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PHM BSc - Resus Science > Sudden Cardiac Death And Catecholaminergic Arrest > Flashcards

Sudden Cardiac Death And Catecholaminergic Arrest Flashcards

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1
Q

What is sudden cardiac death

A

Death within 6 hours of witnessed normal heath due to SCA

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2
Q

What is sudden arrhythmic death syndrome

A

Death from SCA with no cause on PM

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3
Q

Name some causes of SCD

A

Coronary artery disease
Structural - LV hypertrophy, HF, myocarditis
Arrhythmias
Noncardiac -drug OD, PE

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4
Q

Describe hypertrophic cardiomyopathy

A

Asymetrical thickening of the myocardium (particularly AV septum) which can lead to LV outflow obstruction. The myocytes are chaotic and there can be an element of fibrosis

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5
Q

What are the results of the hypertrophy seen in HCM

A

LV outflow obstruction
Risk of VT and VF
Reduced pumping efficiency
Mitral valve abnormalities

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6
Q

What are the genetics of HCM

A

AD mutation in genes encoding sarcomeric proteins eg B-myosin heavy chain and troponin

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7
Q

what is your typical HCM patient

A

Black, male, 20-30 y/o

Syncope, chest pain SOB etc on physical exertion

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8
Q

What does an ECG of a HCM patient look like

A

Non-specific changes
Dagger Q waves (more activity but more muscle to pass through)
ST segment often goes in the opposite direction to QRS
T wave inversion
AF and SVT

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9
Q

How is HCM managed

A 
Amiodarone
B blockers
Verapamil
Anticoagulant and catheter ablation for AF
ICD
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10
Q

What is ARVC

A

Arrhythmogenic RV cardiomyopathy

Fibro-fatty replacement of RV myocytes meaning RV free wall is thin

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11
Q

What are the genetics of ARVC

A

AD mutations in desmosomal genes

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12
Q

What is the typical ARVC patient

A

Northern Italy/Greece, teens/20’s, males, during competitive sport
Palpitations and syncope
Eventually get HF

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13
Q

What does the ECG of ARVC show

A 
Epsilon waves (blip at the end of QRS)
VT with LBBB or ectopics cause the symptoms
V1-V3 show T inversion, prolonged S wave upstroke, wide QRS
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14
Q

How is ARVC managed

A

Amiodarone and b-blockers
ICD
Radio frequency ablation

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15
Q

What is dilated cardiomyopathy

A

LV enlarges and has contractile dysfunction (reducing ejection fraction) but LV wall thickness is normal
RV may also be involved

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16
Q

What are the genetics of dilated cardiomyopathy

A

AD
Genes encoding sarcomeric or lamin A or C
(Only 30% of cases are genetic - lots of other things cause it)

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17
Q

What is a typical dilated cardiomyopathy patient

A

Black,male, 20-60 y/o

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18
Q

How would dilated cardiomyopathy present

A

Often as congestive HF

AF or stroke as a result

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19
Q

What would investigations for dilated cardiomyopathy show

A

CXR: cardiomegaly and pulmonary oedema
ECG: very non specific sinus tachy, LBBB
Echo: LV dilation, reduced systolic and diastolic function, mitral/tricuspid regurg

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20
Q

How is dilated cardiomyopathy managed?

A

As HF so ACEi, b-blockers, digoxin

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21
Q

What is brugada syndrome

A

Arrythmias (VF or pVT) leading to SCD in the presence of a structurally normal heart

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22
Q

What are the genetics of brugada syndrome

A

AD mutation affecting sodium ion channels

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23
Q

What is the typical brugada syndrome presentation

A

East Asian

Syncopal episodes when high vagal tone, fever or alcohol

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24
Q

What are the ECG features of brugada syndrome

A

Coved ST + inverted T + J point elevation in V1-3

May have prolonged PR

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25
Q

How can the ecg changes of brugada be induced

A

Ajmaline

26
Q

How is brugada syndrome diagnosed?

A 
ECG changes + one of:
Documented pVT or VF
Family history of SCD <45 
Family members with coved ST
syncope
Nocturnal agonal respiration
27
Q

How is brugada syndrome managed

A

ICD + avoidance of flecainide, verapamil, amytiptiline, propranolol, hypokalaemia, fever

28
Q

What is the normal QT interval

A

<440 males

<460 females

29
Q

What causes the SCD in long QT

A

Ventricular tachyarrhythmia

30
Q

What is LQTS

A

Encompasses a range of syndromes all leading to prolonged myocardial repolarisation
Also encompasses acquired LQTS

31
Q

What can cause acquired LQTS

A

Drugs, hypokalaemia/magnasaemia/calcaemia, hypothermia, MI, SAH

32
Q

What are the genetics of LQTS 1-3 and the affect on the ion channels

A

LQT1 and LQT2: KCNQ1 and KCNH2 (K leaves cell too slowly)

LQT3: SCN5a (Na enters cell too quickly)

33
Q

In which situations would LQT1-3 present themselves

A

1 - increased adrenergic tone (particular swimming)
2 - startling
3 - resting and bradycardia

34
Q

Describe the T wave ECG features of LQTS 1-3

A

1 - broad based T
2 - notched T
3 - prolonged ST

35
Q

Describe the generic ECG changes for all LQTS

A

Prolonged QTc
T wave abnormalities (specific to each type)
TdP
T wave alternans

36
Q

How is the QTc interval calculated?

A

Bazetts formulae
QT/ square root of RR interval
(QT is measured from initial wave of QRS to T wave return to baseline

37
Q

How does LQTS present

A

Young people with syncope

Often have prodrome of palpitations, chest pain and SOB

38
Q

How is LQTS managed?

A

B blocker
ICD
Lifestyle changes

39
Q

What is romana ward

A

The phenotypic classification of LQTS 1-6, 9-12

40
Q

What is Jervell and Lange Nielsen

A

AR mutation. 2 inherited copies of KCNQ1 (whereas 1 copy = Romano ward)

41
Q

Aside from cardiac features, what else do jervell and Lange Nielsen patients have

A

Bilateral sensorineural deafness

42
Q

What is Anderson Tawil syndrome

A

Phenotypic name for LQTS 7

43
Q

Which gene is effected in LQT7 (Anderson Tawil)

A

KCNJ2

44
Q

How does Anderson Tawil present (ecg and features)

A 
Bidirectional VT
Low set ears and wide spaced eyes
Clinodactyly
Syndactyly
Short
Scoliosis
Hypokalaemic periodic paralysis
45
Q

What is Timothy syndrome and it’s genetics

A

Phenotypic name for LQTS8

CACNA1C

46
Q

What ion channel is affected and what is the implication in Timothy syndrome

A

Delayed calcium channel closing (so more calcium in) leading to increased intracellular exciteability

47
Q

How does Timothy syndrome present

A

Syndactyly, congenital heart malformation, autism

In atypical they also have joint issues and AF

48
Q

What is CPVT

A

Catecholaminergic polymorphic ventricular tachycardia

49
Q

Talk through the genetic mutation and resulting ion channel abnormality that leads to biderectional VT in CPVT

A

AD mutation of RyR2 = leaky ryandadine receptor channel = Ca leaks out of SR in diastole = afterdepolarisation = bidirectional VT

50
Q

How do adrenergics worsen the situation in CPVT

A

More Ca in the SR so more to leak out + adrenergics increase the sensitivity of the ryanadine receptor channel

51
Q

What is your typical CPVT patient

A

Child/adolescent with FH of SCD and person history of “seizures”

52
Q

What ECG features are seen in CPVT

A

Normal at rest!

Bidirectional VT or VF on exercise or emotional stress

53
Q

What is the immediate management of CPVT

A

Adrenaline will worsen the VT

Give B blockers

54
Q

What is the long term management of CPVT

A

ICD
B-Blocker
Fleccainide, verapamil

55
Q

What is Lev-Lenegres/PCCD, it’s genetic mutation and ion channel involved

A

Progressive cardiac conduction defect
SCN5A
Sodium channel affected

56
Q

What are the ECG features of PCCD

A

Over time they progress to a complete heart block with resulting arrythmias

57
Q

How is PCCD managed

A

Pacemaker for bradycardia

Anti arrhythmics

58
Q

What is adrenalines affect on a1 receptors

A

Vasoconstriction
Increased aortic diastolic pressure to increase coronary blood flow
BUT decreased cerebral perfusion pressure

59
Q

What does adrenaline acting on A2 result in

A

Platelet activation = damage to cerebral vasculature

60
Q

What does adrenaline acting on B1 result in

A

Increased inotropy and chonotropy which increases myocardial metabolic demand

61
Q

What were the results of paramedic 2 trial

A

Adrenaline increased 30 day survival but decreases neurological outcome

PHM BSc - Resus Science (29 decks)

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