Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the types of cardiomyopathies

A

hypertrophic cardiomyopathy
arrhythmogenic right ventricular cardiomyopathy (ARVC)
dilated cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is a channelopathy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do cardiomyopathies cause arrhythmias

A

due to scar/ electrical barrier formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what can after depolarisations cause

A

can lead to triggered activity seen as sustained cardiac arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what can early afterdepolarisation cause

A

torsades de pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what can cause early after depolarisations

A 
hypokalaemia 
drugs that prolong QT interval- clarithromycin, class Ia and III antiarrhythmic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what gene causes long QT syndrome

A

potassium voltage gate channel - KCNQ1 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what gene causes brugada syndrome

A

sodium channel voltage gated alpha subunit - SCN5A

calcium channel CACN1Ac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what receptor is affected in catecholamingeric polymorphic VT

A

ryanodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

is short QT syndrome common

A

very rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how common is congenital LQTS

A

1 in 2000 are carriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what can trigger LQTS

A

exercise - LQTS1
emotional stress
sleep
loud noises - LQTS2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what score to calculate long QT risk

A

scwartz score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what gene causes congenital short QT syndrome

A

mutation in cardiac K+ channels

25
what are features of congenital short QT syndrome
QT <300ms at a heart rate <80bpm may be associated with AF may present in young children VERY MALIGNANT
26
what is the management for congenital short QT syndrome
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
what are the risks in brugada syndrome
polymorphic VT, VF AF arrhythmia incdence 1% if asymptomatic, 3.2% in patients with syncope, 13.5 if previous cardiac arrest
28
what inheritance does brugada syndrome follow
autosomal dominant men 8x more likely to get it (genotype and family history of SCD does not influence progosis)
29
what are the features of brugada syndrome on ECG
ST elevation in V1 and 2 RBBB in V1-3 two R waves in V1= RSR may be intermittent and change over time
30
how can a diagnosis of brugada be made
only with provocative testing with flecainide or ajmaline (drugs that block the cardiac sodium channel)
31
What triggers VF In brugada syndrome
abnormal rest or sleep fever excessive alcohol large meals
32
what is the management of brugada syndrome
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
what drugs should you avoid in brugada syndrome
antiarrhythmics psychotrophics analgesics anaesthetics
34
what is catecholaminergic polymorphic ventricular tachycardia
adrenergic induced bidirectional and polymorphic VT and SVTz
35
what triggers CPVT
emotional stress, physical activity
36
what are the types of CPVT
Autosomal dominant- ryanodine receptor mutation recessive- cardiac calsequestrin gene (CASQ2)
37
what are the features of CPVT on IX
normal ECG and echo
38
what is the management for CPVT
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
what are the features of wolffparkinson white syndrome on ECG
short PR wave delta wave slurring into QRS complex ventricular preexcitation
40
what are the risks in WPW
AV reentrant tachycardia most common arrhythmia AF small risk of SCD
41
what causes WPW
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
what test to assess the risk in WPW
exercise ECG- see if able to maintain normal conduction in exertion if risk then ablate pathway
43
what mutation causes hypertrophic cardiomyopathy
mutation in sarcomeric genes
44
what are the problems in hypertrophic cardiomyopathy
rhythm problems and obstruction to outflow of blood
45
how might hypertrophic cardiomyopathy present
sudden death HF/ end stage HF AF
46
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)
implant cardiac device
47
what should you avoid in hypertrophic cardiomyopathy
competitive sport
48
who gets dilated cardiomyopathy
1 in 2500 low in childhood more common in males
49
what genes cause dilated cardiomyopathy
sarcomere and desomal genes, laminA/C and desmin if conduction disease, dystophin if x linked
50
what is the risk on dilated cardiomyopathy
LVEF = 35%
51
what is arrhythmogenic right ventricular cardiomyopathy (ARVC)
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
what mutations in ARVC
AD mutations in genes for desmosomal proteins AR mutations in nondesmosomal genes
53
what increases risk of SCD in ARVC
FHx of premature SCD severity of R and LV function frequent non-sustained VT
54
what are the features of ARVC
on ecg QRS prolongation with late blip in it = epsilon waves VT induction on electrophysiology studies affects males more
55
what is the treatment for ARVC
``` usually get ICD avoid competitive sports beta blockers amiodarone if symptomatic/ CI to BB catheter alblation if symptomatic ```
56
how does an ICD work - what are the complications
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
why is it important to identify pre symptomatic patients at risk of SCD
SCD may be only presentation young age group at risk effective therapies available- lifestyle, BBs, ICD to find other family members at risk
58
when should a QT interval usually finish
before halfway point of RR interval
59
what is seen on ECG in hypertrophic cardiomyopathy
inverted T waves

CLASP Sudden Death (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions