Sudden Cardiac Death - PowerPoint PPT Presentation

1 / 44
About This Presentation
Title:

Sudden Cardiac Death

Description:

Sudden cardiac death (SCD) is a syndrome defined by its clinical presentation ... of patients have idiopathic ventricular fibrillation ('primary electrical disease' ... – PowerPoint PPT presentation

Number of Views:296
Avg rating:3.0/5.0
Slides: 45
Provided by: suhailqadi
Category:

less

Transcript and Presenter's Notes

Title: Sudden Cardiac Death


1
Sudden Cardiac Death
  • Suhail Allaqaband, MD
  • University of Wisconsin-Milwaukee Clinical Campus
  • Sinai Samaritan Medical center

2
  • Sudden cardiac death (SCD) is a syndrome defined
    by its clinical presentation rather than by a
    discrete pathophysiology
  • The World Health Organization definition has been
    widely accepted sudden collapse occurring within
    one hour of symptoms
  • However, as the name implies, SCD is
    instantaneous and most individuals become
    unconscious within seconds to minutes as a result
    of insufficient cerebral blood
  • Underlying heart disease is present the vast
    majority of patients with SCD

3
Sudden Cardiac Death
  • Incidence
  • 400,000 - 500,000/year in U.S.
  • Only 2 - 15 reach the hospital
  • Half of these die before discharge
  • High recurrence rate

4
Underlying Arrhythmia of Sudden Death
Primary VF 8
Torsades de Pointes 13
VT 62
Bradycardia 17
5
ARRHYTHMIC MECHANISM OF SUDDEN CARDIAC DEATH
  • In approximately 80 percent of cases, a sustained
    ventricular arrhythmia is preceded by an increase
    in ventricular ectopy
  • These spontaneous arrhythmias are present for a
    variable period of time prior to the development
    of a sustained ventricular tachyarrhythmia
  • In about one-third of cases, the tachyarrhythmia
    is initiated by an early R on T ventricular
    premature beat in the remaining two-thirds, the
    arrhythmia is initiated by a late cycle VPB

6
ARRHYTHMIC MECHANISM OF SUDDEN CARDIAC DEATH
  • A bradyarrhythmia or asystole is an important but
    less common cause of SCD, being observed in only
    about 10 percent of cases
  • A bradyarrhythmia is more often associated with a
    nonischemic cardiomyopathy

7
ETIOLOGY OF SUDDEN CARDIAC DEATH
  • There are many cardiac and noncardiac causes for
    a sustained ventricular tachyarrhythmia that can
    result in SCD
  • In one study of 809 patients with a cardiac
    arrest, 34 percent had a noncardiac origin, most
    commonly due to trauma, nontraumatic bleeding,
    intoxication, near drowning, or pulmonary
    embolism

8
Causes of Sudden Cardiac Death
  • Nonischemic Heart Disease (cont)
  • myocarditis
  • acute pericardial tamponade
  • acute myocardial rupture
  • Noncardiac Disease
  • sudden infant death syndrome
  • drowning
  • Pickwickian syndrome
  • pulmonary embolism
  • drug-induced
  • airway obstruction
  • no structural heart disease - primary electrical
    disease, chest wall trauma (commotio cordis),
    Brugadas syndrome (right bundle branch block
    and ST segment elevation V1 to V3)
  • Ischemic Heart Disease
  • CAD with MI or angina
  • coronary artery embolism
  • nonathogenic coronary artery disease
  • coronary artery spasm
  • Nonischemic heart disease
  • CAD without MI or angina
  • cardiomyopathy - obstructive, nonobstructive,
    nonischemic
  • valvular heart disease
  • congenital heart disease
  • prolonged QT syndrome
  • preexcitation syndrome
  • complete heart block
  • arrhythmogenic RV dysplasia

9
ETIOLOGY OF SUDDEN CARDIAC DEATH
  • Most patients who experience SCD have an
    underlying cardiac abnormality, particularly
    coronary heart disease
  • The incidence of SCD increases with age in both
    men and women
  • However, at any level of multivariate risk, women
    are less vulnerable to sudden death than men and
    a higher fraction of SCDs in women occur in the
    absence of prior overt coronary heart disease

10
Incidence of Sudden Death Increases with Age
During a 38 years follow-up of subjects in the
Framingham Heart Study, the annual incidence of
sudden death increased with age in both men and
women.However, at each age, the incidence of
sudden death is higher in men than women. (Am
Heart J 1998 136205)
11
ETIOLOGY OF SUDDEN CARDIAC DEATH
  • Symptoms of an acute ischemic episode are
    generally absent, and the collapse is typically
    instantaneous, without any warning
  • Approximately 75 to 80 percent of patients have
    no ECG changes or enzyme abnormalities after
    resuscitation that are suggestive of an acute
    myocardial infarction as a precipitating factor

12
Clinical Substrates Associated with VF Arrest
  • Myocardial ischemia and infarction
  • Acute myocardial infarction is associated with an
    approximate 15 risk of VF within the first 24 to
    48 hours, with the incidence falling to only 3
    percent over the next several days
  • When VF is provoked by an AMI, symptoms of the
    infarction are present for minutes to hours
    before sudden death occurs over 80 percent of VF
    episodes occur within the first 6 hours

13
Clinical Substrates Associated with VF Arrest
  • Congestive heart failure
  • The presence of CHF increases overall mortality
    and the incidence of SCD in both men and women

14
CHF Predict Increased Sudden Death and Overall
Mortality
During a 38 years follow-up of subjects in the
Framingham Heart Study, the presence of CHF
significantly increased sudden death and overall
mortality in both men and women. P lt0.001.
15
Risk of Sudden Death Data from GISSI-2 Trial
1.00
1.00
0.98
0.98
p log-rank 0.002
0.96
0.96
0.94
0.94
Survival
Survival
0.92
0.92
p log-rank 0.0001
0.90
0.90
0.88
0.88
A
B
0.86
0.86
0
30
60
90
120
150
180
0
30
60
90
120
150
180
Days
Days
  • Patients withoutLV Dysfunction

Patients withLV Dysfunction
No PVBs1-10 PVBs/hgt 10 PVBs/h
16
Clinical Substrates Associated with VF Arrest
  • Left ventricular hypertrophy
  • Hypertension with LVH appears to increase the
    risk of SCD
  • In one study, patients with hypertension and LVH
    who died suddenly had less extensive coronary
    disease than normotensives who had SCD
  • These findings suggest that the hypertrophied
    myocardium is more susceptible than normal
    myocardium to the the effects of ischemia

17
Clinical Substrates Associated with VF Arrest
  • Absence of structural heart disease (primary
    electrical disease)
  • Rarely, SCD occurs in patients younger than 40
    years of age who have no evidence of structural
    heart disease
  • However, in approximately 90 percent of these
    cases autopsy reveals evidence of underlying
    heart disease that was unrecognized, including
    myocarditis, hypertrophic cardiomyopathy,
    arrhythmogenic RV dysplasia, sarcoidosis, or
    asymptomatic coronary heart disease
  • The remaining 10 percent of patients have
    idiopathic ventricular fibrillation ("primary
    electrical disease)

18
Clinical Substrates Associated with VF Arrest
  • Brugada's syndrome
  • One interesting subgroup are patients with
    Brugada's syndrome who have a peculiar ECG
    pattern consisting of a RBBB and ST segment
    elevation in V1 to V3
  • One study reported data on 63 such patients, 41
    of whom were diagnosed after an episode of SCD
  • During a 34 month follow-up, a recurrent
    arrhythmic event occurred in 34 percent of
    symptomatic patients and in 27 percent of
    asymptomatic patients

19
Clinical Substrates Associated with VF Arrest
  • Commotio cordis
  • Sudden death has been described in young athletes
    who have been struck in the precordium with a
    projectile object such as a baseball, hockey
    puck, or fist
  • One study described an animal model in which
    low-energy blows to the chest wall delivered
    during repolarization, just before the peak of
    the T wave, produced ventricular fibrillation

20
Clinical Substrates Associated with VF Arrest
  • Family history
  • A family history of myocardial infarction or SCD
    is associated with an increased risk for SCD
  • Genetic abnormality
  • A defect located on chromosome 1p1-1q1, has been
    associated with sudden death
  • Affected individuals have progressive cardiac
    conduction abnormalities and symptomatic sinus
    bradycardia, requiring pacemaker therapy
  • Sudden death generally occurs beyond the age of
    30 and is not prevented by pacemaker therapy

21
OUTCOME OF RESUSCITATION
  • When the initial rhythm is asystole, the
    likelihood of successful resuscitation is low
    and, when performed out of hospital, less than 10
    percent survive to hospitalization
  • The outcome is much better when the initial
    rhythm is a sustained VT (65 to 70 survival)
  • Approximately 25 percent of patients with VF
    survive to be discharged in the majority of
    these patients an acute myocardial infarction is
    the underlying mechanism
  • Patients who have SCD due to PEA also have a poor
    outcome

22
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION
  • The only effective way to reestablish organized
    electrical activity and myocardial contraction is
    prompt electrical defibrillation
  • It has been estimated that organ damage becomes
    irreversible after approximately 4 minutes of VF
  • As a result, the longer the duration of the
    cardiac arrest, the lower the likelihood of
    resuscitation or survival even if initial
    resuscitation is successful

23
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION
  • The Seattle Heart Watch program has reported on
    the outcome of patients resuscitated at the scene
    by a bystander trained in CPR compared with CPR
    initiated by emergency medical personnel
  • There was no difference in the percentage of
    patients resuscitated at the scene and admitted
    alive to the hospital (67 versus 61 percent)
  • However, the percentage discharged alive was
    significantly higher among those with
    bystander-initiated CPR (43 versus 22 percent, plt
    0.001)

24
Bystander-initiated CPR Improves Outcome
25
Causes of in-hospital mortality
  • The cause of death in hospital is most often
    noncardiac, usually being due to anoxic
    encephalopathy or to respiratory complications
    from long-term respirator dependence
  • Only about 10 percent of patients die from
    recurrent arrhythmia, while approximately 30
    percent die from a low cardiac output or
    cardiogenic shock

26
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION
  • In addition to later onset of CPR, there are a
    number of other factors that are associated with
    a poor outcome with CPR
  • Cancer or Alzheimer's disease
  • History of gt2 chronic diseases
  • A history of cardiac disease
  • Absence of any vital signs
  • Sepsis
  • An initial rhythm of asystole or PEA
  • CPR lasting gt5 minutes
  • CVA with severe neurologic deficit

27
ACUTE THERAPY FOR THE SCD VICTIM
  • The only effective approach for terminating VF is
    defibrillation using 200 to 400 J of energy
    delivered transthoracically in a nonsynchronized
    fashion
  • The initial success of defibrillation depends
    upon the duration of the arrhythmia and
    promptness of defibrillation
  • When VF has been present for seconds to a few
    minutes, the success rate is high

28
ACUTE THERAPY FOR THE SCD VICTIM
  • Intravenous amiodarone
  • The ARREST trial (Amiodarone in the
    Out-of-hospital Resuscitation of Refractory
    Sustained Ventricular Tachyarrhythmias)
    randomized 504 patients with a cardiac arrest due
    to VF or pulseless VT who were not resuscitated
    after at least three defibrillation shocks to
    intravenous amiodarone (300 mg) or placebo
  • Survival to hospitalization was greater in the
    amiodarone group (44 versus 35 percent)
  • Time to therapy with the study drug was an
    independent predictor of survival to hospital
    faster treatment was associated with a better
    outcome
  • More than 50 percent of patients who survived to
    discharge had no neurological impairment

29
Evaluation of the survivor of SCD
  • The evaluation begins immediately after
    resuscitation
  • The first concern is to establish any obvious
    provoking factors that may have led to the event
    and which need to be corrected so as to prevent
    an immediate recurrence
  • The patient or/and family should be questioned
    about previous diagnoses of heart disease the
    use of any medication, especially antiarrhythmic
    agents, diuretics, or digoxin and antecedent
    symptoms

30
PROVOKING FACTORS
  • Electrolyte disturbances
  • Any reversible metabolic abnormalities should be
    identified and corrected, particularly
    hypokalemia and hypomagnesemia which may
    predispose to ventricular tachyarrhythmias
  • Antiarrhythmic drugs
  • Whenever possible, antiarrhythmic drugs should be
    discontinued prior to any diagnostic studies

31
PROVOKING FACTORS
  • Use of an illicit drug such as cocaine can
    directly cause arrhythmia or produce coronary
    artery vasospasm and ischemia
  • A prolonged QT interval which may be acquired
    (due, for example, to a drug or electrolyte
    disturbance) or inherited

32
CARDIAC EVALUATION
  • It is essential that the patient undergo a
    complete cardiac examination to establish the
    nature and extent of underlying heart disease
  • The LV function and coronary anatomy should be
    assessed utilizing physical examination, echo,
    cardiac catheterization, and, if warranted,
    myocardial biopsy
  • Since global LV dysfunction due to myocardial
    stunning may be present as a result of the
    cardiac arrest, baseline evaluation of left
    ventricular function should be performed at least
    48 hours after resuscitation

33
ARRHYTHMIA EVALUATION
  • There are different approaches (termed
    conservative and aggressive) to the evaluation
    and treatment of SCD
  • Ongoing controlled trials may in the future
    provide information as to which of these
    approaches is associated with the best outcome

34
Conservative approach
  • The conservative approach involves a complete
    arrhythmia evaluation to establish at baseline
    the type, frequency, and reproducibility of
    spontaneous ventricular ectopy, and the
    inducibility of a ventricular tachyarrhythmia
  • This involves the use of noninvasive ambulatory
    monitoring for 48 hours, an exercise test, and an
    invasive electrophysiologic study

35
Conservative approach
  • For patients with SCD, in whom sustained
    monomorphic VT is induced at baseline, the use of
    antiarrhythmic agents to prevent the induction of
    sustained VT may be an adequate and effective
    first approach
  • For those patients who have recurrent arrhythmia,
    the ICD could be considered as an additional or
    alternative therapy

36
Aggressive approach
  • The aggressive approach uses the ICD in all
    victims of SCD whose chance of recurrence with
    therapy cannot be accurately predicted
  • High, medium and low risk are all objective,
    since recurrence of ventricular fibrillation is
    often lethal

37
Aggressive approach
  • When using an aggressive approach, the value of
    diagnostic testing is to find conditions that do
    not require ICD insertion, like episodic
    prolonged sinus arrest, severe AV nodal or
    infranodal disease causing intermittent third
    degree AV block, and preexcitation with AF
    leading to VF
  • These and some other arrhythmias should be
    treated with pacemaker, radiofrequency ablation
    or therapies other than ICD

38
Nonpharmacologic therapy in survivors of sudden
cardiac death
  • RADIOFREQUENCY ABLATION
  • There are a small number of sudden death
    survivors in whom sustained monomorphic VT
    appears to be the primary arrhythmia and in whom
    a single, discrete arrhythmogenic focus can be
    localized by electrophysiologic mapping
  • In such patients radiofrequency ablation is an
    option for destroying the fixed anatomic lesion
    responsible for the arrhythmia

39
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR
  • The ICD is a well-established and highly
    effective therapy for patients who have
    experienced SCD
  • While a device does not prevent the arrhythmia,
    it reverses it automatically and promptly when it
    occurs
  • There are many reports showing an impressive
    improvement in expected arrhythmia mortality
    (ranging from one to five percent per year) in
    patients who have received an ICD
  • However, there is still a substantial cardiac
    mortality (approximately 5 to 10 percent per
    year) as a result of progressive CHF

40
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR
  • The ICD would not be expected to reduce death
    from heart failure or non-cardiac causes what it
    may do is shift the cause of death from sudden to
    non-sudden cardiac death
  • As a result, the only appropriate endpoint is
    total mortality which has now been reported in
    three trials, CASH, CIDS, and AVID

41
The Cardiac Arrest Survival in Hamburg (CASH
trial )
  • German prospective randomized trial of ICD versus
    antiarrhythmic drugs
  • In this study, patients were randomized to
    receive an ICD, metoprolol, propafenone, or
    amiodarone
  • In an interim two year analysis, the SCD rate was
    lower with the defibrillator than with amiodarone
    or metoprolol (0 versus 8 percent)
  • However there was no difference in total
    mortality with the defibrillator, metoprolol, or
    amiodarone (12 percent)

42
The Canadian ICD Study (CIDS)
  • 659 patients with VT, VF, or syncope deemed to be
    secondary to arrhythmia were randomized to
    amiodarone or an ICD
  • After a five-year follow up, the total mortality
    with the ICD was reduced compared to amiodarone
    (25 versus 30 percent, p0.072)

43
The Antiarrhythmic Drug Versus Defibrillator
(AVID) trial
  • Enrolled patients with a history of VT,VF, or
    syncope judged to be secondary to arrhythmia
  • Survival benefit was noted in the 507 patients
    receiving the ICD compared to the 509 patients
    receiving sotalol or amiodarone
  • The unadjusted survivals for the ICD versus drug
    groups were 89 versus 82 percent at one year, 82
    versus 75 percent at two years and 75 versus 65
    percent at three years
  • The total cost for the ICD was 27,500 more than
    for drug therapy and the cost for additional year
    of survival was 127,000

44
(No Transcript)
Write a Comment
User Comments (0)
About PowerShow.com