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Heart, Blood, & Lymph Disease AH 120 Atherosclerosis The buildup of fatty plaque in the arteries and arterioles. The plaque decreases the lumen of the affected vessel and causes decreased and sluggish blood flow Coronary Artery Disease, (CAD) Atherosclerosis in the coronary arteries Early Atherosclerosis in the Aorta Advanced Atherosclerosis in the Aorta Atherosclerosis Risk Factors Smoking High cholesterol (especially LDL) Obesity High fat diet Lack of exercise Hypertension Diabetes Stress Age Gender Heredity Ischemia: decreased oxygen to a tissue usually because of decreased blood flow Atherosclerosis and the tendency to form clots may cause significant myocardial ischemia Symptoms of cardiac ischemia may not be present until there is 70-75% occlusion of a coronary artery Angina Pectoris: Transient myocardial ischemia Triggers of angina in a person with CAD: Exertion Emotion Environment Eating Angina Pectoris is a warning! It is like a “practice heart attack”! Myocardial Infarction (Heart Attack) Ischemia that is severe enough and lasts long enough to cause death of myocardium cells Usually occurs when atherosclerosis causes thrombus formation Zones of Damage in an M.I. Zone 3 (outer): ischemia Zone #2 (middle): injury Zone #1 (inner): necrosis M.I.’s can occur anywhere on the heart Most occur on the left ventricle The body responds to ischemic damage, eg, M.I., by Phagocytosing necrotic tissue In the heart this tissue is replaced with scar tissue (fibrosis) Generating collateral circulation May not occur quickly enough or effectively enough to sustain life M.I. Signs and Symptoms Chest pain that may radiate into the arms and shoulders, neck, jaw and upper back, and into the abdomen Is a constant pressure sensation Dyspnea Profuse diaphoresis N&V Denial Feeling of Impending Doom M.I. Signs & Symptoms (cont.) Increased Increased Increased Increased Increased temperature WBCs troponin CRP (C-reactive protein) cardiac enzymes SGOT, CPK, LDH Arrhythmias Immediate Treatment for M.I. Analgesic for pain (usually morphine) Oxygen Clot dissolving drugs TPA (Activase) Diagnosing the Severity (Heart cath) Diagnosing (cont.) Swan-Ganz Catheter Swan-Ganz Data Pulmonary artery pressure (PAP) Pulmonary capillary wedge pressure (PCWP) Mixed venous PO2 Cardiac Output (C.O.) An M.I. Will usually make the pressures higher than normal and C.O. and mixed venous PO2 lower than normal Long Term Treatments: Coronary Artery Bypass Graft Long Term Treatments: Angioplasty Long term Treatments: Stents – often put in during angioplasty Dietary changes (low fat) Exercise Addressing all risk factors M.I. Complications Arrhythmias Congestive Heart Failure (CHF) Cardiogenic Shock Arrhythmias:Normal EKG P = atrial contraction, QRS = ventricular contraction PVC = Premature Ventricular Contraction Ischemia makes ventricles “irritable” which increases automaticity A PVC is a wasted beat-there is no effective output yet the myocardium consumes oxygen for this beat. It is treated and suppressed by the drug Lidocaine PVCs PVC QRS is usually bigger and wider than normal PVC’s T wave usually goes in opposite direction of PVC’s QRS Dangerous PVCs: more than six per minute, multifocal, coupled, or R-on-T Ventricular Tachycardia (Vtach) 3 or more consecutive PVC’s It may be continuous! Patient often will lose consciousness as blood pressure drops Ventricular Tachycardia Treated like PVCs. IF blood pressure gets too low, patient may need CPR and defibrillation Ventricular Fibrillation (Vfib) Multiple, irritable foci in the ventricles are trying to depolarize Results in chaotic electrical activity Ventricle “quivers” – there is no effective cardiac output The patient is clinically dead and needs CPR and rapid defibrillation The heart is depolarized externally by passing current through it by electrodes placed on the chest over the heart Vfib Congestive Heart Failure (CHF) Definition of CHF: Failure of the heart to pump adequate amount of blood to the tissues After an M.I., the cardiovascular system tries to maintain adequate blood flow by: Slight increase in heart rate (C.O. = rate x stroke volume) Slight increase in systemic vascular resistance Fluid retention (done by the kidney) This is the problem! Pathology of fluid retention Fluid volume increases! Decreased blood flow to kidney causes release of renin This is converted to angiotensin Angiotensin makes the adrenals secrete aldosterone Aldosterone causes the kidney to retain sodium and fluid while releasing potassium into the urine CHF: Manifestations Enlarged ventricle Pulmonary and/or systemic edema Gurgling breath sounds Swollen feet and ankles Increased sodium and lowered potassium CHF: Treatment Oxygen Diuretics for excess fluid Cardiotonic drugs to improve pumping efficiency Digitalis and its derivatives Low sodium diet;possibly supplemental potassium Cardiogenic Shock (Worst Complication of an M.I.) Definition: systolic blood pressure less than 90 mmhg and signs of impaired tissue perfusion Signs of Impaired Tissue Perfusion Pallor Cool, clammy skin Decreased urine output (less than 20 cc/hr) Decreased level of consciousness Etiology of cardiogenic shock after an M.I. Severe damage to the left ventricle and/or: Aneurysm forms on damaged ventricular wall and/or: Ventricle ruptures Cardiogenic Shock: Manifestations Systolic blood pressure less than 90 mmhg Previously listed signs of poor tissue perfusion Dyspnea/S.O.B. Arrhythmias Cardiogenic Shock: Treatment Surgical repair of damaged ventricle (if possible) Intra-Aortic Balloon Pump Transplant Congenital Heart Defects Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD) Tetralogy of Fallot Coarctation of the Aorta Patent Ductus Arteriosus (PDA) Failure of D.A. to close or it re-opens Shunt is usually L- R but can be R- L if pulmonary artery pressure exceeds aorta pressure Treated with Oxygen, NTE, medicine and possibly surgery Valvular Heart Disease Rheumatic Heart Disease Etiology: complication of a strep infection Pathology: reaction to strep immune complex causes vegetations to form on valves (usually mitral or aortic) Vegetations cause the affected valve to become stenotic or insufficient Mitral Stenosis Mitral Stenosis with left atrial hypertrophy Mitral Insufficiency Note: Left Atrial Hypertrophy Aortic Stenosis and Insufficiency Note: left ventricle hypertrophies with either The chamber behind the affected valve hypertrophies! With narrowing (stenosis) or leakage (insufficiency) of the mitral valve, the left atria enlarges With narrowing (stenosis) or leakage (insufficiency) of the aortic valve, the left ventricle enlarges Stenotic or Insufficient Valves Are Surgically Replaced Mitral Valve Replacement Aortic Valve Replacement Bacterial (or Infectious) Endocarditis Sub-acute caused by strep Acute caused by staph Either one causes large and fragile vegetations to form (again, usually on mitral or aortic) Vegetations not only cause stenosis or insufficiency, but may break off and become emboli Mitral Vegetations from Endocarditis Aortic Vegetations from Endocarditis Other Manifestations of Endocarditis Petechiae due to rupture of capillaries from emboli Hematuria from emboli in kidney Positive blood culture Long term, low-grade fever Murmur/abnormal heart sounds Endocarditis Treatment Early antibiotics for strep and staph infections May be systemic and topical Valve replacement Diseases of the Blood Anemia: decreased RBCs and/or decreased hemoglobin RBC: Normal RBC: Microcytic and Hypochromic if decreased hemoglobin RBC: Macrocytic if decreased production Factors Needed for RBC Production Red bone marrow Erythropoietin (Hemopoietin) – hormone used to form hemoglobin that is secreted by renal tubular cells Iron Folic acid Vitamin B-12 A problem with any of these results in anemia! Manifestations of Anemia Pale skin (pallor) S.O.B. and easy fatigue Lab findings: decreased RBCs or hemoglobin, increased reticulocytes, abnormal appearance (macro or microcytic, hypochromic) or abnormal shapes Anemia due to decreased RBC production Pernicious Anemia Etiology: Decreased vitamin B-12 in blood May be due to heredity or chronic atrophic gastritis Pathology: Decreased “intrinsic factor” causes ingested B-12 to not be absorbed Unusual before age 35 Manifestations (besides anemia) and Treatment All due to decreased B-12 levels in blood G.I.: Smooth, sore tongue, diarrhea, and increased risk of gastric CA CNS: numbness and tingling in extremities, balance and coordination problems Lab: macrocytic RBCs, decreased gastric secretion (and hence decreased intrinsic factor), decreased serum B-12, positive Schilling test Treated by giving B-12 injections Iron Deficiency Anemia Etiology: chronic, low-grade blood loss in adults; poor dietary intake in pregnant women and young children Lab: hypochromic, microcytic RBCs Treatment: Oral or IV iron supplement, control blood loss Anemia due to increased RBC Destruction Hemolytic Anemia Fragile RBCs rupture and the fragments cause organ dysfunction as well as anemia Hemolytic Anemia Manifestations and Treatment S.O.B/easy fatigue Pallor Increased reticulocytes Enlarged spleen Increased Bilirubin levels and possibly jaundice Organ dysfunction due to fragmented cells acting as emboli: abdominal pain, fever, swollen & painful joints, neurologic dysfunction Treated by: removal of spleen, steroids Hereditary Hemolytic Anemias Sickle Cell Anemia: abnormally shaped and fragile RBCs seen in blacks Congenital Spherocytic Anemia: fragile RBC membrane that takes in too much fluid Thalassemia (Cooley’s Anemia): fragile RBCs and decreased hemoglobin usually seen in persons with Mediterranean ancestry Hemolytic anemias may also be acquired due to: Exposure to toxins, drug reactions, or cytotoxic hypersensitivity (Erythroblastosis Fetalis) Polycythemia: too many RBCs (or too much hemoglobin) RBC count > 6 million Hgb > 18g Hct > 54% Primary Polycythemia (Polycythemia Vera) For unknown reason bone marrow makes too many RBCs (WBCs and platelets may increase also Blood becomes very thick (increased viscosity) and clots easily Heart also has to work harder to pump Patients are prone to thrombosis and organ infarction (including heart) Spleen enlarges also Treated by periodic phlebotomy Secondary Polycythemia A compensatory polycythemia caused by chronic hypoxia (usually due to high altitude or chronic lung disease) Patients with secondary polycythemia are prone to the problems of hypoxia and polycythemia No phlebotomy! The cause of the chronic hypoxia is treated Bleeding Disorders Normal clotting (coagulation) show all thirteen factors Hemophilia Sex-linked transmission most commonly passed from mother to son. Causes absence of clotting factor VIII or IX Minor trauma causes heavy bleeding Under the skin Into joint capsules, deep tissues and cavities Is very painful! Platelets are usually OK Treated by administering missing clotting factors during crisis Thrombocytopenia Purpura Reduced platelets causing purple skin lesions (petechiae) Normal platelet count is 150,000 to 350, 000 Purpura appears when platelet count is less than 60,000 Etiologies of Thrombocytopenia Purpura Decreased platelet production Shift in platelet distribution Bone marrow disease Chronic liver or spleen disease Increased destruction of platelets Idiopathic; autoantibodies; drug reaction Manifestations of Thrombocytopenia Purpura Petechiae Oozing of blood from mucosal surfaces Excessive menstrual bleeding Excessive bleeding during dental procedures No joint or deep tissue bleeding! Treatment of Thrombocytopenia Purpura Steroids to decrease destruction Splenectomy Packed RBCs with platelets if bleeding is life-threatening Neoplasia of the Blood and Lymphatic System Leukemia A malignancy of the bone marrow that forms WBCs that results in increased production of useless WBCs. Classification of Leukemia Acute or chronic In acute, the tumor cells are more dedifferentiated and the disease progresses more rapidly Abnormal Cells: Myelogenous if abnormal cells are PMNs Lymphocytic if abnormal WBCs are lymphocytes Leukemia Etiology Radiation Viral infection Heredity Leukemia Pathology Bone marrow is taken over by tumor cells Reduced immune function Severe and refractory infections Organ enlargement Increased production of useless WBCs and decreased production of RBCs and platelets Lymph nodes, spleen, some bones (usually cranial) CNS dysfunction due to increased intracranial pressure Death is usually due to complications caused by pathology Sepsis, bleeding, anemia, organ dysfunction from metastasis Leukemia Treatment Initially chemotherapy and radiation Bone marrow transplant Lymphoma A malignancy in lymph nodes or lymphoid tissue The primary symptom, prior to metastasis is lymph node enlargement Hodgkin’s Disease A lymphoma whose cancerous cells are called Reed-Sternberg cells Easily identified by biopsy Disease responds well to chemotherapy and radiation therapy Treatment is similar to Leukemia treatment A macrocytic anemia in which there is reduced gastric secretion, absence of intrinsic factor, and reduced blood levels of vitamin B-12 is: A. Thalassemia B. Thrombocytopenia purpura C. Hemolytic D. Pernicious E. Iron deficiency A Swan-Ganz catheter monitors which of these: A. B. C. D. E. I and IV II, III, and IV I, II, III, and V II, III, IV, and V I, II, III, IV, and V I. II. III. IV. V. Systemic arterial blood pressure Pulmonary artery pressure Pulmonary wedge pressure Cardiac output Venous oxygen levels The abnormality in congenital spherocytic anemia is: A. B. C. D. E. Red blood cells are too small Red blood cells are spherical and swell up easily Platelets are large and ineffective White blood cells attack red blood cells Red blood cells are fragile and halfmoon shaped Select the heart defect from the following list: A. B. C. D. E. Atrial septal defect (ASD) Ventricular septal defect (VSD) Tetralogy of Fallot Patent ductus arteriosus (PDA) Coarctation of the aorta A constriction of the descending portion of the aorta A communication between the pulmonary artery and the aorta Sequential elevation of SGOT, CPK, and LDH may indicate: A. B. C. D. E. Myocardial Infarction Rheumatic heart disease Pericarditis Septicemia Congestive heart failure “Vegetations” on the heart valves are characteristic of: A. B. C. D. E. I only I and II III and IV I, III, and V II, IV, and V I. II. III. IV. V. Rheumatic heart disease Infectious endocarditis Myocardial Infarction Coronary artery disease Pericarditis A Reed-Sternberg cell is diagnostic for: A. B. C. D. E. Myelogenous leukemia Hodgkin’s disease Thalassemia Thrombocytopenia purpura Hemophilia A buildup of cholesterol and other fatty acids in the arteries of the heart is called: A. B. C. D. E. Myocardial infarction Angina pectoris Congestive heart failure Coronary artery disease Ventricular hypertrophy The inability of the heart to pump an adequate amount of blood to meet tissue demands as may occur after an M.I. is called: A. B. C. D. E. Pulmonary edema Heart failure Mitral insufficiency Pericarditis Aortic stenosis