SCD, Definition, epidemiology, risk factors, etiology, pathophysiology, management, prevention.

1. SUDDEN CARDIAC
DEATH
Dr. Abhik Haldar
DM Cardiology resident
SCB Medical College

2. CONTENTS
o DEFINITION
o EPIDEMIOLOGICAL OVERVIEW
o RISK FACTORS
o ETIOLOGIES
o PATHOPHYSIOLOGY
o MANAGEMENT
o PREVENTION

3. DEFINITION
Sudden cardiac death is natural death from cardiac
causes heralded by abrupt loss of consciousness
within 1 hour of the onset of an acute change in
cardiovascular status.
Pre-existing heart disease may or may not have been known
to be present, but the time and mode of death are
unexpected.

4. DEFINITION- Continued…

5. THE TEMPOLARITY OF EVENTS

6. EPIDEMIOLOGY OVERVIEW
• SCD, constitute major public health problems, accounting for approximately
50% of all cardiovascular deaths and with at least 25% being first
symptomatic cardiac events
• In USA when the etiologic definition is limited to coronary heart disease the
incidence of SCD is 250,000 annually and when all causes are included
incidence is 460,000 per annum.
• Annually about 7-lakh SCD cases occur in India.
• The incidence of sudden death has bimodal distribution within the first year
of life (including sudden infant death syndrome [SIDS] and between 45 and
75 years of age.
• Men remain at higher risk than women across the entire age spectrum.

7. AGE RELATED RISK OF SCD
• Increasing age is a strong
predictor of risk for SCA, but
it is not linear.
• The population of children
and adolescents has an
overall annual risk of 1 per
100,000, and there is
somewhat a higher risk of
SCD at the younger end of
that age range.
• Risk in the general
population, over time,
beginning at 35 years of age
has been estimated at 1 per
1000 population per year

8. PARADOX !
The highest risk categories identify the smallest number of total annual events, and the
lowest risk category accounts for the largest number of events per year

9. RISK FACTORS OF SCD

10. ETIOLOGIES OF SCD
Coronary artery abnormalities Hypertrophy of the ventricular
myocardium
Myocardial diseases and
dysfunction
A. Coronary atherosclerosis
B. Congenital abnormalities of
coronary arteries
C. Coronary artery embolism
D. Coronary arteritis
A. Hypertensive heart disease
B. Hypertrophic
cardiomyopathy
C. Primary or secondary
pulmonary hypertension
A. Chronic congestive heart
failure
B. Myocarditis, acute or
fulminant
C. Takotsubo syndrome
D. Acute alcoholic cardiac
dysfunction
Diseases of the cardiac valves Infiltrative, neoplastic, and
degenerative processes
Congenital heart disease
A. Valvular aortic
stenosis/insufficiency
B. Mitral valve prolapse
C. Prosthetic valve
dysfunction
A. Sarcoidosis
B. Amyloidosis
C. Chagas disease
D. Idiopathic giant cell
myocarditis
A. Congenital aortic or
pulmonic valve stenosis
B. Eisenmenger physiology
C. Late after surgical repair of
congenital lesions

11. ETIOLOGIES OF SCD…cont
Electrophysiologic
abnormalities
Electrical instability related
to neurohumoral influences
Miscellaneous
A. Congenital long–QT
interval syndrome
B. Congenital short–QT
interval syndrome
C. Brugada syndrome
D. ERS
A. Catecholaminergic
polymorphic ventricular
tachycardia
B. Psychic stress,
emotional extremes
(takotsubo syndrome)
A. Commotio cordis—
blunt chest trauma
B. Mechanical
interference with
venous return
C. Dissecting aneurysm of
the aorta

12. PATHOPHYSIOLOGY
TACHYARRYTHMIA BRADYARRYTHMIA-
ASYSTOLE
• Ventricular Fibrillation
• Pulseless VT
• Severe Bradycardia ( HR<20 bpm
)
• Pulseless Electrical Activity (PEA)
• Asystole
ELECTROPHYSIOLOGIC EFFECTS OF MYOCARDIAL
INFARCTION
Ischemic and Reperfusion Injury-
• Alterations in cell membrane physiology with efflux of ionized
potassium (K+), influx of ionized calcium (Ca2+), acidosis.
• Reduction of transmembrane resting potentials.
• Formation of superoxide radicals.
• Differential responses of endocardial and epicardial muscle
activation times and refractory periods.
• Uncoupling of myocytes due to alterations of Connexin 43.
First 10 mins post MI
ISCHEMIC
INJURY
10-30 mins post
MI
REPERFUSION
INJURY
50 %
} 25 % } 25 %

13. MANAGEMENT
The response to cardiac arrest is driven by two principles: (1) maintaining continuous
cardiopulmonary
support until ROSC has been achieved and (2) achieving ROSC as quickly as possible.
Post CA
care
ACLS
Early D-
Fib
BLS
Initial
assessme
nt

14. INITIAL ASSESSMENT
A few seconds of evaluation
• Response to voice,
• Observation for respiratory movements and skin color,
• Simultaneous palpation of major arteries for the presence or absence of a
pulse.
Once suspected/ confirmed call help for out of hospital setting &
arrange for early shifting to hospital.

15. BASIC LIFE SUPPORT
The CAB of Cardiopulmonary Resuscitation
CIRCULATION:
30:2 with a rate of 100/m
Palm of one hand over lower half of sternum, heel of other rests dorsum of hand.
Force to depress the sternum at least 5 cm.
AIRWAY:
Tilting head backwads
Lifting chin
Heimlich maneuver
BREATHING:
Mouth to mouth
Ambu bags
ET tubes

16. EARLY DE-Fib BY FIRST
RESPONDERS
The term first responder refers to the person on scene providing initial CPR and has
emerged from minimally trained EMTs allowed to carry out defibrillation in conjunction with
BLS.

17. ACLS
 Defibrillation-Cardioversion
 Bradyarrhythmic and Asystolic Arrest; Pulseless Electrical
Activity
 Pharmacotherapy
 Stabilization

18. S
H
O
C
K
A
B
L
E
R
H
Y
T
H
M

19. N
O
N
S
H
O
C
K
A
B
L
E
R
H
Y
T
H
M

20. STABILIZATION
• Amiodarone: If frequent PVCs and runs of nonsustained VT persist
after restoration of a sinus rhythm, continuous infusion is preferred.
• Lidocaine: Arrhythmias caused by acute ischemic events.
• Procainamide: may be considered if the others fail.
• Isoproterenol: May be used for the treatment of primary or
postdefibrillation bradycardia when heart rate control is the primary
goal of therapy

21. PREVENTION OF SCD
Secondary
prevention
At high risk
because of
advanced
heart disease
Less
advanced
common or
uncommon
structural
heart
diseases
Structurally
normal
hearts, minor
structural
abnormalities
, or
genetically
based
molecular
disorders
General
population

22. STRATEGIES TO REDUCE SCD
• Anti arrhythmic Drugs
• Therapy Guided by Programmed Electrical Stimulation
• Surgical Intervention Strategies
• Catheter Ablation Therapy
• Implantable Defibrillators

23. Anti-arrhythmic drug therapy
• Historically, ambient arrhythmia suppression by AAD therapy enjoyed a short period
of popularity as a strategy for reduction of SCD.
• Currently, with the exception of beta blockers there is no evidence from RCTs that
antiarrhythmic medications improve survival when given for the primary or secondary
prevention of SCD.
• However the use of these medications may be considered in some patients to
control arrhythmias and improve symptoms.
Medications With Prominent Sodium Channel Blockade:
• Intravenous lidocaine for patients with refractory VT/ cardiac arrest.
• Oral mexiletine for congenital long QT syndrome
• Quinidine for patients with Brugada syndrome
• Flecainide for patients with catecholaminergic polymorphic
ventricular tachycardia
• In ICD patients with drug- and ablation-refractory VT.

24. Anti-arrhythmic drug therapy
Beta Blockers:
• Excellent safety profile and effective in treating VA and reducing the risk of SCD.
• Their antiarrhythmic efficacy is related to the effects of adrenergic-receptor
blockade on sympathetically mediated triggering mechanisms
• Reduce all-cause mortality and SCD in patients with HF with reduced EF (HFrEF)
• Reduce mortality after MI
• First-line therapy for some cardiac channelopathies (e.g., long QT syndrome,
catecholaminergic polymorphic ventricular tachycardia).
Class III anti arrythmic agents:
• For primary prevention, in some studies, amiodarone was found to reduce
the risk of SCD and all-cause mortality, but the quality of the supporting
evidence was very low.
• For secondary prevention of SCD, the same systematic review identified
neither risk nor benefit with amiodarone.

25. SCD PREVENTION IN SPECIFIC
SUBSETS

26. ISCHEMIC HEART DISEASE
SECONDARY PREVENTION PRIMARY PREVENTION
MADIT
MADIT II MUSTT
DINAMIT

27. NICM
DEFINITE, SCD-

28. HCM

29. CONGENITAL LONG QT SYNDROME

30. BRUGADA SYNDROME

31. ADULT CONGENITAL HEART DISEASE

32. Why not to consider ICD for all high risk
patients?......ICD Cost effectiveness
• The cost-effectiveness ratio becomes rapidly
unfavorable as the extension in survival time falls below
1 year, particularly below 0.5 year.
• This inverse relation strongly suggests that the value
provided by an ICD will be highest when the risk of
arrhythmic death due to VT/VF is relatively high and the
risk of nonarrhythmic death (either cardiac or
noncardiac) is relatively low.
• Thus, appropriate patient selection is fundamental to
high value care in using the ICD to prevent SCD.

33. THANK YOU..!!