Sudden cardiac death

Sudden cardiac death

• 63% of all deaths from cardiovascular causes
• Only 6% survive to leave hospital neurologically intact
• 30-80% more likely in lower SES groups
• More likely in first few hours of day (increased sympathetic drive) – beta-blockers provide some protection from this
• Peaks in infancy (SIDS) and age 45-50 (60% in males)
• Occurs during exercise in 15%

causes

• Ventricular tachyarrhythmias
  • Mechanism thought to be interaction of structural heart disease with ventricular extrasystoles with subsequent circus re-entrant pathways
    • LVH
    • Myocardial ischaemia/infarction
    • BBB
    • Pre-excitation syndromes
    • Brugada syndrome
    • Long QT syndrome
• Bradyasystole
  • Cardiac rhythm with ventricular rate <60 or periods of absent heart rhythm
  • Occurs commonly in cardiac arrest, either as initial rhythm, during the course of resus or after defibrillation

causes

• Causes of bradyasystole
  • Myocardial ischaemia/infarction
    • RCA supplies sinus node 55% of the time and AV node 90% of the time
    • BBB are supplied by multiple arteries so bilateral BBB due to ischaemia is rare (unless underlying BBB or severe triple-vessel disease)
    • Cardiac vagal and sympathetic afferents can trigger vagal depressor reflexes (Bezold-Jarisch reflex) or sympathetic cardioexcitation
  • Sick sinus syndrome
  • Hypoxia
  • Hypercarbia
  • Suffocation
  • Near drowning
  • Stroke
  • Beta-blocker/CCB 
  • Opiate overdose
  • Digitalis
  • Parasympathomimetic agents
  • Adenosine
  • Massive haemorrhage

prognosis

• Factors that affect outcome in VF
  • Witnessed collapse
  • Prompt CPR
  • Early defibrillation
  • Young age
  • Arrest occurring away from home (much better rate of survival)
    • More likely to be VF out of home (presumably those in the home are older and likely to have one or more chronic illness precluding activity outside home)
• Likelihood of survival is up to 60% if initial VT/VF
• <5% if not

PEA

• More likely in women with unwitnessed arrest, at night, without bystander CPR
• 2% survive to hospital discharge
• Causes
  • Hypovolaemia
  • Tension pneumothorax
  • Cardiac tamponade
  • PE
  • Massive myocardial depression – Infarction, ischaemia, myocarditis, toxins
  • Profound shock of any cause
  • Hypoxia
  • Acidosis
  • Severe hypercarbia
  • Auto-PEEP
  • TCA, beta-blocker, CCB
  • Hypothermia
  • Hyperkalaemia
  • Post-defibrillation pulselessness

Risk factors if over 35yo

• Age
• Male gender
• Coronary artery disease
• LVH
• Impaired LV function (EF <30%)
• Prolonged QTc
• Ventricular arrhythmias, particularly sustained, inducible VT
• Prediction is near impossible with a multitude of diagnostic modalities being employed, all of which lack sensitivity and specificity
• QRS width is an independent predictor
  • Each 10ms increment in QRS has 25% increased risk of SCD

Factors contributing to likelihood (Tintinalli)

• Cardiovascular pathology
  • CAD (80% of cases)
  • Severe LV dysfunction
  • Cardiomyopathy – Hypertrophic, arrhythmogenic RV dysplasia (10-15%) 
  • CHD (esp. coronary artery anomalies)
  • Valvular heart disease
  • Cardiac pacemaker and conducting system disease
• Hereditary channelopathies
  • Brugada
  • Early repolarisation syndrome
  • Long QT syndrome
  • Short QT syndrome
  • Catecholaminergic polymorphic VT
• Risk factors and triggers
  • HTN, dyslipidaemia, smoking, DM, SES
• Unstable atheroslerotic plaque
  • Psychological stress and physical activity

Causes (DUNN)

• Common cardiac causes
  • Structural
    • 80% of sudden cardiac deaths in people under 35
    • Coronary artery disease (35%)
    • HOCM (25%)
    • Myocarditis (15%)
    • Aortic stenosis
    • Valve failure
  • Electrical
    • 20% of cases
    • Prolonged QT
    • Brugada
    • RV dysplasia
    • Inferior early repolarisation phenomenon (if J point elevation > 2mm)
• Non-cardiac
  • SAH/ICH
  • Seizures

Antiarrhythmics

• Cardiac Arrhythmia Suppression Trial (CAST) showed Class I agents increased risk of sudden cardiac death
• Class III agents (amiodarone, sotalol) and beta-blockers may provide some protective benefit

ICD

• More effective than antiarrhythmics at reducing mortality in patients with:
  • Reduced LVEF
  • Documented non-sustained VT
  • Inducible sustained VT
• <$30 000 per year of life saved
• Indicated in high-risk patients
  • Known significant CAD
  • Depressed LVEF
  • Spontaneous, life-threatening and/or inducible ventricular dysrhythmias

Rescue

• Each minute patient remains in VF, odds of survival reduce by 7-10%
• Chain of survival
  • Early call for help
  • Early CPR – Improves survival and neurological outcome
  • Early defibrillation
    • Rationale based on:
      • 1) Ventricular tachydysrhythmias are the most common cause of sudden cardiac arrest
      • 2) Defibrillation is the most effective therapy for this
      • 3) The effectiveness of defibrillation diminishes with time
      • 4) Unless treated promptly, devolves into less treatable fine VF
  • Early ACLS

Coronary Artery disease

• Seen in 80% of patients
• 1/3 have evidence of acute plaque rupture in long segment stenosis
• Documented initial VF (or shockable rhythm if AED) suggests ACS is cause
• Initial VF only present in 23% of cardiac arrests though

Severe LV dysfunction

• Best predictor of sudden cardiac death
• EF <35% are primary candidates for IDC
• But at least 50% occur in patients without reduced EF

Cardiomyopathy

• Regardless of decompensated status, this is another predictor
• Results in islands of depolarisations and re-entry circuits
• IHCA of patients with heart failure are more likely to be initial VF
• NYHA Class II/III more likely die of sudden cardiac death than HF vs. NYHA Class IV
• HOCM has 1% rise in risk of SCD per year
  • Most common CV cause of sudden cardiac death in young athletes (1/3 of such events)
  • ICD recommended if:
    • Prior documented cardiac arrest, VF, VT, first-degree relative SCD, syncope, LV wall thickness >30mm, abnormal BP response to exercise or high-risk children with unexplained syncope/massive LVH/FHx
• Arrhythmogenic RV dysplasia
  • Right-sided heart failure, RV origin ventricular arrhythmias (i.e. VT with LBBB morphology), syncope and SCD
  • Typically TWI in V1-V3
  • ICD is treatment of choice (beta-blockers do not prevent symptomatic ventricular arrhythmias

Congenital heart disease

• 0.8% of live births
• Those associated with SCD are: coronary artery anomalies (anomalous left coronary artery from pulmonary artery syndrome – ALCAPA), aortic stenosis, coarctation, ToF, TGA, Ebstein’s anomaly and single ventricle
• ALCAPA results in left coronary running between aorta and main pulmonary artery with resultant ischaemia, ventricular arrhythmias or SCD triggered by exercise with resultant dilation of pulmonary artery and compression of LCA
• Most episodes occur during exercise and 50% have VF
• Non-ventricular arrhythmias are common after corrective surgery

Valvular heart disease

• Haemodynamically severe aortic stenosis
• Most common causes are bicuspid aortic valve calcification in mid-adulthood or calcified tricuspid aortic valve in 70-80yo

Conducting system disease

• Sick sinus syndrome
• Should be considered diffuse degenerative disease of conducting system
• Lenegre’s disease
  • Idiopathic sclerodegeneration of AV node and bundle branches
• Lev’s disease
  • Invasion of conducting system by fibrosis or calcification spreading from adjacent cardiac structures

Hereditary channelopathies

• Sudden arrhythmic death syndrome
  • Sudden OOHCA in relatively young adults (mostly men), often during sleep or rest, usually with no prior symptoms and no anatomical abnormality on autopsy (50% have channelopathy when family Ix)
• Ion channel disease
  • Brugada’s syndrome
    • Mostly men, prominent J wave with downsloping ST elevation in leads V1-3
    • Resembles RBB and associated with 40-60% incidence of ventricular arrhythmia (particularly polymorphic VT degenerating to VF)
    • Autosomal dominant inheritance with total loss of function or in acceleration of recovery from sodium channel activation
    • Common in Southeast Asia

Hereditary channelopathies

• Early repolarisation syndrome
  • 1-2% of adults (mostly males)
  • Long considered benign normal ventricular repolarisation variant
  • Prevalence up to 10% in athletes and 100% in performance athletes
  • Prominent, notch-like J wave on QRS downslope followed by upsloping ST elevation
  • Most prominent in mid-to-lateral leads but can occur just laterally or inferiorly
  • Commonly reciprocal ST depression in aVR
  • Cardiology referral might be warranted in young adult with syncope of unknown origin or FHx of SCD with this

Hereditary channelopathies

• Long QT
  • May be autosomal recessive (Jervell and Lange-Neilsen syndrome with nerve deafness) or dominant (Romano-Ward syndrome without nerve deafness)
  • Beta-blockers typically prescribed as prophylaxis against SCD
  • If syncope, TdeP or VF despite beta-blockers, should get ICD

Hereditary channelopathies

• Short QT
  • <0.34 seconds. 
  • Hypercalcaemia, hyperkalaemia, acidosis, SIRS, ischaemia or increased vagal tone or inherent autosomal dominant disease
  • Genetic variety associated with atril arrhythmia (AF), syncope, polymorphic VT, VF and SCD
  • Early repolarisation in lateral leads is seen in 65%
  • Candidates for ICD if syncope or ventricular arrhythmias documented

Hereditary channelopathies

• Catecholaminergic polymorphic VT (CPVT)
  • Genetically determined disorder involving defective myocardial cellular calcium handling
  • Exercise and stress-related VT, syncope and SCD
  • Usually in childhood/early adulthood
  • Many affected have sinus bradycardia of unclear cause
  • 50% carry diagnosis of epilepsy as their diagnosis and cause of recurrent syncope
  • Beta-blockers are mainstay prophylaxis and if fails, then ICD

Last Updated on October 13, 2020 by Andrew Crofton