4
Q

Reading an ECG - How to interpret the rhythm

A

If cycles are not clearly regular, use the card method (lay a card along the ECG, marking positions of 3 successive R waves) Slide the card to and from and chest that the intervals are equal - if not, note if:

  • There is slight but regular lengthening and then shortening (with respiration) - sinus arrhythmia, common in the young
  • There are different rates which are multiples of each other - varying block
  • It is 100% irregular - atrial fibrillation or ventricular fibrillation
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5
Q

Atrial fibrillation vs Ventricular fibrillation

A

In AFib, abnormal p waves precede the QRS signal on the ECG.
In VFib, there is a rapid irregular tracing but p waves and the QRS signal are unidentifiable.
In most ECG’s, AFib results in a rapid irregular pulse (QRS signal), while VFib results in no pulse (no clear QRS signal) so the ECG’s are quite different.

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6
Q

What is Ventricular fibrillation (VF)?

A

Ventricular fibrillation (VF) is the most important shockable cardiac arrest rhythm

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7
Q

ECG findings in Ventricular Fibrillation (VF)

A

Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF –> fine VF)

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8
Q

What is the ECG showing?

A

This is a typical rhythm strip of VF (Ventricular Fibrillation)

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9
Q

Sinus rhythm is characterised by a … … followed by a … …

A

Sinus rhythm is characterised by a P wave followed by a QRS complex

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10
Q

In atrial fibrillation, what will the p waves and QRS complexes look like?

A

No P waves

QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction

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11
Q

ECG Features of Atrial Fibrillation

A
  • Irregularly irregular rhythm
  • No P waves
  • Absence of an isoelectric baseline
  • Variable ventricular rate
  • QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
  • Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm)
  • Fibrillatory waves may mimic P waves leading to misdiagnosis
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12
Q

If the rhythm is 100% irregular, it is …

A

Atrial fibrillation or ventricular fibrillation

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13
Q

In AF, there are no discernible … waves and … complexes are …

A

In AF, there are no discernible P waves and QRS complexes are irregularly irregular

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14
Q

Atrial flutter has a ‘…’ baseline of atrial … and regular QRS complexes

A

Atrial flutter has a ‘Sawtooth’ baseline of atrial depolarisation and regular QRS complexes

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15
Q

Ventricular rhythm has … complexes >0. S with P waves following them or absent

A

Ventricular rhythm has QRS complexes >0.12S with P waves following them or absent

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16
Q

What is the axis on an ECG?

A

The axis is the overall direction of depolarisation across the patient’s anterior chest; this is the sum of all the ventricular electrical forces during ventricular depolarisation.

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17
Q

Determining the ECG axis:

A

Each ‘lead’ on the 12-lead ECG represents electrical activity along a particular plane. The axis lies at 90 degrees to the direction of the lead in which the isoelectric (equally +ve and -ve) QRS complex is found. If the QRS is more positive than negative in lead 1 (0), then the axis must be -30 and visa versa. The exact axis matters little - what you need to be able to recognise is whether the axis is normal (-30 to +90), left-deviated (+90). There are many ways of doing this. If the QRS in lead I (0) is predominantly positive (the R wave is taller than the S wave is deep), the axis must be between -90 and +90. If lead II (+60) is mostly positive, the axis must be between -30 and +150. If both I and II are positive, the axis must be between -30 and +90, the normal range. When II is negative, the axis is likely to be left-deviated (<30) and when I is negative, the axis is likely to be right-deviated (>+90) To remember this: Lovers Leaving - Left axis deviation - QRS complex in I and II point away from each other Lovers Returning - Right axis deviation - QRS complexes in I and III +/- II point towards each other

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18
Q

Left axis deviation - the QRS complexes in leads I and II do what?

A

Point away from eachother

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19
Q

Right-axis deviation - the QRS complexes in leads I and III +/- II do what?

A

Point towards each other

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20
Q

Overview of ECG axis - Lead I vs Lead aVF

A
Both positive = normal axis, Both negative = extreme axis
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21
Q

What is a normal QRS axis?

A

Between -30 and +90

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22
Q

Left axis deviation is …

A

A QRS axis less than -30

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23
Q

Right axis deviation is …

A

A QRS axis greater than +90

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24
Q

Extreme axis deviation is …

A

QRS axis between -90 and +180

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25
Q

Causes of right axis deviation:

A

Right ventricular hypertrophy Acute right ventricular strain e.g. due to PE Lateral STEMI Chronic lung disease, e.g. COPD Hyperkalaemia Sodium-channel blockade Wolff-Parkinson-White syndrome

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26
Q

Causes of left axis deviation:

A

Left ventricular hypertrophy Inferior MI Left bundle branch block Wolff-Parkinson-White syndrome Left anterior fascicular block

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27
Q

Causes of extreme axis deviation:

A

Ventricular rhythms e.g. VT, AIVR, Ventricular ectopic Hyperkalaemia Severe right ventricular hypertrophy

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28
Q

The P wave: Usually precedes each QRS complex, and upright in leads II,III and aV but inverted in …

A

aVR

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29
Q

Absent P waves - why?

A

AF, or hidden due to junctional or ventricular rhythm

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30
Q

P mitrale is seen when? (Bifid P wave)

A

In left atrial hypertrophy (LAE produces a broad, bifid P wave in lead II (P mitrale) and enlarges the terminal negative portion of the P wave in V1)

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31
Q

P pulmonale is seen when? (Peaked P wave)

A

Right atrial hypertrophy produces a peaked P wave (P pulmonale) with amplitude:

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32
Q

Pseudo-P-pulmonale is seen when? (Peaked P wave)

A

Peaked P wave but is likely due to hypokalaemia

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33
Q

PR interval: How to measure and interpret

A

Measure from the start of the P wave to the start of QRS Normal range = 3-5 small squares (0.12-0.2s) A prolonged PR interval implies delayed AV conduction (1st degree heart block) A short PR interval implies unusually fast AV conduction down an accessory pathway, e.g. WPW

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34
Q

Normal PR interval?

A

Normal range = 3-5 small squares (0.12-0.2s)

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35
Q

Prolonged PR interval implies …

A

A prolonged PR interval implies delayed AV conduction (1st degree heart block

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36
Q

Short PR interval implies …

A

A short PR interval implies unusually fast AV conduction down an accessory pathway, e.g. WPW

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37
Q

Normal QRS duration

A

0.12s

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38
Q

If QRS is >0.12s, what does this suggest?

A

Ventricular conduction defects, e.g. a bundle branch block, metabolic disturbance or ventricular origin e.g. ventricular ectopic

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39
Q

High amplitude QRS complexes (tall QRS) suggests what?

A

Ventricular hypertrophy

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40
Q

Normal Q waves are how wide and how deep?

A

0.04S wide and <2mm deep

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41
Q

Pathological Q waves (deep and wide) may occur when?

A

Within a few hours of an acute MI

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42
Q

QT interval - how to measure and interpret

A

Start of QRS to end of T wave Varies with rate The corrected QT interval (QTc) is the QT interval divided by the square root of the R-R interval. A normal QTc is 0.38-0.42s.

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43
Q

What is a normal QTc?

A

0.38-0.42s

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44
Q

Long QT can lead to … and …

A

VT and sudden death

45
Q

The ST segment is usually…

A

Isoelectric

46
Q

If the ST segment is … (>1mm) or … (>0.5mm) it usually implies infarction, or ischaemia, respectively

A

If the ST segment is elevated (>1mm) or depressed (>0.5mm) it usually implies infarction, or ischaemia, respectively

47
Q

The T wave is usually inverted in ….

A

aVR V1 and occasionally V2 Normal if inverted in isolation in lead III. Abnormal if inverted in I,II and V4-V6. Peaked in Hyperkalaemia and flattened in hypokalaemia

48
Q

It is abnormal for the T wave to be inverted in which leads?

A

Abnormal if inverted in I,II and V4-V6.

49
Q

T wave is peaked in which electrolyte distubance?

A

Peaked in Hyperkalaemia and flattened in hypokalaemia

50
Q

T wave is flattened in which electrolyte distubance?

A

Peaked in Hyperkalaemia and flattened in hypokalaemia

51
Q

What is a ‘J wave’? (Osborn wave)

A

The Osborn wave (J wave) is a positive deflection seen at the J wave point in precordial and true limb leads. It is most commonly associated with hypothermia. These changes will appear as reciprocal, negative deflection in aVR and V1.

52
Q

J point vs J wave

A

The letter J on the ECG defines 2 totally different and unrelated events. The J point is a point in time marking the end of the QRS and the onset of the ST segment present on all ECGs. The J wave is a much less common, slow deflection of uncertain origin originally described in relation to hypothermia.

53
Q

What causes J waves? (Osborn waves)

A

Characteristically seen in hypothermia, but also in hypercalcaemia, subarachnoid haemorrhage.

54
Q

What is the most specific ECG abnormality found in hypothermia?

A

J waves

55
Q

Sinus tachycardia - define

A

All impulses are initiated in the sinoatrial node, tachycardia means rate >100bpm

56
Q

Sinus bradycardia - define

A

Sinus rhythm at rate <60bpm Causes - physical fitness, vasovagal attacks, sick sinus syndrome, drugs (e.g. beta-blockers, digoxin, amiodarone), hypothyroidism, hypothermia, raised intracranial pressure, cholestasis

57
Q

Causes of sinus bradycardia

A

Causes - physical fitness, vasovagal attacks, sick sinus syndrome, drugs (e.g. beta-blockers, digoxin, amiodarone), hypothyroidism, hypothermia, raised intracranial pressure, cholestasis

58
Q

Causes of sinus tachycardia

A

Exercise Pain Anxiety Hypovolaemia Hypoxia, hypercarbia Acidaemia Sepsis, pyrexia Anaemia Pulmonary embolism Cardiac tamponade Hyperthyroidism Alcohol withdrawal Pharmacological Beta-agonists: adrenaline, isoprenaline, salbutamol, dobutamine Sympathomimetics: amphetamines, cocaine, methylphenidate Antimuscarinics: antihistamines, TCAs, carbamazepine, atropine Caffeine, theophylline, marijuana

59
Q

Common causes of AF

A

IHD, thyrotoxicosis, hypertension, obesity, heart failure, alcohol

60
Q

What is heart block?

A

Disrupted passage of electrical impulse through the AV node

61
Q

First-degree heart block - define

A

The PR interval is prolonged (>200ms) and unchanging, no missed beats. ‘Marked’ first degree heart block is present if PR interval >300ms

62
Q

Second-degree heart block (Mobitz I/Wenckebach) - define

A

The PR interval becomes longer and longer until a QRS is missed, the pattern then resets.

63
Q

Second-degree heart block (Mobitz II) - define

A

QRSs are regularly missed e.g. P-QRS-P—P-QRS-P— This would be Mobitz II with a 2:1 block (2p:1QRS) This is a dangerous rhythm as it may progress to complete heart block

64
Q

Causes of first degree heart block

A

Enhanced vagal tone: often seen in athletes (non-pathological) Post myocardial infarction Lyme disease Systemic lupus erythematosus Congenital Myocarditis Electrolyte derangements Drugs: particularly AV blocking drugs such as beta-blockers, rate-limiting calcium-channel blockers, digoxin and magnesium1 Thyroid dysfunction

65
Q

Causes of second degree heart block (Mobitz I)

A

Increased vagal tone: often seen in athletes (non-pathological) Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone Inferior myocardial infarction Myocarditis Cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

66
Q

Causes of second degree heart block (Mobitz II)

A

Myocardial infarction Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease) Cardiac surgery (especially surgery occurring close to the septum such as mitral valve repair) Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease) Autoimmune (SLE, systemic sclerosis) Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis) Hyperkalaemia Drugs (e.g. beta-blockers, calcium channel blockers, digoxin, amiodarone) Thyroid dysfunction

67
Q

Mobitz type 2 AV block is always pathological, with the block typically occurring at either the … or the …

A

Mobitz type 2 AV block is always pathological, with the block typically occurring at either the bundle of His (20%) or the bundle branches (80%).

68
Q

Third-degree heart block - define

A

Complete heart block - no impulses are passed from atria to ventricles so P waves and QRS waves appear independently from each other. As tissue distal to the AVN paces slowly, the patient becomes very bradycardia, and may develop haemodynamic compromise. Urgent treatment is required.

69
Q

Causes of third-degree heart block

A

Congenital: structural heart disease (e.g transposition of the great vessels), autoimmune (e.g maternal SLE) Idiopathic fibrosis: Lev’s disease (fibrosis of the distal His-Purkinje system in the elderly) and Lenegre’s disease (fibrosis of the proximal His-Purkinje system in younger individuals) Ischaemic heart disease: myocardial infarction, ischaemic cardiomyopathy Non-ischaemic heart disease: calcific aortic stenosis, idiopathic dilated cardiomyopathy, infiltrative disease (e.g. sarcoidosis, amyloidosis) Iatrogenic: post-ablative therapies and pacemaker implantation, post-cardiac surgery Drug-related: digoxin, beta-blockers, calcium channel blockers, amiodarone Infections: endocarditis, Lyme disease, Chagas disease Autoimmune conditions: SLE, rheumatoid arthritis Thyroid dysfunction

70
Q

ST elevation - indicates…

A

Acute MI (STEMI)

71
Q

What is Prinzmetal Angina?

A

Prinzmetal angina (vasospastic angina or variant angina) is a known clinical condition characterized by chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates. These symptoms occur due to abnormal coronary artery spasm.

72
Q

What ECG changes are found in acute pericarditis?

A

Saddle-shaped ST elevation (widespread)

73
Q

ST depression is seen when?

A

Normal variant (upward sloping), digoxin toxicity (downward sloping), ischaemic (horizontal), angina, NSTEMI, acute posterior MI (ST depression in V1-V3)

74
Q

What is the predominant cause of ST depression?

A

Myocardial ischaemia is the predominant cause of ST depression.

75
Q

What drug causes this ECG change? (Downsloping ST segment)

A

Digoxin (therapeutic doses) Other features may include abnormal T waves (Flattened, inverted, or biphasic) and a short QT interval (<350ms)

76
Q

What electrolyte disturbance is characterised by a down slopping ST segment (widespread) in association with T wave flattening or inversion and U waves?

A

Low potassium is characterised by a down slopping ST segment (widespread) in association with T wave flattening or inversion and U waves. U wave are upright deflections of unknown aetiology occurring after the T wave.

77
Q

The ST segment should be …

A

The ST segment is situated between the QRS complex and the T wave. Under normal circumstances, it should remain on the isoelectric line (i.e. be flat).

78
Q

These are showing …

A

ST elevation and ST depression

79
Q

What is the ECG criteria for a STEMI?

A

The ECG criteria for a STEMI is broadly defined as a ≥2 mm ST segment elevation in 2 contiguous chest leads or ≥1mm ST segment elevation in 2 contiguous limb leads (there may be slightly different variations of these ECG definitions based on age and sex).

80
Q

ST elevation - coronary artery vessel territory

A

The ST elevation usually occurs alongside Q waves and will occur in the leads that represent a coronary artery vessel territory: Anteroseptal STEMI: V1-V4 Lateral STEMI: V5-V6, I, aVL Inferior STEMI: II, III, aVF Posterior STEMI: no ST elevation on routine ECG. Dominant R wave V1. May be ST elevation by placing posterior leads V7-V9.

81
Q

During a STEMI, there are usually reciprocal changes. This refers to ST depression in the leads opposite those with ST elevation. Typical examples: Anterolateral STEMI: inferior ST depression (II, III, aVF) Lateral STEMI: inferior ST depression (II, III, aVF) Inferior STEMI: lateral ST depression (aVL, I) Posterior STEMI: anterior ST depression (V1-V3)

A

During a STEMI, there are usually reciprocal changes. This refers to ST depression in the leads opposite those with ST elevation. Typical examples: Anterolateral STEMI: inferior ST depression (II, III, aVF) Lateral STEMI: inferior ST depression (II, III, aVF) Inferior STEMI: lateral ST depression (aVL, I) Posterior STEMI: anterior ST depression (V1-V3)

82
Q

Several characteristic ECG changes occur during the natural history of a STEMI. Minutes to hours: … T-waves 0-12 hours: …-… 1-12 hours: …-wave development Days: T-wave … Weeks: T-wave … and persistent Q-waves

A

Several characteristic ECG changes occur during the natural history of a STEMI. Minutes to hours: hyperacute T-waves 0-12 hours: ST-elevation 1-12 hours: Q-wave development Days: T-wave inversion Weeks: T-wave normalisation and persistent Q-waves

83
Q

ECG findings - PE

A

Sinus tachycardia (commonest), RBBB, Right ventricular strain pattern (R-axis deviation, dominant R wave and T-wave inversion/ST depression in V1 and V2) Rarely, the SI1QIIITIII pattern occurs - deep S waves in I, pathological Q waves in III, inverted T waves in III

84
Q

Digoxin Toxicity - ECG

A

Down-sloping ST depression and inverted T wave in V5-V6 (Reversed tick) In digoxin toxicity, any arrhythmia may occur (Ventricular ectopics and nodal bradycardia are common)

85
Q

Hyperkalaemia - ECG findings

A

Tall, tented T waves, widened QRS, absent P waves, ‘sine wave’ appearance

86
Q

Hypokalamia - ECG findings

A

Small T waves, prominent U waves, peaked P waves

87
Q

Hypercalcaemia - ECG findings

A

Short QT interval

88
Q

Hypocalcaemia - ECG findings

A

Long QT interval, small T waves

89
Q

ECG territories - what leads, what territory, what artery?

A

I, aVL, V4-V6 = lateral heart territory - circumflex artery V1-V3 = anterioseptal - left anterior descending II, III, aVF = inferior - right coronary artery in 80%, circumflex 20% ‘left-dominant’ V7-V9 = posterior - circumflex

90
Q

Right Bundle Branch Block - what is it?

A

QRS >0.12Sm ‘RSR’ pattern in V1-V3 (“M-shaped” QRS complex) Wide, slurred S wave in lateral leads (I, aVL, V5-V6) MaRRoW (M = V1, RR = RBBB, W = V6)

91
Q

Left Bundle Branch Block - what is it?

A

QRS>0.12s, ‘M’ pattern in V6, W in V1, WiLLiaM - Wi = V1, LL = LBBB, M = V6

92
Q

Causes of LBBB

A

Aortic stenosis Ischaemic heart disease Hypertension Dilated cardiomyopathy Anterior MI Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system Hyperkalaemia Digoxin toxicity

93
Q

Causes of RBBB

A

Right ventricular hypertrophy / cor pulmonale Pulmonary embolus Ischaemic heart disease Rheumatic heart disease Congenital heart disease (e.g. atrial septal defect) Myocarditis Cardiomyopathy Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system

94
Q

Is this RBBB or LBBB?

A

RBBB with LAFB. Broad QRS > 120ms Note the prominent delayed RV conduction, manifested as a tall, broad R wave (R’) best seen in lead V1 Widened S wave is best appreciated in lead I There is appropriate discordance in the right precordial leads with T-wave inversion

95
Q

Is this RBBB or LBBB?

A

LBBB Broad notched R waves are best appreciated in leads aVL and I here. There is absence of Q waves in leads V5-6.

96
Q

If there is LBBB, no comment can be made on what?

A

ST segment and T wave

97
Q

New LBBB may represent what?

A

STEMI

98
Q

What is bifascicular block?

A

The combination of RBBB and left bundle hemiblock, manifest as an axis deviation e.g. left axis deviation in the case of left anterior hemiblock

99
Q

What is trifascicular block?

A

Bifascicular block plus 1st-degree heart block - might need pacing

100
Q

Suspect LVH if the R wave in V6 is >… or the sum of the S wave in V1 and the R wave in V6 is >…

A

Suspect LVH if the R wave in V6 is > 25mm or the sum of the S wave in V1 and the R wave in V6 is >35mm

101
Q

Suspect … if dominant R wave in V1, T wave inversion in V1-V3 or V4, deep S wave in V6, right axis deviation

A

Suspect RVH if dominant R wave in V1, T wave inversion in V1-V3 or V4, deep S wave in V6, right axis deviation

102
Q

Causes of low voltage QRS complex (<5mm in all limb leads)

A

Hypothyroidism COPD Increased haematocrit Changes in chest wall impedance (e.g. in renal failure and subcutaneous emphysema but not in obesity) PE Bundle branch block Carcinoid heart disease Myocarditis Cardiac amyloid Doxorubicin cardiotoxicity Pericardial effusion Pericarditis

103
Q

The P wave on an ECG represents electrical activity from

A

atrial depolarisation.

104
Q

Ventricular depolarisation =

A

QRS complex

105
Q

Absent electrical activity On ecg

A

flat line (i.e. asystole)

106
Q

Electrical pause at the AV node

A

PR interval

107
Q

Ventricular repolarisation

A

T wave

108
Q

Axis overview

A

Cardiovascular Medicine (28 decks)

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