Cardiovascular system presentation. pptx

CVS practical

1. GOVERNMENT MEDICAL COLLEGE NAGPUR CARDIOVASCULAR SYSTEM

2. Topic to be covered Specimens Atherosclerosis Aneurysms Mitral stenosis , aortic stenosis Infective indocarditis Fibrinous pericarditis Syphilitic aortitis Myocardial infaction Slides Atherosclerosis Arteriosclerosis Coronary atheroma with thrombus Myocardial infarction

3. Histology of blood vessel

4. Arteriosclerosis Thickening and loss of elasticity of arterial wall 3 variants Monckeberg medial calcific sclerosis Arteriolosclerosis –small arteries and arterioles (hypertension and DM) Atherosclerosis : The dominant pattern of arteriosclerosis Primarily affects the elastic (aorta, carotid, iliac) and large to medium sized muscular arteries (coronary, popliteal )

5. Monckeberg medial calcific sclerosis >50 years of age , muscular arteries, does not encroach on the vessel lumen clinically insignificant Calcification in media of artery in ring like fashion- stiff pipe stem arteries

6. Arteriolosclerosis Hyaline thickening and proliferative changes of small arteries and arterioles especially in kidney Associated with DM,HT Hyaline arteriosclerosis in benign HT Hyperplastic arteriolitis in Malignant HT Fibrinoid necrosis in malignant HT

7. Atherosclerosis Atherosclerosis is a generic term for thickening and loss of elasticity arterial wall. Atherosclerosis is characterized by intimal lesion called atheroma or atheromatous or fibrofatty plaques which protrude into and obstruct vascular lumen and weaken the underlying media. Greek word – hardening, formation of atheromatous plaque

8. Distribution of atherosclerosis in descending order of heavily involved vessels : Lower abdominal aorta. Coronary arteries. Poptiteal arteries. Internal carotid arteries. Vessels of circle of willis . Vessels rarely usually spared are except their ostia Vessels of the upper extremities. Mesenteric artery. Renal artery

9. Pathogenesis of atherosclerosis Response to injury hypothesis : The response to injury hypothesis considers atherosclerosis to be a chronic inflammatory response of the arterial wall initiated by injury to the endothelium. Moreover, lesion progression is sustained by interaction between modified lipoproteins monocyte derived macrophages T lymphocytes and the normal cellular constituents of the arterial wall.

10. Normal vessel

11. An atheromatous plaque consists of a raised lesion with a soft grumous core of lipid (mainly cholesterol and cholesterol esters) covered by a fibrous cap Mechanical obstructing blood flow, atherosclerotic plaques can rupture leading to catastrophic obstructive vascular thrombosis. increase the diffusion distance from the lumen to the media, ischemic injury and weakening of the vessel wall, changes that may result in aneurysm formation . Morphology Fatty streaks- multiple minute flat yellow spots,(lipid-filled  foamy  macrophages).1 cm long or  longer

12. Vasa vasorum ulceration Yellowish white raised plaque Complicated atherosclerotic lesion Gross of Cut section of aorta

13. Atherosclerosis- Gross eccentrically located, yellowish white plaques – bulges into the lumen may ulcerate Cut section – yellowish white soft core, gritty to cut due to calcification.

14. Microscopy-Components of Atherosclerotic Plaque Vessel wall

15. lumen Near complete occlusion of lumen

16. Complications Rupture Ulceration Haemorrhage Thrombosis and embolism Aneurysm

17. Whitish yellow plaques Adventitial surface Intimal surface Vasa vasorum

18. Microscopy of coronary atherosclerosis W lumen Atheromatous plaque Cholesterol clefts Calcification

19. AHA Classification of atherosclerosis

20. Vasculitis Inflammatory process of blood vessel. Many causes – infectious, chemical mechanical, immunological and radiation INFECTIOUS – Bacterial and syphilis NONINFECTIUOS : ,PAN Hypersensitive leucocytoclastic Wegener's granulomatosis Temporal arteritis / Giant cell arteritis Takayasu’s Dis. / pulseless Dis.. Burger's disease ( Thromboangitis oblita ) Miscellaneous – Rheumatoid arteritis Raynaud’s phenomenon and Raynaud’s disease

21. Syphilitic aortitis Syphilitic – 4 th to 5 th decade Tertiary stage of syphilis Mainly aorta and cerebral vessels AA, Arch and DA involved. Pathogenesis is – begins as  inflammation  of the adventitia, including the vasa vasorum . As it worsens, the vasa vasorum show hyperplastic thickening of their walls that restricts blood flow and causes ischemia of the outer two-thirds of the aortic wall. Starved for oxygen and nutrients,  elastic fibers  become patchy and  smooth muscle cells  necrosis. The wall weakens and scars. If the disease progresses,  syphilitic aortitis  leads to an aortic aneurysm.

22. Gross - Aorta intima has irregular wrinkling, fine or coarse, with irregularities of surface produced by scattered inflammatory fibrosis, producing the characteristic tree bark appearance Microscopy – Endarteritis and periarteritis

23. Intimal surface of aorta show patchy irregular whitish areas Heart with part of ascending aorta

24. Aneurysm permanent abnormal dilatation of vessels due to weakening of wall. Classification - 1)congenital/acquired 2)True / False 3)Depending upon gross appearance fusiform , saccular , cylindrical, arterial dissection, arteriovenous 4) Based on etiopathogenesis Atherosclerosis Syphiltic Dissecting Mycotic Berry aneurysms

25. Atherosclerotic aneurysm : Male > 50 yrs Abdominal aorta & branches Pathogenesis - loss of elastic tissue and atrophy of media Effect - Rupture, compression & occlusion Syphilitic aneurysm : Develop in tertiary stage Male > 50 yrs Arch, ascending aorta & dissecting aorta Pathogenesis - ischemic due to endarteritis & periarteritis

26. Dissecting aneurysms Blood enters the separated (dissected )blood vessels. Aorta and rarely in other vessels Male between 50-70 yrs In female it may occurs during pregnancy Causes: Hypertensive / Non-hypertensive , Marfan’s syndrome,Cystic medial necrosis,Iatrogenic trauma during cardiac catheterisation or CABG,Pregnancy,Chemical toxin

27. Pathogoly : Intimal tear –Ascending Aorta Dissection variable length-Type - I,II & III Debakey’s classification Histology-Focal separation of fibro muscular & elastic tissue

28. Ischaemic heart disease Ischaemic heart disease is the generic designation for a group of closely related syndromes resulting from myocardial ischemic - an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood. The C/M of IHD be divided into four syndromes. ( i ) Myocardial infarction (M1) (ii) Angina pectoris (iii) Chronic IHD with heart failure. (iv) Sudden cardiac death.

29. Myocardial infarction Heart attack 90 % are deaths occurred within first few hours if not treated on time. 10-25% of all deaths Caused by Coronary artery obstruction by Atheromatous plaque, Vasospasm Emboli – left sided intramural thrombi, infective endocarditis , prosthetic material

30. Myocardial response Decrease in blood supply(ischemia) Myocardial dysfunction and death of myocytes in the area supplied by the occluded coronary artery (area of risk) First 20-30 minutes – reversible injury- (proper treatment is given further damage can be prevented (ultra structural damage- <ATP and mitochondrial swelling) Disruption of the sarcolemmal membrane- intracellular enzymes to leak in the circulation (basis for the blood tests)

31. Types of MI Age related- recent/ old healed Location – anterior / posterior/ septal Thickness of myocardium – transmural , subendocarial , multifocal Subendocardial region if first affected by ischemia.

32. Features Transmural Subendocardial Definition Full thickness Inner third to half Frequency More frequent Less Distribution Specific area of supply Circumferential Pathogenesis >75% coronary obstruction Hypoperfusion Coronary thro mbosis Common Rare Epicarditis Common None ECG ST elevation myocardial infarct” (STEMI ) “non–ST elevation infarct” (NSTEMI) Differences between Transmural and Subendocardial MI

33. Patterns of MI Transmural Subendocardial Multifocal microinfarct the necrosis involves virtually the full thickness of the ventricular wall ECG--- “ST elevation myocardial infarct” (STEMI ) Inner third of the ventricular wall — “non–ST elevation infarct” (NSTEMI). Smaller intramural vessels. nonspecific changes or can even be electrocardiographically silent.

34. Left  anterior  descending  coronary  artery (40%  to  50%):  infarcts anterior wall of left ventricle, near the  apex the anterior portion of ventricular septum Right coronary artery   (30% to 40%):  Infarcts -inferior/posterior  wall  of  left  ventricle;  posterior  portion  of  ventricular septum; inferior/posterior right ventricular Left circumflex coronary artery  (15% to 20%):  infarcts involving the lateral wall of left ventricle  except at the apex Infarct location with involved CA

35. Sequence of changes in MI

36. Normal myocardium

37. brick-red  color  (normal ) where  lactate  dehydrogenase  activity is preserved.  Dehydrogenases  leak out  through the damaged membranes  of dead  cells, infarct -unstained pale zone By 2- 3 hours -

38. 4-5 hours – dark mottling Myocardial necrosis along with neutrophilic infiltrate

39. 3-7 days Hyperemic   border; central yellow-tan softening disintegration of dead  myofibers , with dying  neutrophils ;  early  phagocytosis  of dead cells by  macrophages  at infarct border

40. 2-8 weeks White fibrous scar 2-8 weeks Increased collagen deposition,  With decreased cellularity

41. Complication Arrhythmias and conduction defects, Extension of infarction, or re-infarction Congestive heart failure ( pul edema) Cardiogenic shock Pericarditis Mural thrombosis, - embolization Myocardial wall rupture, tamponade Papillary muscle rupture, Ventricular aneurysm

42. MI Ruture

43. Laboratory diagnosis of MI Myocardial cell necrosis leads to membrane damage and leakage of cell contents into the bloodstream This forms the basis for measurement of biochemical markers of myocardial injury in blood The essential parameters for diagnosis of MI are clinical features, electrocardiographic changes, and detection of biochemical markers released in blood from myocardial damage .

44. Clinical features Severe retrosternal chest pain, radiating to back and left arm Rapid, weak pulse Profuse sweating Dyspnea 10-15% may be entirely asymptomatic Electrocardiographic changes Q Waves ST segment changes T wave inversion

45. Biochemical markers Creatine kinase (CK) – Total CK Isoenzymes – CK-MB (activity) and CK-MB (mass)* Aspartate aminotransferase (AST) activity and Lactate dehydrogenase (LDH) – Cardiac troponins ( cTn )* – cTnT – cTnI Myoglobin Currently, myoglobin (an early marker) and cardiac troponin (a definitive marker) are the recommended markers for diagnosis of MI; if cardiac troponin is not available, CK-MB (mass assay) is the next best alternative.

46. Timeline of cardiac markers after acute myocardial infarction Marker Time for detection Peak Return to norma Myoglobin 1-3hr 6-9hrs 1day CK-MB 3-6hrs 12-24hrs 2-3days Troponin 4-8hrs 12-24hrs 5-10days

47. The term acute coronary syndrome comprises of conditions characterized by acute myocardial ischemia and includes ( i ) unstable angina, (ii) non-ST segment elevation myocardial infarction ( NSTEMI ) and (iii) ST segment elevation myocardial infarction (STEMI )

48. Parameter Unstable angina (UA) Non-ST segment elevation myocardial infarction(NSTEMI) ST segment elevation myocardial myocardial infarction (STEMI) 1. Clinical features New angina of severe onset, Angina at rest 3. Recent increase in frequency Similar to UA or STEMI Pain similar to angina but more severe and persistent; not completely relieved by rest or nitroglycerin ; nausea, sense, of apprehension, and sweating;; asymptomatic in 25% 2. ECG ST depression and/or T wave inversion OR Normal ST depression and/or T wave inversion OR Normal ST segment elevation followed by appearance of Q wave and wave inversion 3. Biomarkers Not raised Raised Raised Difference Between Unstable angina, NSTEMI&STEMI

49. Rheumatic fever It is an acute , immunologically mediated, multisystem inflammatory disease classically occurring a few weeks after an episode of group A streptococcal pharyngitis ; skin infection Acute rheumatic carditis is a common manifestation of active RF – pancarditis Chronic rheumatic heart disease (RHD), mainly manifesting as valvular abnormalities.

50. Acute rheumatic fever -host immune responses to group A streptococcal antigens that cross-react with host proteins . antibodies and CD4+ T cells directed against streptococcal M proteins can also in some cases recognize cardiac self-antigens. Antibody binding can activate complement, as well as recruit Fc -receptor bearing cells ( neutrophils and macrophages); cytokine production by the stimulated T cells leads to macrophage activation (e.g ., within Aschoff bodies ). Damage to heart tissue may thus be caused by a combination of antibody- and T cell–mediated reactions

51. Aschoff body (ARC)   Myocardium-  (circumscribed nodule of (mixed mononuclear  inflammatory cells with  associated necrosis)   large activated  Macrophages prominent nucleoli, ( Anitschkow cells )  Chromatin condensed into long, wavy  ribbons (caterpillar cells) Pancarditis 1.Pericarditis 2.Myocarditis 3.Endocarditis- MacCallum plaques,-usually in the left atrium.

52. Acute rheumatic fever: Aschoff body (AB) contains plump histiocytes ( Aschoff cells), Aschoff giant cells may also contain lymphocytes and plasma cells. A central zone of fibrinoid necrosis CUTE RHEUMATIC FEVER (ARF) an Aschoff body (AB) contains plump histiocytes (Aschoff cells),Aschoff giant cells may also contain lymphocytes and plasma cells. A central zone of fibrinoid necrosis

53. CARDIAC LESION Rheumatic endocarditis Rheumatic Valvulitis endocarditis Rheumatic Mural endocarditis Rheumatic Myocarditis Rheumatic Pericarditis

54. Rheumatic valvulitis endocarditis tic VALVULITIS ENDOCARDITIS Fusion and thickening of the chordae tendineae .   Postrheumatic mitral stenosis Fibrotic thickening of the valve leaflets

55. RHEUMATIC VALVULITIS ENDOCARDITIS Aortic stenosis : The severe cuspal thickening and fusion of the commissures have distorted the three cusps of the valve e

56. Pericarditis Inflammation of the pericardium Infections- viral ,bacterial, TB,fungal Immune mediated –RF, SLE,POST MI(Dressler syndrome) Other – MI,uremia,neoplasm Most common cause – viral infection

57. Types of pericarditis 1.Acute pericarditis –fluid accumilation fibrinous and serofibrinous –acute MI, Dressler syndrome, uremia , RF, SLE Serous pericarditis -serous fluid Purulent pericarditis - pyogenic organisms Haemorrhagic pericarditis – neoplastic involvement Caseous pericartis -TB 2.Chronic pericarditis - Adhesive and constrictive

58. Fibrinous pericarditis Characteristically seen in rheumatic heart disease Also called as bread and butter pericarditis Groosly : loss of normal shiny pericardial surface due to deposition of fibrinous exudate in the pericardial sac. The pericardium becomes thick, shaggy due to thick fibrinous exudate

59. Fibrinous Pericarditis

60. Endocarditis Inflammation of the endocardium (the inner layer of the heart) Endocarditis is characterized by the presence of vegetations/ verrucae which have distinct features. Vegetations (thrombotic debris, organisms, with destruction of the underlying cardiac tissues)

61. Classification of Endocarditis Non infective 1. Rheumatic endocarditis 2. Libman - Sacks endocarditis 3.Non bacterial endocarditis Infective 1. Infective /Bacterial endocarditis 2.Other infective – tuberculous,syphilitic , fungal,viral,rickettsial .

62. Infective/Bacterial endocarditis It is a microbial infection of the heart valves or the mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms , often associated with destruction of the underlying cardiac tissues. Classified as Acute bacterial endocarditis (ABE ) is the fulminant and destructive acute infection of the endocardium by highly virulent bacteria in a previously normal heart and almost invariably runs a rapidly fatal course in a period of 2-6 weeks. Subacute bacterial endocarditis (SABE ) is caused by less virulent bacteria in a previously diseased heart and has a gradual downhill course in a period of 6 weeks to a few months and sometimes years

63. The vegetations of BE vary in size from a few millimeters to several centimeters . greenish, irregular, single or multiple, and typically friable. They may appear flat, filiform , fungating or polypoid . The vegetations in ABE tend to bulkier and globular are located more often on previously normal valves cause ulceration or perforation of the underlying valve leaflet, or may produce myocardial abscesses.

64. Heart valves The four cardiac valves— Mitral left side Aortic Tricuspid right side Pulmonary All maintain unidirectional blood flow. Valve function depends on the mobility, pliability, and structural integrity of the leaflets of the atrioventricular valves (tricuspid and mitral) or cusps of the semilunar valves (aortic and pulmonary). Cardiac valves are lined by endothelium

65. Mitral stenosis -Causes 40%patients of RHD (70% females) About 2 decades for the development of MS in RHD Other valvular diseases – Bacterial endocarditis , Libman Sac endocarditis

66. Mitral valve stenosis normal area of the mitral valve orifice  is about 4 to 6 cm 2 Mitral stenosis – < 1 cm 2 narrowing of the left ventricular inflow tract at the level of the mitral valve resulting from a structural abnormality of the mitral valve apparatus

67. Gross of mitral stenosis Early - purse string puckering- base of leaflet is free but the free margins are puckered thickened Advances cases – fish mouth button hole

68. 1.leaflet thickening, 2.commissural fusion

69. What happens with Mitral Stenosis Mitral  stenosis , calcification and fibrous bridging  across the  valvular   commissures  create “fish mouth” or “buttonhole”  stenoses .   left atrium progressively dilates, hypertrophy  and may  harbor  mural thrombi that can  embolize . Long-standing  congestive changes in the lungs may  induce  pulmonary  vascular  and  parenchymal   changes   right ventricular hypertrophy dilatation and right heart failure.   The left  ventricle is largely unaffected by isolated pure mitral  stenosis . 

70. Aortic valve stenosis The aortic valve normally has three cusps or leaflets, although in 1–2% of the population it is found to  congenitally have two leaflets . Normal Area 2.5-4.5 cm2 Mild Stenosis 1.0-2.5 cm2 Moderate Stenosis 0.75-1.0 cm2 Severe Stenosis < 0.75 cm2

71. Aortic Stenosis 1/4 th patients of chronic valvular heart disease 80% symptomatic patients are males Types A.Calcific AS- more common- age related ‘wear and tear’ healing followed by calcification (RVHD), healed congenital malformation familial hypercholesterlaemic xanthomatosis . B. Non- calcific AS- Ch. RH heart disease, congenital bicuspid aortic VD

72. Aortic valve stenosis

73. Effects and Symptoms Symptomatic when the valve orifice is reduced to less than 1cm 2(Normal-3-4.5 cm2) Outflow obstruction Concentric hypertrophy of left ventricle dilatation and hypertrophy of left ventricle Symptoms – exertional dyspnoea, angina pectoris and syncope, sudden death.

74. Case based disscusion 68 Yrs old male a know case of DM &HT, Came to casualty with history of gradually developed left sided chest pain radiating to shoulder, sweating and shortness of breath since 3-4 hrs He had an episode of vomiting non projectile No Histrory of fever, cough or pedal edema Patient is a chronic bidi smoker Past history- had similar complaint

75. General examination – conscious oriented B.P: 180/100mmHg in lying position Pulse: 115 b/m, regular, tachycardia Temp: 99 F Resp : 35/min No paller , icterus , LN pathy , or Organomegaly Systemic Examination CVS: Tachycardia RS, P/A,CNS-NAD

76. ECG Changes: • V1 to V6, AvL • Changes include: • ST Segment Elevation • Q wave development • Loss of R Wave • T wave inversion Investigations CBC-WNL Sr.LDH -Raised Cardiac biomarkers • Trop T raised CK-MB raised Chest Xray • Cardiothoracic ratio increased showing LV Dilatation • Pulmonary edema

77. Diagnosis

78. Assignment 1.Hyaline arteriosclerosis is a feature of A)Malignant HT B)Benign HT C)Both of above D)None of above 2) True about Syphilitic aortitis except A)Tree bark appearance B) Endarteitis C)Seen in secondary syphilis D)Leads to aneurysm

79. 3.In myocardial infarction microscopic picture of coagulative necrosis with neutrophillic infiltration is seen in --- A) 4-12 hours B) 12-24 hours C) 1-3 days D) 3- 7 days 4.Earliest histological change in myocardial infarction is A) Macrophage infiltration B) Neutrophilic infiltration C) Waviness of fibers D) Coagulative necrosis

80. 5. What is the mechanism of acute rheumatic fever- A) Innocent by slender effect B) Due to toxin secretion by streptococci C) Release of pyrogenic cytokines D) Cross reactivity with endogenous antigen 6.Which type of endocarditis has vegetations on both the sides of the valve A) infective endocarditis B) Libman Sack’s endocarditis C) Rheumatic fever D) none

81. 7) Most specific and sensitive marker for MI A)LDH B)CK-MB C) Troponin D)AST 8)Most common cause of mitral stenosis A)Chronic RHD B)Acute rheumatic fever C)Infective endocarditis D)Congenital Heart disease