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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
What is the inheritance of catecholaminergic polymorphic ventricular tachycardia?
AD; ryanodine receptor mutation | Recessive; cardiac calsequestrin gene
26
What is the risk stratification and management of CPVT?
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
27
What are the clinical features of WPW syndrome?
``` Short PR Delta wave Ventricular preexcitation AVRT most common arrhythmia AF more common ```
28
How can the risk be stratified in WPW syndrome?
Exercise stress ECG to assess if the delta wave is still present under stress
29
What can cause hypertrophic cardiomyopathy?
Mutation in sarcomeric genes; arrhythmia +
30
Describe the progression of HOCM
Sudden death Heart failure End stage HF AF
31
What is the broad management of HOCM?
Control BP ICD to protect from sustained, pulseless VT USE HOCM SCD risk calculator Avoid competitive sport
32
What can cause inherited dilated cardiomyopathy?
Sarcomere and desmosomal genes Lamin A/C and desmin Dystrophin if X-linked
33
What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
Fibro-fatty replacement of cardiomyocytes | LV involvement in 50% of cases
34
What can cause ARVC?
AD mutations in genes for desmosomal proteins | AR in non desmosomal genes
35
What arrhythmia is assoc with ARVC?
Re-entrant VT | Usually implanted with ICD
36
How are inherited cardiac conditions generally managed?
Diagnosis; clinical testing and genetic testing Risk management; lifestyle, pharma, non-pharm Family (cascade) screening
37
Describe an ICD?
Subcutaneously placed 2 leads; one in RA and on ein RV Delivers 40 joules
38
What are complications from an ICD?
``` Endocarditis Perforation Haemothorax Pneumothorax Thromboembolic events Vascular problems Lead fractures Lead extraction Lead dislodgement ```
39
What is a classic ecg sign for hypertrophic cardiomyopathy?
Inverted T waves across all chest leads
40
What % of cardiac output does the atrial kick contribute?
30%
41
What is preload?
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
What is afterload?
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
What effect will preload have on Starling's law?
The most the heart muscles stretch in diastole, the more forcefully they contract in systole
44
What are the phases in the cardiac cells?
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
What phases of the cardiac cycle are the absolute refractory period?
Phase 1,2 and 3
46
What phases of the cardiac cycle are the relative refractory period?
Phase 4
47
In what phase of the cardiac cycle do the coronary arteries fill?
Ventricular diastole
48
What is the p wave
Atrial depolarization Location; precedes each QRS Amplitude; 2.5 small squares Duration <0.12 seconds (3 small squares each 0.04 seconds)
49
What is the PR interval?
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
What do changes in the PR interval indicate?
Altered impulse formation or a conduction delay such as AV block
51
What does a short or long PR interval indicate?
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
What is the QRS complex?
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
What do deep and wide QRS complexes represent?
MI
54
What is the ST segment?
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
What is the T wave
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
What is the QT interval?
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
What is the importance of the QT interval?
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
Was are some examples of drugs that can prolonged the QT interval?
``` Amiodarone Amitriptyline Clarithromycin/ erythromycin Citalopram Haloperidol Ketoconazole Levofloxacin Methadone Sumatriptan Sotalol ```
59
What can cause a short QT interval?
Famililal abnormalities Digoxin toxicity Hypercalcaemia
60
What is the U wave?
Recovery period of purkinje or ventricular contraction fibres Small deflection following T wave
61
What can a prominent U wave indicate?
Hypercalcaemia Hypokalaemia Digoxin toxicity
62
What is the blood supply to the SA node?
RCA most commonly | In 30% of people; left circumflex artery
63
Which antiarrhythmic drugs can be used to slow ventricular contraction?
Diltiazem, verapamil, digoxin
64
Which antiarrhythmic can be used to slow the heart rate and convert the rhythm back to sinus?
Amiodarone
65
What is first degree heart block?
Occurs when impulses from the atria are consistently delayed during conduction through the AV node
66
What are the classical ecg findings of 1st degree heart block?
Prolonged PR interval
67
What are the classical ecg findings of mobitz type 1 2nd degree heart block?
PR interval gradually gets longer with each successive beat until a P wave fails to conduct resulting in a dropped beat
68
What are the classical ecg findings of mobitz type 2 2nd degree heart block?
May be 2:1 or 3:1; | 2 p waves before every QRS
69
What are the classical ecg findings of complete heart block?
Normal P and QRS complexes but they have no pattern or regularity Slow ventricular rate
70
Describe class 1a antiarrhythmics
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
Describe class 1b antiarrhythmics
Suppress ventricular ectopy Slow phase 0 depolarization Shorten phase 3 depolarization and action potential Lidocaine; suppression of ventricular arrhythmias
72
Describe class 1c antiarrhythmics `
Slow conduction Flecainide; used for paroxysmal AF or flutter in patients without structural abnormalities Prevents SVT
73
Describe class 2 antiarrhythmics
Beta-adrenergic blockers Block sympathetic nervous system beta receptors and decrease HR Used to treat SVT, used in inherited channelopathies
74
Describe class 3 antiarrhythmics
``` 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
Describe class 4 antiarrhythmics
Calcium channel blockers Prolong conduction time and refractory period in AV node Decrease contractility Verapamil and diltiazem
76
Describe adenosine
Slows AV nodal conduction and inhibits re-entry pathways | Used to treat SVT
77
Describe atropine
Anticholinergic drug that blocks vagal effects on SA and AV node Used to treat symptomatic bradycardia and asytole
78
Describe digoxin
Enhances vagal tone and slows conduction through the SA and AV node USed to treat SVT, AF and flutter
79
Describe magnesium sulfate
Decreases cardiac cell excitability and conduction; slows conduction through AV node and prolongs the refractory period
80
Describe left axis deviation
Positive QRS in lead 1 | Negative QRS in lead aVF
81
Describe right axis deviation
Negative QRS in lead 1 | Positive QRS in lead aVF
82
What can cause left axis deviation?
``` Normal variation Inferior MI Left anterior hemiblock WPW syndrome Mechanical shifts; ascites, pregnancy, tumours LBBB LVH Ageing ```
83
What can cause right axis deviation?
``` Normal Dextrocardia Lateral wall MI Left posterior hemiblock RBBB COPD Acute PE RVH Hyperkalaemia VT ```
84
Describe RBBB and the causes
``` 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
Describe LBBB and the causes
``` 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
Anterior MI ECG
ST elevation in leads V3-4 | LAD
87
Lateral MI ECG
ST elevation in leads 1, aVL, V5-6 | Circumflex artery
88
Inferior MI ECG
ST elevation in 2,3, aVF | RCA
89
Septal MI ECG
ST elevation in V1-2 | LAD
90
Anterolateral MI ECG
ST elevation in 1, aVL, V3-6 | LAD, circumflex
91
What are the characteristic ECG changes seen with hyperkalemia?
Tall, peaked T waves ST segment depression Shortened QT

CLASP - Sudden Death (6 decks)

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