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module 103 - theme 3 > sudden cardiac death > Flashcards

sudden cardiac death Flashcards

1
Q

what is sudden death?

A
  • natural, rapid, unexpected
  • not trauma, toxicity or poison
  • not due to chronic illness
  • natural death within one hour of the onset of acute symptoms
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2
Q

what are the causes of sudden death?

A
  • heart and/or its vessels
  • noncardiac vessels
  • pulmonary system (PE)
  • central nervous system
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3
Q

what causes sudden cardiac death?

A

sudden death due to cardiovascular/coronary vessel causes

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4
Q

what are the direct causes of sudden cardiac death?

A
  • coronary obstruction: infarct, embolism

- arrhythmia/dysrhythmia

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5
Q

what are the disorders leading to risks for sudden cardiac death?

A
  • CHD/low LVEF
  • structural heart disease
  • primary arrhythmia
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6
Q

what is the definition of a cardiac arrest?

A

a sudden stop in effective blood circulation due to the failure of the heart to contract effectively or at all

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7
Q

what is an acute myocardial infarction?

A

when blood flow to some heart muscle is impaired. Usually the heart continues pumping but less effectively

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8
Q

what is the definition of heart failure?

A

when the circulation is substandard, but the heart is still pumping sufficient blood to sustain life

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9
Q

what is arrhythmia/dysrhythmia?

A

a variation in the normal beating pattern of rhythm of the heart

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10
Q

what are the 3 broad categories of arrhythmia causes?

A
  • electrical
  • structural
  • ischaemic
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11
Q

how do the electrical causes link to arrhythmia?

A
  • ion channels and electrical issues at cellular level

- extra conduction pathways at the organ level

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12
Q

how do the structural causes link to arrhythmia?

A
  • unusual shape or size of cardiac tissue that changes signal pathway
  • can lead to signal delays that interfere with cardiac conduction cycle
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13
Q

how do the ischaemic causes link to arrhythmia?

A
  • hypoxia makes local heart tissue electrically unstable

- effectively changes signal pathway, leading to delays that interfere with cardiac conduction cycle

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14
Q

what are the causes of primary arrhythmia?

A
  • unstable myocardium: often due to damaged or hypoxic tissue
  • ion channel pathologies: long QT syndrome
  • accessory conduction pathways
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15
Q

what is cardiomyopathy?

A
  • pathology when heart size, shape or thickness is abnormal
  • this excludes heart disease due to coronary artery disease, hypertension, abnormalities of the heart valves, and heart disease present at the time of birth
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16
Q

what are the consequences of cardiomyopathy?

A
  • risk of pumping dysfunction or low output heart failure

- conduction abnormalities because the normal pathways or electrical conduction are altered

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17
Q

what are the 2 types of cardiomyopathy?

A
  • dilated (eccentric)

- hypertrophic (concentric)

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18
Q

what is associated with tetralogy of fallot?

A

a developmental defect associated with high risk of sudden death even after surgical correction in childhood

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19
Q

what is trigger?

A

brief event required to initiate a period of arrhythmia

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20
Q

what is substrate?

A
  • ongoing, underlying tissue instability that increases triggers or allows for maintenance and amplification or dysrhythmia.
  • it can be and electrical or structural defect
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21
Q

what is R on T (ECG phenomenon)?

A
  • a type of potential trigger for arrhythmias
  • on the ECG, when a premature QRS complex occurs during the previous T wave
  • the T wave is a ‘vulnerable period’ during depolarisation of ventricular AP, refractory period is ending
  • resulting QRS wave is a premature ventricular contraction
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22
Q

what is a pacemaker?

A
  • implanted electronic device that had electrodes that can stimulate the heart
  • consistently applies impulses for each heart beat
23
Q

what is a pacemaker used for?

A

bradyarrhythmias and heart block

24
Q

what is an implantable cardioverter defibrillator?

A
  • implanted electronic device that has electrodes that can stimulate the heart
25
Q

how does an implantable cardioverter defibrillator work?

A
  • applies electrical impulses ONLY when ventricular dysrhythmias detected
  • protects from fast or uncontrolled rhythms
26
Q

what are the indications for implanting an ICD?

A
  • cardiac arrest due to ventricular fibrillation
  • symptomatic heart failure with low LVEF
  • cardiomyopathies
  • congential
  • channelopathies
27
Q

how do antiarrhythmic drugs work?

A

usually affect ion channel activity or sympathetic drive

28
Q

what is reperfusion injury?

A

tissue damage caused when blood supply returns to the tissue after a period of ischemia or hypoxia

29
Q

what causes reperfusion injury?

A

the restoration of circulation results in inflammation and oxidative damage

30
Q

what are the preventative treatments for reperfusion injury?

A
  • cooling
  • immunosuppression
  • oxygen radical scavengers
31
Q

what are the difference between syncope and seizures?

A
  • can be difficult to differentiate from a patient’s description
  • both may have no symptoms
  • syncope may be registered by Holter monitor
  • seizure may be registered by EEG
  • seizures tend to be associated with stiffness and unusual postures/movements
  • syncope patients ‘crumple’ and seizure patients tip over
32
Q

what is vasovagal syncope?

A

vagal increase and symp decrease leading to vasodilation and low heart rate

33
Q

what is exertional syncope?

A
  • neurocardiogenic origin

- benign

34
Q

what is the index case?

A
  • the initial patient in the population of an epidemiological investigation
  • the case of the original patient that stimulates investigation of other members of the family
35
Q

what is penetrance?

A

the proportion of individuals carrying a particular variant (or allele) of a gene (the genotype) that also express an associated trait (the phenotype)

36
Q

what happens with incomplete or reduced penetrance?

A
  • some individuals will not express the trait even though they carry the allele
  • many channelopathies can vary from patient to patient
  • an individual disease can have different phenotypes
  • most phenotypes of polygenic, especially in genes for ‘risk’
37
Q

what are the mechanisms of arrhythmia?

A
  • substrate for arrhythmia: structural or electrical
  • ectopic activity: early after depolarisation, short coupling interval, delayed after depolarisation
  • re-entry
  • wave break
38
Q

what are the clinical scenarios with sudden cardiac death?

A
  • ischaemic heart disease
  • structural heart disease
  • arrhythmic SCD
39
Q

what are the key characteristics of ischaemic heart disease?

A
  • acute ischaemia
  • ventricular remodelling
  • scar formation
  • myocardial fibrosis
  • coupling
  • dilatation
  • poor function
40
Q

what are the key characteristics of dilatated cardiomyopathy?

A
  • accounts for 10% of SCD
  • non-ischaemic dilatation of ventricle
  • causes: idiopathic, viral, alcohol, drugs (chemotherapy), autoimmune
41
Q

what is the pathophysiology of structural heart disease?

A
  • subendocardial myocardial fibrosis
  • neurohormonal activation
  • increased sympathetic tone
  • electrode disturbances
  • leads to: ectopy, re-entry, VT/VF
42
Q

what are the key characteristics of hypertrophic cardiomyopathy?

A
  • most common cause of SCD in young athletes
  • autosomal dominant, incomplete penetrance
  • mutation of cardiac muscle sarcomere genes
  • > 45 mutations identified
  • most commonly beta-myosin or troponin-T
  • asymmetrical septal hypertrophy
  • systolic anterior motion of mitral valve
  • LV outflow tract obstruction
43
Q

what are the symptoms of hypertrophic cardiomyopathy?

A
  • may be asymptomatic
  • exertional chest pain/dyspnoea
  • exteriontal syncope
  • palpitations
  • mechanism of SCD unclear
44
Q

what is ARVC?

A

arrhythmogenic RV cardiomyopathy

45
Q

what happens with ARVC?

A
  • replacement of RV myocardium with fibro-fatty tissue
  • RV hypertrophy and dilatation
  • VT/VF due to re-entry around interstitial fibrosis
46
Q

what are the symptoms of ARVC?

A
  • often asymptomatic
  • exertional syncope of SCD
  • atrial arrhythmia common
  • epsilon wave of ECG
47
Q

what are the other structural SCD?

A
  • aortic stenosis
  • mitral stenosis
  • mitral valve prolapse
  • congenital heart disease: anomalous coronary arteries, ebstein’s abnormally, complex
48
Q

what are the key characteristics of primary arrhythmia?

A
  • non-ischaemic
  • structurally normal heart
  • syndromes include: long QT, wolff-parkinson-white, brugada, primary VT/VF
49
Q

what is Wolff-Parkinson-White?

A
  • accessory pathway from atria to ventricle
  • atrial arrhythmia
  • ventricular pre-excitation
  • VT/VF
  • often clues on resting ECG
50
Q

what is Brugada?

A
  • channelopathy
  • most commonly SCN5A
  • affects fast-type sodium channels
  • reduces conduction velocities
  • particularly affects RVOT
  • prone to VT arising from RVOT
51
Q

how do you treat sudden cardiac death?

A
  • identify at-risk groups
  • preventative treatment
  • treat underlying cause
  • avoid precipitants
  • anti-arrhythmic medication
  • implantable defibrillators
  • family screening where appropriate
52
Q

how do you select the patients for ICD?

A
  • survivors of cardiac arrest (not MI)
  • VT with haemodynamic compromise
  • high risk groups: coronary disease, poor LV function +/- large scar, broad QRS complex on ECG
  • some HCM/long QT/Brugada/ARVC
  • congenital heart disease
53
Q

what are the indications in HCM?

A
  • survived cardiac arrest
  • one or more of: VF or spontaneous sustained VT, unexplained syncope, LV wall thickness more than 30mm, spontaneous NSVT, abnormal exercise BP, family history of premature sudden death

module 103 - theme 3 (17 decks)

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