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Sudden cardiac death


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presentation of sudden death and death due to cardiac causes

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Sudden cardiac death

  1. 1. Rijen ShReStha 21-09-2066M.D. ReSiDent, 1St YeaR
  2. 2.  Define sudden death Principles of examination in case of a sudden death Causes of sudden death Discussion on cardiac causes of sudden death
  3. 3.  Sudden death is any death that occurs within 24 hours of onset of symptoms. ▪ Primary or unpredictable or unexpected ▪ Predictable ▪ Most cases of sudden unexpected death are due to failure to seek timely medical intervention. ▪ If proper medical attention was availed of, death might have been not only predictable but also preventable.
  4. 4.  Age: ▪ 1 month – 30 years ▪ > 70 years Aetiology ▪ Most common: clinically silent degenerative diseases ▪ May be over-looked if evidences are not supportive ▪ Electrocution with household current ▪ Unsuspected drug overdose / poisoning ▪ Concealed trauma with no findings.
  5. 5.  Anatomical examination ▪ Disease ▪ Injury ▪ Evidence of temporal cause Microscopic examination ▪ Disease completely unrecognized on gross Toxicology Lab studies Microbiological cultures
  6. 6.  Failure to examine the sinuses of valsalva and coronary ostia Failure to section coronary arteries at regular, close intervals. Failure to examine entire length of the coronary arteries. Failure to examine ALL the coronary arteries.
  7. 7. Cardiac Causes  Coronary artery disease ▪ Coronary atherosclerosis ▪ Developmental anomalies ▪ Coronary artery embolism ▪ Others ▪ Vasculitis ▪ Dissection  Myocardial diseases ▪ Cardiomyopathies ▪ Myocarditis and other infiltrative processes ▪ Right ventricular dysplasis  Valvular diseases ▪ Mitral valve prolapse ▪ Aortic stenosis and other forms of left ventricular outflow obstruction ▪ Endocarditis  Conduction system abnormalities Modified from Virmani R, Roberts WC: Sudden cardiac death. Hum Pathol 18:485,
  8. 8. Non-cardiac causes Hemorrhage Intra cranial hemorrhage Diseases of the aorta G.I. bleeding Respiratory tract bleeding Intra-cranial causes other than hemorrhage Epilepsy Intracranial Tumors Meningitis Miscellaneous Primary Pulmonary Hypertension Bronchial Asthma Psychiatric Pulmonary thrombo-embolism Epiglottitis Senescence
  9. 9. > 300,000 deaths per year ▪ 80% of which are due to Coronary arterioscleriosisLess due to ▪ Hypertensive Cardio-vascular disease ▪ Cardio-myopathies ▪ Valvular diseases ▪ Myocarditis ▪ Others including Congenital Deformities.
  10. 10.  WHO DALY Report 2004 Nepal India U.S.ACardio-vascular disease 49.9 2810.0 922.7Rheumatic Heart Disease 1.6 103.9 3.5Hypertensive Heart Disease 6.2 49.7 43.7Ischaemic Heart Disease 23.3 1531.5 514.4Inflammatory Heart Disease 0.8 57.8 33.4
  11. 11.  Electrophysiological disturbances leave no anatomical traces, gross or microscopic.  Circumstances  Surroundings  Medical History
  12. 12. Common mechanisms for electro-mechanical decoupling: Myocardial hyper-excitability causing propagation of ectopics.  Ectopic beats causing ventricular tachycardia or premature ventricular contractions.  Presence of circus pathways leads to development of ventricular fibrillation  Ineffective circulation leading to rapid death. Myocardial depression causing failure of propagation of electrical impulses.  Ectopic pace-maker may produce impulse ▪ Failure to establish ectopic pace-maker leads to cardiac asystole and death.
  13. 13. Nervous system can produce strong or electro- chemical discharges that cause ▪ Asystole ▪ Ventricular fibrillation ▪ Vascular redistribution
  14. 14.  On cessation of circulation,  Consciousness lost within 15 seconds  Irreversible cessation of cerebral function within 5 minutes. In case of respiratory arrest, cerebral response is the same. Cardiac function will continue  Initial tachycardia  Bradycardia  Electromechanical dissociation with presence of electrical activity but no circulation.
  15. 15.  Other bio-chemical changes leading to sudden cessation of vital functions:  Electrolyte disturbances  Diabetic ketoacidosis  Drugs
  16. 16. Death due to functional abnormality  Deaths in which there is a significant anatomic alteration from which functional disturbance is obvious or can be referred.  Deaths in which no anatomic alteration can be demostration by routine autopsyThe term ‘functional death’ is used for the latter i.e. apparentsudden cardiac deaths that occur withour any anatomicallysignificant findings by customary autopsy techniques.
  17. 17.  Lesions of the conducting system ▪ Fibrous replacement of the bundle branches (Lev’s Disease) ▪ Aged and hypertrophied hearts ▪ Premature sclerosis of basal septum ▪ Diagnosed following microscopy of conducting system ▪ Calcification of mitral anulus ▪ Impingement of the atrio-ventricular node by calcific deposits ▪ Elderly women ▪ Rheumaroid arthritis, ankylosing spondylitis and scleroderma ▪ ventricular endocardial disease may involve left bundle branch. ▪ Collagen vascular diseases ▪ Infiltrative and inflammatory conditions
  18. 18. Common anomalies found in healthy individuals ▪ Persistent fetal dispersion of atrio-ventricular node. ▪ Ectopic connections between the node and ventricles ▪ Ectopic His bundle ▪ Ectopic atrio-ventricular tracts ▪ Marked sclerosis of artery to the atrio-ventricular node.Role of these anomalies in sudden cardiac death is debatable and undecided.
  19. 19.  Origin of the left coronary artery from the right sinus of Valsalva with the artery passing between the aorta and pulmonary artery. Only a single coronary ostium in the right sinus of Valsalva with the left coronary artery arising from the proximal right coronary artery Origin of the right coronary artery from the left sinus of Valsalva. Origin of the left coronary artery from the right sinus of Valsalva with the artery passing dorsal to the aorta rather than between the aorta and pulmonary artery. Coronary artery hypoplasia  no diagnostic criteria has been set forth for this entity.
  20. 20.  Bridging of coronary arteries: ▪ anomalous pathway of the epicardial arteries ▪ intramural course. ▪ On contraction of the myocardium, the artery gets occluded causing ischaemia. Dissecting coronary aneurysm ▪ Primary ▪ secondary to extension of aortic root dissection ▪ Could be spontaneous ▪ Could be due to trauma Coronary artery spasm ▪ Angina coupled with symptoms similar to acute MI ▪ Autopsy shows no infarct ▪ Coronary artery patent without significant atherosclerosis, narrowing or coronary spasm
  21. 21.  A diverse group of disease of both known and unknown aetiology, characterised by myocardial dysfunction. Diseases not the result of arteriosclerotic, hypertensive, congenital or valvular disease.3 types ▪ Dilated or congestive ▪ Hypertrophic ▪ Restrictive or obliterative
  22. 22.  Gross ▪ Enlargement of the heart with dilatation of all four chambers ▪ Endocardial thrombi is commonly seen Microscopically ▪ Extensive interstitial and peri-vascular fibrosis ▪ Most common cause: ▪ Chronic alcoholism  Direct toxic effects of alcohol  Nutritional effects of alcohol  Toxic effects of additives – E.g. Cobalt ▪ Peripartum cardiomyopathy ▪ Chronic myocarditis ▪ Idiopathic
  23. 23.  Genetic inheritance – autosomal dominant Most common cause of sudden death in adolescents and young adults Gross ▪ Hypertrophied, non-dilated left ventricle ▪ Disproportionate, asymmetrical hypertrophy of inter-ventricular septum as compared to free left ventricular wall ▪ Obstruction of the outflow track ▪ May also present as concentric left ventricular hypertrophy Microscopically ▪ disarray of ventricular myocardial fibers ▪ hypertrophied bizzare myocardium cells. ▪ Seen typically in the septum
  24. 24.  Mitral Valve prolapse  Floppy mitral valve  Myxomatous degeneration of the mitral valve  Barlow’s Syndrome Aortic stenosis  Congenital  Rheumatic inflammation with fusion of cusps  Secondary calcification of congenital bicuspid valves  Primary degenerative calcification of normal aortic valves Acute bacterial valvulitis ▪ involves the tricuspid valve ▪ IV drug abusers
  25. 25.  Clinical Features Could range from no symptoms to non-specific symptoms and may also result in death.  None  Acute fulminating Congestive Heart Failure  Sudden Death
  26. 26.  Aetiology  Infective: ▪ Bacterial ▪ Rickettsial ▪ Viral ▪ Protozoal ▪ Fungal  Connective tissue disorders: ▪ Rheumatic Disease ▪ Rheumatoid Arthritis  Physical agents  Chemical poisons or drugs  Idiopathic
  27. 27.  Associated with a 9x increase in mortality Increased incidence with increasing age. More in men than in women of all ages. Positive Treadmill/Exercise Stress Test associated with increased riskSymptoms: ▪ Vague symptoms including tiredness and fatigue ▪ Chest pain ▪ Palpitations ▪ Shortness of breathIn one-fourth of patients, first symptom is sudden death.Approximately Half of all sudden death victims present with history of Atherosclerotic Heart Disease.
  28. 28. “ANY TIME and ANY PLACE” Sudden death is the first and last symptom in ¼ of individuals with cardiovascular disease. Half of individuals with coronary atherosclerosis die suddenly. Sudden dysarythmias occur in people with no distress previously.
  29. 29.  Sudden death, in an individual with significant coronary atherosclerosis, occurs due to  Myocardial ischemia  Acute electrical event – a ventricular tachydysrhythmia  “Super-imposed transient risk factor”
  30. 30.  Transient rise in Blood pressure Sympathetic discharge Coronary artery spasm Embolism Sympathomimetic stimulation of heart ▪ Caffeine ▪ Epinephrine ▪ Cocaine
  31. 31.  Exercise ▪ Increased heart rate ▪ Increased myocardial oxygen demand ▪ Increased catecholamine levels – ‘hyper-excitability’ Majority of cases of acute cardiac event presents with only electrical instability with only a few showing signs of infarction. Only a small percentage of sudden death is associated with acute coronary artery occlusion with thrombus and myocardial infarct Majority of cases of coronary artery disease who die in the hospital are associated with thrombotic occlusion and infarct.
  32. 32.  Hypertensive cardiovascular disease – concentric thickening Plaque formation – eccentric thickening In elderly, vessel walls rigidly calcified but with patent lumina. Most individuals, 2 vessel involvement  Left main coronary artery  Proximal left anterior descending coronary artery Consider terminal circumstances of death and exclude other causes beyond reasonable doubt.
  33. 33. < 5 hours: Impossible by H&E : possible by PAS (decreased glycogen)5 – 24 hours: Appearance of neutrophils to appearance of degenerating neutrophils1 – 3 days: Exclusively neutrophils and their degenerating forms4 – 6 days: Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries (NO lymphocytes)7 – 14 days: Neutrophils, eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells2 – 8 weeks: Eosinophils, macrophages, pigment, fibroblasts, capillaries, lymphocytes, plasma cells (NO neutrophils)> 2 months: Connective tissue condensed; minute foci of necrosis may still persist. Exudate has essentially disappeared, but a small number of lymphocytes and pigmented macrophages may be seen until one year
  34. 34. Hours Days Weeks1 5 6 12 24 2 3 4 5 6 10 12 14 18 3 4 8 52 Mural Thrombus (Completely organized after 3 weeks) Fibrinous Pericarditis (Organisation beginning at 5 days) Lymphocytes, Plasma Cells Fibroblasts Capillaries Scar Tissue Necrosis Collagen Pigmented Macrophages Eosinophils Neutrophils (with degenerating forms beginning at 24 hours) Adapted from Mallory et al. American Heart Journal 18:647-71, 1939
  35. 35.  Mallory describes that histological features could be determined on gross examination as well:  First 72 hours: Infarction appears pale and drier. Sometimes, hemorrhage is observed.  4 days: Yellow line appears at the periphery due to leukocytic infiltration. Infarct becomes yellow brown.  6 – 8 days: Band becomes broader and sometime yellow-green  8-10 days: Granulation tissue is formed around the infarct forming a reddish-purple zone. Size of infarct decreases, depression may be seen around the infarct  2 – 3 weeks: Healing continues, band of granulation tissue increases and central mass of necrotic muscles decrease. Infarct appears pale and red-brown color.  3-4 weeks: Small islands of necrotic muscle surrounded by granulation tissue.  >1 month: Granulation tissue become older, collagen content increases. Capillaries become compressed and less prominent. Infarct appears paler and gelatinous.  2 – 3 months Infarct contracts to form a white fibrous shrunken and firm scar.
  36. 36.  Perforated Myocardial infarct forming massive hemopericardium with cardiac tamponade.  Distended, taut, blue pericardial sac.  Usually associated with transmural myocardial infarct that is extremely necrotic and inflamed  Occurs between 5 – 7 days before connective tissue replaces necrotic muscle.  History of minimal or no chest discomfort.  Rapid death
  37. 37.  Sudden death – any death that occurs within twenty four hours of onset of symptoms. Common causes of sudden death are cardiac in nature.  In infants – congenital  In children, adolescents and young adults ▪ Cardiomyopathies ▪ Myo carditis ▪ Coronary artery anomalies  In adults – coronary insufficiency caused by coronary artery disease. – Valvular diseases – Myocardial diseases – Diseases of the conduction system