CVS-2_removed.pdf

Normal heart • Weight: • 250-300 gr for females • 300-350 gr for males • The thickness of the walls: • Right ventricule wall thickness: 0,3-0,5 cm • Left ventricule wall thickness: 1,3-1,5 cm • Valves: • Semilunar valves: Aortic and pulmonary • Atrioventricular valves: Mitral and tricuspid • Peri...

Normal heart • Weight: • 250-300 gr for females • 300-350 gr for males • The thickness of the walls: • Right ventricule wall thickness: 0,3-0,5 cm • Left ventricule wall thickness: 1,3-1,5 cm • Valves: • Semilunar valves: Aortic and pulmonary • Atrioventricular valves: Mitral and tricuspid • Pericardium contains 30-50 ml of clear fluid Blood supply to the heart • Left coronary artery: – Anterior descending branch: – – – – Most of the apex Anterior surface of LV 1/3 of anterior RV 2/3 anterior interventricular septum – Circumflex branch: – Lateral wall of LV • Right coronary artery: – – – – Remainder of the anterior surface of RV Posterior aspect of RV Half of the posterior wall of LV Posterior 1/3 of the septum Neoplastic heart disease • Primary tumors: – – – – – Myxoma Lipoma Papillary fibroelastoma Rhabdomyoma Angiosarcoma – – – – Lung carcinoma Breast carcinoma Malignant melanoma Leukemia and lymphomas • Metastatic (more common): • Myxomas occur the most common adult age group • 90% of cases are located in atrium • 80%  left atrium • Single mass/ origin from fossa ovalis • 1-10 cm diameter/ stalk or sessile • Soft, translucent, gelatinous • Origin from Multipotent mesenchymal cell differentiation • Star-shaped, hyperchromatic nucleus, endothel with multiple nucleus, smooth muscle cells and/ or fibroblastic cells • • • • • • • • Rhabdomyomas, occur the most commoninfants and children Often show spontaneous regression (hamartoma???) 1-2 cm diamater/ ventricular/gray-white color mass Nucleus; Large round or polygonal with spider extension Cytoplasm with glucose-loaded vacuoles it can cause ball-valve obstructions Lipomas, usually do not cause symptoms Papillary fibroelastomas usually localized on the heart valve Causes of pericarditis Infections – Viruses – Pyogenic bacteria – Tuberculosis – Fungi – Other parasites Causes of pericarditis Immun-mediated reactions – Rheumatic fever – SLE – Scleroderma – Postcardiotomy – Post-myocardial infarction (Dressler) syn. – Drug hypersensitivity reaction Causes of pericarditis Others – Myocardial infarction – Uremia – After cardiac surgery – Neoplasia – Trauma – Radiation Pericarditis According to clinicopathologic findings: – Acute pericarditis – Healed pericarditis • Adhesive mediastinopericarditis • Constrictive pericarditis Pericarditis According to inflammatory change: – Serous – Serofibrinous – Fibrinous – Suppurative – Hemorrhagic Serous pericarditis • Causes: – – – – Nonbacterial inflammation (RF, SLE, tumors) Early stages of bacterial inflammation Viral infections Unknown • Inflammatory reaction with scant PNL, lymphocytes and histiocytes • Fluid accumulation (50-200 ml) • Increased vascular permeability and protein rich fluid • Organization is rare, healing with resolution Fibrinous/serofibrinous pericarditis • Most frequent type of pericarditis • Causes: – – – – – – – Myocardial infarction Uremia Radiation RF SLE Trauma Bacterial or viral infarctions Uremic pericarditis Fibrinous/serofibrinous pericarditis • • • In fibrinous pericarditis, there is fine granuler precipitate of fibrin on the surfaces (“bread and butter sign”) Heal with resolution or organization When organized: – Plaque-like fibrous thickenings on the surface – Large areas of fibrosis and due to that, adhesive pericarditis • A loud pericardial friction rub Purulent or suppurative pericarditis • Invasion of the pericardial sac by infective organisms: – Direct extension from neighboring infection (e.g. Empyema of the pleural cavity, lobar pnemonia, mediastinal infections, infective endocarditis) – Seeding from blood – Lymphatic extension – Direct introduction during cardiac surgery • • Thin creamy pus (400-500 ml) Serasal surfaces are reddened, granular, yellow-green color of the exudate Purulent or suppurative pericarditis • Healing: – Resolution (rare) – Organization – Constrictive pericardities due to organization Hemorrhagic pericarditis • Exudate mainly composed of blood intermingled with fibrinous or suppurative effusion • Causes: – Tuberculosis – Malignant neoplastic involvement – Cardiac surgery Caseous pericarditis • Caseation within the pericardial sac • Main cause is tuberculosis • Rarely due to mycotic infections • Direct spread from tuberculous foci within the tracheabronchial nodes • As a consequence, fibrocalcific, chronic constrictive pericarditis Adhesive mediastinopericarditis • Follow suppurative or caseous pericarditis, previous cardiac surgery or radiation • Pericardial sac is obliterated • Adherence of parietal pericard to surrounding structures • Great strain on cardiac function during systole • Increased workload • Cardiac hypertrophy and dilatation Constrictive pericarditis • Heart is encased in a dense, fibrous or fibrocalcific scar • Limitation in diastolic expansion • Restriction in cardiac output • Pericardial sac becomes a dense layer of scar with or without calcification (Concretio cordis) • No cardiac hypertrophy or dilatation • Small, quite heart with reduced cardiac output Cardiac dysfunction • • • • • • Pump failure. Flow obstruction. Regurgitant flow. Shunted flow. Disorders of cardiac conduction. Rupture of the heart or a major vessel. Heart failure • congestive heart failure • heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure • several physiologic mechanisms maintain arterial pressure and organ perfusion – Frank-Starling mechanism: which increased filling volumes dilate the heart and thereby increase subsequent actin-myosin cross-bridge formation, enhancing contractility and stroke volüme – Myocardial adaptations, including hypertrophy with or without cardiac chamber dilation – Activation of neurohumoral systems • Release of norepinephrine • Activation of the renin-angiotensin-aldosterone system • Release of atrial natriuretic peptide Left sided heart failure • • • • Major causes – Ischemic heart disease – Hypertension – Aortic and mitral valvular diseases – Primary myocardial diseases Pulmonary congestion and edema due to impaired pulmonary outflow Reduced renal perfusion – Salt retention&expand blood volüme – ATN – Azotemia: impaired waste excretion Reduced CNS perfusion: hypoxic ensefalopathy Right sided heart failure • • • • • most commonly caused by left-sided heart failure Pure: tricuspid& pulmonary valve disease, cor pulmonale Portal systemic, peripheral congestion and edema Hepatomegaly splenomegaly Cardiomyopathy • Heart disease resulting from a primary abnormalities of the myocardium • Mostly idiopathic • Some have well-known causes • 3 types according to pathologic findings: – Dilated cardiomyopathy 90% – Hypertrophic cardiomyopathy – Restrictive cardiomyopathy Dilated cardiomyopathy • Progressive cardiac hypertrophy, dilatation and contractile (systolic) dysfunction • Causes: – Myocarditis (mostly viral) – Toxic effect of alcohol or its metabolics – Pregnancy associated type (hypertension, volume overload, nutritional deficiency?) – Genetic influences (familial DCM) – Idiopathic Dilated cardiomyopathy • Increase in weight (2-3 times) • Dilatation of chambers • Normal or decreased ventricular wall thickness • Mural thrombi, thromboembolism • Although valvular alteration is absent, there is a functional regurgitation • Microscopically, myocytes are hypertrophic, interstitial and endocardial fibrosis • Sometimes small subendocardial scars due to healing of ischemic necrosis Hypertrophic cardiomyopathy Restrictive cardiomyopathy • Idiopathic • Radiation fibrosis • Amyloidosis • Sarcoidosis • Metastatic tumors Restrictive cardiomyopathy • Primary decrease in ventricular compliance, resulting in impaired ventricular filling during diastole • Ventricules are of normal size, the cavities are not dilated