Sudden cardiac death

Sudden cardiac death

1. SUDDEN CARDIAC DEATH Chairperson Dr Praveen Kusubi Student Dr Ibin Shah

2. Definition SCD is natural death from cardiac causes heralded by abrupt loss of consciousness within 1 hour of the onset of an acute change in cardiovascular status Preexisting heart disease may or may not have been known to be present, but the time and mode of death are unexpected

3. Risk factors Age. The incidence of sudden death has two peak ages: within the first year of life (including sudden infant death syndrome and between 45 and 75 years of age. Race higher risk for cardiac arrest and SCD in blacks than in whites Sex . SCD syndrome has a large preponderance in men relative to women during the young adult and early middle-age years

4. Hereditary

5. Lifestyle Factors 1 .Smokers have a two fold to threefold increase in risk for sudden death 2 . Obesity 3. 17-fold relative increase in SCD associated with vigorous exercise as opposed to lower level activity or inactive states habitual vigorous exercise reduces the risk

6. Left Ventricular Ejection Fraction in Chronic Ischemic Heart Disease Ejection fraction of 30% or lower is the single most powerful independent predictor of SCD Ventricular Arrhythmias in Chronic Ischemic Heart Disease Exercise-induced PVCs and short runs of nonsustained VT

7. CAUSES OF SUDDEN CARDIAC DEATH 1 Atherosclerotic Coronary Artery Disease 2 . Nonatherosclerotic Coronary Artery Abnormalities Anomalous Origin of Coronary Arteries from the Wrong Sinus of Valsalva. Embolism to the Coronary Arteries.

8. Coronary Arteritis.- Kawasaki disease , polyarteritis nodosa ,syphilitic aortitis Mechanical Obstruction of Coronary Arteries. –Coronary artery dissection, prolapse of myxomatous polyps, dissection or rupture of a sinus of Valsalva aneurysm Deep myocardial bridges over coronary arteries- common in association with hypertrophic cardiomyopathy

9. Coronary artery spasm. 3.Ventricular Hypertrophy and Hypertrophic Cardiomyopathy Left ventricular hypertrophy is an independent risk factor for SCD -hypertensive heart disease with or without atherosclerosis, valvular heart disease, obstructive and nonobstructive hypertrophic cardiomyopathy ,primary pulmonary hypertension with right ventricular hypertrophy, and advanced right ventricular overload secondary to congenital heart disease.

10. 4 . Acute Heart Failure massive acute myocardial infarction , acute myocarditis, acute alcoholic cardiac dysfunction , acute pulmonary edema massive pulmonary embolism, mechanical disruption of intracardiac structures secondary to infarction or infection

11. 5 .Electrophysiologic Abnormalities Long QT syndrome Short QT syndrome Brugada stndrome Catecholaminergic Polymorphic Ventricular Tachycardia. Central Nervous System Influences

12. PATHOLOGY More than 80% of SCD victims have pathologic findings of CHD 70–75% of males who die suddenly have preexisting healed MIs, whereas only 20–30% have recent acute MIs Transient ischemia Is the mechanism of onset.

13. CLINICAL FEATURES OF PATIENTS WITH CARDIAC ARREST Prodromal Symptoms chest pain, dyspnea , weakness or fatigue, palpitations, syncope,

14. Onset of the Terminal Event Increasing heart rate and advancing grades of ventricular ectopy are common antecedents of VF. Alterations in autonomic nervous system activity

15. Cardiac Arrest most common electrical mechanism is VF, followed by asystole or PEA and pulseless VT Mechanical mechanisms include rupture of the ventricle, cardiac tamponade, acute mechanical obstruction to flow, and acute disruption of a major blood vessel

16. Progression to Biologic Death The onset of irreversible brain damage usually begins within 4 to 6 minutes after loss of cerebral circulation Death is biologically, legally, and literally an absolute and irreversible event

17. MANAGEMENT OF CARDIAC ARREST The response to cardiac arrest is driven by two urgent principles : (1) maintenance of continuous artificial cardiopulmonary support until return of spontaneous circulation has been achieved (2) restoration of spontaneous circulation as quickly as possible.

18. Five elements to achieve this (1) initial assessment and summoning of an emergency response team (2) basic life support (3) early defibrillation by a first responder (if available) (4) advanced life support (5) post–cardiac arrest care.

19. Initial Assessment and Basic Life Support The first action must be confirmation of a cardiac arrest. response to voice, observation for respiratory movements and skin color , and simultaneous palpation of major arteries for the presence or absence of pulse

20. Chest Thump The thumpversion technique involves one or two blows delivered firmly to the junction of the middle and lower thirds of the sternum from a height of 8 to 10 inches. it is recommended to use precordial thumps as a life support technique only when monitoring and defibrillation are available

21. Basic Life Support—The Initial Steps in Cardiopulmonary Resuscitation Goal of this activity is to maintain viability of the central nervous system, heart, and other vital organs until definitive return of spontaneous circulation can be achieved

22. Circulation . The palm of one hand is placed over the lower half of the sternum and the heel of the other rests on the dorsum of the lower part of the hand. The sternum is then depressed, with the resuscitator’s arms straight at the elbows to provide a less tiring and more forceful fulcrum at the junction of the shoulders and back sufficient force is applied to depress the sternum at least 2 inches (>5 cm), with abrupt relaxation, and the cycle is carried out at a rateof about 100 compressions/min

23. For single responders to victims from infancy through adulthood and for adults responded to by two rescuers, a compression- ventilationratio of 30:2 is recommended Two -rescuer CPR in infants and children,compression -ventilation ratio is 15:2

24. Airway . Clearing of the airway includes tilting the head backward and lifting the chin, in addition to exploring the airway forbforeign bodies, including dentures, and removing them

25. Heimlich maneuver

26. Breathing . mouth-to-mouth resuscitation is initiated if no specific rescue equipment is available Intubation is the preferred procedure

27. Advanced Cardiac Life Support The general goals of advanced life support are to restore cardiac rhythm to one that is hemodynamically effective, to optimize ventilation, and to maintain and support the restored circulation A short period of closed-chest cardiac compression 60-90 sec immediately before defibrillation enhances the probability of survival

28. Intubate the patient and start oxygenation Establish Intravenous line

29. Ecg patterns in cardiac arrest

30. Defibrillation-Cardioversion VF or VT that is pulseless and/or accompanied by loss of consciousness is recognized on a monitor or by telemetry, defibrillation should be carried out immediately monophasic devices 360 J initially Biphasic devices 120 to 200 J Failure of the initial shock to provide an effective rhythm is a poor prognostic sign.

31. Failure of a single adequate shock to restore a pulse should be followed by continued CPR and a second shock delivered after five cycles of CPR. If cardiac arrest still persists Epinephrine 1mg i.v followed by repeated defibrillation attempts at 360 J (monophasic) or 200 J or higher (biphasic).

32. Meanwhile secure airway and maintain ventilation Correct electrolyte imbalances and acidosis if present Sodium bicarbonate( 1meq /kg ) is recommended for circumstances of known or suspected pre-existing bicarbonate-responsive causes of acidosis, certain drug overdoses, prolonged resuscitation

33. Pharmacotherapy For patients who continue to have persistent or recurrent VT or VF despite direct-current cardioversion after epinephrine Electrical stability of the heart may be achieved by the intravenous administration of antiarrhythmic agents Amiodarone is the drug of choice (300mg bolus, second dose150 mg , followed by 1 mg/min for up to 6 h and 0.5 mg/min thereafter) If amidarone fails lidocaine is the second choice ( 1mg/kg)

34. If acute hyperkalemia is the triggering event for resistant VF 10% calcium gluconate will be helpful For resistant forms of polymorphic VT or torsades de pointes, rapid monomorphic VT or ventricular flutter (rate ≥260/min), or resistant VF may respond to intravenous beta blocker therapy or intravenous magnesium sulfate .

35. Bradyarrhythmic and Asystolic Arrest; Pulseless Electrical Activity When a person develops this form of cardiac arrest we should focus on establishing cardiorespiratory status i.e., continue CPR, intubate, and establish intravenous access

36. Possible reversible causes Hypovolemia hypoxia cardiac tamponade tension pneumothorax preexisting acidosis drug overdose hypothermia hyperkalemia

37. Epinephrine 1mg i.v is commonly used in an attempt to elicit spontaneous electrical activity or to increase the rate of a bradycardia. Sodium bicarbonate, 1 mEq /kg, may be tried for known or strongly suspected preexisting hyperkalemia or bicarbonate-responsive acidosis

38. Stabilization of Cardiac Rhythm after Initial Return of Spontaneous Circulation If frequent PVC and VT persist – use antiarrythmic drugs First choice is amiodarone In arrythmia due to acute ischemic events lidocaine is preferred For recurrent episodes of polymorphic VT unresponsive to amiodarone , use magnesium sulphate

39. Post cardiac arrest syndrome and post resuscitation care The four components of post-cardiac arrest syndrome include brain injury myocardial dysfunction systemic ischemia/reperfusion responses and control of persistent precipitating factor The goal is to maintain a stable electrical, hemodynamic, and central nervous system status

40. Post resuscitation care Mild therapeutic hypothermia is indicated for resuscitated cardiac arrest victims who are hemodynamically stable, but remain comatose Core body temperature is decreased to 32–34°C, by several available techniques as soon as practical after resuscitation and maintained for a minimum of 12–24 h. It reduces metabolic demands and cerebral edema , and improves probability of survival with better neurologic outcome.

41. Primary prevention of SCD in patients with ischemic heart disease

42. Indications for Implantable Cardioverter-Defibrillators in Genetic Disorders Associated with Risk for Sudden Cardiac Death

43. References 1. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death 2 . Braunwald’s heart disease 3. Harrisons principles of internal medicine 4. Paul l marino ICU Book

44. THANK YOU