SCD.pptx..causes ,and management of sudden cardiac death

Causes of sudden cardiac death

1. SUDDEN CARDIAC DEATH PRESENTOR: DR.VISHALEE DNB 2 ND YEAR RESIDENT MODERATOR: DR.GOVINDAPPA.D, (SR.CONSULTANT PHYSICIAN) DR.S.I.SINGHA (CARDIOLOGIST) DR.ANUSHA BUCHADE (CARDIOLOGIST)

2. SUDDEN CARDIAC DEATH: Sudden cardiac death is the natural death from cardiac causes heralded by abrupt loss of consciousness within 1 hour of onset of an acute change in cardiovascular status. Preexisting heart disease may or may not have been present, but the time and the mode of death are unexpected. To satisfy clinical, legal and social considerations, four temporal elements must be considered: 1.Prodromes 2.Onset 3.Cardiac arrest 4.Biologic death

3. Time references in sudden cardiac death Prodromes biological death onset of terminal events cardiac arrest Days to months Up to 1hour Minutes to weeks

4. ETIOLOGY: Coronary Artery–Related Causes: Myocardial infarction or ischemia Anomalous coronary artery origin Coronary spasm Myocardial bridging Cardiomyopathies: Hypertrophic cardiomyopathy (HCM) Arrhythmogenic right ventricular cardiomyopathy (ARVC) Myocarditis Idiopathic dilated cardiomyopathy Restrictive cardiomyopathy Alcohol-related cardiomyopathy Peripartum cardiomyopathy Tokatsubo cardiomyopathy Primary Arrhythmogenic Diseases:    Long QT syndrome (LQTS) Short QT syndrome (SQTS) Brugada syndrome Early repolarization syndrome Catecholaminergic polymorphic ventricular tachycardia (CPVT) Idiopathic ventricular fibrillation Congenital heart blocks Wolf-Parkinson-White syndrome

5. Congenital Heart Diseases: Tetralogy of Fallot Transposition of great arteries Ebstein anomaly Eisenmenger syndrome Single ventricular physiology Coarctation of aorta Double-outlet right ventricle Interrupted aortic arch Tricuspid atresia Pulmonary atresia Total anomalous pulmonary venous connection Valvular Heart Diseases: Aortic stenosis Mitral valve prolapse Heart Failure: Heart failure with reduced ejection fraction Heart failure with preserved ejection fraction Miscellaneous: Cardiac tamponade Aortic dissection Ruptured aortic aneurysm Pulmonary embolic Left atrial myxoma

6. PATHOPHYSIOLOGY: PATHOLOGY OF SUDDEN CARDIAC DEATH CAUSED BY CORONARY ARTERY ABNORMALITIES: Extensive atherosclerosis has been recognized as the common pathologic finding in the coronary arteries of victims of SCD. The role of coronary artery lesions characterized by plaque fissuring, plaque erosion or rupture, platelet aggregation and thrombosis as a major pathophysiologic mechanism of the onset of cardiac arrest has been clarified. Coronary artery spasm , an established cause of acute ischemia and SCD is commonly associated with non obstructive plaque and spasm itself has been recognized at postmortem examination in rare cases.

7. ELECTRO PHYSIOLOGICAL ABNORMALITIES: Acquired disease of the AV node and HIS Purkinje system and the presence of accessory pathways of conduction are the two grops of structural abnormalities of specialized conduction that may be associated with SCD. Primary fibrosis ( Lenegre disease) or injury secondary to other disorders (Lev disease) of the HIS Purkinje system is commonly associated with intraventricular conduction abnormalities and symptomatic AV block. LONG QT SYNDROME : Congenital long QT syndrome is a congenital abnormality usually caused by inherited mutations affecting the molecular structure of an ion channel proteins and is associated with environmental or neurogenic triggers that can initiate symptomatic or lethal arrythmias

8. BRUGADA SYNDROME: This disorder is characterized by an atypical right bundle branch block pattern and unusual forms of non ischaemic ST-T wave elevations in the precordial leads. It is a familial disorder associated with risk for SCD nad occurs mostly in young and middle aged.Mutations involving the cardiac Na channel gene (SCN5A) are the most commonly observed variants but are identified in only a minority of cases. CATECHOLAMINERGIC POLYMORPHIC VENTRICULAR TACHYCARDIA: CAPT is an inherited syndrome associated with catecholamine- dependent lethal arrhythmias in the absence of forewarning electrocardiographic abnormalities and with atleast partial control by beta adrenoceptor- blocking agents. An autosomal dominant pattern involving the ryanodine receptor locus was initially described predominantly in younger patients, usually men with bidirectional or polymorphic VT associated with risk for SCD.

9. ELECTROPHYSIOLOGICAL EFFECTS OF ACUTE ISCHEMIA: At the level of myocyte, the immediate consequences of ischemia, which includes alterations in cell membrane physiology, with efflux of potassium, influx of calcium, acidosis, reduction in transmembrane potential and enhanced automaticity in some tissues are followed by separate series of changes during reperfusion. At an intercellular level , ischemia alters the distribution of Connexin 43, the primary gap junction protein between myocytes. This alteration results in uncoupling of myocytes, a factor that is arrhythmogenic because of altered patterns of excitation and regional changes in conduction velocity. Clinical relevance is the suggestion that potassium depletion by diuretics and clinical hypokalemia may make the ventricular myocardium more susceptible to potentially lethal arrhythmias.

10. EVALUATION: HISTORY: People with SCA present to the hospital unconscious, with no cardiac tone and respirations. Immediate resuscitation is warranted in patients in cardiorespiratory arrest, regardless of cause. Airway, breathing, circulation, disability, and exposure must be evaluated during a quick primary survey and addressed without delay. On history, patients may experience palpitations, dizziness, or near-syncope before SCA. Almost half of people who had SCA report no symptoms before losing consciousness. 

11. Other signs and symptoms that may be reported by a person who had SCA include the following: Chest pain, discomfort, tightness, pressure related to exertion Excessive exertional and unexplained dyspnea, fatigue, or palpitations associated with exercise Prior recognition of a heart murmur Elevated systemic blood pressure Sensorineural deafness, which may indicate LQTS

12. Relevant information that may be elicited during history-taking includes a prior history of cardiogenic or arrhythmia-related syncope or SCA and a family history of SCD or inherited cardiac arrhythmias. Other information that a person who had SCA may disclose in their past medical and family history includes the following: Prior restriction from sports participation Prior physician-ordered cardiac testing Premature death (before age 40) in more than 1 relative attributed to heart disease  Disability from heart disease in a close relative younger than 50 Hypertrophic or dilated cardiomyopathy, LQTS or other ion channelopathies, Marfan syndrome, clinically significant arrhythmia, or specific knowledge of certain cardiac conditions in family members

13. The relevant history provides clues to certain high-risk patients. In individuals with CAD leading to cardiomyopathy and severe left ventricular systolic dysfunction, a history of syncope with a documented ventricular arrhythmia episode, New York Heart Association (NYHA) class III or IV classification, ventricular arrhythmia immediately after myocardial infarction, and previous myocardial infarctions predict high future SCA and SCD risks.  A family history of SCD increases the risk of SCD in those with inherited cardiac channelopathies and primary cardiomyopathies.

14. PHYSICAL EXAMINATION: Physical examination findings in people with SCA include unresponsiveness and pulselessness. Blood pressure and cardiac tone are absent. Patients may display agonal respirations or apnea. The skin is usually cyanotic and cold to the touch. Pupils are dilated and nonreactive to light. Muscles become flaccid, with absent bladder and bowel control. Cardiac monitoring may show arrhythmias, commonly asystole, PEA, or ventricular fibrillation.

15. Individuals with ACS often have normal neurologic function. However, ACS and stroke may cooccur, with patients exhibiting cardiac abnormalities, eg , new-onset atrial fibrillation, alongside neurologic deficits, eg , new-onset dysphonia or slurred speech. The onset of these signs must be ascertained before deciding to include neuroimaging in the cardiovascular workup. Importantly, people who survive SCA may also manifest neurologic symptoms from brain hypoxia during the arrested state. Specific physical examination findings may point toward other potential causes of cardiac arrest. A mitral valve prolapse's mid-to-late systolic murmur, HCM's ejection systolic murmur, cyanosis, Tetralogy of Fallot right ventricular outflow murmur, and sarcoidosis' skin signs may help identify the underlying cardiac cause.

16. Heart murmurs should be evaluated in both supine and standing positions during the cardiovascular examination. Femoral pulses must be evaluated and compared to exclude aortic coarctation. Brachial artery blood pressure may be taken in the sitting position, preferably on both arms. SCA may be the first manifestation of CAD and other cardiac conditions. Full cardiac assessment is required for individuals who survive this event. Diagnostic tests should include the following: Electrocardiogram (ECG) to evaluate for myocardial ischemia or infarction and inherited channelopathies Echocardiogram to assess for preexisting heart failure, cardiomyopathies, valvular heart diseases, and congenital cardiac abnormalities

17. Coronary angiography for diagnosing ASCVD, coronary artery anomalies, and coronary artery spasms Exercise tests in selected patients to evaluate exercise-induced ventricular arrhythmias and ischemia Electrophysiology testing in select groups of people to search for cardiac conduction diseases and risk stratification Cardiac magnetic resonance imaging (MRI) to establish the diagnosis of cardiomyopathies and assess the risk of SCD Genetic testing if the patient has arrhythmogenic right ventricular cardiomyopathy (ARVC), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), or LQTS A cardiac biopsy may be considered if no other cause is found

18. MANAGEMENT: Initial Management: SCA's initial management is a critical and time-sensitive process aimed at restoring cardiac function and improving the chances of survival. Immediate intervention is crucial to increase the likelihood of a positive outcome. Basic (BLS) and Advanced Cardiac Life Support (ACLS) protocols must be performed by trained healthcare professionals.

19. Resuscitation for cardiac arrest: The initial management steps for SCA resuscitation include rapid recognition of cardiac arrest, early and effective CPR, defibrillation, postcardiac arrest care, and treatment of underlying causes. CPR with effective chest compressions and appropriate defibrillator use is paramount for treating SCD. CPR should be performed according to published BLS and ACLS Early CPR and defibrillation and rapid arrival of emergency medical services (EMS) during cardiac arrest are the major determinants of successful resuscitation.

20. Strategies that may improve the chances of survival include early CPR initiation for witnessed cardiac arrest, bystander CPR, and rapid defibrillation.  Survival after in-hospital cardiac arrest (IHCA) is as high as 90%, especially in intensive care units where the response to ventricular fibrillation is quick. However, survival after OHCA decreases rapidly after the first few minutes from the onset of cardiac arrest. Less than 25% survive at 5 minutes, and close to zero survive 10 minutes after OHCA.  Intravenous or intraosseous epinephrine every 3 to 5 minutes is an important ACLS component, improving the odds of successful resuscitation. Epinephrine's favorable effects are produced by the α-adrenergic mediated vasoconstriction, which improves coronary and cerebral perfusion pressure during CPR.

21. Amiodarone administration after at least 3 defibrillation attempts in refractory ventricular fibrillation cases increases the rate of successful resuscitation as compared to lidocaine and placebo. However, amiodarone does not improve survival to discharge compared to placebo. Procainamide administration in OHCA with a shockable rhythm does not have favorable outcomes. The drug has been associated with a higher number of shocks, longer resuscitation times, and a lower survival rate. CPR with effective chest compression, epinephrine, and treatment of reversible etiologies is the only way of survival

22. POST CARDIAC ARREST CARE : Patients are evaluated for possible SCA causes after successful resuscitation and return of spontaneous circulation (ROSC). The initial evaluation includes an assessment of airway, hemodynamics, and neurologic status, followed by a 12-lead ECG, baseline laboratory investigations, chest radiograph, ECG, and brain imaging. Cardiac arrest results in multiorgan dysfunction. Death can also occur from shock or dysfunction of organs other than the heart. Postcardiac arrest care is complex. Thus, an interprofessional team with expertise in cardiac arrest care and dedicated postcardiac arrest treatment protocols are critical to improving survival and neurological outcomes after ROSC. 

23. ST-elevation myocardial infarction (STEMI)—diagnosed based on clinical presentation, ECG, and cardiac enzyme levels—should be managed with immediate coronary angiography followed by revascularization Percutaneous revascularization can be achieved safely when a postcardiac arrest angiogram reveals significant CAD. Observational studies report improved survival after successful revascularization in patients with SCA.  However, in the absence of STEMI, immediate coronary angiography and revascularization do not provide added benefit.

24. Hypotension may worsen brain injury and outcomes after cardiac arrest due to decreased tissue perfusion. Maintaining systolic blood pressure above 90 mm Hg and mean arterial pressure above 65 mm Hg with proper fluid resuscitation and vasopressor therapy is recommended. Avoiding hypoxia and hypoglycemia is vital in the post-cardiac arrest period, particularly in comatose patients, as these conditions can worsen tissue damage and impact long-term survival. Targeted temperature management (32 °C to 35 °C) is recommended for at least 24 hours in patients not following commands after ROSC. Multiple studies document survival and positive neurologic outcomes when targeted temperature management is used after IHCA and OHCA, even in patients with an initially nonshockable rhythm. Fever in the postcardiac arrest period is associated with poor neurological outcomes and thus must be prevented or treated immediately.

25. Hypoxic brain injury is the major contributor to morbidity and mortality in survivors of OHCA and IHCA. A detailed neurological assessment and appropriate prognostication are required to avoid premature withdrawal of life-saving measures in patients who may otherwise achieve neurological recovery. Avoiding unnecessary treatment when a poor outcome is inevitable is helpful. Neuroprognostication is recommended in every comatose patient after 5 days of targeted temperature management. A multimodal approach, including clinical examination, electroencephalogram, and brain imaging, is recommended for neuroprognostication , as a single test may yield false positive or false negative results.

26. LONG TERM MANAGEMENT: The long-term management of patients who survive SCA focuses on reducing the risk of recurrence, improving overall prognosis, and addressing potential underlying causes or contributing factors. Patients who survive SCA face unique challenges, including the risk of recurrent arrhythmias, underlying cardiovascular disease, and psychological consequences. Therefore, a comprehensive and interprofessional approach to long-term management is crucial to optimize outcomes and enhance quality of life.  SCD prevention is critical after survival from SCA. Patients have a high risk of SCA recurrence or SCD, especially in the presence of underlying structural heart diseases and primary cardiac arrhythmias.

27. Medical treatment has a limited role in preventing SCD. No antiarrhythmic drugs except for β-adrenergic blocking agents have documented evidence for preventing SCD. However, the use of antiarrhythmic medications and heart failure therapy is essential in some patients to control arrhythmias and improve symptoms. β-blockers improve survival and reduce SCD risk in patients with left ventricular systolic dysfunction or previous acute myocardial infarction. β-blockers, especially propranolol and nadolol, are also recommended as the first-line therapy for preventing the recurrence of arrhythmias and SCA in patients with cardiac channelopathies, eg , LQTS and catecholaminergic polymorphic ventricular tachycardia.

28. The recommended cardioprotective agents in patients with cardiomyopathy and severely reduced left ventricular systolic function include β-blockers, mineralocorticoid receptor antagonists, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, angiotensin receptor-neprilysin inhibitors, and sodium-glucose cotransporter-2 inhibitors. These drugs have demonstrated a significant reduction in SCD rate in studies. Contemporary guidelines recommend these drugs for preventing SCD in all patients with heart failure with reduced ejection fraction, irrespective of the underlying cause of left ventricular systolic dysfunction. 

29. Randomized trials demonstrate that ICDs effectively prevent SCD and improve survival in patients who survive SCA due to fatal arrhythmia, as compared to antiarrhythmic drugs . ICD placement is advised to prevent SCD in patients who survive SCA due to ventricular tachycardia or fibrillation without an identified reversible cause. This intervention is supported by class IA recommendations in all contemporary guidelines

30. PROGNOSIS: The overall survival of cardiac arrest depends on multiple factors. The global OHCA survival rate is very low. Only 22% of the patients with OHCA reach the emergency department, and only 8.8% survive until hospital discharge. The 1-year survival rate of OHCA is less than 8% in developed countries. SCA survival rate may be improved with early resuscitation, bystander CPR, and defibrillator access in public places. Periodic education of public officials and community members about the role of bystander CPR and early defibrillation is critical to improving OHCA survival rates.

31. COMPLICATIONS: SCA's complications include anoxic brain injury and multiorgan dysfunction. Mental health disorders are also reported in patients who survive SCA and their families. The literature suggests that a significant number of patients who survive cardiac arrest develop anxiety, depression, and PTSD.  The incidence of depression is reported to be as high as 45%, while 6% to 15% of patients develop anxiety. PTSD is diagnosed in up to 27% of the survivors of cardiac arrest.

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