This document summarizes a seminar on the management of cardiac arrest and cardiac arrest survivors. It defines cardiac arrest and discusses mechanisms and causes. It reviews changes to CPR guidelines including a compression to ventilation ratio of 30:2. It discusses factors that affect blood flow during CPR and prognostic factors for poor outcomes. Management strategies are outlined for defibrillation, antiarrhythmic drugs, vasopressors, steroids and extracorporeal CPR. Adjuncts to CPR like oxygen support and monitoring techniques are also summarized.

1. SEMINAR
TOPIC:
Management of Cardiac
Arrest and Cardiac Arrest
Survivors
Moderatedby: Dr. B Dutta
Presentedby: Dr. Swapnil Garde

2. Definition
• “ Abrupt cessation of cardiac mechanical function,
which may be reversible with prompt intervention
but will lead to death in its absence”
Sudden Cardiac Death
Sudden, irreversible cessation of all biologic functions

3. Mechanisms of Cardiac Arrest
• Ventricular fibrillation
• Ventricular tachycardia
• Asystole
• Bradycardia
• Pulseless Electrical Activity
• Mechanical factors.

4. Causes of VF/pVT

5. Presentation
Differences in Clinical Status Immediately before Death in Patients Dying Primarily of
Arrhythmia versus Circulatory Failure
Clinical Status Immediately
Before Death
Arrhythmic Deaths (n = 82) Circulatory Failure Deaths (n
= 59)
Comatose 0/82 (0%) 56/59 (95%)
Standing or actively moving 39/82 (48%) 0/59 (0%)
Terminal arrhythmia
Ventricular fibrillation 15/18 (83%) 3/9 (33%)
Asystole 3/18 (17%) 6/9 (67%)
Duration of terminal illness
<1 h 53/82 (65%) 4/59 (7%)
>24 h 17/82 (21%) 48/59 (81%)
Nature of terminal illness
Acute cardiac events 80/82 (98%) 8/59 (14%)
Noncardiac events 1/82 (1%) 51/59 (86%)

6. • One minute into persistent VF, coronary blood
flow (myocardial perfusion) declines to zero,
and by 4 minutes, carotid blood flow (cerebral
perfusion) is also nil.
• After about 12 minutes, defibrillation for VF is
rarely effective in the absence of chest
compressions.

7. • Although VF in an adult is persuasively
associated with CAD, PEA, and asystole usually
are not. The exception is when they are seen
in the terminal phase of VF arrests.

8. • One has to consider secondary causes of
cardiac arrest when PEA is otherwise the
primary rhythm.

9. • Recognition of Life Extinct (ROLE) guidelines in
England and Wales deem 20 minutes of
asystole, despite advanced resuscitative
measures, as grounds for termination of
resuscitative efforts.
• Even after successful ROSC, more than 60% of
patients do not survive to hospital discharge.

10. Predictors of poor outcomes for
OHCA include
(1) advanced age;
(2) severe comorbidities, including cancer or
stroke;
(3) preexisting cardiac disease or left ventricular
systolic dysfunction;
(4) CPR greater than 5minutes duration;
(5) development of sepsis;
(6) recurrence of arrhythmias;
(7) PEA or asystole on presentation;
(8) persistent coma; and
(9) unwitnessed arrest or lack of bystander CPR

11. MANAGEMENT

13. • The previous sequence of the “ABC” of basic
life support—airway, breathing,compression—
has been changed to “CAB”—compression,
airway, breathing—based on the recognition
that compression alone is the better strategy
because it minimizes interruptions in
perfusion and avoids excessive ventilation

14. 2000 Guidelines 2005 Guidelines
1 Alerting EMS (only
children)
Phone EMS first and then do
CPR
CPR for 2 min and then call
EMS
2 Unwitnessed adult Shock first 200 CC, then shock
3 Rescue breath Take a deep breath Take a normal breath
4 Rescue breath duration 1–2 s <1 s
5 Ventilation rate 12-15/min 8-10/min
6 CC Ratio 15:2 30:2
7 Two-person CPR Switch when fatigued Every 2 min or 5 cycles (150
CC)
8 Defibrillation Three shocks without CC One shock followed by CC
9 Defibrillation energy Three monophasic stacked 360 J monophasic or 150-
200 J biphasic
10 Postdefibrillation Pulse and rhythm analyses Immediate CC
11 Intubated patients Pause CPR to give breaths Give breaths during CC
12 Drug delivery Drug–CPR–shock Drugs not to interrupt CC
13 High-dose epinephrine May be used Not recommended

15. • For single responders to victims from infancy
(excluding newborns) through adulthood and
for adults responded to by two rescuers, a
compression-ventilation ratio of 30:2 is now
recommended.

17. • Of the factors identified as being responsible
for forward flow with chest compression,
perhaps the most important is the
duration between the onset of VF arrest and
initiation of chest compressions. Other
important factors are the technique used for
chest compressions and the patient's chest wall
configuration.
• It is important to remember that even with
optimal chest compressions, total coronary
flow is only around 20% to 40% of pre-
arrest values

18. Management of Cardiac Arrest
• Defibrillation Strategies for Ventricular Fibrillation or Pulseless
Ventricular Tachycardia: Waveform Energy and First-Shock Success.
• Defibrillation Strategies for Ventricular Fibrillation or Pulseless
Ventricular Tachycardia: Energy Dose for Subsequent Shocks.
• Defibrillation Strategies for Ventricular Fibrillation or Pulseless
Ventricular Tachycardia: Single Shocks Versus Stacked Shocks.
• Antiarrhythmic Drugs During and Immediately After Cardiac Arrest.
• Vasopressors in Cardiac Arrest.
• Steroids.
• Prognostication During CPR.
• Overview of Extracorporeal CPR.

21. ADJUNTS TO CPR:
1. OXYGEN SUPPORT
• When supplementary oxygen is available, it
may be reasonable to use the maximal feasible
inspired oxygen concentration during CPR
(Class IIb, LOE C-EO).

22. 2. Physiologic parameters of
monitoring
• Although no clinical study has examined whether
titrating resuscitative efforts to physiologic
parameters during CPR improves outcome, it may
be reasonable to use physiologic parameters
(quantitative waveform capnography, arterial
relaxation diastolic pressure, arterial pressure
monitoring, and central venous oxygen saturation)
when feasible to monitor and optimize CPR
quality, guide vasopressor therapy, and detect
ROSC (Class IIb, LOE C-EO).

23. 3.Ultrasound During Cardiac Arrest
• Ultrasound (cardiac or noncardiac) may be
considered during the management of cardiac
arrest, although its usefulness has not been well
established (Class IIb, LOE C-EO).
• If a qualified sonographer is present and use of
ultrasound does not interfere with the standard
cardiac arrest treatment protocol, then ultrasound
may be considered as an adjunct to standard
patient evaluation (Class IIb, LOE C-EO).

24. Defibrillation Shock
• All published studies support the effectiveness
(consistently in the range of 85%–98%) of biphasic
shocks using 200 J or less for the first shock.
• Defibrillators using the RLB waveform typically
deliver more shock energy than selected, based on
patient impedance.
• For the RLB, a selected energy dose of 120 J
typically provides nearly 150 J for most patients.

25. • Defibrillators (using BTE, RLB, or monophasic
waveforms) are recommended to treat atrial and
ventricular arrhythmias (Class I, LOE B-NR).

26. • Based on their greater success in arrhythmia
termination, defibrillators using biphasic waveforms
(BTE or RLB) are preferred to monophasic defibrillators
for treatment of both atrial and ventricular arrhythmias
(Class IIa, LOE B-R).
• In the absence of conclusive evidence that 1 biphasic
waveform is superior to another in termination of VF, it
is reasonable to use the manufacturer’s recommended
energy dose for the first shock. If this is not known,
defibrillation at the maximal dose may be considered
(Class IIb, LOE C-LD).

27. Defibrillation Strategies for Ventricular Fibrillation
or Pulseless Ventricular Tachycardia: Energy Dose
for Subsequent Shocks
• It is reasonable that selection of fixed versus
escalating energy for subsequent shocks be based
on the specific manufacturer’s instructions (Class
IIa, LOE C-LD).
• If using a manual defibrillator capable of escalating
energies, higher energy for second and subsequent
shocks may be considered (Class IIb, LOE C-LD).

28. Defibrillation Strategies for Ventricular Fibrillation
or Pulseless Ventricular Tachycardia: Single Shocks
Versus Stacked Shocks
• A single-shock strategy (as opposed to stacked
shocks) is reasonable for defibrillation (Class IIa, LOE
B-NR).

29. Antiarrhythmic Drugs During and Immediately
After Cardiac Arrest
• Antiarrhythmic Drugs During and Immediately After
Cardiac Arrest: Antiarrhythmic Therapy for Refractory
VF/pVT Arrest
the principal objective of antiarrhythmic drug therapy in
shock-refractory VF/Pvt is to facilitate the restoration and
maintenance of a spontaneous perfusing rhythm in concert
with the shock termination of VF.
Amiodarone may be considered for VF/pVT that is
unresponsive to CPR, defibrillation, and a vasopressor
therapy (Class IIb, LOE B-R).
Lidocaine may be considered as an alternative to
amiodarone for VF/pVT that is unresponsive to CPR,
defibrillation, and vasopressor therapy (Class IIb, LOE C-LD).

30. The routine use of magnesium for VF/pVT is
not recommended in adult patients (Class
III: No Benefit, LOE B-R).
No antiarrhythmic drug has yet been shown
to increase survival or neurologic outcome
after cardiac arrest due toVF/pVT.

31. Antiarrhythmic Drugs After
Resuscitation
• There is inadequate evidence to support the
routine use of a β-blocker and lidocaine after
cardiac arrest.
• However, the initiation or continuation of an oral
or intravenous β-blocker may be considered early
after hospitalization from cardiac arrest due to
VF/pVT (Class IIb, LOE C-LD).

32. Steroids
• In IHCA, the combination of intra-arrest
vasopressin, epinephrine, and methylprednisolone
and post-arrest hydrocortisone as described by
Mentzelopoulos et al may be considered; however,
further studies are needed before recommending
the routine use of this therapeutic strategy (Class
IIb,LOE C-LD).
• For patients with OHCA, use of steroids during CPR
is of uncertain benefit (Class IIb, LOE C-LD).

33. Cardiac Arrest During
Percutaneous Coronary Intervention
• Cardiac arrest during PCI is rare, occurring in approximately
1.3% of catheterization procedures.
• Cardiac arrest during PCI is present in both elective and
emergency procedures.
• cardiac arrest during PCI have superior outcomes to
patients in cardiac arrest that occurs in other settings
• Rapid defibrillation (within 1 minute) is associated with
survival to hospital discharge rates as high as 100% in this
population.

34. • The combination of ECPR and IABP has been associated
with increased survival when compared with IABP alone for patients
who present with cardiogenic shock, including those who have a
cardiac arrest while undergoing PCI.

35. Vasopressors in Cardiac arrest
• Standard-dose epinephrine (1 mg every 3 to 5
minutes) may be reasonable for patients in
cardiac arrest (Class IIb, LOE B-R).
• Vasopressin offers no advantage as a substitute
for epinephrine or in combination with
epinephrine in cardiac arrest (Class IIb, LOE
B-R). The removal of vasopressin has been
noted in the Adult Cardiac Arrest Algorithm

37. Recommendations
• Institutional guidelines should include the selection of
appropriate candidates for use of mechanical support
devices to ensure that these devices are used as a bridge to
recovery, surgery or transplant, or other device (Class I, LOE
C-EO).
• It may be reasonable to use mechanical CPR devices to
provide chest compressions to patients in cardiac arrest
during PCI (Class IIb, LOE C-EO).
• It may be reasonable to use ECPR as a rescue treatment
when initial therapy is failing for cardiac arrest that occurs
during PCI (Class IIb, LOE C-LD).

38. Special Circumstances of Resuscitation
1. Cardiac arrest associated with pregnancy .
2. Pulmonary embolism (PE).
3. Cardiac arrest during PCI.

39. PREGNANCY
• Survival of the mother has been reported up to 15
minutes after the onset of maternal cardiac arrest.
Neonatal survival has been documented with PMCD
performed up to 30 minutes after the onset of
maternal cardiac arrest.
• In general, aortocaval compression can occur for
singleton pregnancies at approximately 20 weeks of
gestational age.
• Manual left lateral uterine displacement (LUD)
effectively relieves aortocaval pressure in patients
with hypotension

41. CAUSES
• The most common causes of maternal cardiac
arrest are
1. Hemorrhage
2. Cardiovascular diseases (including myocardial
infarction, aortic dissection, and myocarditis)
3. Amniotic fluid embolism
4. Sepsis
5. Aspiration pneumonitis,
6. Eclampsia.
7. Important iatrogenic causes ofmaternal cardiac
arrest include hypermagnesemia from
magnesium sulfate administration and
anesthetic complications.

42. 2015 Recommendations—New and
Updated
• BLS Modification: Relief of Aortocaval Compression
• Priorities for the pregnant woman in cardiac arrest
are provision of high-quality CPR and relief of
aortocaval compression (Class I, LOE C-LD).
• If the fundus height is at or above the level of the
umbilicus, manual LUD can be beneficial in relieving
aortocaval compression during chest
compressions(Class IIa, LOE C-LD).

43. ALS Modification: Emergency Cesarean
Delivery In Cardiac Arrest
• Because immediate ROSC cannot always be achieved, local resources for a
PMCD should be summoned as soon as cardiac arrest is recognized in a
woman in the second half of pregnancy (Class I, LOE C-LD).
• Care teams that may be called upon to manage these situations should
develop and practice standard institutional responses to allow for smooth
delivery of resuscitative care (Class I, LOE C-EO).
• During cardiac arrest, if the pregnant woman with a fundus height at or
above the umbilicus has not achieved ROSC with usual resuscitation
measures plus manual LUD, it is advisable to prepare to evacuate the
uterus while resuscitation continues (Class I, LOE C-LD).
• PMCD should be considered at 4 minutes after onset of maternal cardiac
arrest or resuscitative efforts (for the unwitnessed arrest) if there is no
ROSC (Class IIa, LOE C-EO).

44. PULMONARY EMBOLISM
• Pulseless electrical activity is the presenting
rhythm in 36% to 53% of PE-related cardiac
arrests, while primary shockable rhythms are
uncommon.
• Current advanced treatment options include
systemic thrombolysis, surgical or percutaneous
mechanical embolectomy, and extracorporeal
cardiopulmonary resuscitation (ECPR).
• Systemic thrombolysis is associated with ROSC

45. • accelerated emergency thrombolysis dosing
regimens for fulminant PE include alteplase
50 mg intravenous (IV) bolus with an option
for repeat bolus in 15 minutes, or single-dose
weight-based tenecteplase; thrombolytics are
administered with or followed by systemic
anticoagulation.

46. 2015 Recommendations
• Confirmed Pulmonary Embolism
• In patients with confirmed PE as the precipitant of
cardiac arrest, thrombolysis, surgical embolectomy,
and mechanical embolectomy are reasonable
emergency treatment options (Class IIa, LOE C-LD).
• Thrombolysis can be beneficial even when chest
compressions have been provided (Class IIa, LOE C-
LD).

47. Post–Cardiac Arrest Care
2015 American Heart Association
Guidelines Update for
Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care

48. Hemodynamic Goals
• Avoiding and immediately correcting hypotension
(systolic blood pressure less than 90 mm Hg,
MAP less than 65 mm Hg) during post-
resuscitation care may be reasonable (Class IIb,
LOE C-LD).
• In the absence of evidence for specific targets,
the writing group made no recommendations to
target any hemodynamic goals other than those
that would be used for other critically ill patients.

49. Targeted Temperature Management
• Induced Hypothermia
• AHA recommends that comatose (ie, lack of
meaningful response to verbal commands) adult
patients with ROSC after cardiac arrest to be
considered for TTM(Class I, LOE B-R for VF/pVT
OHCA;Class I, LOE C-EO for non-VF/pVT (ie,
“nonshockable”) and in-hospital cardiac arrest).
• AHA recommends selecting and maintaining a
constant temperature between 32ºC and 36ºC
during TTM (Class I, LOE B-R).

50. • It is reasonable that TTM be maintained for at
least 24 hours after achieving target
temperature (Class IIa, LOE C-EO).

51. COOLING METHODS
• Cooling methods include the following:
1. Surface cooling with ice packs.
2. Surface cooling with blankets or surface heat
exchange device and ice.
3. Surface cooling helmet.
4. Internal cooling methods using catheter based
technology.
5. Internal cooling methods using infusion of cold
fluids.

52. • Of note, there are essentially no patients for
whom temperature control somewhere in the range
between 32oC and 36oC is contraindicated.
• Higher temperatures might be preferred in patients
for whom lower temperatures convey some risk (eg,
bleeding), and lower temperatures might be
preferred when patients have clinical features that
are worsened at higher temperatures (eg, seizures,
cerebral edema).

53. Hypothermia in the Prehospital
Setting
• AHA recommends against the routine
prehospital cooling of patients after ROSC
with rapid infusion of cold intravenous fluids
(Class III: No Benefit, LOE A).

54. Avoidance of Hyperthermia
• It may be reasonable to actively prevent fever
in comatose patients after TTM (Class IIb, LOE
C-LD).

55. Oxygenation
• 2015 Recommendations
• To avoid hypoxia in adults with ROSC after
cardiac arrest, it is reasonable to use the
highest available oxygen concentration until
the arterial oxyhemoglobin saturation or the
partial pressure of arterial oxygen can be
measured (Class IIa, LOE C-EO).

56. Glucose Control
• The benefit of any specific target range of glucose
management is uncertain in adults with ROSC after
cardiac arrest (Class IIb, LOE B-R).

57. Prognostication Time
• The earliest time for prognostication using clinical
examination in patients treated with TTM, where
sedation or paralysis could be a confounder, may be
72 hours after return to normothermia (Class IIb,
LOE C-EO).
• We recommend the earliest time to prognosticate a
poor neurologic outcome using clinical examination
in patients not treated with TTM is 72 hours after
cardiac arrest (Class I, LOE B-NR).

58. • Major management categories:
1. Primary Cardiac Arrest in patients with
AMI
2. Secondary Cardiac arrest in patients with
AMI
3. Due to non-cardiac diseases.
4. Survival after out of hospital cardiac
arrest.

59. • For successfully resuscitated patients, whether
OHCA or IHCA, post cardiac arrest care
includes admission to ICU and continous
monitoring for a minimum of 48-72 hrs.

60. Treatment Options For patients SCD
• ACUTE CARDIOVASCULAR INTERVENTIONS
• PHARMACOLGICAL
• DEVICE THERAPY
• SURGICAL INTERVENTIONS

61. Acute Cardiovascular Interventions
• Coronary angiography should be performed emergently (rather than
later in the hospital stay or not at all) for OHCA patients with
suspected cardiac etiology of arrest and ST elevation on ECG
(ClassI, LOE B-NR).
• Emergency coronary angiography is reasonable for select (eg,
electrically or hemodynamically unstable) adult patients who are
comatoseafter OHCA of suspected cardiac origin but without
ST elevation on ECG (Class IIa, LOE B-NR).
• Coronary angiography is reasonable in post–cardiac arrest patients
for whom coronary angiography is indicated regardless of whether
the patient is comatose or awake (Class IIa,LOE C-LD).

62. Beta-
Blockers
ACE
Inhibitors
Statins Amiodarone

63. Beta Blockers
• Universally applicable and better established
for prevention of SCD.
• The Metoprolol CR/XL Randomized
Intervention Trial in Congestive Heart Failure
(MERIT-HF) demonstrated a 34% decrease in
the all-cause mortality rate, 38% decrease in
the cardiovascular mortality rate, and a 41%
decrease in the sudden death rate.

64. • Beta Blockers are effective in the setting of
ventricular arrhythmias provoked by a high
sympathetic tone, as in patients with
congenital long-QT syndrome, arrhythmogenic
right ventricular dysplasia, or CHF.
• Importantly, the beneficial effects of Beta-
blockers on cardiac mortality are most
pronounced in patients who are at higher risk
for sudden cardiac death, such as those with
CHF, atrial and ventricular arrhythmias, post-
myocardial infarction, and diabetes

65. ACE INHIBITORS
• Although data from individual trials has
conflicted on this issue, a meta-analysis
including more than 15,000 post–myocardial
infarction patients reported a 20% reduction in
sudden cardiac death in ACE-inhibitor treated
subjects

66. • Whether these results also pertain to
angiotensin receptor blockers is not known.
• The protection afforded by ACE inhibitors may
extend to patients with vascular disease in
general.

67. STATINS
• Reports suggest that, in addition to preventing
vascular events, statins reduce SCD and
appropriate shocks in patients with ICDs.
[Chiu JH, Abdelhadi RH, Chung MK, et al. Effect of statin therapy on risk of ventricular arrhythmia
among patients with coronary artery disease and an implantable cardioverter-defibrillator.
Am J Cardiol. 2005;95(4):490-491. [PMID: 15695135]
• A report from the MADIT II trial found that time-
dependent exposure to statins was associated with a
nearly 30% reduction in appropriate ICD therapy for
VT/VF or cardiac death, after adjustment for other
factors

68. AMIODARONE
• Amiodarone was shown to significantly reduce SCD
rates among post–myocardial infarction and heart
failure patients in several placebo-controlled
randomized studies, but its effects on total
mortality are questionable, with some individual
trials showing improved survival, but others not.
• Unlike with other antiarrhythmic drugs, no study
showed increased mortality with amiodarone in
these populations.

69. • Amiodarone is the drug of choice(DOC) when
antiarrhythmic drug treatment is required in
patients with left ventricular dysfunction and
congestive heart failure.

70. • In contrast to the oral version, relatively
strong evidence supports the use of
intravenous amiodarone for out-of-hospital
cardiac arrest and recurrent unstable
ventricular arrhythmias.

71. Implantable Defibrillators
• Primary prevention of Sudden Cardiac arrest in
Patients with Advanced Heart Disease.
• Secondary prevention Of Sudden Cardiac
Death after Survival Of Cardiac Arrest.

73. Primary Prevention of Sudden Cardiac Death in Patients
with Advanced Heart Disease

74. Secondary Prevention of Sudden Cardiac Death after
Survival of Cardiac Arrest

75. SURGICAL INTERVENTION
• REVASCULARIZATION
• There is a reduced prevalence of SCD after CABG,and attempts
should be made to identify and revascularize ischemic myocardium
in order to mitigate arrhythmic risk.
• Among the 13,476 patients in the Coronary Artery Surgical Study
(CASS) registry, all of whom had significant coronary artery disease,
operable vessels, and no significant valvular disease, the mean
incidence of SCD during the 4.6-year average follow-up was 5.2% in
patients treated medically and 1.8% in those treated surgically. The
beneficial effect of CABG was even more pronounced in the
subgroup of patients with reduced left ventricular ejection fraction
and multivessel disease.
• The protective effect of CABG against recurrent cardiac arrest
appears to be best in patients with reversible ischemia as the major
pathophysiologic factor in SCD.

76. Antiarrhythmia Surgery
• Electrophysiologically guided subendocardial
resection and cryoablation are potentially curative
surgical options in patients with recurrent
monomorphic VT in whom areas of slow conduction
around myocardial scars are critical for sustaining VT.
• Long-term follow-up of this operative technique has
yielded a clinical success rate of nearly 90% in
eliminating the presenting rhythm in patients who
survive surgery.
• The best candidates for electrophysiologically guided
subendocardial resection are patients who require
coronary revascularization and have a well-defined left
ventricular aneurysm.

77. Catheter Ablation Therapy
• Catheter ablation of arrhythmias has emerged as a
curative approach for many supraventricular
arrhythmias and a few specific forms of VT.
• The role of catheter ablation in the prevention of
SCD is less well established, but this therapy form
has been successfully used in selected cases.
• Radiofrequency catheter ablation can potentially
prevent SCD in patients with documented and
inducible bundle-branch reentrant VT as
the only mechanism of cardiac arrest.
• But high rates of recurrent VT after apparently
successful VT ablations suggest that few of these
patients can safely be managed without ICDS.

78. The 2016 American Heart Association (AHA)/American College of Cardiology
(ACC) Clinical Performance and Quality Measures for Prevention of Sudden
Cardiac Death (SCD) propose 10 key measures in the domains of preventative
cardiology, resuscitation/emergency cardiovascular care, heart failure/general
cardiology, and electrophysiology:
1. Smoking cessation intervention in patients who suffered sudden cardiac
arrest (SCA), have ventricular arrhythmias, or are at risk for SCD.
2. Screening for family history of SCD.
3. Screening for asymptomatic left ventricular dysfunction among individuals
who have a strong family history of cardiomyopathy and SCD.
4. Referring for cardiopulmonary resuscitation (CPR) and automatic external
defibrillator (AED) education those family members of patients who are
hospitalized with known cardiovascular conditions that increase the risk of
SCA (any acute myocardial infarction, known heart failure [HF], or
cardiomyopathy).
5. Use of an implantable cardioverter-defibrillator (ICD) for prevention of
SCD in patients with HF and reduced ejection fraction (HFrEF) who have an
anticipated survival of >1 year.

79. 6. Use of guideline-directed medical therapy: angiotensin-converting
enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB) or
angiotensin-receptor/neprilysin inhibitor (ARNI), and beta-blocker,
and aldosterone receptor antagonist) for prevention of SCD in
patients with HFrEF.
7. Use of guideline-directed medical therapy (ACE-I or ARB or ARNI,
and beta-blocker, and aldosterone receptor antagonist) for the
prevention of SCD in patients with myocardial infarction and
reduced EF.
8. Documenting the absence of reversible causes for cardiac arrest
and/or sustained ventricular tachycardia before a secondary-
prevention ICD is placed.
9. Counseling eligible patients about an ICD.
10. Counseling first-degree relatives of survivors of SCA associated
with an inheritable condition.

80. Thank you.