This document provides information on sudden cardiac death (SCD), including its definition, epidemiology, risk factors, etiologies, and prevention. Some key points: - SCD is defined as a natural death from cardiac causes within 1 hour of symptoms. It is a major cause of mortality, accounting for 10-15% of natural deaths. - Risk factors include prior heart disease, low ejection fraction, family history, and cardiomyopathy. The risk is bimodal with peaks under 1 year old and over 65 years old. - Causes include ventricular arrhythmias, asystole, and pulseless electrical activity. Prevention strategies include implantable defibrillators, antiarrhythmic drugs

1. Dr. Pritam Kr Chatterjee

2.  Definition
 Epidemiological Overview
 Risk Factors
 Etiologies
 SIDS & SCD in Children
 Clinical Features
 Management
 Prevention of SCD

3. SCD is a natural death from cardiac causes heralded by
abrupt loss of consciousness within 1 hr of the onset of an
acute change in cardiovascular status.
Preexisting heart disease may or may not have been known to be
present but time & mode of death are unexpected.
Key Elements– NATURAL, RAPID , UNEXPECTED

4. In the context of time, sudden is defined for most
clinical and epidemiologic purposes as 1 hour or less
between a change in clinical status heralding the
onset of the terminal clinical event and the cardiac
arrest itself.
To satisfy clinical, scientific, legal, and social
considerations, four temporal elements must be
considered: (1) prodromes, (2) onset of terminal
event, (3) cardiac arrest, and (4) biologic death

5. SCD viewed from four temporal
perspectives

6. TERM DEFINITION MECHANISMS
Sudden
cardiac
death
Sudden, irreversible cessation of all
biologic functions
—
Cardiac
arrest
Abrupt cessation of cardiac
mechanical function, which may be
reversible by a prompt intervention
but will lead to death in its absence
Ventricular fibrillation,
ventricular tachycardia,
asystole, bradycardia,
pulseless electrical activity,
mechanical factors
Cardiovas
cular
collapse
Sudden loss of effective blood flow
due to cardiac and/or peripheral
vascular factors that may reverse
spontaneously (e.g.,
neurocardiogenic syncope; vasovagal
syncope) or require interventions
(e.g., cardiac arrest)
Same as cardiac arrest, plus
vasodepressor syncope or
other causes of transient
loss of blood flow

7. EPIDEMIOLOGY OF SCD
 Approx. 5,00,000 CASES IN U.S.A PER ANNUM
 In India its around 7 Lakhs per year
 Accounts for 10-15% of natural deaths and 50 % deaths
from cardiac causes.
 BIMODAL AGE DISTRIBUTION with peaks between
birth and 6 months of age & after 65 yrs of age
 Male preponderance
 May be the first presentation of cardiovascular disease
in 25% of patients

8. AGE RELATED RISK FOR SCD

9.  Prior Episode of V.TACH
 Low LVEF.
 Previous Myocardial Infarction.
 Coronary Artery Disease
 Family History of SCD.
 Cardiomyopathy
 Congestive Heart Failure
 Long QT Syndrome.
 Right Ventricular Dysplasia.
Risk Factors of Sudden Cardiac Death (SCD)

10. Emerging markers of SCD:
 Microvolt T wave alternans
 Contrast enhanced MR imaging of
postinfarction border
 QT Variability
 MIBG Imaging
 Derivatives of heart rate variability methods
 Familial clustering

12. Three Basic ECG Patterns with
Cardiac Arrest
 Ventricular tachyarrhythmia-- ventricular fibrillation
(VF)/sustained type of pulseless ventricular
tachycardia
 Ventricular asystole or a brady-asystolic rhythm with
an extremely slow rate
 Pulseless electrical activity (PEA), previously referred
to as electromechanical dissociation.

15. Ventricular Tachycardia

16. Indian study
 Most of SCD
occurred in the first
year
VALIANT study
 ~25% of SCD
occurred in the first
month
 65% occurred after
90 days
Rao B H . Global burden of Sudden Cardiac Death and insights from India. Indian heart journal 6 6 ( 2 0 1 4 ) s 1 8 es 2 3

17. CORONARY ARTERY DS HYPERTROPHIC CMP
•Previous cardiac arrest
•Syncope
•Prior AMI within 6 months
•EF < 30%
•History of frequent ventricular
ectopics
•Family H/O SCD
•Previous cardiac arrest
•Syncope
•LV Wall thickness> 30 mm
•Drop in SBP on exercise
•Repetitive NSVT on holter
•Extensive/diffuse late gadolinium
enhancement in contrast CMR

18. DCMP VAVULAR HEART DS LONG QT
SYNDROME
•Previous cardiac
arrest
•Syncope
•EF of 30-35%
•Use of inotropes
•Valve replacement
within past 6 months
•Syncope
•H/O frequent
Ventricular ectopics
•Symptoms a/w severe
uncorrected AS or MS
•Family H/O long QT &
SCD
•Medications that
prolong QT
•Bilateral deafness

19.  Acquired disease of the AV node and His-Purkinje system
& the presence of accessory pathways of conduction
Risk group-
 Anterior AMI with RBBB/Bifascicular block
 Primary fibrosis/secondary(Lenegre/Lev)with intramural
conduction defect
 Aberrant pathway with short anterograde pathway
SYNDROMIC PESENTATION-
Long-QT Syndromes
Short-QT Syndrome
Brugada Syndrome
Early Repolarization Pattern and SCD
Catecholaminergic Polymorphic Ventricular Tachycardia
Electrical Instability Resulting from Neurohumoral and Central
Nervous System Influences

20. SIDS (birth and 6 months ) had an incidence of 1.2
deaths/1000 live births
SIDS deaths related to longer QT intervals and related
arrhythmias-mutation of Na channel(SCN5A)
Beyond SIDS age group:
• Post CHD
surgery
25%
• 25-65%
• Older children(1-
21yrs)
cardiac causes of
sudden death • congenital aortic stenosis,
Eisenmenger syndrome,
pulmonary stenosis or
atresia, or HOCM
75%

21.  Massive pulmonary embolism
 Holiday heart syndrome
 Heat-stroke
 Aortic dissection

22. Before Arrest
Hypotension (systolic
BP < 100 mm Hg)
Pneumonia
Renal failure
(BUN > 50 mg/dL)
Cancer
Homebound
lifestyle
During Arrest
Arrest duration
>15 min
Intubation
Hypotension
(systolic BP <
100 mm Hg)
Pneumonia
Homebound
lifestyle
After Resuscitation
Coma
Need for
pressors
Arrest duration
> 15 min

23.  The response to a cardiac arrest is driven by two urgent
principles:
(1) maintenance of continuous artificial
cardiopulmonary support until return of spontaneous
circulation
(2) restoration of spontaneous circulation as quickly
as possible.
(1) initial
assessment
&
summoning
of an
emergency
response
team;
(2) basic
life
support
3) early
defibrillation
by a first
responder (if
available)
(4)
advanced
life
support;
(5) post–
cardiac
arrest
care.
long-
term
manag
ement

24.  Observe for respiratory movement
 Look at the skin color
 Simultaneous palpation of major arteries
Once suspected/ confirmed call help for out of
hospital setting & arrange for early shifting to
hospital.

25.  Chest Thump( Thump version):
One/two blows delivered to the junction of
middle & lower third of sternum from a height
of 8-10 inches.
If conscious forceful cough increases
intrathoracic pressure which increases forward
flow & finally convert VT/VF.

26. 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

27. Opening the airway

28. Summary of Key BLS Components for Adults,
Children and Infants

33. Trained security guards, police , laypersons
knowledgeable in CPR with access to AEDs.

34.  Defibrillation-Cardioversion
 Pharmacotherapy
 Bradyarrhythmic and Asystolic Arrest;
Pulseless Electrical Activity
 Stabilization

35. DEFIBRILLATION-CARDIOVERSION

37.  Amiodarone: Continuous infusion is preferred
 Lidocaine: Particularly after ischemic events
 Procainamide: If other fails
 Propranolol/Esmolol: For polymorphic VT /VT
Storm in conjunction with Magnesium
Sulphate unresponsive to Amiodarone
 Isoproterenol: For post defibrillation
bradycardia

38.  Primary Cardiac Arrest in Acute Myocardial
Infarction(free of hemodynamic dysfunction):
Urgent intervention
 Secondary Cardiac Arrest in Acute Myocardial
Infarction(with hemodynamic instability):
Aggressive hemodynamic, anti ischemic, anti arrhythmic
measures.
 Cardiac Arrest Among in-Hospital Patients with Non
cardiac Abnormalities:
Withdrawal of offending drugs, correction of
electrolytes, acidosis & hypoxia.

39.  The goals of the workup are to identify the specific causative
and triggering factors of the cardiac arrest, to clarify the
functional status of the patient's cardiovascular system, and to
establish long-term therapeutic strategies-
General Care-
 CABG Patch trial revealed no mortality benefit of ICD after
revascularization & indications limited to generally accepted
indication for angioplasty or surgery
 Cardiac arrest survivors a significant improvement in long-
term outcome observed who had received beta blockers.
 MRFIT suggested a higher mortality rate in the special
intervention group, related to diuretic use and K+ depletion
 Various pharmacologic strategies (ACEI,β-blocker etc) provide
SCD benefit in conjunction with total mortality benefit

40. Prevention of Cardiac
Arrest and Sudden
Cardiac Death

41. A. Anti arrhythmic Drugs
B. Therapy Guided by Programmed Electrical
Stimulation
C. Surgical Intervention Strategies
D. Catheter Ablation Therapy
E. Implantable Defibrillators

42.  Historically, assumption that a high frequency of ambient ventricular
arrhythmias constituted triggering mechanism for lethal arrhythmias and
suppression by anti arrhythmic drugs was protective.
 Ambient arrhythmia suppression and empiric anti arrhythmic drug
therapy enjoyed a short period of popularity as a strategy for reduction
of risk among VT/VF survivors
Results of CAST demonstrated certain class I anti
arrhythmic drugs are neutral or harmful
Secondary analysis of a small number of events ,combination of
amiodarone and beta blocker in the post–MI patient provides greater
benefit from subgroup analysis of the EMIAT and CAMIAT Study
another study reinforced the benefit of beta blockers
for the specific prevention of SCD in unselected post–MI
patients.

43.  The use of programmed electrical stimulation to identify
benefit on the basis of suppression of inducibility by an anti
arrhythmic drug gained popularity for evaluation of long-term
therapy among survivors of out-of-hospital cardiac arrest.
 Nonetheless, most studies have demonstrated limitations
based on observations that a relatively small fraction of cardiac
arrest survivors had inducible arrhythmias.
 Drug suppression of inducibility during electrophysiologic
testing as an endpoint for secondary prevention of SCD/
primary prevention in high-risk post–myocardial infarction
patients has yielded to the benefits of ICD therapy in most
subgroups

44.  Intraoperative map-guided cryoablation may
be used for patients who have –
inducible, hemodynamically stable sustained
monomorphic VT during electrophysiologic
testing
and have suitable ventricular and coronary
artery anatomy amenable to catheter ablation.
 It can be used as adjunctive therapy for ICD
recipients whose arrhythmia burden requires
frequent shocks.

45.  Catheter ablation techniques to treat VT most
successful for the benign focal tachycardias
that originate in the right ventricle or left side
of the IVS
 VT caused by bundle branch reentrant
mechanisms, ablation of the right bundle
branch to interrupt the reentrant cycle
 catheter ablation techniques are not used for
the treatment of higher risk ventricular
tachyarrhythmias or for definitive therapy

46. SECONDARY PREVENTION BY ICD

49. A. LVEF ≤ 35%
Prior AMI≥ 40 days
NYHA class II- III
B. LVEF ≤ 30%
Prior AMI ≥40 days
NYHA class I
C. LVEF ≤ 40%
Prior AMI
Inducible VT/VF at EP study
NSVT

50. ICD Indications in Genetic Disorders Associated with Sudden Cardiac Death Risk

51.  Can the young of SCD be the donor of
heart transplantation ?
Answer: NO

52.  The vast majority of cases of SCD are due to ventricular
arrhythmias
 The causes of SCD is different in different age groups
 The most effective strategy for prevention of SCD is
implantable cardioverter defibrillator (ICD)
 Strictly speaking, most victims of SCD can not be the donor of
heart transplantation