This document discusses sudden cardiac death (SCD), defined as unexpected death from cardiac causes within one hour of symptom onset or within 24 hours of being asymptomatic. The main causes of SCD are cardiac arrhythmias and hemodynamic catastrophes due to structural heart disease, ischemic heart disease, or inherited arrhythmia syndromes. Risk factors for SCD include age over 35, male sex, left ventricular dysfunction, ventricular arrhythmias, hypertension, diabetes, smoking, and family history of cardiac disease or sudden death. Mechanisms of SCD include abnormal automaticity, triggered activity due to early or late afterdepolarizations, and reentry phenomena involving scar tissue or functional conduction blocks. High-risk patients should undergo evaluation including

1. Sudden Cardiac Death
By Dr Niraj

2. Definition
• Sudden and unexpected death
• Occurring within 1 hour of symptom onset
Or
• In patients found dead within 24 hours of
being asymptomatic
• Presumably due to:
– Cardiac arrhythmia
– Haemodynamic catastrophe
Natural, Rapid and Unexpected

3. Incidence of SCD
• Almost 50% of all CV deaths
• At least 25% -first symptomatic event
• M>F
• 70%- out-of-hospital*
• Out-of-hospital SR- 6%
• In-hospital SR-24%
• Rapid emergency response, public knowledge
• Prognosis better in shockable > PEA/asystole

4. Incidence of SCD
• India- >7,00,000 deaths/year and approx 10.3% of mortality (Rao et
al.)
• Peak age – 45 to 75 yrs, M>F (3:1)
• SR <1%
• Vital data esp. from rural areas – unaccounted for
• Rural-urban gradient in CAD (7.6-12% v 3.1-7.4%) - different risk
factors
• Urban India and Western SCD trends similar- Gupta et al. (2007)
• Prevailing RFs- HTN, DM, smoking

5. Four temporal elements
1. Prodrome- Predictors of an impending
cardiac event
2. Onset of terminal event- from onset of
1st symptom to SCA
3. Cardiac arrest
4. Biologic death- upto 1 hour from
terminal event

6. diagram

7. Etiology of SCD
Structural HD Cardiomyopathy
HCM, NIDCM, ARVC
Myocardial scarring and fibrosis
Inherited Arrhythmia syndromes BrS, LQTS, WPW, CPVT
Channelopathies
Ischaemic Heart Disease** - X 2.8-5.3 risk (Framingham)
LVEF < 30-35% *
Valvular HD AS, MVP, Prosthetic valve dysfunction
Mechanical pathologies Acute cardiac tamponade, Massive PE, Acute
intracardiac thrombus, Commotio cordis
Congenital HD Congenital AS, PS, VSD+Eisenmenger
physiology, Anomalous origin of coronary
arteries, post-TOF repair
SIDS- Sudden infant death syndrome - <0.5/1000 live births, M>F infants

8. Contributory Risk factors
1. Hypertension
2. Type 2 DM
3. Dyslipidaemia
4. CKD
5. Obesity
6. OSA
7. Seizures
8. Smoking
9. Type A personality
10. Nutritional deficiencies

9. Risk analysis
1. Age
– 2 peaks- <1 year (SIDS) and 45-75 yrs
– Strong predictor, non-linear, >35 yrs, 1 in 1000/yr
– Risk decreases in later years >75 yrs, Framingham
– Steep increase- adolescent to middle-age (IHD)
– HCM, BrS, LQTS, ARVC- important considerations
2. IHD
– MC substrate a/w SCD
– Transition from mid-20s to mid-30s (>40% of cases)

10. diagram

11. Risk analysis
3. Diseases presenting in young-
– Myocardial fibrosis and remodelling
– Channelopathies
– CHD
– Myocarditis
– Genetic structural disorders
4. Race-
SCA and SCD risk higher in black >
white/asian > hispanic

12. Risk analysis
5. Gender
– <65 years- M>F by x 4-7
– 65 + years- M>F – 2:1
– Protection against CAD before menopause
– Severe LV dysfunction- ↓ 50%
– CAD- ↓66% before SCD
6. Heredity
– Inherited arrhythmia syndromes
– Gene loci-encoding ion channel protein mutations
– CAD: Atherogenesis, plaque destabilisation, thrombosis, arrhythmia

13. diagram

14. Risk analysis
7. LVEF
– <30%- single most powerful independent predictor of SCD
– MR rate changes the most btw 30-40%
– Infarct size, fibrosis- better predictor of cardiac events
– LV dysfunction- modulates risk in Post-MI pts with VPCs
8. Ventricular arrhythmias
– Benign- most VPCs, NSVT (short runs)- in absence of structural HD
– If present during TMT (peak/recovery)- higher risk
– VPCs in Post-ACS pts- increased risk (>10/hour)
– Polymorphic NSVT- drug/electrolyte/functional

15. Mechanisms of SCD
1. Automaticity
– Enhanced normal
– Abnormal
2. Afterdepolarisations  Triggered activity
– Early
– Late
3. Re-entry phenomenon

16. Automaticity
• Phase 4- spontaneous depolarisation of
transmembrane AP
• In MI/ischaemia:↑ EC K+ causes partial
depolarisation of RMP
• Injury currents develop btw healthy and
infarcted/ischaemic myocardium
• This initiates spontaneous activity
• Purkinje fibres and Ventricular myocytes

17. Triggered Activity
• AP prolongation may occur due to
– ↑ inward currents (Na+/Ca2+/Na+-Ca2+ exchange)
– ↓ repolarising K curents
• Early afterdepolarisations- late phase 3/early
phase 3 of AP
• TdP VT associated with QT-Prolongation
(medications/hereditary)
• Delayed afterdepolarisations- after complete
membrane repolarisation, due to Ca2+ overload
• CPVT, Digoxin toxicity, idiopathic outflow tract VA

18. Re-entry phenomenon
• Most sustained VA in the presence of
structural HD
• Ischaemia, Brugada syndrome
• Re-entry requires a trigger to initiate the
arrhythmia and a substrate to sustain it
• Trigger- VPC (automaticity)
• Substrate-
1. Fixed anatomical obstacle- patchy fibrosis, scar
(post-MI or post-surgery, CM, hypertrophy)
2. Functional block- functional re-entry. Rotor vs.
Multiple wavelet re-entry

19. Approach in high-risk patients
• Symptoms of VA:
– Palpitations
– Skipped/extra beats
– Breathlessness (at
rest/on exertion)
– Chest pain
– Syncope/near-syncope
– Lightheadedness
•Symptoms related to
underlying heart disease:
•Exertional dyspnoea
•Orthopnoea/PND
•Chest pain
•Pedal oedema
Precipitating factors: Exercise, emotional stress,
concurrent illness

20. Approach in high-risk patients
• Medications:
– Anti-arrhythmics
– QTc and TdP
– Alcohol
– Stimulants-
cocaine,
amphetamines
– Anabolic steroids
• Past medical history:
• Thyroid disease
• AKI/CKD
• CVA/embolic events
• Epilepsy
• Unexplained RTA

21. Clinical examination
• Bigeminy/Trigeminy-
– Effective bradycrdia
– Apico-Radial deficit
– Relative HTN, wide PP
• Carotid bruits
• Peripheral pulses
• JVP
• Peripheral oedema
• S3 gallop
• Cardiac murmurs
• Crepitations

22. Approach in high-risk patients
• Family history:
– Cardiac channelopathies-LQTS, CPVT, BrS
– Arrhythmias
– Conduction disorders, pacemakers/ICDs
– N-M junction disorders
– Muscular dystrophy
– Epilepsy

23. Evaluation
• Non-invasive
1. ECG-
– VT, high-grade AV block, sinus brady + pauses, SVT, PPM
malfunction
– Chamber enlargement, previous MI, inherited arrhythmia
disorders
– QRS duration- prognostic
– Microvolt T-wave alternans - predictive
2. Exercise testing-
– Abnormal recovery
– External/implantable recorders
– CPVT

24. Emerging markers of risk for SCD
• Cardiac MRI-
– Infarct area
– Fibrosis patterns (delayed hyperenhancement)
• Sympathetic imaging-
– 11C-hydroxyephedrine
– MIBG
• Genetic/Familial testing
– Risk profiling
– Familial clustering- CAD