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CLASP - Sudden Death > ECG interpretation, cardiac arrhythmias and management of risk > Flashcards

ECG interpretation, cardiac arrhythmias and management of risk Flashcards

1
Q

What is a sudden cardiac death?

A

Defined as an event that is non-traumatic, non-violent, unexpected and resulting from sudden cardiac arrest within 6 hours of previously witnessed normal health

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2
Q

What are the different forms of arrhythmias that commonly result in SCD?

A

Inherited arrhythmia syndrome
Inherited cardiomyopathies
Interited multi-system disease with CVS involvement; myotonic dystrophy, marfans, ehlers danlos

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3
Q

What are the different forms of channelopathies?

A 
Congenital long QT syndrome
Brugada syndrome
Catecholaminergic polymorphic ventricular tachycardia 
Short QT syndrome
Progressive familial conduction 
Familial AF 
Familial WPW
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4
Q

What are the different forms of cardiomyopathies?

A

Hypertrophic cardiomyopathy
Arrhythmogenic Right Ventricular Cardiomyopathhy (ARVC)
Dilated cardiomyopathy

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5
Q

What is an early afterdepolarization?

A

Occur with abnormal depolarization during phase 2 or 3
Caused by an increase in frequency of abortive action action potentials before normal repolarization is completed
Phase 2 may be interrupted due to augmented opening of calcium channels
Phase 3 may be interrupted due to opening of sodium channels

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6
Q

What arrhythmia can early afterdepolarization result in?

A

Torsades De Pointes

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7
Q

What can potentiate an EAD?

A

Hypokalaemia and drugs that prolong the QT interval including class 1a and 3 antiarrhythmic drugs

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8
Q

What is a channelopathy?

A

Arrhythmogenesis related to ioin current imbalance and development of early and late depolarisations

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9
Q

What is brugada syndrome?

A

Inherited problem with sodium channels in cardiac myocytes resulting in specific characteristic ECG appearances

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10
Q

In LQTS what will trigger torsades de pointes?

A

Adrenergic stimulation

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11
Q

What are the management strategies for LQTS?

A

Beta blocker

ICD

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12
Q

What is the threshold for implantation of an ICD in terms of SCD?

A

4%

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13
Q

What are the different types of LQTS?

A

Autosomal dominant; isolated LQTS (romano ward syndrome)

Autosomal recessive; if assoc with deafness - Jervell and Langer-Nielsen Syndrome

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14
Q

What scoring system can be used to diagnose LQTS?

A

Schwartz score

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15
Q

What is the cut off for a prolonged QT for diagnosis of LQTS?

A

QTc >480 ms in repeated 12 lead ECGs

Can be diagnosed in the presence of a confirmed pathogenic LQTS mutation irrespective of QT duration

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16
Q

What lifestyle modifications are recommended for people with LQTS?

A

Avoid QT prolonging drugs
Correct electrolyte abnormalities (hypokalaemia, hypomagnesaemia, hypocalcaemia) that may occur due to diarrhoea, vomiting or metabolic conditions
Avoid strenuous swimming= LQTS 1
Avoid exposure to loud noises (alarm clocks) = LQTS 2

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17
Q

What causes short QT syndrome?

A

Mutation in cardiac K+ cells

QT <300ms

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18
Q

What arrhythmias does brugada syndrome predispose you to?

A

Polymorphic VT and VF

AF

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19
Q

What is the characteristic ecg pattern seen with brugada syndrome?

A

ST elevation and RBBB in V1-3

May only see changes with provocative testing with flecainide or ajmaline (drugs that block cardiac sodium channel)

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20
Q

What is the inheritance of brugada syndrome?

A

Autosomal Dominant; adult males 8x more common

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21
Q

What can trigger VF in brugada syndrome?

A

Rest or sleep
Fever
Alcohol excess, large meals

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22
Q

What is the management of brugada syndrome?

A

Avoid drugs that induce ST segment elevation in the right precordial leads - antiarrhythmics, psychotropics, analgesics, anaesthetics
Early paracetamol for fever
Avoid excessive alcohol and large meals
ICD

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23
Q

What is catecholaminergic polymorphic ventricular tachycardia?

A

Adrenergic induced bidirectional and polymorphic VT

SVTs triggered by emotional stress and/or physical activity

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24
Q

Are there ECG or echo findings with catecholaminergic polymorphic ventricular tachycardia?

A

No

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25
Q

What is the inheritance of catecholaminergic polymorphic ventricular tachycardia?

A

AD; ryanodine receptor mutation

Recessive; cardiac calsequestrin gene

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26
Q

What is the risk stratification and management of CPVT?

A

Avoid competitive sports, strenuous exercise and stressful environments
Beta blockers are recommended in all pts with CPVT
ICD implantation +/- flecainide if experienced cardiac arrest, recurrent syncope or bidirectional VT
Therapy with beta blockers should be considered for genetically positive family members ever after a negative exercise test

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27
Q

What are the clinical features of WPW syndrome?

A 
Short PR 
Delta wave
Ventricular preexcitation 
AVRT most common arrhythmia
AF more common
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28
Q

How can the risk be stratified in WPW syndrome?

A

Exercise stress ECG to assess if the delta wave is still present under stress

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29
Q

What can cause hypertrophic cardiomyopathy?

A

Mutation in sarcomeric genes; arrhythmia +

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30
Q

Describe the progression of HOCM

A

Sudden death
Heart failure
End stage HF
AF

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31
Q

What is the broad management of HOCM?

A

Control BP
ICD to protect from sustained, pulseless VT
USE HOCM SCD risk calculator
Avoid competitive sport

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32
Q

What can cause inherited dilated cardiomyopathy?

A

Sarcomere and desmosomal genes
Lamin A/C and desmin
Dystrophin if X-linked

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33
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A

Fibro-fatty replacement of cardiomyocytes

LV involvement in 50% of cases

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34
Q

What can cause ARVC?

A

AD mutations in genes for desmosomal proteins

AR in non desmosomal genes

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35
Q

What arrhythmia is assoc with ARVC?

A

Re-entrant VT

Usually implanted with ICD

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36
Q

How are inherited cardiac conditions generally managed?

A

Diagnosis; clinical testing and genetic testing
Risk management; lifestyle, pharma, non-pharm
Family (cascade) screening

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37
Q

Describe an ICD?

A

Subcutaneously placed
2 leads; one in RA and on ein RV
Delivers 40 joules

38
Q

What are complications from an ICD?

A 
Endocarditis 
Perforation 
Haemothorax
Pneumothorax
Thromboembolic events
Vascular problems 
Lead fractures 
Lead extraction 
Lead dislodgement
39
Q

What is a classic ecg sign for hypertrophic cardiomyopathy?

A

Inverted T waves across all chest leads

40
Q

What % of cardiac output does the atrial kick contribute?

A

30%

41
Q

What is preload?

A

Stretching of muscle fibres in ventricles and is determined by the pressure and amount of blood remaining in the left ventricle at the end of diastole

42
Q

What is afterload?

A

Amount of pressure the left ventricle must work against to pump blood into the circulation
The greater this resistance, the more the heart works to pump out blood

43
Q

What effect will preload have on Starling’s law?

A

The most the heart muscles stretch in diastole, the more forcefully they contract in systole

44
Q

What are the phases in the cardiac cells?

A

Phase 0 = sodium move rapidly into cell
Phase 1 = L-type sodium channels close
Phase 2 = calcium flows in, potassium flows out
Phase 3 = calcium channels close, potassium flow out rapidly
Phase 4 = Cell membrane impermeable to sodium

45
Q

What phases of the cardiac cycle are the absolute refractory period?

A

Phase 1,2 and 3

46
Q

What phases of the cardiac cycle are the relative refractory period?

A

Phase 4

47
Q

In what phase of the cardiac cycle do the coronary arteries fill?

A

Ventricular diastole

48
Q

What is the p wave

A

Atrial depolarization
Location; precedes each QRS
Amplitude; 2.5 small squares
Duration <0.12 seconds (3 small squares each 0.04 seconds)

49
Q

What is the PR interval?

A

Beginning of the P wave to the beginning of QRS
Tracks atrial impulse from atria through the AV node, bundle of his and left/right bundle branches
Should be 0.12-0.20 seconds (3-5 small squares)

50
Q

What do changes in the PR interval indicate?

A

Altered impulse formation or a conduction delay such as AV block

51
Q

What does a short or long PR interval indicate?

A

Short; impulse is generated separate from SA node
Prolonged; slowing through atria or AV junction, can represent a conduction delay due to digoxin toxicity, heart block, MI

52
Q

What is the QRS complex?

A

Ventricular depolarisation and contraction = systole
Transmitted from AV node to bundle of his and purkinje fibres in ventricular walls
Should be 0.06-0.12 seconds long

53
Q

What do deep and wide QRS complexes represent?

A

MI

54
Q

What is the ST segment?

A

End of ventricular depolarization and beginning of repolarisation
The point that marks the end of the QRS and beginning of ST is known at the J point

55
Q

What is the T wave

A

Ventricular repolarization
The peak of the T wave represents the relative refractory period of the cell, a time when the cells are vulnerable to extra stimuli

56
Q

What is the QT interval?

A

Ventricular depolarization and repolarization
Varies depending on heart rate
Should be 0.36-0.44 seconds and should not be greater than half the distance between R-R

57
Q

What is the importance of the QT interval?

A

Shows time needed for the ventricular depolarization/ repolarization cycle
An abnormality in duration may indicate myocardial problems
Prolonged QT intervals indicate that the relative refractory period is longer

58
Q

Was are some examples of drugs that can prolonged the QT interval?

A 
Amiodarone 
Amitriptyline 
Clarithromycin/ erythromycin
Citalopram
Haloperidol 
Ketoconazole 
Levofloxacin 
Methadone
Sumatriptan 
Sotalol
59
Q

What can cause a short QT interval?

A

Famililal abnormalities
Digoxin toxicity
Hypercalcaemia

60
Q

What is the U wave?

A

Recovery period of purkinje or ventricular contraction fibres
Small deflection following T wave

61
Q

What can a prominent U wave indicate?

A

Hypercalcaemia
Hypokalaemia
Digoxin toxicity

62
Q

What is the blood supply to the SA node?

A

RCA most commonly

In 30% of people; left circumflex artery

63
Q

Which antiarrhythmic drugs can be used to slow ventricular contraction?

A

Diltiazem, verapamil, digoxin

64
Q

Which antiarrhythmic can be used to slow the heart rate and convert the rhythm back to sinus?

A

Amiodarone

65
Q

What is first degree heart block?

A

Occurs when impulses from the atria are consistently delayed during conduction through the AV node

66
Q

What are the classical ecg findings of 1st degree heart block?

A

Prolonged PR interval

67
Q

What are the classical ecg findings of mobitz type 1 2nd degree heart block?

A

PR interval gradually gets longer with each successive beat until a P wave fails to conduct resulting in a dropped beat

68
Q

What are the classical ecg findings of mobitz type 2 2nd degree heart block?

A

May be 2:1 or 3:1;

2 p waves before every QRS

69
Q

What are the classical ecg findings of complete heart block?

A

Normal P and QRS complexes but they have no pattern or regularity
Slow ventricular rate

70
Q

Describe class 1a antiarrhythmics

A

Sodium channel blockers
Reduce excitability of cardiac cells and decrease contractility
Have anticholinergic and proarrhythmic effects
Depress phase 0 and prolong repolarisation
Procainamide
Used in SVT and ventricular arrhythmias

71
Q

Describe class 1b antiarrhythmics

A

Suppress ventricular ectopy
Slow phase 0 depolarization
Shorten phase 3 depolarization and action potential
Lidocaine; suppression of ventricular arrhythmias

72
Q

Describe class 1c antiarrhythmics `

A

Slow conduction
Flecainide; used for paroxysmal AF or flutter in patients without structural abnormalities
Prevents SVT

73
Q

Describe class 2 antiarrhythmics

A

Beta-adrenergic blockers
Block sympathetic nervous system beta receptors and decrease HR
Used to treat SVT, used in inherited channelopathies

74
Q

Describe class 3 antiarrhythmics

A 
Potassium channel blockers 
Block potassium movement in phase 3 
Increase duration of action potential 
Prolong effective refractory period 
Amiodarone; used for SVT, AF, atrial flutter; WPW syndrome and ventricular arrhythmias
75
Q

Describe class 4 antiarrhythmics

A

Calcium channel blockers
Prolong conduction time and refractory period in AV node
Decrease contractility
Verapamil and diltiazem

76
Q

Describe adenosine

A

Slows AV nodal conduction and inhibits re-entry pathways

Used to treat SVT

77
Q

Describe atropine

A

Anticholinergic drug that blocks vagal effects on SA and AV node
Used to treat symptomatic bradycardia and asytole

78
Q

Describe digoxin

A

Enhances vagal tone and slows conduction through the SA and AV node
USed to treat SVT, AF and flutter

79
Q

Describe magnesium sulfate

A

Decreases cardiac cell excitability and conduction; slows conduction through AV node and prolongs the refractory period

80
Q

Describe left axis deviation

A

Positive QRS in lead 1

Negative QRS in lead aVF

81
Q

Describe right axis deviation

A

Negative QRS in lead 1

Positive QRS in lead aVF

82
Q

What can cause left axis deviation?

A 
Normal variation 
Inferior MI 
Left anterior hemiblock 
WPW syndrome 
Mechanical shifts; ascites, pregnancy, tumours 
LBBB
LVH 
Ageing
83
Q

What can cause right axis deviation?

A 
Normal 
Dextrocardia 
Lateral wall MI 
Left posterior hemiblock 
RBBB
COPD 
Acute PE 
RVH
Hyperkalaemia
VT
84
Q

Describe RBBB and the causes

A 
Anterior wall MI
Cardiomyopathy
Cor pulmonale 
PE 
IHD 
ECG: 
Lead V1; rsR QRS complex and T wave inversion 
Lead V6; widened S wave and upright T wave
85
Q

Describe LBBB and the causes

A 
Hypertensive heart disease 
Aortic stenosis 
Degenerative changes of conduction system 
IHD
ECG: 
All leads have prolonged QRS
V1; QS wave pattern 
V6; slurred R wave and T wave inversion
86
Q

Anterior MI ECG

A

ST elevation in leads V3-4

LAD

87
Q

Lateral MI ECG

A

ST elevation in leads 1, aVL, V5-6

Circumflex artery

88
Q

Inferior MI ECG

A

ST elevation in 2,3, aVF

RCA

89
Q

Septal MI ECG

A

ST elevation in V1-2

LAD

90
Q

Anterolateral MI ECG

A

ST elevation in 1, aVL, V3-6

LAD, circumflex

91
Q

What are the characteristic ECG changes seen with hyperkalemia?

A

Tall, peaked T waves
ST segment depression
Shortened QT

CLASP - Sudden Death (6 decks)

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