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SUDDEN CARDIAC DEATH

Prof. Lotfy Hamed Abo dahab . Professor Of Internal Medicine and Cardiology. Sohag University. SUDDEN CARDIAC DEATH. DEFINITION.

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SUDDEN CARDIAC DEATH

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  1. Prof. LotfyHamedAbodahab. Professor Of Internal Medicine and Cardiology. Sohag University SUDDEN CARDIAC DEATH

  2. DEFINITION Sudden cardiac death (SCD) generally refers to an unexpected death from a cardiovascular cause in a person with or without preexisting heart disease occurring within 1 hour of an acute change in clinical status.

  3. INCIDAENCE • The incidence of SCD in the United States ranges between 180 000 and 450 000 cases annually • SCD still accounts for 50% of all CAD deaths and 15% to 20% of all deaths. • Despite major advances in cardiopulmonary resuscitation and post resuscitation care, survival to hospital discharge after cardiac arrest remains poor only 7.9% • 2016 American Heart Association

  4. Causes 1- Coronary artery disease 2-Cardiomyopathies Dilated Hypertrophic Arrhythmogenic right ventricular 3-Primary electric disorders related to channelopathies: Long QT syndrome Brugada syndrome 4-Valvular and congental heart diseas 5- Acute myocarditis 6- Over dose of any cardiac medication or illegal use of amphetamines 4-Commotiocordis 5- Coronary anomaly

  5. Demographics: Age, Sex, and Race Age • The incidence of SCD increases markedly with age regardless of sex or race • For example, the annual incidence for 50-year-old men is 100 per 100 000 population compared with 800 per 100 000 for 75-year-old men

  6. Sex • At any age, women have a lower incidence of SCD than men, even after adjustment for CAD risk factors. • This discrepancy may be decreasing over time. • Approximately two-thirds of women who present with SCD have no known history of heart disease compared with 50% of men.

  7. Race • There are also racial differences in the incidence of SCD that are not well understood. • American black men and women appear to had higher rates (relative risk1.3–2.8) of cardiac arrest than whites

  8. In addition, survival rates after cardiac arrest are lower for African blacks • In all studies of racial differences, it is difficult to separate socioeconomic influences from a true genetic predisposition.

  9. Incidence of SCD according to age, sex and race Chicago CPR Project (6451 pt: 3207 whites and 2910 blacks)

  10. The proportions of underlying cardiac disease among men and women who survived after SCD (Albert et al.).

  11. Underlying Pathophysiology • The pathophysiology of SCD is complex and is believed to require the interaction between a transient event and underlying substrate. • This process induces electric instability and lethal ventricular arrhythmias followed by hemodynamic collapse. • Although the challenge remains to predict when such interactions prove harmful, a variety of risk factors have been proposed.

  12. CAD is the most common substrate underlying SCD in the Western world, being responsible for 75% of SCDs. • Cardiomyopathies (dilated, hypertrophic, and arrhythmogenic right ventricular cardiomyopathy) • Primary electric disorders related to channelopathiesaccount for most of the remainder. • In 5% of SCDs or cardiac arrests, a significant cardiac abnormality is not found after extensive evaluation or at autopsy.

  13. CAD predisposes to SCD in 3 general settings: (1) acute myocardial infarction (2) ischemia without infarction (3) structural alterations such as scar formation or ventricular dilatation secondary to infarction or chronic ischemia. • The mechanism of SCD in cases without acute MI is an electric event due to a ventricular arrhythmia triggered by ischemia or other arrhythmogenic stimuli in the setting of a chronically diseased heart

  14. Ventricular fibrillation degenerates to asystole over several minutes; • AS a result, the majority of SCD patients demonstrate asystole or pulseless electric activity when first examined by rescue teams.

  15. First cardiac rhythm documented at time of SCD (Bayes de Luna et al.).

  16. Risk Factors 1- Structural Heart Disease • Coronary artery disease or congestive heart failure markedly increases SCD risk in the population • After experiencing an MI, women and men have a 4- to 10-fold higher risk of SCD, respectively The absolute rate is highest in the first 30 days after MI and decreases gradually with time

  17. Both left ventricular dysfunction and New York Heart Association class are powerful risk factors for SCD in patients with either ischemic or nonischemiccardiomyopathy, and implantable cardioverter defibrillators prolong life in these high-risk patients.

  18. Other markers of structural heart disease associated with elevated SCD risk include left ventricular hypertrophy, QTc prolongation, and abnormal heart rate profile during exercise. • At the present time, none of these markers have been incorporated into risk stratification algorithms.

  19. 2- CAD Risk Factors • Because 80% of men who experience SCD have underlying CAD, it follows that the standard CAD risk factors are predictive of SCD in the general population. • Modifiable CAD risk factors that predict SCD include hypertension, dyslipidemia, diabetes , kidney dysfunction, obesity, and smoking.

  20. 3- Electrocardiographic Measures of Risk • Standard 12-lead electrocardiographic measures including: • Heart rate • QRS duration • QT interval • Early repolarization(ER) have been assessed as risk factors for SCD.

  21. An elevated resting heart rate and prolonged QT interval increase SCD risk in the general population. • Similarly, a prolonged QRS duration has also been associated with SCD. • An interest has focused on early repolarization (ER) as a novel risk factor for SCD and cardiovascular death.

  22. ER is defined as an elevation of the junction between the end of the QRS complex and the beginning of the ST segment (J point), • Its presence in the inferior or lateral ECG leads has been associated with a history of SCD and idiopathic VF in case control studies

  23. 4- Nutritional Risk Factors • Dietary intake and blood-based measures of selected nutrients have been specifically associated with SCD in several observational studies. • Increased consumption of polyunsaturated fatty acidsas in olive-peanut oils and avocadosis is inversely associated with SCD to a greater extent than nonfatal MI.

  24. Consuming fish 1 to 2 times per week was associated with 42% to 50% reductions in SCD risk. • Alcohol intake may also have a selective effect on SCD risk. • Heavy alcohol consumption (5 drinks per day) is associated with an increased risk of SCD but not nonfatal MI. • In contrast, light-to-moderate levels of alcohol consumption ( 1⁄2 to 1 drink per day) may be associated with reduced risks of SCD

  25. Magnesium intake as in almonds-spinach-peanuts-creals - milk-salmon-avocadsas may also be related to SCD rates. • Each 0.25 mg/dL increase in plasma magnesium was associated with a 41% reduced risk of SCD.

  26. Finally, there is some evidence that certain dietary patterns are associated with lower SCD risk. • A Mediterranean-style diet consisting of higher intake of vegetables, fruits, nuts, whole grains, fish, moderate intake of alcohol, and low intake of red/processed meat, has been associated with lower risks of cardiovascular disease and SCD in clinical trials and observational studies.

  27. 5- Biological Markers • The early stages of hemodynamic stress, atherosclerotic plaque instability, and cardiac remodeling may only be detectable with biomarkers that are associated with: • Inflammatory processes (CRP) • Metabolic factors (aldosterone, cystatin C, renin, vitamin D, parathyroid hormone) • Neurohormonal regulation (BNP)

  28. Triggers • SCD risk is not only a function of the underlying substrate and its vulnerability to arrhythmias but also the frequency of exposure to acute precipitants or triggers. • These triggers tend to increase sympathetic activity, which in turn may precipitate arrhythmias and SCD.

  29. 1-Diurnal/Seasonal Variation • Several studies have demonstrated a circadian pattern to the occurrence of SCD • The peak incidence occurs in the morning hours from 6 AM with a smaller peak in the late afternoon • This morning peak in SCD is blunted by Beta-blockers, supporting the concept that excessive activation of the sympathetic nervous system in the morning hours may be responsible.

  30. Weekly patterns to SCD onset have also been appreciated. The risk of SCD appears to be highest on Monday with a nadir over the weekend. • These patterns of onset suggest that activity and psychological exposures play roles in triggering SCD.

  31. There have also been reports of seasonal variation in SCD rates with lower rates in the summer and higher rates in winter months . • SCD may be associated with endogenous rhythms and environmental factors including temperature, sunlight exposure, and other climatic conditions.

  32. 2- Physical Activity • Physical activity has both beneficial and adverse effects on SCD risk. • Most studies, , have found inverse associations between increasing regular physical activity and SCD . • Results of majority of studies have documented moderate levels of exertion have a favorable associations.

  33. Despite the long-term benefits of exercise, it is also well known that SCD occurs with a higher-than-average frequency during or shortly after vigorous exertion. • The effect of exertion on plaque vulnerability and the sympathetic nervous system could account for both the transiently increased risk of SCD during a bout of exertion and the ability of habitual vigorous exercise to modify this excess risk.

  34. Acute bouts of exercise decrease vagal activity leading to an acute increase in susceptibility to ventricular fibrillation, whereas habitual exertion increases basal vagal tone, resulting in increased cardiac electric stability. • Despite these transiently elevated relative risks, the absolute risk of SCD during any particular episode of exertion is extremely low in most series, and exertion-related SCDs are felt to be relatively rare outcomes.

  35. 3- Psychosocial Determinants • Lower socioeconomic status, depression, anxiety, social isolation, and psychological stress have all been linked to an increase in cardiovascular mortality . • Arrhythmic mechanisms have been postulated for these associations.

  36. 4- Genetic Predisposition to SCD • The discovery of novel genes implicated in inherited arrhythmic diseases (IADs) may account for part of the familial component of SCD risk observed in epidemiological studies.

  37. Management • A cardiologist and cardiac electrophysiologist always should be participating with the rescue team in the care of patients with SCD which generally involves ICD implantation. • Other consultations for expertise include an interventional cardiologist and cardiac surgeon and are made on an individual basis.

  38. Advanced cardiac life support (ACLS): • In the event of cardiac arrest, the immediate implementation of ACLS guidelines is indicated. Through these measures, the greatest benefits can be achieved in the fight against sudden death. • In general, ACLS guidelines should be followed in all cases of SCA; however, depending on the presented rhythm, the following should be considered in acute therapy of SCA:

  39. Bystander CPR • Recent data suggest, that compression-only CPR may be of equal or greater effectiveness than traditional compression plus ventilation techniques. • Known facts that the main initiating mechanisms of SCD are V T and V F and so defibrillation is a critical factor in restoring the rhythm. • Immediate chest compression and defibrillation are the most important interventions to improve the outcome in SCD, whereas ventilation does not play an important role.

  40. Ventricular arrhythmia (VF and VT) • Defibrillation is the mainstay of the acute therapy of SCA due to VF or VT. • Epinephrine (1 mg q3-5min) or vasopressin (40 U single dose) are given. • Amiodarone (300 mg IV push and 150 mg repeat IV push if needed) and lidocaine (1 mg/kg IV push q3-5min up to 3 doses) can be used as antiarrhythmic drugs if defibrillation does not control the VF/VT. • In case of polymorphic VT or suspected hypomagnesemia, 1-2 g IV push of magnesium is recommended.

  41. Pulseless electrical activity (PEA) • Epinephrine (1 mg q3-5min) can be used as there is no evidence supporting the use of vasopressin in PEA. • Atropine (1 mg q3-5min) should be used in case of bradycardia. • Sodium bicarbonate (1 meq/kg) should be given if there is associated hyperkalemia and its use may be considered in long arrest intervals and suspected metabolic acidosis.

  42. Asystole • One study suggested that vasopressin is more effective in acute therapy of asystole than epinephrine. • Atropine and sodium bicarbonate are used with similar indications in PEA.

  43. Medical stabilization • Careful post resuscitative care is essential because studies have shown a 50% repeat SCA after resuscitation . • Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of many studies.

  44. Empiric beta-blockers are reasonable in many circumstances because of favorable properties. • Empiric antiarrhythmics, including amiodarone, should not supersede ICD implantation unless control of recurrent VT is needed while the patient is in the hospital.

  45. Therapeutic hypothermia • This intervention limits neurologic injury associated with brain ischemia during a cardiac arrest and reperfusion injury associated with resuscitation . • Hypothermia prevent neurologic injury,by several mechanisms including reduction in metabolism and oxygen consumption of the brain, inhibition of glutamate and dopamine release, and prevention of oxidative stress and apoptosis.

  46. Therefore, therapeutic hypothermia should be considered for patients who have been successfully resuscitated from SCA and who are comatose. • Therapeutic hypothermia is more effective in patients with initial rhythm of VF/VT but is also recommended for patients presenting with asystole and PEA.

  47. Patients who should not receive therapeutic hypothermia • Those with tympanic membrane temperature of below 30ºc at the time of presentation. • Those who were comatose before SCD. • Those who are pregnant. • Those who have inherited coagulation disorders. • Those who are terminally ill.

  48. Two main techniques for induction of therapeutic hypothermia: • Surface cooling methods with the use of precooled surface cooling pads • Core cooling methods with the use of cold intravenous fluids.

  49. Primary prevention of SCD • Several studies have evaluated the use of prophylactic ICD for primary prevention in patients who at high risk for future SCD. • The Home Automated Defibrillator Trial (HAT) demonstrated no survival benefit for the use of a home automated external defibrillator AED in patients surviving after a recent anterior MI who were not candidates for an ICD.

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