Cardiovascular Disease Presentation PDF

1 Cardiovascular Disease By: Fatma Ali Alashkham  2 What is Cardiovascular Disease (CVD)? “ Cardiovascular Disease is an abnormal function of the heart involving the narrowing or blocking of blood vessels.” ...

1 Cardiovascular Disease By: Fatma Ali Alashkham  2 What is Cardiovascular Disease (CVD)? “ Cardiovascular Disease is an abnormal function of the heart involving the narrowing or blocking of blood vessels.”  3 Blood vessels Vasculitis: Types * Blood vessel Localized: due to inflammation. trauma, infections or toxins. Systemic: multifocal nercrosis in multiorgans.  4 Why is polyarteritis Nodosa? ‫باهتلا‬ ‫بايابشلا باقعلا‬ 5  6 Wegener, s granulomatosis ‫مرو‬ ‫يبلبح مشنغاا‬ ❑Age: 40 yrs. ❑Clinical : a necrotizing granulomatous  Ulcer in nose. vasculitis of: ‫ بالطضابا باغللر بالا‬ Sinusitis. ‫ شهسبي يح باهتلا باعمألا بالمدشا م شثؤا‬ Recurrent pneumonia. ‫ألح باهليا بالمدا‬  Renal insufficiency. I. Upper / lower respiratory tract. II.Kidney { glomerulonephritis}. ❑Cause: unclear III.Arteries & veins.  7 Temporal (giant cell,cranial) arteritis.‫باهتلا باياشلا وم بااللشل باقللللا‬ Inflammatory arteritis affecting large vessels Fever. mainly head arteries. Fatigue. Age: above 50 yrs & more Weight loss. common in women. Unilateral headache. Site: temporal artery & Facial pain & morning extracranial branches of stiffness of neck, carotid artery. shoulder, and hip, There is multifocal unilateral blindness. granulomatous vasculiti Fibrosis= vessel wall thickness.  8 Takayasu,s arteritis ( pulseless disease). Age: 15 to 40 yrs, mainly females.  a granulomatous vasculitis affects mainly aotra and its main branches. Absent pulse in upper extremity+coldness or numbness of fingers. Bp is low in upper extremity (than in lower). Involvement of : Pulmonary arteries pulm hypertension cor pulmonale. Of retinal arteries hge blindness.  9 Kawasaki,s disease Age: infants and young children 2- 5 years male more then female and unknown cause.  acute febrile illness. (is the medical term used to describe a sudden fever or elevation in body temperature) Transmural inflammation of vessels with fibrinoid necrosis aneurysm / thrombosis. Acute myocardial infarction ( the most common cause of MI in children). 10  11 Thromboangitis obliterans Age: 25 to 50 yrs, cigarette smoking males. Remitting & relapsing inflammatory disorder may lead to thrombosis of medium- sized vessls.  ‫لل شثلا بالطضابا بالاهتللح بالغقلا مباهللاو ىاإ طللت‬.‫باعمألا بالمدشا مهداضا باحلا‬ Clinical: Intermittent claudication in feet & hands, Raynaud,s phenomenon )is a problem that causes decreased blood flow to the fingers(, and distal gangrene. 12  13 Atherosclerosis (AT). Is a degenerative disease of large and median sized arteries, characterized by intimal plaques, called atheroma that press on, and weaken the underlying media, & superadded serious complications. a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls. 14  15 Atherosclerosis (AT). Acquired risk factors:  Hyperlipidemia.  Hypertension.  Cigarette smoking.  Diabetes mellitus. Minor acquired risk factors:  Sedentary life- style e.g., lack of physical exercise.  Obesity, stress, type 1 personality, low socio- economic status.  Oral contraceptive pils, hyperuricemia & high carbohydrate intake.  16 Atherosclerosis (AT). Pathogenesis.  AT lesions start in response to endothelial cell injure, which may be caused by: Hyperlipidemia. Hypertension Smoking. Toxins.  The endothelial injury results in dysfunction of their lining endothelial cells permeability, leukocyte adhesion & thrombotic potential.  17 Atherosclerosis (AT).  Accumulation of plasma lipoproteins, mainly low-density lipoprotein(LDL) with it is high content of cholesterol, in the vessel wall.  Migration of macrophages to intima, and smooth muscle cells from media to intima, to engulf lipids forming foam cells (Moncytes).  Atheromatous plaques: a fibro- fatty lesion, irregular and raised plaques may coalesce to form map- like configuration.  ‫‪18‬‬ ‫طابرا بابامطلغلا بالهغلا يح بابللبمل ‪ ،‬مصلخا بابامطلا ‬ ‫مم مودل اسبا ألالا )‪ (LDL‬بالهغح مغانم بالثليا‬ ‫ما بالدالسهاما ‪ ،‬يح ولبر بادألا بالمدا‪.‬‬ ‫هلاه باالما ىاإ بابضلاا بالبصللا ‪ ،‬مصللشل باقاللا ‬ ‫باللسلا ما‬ ‫بادات ىاإ بابضلالا ‪ ،‬اهبهلم بااللشل بالهغلا باللداا الاللشل‬ ‫بااغدشا‬ ‫ادشحلا أدلله‪ :‬ةيا لهغلا ‪ ،‬ادشحلا غلا مغهتلا ‪.‬‬ ‫ابلتل للاااشضا‪.‬‬ ‫ب‬ ‫مماطنقا لل طهحل اهيلل طلدشغبل‬  19 Atherosclerosis (AT).  Proliferation of SMCs , and some of them change to foam cells+ collagen.  Foam cells ( SMCs & macrophages) are responsible for the yellow discoloration that are seen in early AT and are known as fatty streaks. fatty streaks are reversible change.  20 Atherosclerosis (AT). Morphology of AT:  fatty streak : appear at orifices of branches (linear elevations ) of aorta, coronaries, and cerebral arteries. They appear in some children.  Fibro- fatty (atheromatous) plaques: these are irregularly raised plaques, of several cm, may coalesce to form map- like configuration. They mainly arise in abdominal aorta, coronaries, popliteal arteries, internal carotids, & mesenteric arteries.  21 Atherosclerosis (AT).  Advanced (complicated ) plaques: are plaques that may show in Calcification. Fissuring or ulceration. Thrombus formation. He into the plaque results from rupture of overlying fibrous cap. Anrurysmal dilation.  22 Atherosclerosis (AT).  Clinical effects ( complication ) of AT:  ischemic heart disease.  Cerebral stroke ( cerebral infarction).  Gangrene of foot and intestines.  Abdominal aorta aneurysm.  Intermittent claudication ( ischemia of lower limb vessels pain on walking relieved by rest).  23 Aneurysm It is a localized permanent dilation of blood vessels, or hear, due to weakness of the wall and mainly affects the aorta. ‫هد طدام مدطقح لباا العمألا بالمدشا‬ ،.‫ لسبي طقض باللبر مشثؤا ليلل رالسح ألإ باياشلا باعمرلح‬، ‫وم الم‬ Causes:  Atherosclerosis.  Syphilis. is a bacterial infection usually spread by sexual contact.‫مام باههاا‬  Congenital abnormality in circle willis, known as berry aneurysm.  Trauma.  Inflammatory.  Idiopathic.  24 is a circulatory anastomosis that supplies blood to the brain and surrounding structures. A circulatory anastomosis is a connection (an anastomosis) between two blood vessels, such as between arteries (arterio-arterial anastomosis), between veins (veno-venous anastomosis) or between an artery and a vein (arterio-venous anastomosis)  25 Aneurysm Types:  According to compositions of the wall OR histological:  true aneurysm: formed of all layers of the vessel. False aneurysm: formed of a fibrous wall, lacking normal structures & connected to the vessel lumen.  ‫ شهلدا ما‬:‫ طللل باعمألا بالمدشا باحعلعح‬:‫يسي طابرلي باللبر‬ ‫ شهلدا‬:‫طللل باعمألا بالمدشا باللوا‬.‫وللم لبعلا بادألا بالمدا‬ ‫ما ولبر النح شنهعا ىاإ باتللرل باضبلقلا ممهدل لهلدشض بادألا‬.‫بالمدا‬  According to morphology: saccular, fusiform, serpentine or varicose,& cylindrical. ‫ بأدبا بم مهقاا‬، ‫ منهاح‬، ‫رلسلا‬.‫ واضدبالا‬، ‫وم لمباح‬  26 Aneurysm  According to etiology: Atherosclerotic Aneurysm :affecting the abdominal portion of the aorta, common iliac and other large arteries, particularly with age. Dissecting aneurysm: An aneurysm in which the wall of an artery rips (dissects) longitudinally. This occurs because bleeding into the weakened wall splits the wall. Dissecting aneurysms tend to affect the thoracic aorta. They are a particular danger in Marfan syndrome. (MFS) is a multi-systemic genetic disorder that affects the connective tissue  27 A berry aneurysm: which looks like a berry on a narrow stem, is the most common type of brain aneurysm. They make up 90 percent of all brain aneurysms, according to Stanford Health Care. Berry aneurysms tend to appear at the base of the brain where the major blood vessels meet, also known as the Circle of Willis.  28 A mycotic aneurysm is a dilation of an artery due to damage of the vessel wall by an infection. It is also referred to as infected aneurysm. The term “mycotic” referring to fungal is a misnomer as various organisms including predominantly bacterial can cause the aneurysm.  29 Varicose veins It is abnormal dilated, elongated and tortuous vein..‫مهد بادرشل بالهدام مبالللمل مبالهقاا‬ Types are:  Varicose veins of leg: affects mainly the saphenous veins in females due to incompetence of vein valves, repeated pregnancies.  Complication: Cosmetic disorder. Ulceration. Embolism. Squamous cell carcinoma.  30 Varicose veins  esophageal varicose veins: occurs due to portal hypertension in liver cirrhosis and this lead to hematmesis. ‫شحلي لسبي برطنلا طنت بالو بابللح يح طللض بالبل مهلب شثلا ىاإ‬.‫لحا لمدا‬  Hemrrhoide ( piles) : varicosity of venous plexus of superior & inferior rectal veins bleeding.  Varicocele of spermatic venous plexus in spermatic cord causing scrotal enlargement, and male infertility.  31 Hypertension Reflects a health problem because:  It is very common.  It has wide spread consequences.  It is asymptomatic for long period.  It is one of the commonest important risk factor in coronary heart disease and cerebrovascular accidents.  It causes left ventricular, hypertrophy & congested heart failure, renal failure, and aortic dissecting aneurysm.  32 Hypertension Normal blood pressure is controlled by:  Cardiac output.  Peripheral resistance; regulated by the vasoconstrictors as angiotensin-II, catecholamines, thromboxane, leukotreins, and adrenergics.  ، ‫ بالللدطاشغلا‬، ‫ باثامدلدرسلا‬، ‫ باللطللدالملغلا‬، 2 ‫واللدطغسلا‬.‫مباعلرشغلالا‬  33 Hypertension  role of kidney in HTN:  Kidney secrets Renin-angiotension system.  It regulates sodium homeostasis.  It synthesizes renal vasodepressor substances, such as PGs, urinary kallikrein, PAF, & nitric oxide.  34 Hypertension  classification of HTN: according to aetiology  Primary or essential HTN: comments type 85-90 % of cases of this type. Unknown aetiology but main theories suggested are:- Renal ischemia ( humoral mechanism) is activation renin system angiotensinogen angiotensin ( arteriolar spasm & hyperaldosteronism). Neurogenic mechanism is ( psychic and emotional stimuli sympathetic tone peripheral vasoconstriction 95% hypertension, 90% benign, 10% malignant.  35  Secondary HTN: secondary to pre-existing diseases. 5% hypertension, 80% benign, 20% malignant.  36 Hypertension  Causes of secondary HTN:  Renal: acute & chronic glomeriolonephritis, chronic pyelonephritis ‫باهتلا يح يدم باللح‬, polycystic kidney ‫طااا بم باهنلا ولبر باللح‬, renal artery stenosis & rennin producing tumour.  Endocrine: thyrotoxicosis, hypothroidism, primary hyperaldosteronism,& pheochromoctoma. ، ‫باهسلا بالرلح‬ ‫ مرو باعدبطا‬، ‫ ياف باعالماهلامالا باعماح‬، ‫لددر بانله بالرللا‬  Vasccular: coarctation of aorta, vasculitis ( polyarteritis).  Others: preeclampsia, increased intracranial tension and acute stress. ‫ باهتلا باعمألا بالمدشا (باهتلا‬، ‫طالا باعلتا‬ ‫ مبشلله باهدطا لبصل‬، ‫ طسلا باحلل‬:‫ةصاما‬.)‫بايابشلا بالهقلله‬  37 Hypertension Pathogenesis of HTN: ( genetic factors). Defective sodium Theory 1 excretion Salt intake ‫صلل يح‬ ‫ىيابب‬ Na++ ‫باددلشدو‬ retention ‫باليهبلا‬ Plasma HTN COP volume  38 Hypertension Neurhormonal Theory 2 activity ‫ايلف‬ Salt intake ‫هامداح أدبح‬ Peripheral Neural HTN resistance activity  39 Hypertension Environmental factors :  stress, obesity, heavy use of salt, smoking & lack of physical activity.  40 Hyperaldosteronism is a disease in which the adrenal gland(s) make too much aldosterone which leads to hypertension (high blood pressure) and low blood potassium levels. Pheochromocytoma is a type of neuroendocrine tumor that grows from cells called chromaffin cells. These cells produce hormones needed for the body and are found in the adrenal glands. The adrenal glands are small organs located in the upper region of the abdomen on top of the kidneys  41 Hypertension ❑According to clinical manifestations:  Benign HTN: usually primary if secondary it is caused by endocrinal diseases.  age: above 45 yrs.  It is associated with hyaline arteriolosclesrosis: a homogeneous pink hyaline thickening of the wall of arterioles with narrowing of the lumen.  Symptoms: palpitation, audible pulsation in the head, headache, attacks of dizziness. ‫ ابم‬، ‫ صنعلا‬:‫باعأابم‬.‫ ادللا لمبر‬، ‫ خلبا‬، ‫مسلدا يح بااوا‬  42 Hypertension  complications are:  Left ventricular hypertrophy congestive heart failure.  Cerebral hemorrhage infarction.  nephrosclerosis proteninurea.  Cause of death: heart failure, cerebral hemorrhage, renal failure.  43 Hypertension  malignant HTN: usually secondary caused by renal diseases.  Malignant termination of benign hypertesion& it may follow essential HTN, & It is much less than the benign HTN.  Age: 30-35 yrs and equal sex incidence.  Morphology: it is associated with arteriolar fibrinoid necrosis ‫صلخا للرداللا‬, hyperplastic arteriolosclerosis which appear as onion- skin.  44 Hypertension  complication of HTN:  Heart left ventricular hypertrophy H.F, & focal myocardial necrosis.  Kidneys= nephrosclerosis renal failure.  Eye: retinopathy= microaneurysm, retinal hge, papiledema. swelling that is caused by increased intracranial pressure due to any cause.  Brain cerebral hge, & encephalopathy. ‫بأهللا‬ ‫لملغح‬  45 Hypertension Main cause of death in:  benign essential HTN: heart failure, followed by cerebral hge.  Malignant HTN: Renal failure.  46 The heart  Hypertensive heart disease:  Systemic Hypertensive heart disease: it affects the left ventricle leading to adaptive response to the high blood prssure in the form of hypertrophy, usually concentric hypertrophy. )is a hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ are thickened and its capacity or volume is diminished(  Myocardial dysfunction, cardiac dilation,& chronic H F.  Pulmonary Hypertensive heart disease: Cor pulmonale.  47 The heart  48 The heart  Causes of cor pulmonale:  Lung parenchyma diseases such as ( chronic obstructive pulmonary disease, diffuse pulmonary fibrosis, & cystic fibrosis).  Lungvascular diseases such as ( pulmonary embolism, primary pulmonary vein sclerosis, wegener,s granulomatosis, vascular sclerosis secondary to drugs, toxins or radiation. & disseminated lung metastases).  49 The heart Heart failure ‘H F’: It is inability or failure of the heart to maintain an output sufficient for metabolic requirement of tissues.  50 The heart  pathophysiology of H F:  Backward failure: occurs when a ventricle fails to pump an adequate volume, blood accumulates in the atrium and the connecting venous system, e.g., in aortic stenosis, or essential HNT.  Forward failure: occurs when the heart in unable to deliver a sufficient output to the peripheral tissue, e.g., myocardial infarction.  51 The heart  Low output failure: occur when the cardiac output is reduced, this occurs in most patients of heart failure.  High output failure: occurs in thyrotoxicosis, severe anemia, and pregnancy.  52 The heart ❑ H F, may be acute or chronic, left or right side.  Causes acute H F:  Sudden occlusion of coronary artery.  Massive pulmonary embolism.  Hemopericardium.  Acute toxic myocarditis.  Rupture of ventricular aneurysm.  Chronic H F: left or right side.  53 The heart Left sided chronic H F: causes are  Ischemic heart disease.  Essential HNT.  Myocardial infarction diseases.  Aortic valve stenosis & incompetence.  Mitral valve incompetence.  54 The heart  effects of chronic left HF:  Lung: chronic venous congestion of lung and pulmonary edema.  Kidney: COP leads to renal perfusion, and this in turn leads to pre- renal azotemia. occurs when fluid isn't flowing enough through the kidneys Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood.  Brain: COP leads to cerebral hypoxia which leads to hypoxia encephalopathy with irritability, restlessness, then stupor and coma..‫باهتلا مباعرو ؤا بالهدا مبانلبدلا‬  55 The heart Right sided H F: occurs either on top of L V F or a pure form.  Causes :  Cor pulmonale.  Mitral stenosis.  Congenital heart disease with left to right shunt.  56 The heart  effects of Right chronic H F:  Chronic Venous Congestion  CVC liver: nutmeg liver, long standing cases lead to cardiac sclerosis. CVC spleen ( congestive splenomegaly). Ascitis and pleural effusion. Subcutaneuos tissue edema, appears around ankles or sacral region if patients is recumbent.Chronic Venous Congestion CVC liver: nutmeg liver, long standing cases lead to cardiac sclerosis.  hronic Venous Congestion  57 Rheumatic fever ‘R F’:  Is autoimmune collagen diseases its meaning inflammation and degeneration of collagen fibers affects mainly heart and joints its an acute recurrent inflammatory disease occurs principally at childhood and usually infection follows Beta- hemolytic streptococcal group A pharyngitis ( sore throat) & tonsillitis. R F declines due to use of antibiotics and improvement of socioeconomic living conditions.  58 Rheumatic fever ‘R F’:  etiopathogenesis of R F: it is a post infectious immunologic disorder it results from either:  immune reaction to streptococal hyaluronate capsule Ags that evokes antibotic cross reaction with human tissue Ags or:  Auto immune reaction incited by streptococcal.  59 Rheumatic fever ‘R F’: Acute rheumatic carditis:  It is due to the immune reaction with a widely distributed focal inflammatory lesions found in connective tissue of heart, these are known as Aschoff bodies.  Aschoff bodies are formed of central fibrinoid necrosis, surrounding by lymphocytes and plasma cells.  60 Rheumatic fever ‘R F’: Rheumatic pancarditis: 3 layers of heart affected at same time  Pericarditis: a fibrinous or serofibrinous inflammation, gives a shaggy or bread and butter appearance.  Myocarditis: scattered aschoff bodies within the interstitial connective tissue, usually perivascular it may cause arrhythmia.  Endocarditis: there is fibrinoid necrosis within the cusps or chordenae.  61 Rheumatic fever ‘R F’:  chronic rheumatic heart disease:  It is characterized by organization of the repeated attacks of pancarditis ended by fibrosis which leads to deformity of the cardiac valves and fusion of the commissures, shortening of chordae tendineae leading to stenosis or incompetence of affected valve.  Mitral stenosis occurs in 65-70% of cases.  62 Rheumatic fever ‘R F’: mitral and aortic stenosis occurs in 25%. The affected valve appears as fish- mouth, button-hole, or funnel stenosis. Valves are either stenosed or incompetence.  63 Rheumatic fever ‘R F’:  complications of R H D:  Valvular deformity; stenosis or incompetence.  Arrhythmia; atrial fibrillation.  Mitral stenosis leads to pulmonary hypertension, C V C of lung and congestive heart failure. 64  65 Ischemic heart disease ‘IHD’  coronary heart disease ‘C H D’.  coronary Artery disease ‘C H D’.  it is a group of related syndromes caused by ischemia due to coronary insufficiency in about 90% of cases.  66 Ischemic heart disease ‘IHD’ Ischemic heart disease ‘IHD’:  angina pectoris.  Myocardial infarction ‘MI’.  Sudden death.  Chronic I H D with congestive heart failure.  67 Ischemic heart disease ‘IHD’  pathogenesis:  more than 90% of patients with IHD have fixed stenosing coronary, caused by atherosclerosis.  Common sites for atherosclerosis are; Left anterior descending coronary artery. Left circumflex coronary artery. Right coronary artery: stenosis affects the proximal & distal thirds.  68 Ischemic heart disease ‘IHD’  angina pectoris:  It is a paroxysmal attacks of substernal or precordial chest discomfort in the form of constricting, squeezing, choking or knife- like stabbing.  Etiology: it is due to myocardial ischemia, lasts for 15 seconds to 15 minutes.  69 Ischemic heart disease ‘IHD’  Types of angina: Stable,or typical angina. prinzmetal’s or variant angina. Unstable, or crescendo angina.  70 Ischemic heart disease ‘IHD’ Stable,or typical angina.  Most common type of angina. It is caused by ischemia ( athromatous plaque) plus increased demand of blood due to physical activity or emotion. atheromatous plaque ("plaque"), is an abnormal accumulation of material in the inner layer of the wall of an artery  It is relieved by rest or nitroglycerin  71 Ischemic heart disease ‘IHD’  Prinzmetal’s or variant angina:  Occurs at rest and is caused by coronary spasm in addition to the atheromatous plaque.  It is relieved by vasodilators such as nitroglycerin or calcium blockers.  72 Ischemic heart disease ‘IHD’  Unstable, or crescendo angina:  Occurs at rest and is caused by acute changes in atheromatous plaque such as ulceration or fissuring.  it is the more sever and prolonged angina, that’s why it is called pre- infarction angina, or acute coronary insufficiency.  73 Ischemic heart disease ‘IHD’ Myocardial infarction ‘MI’:  Heart attack & tow types.  Transmural MI: it affects the full or nearly thickness of ventricular wall.  It is usually associated with coronary atheromatous plaque complicated by rupture and superimposed thrombus.  Subendocardial MI: the ischemic necrosis is limited to the inner third or at most inner half of the ventricular wall.  74 Ischemic heart disease ‘IHD’ Risk factors MI:  constitutional factors:  age: can occur at any age but frequency rises progressively with increasing age; 5% of MI occurs in patients under age 40 yr and 45% occurs in patients under age 65yr. Sex: until age of 50 years males are affected more than females; women are protected against MI during reproductive life. But risk is increased in females using oral contraceptive.  75 Ischemic heart disease ‘IHD’  acquired risk factors:  Atherosclerosis.  Hypertension.  Genetic hypercholesterolemia.  Diabetes mellitus.  Cigarette smoking.  76 Ischemic heart disease ‘IHD’  pathogenesis:  coronary artery occlusion; in about 90% of transmural MI the obstruction is caused by a thrombus on top of atheromatous plaque with fissuring or ulceration.  77 Ischemic heart disease ‘IHD’  Morphology: the site of infarction depends on which coronary artery is obstructed; left ascending coronary artery.  Occlusion leads to infarction of anterior wall of left ventricle near the apex, and anterior two- thirds of inter- ventricular septum. It is the common site to be affected and seen in 40-50% of cases.  78 Ischemic heart disease ‘IHD’  right coronary artery occlusion occurs in 30-40% of cases, and infarction affects posterior wall of left ventricle, posterior third of interventricular septum. Diagnosis of MI:  Symptoms  Raised serum enzymes.  E C G changes.  M R I.  79 Ischemic heart disease ‘IHD’  clinical features:  asymptomatic, i.e., silent MI.  Pain: sever, crushing substernal chest pain, may radiate to neck, jaw, shoulder left arm, or epigastrum, usually continues for hours or days & not respond well to nitroglycerin.  Pulse: rapid & weak.  Sweating, nausea& vomiting.  Anxiety, dizziness& faintness.  Laboratory abnormalities.  80 Ischemic heart disease ‘IHD’  complications:  Cardiac arrhythmia: occurs in 75-95% of cases:  ventricular or atrial extrasystole. Sinus tachycardia. Complete heart block. Ventricular fibrillation.  Acute myocardial failure + pulmonary edema: in 60% of MI.  81 Ischemic heart disease ‘IHD’  Cardiac shock: pump failure, 10-15%.  Rupture: of anterior wall of LV hemopericardium. & rupture of postero-medial papillary muscle acute mitral regurgitation and heart failure and rupture of ventricular septum left or right shunt.  Mural thrombi systemic embolism.  82 Ischemic heart disease ‘IHD’  Fibrinous pericarditis occurs in first week of transmural infarction friction rub.  Ventricular aneurysm: late complication due to scar tissue heart failure + thrombus formation.  Recurrence of MI as the etiological cause is still there.  83 Ischemic heart disease ‘IHD’  sudden cardiac death:  Unexpected death due to cardiac causes, occurs within one hour.  The commonest cause is MI { acute plaque change fatal arrhythmia}  Other causes: myocarditis, cardiomyopathy, mitral prolapse, aortic valve stenosis, and congential structural abnormality.  84 Ischemic heart disease ‘IHD’  chronic IHD:  Chronic heart failure which results as a consequence of ischemic heart damage, and usually there is a history of angina.  Repeated subclinical or mild attacks myocardial scaring weaken the myocardium chronic heart failure.  85 Valvular lesions  mitral stenosis:  Etiology:  calcified congenital bicuspid valve.  Chronic rheumatic heart disease.  Degenerative change in old age.  Rheumatoid arthritis.  86 Valvular lesions  Pathophysiology:  There is volume ovrload in left atrium, this is reflected on lungs ( back pressure) chronic venous congestion pulmonary hypertension pulmonary edema.  Decreased cardiac output due to underfilling of L V.  87 Valvular lesions Clinical features:-  dyspnea, and hemoptysis secondray to pulmonary congetion.  Atrial fibrillation, secondray to LA dialation/ hypertrophy.  Dysphagia for solid food due to LA enlargement pressing on esophagus.  88 Valvular lesions  Horsness of voice due to irritation of recurrent laryngeal nerve.  Atrial thrombosis associated with atrial fibrilltiuon.  Thrombosis in appendages thrombo- emblism Cerebral infarction.  89 Valvular lesions Mitral valve prolapse:-  Affects young people.  Caused by increased glycosaminoglycans (a loose ground substance within leaflets and cordae of mitral valve redundant voluminous valve.  Tricusped valve is involved in 25-30 %.  Leaflets prolapse into LA during systole.  90 Valvular lesions Mitral regurgitation:- Etiology  Mitral valve prolapse (MVP), chronic rheumatic heart disease, bacterial endocarditis and rupture of papillary muscle in myocardial infarction MI.  pathphysiology:-  Reflux of blood into LA during systole.  Volume overload in LV&LA leads to hypertrophy/ dilation of both chambers and chronic venous congestion (CVC) lung.  91 Valvular lesions Aortic stenosis: Etiology:  Calcified congential bicuspid valve.  Chronic rheumatic heart disease.  Degenerative change associated with old age ( calcific aortic stenosis).  92 Valvular lesions  Pathophysiology:  Increased resistance to ejection of blood during systole leads decreased COP, i.e., decreased stroke volume, and this lead to narrow pulse pressure.  Concentric LV hypertrophy.  93 Valvular lesions  Clinical features:  Angina: due to decreased COP less filling of coronary arteries, hypertrophic heart receives less blood.  Syncope with exercise due to decreased COP less blood in brain.  94 Valvular lesions  Calcific aortic stenosis:  Age related degenerative change, due to ‘ wear and tear’.  The most common cause of aortic stenosis.  Age: depends if there is congenital anomaly:  At age of 60 to 70 if there is congenital bicuspid valve.  At age of 80 with previously normal valves  There is gradual increase in pressure in the left ventricle Hypertrophy.  95 Valvular lesions  Aortic regurgitation:- Etiology:  chronic rheumatic heart disease.  Long standing essential hypertension.  Bacterial endocarditis.  Dilatation of aortic valve ring in syphilis, dissecting aneurysm, or coarctation of aorta.  96 Valvular lesions  Pathophysiology:-  LV hypertrophy/ dilatation.  Left heart failure.  Increased stroke.  Increased pulse pressure  97 Valvular lesions Tricusped stenosis:-  Etiology: usually associated with mitral stenosis in chronic rheumatic heart disease.  Effects: systemic venous congestion neck vein distension, congestive splenomegaly, and depending pitting edema =ch Rt ht failure.  98 Valvular lesions  Tricusped regurgitation:-  Etiology: stretching of the tricusped valve ring in Rt ht failure, chronic rheumatic heart disease, carcinoid syndrome and bacterial endocarditis.  Effects: volume overload in RV& RA hypertrophy/ dilation.  99 Valvular lesions Pulmonary stenosis:-  Etiology: congenital and carcinoid syndrome.  Effects:pressure overload on RV. Pulmonary regurgitation:-  Etiology: usually functional due to congestive heart failure & heart dilation.  Effects: pulmonary hypertension volume overload on RV.  100 Congenital heart disease Children with significant congenital anomalies may show:  Failure to thrive.  Retarded development.  Cyanosis.  Risk of recurrent illness ( e,g., bacterial endocarditis).  types: * shunts, or * obstructions.  101 Congenital heart disease  shunts:  right to left shunt cyanosis.  Left to right shunt right heart overload, secondray pulmonary hypertension and RV hypertrophy; it ended by cyanosis because pressure in right side will become more than left side.  Long standing Cyanosis clubbing of fingers and toes, hypertrophic osteoarthropathy, and polycythemia.  102 Congenital heart disease Obstructions:  coarctation & valvular stenosis or atresia.  right to left shunts: cyanotic congenital heart disease.  Tetralogy of fallot:  Ventricular septal defect ‘VSD.’  Dextroposed aorta over-riding VSD.  Pulmonary stenosis with RV outflow obstruction.  RV hypertrophy.  103 Congenital heart disease  translocation of great arteries: { more common in children of diabetic mothers}.  aorta & pulmonary artery inversions relative to the ventricles.  Atrial inversions relative to the ventricles.  Ventricles inversions relative to the atria.  Origins of great vessels from the same ventricle.  104 Congenital heart disease  Truncus arteriosus:  developmental failure of aorta & pulmonary artery to separate.  There is early cyanosis, then flow will be reversed to lead to RV hypertrophy + pulmonary hypertension.  105 Congenital heart disease  left to right shunt: Ventricular septal defect ( VSD).  The most common anomaly, associated with tetralogy of Fallot, increased risk of bacterial endocarditis, prognosis varies from spontaneous closure to fatal heart failure.  106 Congenital heart disease  Atrial septal defect ( ASD).  Occurs in female < males, asymptomatic until adulthood: when there is right side hypertrophy ends by right to left shunt cyanosis.  patent ductus arteriosus( PDA).  Occurs as isolated defect in 85-90% of cases, early asymptomatic, later pulmonary hypertension + RV hypertrophy ends by right to left shunt cyanosis. 107  108 Test Q1- Different between Apoptosis and Necrosis? Q2- What are the stages and types of shock? Q3- Define the following terms? 1- Edema. 2- Hyperemia and Congestion. 3- shock. Q4- mention the define Thrombosis and types? Q5- mention Causes of Cell Injury? Good luck