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Supporting Life > Abnormal ECG - Arrhythmias > Flashcards

Abnormal ECG - Arrhythmias Flashcards

1
Q

How are arrhythmias dangerous?

A

Reduction in cardiac output

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2
Q

What allows all parts of the heart to become latent pacemakers?

A

Phase 4 depolarisation

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3
Q

Bradyarrhythmia:

A

< 60 bpm

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4
Q

Tachyarrhythmia:

A

> 100 bpm

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5
Q

Which types of arrhythmias are easiest to treat?

A

Supraventricular rather than ventricular

Those of atrial or AVN origin

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6
Q

What is complete (third degree) heart block?

A

Complete dissociation of beating between the atria and the ventricles

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7
Q

What dictates the speed of the bradyarrhythmia in third degree heart block?

A

The location of the ectopic pacemaker: slower more distal to the SAN

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8
Q

What causes complete (third degree) heart block?

A

Atherosclerosis
CHD
Dilated cardiomyopathy
Idiopathic

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9
Q

ECG findings in complete (third degree) heart block?

A

QRS complex and T waves completely dissociated from the P waves as the ventricles beat independently of the SAN firing

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10
Q

How does re-entry cause arrhythmia?

A

Because the wave of depolarisation in the heart is no longer homogenous and the rate becomes too rapid

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11
Q

How can you treat a unidirectional bundle branch block?

A

Deepen the block to prolong the refractory period with a drug

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12
Q

What paradoxically can cause early afterdepolarisations?

A

Anti-arrhythmics e.g. digoxin (also too much calcium and catecholamines)

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13
Q

What do both early and delayed after-depolarisations cause?

A

Re-entry

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14
Q

In atrial fibrillation, where is the ectopic pacemaker located?

A

Atria / pulmonary artery / pulmonary vein

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15
Q

Why does atrial fibrillation cause decreased cardiac output?

A

Ventricles beat too quickly and are not primed with blood

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16
Q

What drugs can treat atrial fibrillation?

A

Adenosine and digoxin

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17
Q

How do adenosine and digoxin treat atrial fibrillation?

A

Slow AVN conduction

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18
Q

How do you describe the rhythm of beating in atrial fibrillation?

A

Regularly irregular

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19
Q

Describe the ECG of atrial fibrillation

A

No p waves
F waves of varying amplitudes
Very frequent QRS complexes

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20
Q

Why is the QRS complex in ventricular fibrillation broader than in a normal patient?

A

Ectopic site in the ventricle wall and muscle conducts slower than the conduction system

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21
Q

Why can ventricular fibrillation occur post-MI

A

MI scar allows re-entry

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22
Q

Describe the ECG of ventricular fibrillation

A

Either: Broad QRS which can be regular (monomorphic0 or irregular (polymorphic) and p waves don’t capture

Or: No ventricular beat so disorganised and chaotic activity reflected in the ECG

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23
Q

How does an implanted defibrillator work?

A

Cardioversion back to sinus rhythm

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24
Q

Class 1 drugs:

A

Na channel blockers, suppress conduction

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25
Q

Give an example of a class 1 drug:

A

Flecainide

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26
Q

Class 2 drugs:

A

Beta receptor blockers, reduce excitability and inhibit AVN conduction (-olol)

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27
Q

Give an example of a class 2 drug:

A

Bisoprolol

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28
Q

Class 3 drugs:

A

Drugs which prolong the AP and refractory period

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29
Q

Give an example of a class 3 drug:

A

Amiodarone

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30
Q

Class 4 drugs:

A

Ca channel blockers, inhibit AVN conduction

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31
Q

Give an example of a class 4 drug:

A

Verapamil

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32
Q

Function of adenosine:

A

Slows AVN conduction

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33
Q

Function of digoxin:

A

Stimulates the vagus and thus slows AVN conduction

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34
Q

What drugs could be used to slow AVN conduction as a rate control strategy for treatment?

A

Class 2 (bisoprolol), class 4 (verapamil), adenosine and digoxin

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35
Q

What drugs could be used to block the re-entrant pathway and treat the source of the arrhythmia as a rhythm control strategy for treatment?

A

Class 1 (flecainide), class 3 (amiodarone)

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36
Q

Name class 2 drugs:

A 
Carvedilol
Propranolol
Esmolol
Timolol
Metoprolol
Atenolol
Bisoprolol
Nebivolol
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37
Q

Name class 1 drugs:

A

1a: Quinidine
Procainamide
Disopyramide
Ajmaline

1b: Lidocaine
Mexiletine

1c: Flecainide
Propafenone

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38
Q

Name class 3 drugs:

A 
Amiodarone
Dronedarone
Sotalol
Bretylium
Ibutilide
Dofetilide
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39
Q

Name class 4 drugs:

A

Verapamil
Diltiazem
Nifedipine

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40
Q

The majority of paroxysmal tachycardias are caused by what?

A

Re-entry

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41
Q

Chronic degenerative cause of bradycardia?

A

Sick sinus syndrome / sinoatrial disease

42
Q

What is sick sinus syndrome?

A

Fibrosis of the SAN (usually idiopathic)

43
Q

Important prophylaxis in tachy-brady syndrome?

A

Anti-coagulation

44
Q

Drugs used for vasovagal attacks:

A

Beta-blockers, alpha-blockers (e.g. amiodarone) and myocardial negative inotropes (e.g. disopyramide)

45
Q

First degree AV block =

A

Prolongation of the PR interval to > 0.22s

Every atrial depolarisation is followed by ventricular depolarisation but with delay

46
Q

Second degree AV block =

A

Some p waves conduct and others do not

47
Q

Progressive PR interval prolongation until a p wave fails to conduct is which type of heart block?
PR interval before the p wave fails is broader than after

A

Second degree AV block: Mobitz I block

48
Q

Dropped QRS complex not preceded by a progressive PR interval prolongation. QRS complex is wide > 0.12s
Which type of heart block?

A

Second degree AV block: Mobitz II block

49
Q

Every second or third p wave conducts to the ventricles.

Which type of heart block?

A

Second degree AV block: 2:1 / 3:1 / advanced block

50
Q

What does a broad complex escape rhythm > 0.12s imply?

A

That the escape rhythm occurs below the bundle of His more distally in the His-purkinje system

51
Q

Narrow onset escape rhythm is characterised by which differential?

A

QRS complex < 0.12s

52
Q

Narrow onset escape rhythm suggests what?

A

Escape rhythm lies in the bundle of His more proximal to the AVN

53
Q

Treatment for narrow onset escape rhythm?

A

IV atropine for recent and transient onset, pacemaker for for chronic onset AV block

54
Q

Which drugs can induce complete heart block?

A

Digoxin, beta-blockers, CCBs (non-dihydropyridine) amiodarone

55
Q

What is the commonest cause of re-entry in patients with normal hearts?

A

AVN re-entry (AVNRT)

56
Q

ECG of AVNRT? (or accelerated junctional tachycardia)

A

No visible p wave or inverted p wave immediately before or after the QRS complex

57
Q

ECG of AV reciprocating tachcardia?

A

P wave visible between QRS complex and t wave

58
Q

ECG of atrial flutter?

A

Flutter waves of 300/min usually with a 2:1 AVN conduction rate

59
Q

ECG of atrial tachycardia?

A

Organised atrial activity with p wave morphology different to sinus rhythm preceding the QRS

60
Q

ECG of multifocal atrial tachycardia?

A

P waves of differing morphologies and irregular RR interval

61
Q

Why should amiodarone be reserved until last as a rhythm control treatment in a heart with no significant disease?

A

Adverse extra cardiac effects

62
Q

When is amiodarone only recommended treatment for rhythm control?

A

When the patient has heart failure or left ventricular hypertrophy

63
Q

Where are the ectopic triggers for atrial fibrillation typically found?

A

Pulmonary veins

64
Q

Drug causes of long QT syndrome:

A

Quinidine, disopyramide, sotalol, amiodarone, TCAs (e.g. amitriptyline)
Phenothiazine drugs (e.g. chlorpromazine)
Antipsychotics (e.g. haloperidol, olanzapine)
Macrolides (e.g. erythromycin)
Quinolones (e.g. ciprofloxacin)
Methadone

65
Q

Cardiac causes of long QT syndrome:

Other causes: diabetes, fasting and liquid protein diets

A

Bradycardia
Mitral valve prolapse
Acute MI

66
Q

Treatment for long QT syndrome?

A

Beta blokade, pacemaker, left cardiac sympathetic denervation

67
Q

Arrhythmogenic right sided cardiomyopathy ECG and treatment?

A

ECG: abnormality/inverted t waves in V1-3 and terminal notch in the QRS
Treatment: solatolol, ablation, defibrillator

68
Q

What is a differential for ST elevation in inferior ECG leads?

A

Aortic dissection

69
Q

Adverse complication of beta blockers?

A

Worsen peripheral vascular disease if this is present

70
Q

Contraindications for beta blockers?

A

Uncontrolled heart failure
Asthma
Sick sinus syndrome
Concurrent verapamil use; may precipitate severe bradycardia

71
Q

Side-effects of beta-blockers?

A 
Bronchospasm
Cold peripheries
Fatigue
Sleep disturbance (nightmares)
Erectile dysfunction
72
Q

Indications for beta blockers?

A 
Angina
Post-MI
Heart failure
Arrhythmias
Hypertension
Thyrotoxicosis
Migraine prophylaxis
Anxiety
73
Q

ECG showing ST wave going down with inverted T wave =

A

Subendocardial ischaemia
Innermost layer has most resistance due to contraction of the myocardium - this innermost layer is ischaemic so repolarises slower so heart wall depolarises from the outer layer in rather than in-out causing inversion

74
Q

How does ischaemia cause SOB?

A

Slower relaxation in diastole so pressure in LA increases as not properly relaxed and blood is entering from lungs so this pressure is backed up to the lungs

75
Q

What do pathologic Q waves indicate?

A

Previous MI

76
Q

Detecting ischaemia?

A

Look for abnormal signs of repolarisation such as ST segment abnormalities or T wave inversion

77
Q

Test for left bundle branch block?

A

Cannot trust ECG, must move on to CTCA as cannot properly assess ST and T wave as depolarisation is already delayed so repolarisation follows in an inverted direction

78
Q

When do you offer CTCA?

A

If clinical assessment includes typical or atypical angina
or if assessment indicates non-anginas chest pain but the 12-lead resting ECG has been done and indicates ST-T changes or Q waves

79
Q

What is CTCA?

A

Perfusion X-ray imaging that allow you to visualise contrast in the coronary arteries
Anatomical assessment, not a functional assessment
Give stressor e.g. bicycle or vasodilatory/inotropic drug a d image again

80
Q

Second-line non-invasive functional testing?

A

MPS with SPECT

(first pass contrast enhanced MRI perfusion or MRI for stress induced wall motion abnormalities

81
Q

Invasive functional assessment:

A

> 20% drop in perfusion pressure will be angina causing

If a positive fractional flow reserve is measured from the pressures, this is an indication for re-vascularisation

82
Q

Anatomical assessment of CAD:

A

CTCA

Invasive angiography

83
Q

Functional assessment of CAD:

A 
ECG, exercise ECG
Nuclear medicine: SPECT and PET
Stress ECHO
Stress MRI
CT FFR
Invasive coronary physiology
84
Q

What drug is used for functional wall motion testing?

A

Dobutamine which causes inotropic stimulation

Induces true ischaemia

85
Q

Which drugs are used to measure perfusion?

A

Vasodilators: adenosine, regadenoson, dipyridamole

Induction of true ischaemia is exceptional

86
Q

Side effects of adenosine?

A

Bronchospasm
AV block I, II and III
Hypotension
Hyperventilation

87
Q

Side effects of dobutamide?

A 
Sustained or non-sustained VT
Paroxysmal AF
Transient 2:1 block
Severe hypertensive reaction
Hypotension
Nausea
88
Q

Mechanism of amiodarone:

A 
Class III anti-arrhythmic, blocks K channels and thus prolongs the AP
(also has a class I effect and blocks Na channels)
Used in the treatment of atrial, nodal and ventricular tachycardias
89
Q

S1:

A

Closure of mitral and tricuspid valves
Soft if long PR or mitral regurgitation
Loud in mitral stenosis

90
Q

S2:

A

Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal

91
Q

S3 (third heart sound):

A

Caused by diastolic filling of the ventricles
Normal <30 (up to 50 in women maybe)
Heard in dilated cardiomyopathy (aka left ventricular failure), constrictive pericarditis (aka pericardial knock) and mitral regurgitation

92
Q

S4 (fourth heart sound):

A

Heard in aortic stenosis, HOCM and hypertension
Caused by atrial contraction against a stiff ventricle
In HOCM a double palpable pulse may be felt as a result of S4

93
Q

Problems with amiodarone?

A

Interacts with warfarin, increasing warfarin concentration
May cause statin-induced rhabdomyolysis (raised CK)
Pro-arrhythmic affect of prolonging QT interval
Pulmonary/liver fibrosis, thyroid dysfunction, bradycardia, myopathy, neuropathy

94
Q

Which coronary artery blockage would present ECG changes in leads V1 to V4? (anteroseptal)

A

Left anterior descending

95
Q

Which coronary artery blockage would present ECG changes in leads II, III and aVF? (inferior)

A

Right coronary

96
Q

Which coronary artery blockage would present ECG changes in leads V4-6, I and aVL? (anterolateral)

A

Left anterior descending or left circumflex

97
Q

Which coronary artery blockage would present ECG changes in leads I, aVL +/- V5-6? (lateral)

A

Left circumflex

98
Q

Which coronary artery blockage would present ECG changes in leads V1-2 with tall R waves? (posterior)

A

Usually left circumflex, also right coronary

99
Q

S1:

A

Closure of mitral and tricuspid valves
Soft if prolonged PR or mitral regurgitation
Loud in mitral stenosis

100
Q

S2:

A

Closure of aortic and pulmonary valves
Soft in aortic stenosis
Splitting during inspiration is normal

101
Q

S3 (third heart sound):

A

Caused by diastolic filling of the ventricle
Normal if <30 y/o (women up to 50)
Left ventricular failure e.g. dilated cardiomyopathy
Constrictive pericarditis
Mitral regurgitation

102
Q

S4 (fourth heart sound):

A

Atrial contraction against a stiff ventricle
Aortic stenosis, HOCM, hypertension
HOCM may have palpable double apical pulse due to S4

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