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SUDDEN CARDIAC DEATH

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SUDDEN CARDIAC DEATH Yuanxiu Chen, MD, Ph.D DEPT. OF CARDIOLOGY RENMIN HOSPITAL WUHAN UNIVERSITY DEFINITION Sudden cardiac death unexpected natural death due to a ... – PowerPoint PPT presentation

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Title: SUDDEN CARDIAC DEATH


1
SUDDEN CARDIAC DEATH
  • Yuanxiu Chen, MD, Ph.D
  • DEPT. OF CARDIOLOGY
  • RENMIN HOSPITAL
  • WUHAN UNIVERSITY

2
DEFINITION
  • Sudden cardiac deathunexpected natural death due
    to a cardiac cause within a short time period
    from the onset of symptoms in a person without
    any prior condition that would appear fatal

3
Key points
  • Time
  • 1 hour (24hours) from the onset
  • Cardiac arrest Discontinuation of blood
    supply to brain
  • Die or survive
  • History of heart disease
  • with or without

4
 Pathophysiological Mechanism ??????
  • Life threaten arrhythmias arising from several
    pathological condition
  • Tachyarrhythmias
  • Bradyarrhythmias or asystolic arrest
  • Pulseless electrical activity,PEA

5
  • Tachyarrhythmias
  • ???????
  • Ventricular fibrillation 70 ????

6
  • Sustained ventricular tachycardia lt2
  • ?????

7
  • Bradyarrhythmias or asystolic arrest
  • ??????? ????
  • Sinus asystole

8
  • Pulseless electrical activity,PEA
  • (???????)
  • Electromechanical dissociation
  • (?????)

9
EPIDEMIOLOGY(????)
  • Incidence ??? 300,000-400,000 yearly in USA
  • Account for gt50 cardiac death
  • In China
  • no accurate figure
  • huge population
  • victims must might be numerous

10
Influence of Age, Race, and Gender
  • AGE ?? The incidence of sudden cardiac death
    increases with age, in both men and women as well
    as whites and nonwhites because of the higher
    prevalence of ischemic heart disease at older age

11
  • RACIAL DIFFERENCES ???? rate of sudden coronary
    death is higher in blacks than in whites
  • GENDER ?? Higher in men than in women

12
ETIOLOGY( ???)
  • The relationship between structure and function
    of the heart in sudden cardiac death Cardiac
    death is related to a
  • lot of heart diseases

13
Coronary Heart Disease ???
  • Account for more than 80 of SCDs in western
    countries
  • First manifestation in 25 of CHD patients
  • LVEFlt30 is a strong predict factor for SCD in
    patients with coronary heart disease
  • Atherosclerosis of multiple coronary arteries is
    the underlying pathophysiologic changes in such
    patients

14
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15
Major Risk factors for CHD ??????????
  • Risk factors of atherosclerosis
  • Not well confirmed, but lots of evidence prove
    that there are some factors might be related to
    CHD
  • Multiple factors work together but at different
    aspects to cause CHD to happen

16
  • Age
  • gt40 years
  • older than 49 years speed up
  • some young people

17
  • Gender
  • more male suffer than female,21
  • female suffer after menopause (????)
  • because of decrease of Estrogens(???) in
  • the circulation, with resulted in a drop of
  • HDL (high density lipoprotein)
  • (Estrogens) provides a protection for women
    against CHD?

18
  • Abnormal in blood lipid ????
  • Hyperlipedamia ????
  • Total cholesterol ????
  • Triglyceride ????
  • Low density lipoprotein LDL ??????
  • Very low density lipoprotein ???????
  • Apoprotein B????B
  • Apoprotein A????A
  • High density lipoprotein ??????

19
  • Hypertension
  • 60-70CHD patients have hypertension
  • 4 times than normal blood pressure pts
  • both SBP and DBP are significant

20
  • Smoking ??
  • risk raises 2-6 times

21
  • Diabetes mellitus ???
  • 2 times danger than the non-diabetes patient

22
  • Body weight ?? (Obesity??)

23
  • Occupation ??
  • Diet ??
  • Heredity ??
  • Others

24
Cardiomyopathies
  • Idiopathic dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Hypertensive cardiomyopathy
  • Arrhythmogenic right ventricular dysplasia
    (????????????)

25
Valvular heart disease
  • Mitral valve prolapse syndrome
  • ????????
  • Other valvular heart diseases
  • Aortic stenosis(??????)

26
Inflammatory myocardial disease
  • Myocarditis ???
  • several kind of arrhythmia might develop
  • atrioventricular block

27
Congenital heart disease ??????
  • Arrhythmia
  • Hemodynamic changes ???????

28
Long QT syndrome
  • Congenital
  • Acquired
  • torsades de points (TDP, ???????)twisting (??) of
    the peaks and troughs of the QRS complexes in
    relation to the baseline

29
Brugada Syndrome
  • Died suddenly during night
  • Young patient without any evidence of heart
    disease
  • Family histroy
  • Elevated ST segment (V1-3) with right bundle
    block
  • Some defect in certain gene

30
Wolff-Parkinson-white syndrom
  • Accessory AV pathway ????
  • Also called preexciteation syndrome

31
  • paroxysmal supraventricular tachycardia
  • ??????????

32
  • Atrail fibrillation ----ventricular fibrillation

33
Idiopathic ventricular fibrillation ?????
34
Drugs and other toxic agents Proarrhythmia
???????
  • Antiarrhythmic agents
  • quinidine(???)
  • flecainide (???)
  • encainide(???)
  • CAST(Cardiac Arrhythmia Suppression Trail)
  • Evidence Based Medicine

35
Evidence Based Medicine ????
  • Multicenter
  • Randomized
  • Double blind
  • Placebo controlled

36
Cocaine and alcohol ??????
  • Drug abuseCocaine Marihuana(??)
  • Alcoholic excessive drinking

37
Electrolyte abnormalities ????? 
  • Hypokalemia ????
  • Magnesium deficiency ??
  • Increase in intracellular calcium

38
Pathology of SCD Caused by CHD
  • The coronary arteries
  • Extensive atherosclorosis
  • Acute atherothrombosis
  • Coronary arteries spasm

39
What is Atherothrombosis?
  • Atherothrombosis is characterized by a sudden
    (unpredictable) atherosclerotic plaque disruption
    (rupture or erosion) leading to platelet
    activation and thrombus formation

Plaque rupture1
Plaque erosion2
1. Falk E et al. Circulation 1995 92 65771. 2.
Arbustini E et al. Heart 1999 82 26972.
40
  • Atherothrombosis is the underlying condition that
    results in events leading to myocardial
    infarction, ischemic stroke, and vascular death

41
  • Atherothrombosis

42
The Development of Atherothrombosis a
Generalized and Progressive Process
Adapted from Drouet L. Cerebrovasc Dis 2002
13(suppl 1) 16.
43
Atherothrombosis and Microcirculation
Plaque rupture
Microvascular obstruction
Embolization
Adapted from Topol EJ, Yadav JS. Circulation
2000 101 57080, and Falk E et al. Circulation
1995 92 65771.
44
Major Clinical Manifestations of Atherothrombosis
Ischemic stroke
Transient ischemic attack
Myocardial infarction
  • Angina
  • Stable
  • Unstable
  • Peripheral arterial
  • disease
  • Intermittent claudication
  • Rest Pain
  • Gangrene
  • Necrosis

Adapted from Drouet L. Cerebrovasc Dis 2002
13(suppl 1) 16.
45
  • The myocardium(of sudden cardiac death by
    autopsy)
  • Healed myocardial infarction is a common finding
    of autopsy in the victims
  • Frequency ranging from 40-70
  • Acute myocardial infarction is about 20

46
Mechanism and Pathophysiology of SCD
  • Mechanism of tachyarrhythmias resulted from
    coronary atherosclorosis is not clear
  • Coronary artery disease caused the blood flow to
    myocardium decrease, which resulted in metabolic
    change and electrophysiological(???) instability,
    both could lead to ventricular fibrillation

47
  • Long term left ventricle overload (????)and
    ischemic injury could cause the disturbance of
    cellular electrophysiology, resulted in
    ventricular fibrillation

48
  • At the level of myocyte, acute ischemia cause
  • Loss of integrity of cell membranes
  • Efflux of K
  • Influx of Ca2
  • Acidosis
  • Reduction of transmembrane resting potentials
  • Alpha- and/or beta-adrenocepter and autonomous
    never activity alteration
  • As the result, the electrical instability
    increased

49
  • Ischemia increases the dispersion (???)of
    repolarization(??) between the normal and
    diseased tissue, induces afterpolarization(???)
    as triggering response for Ca2-dependent
    arrhythmia, finally leads to ventricular
    fibrillation

50
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51
  • SCD caused by bradyarrhythmias and asystolic
    arrest often appeared in severely diseased hearts
  • Probably represent diffuse(??)involvement of
    subendocardial Purkinje fibers

52
  • Systemic influences that increase extracellular
    K concentration including
  • Acidosis
  • Shock
  • renal failure
  • Trauma
  • Hypoxia
  • Result in partial depolarization of cells in
    His-Purkinje system, with a decrease in the
    slope(??) of spontaneous phase 4 depolarization
    and ultimate loss of automaticity(???)

53
  • Long time asystolic arrest may degenerate to
    ventricular fibrillation or persistent asystole

54
  • Pulseless electrical activity (PEA)
  • Electromechanical dissociation(EMD)
  • Could be separated into
  • Primary form
  • Secondary form

55
  • Primary form
  • Failure of electromechanical coupling
  • Usually occurs as an end-stage event of advanced
    heart disease, acute ischemic events or after
    electrical resuscitation from a prolonged cardiac
    arrest

56
  • Secondary form
  • Result from abrupt cessation of cardiac venous
    return(??????)
  • Massive pulmonary embolism(?????)
  • Acute mulfunction of prosthetic valves(????????)
  • Cardiac tamponade from hemopericardium????

57
How to?
  • Pulseless electrical activity (PEA) is related to
    metabolic disorder of intracellular
    Ca2,intracellular acidosis and deficiency of ATP

58
Clinical presentation
  • Prodromes ( ????)
  • Onset of terminal events (??????)
  • Cardiac arrest (????)
  • Biological death (?????)
  • ---- Differ greatly from one to another

59
OMENOUS SYMPTOMS????
  • Chest pain ??
  • Dyspnea ????
  • Fatigue ??
  • Palpitation ??
  • Some patients may not have prodromes and cardiac
    arrest might be the first manifestation

60
Terminal events
  • Beginning of cardiac arrest
  • Due to the abrupt change of cardiovascular
    function
  • Duration within 1 hour
  • Heart rate increase, ventricular ectopic beat,
    ventricular tachycardia might develop

61
Cardiac arrest
  • Abrupt loss of consciousness ????
  • Cardiac arrest cause the blood supply to
    tbe brain drop abruptly
  • Pulse at carotid artery (???) or femoral artery
    (???) disappeared
  • Breath stoped (????)
  • Heart sound disappeared (????)
  • Paleness of the skin (????)
  • Observation should be done rapidly
  • so that resuscitation (??) could
  • begin in short time

62
Biological death
  • Time from cardiac death to biological death
    depends on
  • Underlying disease
  • Time from SCD to the beginning CPR

63
  • Irreversible brain injure occurs 4-6 min after
    ventricular fibrillation biological death
    gradually

64
  • Time from VT to biological death longer, VT
    might turn to VF or asystolic arrest (????) if
    not terminated automatically of by
    therapy(medical, electrical)

65
  • Asystolic arrest or bradyarrhythmias biological
    death occurs shortly

66
MANAGEMENT OF CARDIAC ARREST ???????
  • Outside hospital
  • Community emergency system important??????

67
TRY FOLLOWING MEARSURES IMMEDIATELY
  • THUMPVERSION(????)
  • using fist (??) to hit the victim at
  • the middle-lower part of the breast bone
    (????????)
  • COUGH-VERSION (????)
  • increasing of intra-thoracic pressure
    (????)might stop the tachyarrhythmias
  • KEEP THE AIRWAY OPEN

68
BASIC LIFE SUPPORT cardiac pulmonary
resuscitation(????)
  • Airway
  • Breathing
  • Circulation
  • Defibrillation

69
  • Airway
  • head tilt chin lift (????)
  • if trauma is present, use jaw thrust
  • (??????,?????)

70
  • Breathing
  • look, listen, and feel for no more than 10
    seconds
  • mouth-to-mouth artificial breath ????
  • 10-12 breaths/min
  • intubation if possible
  • (better)

71
  • Circulation
  • Check for sign of circulation (breathing, cough,
    movement) including pulse for no more than 10
    seconds

72
  • If signs of circulation/pulse present but no
    breathing, provide rescue breathing
  • If signs of circulation/pulse absent, begin chest
    compression interposed with breaths
  • If signs of circulation/pulse present but lt 60bpm
    in child or infant with poor perfusion, begin
    chest compression

73
  • Compression landmarks
  • lower half of sternum
  • Compression method
  • heel of one hand, other hand on top
  • Compression depth
  • 11/2 to 2 inches
  • Compression rate
  • approximate 100/min
  • Compression/ventilation ratio
  • 152(single rescuer or two rescuers.)

74
  • Defibrillation
  • Using automated external defibrillators is
    now considered an integral part of adult basic
    life support by healthcare provider
  • VT synchronized
  • VF non-synchronized

75
ADVANCED LIFE SUPPORT
  • IV ACCESS Drug therapy
  • anti-arrhythmic agents
  • tachycardia
  • bradycardia
  • MORNITORING AFTER CPR
  • PREVENTION AND TREADMENT OF
  • ENCEPHALO edema
  • prevention and treatment of renal failure

76
  • Cardiopulmonary resuscitation(CPR) Airway ??
    Breath ???? Circulation ??(Chest compression
    ???) Defibrillation,Drugs ??,?? Electrolyte
    ??? Fluids ?? Gas ?? 

77
Treatment of Ventricular fibrillation?????
  • Witnessed arrest Unwitnessed
    arrest Check pulseif no pulse check
    pulseif no

  • pulse Precordial thump Check
    pulseif no pulse CPR until a defibrillator is
    available Check monitor for rhythmif Vf or VT
    Defibrillate, 200J Defibrillate, up to 360J CPR
    if no pulse

78
  • Establish IV access Epinephrine,
    110,000,0.5-1mg iv PUSH Intubate, if
    possible Defibrillate with up to 360J Lidocaine,
    1mg/kg IV PUSH Defibrillate with up to
    360J Bretylium, 5mg/kg IV PUSH (Consider
    bicarbonate) Defibrillate with up to
    360J Bretylium, 10mg/kg IV PUSH Defibrillate
    with up to 360J Repeated lidocaine or
    bretylium Defibrillate with up to 360J

79
  • MENAGEMENT FOR ASYSTOLE If rhythm is unclear
    and possibly ventricular Fibrillation,
    defibrillate as for ventricular fibrillation. If
    asystole is present Continue CPR Establish IV
    access Epinephrine,110,000, 0.5-1mg IV
    PUSH Intubate when possible Atropine, 1.0mg IV
    PUSH(repeated in 5 min) (Consider
    bicarbonate) Consider pacing

80
  
  • MANEGEMENT FOR ELECTRO-MECHANICAL
    DISSOCIATION
  • (Pulseless electrical activity??????)
  • Continue CPR Establish IV access Epinephrine,
    110,000,0.5-1.0mg IV PUSH Intubate when
    possible Consider bicarbonate Consider
    hypovolemia????, cardiac tamponade????, tension
    pneumothorax?????, hypoxemia????,acidosis???,pulm
    onary embolism???

81
Some advance in CPR
  • Amiodarone(???)or lidocaine
  • Intubation(??) or mask(??)

82
Monitoring after CPR
  • 48-72h monitoring in ICU (CCU)after CPR
  • Treatment of original disease leading to SCD
  • Maintenance of effective circulation and
    respiration
  • Prevention of recur of SCD
  • Balance of fluid,electrolyte and acid-base
  • Prevention of cerebral edema and acute renal
    failure

83
Prognosis??
  • Associated with the cause
  • Structural heart diseasepoor
  • Nonstructural heart disease depends
  • resulting from severe illness such as
    cancer,
  • multiple organs failure(?????)poor
  • arising from intoxication??, Electrolyte
  • abnormalities(?????), etc might be
    better

84
Prevention
  • Medicine
  • RFCA
  • Implantable cardioversor defibrillator (ICD)
  • Revascularization (PTCA,Surgery )

85
Medicine
  • Prevention of coronary heart disease
  • Antihypertensive agents
  • Lipid lowering medicine
  • Blood sugar lowering madicine
  • Aspirin
  • Antiarrhythmic agents

86
  • Antiarrhythmic agents
  • Flecainide,encainide,sotalol have been proven to
    increase the death rate in ischemic heart disease
  • ß-blocker Metolol is said to be benefit for
    patients with myocardial infarction in lowering
    arrhythmic mortality and total mortality
  • Amiodarone lowering arrhythmic mortality

87
ICD
  • Implantable cardioverter and difibrillator

88
?????????
602 AM
605 AM
607 AM
611 AM
  • Source After Josephson, ME

89
ICD???????
  • ?????? Save patients life
  • ????? decrease the mortality
  • ?????? Improve the quality of life
  • ???????? worry
  • ??VT???? expense
  • ??????? side effect
  • ????-?????,?????safety

90
ICD????Main function
  1. ???????Anti-bradycardia pacing
  2. ??????????Recognizing VT/VF
  3. VF??????? Difibrillation
  4. VT???ATP(Anti-tachycardia pacing)?????Synchronize
    d cardioversion)
  5. ???????????Storage of events

91
91
92
???????A real case
  • 60?,??
  • 1978??1??????
  • 1984??2??????
  • 1988??3???????,??????????
  • 2000?11?,?4?????????,??PTCA??
  • 2001?3?,??,????PTCA??,??????????
  • 2001?6?,Holter????2 s??135bpm ??????

93
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94
2001?6?30?(???) 800am Dick Cheney ?????????,????
??????????
95
ICD?? ??? GEM III
96
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97
??????1?? Dick Cheney???????????,??300pm????,???
???
98
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99
(No Transcript)
100
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101
2001?7?2?(???)?? ????????????
102
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103
PTCAStent
  • Percutaneous transluminal coronary angioplasty
  • Percutaneous intracoronary stent implantation

104
(No Transcript)
105
?????????
106
??????
107
?????,????
108
??????????????
109
Question
  • What is SCD?
  • Whats the major cause of SCD?
  • Whats the pathophysiological mechanism of SCD?
  • What is CPR? How to perform CPR?

110
THANK YOU !
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