Symposium 7 Sudden Cardiac Death Flashcards

1
Q

Conditions of sudden cardiac 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

Causes of sudden death

A

Heart and/or its vessels
Non-cardiac vessels (stroke or aneurysm)
Pulmonary system (PE)
Centra Nervous system (rare seizures in epilepsy)

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3
Q

Sudden Cardiac Death

A

Due to cardiovascular/coronary vessel causes: coronary obstruction (infarct/embolism); arrhythmia/dysrhythmia
Disorders leading to risks for sudden death: CHD/low LVEF (left ventricular ejection fraction), structural heart disease (cardiomyopathies) (and developmental/genetic structural pathologies of heart), primary arrhythmia

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4
Q

Cardiac Arrest

A

A sudden stop in effective blood circulation due to the failure of the heart to contract effectively or at all
Not same as an acute myocardial infarct - can sometimes result from an AMI (when blood flow to some heart muscle is impaired)
Not the same as heart failure (when circulation is substandard, but the heart is still pumping sufficient blood to sustain life)

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5
Q

Broad Categories of arrhythmia causes

A

electrical: ion channels and electrical issues at cellular level; extra conduction pathways at 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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6
Q

Causes of primary arrhythmia

A

Unstable myocardium: often due to damaged or hypoxic tissue (eg AF)
Ion channel pathologies: long QT syndrome, accessory conduction pathways

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7
Q

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 time of birth
Consequences: risk of pumping dysfunction or low output heart failure; conduction abnormalities (because normal pathways of electrical conduction are altered)

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8
Q

Substrate vs Trigger

A

To have an arrhythmia, you need both a substrate and trigger
Trigger: brief event required to initiate a period of arrhythmia (precipitating event, e.g. extrasystole or nearby focus of rapid firing)
Substrate: ongoing, underlying tissue instability that increases triggers or allows for maintenance and amplification of dysrhythmia (predisposing factor, electrical/structural defect - fibrosis/problems with ion channels)
R on T is a potential trigger for arrhythmias - when premature QRS complex occurs during the previous T wave - this QRS wave is a premature ventricular contraction

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9
Q

Pacemakers and Implantable Cardioverter Defibrillator

A

Pacemaker: implanted electronic device - has electrodes that can stimulate the heart; consistently applies impulses for each heart beat; mostly used for bradyarrhythmia and heart block
Implantable Cardioverter Defibrillator: has electrodes that can stimulate the heart; applies electrical impulses only when ventricular dysrhythmias detected; protects from fast or uncontrolled rhythms
Indications for ICD: cardiac arrest due to ventricular fibrillation; symptomatic HF with low LVEF (low output HF after MI (40 days later); cardiomyopathies (dilated cardiomyopathy); congenital (Tetralogy of Fallot); Channelopathies (long QT syndrome)

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10
Q

Reperfusion injury

A

Tissue damage caused when blood supply returns to the tissue after a period of ischaemia or hypoxia - leads to electrical irregularities and risk
Contexts: myocardium after angioplasty, brain tissue after ischaemic stroke
Cause: the restoration of circulation results in inflammation and oxidative damage
Preventative treatments: cooling, immunosuppression, oxygen radical scavengers

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11
Q

Syncope Seizures

A

Loss of consciousness: symptoms described as ‘black outs’ - figuring out which is which - delays diagnosis
Syncope vs seizure: can be difficult to differentiate from a patient’s description; both may have no symptoms when not occurring - syncope may be registered by Holter monitor (24 hour ECG) and seizure may be registered by EEG (brain imaging is also important);
seizures tend to be associated with stiffness and unusual postures/movements - syncope patients ‘crumple’, seizure patients ‘tip over’

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12
Q

Vasovagal vs Exertion syncope

A

Vasovagal syncope: vagal increase (and symp decrease) -> vasodilation and low heart rate - triggered centrally brain not triggered at level of heart
Most common form of syncope: recurrent, common in young adults, recurrent
Exertional syncope: neurocardiogenic origin or benign

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13
Q

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) - if a mutation in the gene responsible for a particular autosomal dominant disorder has 95% penetrance, then 95% of those with the mutation will develop the disease, while 5% will not.
Incomplete or reduced penetrance: some individuals will not express the trait even if the carry the allele; many channelopathies can vary from patient to patient - an individual disease can have different phenotypes, and most phenotypes are polygenic

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