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103-theme 3 > sudden cardiac death > Flashcards

sudden cardiac death Flashcards

1
Q

what is sudden death? 4

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 can cause sudden death? 4

A
  • Heart and/or its vessels
  • Non-cardiac vessels (stroke or aneurysm)
  • Pulmonary system (PE)
  • Central nervous system (CNS) (rare seizures in epilepsy)
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3
Q

what is sudden cardiac death? 3

A
  • Sudden death due to cardiovascular/ coronary vessel causes
  • Coronary obstruction (infarct/ embolism)
  • Arrhythmia/ dysrhythmia
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4
Q

what disorders can lead to an increased risk of SCD? 3

A
  • CHD/ low LVEF
  • Structural heart disease (cardiomyopathies), also developmental/ genetic pathologies of the heart)
  • Primary arrhythmia
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5
Q

what is cardiac arrest? 4

A
  • Also known as cardiopulmonary arrest or circulatory arrest
  • A sudden stop in the effective blood circulation due to the failure of the heart to contract effectively or at all
  • Not the same as an acute myocardial infarct also it can result from AMI sometimes, AMI is when the blood flow to some heart muscles is impaired, usually the heart continues pumping but less effectively
  • Not the same as heart failure= HF is when the circulation is substandard, but the heart is still pumping sufficient blood to sustain life
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6
Q

what is arrhythmia/ dysrhythmia? 4

A
  • A variation in the normal beating pattern or rhythm of the heart
  • There is no difference in meaning between the two terms
  • Arrhythmia is usually due to disorganisation of the electrical signals running through the heart
  • Can be fast, slow or abnormal
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7
Q

what can cause arrhythmia? 6

A

Electrical (primary of arrhythmogenic):

  • Ion channels and electrical issues at cellular level
  • Extra conduction pathways at the organ level

Structural:

  • Unusual shape or size of cardiac tissue that changes signal pathway
  • Can lead to signal delays that interfere with cardiac conduction cycle

Ischaemic:

  • Hypoxia makes local heart tissue electrically unstable
  • Effectively changes signal pathway leading to delays that interfere with cardiac conduction cycle
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8
Q

what can cause primary arrhythmia? 3

A
  • Unstable myocardium= often due to damaged or hypoxic tissue, AF
  • Ion channel pathologies= channelopathies, long QT syndrome
  • Accessory conduction pathways Wolff Parkinson white
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9
Q

what is cardiomyopathy? 4

A
  • Pathology when heart shape, size 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
  • Risk of pumping dysfunction of low output heart failure
  • Conduction abnormalities because the normal pathways of electrical conduction are altered
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10
Q

what is tetralogy of Fallot? 2

A
  • Developmental defect

- Associated with higher risk of sudden death even after surgical correction in childhood

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11
Q

describe substrate vs trigger? 3

A
  • To have arrhythmia, you usually need both substrate and trigger
  • Trigger= brief event required to initiate a period of arrhythmia precipitating event, like an extrasystole of a nearby focus of rapid firing
  • Substrate= ongoing, underlying tissue instability that increases triggers or allows for the maintenance and amplification or dysrhythmia. Predisposing factor, electrical or structural defect such as fibrosis or inflammation caused by IHD (structural) and genetic or pharmalogical problems with ion channels or electrolytes (electrical)
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12
Q

describe R on T, ECG phenomenon? 4

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 repolarisation of ventricular AP when the refractory period is ending
  • Resulting QRS wave is a premature ventricular contraction (PVC)
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13
Q

what is a pacemaker? 3

A
  • Implanted electronic device that has electrodes which can stimulate the heart
  • Consistently applies impulses for each heartbeat
  • Mostly used for bradyarrhythmia’s and heart block
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14
Q

what is an implantable cardioverter defibrillator? 4

A

mplanted electronic device

  • Has electrodes which can stimulate the heart
  • Applies electrical impulses only when ventricular dysrhythmias detected
  • Protects from fast or uncontrolled rhythms
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15
Q

what are the indications for implanting an ICD? 12

A
  • Cardiac arrest due to ventricular fibrillation
  • Symptomatic heart failure with low LVEF low output heart failure after MI
  • Cardiomyopathies dilated cardiomyopathy
  • Congenital tetralogy of Fallot
  • Channelopathies
  • VF or spontaneous sustained VT
  • Unexplained syncope
  • LV wall thickness more than 30mm
  • Spontaneous NSVT
  • Abnormal exercise BP
  • Family history of premature sudden death
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16
Q

describe antiarrhythmic drugs? 5

A
  • Usually affect ion channel activity or sympathetic drive
  • Amiodarone
  • Beta blockers
  • Digoxin
  • Mostly for supra-ventricular arrhythmias arising from atria or AV node
17
Q

describe a reperfusion injury? 5

A
  • Tissue damage caused when blood supply returns to the tissue after a period of ischemia or hypoxia tissue damage and/or hypoxia leads to electrical irregularities and risk
  • Myocardium after PCI
  • Brain tissue after ischaemic stroke
  • Cause: the restoration of circulation causes inflammation and oxidative damage
  • Preventative treatments: cooling, immunosuppression, oxygen radical scavengers
18
Q

describe syncope vs seizures? 7

A
  • Loss of consciousness: symptoms described as black outs
  • Can be difficult to differentiate from a patient’s description, both may have no symptoms when not occurring
  • Syncope may be registered be a Holter monitor (24hr ECG)
  • Seizure may be registered by ECG
  • Seizures tend to be associated with stiffness and unusual postures
  • Syncope patients crumple, seizure patients tip over
  • However convulsive syncope features tipping over
19
Q

what is vasovagal syncope? 6

A
  • Vagal increase and sympathetic decrease vasodilation and low heart rate
  • Triggered centrally not triggered at level of heart
  • Common in young adults
  • Most common form of syncope
  • Recurrent
  • Recover shortly after lying supine with head and trunk at same height treatment is mostly avoidance and education, prognosis is excellent
20
Q

what is exertional syncope? 2

A
  • Neurocardiogenic origin

- Benign

21
Q

what is an index case (proband)? 2

A
  • Index case= the initial patient in the population of an epidemiological investigation
  • The case of the original patient that stimulated investigation of other members of the family
22
Q

describe penetrance? 3

A
  • The proportion of individuals carrying a particular variant (or allele) of a gene that also express an associated trait
  • Incomplete or reduced penetrance= some individuals will not express the trait even though they carry the allele
  • Many channelopathies can vary from patient to patient
23
Q

what is dilated cardiomyopathy? 8

A
  • 10% of sudden cardiac death
  • Non-ischaemic dilation of ventricle
  • Causes: idiopathic, viral, alcohol, drugs (chemotherapy), autoimmune

Pathology:

  • Subendocardial myocardial fibrosis
  • Neurohumoral activation
  • Increased sympathetic tone
  • Electrolyte disturbances
  • Leads ectopy, re-entry, VT/VF
24
Q

what is hypertrophic cardiomyopathy? 7

A
  • Most common cause of sudden cardiac death 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
25
Q

what are the symptoms of hypertrophic cardiomyopathy? 5

A
  • May be asymptomatic
  • Exertional chest pain/dyspnoea
  • Exertional syncope
  • Palpitations
  • Mechanism of SCD unclear
26
Q

what is ARVC? 9

A
  • Arrhythmogenic RV cardiomyopathy
  • 30-50% familial
  • Replacement of RV myocardium with fibro-fatty tissue
  • RV hypertrophy and dilation
  • VT/VF due to re-entry around interstitial fibrosis
  • Often asymptomatic
  • Exertional syncope and SCD
  • Atrial arrhythmia common
  • Epsilon wave on ECG
27
Q

what is wolff-parkinson-white? 5

A
  • Accessory pathway from atria to ventricle
  • Atrial arrhythmia
  • Ventricular pre-excitations
  • VT/VF
  • Often clue on resting ECG
28
Q

what is brugada? 6

A
  • Channelopathy
  • Most commonly SCN5A
  • Affects fast-type sodium channels
  • Reduces conduction velocities
  • Particularly affects RVOT
  • Prone to VT arising from RVOT
29
Q

how do we treat SCD? 7

A
  • Identify at risk groups
  • Preventative treatment
  • Treat underlying cause
  • Avoid precipitants
  • Anti-arrhythmic medication
  • Implantable defibrillators
  • Family screening where appropriate
30
Q

how do we select patients for ICD? 3

A
  • Survivors of cardiac arrest (not MI)
  • VT with haemodynamic compromise
  • High-risk group: coronary disease, poor LV function +/- large scar, broad QRS complex on ECG

103-theme 3 (18 decks)

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