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Cardiac arrest seminar

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CARDIAC ARREST AND CPR SEMINAR CONDUCTED AT GMCH GUWAHATI. (SHORT NOTE).

Publicado en: Salud y medicina
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Cardiac arrest seminar

  1. 1. SEMINAR TOPIC: Management of Cardiac Arrest and Cardiac Arrest Survivors Moderatedby: Dr. B Dutta Presentedby: Dr. Swapnil Garde
  2. 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. 3. Mechanisms of Cardiac Arrest • Ventricular fibrillation • Ventricular tachycardia • Asystole • Bradycardia • Pulseless Electrical Activity • Mechanical factors.
  4. 4. Causes of VF/pVT
  5. 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. 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. 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. 8. • One has to consider secondary causes of cardiac arrest when PEA is otherwise the primary rhythm.
  9. 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. 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. 11. MANAGEMENT
  12. 12. • 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
  13. 13. 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
  14. 14. • 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.
  15. 15. • 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
  16. 16. 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.
  17. 17. 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).
  18. 18. 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).
  19. 19. 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).
  20. 20. 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.
  21. 21. • Defibrillators (using BTE, RLB, or monophasic waveforms) are recommended to treat atrial and ventricular arrhythmias (Class I, LOE B-NR).
  22. 22. • 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).
  23. 23. 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).
  24. 24. 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).
  25. 25. 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).
  26. 26. 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.
  27. 27. 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).
  28. 28. 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).
  29. 29. 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.
  30. 30. • 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.
  31. 31. 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
  32. 32. 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).
  33. 33. Special Circumstances of Resuscitation 1. Cardiac arrest associated with pregnancy . 2. Pulmonary embolism (PE). 3. Cardiac arrest during PCI.
  34. 34. 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
  35. 35. 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.
  36. 36. 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).
  37. 37. 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).
  38. 38. 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
  39. 39. • 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.
  40. 40. 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).
  41. 41. Post–Cardiac Arrest Care 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
  42. 42. 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.
  43. 43. 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).
  44. 44. • It is reasonable that TTM be maintained for at least 24 hours after achieving target temperature (Class IIa, LOE C-EO).
  45. 45. 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.
  46. 46. • 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).
  47. 47. 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).
  48. 48. Avoidance of Hyperthermia • It may be reasonable to actively prevent fever in comatose patients after TTM (Class IIb, LOE C-LD).
  49. 49. 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).
  50. 50. 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).
  51. 51. 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).
  52. 52. • 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.
  53. 53. • 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.
  54. 54. Treatment Options For patients SCD • ACUTE CARDIOVASCULAR INTERVENTIONS • PHARMACOLGICAL • DEVICE THERAPY • SURGICAL INTERVENTIONS
  55. 55. 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).
  56. 56. Beta- Blockers ACE Inhibitors Statins Amiodarone
  57. 57. 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.
  58. 58. • 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
  59. 59. 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
  60. 60. • 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.
  61. 61. 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
  62. 62. 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.
  63. 63. • Amiodarone is the drug of choice(DOC) when antiarrhythmic drug treatment is required in patients with left ventricular dysfunction and congestive heart failure.
  64. 64. • 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.
  65. 65. 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.
  66. 66. Primary Prevention of Sudden Cardiac Death in Patients with Advanced Heart Disease
  67. 67. Secondary Prevention of Sudden Cardiac Death after Survival of Cardiac Arrest
  68. 68. 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.
  69. 69. 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.
  70. 70. 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.
  71. 71. 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.
  72. 72. 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.
  73. 73. Thank you.

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