Transcript Heart, Blood, & Lymph Disease

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
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Smoking
High cholesterol
(especially LDL)
Obesity
High fat diet
Lack of exercise
Hypertension
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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.
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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
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Phagocytosing necrotic tissue
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In the heart this tissue is replaced with
scar tissue (fibrosis)
Generating collateral circulation
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May not occur quickly enough or effectively
enough to sustain life
M.I. Signs and Symptoms
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Chest pain that may radiate into the arms
and shoulders, neck, jaw and upper back,
and into the abdomen
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Is a constant pressure sensation
Dyspnea
Profuse diaphoresis
N&V
Denial
Feeling of Impending Doom
M.I. Signs & Symptoms (cont.)
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Increased
Increased
Increased
Increased
Increased
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temperature
WBCs
troponin
CRP (C-reactive protein)
cardiac enzymes
SGOT, CPK, LDH
Arrhythmias
Immediate Treatment for M.I.
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Analgesic for pain (usually morphine)
Oxygen
Clot dissolving drugs
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TPA (Activase)
Diagnosing the Severity
(Heart cath)
Diagnosing (cont.)
Swan-Ganz Catheter
Swan-Ganz Data
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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:
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Stents – often put in during angioplasty
Dietary changes (low fat)
Exercise
Addressing all risk factors
M.I. Complications
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Arrhythmias
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Congestive Heart Failure (CHF)
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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
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PVC QRS is usually bigger and wider than normal
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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)
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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
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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)
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This is the problem!
Pathology of fluid retention
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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
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Enlarged ventricle
Pulmonary and/or systemic edema
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Gurgling breath sounds
Swollen feet and ankles
Increased sodium and lowered
potassium
CHF: Treatment
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Oxygen
Diuretics for excess fluid
Cardiotonic drugs to improve pumping
efficiency
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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
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Pallor
Cool, clammy skin
Decreased urine output (less than 20
cc/hr)
Decreased level of consciousness
Etiology of cardiogenic shock
after an M.I.
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Severe damage to
the left ventricle
and/or:
Aneurysm forms on
damaged ventricular
wall and/or:
Ventricle ruptures
Cardiogenic Shock:
Manifestations
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Systolic blood pressure less than 90
mmhg
Previously listed signs of poor tissue
perfusion
Dyspnea/S.O.B.
Arrhythmias
Cardiogenic Shock: Treatment
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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)
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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
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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!
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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
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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
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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
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Early antibiotics for strep and staph
infections
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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
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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
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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
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Etiology: Decreased vitamin B-12 in
blood
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May be due to heredity or chronic atrophic
gastritis
Pathology: Decreased “intrinsic factor”
causes ingested B-12 to not be
absorbed
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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
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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
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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
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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)
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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)
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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
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Under the skin
Into joint capsules, deep tissues and cavities
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Is very painful!
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Platelets are usually OK
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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
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Decreased platelet production
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Shift in platelet distribution
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Bone marrow disease
Chronic liver or spleen disease
Increased destruction of platelets
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Idiopathic; autoantibodies; drug reaction
Manifestations of
Thrombocytopenia Purpura
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Petechiae
Oozing of blood from
mucosal surfaces
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Excessive menstrual
bleeding
Excessive bleeding during
dental procedures
No joint or deep
tissue bleeding!
Treatment of
Thrombocytopenia Purpura
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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
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Acute or chronic
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In acute, the tumor cells are more
dedifferentiated and the disease
progresses more rapidly
Abnormal Cells:
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Myelogenous if abnormal cells are PMNs
Lymphocytic if abnormal WBCs are
lymphocytes
Leukemia Etiology
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Radiation
Viral infection
Heredity
Leukemia Pathology
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Bone marrow is taken over by tumor cells
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Reduced immune function
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Severe and refractory infections
Organ enlargement
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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
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Sepsis, bleeding, anemia, organ dysfunction from
metastasis
Leukemia Treatment
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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
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A lymphoma whose cancerous cells are
called Reed-Sternberg cells
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Easily identified by biopsy
Disease responds well to chemotherapy
and radiation therapy
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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
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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