SUDDEN CARDIAC DEATH

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SUDDEN CARDIAC DEATH

• Yuanxiu Chen, MD, Ph.D
• DEPT. OF CARDIOLOGY
• RENMIN HOSPITAL
• WUHAN UNIVERSITY

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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

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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

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 Pathophysiological Mechanism??????

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

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

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• Sustained ventricular tachycardia lt2
• ?????

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

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

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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

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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

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

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ETIOLOGY( ???)

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

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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

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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

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

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• 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?

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• 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 ??????

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

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• Smoking ??
• risk raises 2-6 times

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

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• Body weight ?? (Obesity??)

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

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Cardiomyopathies

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

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Valvular heart disease

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

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Inflammatory myocardial disease

• Myocarditis ???
• several kind of arrhythmia might develop
• atrioventricular block

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Congenital heart disease ??????

• Arrhythmia
• Hemodynamic changes ???????

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Long QT syndrome

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

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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

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Wolff-Parkinson-white syndrom

• Accessory AV pathway ????
• Also called preexciteation syndrome

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

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• Atrail fibrillation ----ventricular fibrillation

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Idiopathic ventricular fibrillation?????
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Drugs and other toxic agents Proarrhythmia
???????

• Antiarrhythmic agents
• quinidine(???)
• flecainide (???)
• encainide(???)
• CAST(Cardiac Arrhythmia Suppression Trail)
• Evidence Based Medicine

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Evidence Based Medicine????

• Multicenter
• Randomized
• Double blind
• Placebo controlled

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Cocaine and alcohol ??????

• Drug abuseCocaine Marihuana(??)
• Alcoholic excessive drinking

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Electrolyte abnormalities ????? 

• Hypokalemia ????
• Magnesium deficiency ??
• Increase in intracellular calcium

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Pathology of SCD Caused by CHD

• The coronary arteries
• Extensive atherosclorosis
• Acute atherothrombosis
• Coronary arteries spasm

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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.
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• Atherothrombosis is the underlying condition that
  results in events leading to myocardial
  infarction, ischemic stroke, and vascular death

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• Atherothrombosis

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The Development of Atherothrombosis a
Generalized and Progressive Process
Adapted from Drouet L. Cerebrovasc Dis 2002
13(suppl 1) 16.
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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.
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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.
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• 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

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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

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

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• 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

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• 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

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

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• 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(???)

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

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

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• 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

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

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How to?

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

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Clinical presentation

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

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OMENOUS SYMPTOMS????

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

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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

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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

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Biological death

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

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

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

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• Asystolic arrest or bradyarrhythmias biological
  death occurs shortly

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MANAGEMENT OF CARDIAC ARREST???????

• Outside hospital
• Community emergency system important??????

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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

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BASIC LIFE SUPPORTcardiac pulmonary
resuscitation(????)

• Airway
• Breathing
• Circulation
• Defibrillation

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

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

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

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• 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

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• 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.)

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

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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

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

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Treatment of Ventricular fibrillation?????

• Witnessed arrest Unwitnessed
  arrestCheck pulseif no pulse check
  pulseif no
• 
  pulsePrecordial thump Check
  pulseif no pulseCPR until a defibrillator is
  availableCheck monitor for rhythmif Vf or VT
  Defibrillate, 200JDefibrillate, up to 360JCPR
  if no pulse

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• Establish IV accessEpinephrine,
  110,000,0.5-1mg iv PUSHIntubate, if
  possibleDefibrillate with up to 360JLidocaine,
  1mg/kg IV PUSHDefibrillate with up to
  360JBretylium, 5mg/kg IV PUSH(Consider
  bicarbonate)Defibrillate with up to
  360JBretylium, 10mg/kg IV PUSHDefibrillate
  with up to 360JRepeated lidocaine or
  bretyliumDefibrillate with up to 360J

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• MENAGEMENT FOR ASYSTOLEIf rhythm is unclear
  and possibly ventricular Fibrillation,
  defibrillate as for ventricular fibrillation.If
  asystole is presentContinue CPREstablish IV
  accessEpinephrine,110,000, 0.5-1mg IV
  PUSHIntubate when possibleAtropine, 1.0mg IV
  PUSH(repeated in 5 min)(Consider
  bicarbonate)Consider pacing

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• MANEGEMENT FOR ELECTRO-MECHANICAL
  DISSOCIATION
• (Pulseless electrical activity??????)
• Continue CPREstablish IV accessEpinephrine,
  110,000,0.5-1.0mg IV PUSHIntubate when
  possibleConsider bicarbonateConsider
  hypovolemia????, cardiac tamponade????, tension
  pneumothorax?????, hypoxemia????,acidosis???,pulm
  onary embolism???

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Some advance in CPR

• Amiodarone(???)or lidocaine
• Intubation(??) or mask(??)

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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

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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

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Prevention

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

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Medicine

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

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• 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

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ICD

• Implantable cardioverter and difibrillator

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?????????
602 AM
605 AM
607 AM
611 AM

• Source After Josephson, ME

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ICD???????

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

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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

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???????A real case

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

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2001?6?30?(???) 800amDick Cheney?????????,????
??????????
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ICD?? ??? GEM III
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??????1??Dick Cheney???????????,??300pm????,???
???
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2001?7?2?(???)??????????????
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PTCAStent

• Percutaneous transluminal coronary angioplasty
• Percutaneous intracoronary stent implantation

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?????????
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??????
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?????,????
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??????????????
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Question

• What is SCD?
• Whats the major cause of SCD?
• Whats the pathophysiological mechanism of SCD?
• What is CPR? How to perform CPR?

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THANK YOU !