1
Q

Sudden death

A

A natural, rapid and unexpected death.

Not caused by:
Trauma
Toxic or poisonous substances.

Not as a result of a chronic illness

Natural death within an hour of an acute onset of symptoms.

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2
Q

Causes of sudden death (4)

A

Cardiac causes and its vessels.

Non-cardiac vessels- i.e stroke or aneurysm

Pulmonary- i.e PE

CNS- some seizures in epilepsy.

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3
Q

Sudden cardiac death

A

Sudden death due to cardiac/ coronary vessels.

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4
Q

Direct causes of sudden cardiac death

2

A

Coronary obstruction

Arrhythmias

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5
Q

Disorders that increases risk of sudden cardiac death (3)

A

Coronary heart disease- low ventricular ejection fraction (LVEF)

Cardiomyopathies

Primary arrhythmias- inherited cardiac symptom.

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6
Q

Cardiac arrest

A

The heart stops contracting effectively or not at all- is not the same as an MI

Causes sudden stop in effective blood circulation.

Can result from heart failure or an MI.

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7
Q

Three causes of arrhythmias

A

Electrical

Structural

Ischaemic

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8
Q

Electrical cause of arrhythmias

3

A

Primary arrhythmia due to:

Unstable myocardium due to damaged/ hypoxic tissue (i.e after an MI).
Example- AF

Channelopathies:
Genetic disorders which prevents ion channels from functioning correctly
i.e long QT syndrome

Accessory conduction pathways:
Example- Wolff-Parkinson-
White

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9
Q

Wolff-Parkinson-White

  • Pathology
  • Symptoms (4)
A

Cardiac conduction abnormality where there is an abnormal accessory electrical conduction pathway b/w atria and ventricles.

Bundle of Kent- abnormal pathway- stimulates premature ventricular contraction.

Symptoms may occur:
Dizziness
Palpitations
Syncope
Dyspnoea
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10
Q

Long QT syndrome

  • Pathology
  • Treatment
A

A arrhythmogenic disorder than can cause fatal cardiac arrhythmia.

Cause by genetic abnormalities.

Treatment- beta-blockers, ICDs (implantable cardioverter defibrillator).

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11
Q

Cardiomyopathy

  • Pathology
  • Complications
A

Heart muscle is structurally and functionally abnormal.

Change in heart size, shape or thickness that is abnormal.
Types: Dilate vs concentric

Excludes reasons:
CHD
Hypetension
Heart valve abnormality

Leads to:
Low output heart failure
Conduction abnormalities.

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12
Q

Restrictive cardiomyopathy

A

Stiffing and rigid ventricles due to abnormal tissue replacing cardiomyocytes.

This prevents ventricles from filling with blood properly- enlarges the atria.

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13
Q

Arrhythmogenic right ventricular dysplasia

A

Disorder where some cardiomyocytes die and is replaced with scar tissue.

Can cause arrhythmias by disrupting electrical signal pathways.

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14
Q

Tetralogy of Fallot

A

Four development defects often co-occurring:

  • Ventricular septal defect, hole between ventricles
  • Pulmonary valve stenosis
  • RV hypertrophy
  • Overriding aorta, displaced or moved aorta.

This condition is associated with a higher risk of sudden cardiac death even after surgical correction.

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15
Q

Trigger

- Include example

A

A brief event required to start a period of arrhythmia.

Examples: An extrasystole, nearby focus of rapid firing (atrial flutter).

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16
Q

Substrate

- 2 types of defects

A

Underlying tissue instability that increases tigger/ amplifies and maintains dysrhythmia.

Electrical defect: genetic or pharmacological problems with ion channels

Structural defect: Fibrosis or inflammation caused by IHD.

17
Q

R on T

A

When a premature QRS complex occurs during the previous T wave.

Potential trigger for arrhythmias

Premature QRS= premature ventricular contraction.

18
Q

Pacemaker

A

Implanted electronic device that contains electrodes to stimulate the heart.

Constantly applies impulse for EVERY SINGLE heart beat

Use: Heart block, bradyarrhythmias.

19
Q

ICD

- Indications

A

Implantable cardioverter defibrillator.

Only applies electrical impulses to the heart when a ventricular arrhythmia is detected.

Use:
Ventricular fibrillation
Ventricular tachycardia

20
Q

Indications for implanting ICD

A

Cardiac arrest from ventricular fibrillation.

Symptomatic HF with low LVEF.

Cardiomyopathies- DCM

Congenital

Channelopathies

21
Q

Amiodarone

A

Antiarrhythmic drug that does so by prolonging the repolarisation phase.

22
Q

Antiarrhythmic drugs

A

Amiodarone

Beta-blockers: bisoprolol, propranolol.

Digoxin in AF

23
Q

Reperfusion injury

A

Tissue damage when blood supply returns to tissue after a period of ischaemia or hypoxia.

The restoration of circulation causes inflammation and oxidative damage.

Example:
Myocardium after percutaneous coronary intervention (MI)

Brain tissue after ischaemic stroke.

24
Q

Preventative treatment for reperfusion injury

A

Cooling

Immunosuppression

Oxygen radical scavengers

25
Q

Syncope indications

A

Loss of postural tone

Lightheadedness

Sweating before faint

Associated with prolonged sitting or standing

26
Q

Seizure indications

A

Maintained/ high postural tone

Bitten tongue

Deja vu/ jamais vu

27
Q

Vasovagal syncope

A

Most common form of syncope where:
Vagal input increase = vasodilation and bradycardia

Triggered by the brain, not heart.

28
Q

Exertional syncope

A

Neurocardiogenic origin

Caused by permutations in homeostatic maintenance of arterial blood pressure and systemic vascular resistance.

29
Q

Index case/ Proband

A

The initial patient in the population being investigated.

Could lead to source of disease- patient 0.

30
Q

Number needed to treat

A

Average number of patients who need to be treated to prevent one additional bad outcome.

31
Q

Predisposing factors that can lead to electrical instability after ventricular remodelling.

A

Low LVEF.

Presence of a myocardial scar.

Autonomic dysfunction.

Genetic polymorphism..

32
Q

Precipitating events that can lead to electrical instability after ventricular remodelling.

A

Acute ischaemia

Worsening heart failure

Metabolic/ electrolyte disturbances

Medication- like QT prolonging drugs.

33
Q

Dilated cardiomyopathy

A

Non-ischaemic dilation of a ventricle

Causes:
Idiopathic
Viral
Alcohol
Chemotherapy
Autoimmune.
34
Q

Pathophysiology of Dilated cardiomyopathy

A
  • Subendocardial myocardial fibrosis
  • Neurohumoral activation: activation of the RAAS system and the sympathetic system.
  • Increased sympathetic tone
  • Electrolyte disturbances
35
Q

3 ways in which an electrical circuit in the heart can show ‘re-entry’

A
  1. Large circuit size, increases circuit time= re-entry.
  2. Atrial refractory time shorter than circuit time= re-entry.
  3. A zone of slow conduction, increases circuit time= re-entry.
36
Q

Hypertrophic cardiomyopathy

A

Caused by genetic disorder which- autosomal dominant.

Mutates cardiac sarcomere genes: mainly beta-myosin and troponin-T

Asymmetrical septal hypertrophy.

Causes the mitral valve to move forward during systole which can completely obstruct outflow tract.

37
Q

Arrhythmogenic RV cardiomyopathy (ARVC)

A

A condition that is 30-50% familial and is muti-genomic

There RV myocardium is replaced with fibro-fatty tissue

Causes RV dilated hypertrophy

Consequence Ventricular fibrillation/ tachycardia.

Shows epsilon wave on ECG.

38
Q

Brugada

A

A channelopathy most commonly caused by SCN5A mutation.

Affects fast-type sodium channels- reduces conduction velocities.

Mainly affects right ventricular outflow tract which is prone to ventricular tachycardia.

39
Q

Patient selection for ICD

A

Survivors of a cardiac arrest that did not occur from MI.

Ventricular tachycardia with haemodynamic compromise.

Some HCM, long QT, brugada and ARVC.

Congenital heart disease

broad QRS complex