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CLASP sudde death > arrhythmias > Flashcards

arrhythmias Flashcards

1
Q

channelopathies

A

problem in conducting system usually due to protein problems that predispose to rhythm problems

arrhythmogenesis is related to ion current imbalance + development of early + late depolarisations

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2
Q

examples of channelopathies

A

congenital long QT syndrome
brugada syndrome
catecholaminergic polymorphic ventricular tachycardia (CPVT)
short QT syndrome
progressive familial conduction disease
familial AF
familial WPW

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3
Q

cardiomyopathies

A

arrythmogenesis is related to scar/electrical barrier formations + subsequent re-entry

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4
Q

examples of cardiomyopathies

A

hypertrophic cardiomyopathy
arrhymogenic right ventricular cardiomyopathy (ARVC)
dilated cardiomyopathy

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5
Q

what causes early after depolarisations (EADs)?

A

increase in frequency of abortive action potetials before normal repolarisation is completed

can result in Torsades de Pointes

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6
Q

when do early after depolarisations occur?

A

occur with abnormal depolarisations during phase 2 or phase 3

  • phase 2 may be interrupted due to augmented opening of Ca channels
  • phase 3 interruptions are due to opening of sodium channels
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7
Q

what can early after depolarisations (EADs) be potentiated by?

A

hypokalamia
drugs that prolong QT interval - amiodarone, sotalol, haloperidol, erythromycin, citalopram

(EADs can result in Torsades de Pointes)

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8
Q

what are delayed after depolarisations caused by?

A

elevated cystolic calcium concentrations
- classically seen with digoxin toxicity

overload of sarcoplasmic reticulum may cause spontaneous Ca2+ release after repolarising
- causing the released Ca2+ to exit the cell through 3Na+/Ca2+ exchanger -> nedepolarising current

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9
Q

classic feature of delayed after depolarisations

A

bidirectional ventricular tachycardia
- also seen in catecholaminergic polymorphic ventricular tachycardia (CPVT)

(CPVT - cardiomyocytes are hypersensitive to adrenaline + other caracholamines)

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10
Q

when do delayed after depolarisations occur?

A

begin during phase 4 after repolarisation but before another action potenitial would normally occur via normal conduction systems of heart

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11
Q

biggest complication of congenital long QT syndrome

A

risk of polymorphic VT (torsades de pointes) triggered by adernergic stimulation

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12
Q

risk of sudden cardiac death in long QT syndrome

A

0.33-0.9%

risk of this happening is related to
- legth of prologations - longer= higher risk
- pre-adolescent males
- adult female
- prior syncope
- response to beta blockers - if respond well risk low

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13
Q

long QT subtypes

A

13 subtypes
- different types appear differently on ECG, different penetrance

  • autosomal dominant - isolated LQT or extra cardiac features
  • autosomal recessive - assoc with deafness
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14
Q

long QT syndrome diagnosis

A

QT >=480ms in repeated ECGs

LQTS risk score >3

-> confirmed pathogenic LQTS mutations irrespective of QT duration

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15
Q

management of long QT syndrome

A

long acting beta blocker (NOT SOTALOL)
lifestyle
- avoid QT prolonging drugs
- correct electrolyte abnormalities
- avoidance of genotype specific triggers

LQTS1 - strenous swimming
LQTS2 - exposure to loud noises

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16
Q

torsades de pointes

A

polymorphic ventricular tachycardia
occurs in patients with prolonged QT interval

will either terminate spontaneously + revert back to sinus rhythm or progress in to ventricular tachycardia which can lead to cardiac arrest

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17
Q

prolonged QT interval

A

ECG finding of prolonged repolarisation of the muscle cells in the heart after contractions

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18
Q

depolarisations

A

electrical process that leads to heart contractions

19
Q

repolarisation

A

period of recovery before myocytes are ready to depolarise again

20
Q

physiology of torsades de pointes

A

waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of myocytes
- these abormal spontaneous depolarisations prior to repolarisation are known as “after depolarisations”

these spread throught the ventricle, leading to ventricular contraction prior to proper repolarisation occuring
- when this occurs + the ventricle continue to stimulate recurrent contractions without normal repolarisation = Torsades de pointes

21
Q

causes of prolonged QT

A

long QT syndrome (inherited)
medications
electrollyte disturbances

22
Q

what medications can cause prolonged QT syndrome

A

antipsychotics
citalopram
flecanide
sotalol
amiodarone
macrolide antibiotics

23
Q

what electrolyte disturbances can cause long QT syndrome

A

hypOkalaemia
hypomagnesaemia
hypocalcaemia

24
Q

management of torsades de pointes

A

acute
- correct cause - electrolyte/medication
- magnesium infusion - even if normal serum magnesium
- defibrillation if VT occurs

long term mx of prolonged QT
- avoids QT long meds
- beta blocker - NOT sotalol
- pacemaker or implantable defibrillator

25
Q

congenital short QT syndrome

A

very rare
caused by mutation in cardiac K+ channels
may be assoc with AF
may present in young kids - most dont survive
very malignant

26
Q

brugada syndrome

A

inherited channelopathy
risk of polymorphic VT, VF
AF commoon
12 assoc genes

autosomal dominant
adults, 8x more common in males
also if previous cardiac arrest

27
Q

ECG changes seen in brugada syndrome

A

ST elevation + RBBB in V1-V3
ECG finfing may be intermittent + change over time

changes may only be seen with provocative testing
-> flecanide or ajmaline - drugs that block the cardiac sodium channel

28
Q

VF triggers in brugada syndrome

A

usually rest or sleep
fever
excessive alcohol, large meals

genotype + fam history of sudde cardiac death DOES NOT influence prognosis

29
Q

management of brugada syndrome

A

lifestyle
- avoid drugs that induce ST elevation in right leads
– anti-arrhythmis drugs
– psychotropics
– analgesics
– anaesthetics
- avoid excessive alcohol + large meals
- prompt treatment of any fever with paracetamol

ICD implantation if
- survived aborted cardiac arrect
- documented spontaneous sustained VT
- considered is spontaneous type I ECG pattern + history of syncope

30
Q

catecholaminergic polymorphic ventricular tachycardia (CPVT)

A

adrenergic induced bidirectional + polymorphic VT, SVTs triggered by emotional stress of physical physical activity

1 in 1000
at rest, normal ECG + ECHO

autosomal dominant + recessive

31
Q

CPVT management

A

lifestyle - avoid competitive sports, strenous exercise, stressful environments

beta blockers for all
- consider for genetically positive family members even after negative exercise test

ICD implantation +/- flecainide
- for patients who experient recurrent syncope, cardiac arrest, polymorphic/bidirectional VT despite optimal therapy

32
Q

Wolff-Parkinson White syndrome

A

accessory pathway connecting atria to ventricles (bundle of kent)
- usually only one pathway -> SA node

small risk of sudden cardiac death (SCD)

33
Q

management of Wolff-parkinson white

A

radiofrequency ablation of accessory pathway

34
Q

hypertrophic cardiomyopathy

A

common
mutation in sarcomere gene that codes for development of cardiac muscle

35
Q

causes of hypertrophic cardiomyopathy

A

40-60% sarcomeric protein gene mutation
Anderson-Fabry
mitochondrial diseases
neuromuscular disease
amyloidosis
new-born of diabetic mother
drug induced - tacrolimu, hydroxycholoquine, teroids

36
Q

hypertrophic cardiomyopathy presentation

A

varies massively
sudden death
heart failure
end stage heart failure
atrial fibrillation

syncope following exercise
jerky pulse, double apex beat
ejection systolic murmur

37
Q

prevention of sudden cardiac death in hypertrophic cardiomyopathy

A

avoid competitive sports
ICD implantation in patient who have survived cardiac arrest due to VT or VF
evaluate 5yr risk every 1-2yrs

38
Q

arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

occurs when fibro-fatty replacement of cardiomyocytes - fatty deposits in RV wall
- current travels around the fat causing reentry VT

LV involvement in >50%

39
Q

inheritance of arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

autosomal dominant mutations in genes from desmosomal proteins

autosomal recessive mutation in nondesmosomal genes

around 50% of patients have a mutation of one of the several genes which encode components of desmosome

(variable expression)

40
Q

management of ARVC

A

1st - beta blockers(sotalol) - titrated to max tolerated dose
- amiodarone if not tolerated

ICD implantation
catheter ablation
avoid competitive sports

ICD depends on risk of SCD
- fam history of premature SCD
- severity of RV + LV function
- frequent non-sustained VT
- ECG = QRS widening
- male
- age of presentation

41
Q

investigations of ARVC

A

ECG - abnormalities in V1-3, typically T wave inversion
- epsilon wave is found in about 50% - best described as a terminal notch in the QRS complex

ECHO
- often subtle in early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall

MRI useful to show fibrofatty tissue

42
Q

drugs to avoid in hypertrophic cardiomyopathy

A

nitrates
ACEi
inotropes

43
Q

features of dilated cardiomyopathy

A

classic findings of heart failure
systolic murmur - stretching of valves may cause mitral + tricuspid regurgitation
S3
“balloon” appearance on CXR

CLASP sudde death (5 decks)

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