Heart, Blood, & Lymph Disease

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Heart, Blood, Lymph Disease

• AH 120

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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

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Coronary Artery Disease, (CAD)

• Atherosclerosis in the coronary arteries

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Early Atherosclerosis in the Aorta
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Advanced Atherosclerosis in the Aorta
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Atherosclerosis Risk Factors

• Smoking
• High cholesterol (especially LDL)
• Obesity
• High fat diet
• Lack of exercise
• Hypertension

• Diabetes
• Stress
• Age
• Gender
• Heredity

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Ischemia decreased oxygen to a tissue usually
because of decreased blood flow

• Atherosclerosis and the tendency to form clots
  may cause significant myocardial ischemia

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Symptoms of cardiac ischemia may not be present
until there is 70-75 occlusion of a coronary
artery
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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!
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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
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Zones of Damage in an M.I.

• Zone 3 (outer) ischemia
• Zone 2 (middle) injury
• Zone 1 (inner) necrosis

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M.I.s can occur anywhere on the heart

• Most occur on the left ventricle

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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

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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

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M.I. Signs Symptoms (cont.)

• Increased temperature
• Increased WBCs
• Increased troponin
• Increased CRP (C-reactive protein)
• Increased cardiac enzymes
• SGOT, CPK, LDH
• Arrhythmias

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Immediate Treatment for M.I.

• Analgesic for pain (usually morphine)
• Oxygen
• Clot dissolving drugs
• TPA (Activase)

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Diagnosing the Severity(Heart cath)
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Diagnosing (cont.)Swan-Ganz Catheter
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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

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Long Term TreatmentsCoronary Artery Bypass Graft
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Long Term Treatments Angioplasty
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Long term Treatments

• Stents often put in during angioplasty
• Dietary changes (low fat)
• Exercise
• Addressing all risk factors

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M.I. Complications

• Arrhythmias
• Congestive Heart Failure (CHF)
• Cardiogenic Shock

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ArrhythmiasNormal EKG
P atrial contraction, QRS ventricular
contraction
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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

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PVCs

• PVC QRS is usually bigger and wider than normal
• PVCs T wave usually goes in opposite direction
  of PVCs QRS
• Dangerous PVCs more than six per minute,
  multifocal, coupled, or R-on-T

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Ventricular Tachycardia (Vtach)

• 3 or more consecutive PVCs
• It may be continuous!
• Patient often will lose consciousness as blood
  pressure drops

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

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Vfib
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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!

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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!
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CHF Manifestations

• Enlarged ventricle
• Pulmonary and/or systemic edema
• Gurgling breath sounds
• Swollen feet and ankles
• Increased sodium and lowered potassium

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CHF Treatment

• Oxygen
• Diuretics for excess fluid
• Cardiotonic drugs to improve pumping efficiency
• Digitalis and its derivatives
• Low sodium dietpossibly supplemental potassium

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Cardiogenic Shock (Worst Complication of an M.I.)

• Definition systolic blood pressure less than 90
  mmhg and signs of impaired tissue perfusion

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Signs of Impaired Tissue Perfusion

• Pallor
• Cool, clammy skin
• Decreased urine output (less than 20 cc/hr)
• Decreased level of consciousness

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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

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Cardiogenic Shock Manifestations

• Systolic blood pressure less than 90 mmhg
• Previously listed signs of poor tissue perfusion
• Dyspnea/S.O.B.
• Arrhythmias

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Cardiogenic Shock Treatment

• Surgical repair of damaged ventricle (if
  possible)
• Intra-Aortic Balloon Pump
• Transplant

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Congenital Heart Defects
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Atrial Septal Defect (ASD)
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Ventricular Septal Defect (VSD)
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Tetralogy of Fallot
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Coarctation of the Aorta
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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

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Valvular Heart Disease
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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)

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Vegetations cause the affected valve to become
stenotic or insufficient
Mitral Stenosis
Mitral Stenosis with left atrial hypertrophy
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Mitral Insufficiency
Note Left Atrial Hypertrophy
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Aortic Stenosis and Insufficiency
Note left ventricle hypertrophies with either
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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

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

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Mitral Vegetations from Endocarditis
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Aortic Vegetations from Endocarditis
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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

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Endocarditis Treatment

• Early antibiotics for strep and staph infections
• May be systemic and topical
• Valve replacement

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Diseases of the Blood
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Anemia decreased RBCs and/or decreased hemoglobin
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RBC Normal
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RBC Microcytic and Hypochromic if decreased
hemoglobin
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RBC Macrocytic if decreased production
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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!

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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

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Anemia due to decreased RBC production
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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

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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

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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

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Anemia due to increased RBC Destruction

• Hemolytic Anemia
• Fragile RBCs rupture and the fragments cause
  organ dysfunction as well as anemia

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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

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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 (Cooleys Anemia) fragile RBCs and
  decreased hemoglobin usually seen in persons with
  Mediterranean ancestry

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Hemolytic anemias may also be acquired due to

• Exposure to toxins, drug reactions, or cytotoxic
  hypersensitivity (Erythroblastosis Fetalis)

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Polycythemia too many RBCs (or too much
hemoglobin)

• RBC count gt 6 million
• Hgb gt 18g
• Hct gt 54

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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

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Secondary Polycythemia

• A compensatory polycythemia caused by chronic
  hypoxia (usually due to high altitude or chronic
  lung disease)

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Patients with secondary polycythemia are prone to
the problems of hypoxia and polycythemia

• No phlebotomy! The cause of the chronic hypoxia
  is treated

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Bleeding Disorders
Normal clotting (coagulation) show all thirteen
factors
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Hemophilia

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

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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
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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

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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

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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!

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Treatment of Thrombocytopenia Purpura

• Steroids to decrease destruction
• Splenectomy
• Packed RBCs with platelets if bleeding is
  life-threatening

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Neoplasia of the Blood and Lymphatic System
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Leukemia

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

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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

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Leukemia Etiology

• Radiation
• Viral infection
• Heredity

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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

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Leukemia Treatment

• Initially chemotherapy and radiation
• Bone marrow transplant

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Lymphoma

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

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Hodgkins 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

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SAMPLE TEST QUESTIONS!
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• A macrocytic anemia in which there is reduced
  gastric secretion, absence of intrinsic factor,
  and reduced blood levels of vitamin B-12 is
• Thalassemia
• Thrombocytopenia purpura
• Hemolytic
• Pernicious
• Iron deficiency

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A Swan-Ganz catheter monitors which of these

• I and IV
• II, III, and IV
• I, II, III, and V
• II, III, IV, and V
• I, II, III, IV, and V

• Systemic arterial blood pressure
• Pulmonary artery pressure
• Pulmonary wedge pressure
• Cardiac output
• Venous oxygen levels

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The abnormality in congenital spherocytic anemia
is

• 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 half-moon shaped

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Select the heart defect from the following list

• 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

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Sequential elevation of SGOT, CPK, and LDH may
indicate

• Myocardial Infarction
• Rheumatic heart disease
• Pericarditis
• Septicemia
• Congestive heart failure

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Vegetations on the heart valves are
characteristic of

• I only
• I and II
• III and IV
• I, III, and V
• II, IV, and V

• Rheumatic heart disease
• Infectious endocarditis
• Myocardial Infarction
• Coronary artery disease
• Pericarditis

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A Reed-Sternberg cell is diagnostic for

• Myelogenous leukemia
• Hodgkins disease
• Thalassemia
• Thrombocytopenia purpura
• Hemophilia

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A buildup of cholesterol and other fatty acids in
the arteries of the heart is called

• Myocardial infarction
• Angina pectoris
• Congestive heart failure
• Coronary artery disease
• Ventricular hypertrophy

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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

• Pulmonary edema
• Heart failure
• Mitral insufficiency
• Pericarditis
• Aortic stenosis