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Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is the difference between a supraventricular and a ventricular arrhythmia?

A

Supraventricular - origin is above the ventricles.

Ventricular - origin is in ventricular muscle (common) or fascicles of the conducting system (uncommon).

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2
Q

What are the forms of supraventricular tachycardia and bradycardia?

A

Tachycardia: AF, atrial flutter, ectopic atrial tachycardia.
Bradycardia: sinus bradycardia, sinus pauses.

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3
Q

What are types of ventricular arrhythmias?

A

Ventricular ectopics or premature ventricular complexes (PVC), ventricular tachycardia, ventricular fibrillation, asystole.

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4
Q

Give some examples of AV node arrhythmias.

A

AVN re-entry tachycardia, AV reciprocating or AV re-entrant tachycardia, AV block.

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5
Q

What abnormal anatomy can cause arrhythmias?

A

LVH, accessory pathways, congenital heart disease.

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6
Q

How can the autonomic nervous system cause arrhythmias?

A

Sympathetic stimulation (stress, exercise, hyperthyroidism), increased vagal tone causing bradycardia.

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7
Q

What are the metabolic causes of arrhythmias?

A

Hypoxia (chronic pulmonary disease, PE), ischaemic myocardium (acute MI, angina), electrolyte imbalances.

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8
Q

What infection can cause arrhythmias and how?

A

Viral myocarditis, causes inflammation.

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9
Q

What are genetic causes of arrhythmias?

A

Mutations of genes encoding cardiac ion channels e.g. congential long QT syndrome.

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10
Q

What causes ectopic beats?

A

Altered automaticity e.g. ischaemia, catecholamines. Triggered activity e.g. digoxin, long QT syndrome.

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11
Q

What is required for re-entry arrhythmia?

A

More than one conduction pathway with a different speed of conduction and recovery of excitability (refractoriness).

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12
Q

What are re-entry arrhythmias caused by?

A

Accessory pathway tachycardia (Wolf Parkinson White syndrome), previous MI, congenital heart disease.

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13
Q

When will an ectopic focus take over the intrinsic rhythm?

A

If beats are faster than sinus rhythm.

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14
Q

What is re-entry?

A

A self perpetuating circuit triggered by an ectopic beat.

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15
Q

What conditions increase the phase 4 slope causing an increase in heart rate?

A

Hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia (prolongs repolarisation).

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16
Q

What conditions decrease phase 4 slope causing slowed conduction (bradycardia, heart block)?

A

Hypothermia, hyperkalaemia.

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17
Q

What is triggered activity?

A

In phase 3 of the action potential a small depolarisation may occur (afterdepolarisation), and if of sufficient magnitude may reach threshold and lead to a sustained train of depolarisations.

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18
Q

What things can cause triggered activity?

A

Digoxin toxicity, Torsades de Pointes in long QT syndrome, hypokalaemia.

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19
Q

What are the causes of re-entry?

A 
Structural abnormalities (accessory pathways, scar from MI, congential heart disease). 
Functional abnormalities (conditions that depress conduction velocity or shorten refractory period promote functional block e.g. ischaemia, drugs).
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20
Q

How can ischaemia cause re-entry?

A

It slows down conduction. Part of the myocardium will be depolarised later which then spreads due to the rest of the muscle being excitable again and causes an extra beat.

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21
Q

What are the symptoms of re-entry tachycardia?

A

Palpitations, SOB, dizziness, syncope, presyncope, sudden cardiac death, angina and heart failure.

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22
Q

What investigations would you do to look for arrhythmias?

A

ECG, CXR, echo, stress ECG (looks for ischaemia), 24 hour ECG, event recorder (captures arrhythmia), electrophysiological study (induce clinical arrhythmia to study mechanism and map arrhythmia).

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23
Q

What are you looking for in an ECG?

A

Signs of previous MI (Q waves), pre-excitation (Wolf Parkinson White syndrome).

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24
Q

What is Wolf Parkinson White syndrome and what would show up on ECG?

A

Congenital accessory conduction pathway between the atria and ventricles. Short PR interval, wide QRS due to delta wave (slope before QRS).

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25
Q

What do you look for in an exercise ECG?

A

Ischaemia, exercise induced arrhythmia.

26
Q

How can an electrophysiological study be used to treat arrhythmia?

A

By delivering radiofrequency ablation to the extra pathway.

27
Q

What causes normal sinus arrhythmia?

A

Reflex changes in vagal tone during the respiratory cycle (inspiration reduces vagal tone and increases HR).

28
Q

What can cause sinus bradycardia?

A

Normal in athletes, beta-blockers, ischaemia (common in inferior STEMIs).

29
Q

What drugs is used to treat acute sinus bradycardia?

A

Atropine.

30
Q

What treatment would you use in sinus bradycardia if there was haemodynamic compromise?

A

Pacing.

31
Q

What is the treatment for sinus tachycardia?

A

Treat underlying cause, B-blockers.

32
Q

What are the symptoms and treatments of atrial ectopic beats?

A

Symptoms: asymptomatic, palpitations.
Treatment: none.

33
Q

How do sinus tachycardia and supraventricular tachycardia differentiate?

A

SVT is much faster and more symptomatic.

34
Q

What can cause supraventricular tachycardia (SVT)?

A

AV nodal re-entrant tachycardia (AVNRT), AV reciprocating tachycardia/AV re-entrant tachycardia (via an accessory pathway, AVRT), ectopic atrial tachycardia (EAT).

35
Q

What is the difference between AVNRT and AVRT?

A

AVNRT - the re-entrant circuit is within the AV node.

AVRT - a circuit using the AV node and a pathway between the atria and the ventricles.

36
Q

What is ectopic atrial tachycardia (EAT)?

A

Where there is an area of atrium that is firing and overtakes the AV node.

37
Q

How would you manage SVT acutely?

A

Increase vagal tone (Valsalva, carotid massage), slow conduction in the AV node (IV adenosine, IV verapamil).

38
Q

What is the chronic management of SVT?

A

Avoid stimulants, electrophysiology study and radiofrequency ablation (first line in young symptomatic patients), beta-blockers, antiarrhythmic drugs.

39
Q

What is radiofrequency catheter ablation (RFCA)?

A

Selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit.

40
Q

Describe how an electrophysiologic study is carried out.

A

ECG catheters placed in heart via femoral veins. Intracardiac ECH recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia. Catheter placed over focus/pathway and tip heated to 55-65*C.

41
Q

What is another name for AV node conduction disease?

A

Heart block.

42
Q

What are the causes of AV node conduction disease (heart block)?

A

Ageing, acute MI, myocarditis, infiltrative disease e.g. amyloid, drugs e.g. B-blockers and Ca channel blockers, calcific aortic valve disease, post-aortic valve surgery.
Genetics: Lenegre’s disease, myotonic dystrophy.

43
Q

What are the ECG findings for 1st degree heart block?

A

PR interval longer than normal (>0.2s).

44
Q

What are the ECG findings for 2nd degree heart block: Mobitz I?

A

Progressive lengthening of PR interval, eventually resulting in a dropped beat (usually vagal in origin).

45
Q

What are the ECG findings for 2nd degree heart block: Mobitz II?

A

Intermittent non-conducted P waves.

46
Q

What may Mobitz II heart block progress to?

A

3rd degree heart block.

47
Q

How would you treat Mobitz II heart block?

A

With a permanent pacemaker.

48
Q

What are the ECG findings in 3rd degree heart block?

A

No APs from the SA node/atria get through the AV node (broad QRS).

49
Q

What is the treatment for 3rd degree heart block?

A

Ventricular pacing.

50
Q

What are the 2 types of pacemakers?

A 
Single chamber (paces the right atria or right ventricle only). 
Dual chamber (paces the RA and RV): maintains AV synchrony (preserves atrial kick), used for AVN disease.
51
Q

What are the types of ventricular arrhythmias?

A

Ventricular ectopic or premature ventricular complex (PVC), VT, VF and asystole.

52
Q

What effect do premature ventricular complexes have on blood pressure?

A

Leads to a transient reduction in blood pressure.

53
Q

What are some causes of ventricular ectopics?

A

Structural: LVH, heart failure, myocarditis.
Metabolic: ischaemic heart disease, electrolytes.

54
Q

When would you need to investigate ventricular ectopics further?

A

If they are worse on exercise.

55
Q

How would you treat ventricular ectopics?

A

Beta-blockers, ablation of focus.

56
Q

What are the causes of ventricular tachycardia?

A

Coronary artery disease, previous MI, cardiomyopathy, inherited/familial arrhythmia syndrome e.g. long QT and Brudaga syndrome.

57
Q

What is monomorphic and polymorphic VT?

A

Monomorphic: complexes are same size.
Polymorphic: complexes are not the same size.

58
Q

What are the treatments of ventricular fibrillation?

A

Defibrillation, cardiopulmonary resuscitation.

59
Q

What are the long term treatments for VT?

A

Correct underlying problem, anti-arrhythmic drugs are inneffective.
Implantable cardiovertor defibrillators if life-threatening or VT catheter ablation.

60
Q

How would you treat stable and unstable VT?

A

Stable: pharmacologic cardioversion with AAD (prepare for DCCV).
Unstable: direct current cardioversion.

61
Q

If you were unsure if it was VT, how could you make the diagnosis?

A

Using adenosine.

62
Q

What are the functions of an impantable cardiac defibrillator?

A

Termination of VT/VF: anti-tachycardic pacing (outpaces the VT, painless), cardioversion, defibrillation.
Atrium and ventricle: pacing for bradycardia.

Cardiovascular (32 decks)

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