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Year 3 Sudden death > Cardiac Conditions that Cause Sudden Death > Flashcards

Cardiac Conditions that Cause Sudden Death Flashcards

1
Q

Define sudden cardiac death

A

Event that is non-traumatic, non-violent, unexpected and resulting from sudden cardiac arrest within 6hrs of previously witnessed normal health

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2
Q

Is Brugada syndrome a channelopathy or cardiomyopathy?

A

Channelopathy

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3
Q

What is a channelopathy?

A

Ion current imbalance + development of early/late depolarizations

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4
Q

What is a cardiomyopathy?

A

Arrhythmogenesis related to scar/electrical barrier formation and subsequent re-entry

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5
Q

Are channelopathies normal or abnormal at screening?

A

Often normal

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6
Q

Are cardiomyopathies normal or abnormal at screening?

A

Often abnormal

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7
Q

What are the mechanisms of arrhythmia?

A

Automaticity - thing that keeps node firing
Trigger
Re-entry e.g. scar

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8
Q

When do ‘after depolarizations’ occur?

A

interrupt phase 2,3 or 4 of cardiac action potential

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9
Q

What do after depolarizations lead to?

A

Triggered activity - sustained cardiac arrhythmia e.g. fibrillation

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10
Q

When do early after depolarizations occur?

A

During phase 2 or 3

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11
Q

What happens during phase 4 of the cardiac action potential?

A

Repolarization phase

Ventricular myocyte at rest

K+ channels open

Resting membrane potential = -90mV

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12
Q

What happens during phase 0 of the cardiac action potential and why?

A

Fast Na+ influx

Depolarization

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13
Q

What happens during phase 1 of the action potential cardiac cycle?

A

Closure of Na+ channels and transient K+ efflux

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14
Q

What happens during phase 2 of the action potential cycle?

A

Ca++ influx

Plateau

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15
Q

What happens during phase 3 of the cardiac action potential cycle?

A

Closure of Ca++ channels and K+ efflux

Rapid repolarization

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16
Q

What type of activity do after depolarizations lead to?

A

Triggered activity - sustained cardiac arrhythmia

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17
Q

What causes an early after depolarization?

A

Increase in the frequencyof abortive action potentials before normal repolarization is complete

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18
Q

Why might phase 2 be interrupted by an early afterdepolarization?

A

Augmented opening of Ca2+ channels

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19
Q

Why might phase 3 be interrupted by an early afterdepolarization?

A

Opening of Na2+ channels

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20
Q

What do early afterdepolarizations cause?

A

Torsades de Pointes

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21
Q

What is Torsades de Pointes?

A

Specific form of VT in patients with long QT syndrome.

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22
Q

What might Torsades de Pointes look like on ECG?

A

Rapid, irregular QRS complexes

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23
Q

What can cause early afterdepolarizations?

A

Hypokalemia

Drugs that prolong QT interval

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24
Q

Are the vast majority of cardiac conditions dominantly or recessively inherited?

A

Dominantly

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25
Q

When do delayed afterdepolarizations occur?

A

Phase 4 after repolarization complete but before another action potential would normally occur

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26
Q

What causes delayed afterdepolarizations?

A

Elevated cytosolic Ca2+ concentrations

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27
Q

What drug toxicity can cause elevated cytosolic Ca2+ concentrations?

A

Digoxin

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28
Q

What causes the delayed afterdepolarization?

A

Overload of sarcoplasmic reticulum causes spontaeous Ca2+ release after repolarization

Causes relased Ca2_ to exit cell through 2Na+/2Ca2+ exchanger

Results in net depolarizing current

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29
Q

Bidirectional ventricular tachycardia is a classical feature of what afterdepolarization?

A

Delayed afterdepolarization

also catecholaminergic polymorphic ventricular tachycardia/CPVT

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30
Q

What causes QT prolongation?

A

Less repolarising current prolongs APD (action potential duration)
OR
More depolarising current prolongs APD

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31
Q

Polymorphic VT is triggered by what in congenital LQTS?

A

Adrenergic stimulation

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32
Q

What is the name of the autosomol dominant congenital LQT syndrome that causes isolated LQT?

A

Romano-Ward syndrome

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33
Q

What is Jervell and Lange-Nielsen-syndrome?

Is it autosomal dominant or recessive?

A

Long QT syndrome associated with deafness

Autosomal recessive

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34
Q

Are you likely to die from LQT syndrome?

A

No

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35
Q

What is the treatment for long QT syndrome?

A

Beta blockers

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36
Q

What should people with LQTS1 avoid?

A

Strenuous swimming

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37
Q

What should people with LQTS2 avoid?

A

Exposure to loud noises

38
Q

How is long QT syndrome diagnosed?

A

QTc >480ms in repeated 12-lead ECG or LQTS risk score >3

39
Q

What criteria is used to diagnose LQT syndrome?

A

Schwartz criteria

40
Q

What is the criteria for diagnosing congenital short QT syndrome?

A

QT < 300ms at HR < 80bpm

41
Q

Congenital short QT syndrome may be associated with what other cardiac condition?

A

AF

42
Q

Are you likely to die from congenital short QT syndrome?

A

Yes

43
Q

What are some of the problems of implanting a cardioverter defibrillator in children?

A

Body size
Psychological
Inappropriate discharges due to T wave oversensing

44
Q

What drugs could you give in congenital short QT syndrome?

A

Anti-arrhythmic drugs e.g. quinidine, flecainide

45
Q

What condition causes RBBB in V1-3 and ST elevation?

A

Brugada syndrome

46
Q

A patient who has brugada syndrome has an increased risk of developing what arrhythmias?

A

VT

VF

47
Q

ECG changes in Brugada syndrome may be intermittent. How can you get a diagnostic ECG in a patient who may have Brugada syndrome?

A

Provocative testing with flecainide or ajmaline

drugs that block the cardiac Na channel

48
Q

Why are flecainide and ajmaline used in the provocative testing of a patient with Brugada syndrome?

A

Block the cardiac sodium channel

49
Q

What 2 gene mutations are associated with Brugada syndrome?

A

SCN5A - sodium channel

CACN1Ac - calcium channel

50
Q

What is the pathophysiology of Brugada syndrome?

A

Channelopathy
Alters transmembrane ion currents
SCN5A gene codes for cardiac voltage gated Na channel
Defect causes reduced Na current available during phase 0 and early repolarization of cardiac potential

51
Q

Is Brugada syndrome inheritance mostly dominant or recessive?

A

Dominant

52
Q

After provocative drug testing, what would you see on the ECG of a patient with Brugada syndrome?

A

ST segment elevation with type 1 morphology in 1 or leads (V1 and/or V2)

53
Q

What can trigger VF in Brugada syndrome?

A

Rest/sleep
Fever
Excessive alcohol
Large meals

54
Q

What lifestyle changes should patients with Brugada syndrome make?

A

Avoid drugs that induce ST segment elevation in right precordial leads
Avoid excessive alcohol + large meals
Prompt treatment of fever

55
Q

When would you consider implanting an ICD in a patient with Brugada syndrome?

A

Previous cardiac arrest

Documented sponatenous sustained VT

56
Q

What drugs would you avoid in Brugada syndrome?

A

Anti-arrhythmics
Psychotropics
Analgesics
Anaesthetics

57
Q

What condition is described:

Adrenergic induced bidirectional and polymporphic VT, SVTs?

A

Catecholaminergic polymorphic ventricular tachycardia

58
Q

What triggers catecholaminergic polymorphic ventricular tachycardia?

A

Emotional stress

Physical activity

59
Q

What can be seen on a patient’s echo and ECG in catecholaminergic polymorphic ventricular tachycardia?

A

Nothing

Normal

60
Q

How is catecholaminergic polymorphic ventricular tachycardia investigated?

A

Autosominal dominant OR recessive (wheyyyyyy u fooled)

61
Q

What gene mutation is associated with dominant inheritance of catecholaminergic polymorphic ventricular tachycardia (CPVT)?

A

Ryanodine Receptor mutation (RyR2)

62
Q

What gene mutatio nis associated with recessive inheritance of catecholaminergic polymorphic ventricular tachycardia?

A

Cardiac calsequestrin gene (CASQ2)

63
Q

What lifestyle changes are recommended for patients with CPVT?

A

Avoidance of competitive sports, strenuous exercise + stressful environments

64
Q

A patient has recently been diagnosed with CPVT. What drug should they be put on?

A

Beta blockers

65
Q

When should you implant an ICD in a patient with CPVT?

A

If they’ve experienced cardiac arrest, recurrent syncope or polymorphic/bidirectional VT despite optimal therapy

66
Q

Beta blockers should be considered for genetically positive family members of a person with CPVT despite a negative exercise test. True or false?

A

True

67
Q

What should be considered in addition to beta blockers in patients with CPVT that have had recurrent syncope or polymorphic/bidirectional VT whilst on beta blockers (who are not suitable for an ICD)?

A

Flecainide

68
Q

What is a last resort therapy for CPVT after drugs and ICD?

A

left cardiac sympathetic denervation

69
Q

What is the pathophysiology of Wolff-Parkinson-White syndrome (WPW)?

A

Presence of accessory pathway between atrium and ventricle

70
Q

AVRT (atrioventricular re-entrant tachycardia) is the most common arrhythmia in what condition?

A

WPW

71
Q

Squatting babies are associated with what cardiac condition?

A

Tetralogy of fallot

72
Q

What are the 4 components of tetralogy of fallot?

A

Pulmonary stenosis
Ventricular septal defect
Right Ventricular hypertrophy
Overriding aorta

73
Q

A mutation in what genes causes hypertrophic cardiomyopathy?

A

Sarcomeric genes (MYH7/MYBPC3)

74
Q

How does hypertrophic cardiomyopathy tend to present? (4)

A

Sudden death
Heart failure
End stage heart failure
AF

75
Q

What is the treatment for hypertrophic cardiomyopathy?

A

ICD if severe (prior cardiac arrest/sustained VT) or lotsa risk factors (FHx in first degree relative, LV wall thickness >30mm, recent unexplained syncope)

76
Q

What can you use if you are unsure of a patient’s risk of sudden cardiac death?

A

HOCM: SCD risk calculator

77
Q

What lifestyle modifications should people with HOCM make?

A

Avoid competitive sports

78
Q

What genes cause dilated cardiomyopathy?

A

Sacromere + desmosomal genes
laminA/C and desmin if conduction disease
Dystrophin if X-linked

79
Q

Who tends to get dilated cardiomyopathy, males or females?

A

Males

not common in childhood

80
Q

Describe the pathogenesis of arrhythmogenic right ventricular cardiomyopathy

A

Fibro-fatty replacement of cardiomyocytes

81
Q

What autosomal dominnat mutations cause arrythmogenic right ventricular cardiomyopathy?

A

Desmosomal proteins

82
Q

What autosomal recessive mutations cause arrhythmogenic right ventricular cardiomyopathy?

A

Nondesmosomal genes

83
Q

What arrhythmia can be caused by arrhythmogenic right ventricular cardiomyopathy?

A

VT

84
Q

What lifestyle modifications are recommended in arrhythmogenic right ventricular cardiomyopathy?

A

Avoidance of competitive sports

85
Q

What is the first line therapy in arrhythmogenic right ventricular cardiomyopathy?

A

Beta blockers

86
Q

What drug can be used in patients intolerant of beta blockers in arrhythmogenic right ventricular cardiomyopathy?

A

Amiodarone

87
Q

Is ICD used in arrhythmogenic right ventricular cardiomyopathy?

A

YEah

In patients with history of aborted SCD and haemodynamiclaly poorly tolerated VT

88
Q

What is the only known treatment for VF?

A

Defibrillation

89
Q

What does defibrillation do?

A

Delivers high energy to all cardiac myocytes causing them to fully depolarise (resets them)

90
Q

Lamin A/C mutations are associated with which inherited condition?

A

Dilated cardiomyopathy
First degree heart block
SVT and VA

91
Q

What is the treatment for all patients with DCm and confirmed disease-causing LMNA mutation and risk factors?

A

ICD

Year 3 Sudden death (5 decks)

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