Sudden cardiac death Flashcards
Sudden death
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.
Causes of sudden death (4)
Cardiac causes and its vessels.
Non-cardiac vessels- i.e stroke or aneurysm
Pulmonary- i.e PE
CNS- some seizures in epilepsy.
Sudden cardiac death
Sudden death due to cardiac/ coronary vessels.
Direct causes of sudden cardiac death
2
Coronary obstruction
Arrhythmias
Disorders that increases risk of sudden cardiac death (3)
Coronary heart disease- low ventricular ejection fraction (LVEF)
Cardiomyopathies
Primary arrhythmias- inherited cardiac symptom.
Cardiac arrest
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.
Three causes of arrhythmias
Electrical
Structural
Ischaemic
Electrical cause of arrhythmias
3
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
Wolff-Parkinson-White
- Pathology
- Symptoms (4)
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
Long QT syndrome
- Pathology
- Treatment
A arrhythmogenic disorder than can cause fatal cardiac arrhythmia.
Cause by genetic abnormalities.
Treatment- beta-blockers, ICDs (implantable cardioverter defibrillator).
Cardiomyopathy
- Pathology
- Complications
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.
Restrictive cardiomyopathy
Stiffing and rigid ventricles due to abnormal tissue replacing cardiomyocytes.
This prevents ventricles from filling with blood properly- enlarges the atria.
Arrhythmogenic right ventricular dysplasia
Disorder where some cardiomyocytes die and is replaced with scar tissue.
Can cause arrhythmias by disrupting electrical signal pathways.
Tetralogy of Fallot
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.
Trigger
- Include example
A brief event required to start a period of arrhythmia.
Examples: An extrasystole, nearby focus of rapid firing (atrial flutter).
Substrate
- 2 types of defects
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.
R on T
When a premature QRS complex occurs during the previous T wave.
Potential trigger for arrhythmias
Premature QRS= premature ventricular contraction.
Pacemaker
Implanted electronic device that contains electrodes to stimulate the heart.
Constantly applies impulse for EVERY SINGLE heart beat
Use: Heart block, bradyarrhythmias.
ICD
- Indications
Implantable cardioverter defibrillator.
Only applies electrical impulses to the heart when a ventricular arrhythmia is detected.
Use:
Ventricular fibrillation
Ventricular tachycardia
Indications for implanting ICD
Cardiac arrest from ventricular fibrillation.
Symptomatic HF with low LVEF.
Cardiomyopathies- DCM
Congenital
Channelopathies
Amiodarone
Antiarrhythmic drug that does so by prolonging the repolarisation phase.
Antiarrhythmic drugs
Amiodarone
Beta-blockers: bisoprolol, propranolol.
Digoxin in AF
Reperfusion injury
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.
Preventative treatment for reperfusion injury
Cooling
Immunosuppression
Oxygen radical scavengers
Syncope indications
Loss of postural tone
Lightheadedness
Sweating before faint
Associated with prolonged sitting or standing
Seizure indications
Maintained/ high postural tone
Bitten tongue
Deja vu/ jamais vu
Vasovagal syncope
Most common form of syncope where:
Vagal input increase = vasodilation and bradycardia
Triggered by the brain, not heart.
Exertional syncope
Neurocardiogenic origin
Caused by permutations in homeostatic maintenance of arterial blood pressure and systemic vascular resistance.
Index case/ Proband
The initial patient in the population being investigated.
Could lead to source of disease- patient 0.
Number needed to treat
Average number of patients who need to be treated to prevent one additional bad outcome.
Predisposing factors that can lead to electrical instability after ventricular remodelling.
Low LVEF.
Presence of a myocardial scar.
Autonomic dysfunction.
Genetic polymorphism..
Precipitating events that can lead to electrical instability after ventricular remodelling.
Acute ischaemia
Worsening heart failure
Metabolic/ electrolyte disturbances
Medication- like QT prolonging drugs.
Dilated cardiomyopathy
Non-ischaemic dilation of a ventricle
Causes: Idiopathic Viral Alcohol Chemotherapy Autoimmune.
Pathophysiology of Dilated cardiomyopathy
- Subendocardial myocardial fibrosis
- Neurohumoral activation: activation of the RAAS system and the sympathetic system.
- Increased sympathetic tone
- Electrolyte disturbances
3 ways in which an electrical circuit in the heart can show ‘re-entry’
- Large circuit size, increases circuit time= re-entry.
- Atrial refractory time shorter than circuit time= re-entry.
- A zone of slow conduction, increases circuit time= re-entry.
Hypertrophic cardiomyopathy
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.
Arrhythmogenic RV cardiomyopathy (ARVC)
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.
Brugada
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.
Patient selection for ICD
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
