Sudden cardiac death

1. SUDDEN CARDIAC DEATH
Chairperson Dr Praveen Kusubi
Student Dr Ibin Shah

2. Definition
• SCD 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
• Preexisting heart disease may or may not have been known to be
present, but the time and mode of death are unexpected

4. Risk factors
• Age. The incidence of sudden death has two peak ages: within the
first year of life (including sudden infant death syndrome and
between 45 and 75 years of age.
• Race higher risk for cardiac arrest and SCD in blacks than in whites
• Sex. SCD syndrome has a large preponderance in men relative to
women during the young adult and early middle-age years

5. • Hereditary

6. • Lifestyle Factors
1.Smokers have a two fold to threefold increase in risk for sudden
death
2. Obesity
3. 17-fold relative increase in SCD associated with vigorous exercise as
opposed to lower level activity or inactive states
habitual vigorous exercise reduces the risk

7. • Left Ventricular Ejection Fraction in Chronic Ischemic Heart Disease
Ejection fraction of 30% or lower is the single most powerful
independent predictor of SCD
• Ventricular Arrhythmias in Chronic Ischemic Heart Disease
Exercise-induced PVCs and short runs of nonsustained VT

8. CAUSES OF SUDDEN CARDIAC DEATH
• 1 Atherosclerotic Coronary Artery Disease
• 2. Nonatherosclerotic Coronary Artery Abnormalities
Anomalous Origin of Coronary Arteries from the Wrong Sinus of
Valsalva.
Embolism to the Coronary Arteries.

9. Coronary Arteritis.- Kawasaki disease , polyarteritis nodosa ,syphilitic
aortitis
Mechanical Obstruction of Coronary Arteries. –Coronary artery
dissection, prolapse of myxomatous polyps, dissection or rupture of a
sinus of Valsalva aneurysm
Deep myocardial bridges over coronary arteries- common in
association with hypertrophic cardiomyopathy

10. Coronary artery spasm.
3.Ventricular Hypertrophy and Hypertrophic Cardiomyopathy
1. Left ventricular hypertrophy is an independent risk factor for SCD -
hypertensive heart disease with or without atherosclerosis,
2. valvular heart disease,
3. obstructive and nonobstructive hypertrophic cardiomyopathy
4. ,primary pulmonary hypertension with right ventricular hypertrophy,
5. and advanced right ventricular overload secondary to congenital heart
disease.

11. 4. Acute Heart Failure
massive acute myocardial infarction
, acute myocarditis,
acute alcoholic cardiac dysfunction
, acute pulmonary edema
 massive pulmonary embolism,
mechanical disruption of intracardiac structures secondary to
infarction or infection

12. • 5 .Electrophysiologic Abnormalities
• Long QT syndrome
• Short QT syndrome
• Brugada stndrome
• Catecholaminergic Polymorphic Ventricular Tachycardia.
• Central Nervous System Influences

16. PATHOLOGY
• More than 80% of SCD victims have pathologic findings of CHD
• 70–75% of males who die suddenly have preexisting healed MIs,
• whereas only 20–30% have recent acute MIs
• Transient ischemia Is the mechanism of onset.

17. CLINICAL FEATURES OF PATIENTS
WITH CARDIAC ARREST
• Prodromal Symptoms
chest pain,
dyspnea,
 weakness or fatigue,
 palpitations,
syncope,

19. • Onset of the Terminal Event
Increasing heart rate and advancing grades of ventricular ectopy are
common antecedents of VF.
Alterations in autonomic nervous system activity

20. • Cardiac Arrest
most common electrical mechanism is VF, followed by asystole or PEA
and pulseless VT
 Mechanical mechanisms include
rupture of the ventricle, cardiac tamponade, acute mechanical
obstruction to flow, and acute disruption of a major blood vessel

21. • Progression to Biologic Death
• The onset of irreversible brain damage usually begins within 4 to 6
minutes after loss of cerebral circulation
• Death is biologically, legally, and literally an absolute and irreversible
event

22. MANAGEMENT OF CARDIAC ARREST
• The response to cardiac arrest is driven by two urgent principles
• : (1) maintenance of continuous artificial cardiopulmonary support
until return of spontaneous circulation has been achieved
• (2) restoration of spontaneous circulation as quickly as possible.

23. • Five elements to achieve this
• (1) initial assessment and 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.

24. • Initial Assessment and Basic Life Support
• The first action must be confirmation of a cardiac arrest.
• response to voice, observation for respiratory movements and skin
color, and simultaneous palpation of major arteries for the presence
or absence of pulse

25. • Chest Thump
• The thumpversion technique involves one or two blows delivered
firmly to the junction of the middle and lower thirds of the sternum
from a height of 8 to 10 inches.
• it is recommended to use precordial thumps as a life support
technique only when monitoring and defibrillation are available

26. • Basic Life Support—The Initial Steps in Cardiopulmonary
Resuscitation
• Goal of this activity is to maintain viability of the central nervous
system, heart, and other vital organs until definitive return of
spontaneous circulation can be achieved

27. • Circulation.
• The palm of one hand is placed over the lower half of the sternum
and the heel of the other rests on the dorsum of the lower part of the
hand.
• The sternum is then depressed, with the resuscitator’s arms straight
at the elbows to provide a less tiring and more forceful fulcrum at the
junction of the shoulders and back
• sufficient force is applied to depress the sternum at least 2 inches (>5
cm), with abrupt relaxation, and the cycle is carried out at a rateof
about 100 compressions/min

29. • For single responders to victims from infancy through adulthood and
for adults responded to by two rescuers, a compression-
ventilationratio of 30:2 is recommended
• Two -rescuer CPR in infants and children,compression-ventilation
ratio is 15:2

30. • Airway.
• Clearing of the airway includes tilting the head backward and lifting
the chin, in addition to exploring the airway forbforeign bodies,
including dentures, and removing them

31. Heimlich maneuver

32. • Breathing.
• mouth-to-mouth resuscitation is initiated if no specific rescue
equipment is available
• Intubation is the preferred procedure

33. • Advanced Cardiac Life Support
• The general goals of advanced life support are to restore cardiac
rhythm to one that is hemodynamically effective, to optimize
ventilation, and to maintain and support the restored circulation
• A short period of closed-chest cardiac compression 60-90 sec
immediately before defibrillation enhances the probability of survival

34. • Intubate the patient and start oxygenation
• Establish Intravenous line

35. • Ecg patterns in cardiac arrest

39. Defibrillation-Cardioversion
• VF or VT that is pulseless and/or accompanied by loss of
consciousness is recognized on a monitor or by telemetry,
defibrillation should be carried out immediately
• monophasic devices 360 J initially
• Biphasic devices 120 to 200 J
• Failure of the initial shock to provide an effective rhythm is a poor
prognostic sign.

41. • Failure of a single adequate shock to restore a pulse should
be followed by continued CPR and a second shock delivered
after five cycles of CPR.
• If cardiac arrest still persists Epinephrine 1mg i.v followed by
repeated defibrillation attempts at 360 J (monophasic) or
200 J or higher (biphasic).

42. • Meanwhile secure airway and maintain ventilation
• Correct electrolyte imbalances and acidosis if present
• Sodium bicarbonate( 1meq /kg ) is recommended for circumstances
of known or suspected pre-existing bicarbonate-responsive causes of
acidosis, certain drug overdoses, prolonged resuscitation

43. Pharmacotherapy
• For patients who continue to have persistent or recurrent VT or VF
despite direct-current cardioversion after epinephrine
• Electrical stability of the heart may be achieved by the intravenous
administration of antiarrhythmic agents
• Amiodarone is the drug of choice (300mg bolus, second dose150 mg ,
followed by 1 mg/min for up to 6 h and 0.5 mg/min thereafter)
• If amidarone fails lidocaine is the second choice ( 1mg/kg)

44. • If acute hyperkalemia is the triggering event for resistant VF 10%
calcium gluconate will be helpful
For resistant forms of polymorphic VT or torsades de pointes, rapid
monomorphic VT or ventricular flutter (rate ≥260/min), or resistant VF
may respond to intravenous beta blocker therapy or intravenous
magnesium sulfate.

46. Bradyarrhythmic and Asystolic Arrest;
Pulseless Electrical Activity
• When a person develops this form of cardiac arrest we should focus
on establishing cardiorespiratory status i.e., continue CPR, intubate,
and establish intravenous access

47. • Possible reversible causes
• Hypovolemia
• hypoxia
• cardiac tamponade
• tension pneumothorax
• preexisting acidosis
• drug overdose
• hypothermia
• hyperkalemia

48. • Epinephrine 1mg i.v is commonly used in an attempt to elicit
spontaneous electrical activity or to increase the rate of a
bradycardia.
• Sodium bicarbonate, 1 mEq/kg, may be tried for known or strongly
suspected preexisting hyperkalemia or bicarbonate-responsive
acidosis

51. • Stabilization of Cardiac Rhythm after Initial Return of
Spontaneous Circulation
• If frequent PVC and VT persist – use antiarrythmic drugs
• First choice is amiodarone
• In arrythmia due to acute ischemic events lidocaine is
preferred
• For recurrent episodes of polymorphic VT unresponsive to
amiodarone , use magnesium sulphate

53. Post cardiac arrest syndrome and post
resuscitation care
• The four components of post-cardiac arrest syndrome include
• brain injury
• myocardial dysfunction
• systemic ischemia/reperfusion responses
• and control of persistent precipitating factor
• The goal is to maintain a stable electrical, hemodynamic, and central
nervous system status

54. • Post resuscitation care
• Mild therapeutic hypothermia is indicated for resuscitated cardiac
arrest victims who are hemodynamically stable, but remain comatose
• Core body temperature is decreased to 32–34°C, by several available
techniques as soon as practical after resuscitation and maintained for
a minimum of 12–24 h.
• It reduces metabolic demands and cerebral edema, and improves
probability of survival with better neurologic outcome.

55. Primary prevention of SCD in patients with
ischemic heart disease

57. • Indications for Implantable Cardioverter-Defibrillators in
Genetic Disorders Associated with Risk for Sudden Cardiac
Death

59. References
• 1. 2017 AHA/ACC/HRS Guideline for Management of Patients With
Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death
• 2 .Braunwald’s heart disease
• 3. Harrisons principles of internal medicine
• 4. Paul l marino ICU Book

60. •THANK YOU