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CLASP Sudden Death > Cardiac Causes and ECG > Flashcards

Cardiac Causes and ECG Flashcards

1
Q

what is sudden cardiac death

A

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 types of genetic conditions can cause arrythmias

A

inherited arrhythmia syndromes
inherited cardiomyopathies
inherited multisystem diseases with CVS involvement (e.g. myotonic dystrophy, collagen problems)

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3
Q

what are the types of channelopathies

A 
congenital long QT syndrome 
brugada syndrome 
catecholamigeric polymorphic ventricular tachycardia (CPVT)
short QT syndrome 
progressive familial conduction disease 
familial AF 
familial WPW
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4
Q

what are the types of cardiomyopathies

A

hypertrophic cardiomyopathy
arrhythmogenic right ventricular cardiomyopathy (ARVC)
dilated cardiomyopathy

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5
Q

what is a channelopathy

A

arrhythmogenesis related to ion current imbalance and development of early and late depolarisation

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6
Q

how do cardiomyopathies cause arrhythmias

A

due to scar/ electrical barrier formation

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7
Q

what are after depolarisations

A

abnormal depolarisations of cardiac myocytes that interrupt phase 2,3 or 4 of the cardiac AP in the conduction system of the heart

(extra electrical activities that cause problems)

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8
Q

what can after depolarisations cause

A

can lead to triggered activity seen as sustained cardiac arrhythmia

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9
Q

what is an early afterdepolarisation (EAD)

A

abnormal depolarisation during phase 2 or 3
caused by an increase in the frequency of abortive action potentials before normal repolarisation is completed

phase 2 interrupted by increased Ca channels opening
phase 3 interrupted by opening of Na channels

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10
Q

what can early afterdepolarisation cause

A

torsades de pointes

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11
Q

what is torsades de pointes

A

polymorphic ventricular tachycardia
associated with a prolonged QT
can be congenital or acquired
caused by ectopic beat landing on the abnormal T wave in prolonged QT syndrome

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12
Q

what can cause early after depolarisations

A 
hypokalaemia 
drugs that prolong QT interval- clarithromycin, class Ia and III antiarrhythmic agents
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13
Q

what gene causes long QT syndrome

A

potassium voltage gate channel - KCNQ1 gene

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14
Q

what gene causes brugada syndrome

A

sodium channel voltage gated alpha subunit - SCN5A

calcium channel CACN1Ac

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15
Q

what receptor is affected in catecholamingeric polymorphic VT

A

ryanodine

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16
Q

is short QT syndrome common

A

very rare

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17
Q

what are the risk of congenital long QT syndrome

A

polymorphic VT (torsades de pointes) triggered by adrenergic stimulation
syncope- 5%
SCD 0.33-0.9%

(risk associated with severity of QT prolongation)

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18
Q

how common is congenital LQTS

A

1 in 2000 are carriers

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19
Q

what are the types of congenital LQTS

A

autosomal dominant:
-isolated LQT-
romano-ward syndrome
-extra cardiac features- anderson- tawil syndrome, timothy syndrome

autosomal dominant:
-associated with deafness- jervell and lange nielsen syndrome

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20
Q

what are the features of LQTS on ECG

A

QTc (corrected QT) >/= 480 ms in the absence of secondary causes in repeated ECG
abnormal T waves- bifid

AF (irregularly irregular) + abnormal T waves= LQTS

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21
Q

what can trigger LQTS

A

exercise - LQTS1
emotional stress
sleep
loud noises - LQTS2

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22
Q

what is the management for congenital long QT syndrome

A

avoid QT prolonging drugs- clarithromycin
correct electrolyte abnormalities (hypokalaemia/ magnesaemia/ calcaemia)
avoid swimming - dangerous
environment
beta blockers
ICD (high morbility)
loud noises - alarm clock in morning

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23
Q

what score to calculate long QT risk

A

scwartz score

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24
Q

what gene causes congenital short QT syndrome

A

mutation in cardiac K+ channels

25
Q

what are features of congenital short QT syndrome

A

QT <300ms at a heart rate <80bpm
may be associated with AF
may present in young children
VERY MALIGNANT

26
Q

what is the management for congenital short QT syndrome

A

hard to manage
?anti-arrhythmic drugs : quinidine, flecainide
ICD hard with children as increased body use, pyschological issues and inappropriate discharges due to T wave oversensing

27
Q

what are the risks in brugada syndrome

A

polymorphic VT, VF
AF

arrhythmia incdence 1% if asymptomatic, 3.2% in patients with syncope, 13.5 if previous cardiac arrest

28
Q

what inheritance does brugada syndrome follow

A

autosomal dominant
men 8x more likely to get it

(genotype and family history of SCD does not influence progosis)

29
Q

what are the features of brugada syndrome on ECG

A

ST elevation in V1 and 2
RBBB in V1-3
two R waves in V1= RSR
may be intermittent and change over time

30
Q

how can a diagnosis of brugada be made

A

only with provocative testing with flecainide or ajmaline (drugs that block the cardiac sodium channel)

31
Q

What triggers VF In brugada syndrome

A

abnormal rest or sleep
fever
excessive alcohol
large meals

32
Q

what is the management of brugada syndrome

A

avoid drugs that indice ST elevatio in right precordial leads
avoid excess alcohol and large meals
prompt treatment of fever with antipyrexials- paracetamol

if had previous cardiac arrest /sustained spontaneous SVT then ICD
consider ICD if history of syncope

33
Q

what drugs should you avoid in brugada syndrome

A

antiarrhythmics
psychotrophics
analgesics
anaesthetics

34
Q

what is catecholaminergic polymorphic ventricular tachycardia

A

adrenergic induced bidirectional and polymorphic VT and SVTz

35
Q

what triggers CPVT

A

emotional stress, physical activity

36
Q

what are the types of CPVT

A

Autosomal dominant- ryanodine receptor mutation

recessive- cardiac calsequestrin gene (CASQ2)

37
Q

what are the features of CPVT on IX

A

normal ECG and echo

38
Q

what is the management for CPVT

A

avoid competitive sports, strenuous exercise, stressful environments

beta blockers +/- flecainide if spontaneous/ stress induced VAs

if previous arrest, recurrent syncope or polymorphicbidirectional CT despite therapy then ICD

beta blockers for genetically +ve family members, even with negative exercise test

39
Q

what are the features of wolffparkinson white syndrome on ECG

A

short PR wave
delta wave slurring into QRS complex
ventricular preexcitation

40
Q

what are the risks in WPW

A

AV reentrant tachycardia most common arrhythmia
AF
small risk of SCD

41
Q

what causes WPW

A

extra bit of conducting tissue, accessory pathway. AV node has build in delay normally but in accessory pathway no conduction delay= ventricles fibrillate at the same rate as artia fibrillating

42
Q

what test to assess the risk in WPW

A

exercise ECG- see if able to maintain normal conduction in exertion
if risk then ablate pathway

43
Q

what mutation causes hypertrophic cardiomyopathy

A

mutation in sarcomeric genes

44
Q

what are the problems in hypertrophic cardiomyopathy

A

rhythm problems and obstruction to outflow of blood

45
Q

how might hypertrophic cardiomyopathy present

A

sudden death
HF/ end stage HF
AF

46
Q

what management for hypertrophic cardiomyopathy if risk of SCD (age, FHx, unexplained syncope, previous arrest due to VT/VF, spontaneous sustained VT causing syncope or haemodynamic compromise)

A

implant cardiac device

47
Q

what should you avoid in hypertrophic cardiomyopathy

A

competitive sport

48
Q

who gets dilated cardiomyopathy

A

1 in 2500
low in childhood
more common in males

49
Q

what genes cause dilated cardiomyopathy

A

sarcomere and desomal genes,
laminA/C and desmin if conduction disease,
dystophin if x linked

50
Q

what is the risk on dilated cardiomyopathy

A

LVEF = 35%

51
Q

what is arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

fatty infiltrations in right ventricle causing fibrofatty replacement of cardiomyocytes
half have LV involvement

causes rhythm problems as signals go round the fat cells- VT
(1 in 1000-5000 prevalence, mortality 0.9%/year)

52
Q

what mutations in ARVC

A

AD mutations in genes for desmosomal proteins

AR mutations in nondesmosomal genes

53
Q

what increases risk of SCD in ARVC

A

FHx of premature SCD
severity of R and LV function
frequent non-sustained VT

54
Q

what are the features of ARVC

A

on ecg QRS prolongation with late blip in it = epsilon waves

VT induction on electrophysiology studies

affects males more

55
Q

what is the treatment for ARVC

A 
usually get ICD
avoid competitive sports 
beta blockers 
amiodarone if symptomatic/ CI to BB
catheter alblation if symptomatic
56
Q

how does an ICD work - what are the complications

A

leads (2) go into right ventricle and artia, monitors rhythm and delivers shock if needed

  • endocarditis
  • perforation
  • hemothorax
  • pneumothorax
  • thromboembolic events
  • vascular complications
  • lead fractures/ extraction complications dislodgements
57
Q

why is it important to identify pre symptomatic patients at risk of SCD

A

SCD may be only presentation
young age group at risk
effective therapies available- lifestyle, BBs, ICD
to find other family members at risk

58
Q

when should a QT interval usually finish

A

before halfway point of RR interval

59
Q

what is seen on ECG in hypertrophic cardiomyopathy

A

inverted T waves

CLASP Sudden Death (6 decks)

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