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) May not occur quickly enough or effectively enough to sustain life
Generating collateral circulation
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)
Swan-Ganz Catheter
Diagnosing (cont.)
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
Bone marrow disease
Shift in platelet distribution
Chronic liver or spleen disease
Idiopathic; autoantibodies; drug reaction
Increased destruction of platelets
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
Increased production of useless WBCs and decreased production of RBCs and platelets Severe and refractory infections Lymph nodes, spleen, some bones (usually cranial)
Reduced immune function
Organ enlargement
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