2. Heart, Blood, & Lymph Disease AH 120

3. 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

4. Coronary Artery Disease, (CAD) Atherosclerosis in the coronary arteries

5. Early Atherosclerosis in the Aorta

6. Advanced Atherosclerosis in the Aorta

7. Atherosclerosis Risk Factors Smoking High cholesterol (especially LDL) Obesity High fat diet Lack of exercise Hypertension Diabetes Stress Age Gender Heredity

8. Ischemia: decreased oxygen to a tissue usually because of decreased blood flow Atherosclerosis and the tendency to form clots may cause significant myocardial ischemia

9. Symptoms of cardiac ischemia may not be present until there is 70-75% occlusion of a coronary artery

10. 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”!

11. 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

12. Zones of Damage in an M.I. Zone 3 (outer): ischemia Zone #2 (middle): injury Zone #1 (inner): necrosis

13. M.I.’s can occur anywhere on the heart Most occur on the left ventricle

14. 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

15. 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

16. M.I. Signs & Symptoms (cont.) Increased temperature Increased WBCs Increased troponin Increased CRP (C-reactive protein) Increased cardiac enzymes SGOT, CPK, LDH Arrhythmias

17. Immediate Treatment for M.I. Analgesic for pain (usually morphine) Oxygen Clot dissolving drugs TPA (Activase)

18. Diagnosing the Severity (Heart cath)

19. Diagnosing (cont.) Swan-Ganz Catheter

20. 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

21. Long Term Treatments: Coronary Artery Bypass Graft

22. Long Term Treatments: Angioplasty

23. Long term Treatments: Stents – often put in during angioplasty Dietary changes (low fat) Exercise Addressing all risk factors

24. M.I. Complications Arrhythmias Congestive Heart Failure (CHF) Cardiogenic Shock

25. Arrhythmias:Normal EKG P = atrial contraction, QRS = ventricular contraction

26. 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

27. 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

28. Ventricular Tachycardia (Vtach) 3 or more consecutive PVC’s It may be continuous! Patient often will lose consciousness as blood pressure drops

29. Ventricular Tachycardia Treated like PVCs. IF blood pressure gets too low, patient may need CPR and defibrillation

30. 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

31. Vfib

32. 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!

33. Pathology of fluid retention 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 Fluid volume increases!

34. CHF: Manifestations Enlarged ventricle Pulmonary and/or systemic edema Gurgling breath sounds Swollen feet and ankles Increased sodium and lowered potassium

35. CHF: Treatment Oxygen Diuretics for excess fluid Cardiotonic drugs to improve pumping efficiency Digitalis and its derivatives Low sodium diet;possibly supplemental potassium

36. Cardiogenic Shock (Worst Complication of an M.I.) Definition: systolic blood pressure less than 90 mmhg and signs of impaired tissue perfusion

37. Signs of Impaired Tissue Perfusion Pallor Cool, clammy skin Decreased urine output (less than 20 cc/hr) Decreased level of consciousness

38. 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

39. Cardiogenic Shock: Manifestations Systolic blood pressure less than 90 mmhg Previously listed signs of poor tissue perfusion Dyspnea/S.O.B. Arrhythmias

40. Cardiogenic Shock: Treatment Surgical repair of damaged ventricle (if possible) Intra-Aortic Balloon Pump Transplant

41. Congenital Heart Defects

42. Atrial Septal Defect (ASD)

43. Ventricular Septal Defect (VSD)

44. Tetralogy of Fallot

45. Coarctation of the Aorta

46. 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

47. Valvular Heart Disease

48. 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)

49. Vegetations cause the affected valve to become stenotic or insufficient Mitral Stenosis Mitral Stenosis with left atrial hypertrophy

50. Mitral Insufficiency Note: Left Atrial Hypertrophy

51. Aortic Stenosis and Insufficiency Note: left ventricle hypertrophies with either

52. 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

53. Stenotic or Insufficient Valves Are Surgically Replaced Mitral Valve Replacement Aortic Valve Replacement

54. 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

55. Mitral Vegetations from Endocarditis

56. Aortic Vegetations from Endocarditis

57. 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

58. Endocarditis Treatment Early antibiotics for strep and staph infections May be systemic and topical Valve replacement

59. Diseases of the Blood

60. Anemia: decreased RBCs and/or decreased hemoglobin

61. RBC: Normal

62. RBC: Microcytic and Hypochromic if decreased hemoglobin

63. RBC: Macrocytic if decreased production

64. 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!

65. 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

66. Anemia due to decreased RBC production

67. 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

68. 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

69. 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

70. Anemia due to increased RBC Destruction Hemolytic Anemia Fragile RBCs rupture and the fragments cause organ dysfunction as well as anemia

71. 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

72. 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

73. Hemolytic anemias may also be acquired due to: Exposure to toxins, drug reactions, or cytotoxic hypersensitivity (Erythroblastosis Fetalis)

74. Polycythemia: too many RBCs (or too much hemoglobin) RBC count > 6 million Hgb > 18g Hct > 54%

75. 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

76. Secondary Polycythemia A compensatory polycythemia caused by chronic hypoxia (usually due to high altitude or chronic lung disease)

77. Patients with secondary polycythemia are prone to the problems of hypoxia and polycythemia No phlebotomy! The cause of the chronic hypoxia is treated

78. Bleeding Disorders Normal clotting (coagulation) show all thirteen factors

79. Hemophilia Sex-linked transmission most commonly passed from mother to son. Causes absence of clotting factor VIII or IX

80. 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

81. 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

82. Etiologies of Thrombocytopenia Purpura Decreased platelet production Bone marrow disease Shift in platelet distribution Chronic liver or spleen disease Increased destruction of platelets Idiopathic; autoantibodies; drug reaction

83. 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!

84. Treatment of Thrombocytopenia Purpura Steroids to decrease destruction Splenectomy Packed RBCs with platelets if bleeding is life-threatening

85. Neoplasia of the Blood and Lymphatic System

86. Leukemia A malignancy of the bone marrow that forms WBCs that results in increased production of useless WBCs.

87. 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

89. Leukemia Etiology Radiation Viral infection Heredity

90. Leukemia Pathology Bone marrow is taken over by tumor cells Increased production of useless WBCs and decreased production of RBCs and platelets Reduced immune function Severe and refractory infections Organ enlargement 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

91. Leukemia Treatment Initially chemotherapy and radiation Bone marrow transplant

92. Lymphoma A malignancy in lymph nodes or lymphoid tissue The primary symptom, prior to metastasis is lymph node enlargement

94. 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

96. 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

97. A Swan-Ganz catheter monitors which of these: A. I and IV B. II, III, and IV C. I, II, III, and V D. II, III, IV, and V E. I, II, III, IV, and V I. Systemic arterial blood pressure II. Pulmonary artery pressure III. Pulmonary wedge pressure IV. Cardiac output V. Venous oxygen levels

98. The abnormality in congenital spherocytic anemia is: A. Red blood cells are too small B. Red blood cells are spherical and swell up easily C. Platelets are large and ineffective D. White blood cells attack red blood cells E. Red blood cells are fragile and half- moon shaped

99. Select the heart defect from the following list: A. Atrial septal defect (ASD) B. Ventricular septal defect (VSD) C. Tetralogy of Fallot D. Patent ductus arteriosus (PDA) E. Coarctation of the aorta A constriction of the descending portion of the aorta A communication between the pulmonary artery and the aorta

100. Sequential elevation of SGOT, CPK, and LDH may indicate: A. Myocardial Infarction B. Rheumatic heart disease C. Pericarditis D. Septicemia E. Congestive heart failure

101. “Vegetations” on the heart valves are characteristic of: A. I only B. I and II C. III and IV D. I, III, and V E. II, IV, and V I. Rheumatic heart disease II. Infectious endocarditis III. Myocardial Infarction IV. Coronary artery disease V. Pericarditis

102. A Reed-Sternberg cell is diagnostic for: A. Myelogenous leukemia B. Hodgkin’s disease C. Thalassemia D. Thrombocytopenia purpura E. Hemophilia

103. A buildup of cholesterol and other fatty acids in the arteries of the heart is called: A. Myocardial infarction B. Angina pectoris C. Congestive heart failure D. Coronary artery disease E. Ventricular hypertrophy

104. 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. Pulmonary edema B. Heart failure C. Mitral insufficiency D. Pericarditis E. Aortic stenosis