Lecture Notes NCM 102: Union Christian College College of Nursing
Lecture Notes NCM 102: Union Christian College College of Nursing
Lecture Notes NCM 102: Union Christian College College of Nursing
COLLEGE OF NURSING
Level III
San Fernando City, La Union
LECTURE NOTES
NCM 102
PREPARED BY:
A. Alterations in Oxygenation
1. GAS TRANSPORT
(Cardiovascular System)
Anatomic and Physiologic Overview (The HEART)
The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the space
between the lungs (mediastinum) and rests on the diaphragm.
It weighs approximately 300g (10.6 oz), although heart weight and size are influenced by age,
gender, body weight, extent of physical exercise and conditioning and heart disease.
Heart pumps blood to the tissues, supplying them with oxygen and other nutrients.
During systole (contraction of the muscle), the chambers of the heart become smaller as the blood is
ejected.
During diastole (relaxation of the muscle), the heart chambers fill with blood in preparation for the
subsequent ejection.
Normal resting adult heart beat is approximately 60 to 80 time per minutes.
Each ventricles ejects approximately 70ml of blood per beat and has an output of approximately 5 L /
minute.
The heart is composed of three layers. The inner layer, or endometrium, consists of endothelial
tissue, which lines the inside of the heart and valves.
The middle layer, or myocardium, is made up of the muscle fibers and is responsible for the
pumping action.
Right ventricle lies anteriorly (just beneath the sternum) and the left ventricle is situated posteriorly.
The left ventricle is responsible for the apex beat or the point of maximal impulse (PMI), which is
palpable normally in the left midclavicular line of the chest wall at the fifth intercostals space.
MYOCARDIAL (CORONARY BLOOD SUPPLY)
1. LCA – located in the upper half of coronary sinus (sinus valsalva of the aorta)
Three branches:
• Left main coronary artery and two
bifurcation which are:
• Left circumflex – supplies left ventricle and
auricle or atrium
• Left Anterior descending artery – supplies
the anterior 2/3 of the septum and right bundle
branch.
2. RCA – supplies SA node, AV junction, posterior
bundle branch, posterior 1/3 of the septum, Right
ventricle and diaphragmatic surface of the Left
ventricle, Branch – posterior descending Artery.
3. Three systems of the Veins in the heart:
• thebesian vein
• anterior cardiac vein
• coronary sinus – primary means of draining from the left ventricle.
CONDUCTIVE SYSTEM
Sino-atrial note (Pace maker of the heart)
atrioventricular node Bundle of His Right
and Left Bundle branch Purkinje Fibers.
Nervous system control – includes the
following:
a. Vagus nerve of the
parasympathetic – slows rate of impulse
formation in the SA node.
b. Sympathetic nerve – increase
the rate of the impulse formation,
conduction, and force of contraction.
OTHERS:
1. Cardiac Output (CO) – it is the volume of blood ejected per minute by each ventricle,
calculated by SV x HR.
2. Heart rate – refers to the actual number of heart beats occurring per minute.
3. Cardiac index – is C.O. divided by Body surface area (BSA); it is more accurate
measurement of cardiac output.
4. Stroke volume – refers to the amount of blood pumped from the ventricles during its
contraction of the heart (about 70ml of blood in an adult) and depends on:
i. Preload – resting force of the myocardium increased in venous return and depends
on two factors:
ii. Stretching potential of the Left ventricle (LV + diastolic pressure).
iii. The volume of blood remaining in the Left ventricle after diastole.
iv. Contractility –refers to the change in force of contraction without changing the resting
length.
v. Ejection Fraction – is the amount of blood ejected by the ventricle at each
contraction.
vi. Afterload – refers to the amount of ventricular tension during systole which is needed
to open the semi lunar valves and eject blood.
- Also refers to the resistance to the ventricular ejection offered by the
peripheral blood vessels minus total peripheral resistance(TPR).
ASSESSMENT
1. Nursing History
i. Health History
A. Non-modifiable risk factors:
1. Age – atherosclerosis is disease of middle age (40 - 50). Cardiovascular disease is
greater in men until 65 when the incidence equalizes.
2. Gender – some theories attributes it to the higher estrogen levels of pre-menopausal
women because there maybe a relationship between increase in estrogen level to high
density lipoproteins which are inversely related to atherosclerosis and ischemic heart disease
(IHD)
3. Race - - IHD is higher in whites; HPN is twice greater in blacks.
4. Genetic History – family history appears to be a significant risk factor for
predisposition to heart disease.
B. Modifiable Risk Factors:
1. Hyperlipidemia – plasma lipids (cholesterol), triglycerides, phospholipids and fatty
acids) are produced from endogenous synthesis in the liver and from the dietary intake of
fats.
Types of Hyperlipidemia:
i. Primary hyperlipidemia – caused by inborn error of lipid metabolism.
ii. Secondary Hyperlipidemia – related to such conditions as DM or hypothyroidism.
iii. For lipids to be used and transported by the body they need to become soluble in
blood by combining with protein to form macromolecules called lipoproteins.
Lipotprotein are vehicle for fat mobilization and transport.
2. Types of lipoproteins:
i. HDLs – contain more protein by weight and less lipid han any other lipoprotein. They
carry lipids away from arteries and to the liver for metabolism. Therefore, high serum
LDL are desirable.
ii. LDLs – contain more cholesterol than any of the other lipoproteins and have an
affinity for arterial walls. Elevated LDL correlate most closely with an increased
incidence of atherosclerosis.
iii. VLDLs – contain most triglycerides. High VLDL concentration may increase the risk
of premature atherosclerosis when associated with other factors such as diabetes,
hypertension and cigarette smoking.
4. Hypertension – known to be a precursor of atherosclerosis.
Prevention: control sodium and caloric intake.
Management: Diuretics; antihypertensive
Sodium restricted diet
Calorie controlled diet
Therapy must be continued for lifetime and compliance on this program is
imperative.
5. Smoking – (Hazard) – the hazard of tobacco smoking are produced by the inhalation
of nicotine, which is a vasoconstrictor and carbon monoxide which reduces the oxygen
carrying capacity of the blood.
Elevated serum lipids, hypertension and cigarette smoking are the (3)
most significant modifiable risk significant.
6. Sedentary lifestyle –
Prevention: Engage in regular exercise; this will promote muscle strength,
flexibility, endurance.
E. ENZYME STUDIES
ASPARTATE AMINOTRANSFERASE (AST)
Formerly SGOT
Elevated level indicates tissue necrosis
Normal range is 7 – 40 mu/ml
Range with Myocardial Infarction
o Initial elevation: 4 – 6 hours
o Peaks: 24 – 36 hours
o Returns to normal: 4 – 7 days
CREATINE PHOSPHOKINASE (CPK)
Is the most cardiac specific enzymes
Is an accurate indicator of myocardial damage
Normal range:
- Males : 50 – 325 mu/ml
- Females: 50 – 250 mu/ml
Range with Myocardial Infarction
- Onset: 3 – 6 hours
- Peaks: 12 – 18 hours
- Returns to normal: 3 – 4 days
LACTATE DEHYDROGENASE (DLH)
Among the five isoenzymes
Is the most sensitive indicator of myocardial damage
In MI, LDH1 is elevated and its level exceeds LDH2 making LDH1 /LDH2
ratio “flipped”
Range with Myocardial Infarction
- Onset: 12 hours
- Peaks: 48 hours
- Returns to normal: 10 – 14 days
HYDROXYBUTYRATE DEHYDROGENASE (HBD)
Its elevation always accompany elevation of LDH1
Is valuable in detecting “Silent MI” because it remains elevated for a long
period of time, even after the other enzymes have returned to normal
The HBD/LDH ratio may be increased in MI
Range with Myocardial Infarction
- Onset: 10 – 12 hours
- Peaks: 48 – 72 hours
- Returns to normal: 12 – 13 days
F. URINALYSIS
Is usually performed to assess the effects of cardiovascular disease on renal
function and the existence of concurrent renal or systemic diseases
Albuminuria is detected in clients with malignant hypertension & CHF
Myoglobinuria supports diagnosis of MI
G. BLOOD URIC ACID
Reflects adequacy of renal tissue perfusion thereby glomerular filtration of
metabolites.
CVD result to decreased renal tissue perfusion
This will cause impairment of the ability of the kidneys to clear the plasma of
end products of metabolism like uric acid
Normal range: 2.5 to 8 mg /dl
H. SEROLOGIC TESTS
VDRL helps indicate presence of syphilis
This involves development of aortic disorders
I. SERUM ELECTROLYTES
Electrolytes affect cardiac contractility, specially Na, K, Ca
Normal range:
- Na - 135 – 145 mEq/L
- K - 3.5 – 5 mEq / L
- Ca - 4.5 – 5.5 mEq /L
B. ELECTROCARDIOGRAPHY (ECG, EKG)
Is the graphical recording of the
electrical activities of the heart
Indicates alterations in myocardial
oxygenation
Is the first test done when CVD is
suspected
WAVES, COMPLEXES AND INTERVALS
P wave
Depolarization of atria
Duration is 0.04 to 0.11 seconds
PR interval
Time of impulse transmission from SA node to the AV node
Duration is 0.12 to 0.20 seconds
QRS complex
Depolarization of the ventricles
Duration is 0.05 to 0.10
ST segment
Represents the plateau phase of action potential
T wave
Ventricular repolarization
Should not exceed 5 mm amplitude
NURSING RESPONSIBILITIES
Inform the client that the procedure is painless and that he will not
experience electrocution or a shock
The 0 level of the manometer is placed at the right, mid – axillary, 4th ICS, the
approximate level of the right atrium when in supine position.
Place the client in supine
position or in the same
position as during the initial
reading.
Swan – Ganz Catheter is inserted via antecubital vein into the right side of the
heart and is floated into the pulmonary artery.
It reflects pressure in the left heart
NURSING RESPONSIBILITIES
Inflate balloon only for PCWP readings, deflate between
readings
Observe catheter insertion site, culture site every 48 hours
Assess extremity for color, temperature, capillary filling and
sensation
E. SONIC STUDIES
1. ECHOCARDIOGRAPHY
Uses ultrasound to assess cardiac structure and mobility
No special preparation is required
It is painless and takes approximately 30 – 60 minutes to complete
The client has to remain still, in supine position slightly turned to the left side, and
with HOB elevated 15 – 20 degrees.
G. RADIOLOGIC TESTS
4. ANGIOGRAPHY
Involves introduction of contrast medium into the vascular system to outline the
heart and blood vessels
It may be done during cardiac catheterization
Nursing interventions are similar to that of cardiac catheterization
Observe for hypotension after the procedure because the contrast medium may
cause profound diuretic effect
Hematologic System:
The hematologic system consists of the blood and the sites where blood is produced, including
the bone marrow and the reticuloendothelial system (RES).
Blood is a specialized organ that differs from other organs in that it exists in a fluid state. Blood is
composed of plasma and various types of cells.
Plasma is a fluid portion of blood; it contains various proteins, such as albumin, globulin,
fibrinogen, and other factors necessary for the clotting as well as electrolytes, waste products
and nutrients.
45% of which is the cellular components of blood which are the Leukocytes (white blood cells,
WBC), Erythrocytes (red blood cells, RBCs), and thrombocytes (platelets).
Hematopoiesis is a continuous process of replenishing the dead blood cells, since most of the
blood cells have short life span.
The primary site for hematopoiesis is the bone marrow. The liver and spleen may also be
involved.
Under normal conditions, the adult bone marrow produces about 175 billion RBCs, 70 million
neotrophils (mature form of white cells), and 175 million thrombocytes (platelets) each day.
The volume of blood is 7% – 10% of the normal body weight and amounts to 5 to 6 liters.
Hemostasis is the balance between two systems which is the clot formation and clot dissolution
or fibrinolysis.
The bone marrow, is the site of hematopoiesis or blood cell formation. In a child, all skeletal
bones are involved, but as he person ages, marrow activity decreases. By adulthood, marrow
activity is usually limited to the pelvis, ribs, and sternum.
Marrow is one of the largest organs of the body, making up 4% to 5% of total body weight. It
consists of islands of cellular components (red marrow) separated by fat (yellow marrow).
In cases of adult disease causing marrow destruction, fibrosis, or scarring, - the liver and spleen
can also resume production of blood cells by a process as extramedullary hematopoiesis.
The marrow is highly vascular. Within it are primitive cells called stem cells.
These stem cells have the ability to self-replicate, thereby ensuring a continuous supply of stem
cells throughout the life cycle.
When stimulated to do so, stem cells can begin a process of differentiation into either myeloid or
lymphoid stem cells.
These stem cells are committed to produce specific types of blood cells.
Thus, with the exception of lymphocytes, all blood cells are derived from the myeloid stem cell,
and thus it is easy to appreciate why a defect in the myeloid stem cell can cause problems not
only with white cell production, but also with red cell and platelet production.
Differentiation of the primitive myeloid stem cell of the marrow into an erythroblast is stimulated
erythropoietin, a hormone produced primarily by the kidney. If the kidney detects low levels of
oxygen, the release of erythropoietin is increased
The increased erythropoietin then stimulates the marrow to increased production of RBCs. The
entire process typically takes 5 days.
The normal erythrocyte production, the bone marrow also requires iron, vitamin B12, folic acid,
pyridoxine (vitamin B6), and other factors. A deficiency of these factors during erythropoiesis can
result in decreased RBC production and thus anemia.
The rate of iron absorption is regulated by the amount of iron already stored in the body and by
the rate of red cell production.
Additional amounts of iron, up to 2mg daily, must be absorbed by the adult female to replace
blood lost during menstruation.
Total body iron content in the average adult is approximately 3mg, most of which is present in
hemoglobin or in one of its breakdown products.
When required, the iron is released into the plasma, binds to transferrin, and is transported into
the membranes of the normoblasts (erythrocyte precursor) within the marrow, where it is
incorporated into the hemoglobin. All these process takes only 6 to 8 minutes.
Iron is lost in the feces, either in bile, blood or mucosal cells from the intestine.
Normally concentration of iron in blood is about 75 to 175µg/dL (13 – 31 µmol/L) for men and 65
to 165µg/dL (11 - 29µmol/L) for women.
With iron deficiency, bone marrow iron stores are rapidly depleted; thus, hemoglobin synthesis is
depressed, and the red cells produced by the marrow are small and low in hemoglobin.
Vitamin B12 and folic acid are required for synthesis of deoxyribonucleic acid (DNA) in many
tissues, but deficiencies of either of these vitamins have the greatest effect on erythropoiesis.
Both B12 and folic acid are derived from the diet.
Folic acid is absorbed in the proximal small intestine, but only small amounts are stored within the
body
Vitamin B12 found only in foods of animal origin, strict vegetarians may ingest little B12. B12
combines with intrinsic factor complex is absorbed in the stomach. The vitamin B12 – intrinsic
factor complex is absorbed in the distal ileum
PLANNING / IMPLEMENTATION FOR HEALTH RESTORATION & MAINTENANCE for CLIENTS WITH
CARDIOVASCULAR PROBLEMS
A. Neonate
1. CONGENITAL HEART DEFECTS
i. are structural or functional anomalies in the heart that occur during fetal development
and are present at birth.
PATHOPHYSIOLOGY
STENOTIC LESIONS
Pulmonary Stenosis
Aortic Stenosis
Coartation of the Aorta
There is decreased blood flow through the major vessels existing the heart – the pulmonary
artery or the aorta. The chamber from which the stenotic vessel exits determines whether
right or left ventricular hypertrophy occurs.
Pulmonary Stenosis
there is obstruction of blood flow into the pulmonary artery due to the thickening and
fusing of the leaflets of the pulmonary artery.
This causes increased pressure into the right ventricle as its workload increases to
try to pump blood against the obstruction.
This leads to right ventricular hypertrophy and back up into the systemic circulation
attempting to return blood to the right atrium.
Aortic Stenosis and Coarctation of the Aorta
obstruction is present in the aorta either into the aortic valve or in the aortic arch.
This causes increased pressure in the left ventricle as it attempts to pump blood into
the systemic circulation against the obstruction.
The resultant increased left – sided pressure causes back pressure in the pulmonary
circulation and pulmonary congestion.
COMPLICATIONS
Congestive Heart Failure
Failure to Thrive
Decreased Cardiac Output
Pulmonary Edema
Hypoxia
Complications associated with surgical repair of defects
CLINICAL MANIFESTATIONS
Left – to – Right Shunts
Murmur
Dyspnea on exertion
Growth Retardation
Failure to Thrive
Diaphoresis
Right Ventricular Hypertrophy
Right sided CHF
Stenotic Lesions
Murmur
Dyspnea in exertion
Right or left sided heart failure and consequent systemic or pulmonary signs and symptoms.
Diagnostic Tests
Cardiac Auscultation
Blood Pressure
Chest X- ray
ECG
Echocardiogram
Cardiac Catheterization
MRI
Laboratory (Preoperative)
CBC
ABG
Electrolyte levels
Coagulation Studies
Cardiac Enzymes
Urinalysis
Therapeutic Management
Medical Management
Digoxin
Furosemide
Propanolol
Enalapril
Captopril
Surgical Management
Open Chest Surgery and Cardiopulmonary Bypass
Nursing Intervention
Promote activity tolerance by minimizing effects of CHF.
Provide information to parents.
Promote parental relaxation and reduce anxiety.
Promote family processes.
Promote normal growth and development.
Provide for adequate tissue perfusion.
Maintain adequate gas exchange.
Maintain adequate cardiac output.
Restore fluid balance and prevent future overload.
Assist in return of body temperature to WNL.
Prevent cardiac dysrhythmias.
Promote adequate gas exchange and patent airway.
Prevent infection.
Promote effective breathing pattern and maintain pain control.
Prevent thrombus formation.
Promote rest and sleep.
Promote health maintenance.
Discharge Teaching
Provide instructions on importance of regular follow – up visits to screen for residual
cardiovascular complications.
Provide instructions on medication administration including dosages, schedule of
administration and adverse effects to report to physician.
Provide information on normal growth and development and importance of normalcy for child.
Provide written instructions for home care after cardiac surgery.
• Age 3 to 7 yr
• A leukemic cell karyotype with chromosomes that are normal in number but abnormal in morphology (pseudodiploid)
Treatment
• Chemotherapy
• Remission induction
• CNS prophylaxis
• Maintenance
Treatment
• Chemotherapy
• Remission induction
• CNS prophylaxis
• Maintenance
Induction therapy:
The goal is to induce remission. Several regimens emphasize early introduction of an intensive multidrug regimen. Remission
can be induced with daily oral prednisone (deltasone)
and weekly IV vincristine (Oncovin) with the addition of an anthracycline or asparaginase (Espar)
. Other drugs and combinations that may be introduced early in treatment are cytarabine(Cytosar)
and etoposide (Etopophos)
as well as cyclophosphamide (Cytoxan)
In some regimens, intermediate-dose or high-dose IV methotrexate (Rheumatrix) is given with leucovorin rescue. The
combinations and their dosages are modified according to the presence of risk factors. Imatinib (Gleevec)
can be added to the drug regimen in patients with Ph chromosome–positive ALL.
CNS prophylaxis: An important site of leukemic infiltration is the meninges; prophylaxis and treatment may include high-dose
intrathecal methotrexate (Rheumatrix), cytosine arabinoside, and corticosteroids. Cranial nerve or whole-brain irradiation may be
necessary and is often used for patients at high risk of CNS disease (eg, high WBC count, high serum LDH, B-cell phenotype)
but has been used less often in recent years.
Consolidation therapy: The goal of consolidation is to prevent leukemic regrowth. Consolidation therapy usually lasts a few
months and combines drugs that have different mechanisms of action than drugs used in induction regimens. Allogeneic stem
cell transplantation is recommended as consolidation of Ph chromosome–positive ALL or in 2nd or later relapses or remissions.
Maintenance therapy: Most regimens include maintenance therapy with methotrexate (Rheumatrix)
and mercaptopurine (Purinethol). Therapy duration is usually 2½ to 3 yr but may be shorter with regimens that are more intensive
in earlier phases and for B-cell (L3) cases. For patients in continuous complete remission for 2½ yr, the risk of relapse after
therapy cessation is about 20%, usually within 1 yr. Thus, when therapy can be stopped, most patients are cured.
Relapse: Leukemic cells may reappear in the bone marrow, the CNS, or the testes. Bone marrow relapse is particularly
ominous. Although a new round of chemotherapy may induce a 2nd remission in 80 to 90% of children (30 to 40% of adults),
subsequent remissions tend to be brief. Only a few patients with late bone marrow relapses achieve long disease-free 2nd
remissions or cure.
If an HLA-matched sibling is available, stem cell transplantation offers the greatest hope of long-term remission or cure (see
Transplantation: Hematopoietic Stem Cell Transplantation). Cells from other relatives or matched, unrelated donors are
sometimes used. Transplantation is rarely used for patients > 65 yr, because it is much less likely to be successful and adverse
effects are much more likely to be fatal.
When relapse involves the CNS, treatment includes intrathecal methotrexate (with or without cytarabine or corticosteroids) twice
weekly until all signs disappear. Most regimens include systemic reinduction chemotherapy because of the likelihood of systemic
spread of blast cells. The role of continued intrathecal drug use or CNS irradiation is unclear.
Testicular relapse may be evidenced clinically by painless firm swelling of the testis or may be identified on biopsy. If unilateral
testicular involvement is clinically evident, the apparently uninvolved testis should undergo biopsy. Treatment is by irradiation of
the involved testis and administration of systemic reinduction therapy as for isolated CNS relapse.
YOUNG
1. HODGKIN’S DISEASE
• a malignant condition characterized by proliferation of abnormal giant,
multinucleated cells, called Reed-Sternberg cells, which are located in lymph
nodes.
• Although the cause of Hodgkin’s lymphoma remains unknown, the main
interacting factors include infection with Epstein-Barr virus, genetic
predisposition, and exposure to occupational toxins.
• The incidence of Hodgkin’s lymphoma is increased in incidence among
human immunodeficiency virus infected patients.
• The nursing care for Hodgkin’s lymphoma is largely based on managing
problems related to the disease (e.g., pain due to tumor), pancytopenia, and
other side effects of therapy.
• Malignancy in the lymphoid system.
S/sx:
painless swelling of lymph nodes
persistent fever
night sweats
weight loss
fatigue/malaise
edema of face & neck
jaundice
Dx:
Lymph node biopsy
CXR
CT scan
Lymphangiography
Tx:
Chemo/radiation therapy
Bone marrow transplant
Blood sternal transfusions
Immunotherapy
Nsg. Dx:
Potential for infection
Interventions:
Instruct the patient to report any signs of infection.
Prepare the patient for chemotherapy and radiation therapy.
Relaxation techniques
Administer meds as ordered
Provide emotional support.
Advise patient taking Prednisone against sudden withdrawal of drug & not to change dosage or
discontinue drug without consent of physician.
Good nutrition
Use soft toothbrush
Avoid crowds & any person with known infection
3. KAWASAKI’S DISEASE
o Multi – system vasculitis primarily affecting the cardiovascular system.
CM: High spiking fever, 5 or more days
Criteria for Dx:
Fever lasting for more than 5 days
Bilateral conjunctivitis
Changes of lips & oral cavity
S/Sx
dry, red fissure lips
strawberry tongue
diffuse erythema of mucous membrane
Changes of peripheral extremities
erythema of the palms & soles
indurative edema of the hands & feet
membranous desquamation from fingertips
Polymorphous rash (primarily on trunk)
Acute non-purulent swelling of cervical lymph node to > 1.5 cm in diameter
Lab. Data: Elevated ESR during the acute stage
Nsg. Dx: Pain
Interventions:
Administer ASPIRIN as ordred
Monitor VS
Offer clear liquid diet like popsicles
Teach the parents to perform CPR
4. PERICARDITIS
is an inflammation of the pericardium.
CAUSES:
bacterial, fungal, or viral infection
Neoplasm
Autoimmune disease
Postcardiac injury
Drugs such as procainamide or Hydralazine
S/Sx:
• pain in the anterior chest
• associated symptoms of dyspnea, fever, sweating and chills
• pericardial friction rub
Dx
• CRX
• Echocardiogram
• ECG
• WBC and differential count
• Tuberculin testing
• Pericardiocentesis
Mx:
• Monitor HR, rhythm, BP and RR
• Assess for cardiac tamponade
• Assess for CHF
• Institute continuous cardiac monitoring
• Encourage bed rest
• Help the patient to a position of comfort
• Provide relief to anxiety
ACUTE PERICARDITIS
sharp, offensive, sudden pain usually starts over the sternum and radiates to the neck,
shoulder, back and arms.
CHRONIC PERICARDITIS
gradual increase in systemic venous pressure and produces symptoms similar to those of
chronic right heart failure.
Dx:
Normal or elevated WBC count
elevated ESR
slightly elevated cardiac enzyme levels
culture of pericardial fluid obtained by open surgical drainage or cardiocentesis
ECG – elevation of ST segment
Interventions:
Provide complete CBR
Assess pain in relation to respiration and body position.
Place the patient in an upright position to relieve dyspnea and chest pain.
Explain tests and treatments to the patient.
Instruct on DBE and coughing exercises.
Clinical manifestations:
Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and
nausea and vomiting are early systemic manifestations of the viral illness.
Early cardiac manifestations appear 7 to 10 days after viral infection and include
pleuritic chest pain with a pericardial friction rub and effusion.
Late cardiac signs relate to the development of HF and may include an S3 heart
sound, crackles, jugular venous distention, syncope, peripheral edema, and angina.
fatigue, dyspnea, palpitation, feveCollaborative care includes the following:
Managing associated cardiac decompensation with:
a. Digoxin (Lanoxin) to treat ventricular failure
b. Diuretics to reduce fluid volume and decrease preload
c. Nitroprusside (Nitropress), inamrinone (Inocor), and milrinone (Primacor) to
reduce afterload and improve cardiac output
d. The use of anticoagulation therapy may be considered in patients with a low
ejection fraction who are at risk for thrombus formation from blood stasis in the
cardiac chambers.
e. Immunosuppressive therapy to reduce myocardial inflammation and to prevent
irreversible myocardial damage.
f. Oxygen therapy, bed rest, and restricted activity.
g. Intraaortic balloon pump therapy and ventricular assist devices.
Dx:
ECG typically shows diffuse ST segment and T wave abnormalities, conduction defects
(prolonged PR interval), and supraventricular arrhythmias.
Stool and throat cultures, endomyocardial biopsy
Cardiac enzyme levels, WBC count and ESR are increased.
Antibody titers are elevated.
Tx:
Antibiotics
modified bed rest
activity restriction
sodium restriction
Diuretics
digitalis glycosides
Interventions:
Nursing interventions focus on assessment for the signs and symptoms of HF and
include assessing the level of anxiety, instituting measures to decrease anxiety, and
keeping the patient and family informed about therapeutic measures.
Most patients with myocarditis recover spontaneously, although some may develop
dilated cardiomyopathy. If severe HF occurs, the patient may require heart
transplantation.
Observe for signs of digitalis toxicity (anorexia, nausea, vomiting, blurred vision, cardiac arrythmias)
Stress the importance of bed rest.
Resume normal activities gradually and avoid competitive sports.
6. ENDOCARDITIS
Infection of the inner lining of the heart caused by direct invasion of bacteria leading to
deformity of the valve leaflets
Endocarditis usually refers to infection of the endocardium (ie, infective endocarditis). The
term can also include noninfective endocarditis, in which sterile platelet and fibrin thrombi
form on cardiac valves and adjacent endocardium. Noninfective endocarditis sometimes
leads to infective endocarditis. Both can result in embolization and impaired cardiac
function.
Endocarditis can occur at any age. Men are affected about twice as often. IV drug
abusers and immunocompromised patients are at highest risk.
Local consequences:
• formation of myocardial abscesses with tissue destruction and sometimes
conduction system abnormalities
• Severe valvular regurgitation
• Aortitis
• Prosthetic valve infections
Systemic consequences (primarily due to embolization)
• septic pulmonary emboli
• Mycotic aneurysms
• Cutaneous and retinal emboli
Treatment
Treatment consists of a prolonged course of antimicrobial therapy.
Surgery may be needed for mechanical complications or resistant organisms.
Antibiotic regimens:
Ampicillin
Nafcillin
gentamicin
vancomycin
rifampin
Prevention
Antimicrobial prophylaxis is recommended for patients at high to moderate risk of infective
endocarditis before procedures associated with bacteremias and subsequent infective
endocarditis
Nursing Interventions:
Record daily weight
Evaluate JVD – this signifies the development of CHF.
Instruct the patient to take antibiotics before dental procedures that can cuse
bleeding.
Avoid sharing of needles.
Teach the women in child bearing years the risks of using IUDs, or birth control
(source of infection).
a. Adult
1. ATHEROSCLEROSIS
Atherosclerosis is patchy intimal plaques (atheromas) in medium-sized and large arteries
The plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue.
Risk factors include dyslipidemia, diabetes, cigarette smoking, family history, sedentary
lifestyle, obesity, and hypertension.
Atherosclerosis can affect all large and medium-sized arteries, including the coronary,
carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities.
It is the leading cause of morbidity and mortality in the US and in most developed countries.
Atherosclerosis is rapidly increasing in prevalence in developing countries, and as people in
developed countries live longer, incidence will increase. By 2020, atherosclerosis is
expected to be the leading cause of death worldwide.
Pathophysiology
The hallmark of atherosclerosis is the atherosclerotic plaque, which contains lipids
(intracellular and extracellular cholesterol and phospholipids), inflammatory cells (eg,
macrophages, T cells), smooth muscle cells, connective tissue (eg, collagen,
glycosaminoglycans, elastic fibers), thrombi, and Ca deposits.
Endothelial injury is thought to have a primary role.
Atherosclerosis preferentially affects certain areas of the arterial tree.
Macrophages elaborate proinflammatory cytokines that recruit smooth muscle cell migration
from the media and that further attract and stimulate growth of macrophages.
The result is a subendothelial fibrous plaque with a fibrous cap, made of intimal smooth
muscle cells surrounded by connective tissue and intracellular and extracellular lipids.
Atherosclerotic plaques may be stable or unstable.
The strength of the fibrous cap and its resistance to rupture depend on the relative balance
of collagen deposition and degradation. Plaque rupture involves secretion of
metalloproteinases, cathepsins, and collagenases by activated macrophages in the plaque.
These enzymes digest the fibrous cap, particularly at the edges, causing the cap to thin and
ultimately rupture. T cells in the plaque contribute by secreting cytokines. Cytokines inhibit
smooth muscle cells from synthesizing and depositing collagen, which normally reinforces
the plaque.
Once the plaque ruptures, plaque contents are exposed to circulating blood, triggering
thrombosis; macrophages also stimulate thrombosis because they contain tissue factor,
which promotes thrombin generation in vivo. One of 5 outcomes may occur:
o The resultant thrombus may organize and be incorporated into the plaque, changing
the plaque's shape and causing its rapid growth.
o The thrombus may rapidly occlude the vascular lumen and precipitate an acute
ischemic event.
o The thrombus may embolize.
o The plaque may fill with blood, balloon out, and immediately occlude the artery.
o Plaque contents (rather than thrombus) may embolize, occluding vessels
downstream.
Risk Factors
Nonmodifiable
1. Age
2. Family history of premature atherosclerosis*
3. Male sex
4. Modifiable, established
5. Certain dyslipidemias (high total or LDL level, low HDL level, increased total-
to-HDL cholesterol ratio)
6. Cigarette smoking
7. Diabetes mellitus
8. Hypertension
Modifiable
1. Alcohol intake (other than moderate)
2. Chlamydia pneumoniae infection
3. High CRP level
4. High level of small, dense LDL
5. High lipoprotein(a) level
6. Hyperhomocysteinemia
7. Hyperinsulinemia
8. Hypertriglyceridemia
9. 5-Lipoxygenase polymorphisms
10. Low intake of fruits and vegetables
11. Obesity or metabolic syndrome
12. Prothrombotic states (eg, hyperfibrinogenemia, high plasminogen activator
inhibitor level)
13. Psychosocial factors (eg, type A personality, depression, anxiety, work
characteristics, socioeconomic status)
14. Renal insufficiency
15. Sedentary lifestyle†
16. CRP = C-reactive protein, HDL = high density lipoprotein, LDL = low density
lipoprotein.
17. *Disease in a first-degree relative before age 55 for men and before age 65
for women.
Treatment
1. Diet: Several changes are beneficial:
Tx:
P – ercutaneous
T – ransluminal
C – oronary
A –ngioplasty
Objective:
To vascularize the myo cardium
To prevent angina
Increase survival rate
C – oronary
A – rterial
B – ypass
G – raft surgery
3. ANGINA PECTORIS
Angina pectoris is a clinical syndrome of precordial discomfort or
pressure due to transient myocardial ischemia without infarction. It is typically
precipitated by exertion or psychologic stress and relieved by rest or sublingual
nitroglycerin.
Etiology and Pathophysiology
1. Atherosclerosis, coronary artery spasm, coronary artery embolism
2. Acute coronary thrombosis
3. angina if obstruction is partial or transient
4. MI.
Because myocardial O2 demand is determined mainly by heart rate,
systolic wall tension, and contractility, narrowing of a coronary artery typically
results in angina that occurs during exertion and is relieved by rest.
In addition to exertion, cardiac workload can be increased by disorders
such as hypertension, aortic stenosis, aortic regurgitation, or hypertrophic
cardiomyopathy. In such cases, angina can result whether atherosclerosis is
present or not. These disorders can also decrease relative myocardial perfusion
because myocardial mass is increased (causing decreased diastolic flow).
A decreased O2 supply, as in severe anemia or hypoxia, can
precipitate or aggravate angina.
2 Walking rapidly
Walking uphill
Climbing stairs rapidly
Walking or climbing stairs after meals
Cold
Wind
Emotional stress
Unstable angina: Because angina characteristics are usually predictable for a given
patient, any changes (ie, rest angina, new-onset angina, increasing angina) should
be considered serious. Such changes are termed unstable angina and require
prompt evaluation and treatment.
Clinical situation
Diagnosis
1. Typical symptoms
Diagnosis is suspected if chest discomfort is typical and is precipitated by exertion
When the resting ECG is abnormal, false-positive ST-segment shifts are common on the
stress ECG, so patients should have stress testing with myocardial imaging. Exercise or
pharmacologic stress (eg, with dobutamine (Dobutrex)
or dipyridamole (Persantine) infusion may be used. The choice of imaging technique
depends on institutional availability and expertise. Imaging tests can help assess LV
function and response to stress; identify areas of ischemia, infarction, and viable tissue; and
determine the site and extent of myocardium at risk. Stress echocardiography can also
detect ischemia-induced mitral regurgitation.
Intravascular ultrasonography provides images of coronary artery structure. This test can
provide more information about coronary anatomy than other tests; it is indicated when the
nature of lesions is unclear or when apparent disease severity does not match symptom
severity. Used with angioplasty, it can help ensure optimal placement of stents.
Imaging: Electron beam CT can detect the amount of Ca present in coronary artery plaque.
The Ca score (from 1 to 100) is roughly proportional to the risk of subsequent coronary
events. However, because Ca may be present in the absence of significant stenosis, the
score does not correlate well with the need for angioplasty or CABG. Current indications for
cardiac MRI include evaluation of cardiac structure and function, assessment of myocardial
viability, and possibly diagnosis and risk assessment of patients with either known or
suspected CAD.
Prognosis
The main adverse outcomes are unstable angina, MI, and sudden death due to
arrhythmias.
Annual mortality rate is about 1.4% in patients with angina, no history of MI, a
normal resting ECG, and normal BP. Women with CAD tend to have a worse
prognosis.
Mortality rate is about 7.5% when systolic hypertension is present, 8.4% when the
ECG is abnormal, and 12% when both are present. Type 2 diabetes about doubles
the mortality rate for each scenario.
Prognosis worsens with increasing age, increasingly severe anginal symptoms,
presence of anatomic lesions, and poor ventricular function.
Lesions in the left main coronary artery or proximal left anterior descending artery
indicate particularly high risk.
Although prognosis correlates with number and severity of coronary arteries affected,
prognosis is surprisingly good for patients with stable angina, even those with 3-
vessel disease, if ventricular function is normal.
Treatment
1. Modification of risk factors (smoking, BP, lipids)
• The main goals are to relieve acute symptoms, prevent or reduce ischemia and
prevent future ischemic events. For an acute attack, sublingual nitroglycerin is the
most effective drug.
• To prevent ischemia, all patients diagnosed with CAD or at high risk of developing
CAD should take an antiplatelet drug daily. β-Blockers, unless contraindicated or not
tolerated, are given to most patients. For some patients, prevention of symptoms
requires Ca channel blockers or long-acting nitrates.
B. β-Blockers limit symptoms and prevent infarction and sudden death better than
other drugs.
• β-Blockers block sympathetic stimulation of the heart and reduce systolic BP, heart
rate, contractility, and cardiac output, thus decreasing myocardial O2 demand and
increasing exercise tolerance.
• They also increase the threshold for ventricular fibrillation. Most patients tolerate
these drugs well.
• Many β-blockers are available and effective. Dose is titrated upward as needed until
limited by bradycardia or adverse effects.
• Patients who cannot tolerate β-blockers are given a Ca channel blocker with
negative chronotropic effects (eg, diltiazem – cardizem, verapamil (Calan, Isoptin).
• Those at risk for β-blocker intolerance (eg, those with asthma) may be tried on a
cardioselective β-blocker (eg, carvedilol – COREG) perhaps with pulmonary function
testing before and after drug administration to detect drug-induced bronchospasm.
. Nitroglycerin
PCI is usually preferred for 1- or 2-vessel disease with suitable anatomic lesions.
Lesions that are long or near bifurcation points are often not amenable to PCI.
However, as stent technology improves, PCI is being used for more complicated
cases.
CABG is very effective in selected patients with angina. The ideal candidate has
severe angina pectoris and localized disease, or diabetes mellitus. About 85% of
patients have complete or dramatic symptom relief. Exercise stress testing shows
positive correlation between graft patency and improved exercise tolerance, but
exercise tolerance sometimes remains improved despite graft closure.
CABG improves survival for patients with left main disease, those with 3-vessel
disease and poor LV function, and some patients with 2-vessel disease. However,
for patients with mild or moderate angina (class I or II) or 3-vessel disease and good
ventricular function, CABG appears to only marginally improve survival. For patients
with 1-vessel disease, outcomes with drug therapy, PCI, and CABG are similar;
exceptions are left main disease and proximal left anterior descending disease, for
which revascularization appears advantageous.
Nursing Interventions:
Administer nitroglycerine sublingually to relieve the pain.
Teach the patient that a burning sensation under the tongue after
nitroglycerine administration indicates that the drug is potent.
The drug may also cause facial flushing and headache.
Prepare the patient for PTCA by informing the patient that a balloon tipped
catheter will be introduced through a guide wire into a coronary vessel.
VARIANT ANGINA
Variant angina is angina pectoris secondary to epicardial coronary artery spasm
(Prinzmetal's angina).
Most patients with variant angina have significant fixed proximal obstruction of at
least one major coronary artery. Spasm usually occurs within 1 cm of the obstruction
(often accompanied by ventricular arrhythmia).
Symptoms are anginal discomfort occurring mainly during rest, often at night, and
only rarely and inconsistently during exertion (unless significant coronary artery
obstruction is also present). Attacks tend to occur regularly at certain times of day.
Average survival at 5 yr is 89 to 97%, but mortality risk is greater for patients with
both variant angina and atherosclerotic coronary artery obstruction. Usually,
sublingual nitroglycerin promptly relieves variant angina. Ca channel blockers may
effectively prevent symptoms. Theoretically, β-blockers may exacerbate spasm by
allowing unopposed α-adrenergic vasoconstriction, but this effect has not been
proved clinically. Oral drugs most commonly used are sustained-release diltiazem
120 to 540 mg once/day, sustained-release verapamil 120 to 480 mg once/day
(dose must be reduced in patients with renal or hepatic dysfunction), or amlodipine
15 to 20 mg once/day (dose must be reduced in elderly patients and patients with
hepatic dysfunction). In refractory cases, amiodarone may be useful. Although these
drugs relieve symptoms, they do not appear to alter prognosis.
SYNDROME X
Syndrome X is cardiac microvascular dysfunction or constriction causing angina
(microvascular angina).
Some patients with typical angina that is relieved by rest or nitroglycerin have normal
coronary arteriograms (eg, no atherosclerosis, embolism, or inducible arterial
spasm). Some of these patients have ischemia detected during stress testing; others
do not. In some patients, the cause of ischemia seems to be reflex intramyocardial
coronary constriction and reduced coronary flow reserve. Other patients have
microvascular dysfunction within the myocardium: The abnormal vessels do not
dilate in response to exercise or other cardiovascular stressors; sensitivity to cardiac
pain may also be increased. Prognosis is good, although symptoms of ischemia may
recur for years. In many patients, β-blockers relieve symptoms. This disorder should
not be confused with variant angina due to epicardial coronary spasm or with
another disorder called syndrome X, which refers to the metabolic syndrome.
SILENT ISCHEMIA
Patients with CAD (particularly diabetics) may have ischemia without symptoms.
Ischemia is evidenced by transient asymptomatic ST-T abnormalities seen during
24-h Holter monitoring. Radionuclide studies can sometimes document
asymptomatic myocardial ischemia during physical or mental stress (eg, mental
arithmetic). Silent ischemia and angina pectoris
5. MYOCARDIAL INFARCTION
destruction of cardiac tissue due to reduced coronary blood flow.
IM:
Lower sternal pain not relieved by rest and nitroglycerine, characterized as
crushing or excruciating.
S/Sx:
Chest pain
dyspnea
hyperthermia
initial in BP
mild restlessness & apprehensions
cool, moist, ashen skin
occasional findings
Dx:
Cardiac Enzymes (CPK-MB, LDH, SGPT, SGOT, Troponin test)
ECG tracing (widening of QRS complexes)
Serum cholesterol & uric acid
CBC
Lab. Data:
Elevated creatinine phosphokinase, and TROPONIN
ECG reveals ST segment elevation or depression and T wave inversion.
Nursing Dx:
Pain related to decreased tissue oxygenation.
Interventions:
Narcotic analgesics : Morphine SO4
Administer O2 inhalation
Enforce CBR without BRP
Avoid valsalva manuever
Semi-Fowler
Provide a general liquid diet that is ↓ in
Monitor V/S, I&O, & ECG tracings
Take 20-30 ml/wk
Assist in surgery: CABG
Provide health teaching
Avoid modifiable risk fx
Prevent complications
Arrhythmias
Shock
Thrombophlebitis
CHF
Dressler’s syndrome
Diet - low fat, low cholesterol, low sodium diet.
Teach importance of follow up care
Resume ADL
Strict compliance to meds
Vasodilators
Anti-arrhythmic
Beta blockers
ACE inhibitors
Ca antagonist
Thrombolytics/fibrinolytics
S/E: (Monitor for bleeding)
♦ Sreptokinase
♦ Urokinase
♦ Tissue plasminogen activating factor
Anti-coagulants
Heparin
↓
PTT
↓
If prolonged bleeding
↓
Antidote: Protamine SO4
Coumadin (Warfarin)
↓
PT
↓
prolonged bleeding
↓
Antidote: Vit K
7. HYPERTENSION
• is defined as a persistent systolic blood pressure (SBP) greater than or equal to 140
mm Hg, diastolic blood pressure (DBP) greater than or equal to 90 mm Hg, or
current use of antihypertensive medication. There is a direct relationship between
hypertension and cardiovascular disease (CVD).
CLASSIFICATION OF HYPERTENSION
• Hypertension is classified as follows:
o Prehypertension: BP 120 to 139 / 80 to 89 mm Hg
o Hypertension, Stage 1: BP 140 to 159 / 90 to 99 mm Hg
o Hypertension, Stage 2: systolic BP greater than or equal to 160 or diastolic
BP greater than or equal to 100 mm Hg.
• Subtypes of hypertension:
o Isolated systolic hypertension (ISH): average SBP greater than or equal to
140 mm Hg coupled with an average DBP less than 90 mm Hg. ISH is more
common in older adults. Control of ISH decreases the incidence of stroke,
heart failure, cardiovascular mortality, and total mortality.
o Pseudohypertension (false hypertension) occurs with advanced
arteriosclerosis. Pseudohypertension is suspected if arteries feel rigid or
when few retinal or cardiac signs are found relative to the pressures obtained
by cuff.
ETIOLOGY OF HYPERTENSION
• Primary (essential or idiopathic) hypertension: elevated BP without an identified
cause; accounts for 90% to 95% of all cases of hypertension.
• Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular disease),
kidney (nephrosclerosis), and eyes (retinal damage).
• Sustained high BP increases the cardiac workload and produces left ventricular
hypertrophy (LVH). Progressive LVH, especially in association with CAD, is
associated with the development of heart failure.
• The retina provides important information about the severity and duration of
hypertension. Damage to retinal vessels provides an indication of concurrent vessel
damage in the heart, brain, and kidney. Manifestations of severe retinal damage
include blurring of vision, retinal hemorrhage, and loss of vision.
DIAGNOSTIC STUDIES
• Basic laboratory studies are performed to (1) identify or rule out causes of secondary
hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular
risk, or (4) establish baseline levels before initiating therapy.
• Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used
to screen for renal involvement and to provide baseline information about kidney
function.
• Lipid profile provides information about additional risk factors that predispose to
atherosclerosis and cardiovascular disease.
• Uric acid levels are determined to establish a baseline, because the levels often rise
with diuretic therapy.
• Lifestyle modifications are indicated for all patients with prehypertension and
hypertension and include the following:
o Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by
approximately 5 to 20 mm Hg.
o Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves
eating several servings of fish each week, eating plenty of fruits and
vegetables, increasing fiber intake, and drinking a lot of water. The DASH diet
significantly lowers BP.
o Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g
of sodium per day.
o This involves avoiding foods known to be high in sodium (e.g., canned soups)
and not adding salt in the preparation of foods or at meals.
o There is evidence that greater levels of dietary potassium, calcium, vitamin D,
and omega-3 fatty acids are associated with lower BP in those with
hypertension.
o Restriction of alcohol to no more than two drinks per day for men and no
more than one drink per day for women
o Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a
day most days of the week. Moderately intense activity such as brisk walking,
jogging, and swimming can lower BP, promote relaxation, and decrease or
control body weight.
o It is strongly recommended that tobacco use be avoided.
o Stress can raise BP on a short-term basis and has been implicated in the
development of hypertension. Relaxation therapy, guided imagery, and
biofeedback may be useful in helping patients manage stress, thus
decreasing BP.
Drug Therapy
• Drug therapy is not recommended for those persons with prehypertension unless it
is required by another condition, such as diabetes mellitus or chronic kidney
disease.
• The overall goals for the patient with hypertension include (1) achievement and
maintenance of the goal BP; (2) acceptance and implementation of the therapeutic
plan; (3) minimal or no unpleasant side effects of therapy; and (4) ability to manage
and cope with illness.
• Drugs currently available for treating hypertension work by (1) decreasing the
volume of circulating blood, and/or (2) reducing SVR.
o Diuretics promote sodium and water excretion, reduce plasma volume,
decrease sodium in the arteriolar walls, and reduce the vascular response to
catecholamines.
o Adrenergic-inhibiting agents act by diminishing the SNS effects that increase
BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor
center and peripherally to inhibit norepinephrine release or to block the
adrenergic receptors on blood vessels.
o Direct vasodilators decrease the BP by relaxing vascular smooth muscle and
reducing SVR.
o Calcium channel blockers increase sodium excretion and cause arteriolar
vasodilation by preventing the movement of extracellular calcium into cells.
o Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of
angiotensin I to angiotensin II and reduce angiotensin II (A-II)–mediated
vasoconstriction and sodium and water retention.
o A-II receptor blockers (ARBs) prevent angiotensin II from binding to its
receptors in the walls of the blood vessels.
o Thiazide-type diuretics are used as initial therapy for most patients with
hypertension, either alone or in combination with one of the other classes.
o When BP is more than 20/10 mm Hg above SBP and DBP goals, a second
drug should be considered. Most patients who are hypertensive will require
two or more antihypertensive medications to achieve their BP goals.
o Side effects and adverse effects of antihypertensive drugs may be so severe
or undesirable that the patient does not comply with therapy.
Hyperuricemia, hyperglycemia, and hypokalemia are common side
effects with both thiazide and loop diuretics.
ACE inhibitors lead to high levels of bradykinin, which can cause
coughing. An individual who develops a cough with the use of ACE
inhibitors may be switched to an ARB.
Hyperkalemia can be a serious side effect of the potassium-sparing
diuretics and ACE inhibitors.
Sexual dysfunction may occur with some of the diuretics.
Orthostatic hypotension and sexual dysfunction are two undesirable
effects of adrenergic-inhibiting agents.
Tachycardia and orthostatic hypotension are potential adverse effects
of both vasodilators and angiotensin inhibitors.
Patient and family teaching related to drug therapy is needed to
identify and minimize side effects and to cope with therapeutic effects.
Side effects may be an initial response to a drug and may decrease
with continued use of the drug.
• Resistant hypertension is the failure to reach goal BP in patients who are adhering to
full doses of an appropriate three-drug therapy regimen that includes a diuretic.
NURSING MANAGEMENT
• The primary nursing responsibilities for long-term management of hypertension are
to assist the patient in reducing BP and complying with the treatment plan. Nursing
actions include patient and family teaching, detection and reporting of adverse
treatment effects, compliance assessment and enhancement, and evaluation of
therapeutic effectiveness.
• Patient and family teaching includes the following: (1) nutritional therapy, (2) drug
therapy, (3) physical activity, (4) home monitoring of BP (if appropriate), and (5)
tobacco cessation (if applicable).
o Home monitoring of BP should include daily BP readings when treatment is
initiated or medications are adjusted and weekly once the BP has stabilized.
A log of the BP measurements should be maintained by the patient. Devices
that have memory or printouts of the readings are recommended to facilitate
accurate reporting.
o A major problem in the long-term management of the patient with
hypertension is poor compliance with the prescribed treatment plan. The
reasons include inadequate patient teaching, unpleasant side effects of
drugs, return of BP to normal range while on medication, lack of motivation,
high cost of drugs, lack of insurance, and lack of a trusting relationship
between the patient and the health care provider.
GERONTOLOGIC CONSIDERATIONS
• The prevalence of hypertension increases with age. The lifetime risk of developing
hypertension is approximately 90% for middle-aged (age 55 to 65) and older (age
>65) normotensive men and women.
• In some older people, there is a wide gap between the first Korotkoff sound and
subsequent beats (auscultatory gap). Failure to inflate the cuff high enough may
result in underestimating the SBP.
• Older adults are sensitive to BP changes. Reducing SBP to less than 120 mm Hg in
a person with long-standing hypertension could lead to inadequate cerebral blood
flow.
• Older adults produce less renin and are more resistant to the effects of ACE
inhibitors and angiotensin II receptor blockers.
HYPERTENSIVE CRISIS
• Hypertensive crisis is a severe and abrupt elevation in BP, arbitrarily defined as a
DBP more than 140 mm Hg.
o Hypertensive crisis occurs most often in patients with a history of
hypertension who have failed to comply with their prescribed medications or
who have been undermedicated.
o Hypertensive crisis related to cocaine or crack use is becoming a more
frequent problem. Other drugs such as amphetamines, phencyclidine (PCP),
and lysergic acid diethylamide (LSD) may also precipitate hypertensive crisis
that may be complicated by drug-induced seizures, stroke, MI, or
encephalopathy.
• Mean arterial pressure (MAP) is generally used instead of systolic and diastolic
readings to guide therapy. MAP is calculated as follows: MAP = (SBP + 2 DBP) ÷ 3.
• The initial treatment goal is to decrease MAP by no more than 25% within minutes to
1 hour. If the patient is stable, the target goal for BP is 160/100 to 110 mm Hg over
the next 2 to 6 hours.
4. Frequently, if pain is severe and persistent, the affected leg feels cold, sweats
excessively, and becomes cyanotic, probably because of sympathetic nerve
overactivity.
7. In young men who smoke and have extremity ulcers, a positive Allen's test
(the hand remains pale after the examiner simultaneously compresses the radial and
ulnar arteries, then alternately releases them) suggests the disorder.
8. Pallor with elevation and rubor with dependency frequently occur in affected
hands, feet, or digits. Ischemic ulceration and gangrene, usually of one or more
digits, may occur early in the disorder but not acutely.
9. Noninvasive tests show greatly decreased blood flow and pressure in the
affected toes, feet, and fingers.
Diagnosis
1. (Other causes of ischemia excluded by testing)
2. Angiography
3. History and physical examination
4. Echocardiography
5. Leg arteriography
6. Allen's test
Treatment
1. Smoking cessation
2. Local measures
3. Sometimes drug therapy
• iloprost (Ventavis) 0.5 to 3 ng/kg/min IV infusion over 6 h may help prevent
amputation.
• Pentoxifylline (Trental)
• Ca channel blockers
• Thromboxane inhibitors
OTHERS:
Part 2
Alterations of Hematologic Functions
1. Anemias are a laboratory definition that implies a low red cell count and hemoglobin or
hematocrit level that is below normal. Physiologically, anemia exists when there is an
insufficient amount of hemoglobin to deliver oxygen to the tissues.
Altered Physiology
i. The appearance of anemia may reflect (1)-decreased production of red cells, (2) red
cell loss, or (3) increased destruction.
ii. Marrow failure may occur as a result of nutritional deficiency, toxic exposure, tumor
invasion, or unknown causes.
iii. Red cells may be lost through hemorrhage or hemolysis (increased destruction).
• This problem may be rooted in an intrinsic red cell defect that is incompatible with
normal red cell survival or is explainable on the basis of some factor extrinsic to the red
cell that promotes red-cell destruction.
• Red cell lysis occurs mainly within the phogocytic cells of the reticuloendothelial system,
notably within the liver and spleen.
• As a by-product of this process, bilirubin, formed by the metabolism of hemoglobin
within the phagocyte, enters the blood stream, and an increase in hemolysis in promptly
reflected by an increase in total plasma bilirubin.
• General Considerations:
• 1. Red cells and hemoglobin are normally formed at the same rate at which they are
destroyed.
• 2. Whenever formation of red cells or hemoglobin is decreased or their destruction is
increased, anemia results.
• 3. The ability of red blood cells to carry hemoglobin is decreased.
• 4. The ability of the hemoglobin to oxygenate the tissues and remove carbon dioxide for
excretion by the lungs is also decreased.
• 5. Less hemoglobin is available to act as a buffer in regulating the pH of the blood.
Clinical manifestations:
(Most manifestations are attributable to a decrease in the oxygen-carrying capacity of the
blood, and are the same regardless of the cause of anemia.)
i. The more rapidly the anemia develops, the more severe its symptoms:
• Pallor
• Susceptibility to fatigue
• Shortness of breath
• Headache; disturbed cerebration; dizziness
• Development of angina pectoris or congestive heart failure in susceptible individuals.
ii. Severity of symptoms dependent on:
• The speed with which and the degree to which the anemia has developed.
• Its prior duration (i.e., its chronicity)
• The metabolic requirements of the particular patient.
• Any other disorders currently afflicting the patient, particularly cardiac conditions, etc.
• Special complications or concomitant features of the condition producing the anemia.
a. Iron Deficiency Anemias are conditions in which the total body iron content is decreased below normal.
Etiology:
Iron deficiency develops when the body’s need for iron exceeds the supply.
Chronic blood loss – gastrointestinal (GI) bleeding (secondary to gastritis, peptic ulcer, hemorrhoids,
malignancy), excessive menstrual bleeding, multiple pregnancies, hookworm infestation.
Impaired GI absorption of iron – small bowel disease, certain gastric resections.
Insufficient intake.
Increased iron requirements – during pregnancy, periods of rapid growth, menstruation (average of
20 mg. Of iron lost per menstrual cycle.)
Excessive ingestion of aspirin (leading to occult GI blood loss).
Iron Balance and Stores:
Approximately 6mg. Of iron is ingested per 1000Kcal. or 16-20 mg / day.
The amount of iron ingested is related to the number of calories consumed. Normally about 5% - 10%
of ingested iron is absorbed by the GI mucosa, bound to transferrin (main iron-binding protein in
plasma), and carried through the blood stream to the bone marrow. In the marrow, iron is transported
to red cells and reticuloendothelial cells.
Normal adult male has iron stores of 900mg.; adult female has 300 mg.
Adult male loses about 1mg. Iron per day; premenopausal woman loses about 1.5-mg iron per day.
Management:
i. Oral Iron Therapy
Allows patient to regenerate hemoglobin. (Hematologic values should return to normal in 4 – 8
weeks) Therapy is continued approximately 6 months following normalization of blood values to
restore to hemoglobin and iron stores. It is continued longer in-patients with continued blood loss.
Choice of iron depends on (1) patient tolerance, (2) GI absorption, and (3) dosage according to
estimate of hemoglobin deficiency.
a. Oral iron preparations
a. Ferrous sulfate (preferred and least expensive)
b. Ferrous gluconate
ii. Parenteral Iron Therapy
Parenteral iron therapy is given only when:
(1) the patient is unable to tolerate iron preparations orally,
(2) the patient has severe GI disorders,
(3) there is continuing negative iron balance while patient is taking maximum oral dose tolerated, or
(4) There is nonadherence by patient.
Parenteral iron preparations:
(1) Iron dextran (Imferon)
(2) Iron sorbitex (Jectofer) – may cause patient’s urine to turn black on standing, since about 50% of
iron is excreted in the urine within 24 hours.
Nursing Alert: Extravasation of iron medication results in painful local induration. An anaphylactic reaction
may occur following either intramuscular or intravenous injection of iron dextran.
Clinical Manifestations:
Reduction in hemoglobin concentration decreases the capacity of the blood to transport and deliver oxygen to
the tissues.
1. Easy fatigability
2. Headache, dizziness, tinnitus
3. Palpitations and dyspnea on exertion
4. Pallor of skin and mucous membranes
5. Smooth, sore tongue associated with burning sensation.
6. Cheilosis (lesions at corners of mouth)
7. Pica (Craving to eat unusual substances)
8. Koilonychia (spoon-shaped fingernails)
Patient Problems / Nursing Diagnoses
1. Fatigue related to anemia
2. Discomfort (headache, etc.) related to anemia
3. Activity intolerance related to reduced energy.
4. Inadequate nutritional intake related to dyspepsia
5. Ineffective individual coping related to related lifestyle resulting from activity limitations.
6. Diarrhea or constipation related to iron ingestion
b. Megaloblastic Anemias
1. A Megaloblast is a nucleated red cell with delayed and abnormal nuclear maturation.
2. B12 deficiency (pernicious Anemia) and / or Folic acid deficiency cause the most common
megalobastic anemias.
3. Anemias due to deficiencies of Vitamin B12 and folic acid show identical bone marrow and peripheral
blood changes. This is because both vitamins are essential for normal DNA synthesis.
* Folic Acid Deficiency is necessary for normal red blood cell production. Folate depletion results in
progressive anemia.
Causes:
1. Inadequate dietary intake
a. Common in alcoholics
b. Elderly individuals who live on “tea and toast”
c. Patients on hyperalimentation or chronic hemodialysis.
2. Impaired absorption – most absorption of folic acid takes place in upper jejunum
3. Increased requirements – chronic hemolytic anemias; pregnancy, etc.
4. Impaired utilization – from folic antagonists (methotrexate)
Clinical Manifestations:
Symptoms of anemia – fatigue, weakness, pallor, sore tongue, cracked lips.
Diagnostic Evaluation:
Assay of serum folate
Management:
1. Give oral folic acid replacement as prescribed.
2. Inform the patient that a proper diet will prevent most instances of folate deficiency: green vegetables
(asparagus, broccoli, and spinach); yeast, liver, organ meats, some fresh fruits.
Megaloblastic Anemias has two types, the Pernicious Anemia and Folic acid deficiency anemia. Folic
acid and vitamin B12 are necessary for the synthesis of nucleoproteins, which are essential for maturation of
red blood cells. So, deficiencies or disturbances in their normal metabolism of these two substances will
interfere with the synthesis of nucleoproteins. As a result, RBC is immature and larger than normal at every
stage of their development and number of circulating RBC is decreased.
* Pernicious Anemias are caused by lack of intrinsic factor, which normally is produced by gastric mucosal
parietal cells. B12 deficiency is also seen in diseases of the small intestine – i.e., malabsorption, blind
loop syndrome, following gastrectomy.)
Altered Physiology:
Pernicious anemia is a type of macrocytic anemia caused by failure of absorption of Vitamin B 12 (cobalamin).
Cobalamin is released form its protein-bound state by an acidic gastric environment. Lack of gastric acid may
lead to pernicious anemia, however; the most common cause is lack of intrinsic factor, a glucoprotein
produced by the parietal cells of the gastric lining. Vit B12 is absorbed in the terminal ileum, so if that part of
the bowel is surgically resected, absorption cannot occur. The cause of pernicious anemia may also be from
an autoimmune response. Without Vitamin B12, deoxyribonucleic acid (DNA) synthesis and cell replication
are impaired. RBC precursors do not divide normally, and large, poorly functioning RBCs are created..
Erythropoiesis (from impaired folic acid from the lack of vitamin B12 directly) is greatly affected.
1. Symptoms due to anemia
a. Pallor
b. Dyspnea, tachycardia, easy fatigability
c. Angina pectoris, arrythmias, CHF
d. Edema of the legs
2. Symptoms due to physiologic changes in gastrointestinal tract
a. Sore mouth with smooth, red, “beefy” tongue
b. Loss of appetite
c. Indigestion and epigastric discomfort
d. Recurring diarrhea or constipation
e. Weight loss
3. Symptoms due to neurologic changes (neuropathy occurs in high percentage of untreated patients)
a. Tingling and numbness or burning pain (paresthesia) involving hands and feet.
b. Loss of position sense, leading to disturbances of gait
c. Disturbances of bladder and bowel function
d. Psychiatric symptoms – from cerebral dysfunction
Diagnostic Evaluation:
1. Blood smear – reveals marked variation in size and shape of cells and a variable number of unusually
large cells containing a normal concentration of hemoglobin.
2. Tests for serum and red cell folate levels and serum Vitamin B12 level
3. Gastric analysis – the gastric juice lacks free hydrochloric acid (achlorhydria).
4. Schilling Test – a test for vitamin B12 absorption.
Purpose:
To prove that the patient cannot absorb oral vitamin B12 unless intrinsic factor is added.
i. The patient is given a small dose of radioactive B12 in water to drink followed by a nonradiocative
intramuscular dose.
ii. When the oral vitamin is absorbed, it will be excreted in the urine; the IM dose helps to flush it into
urine.
iii. A 24-hours urine specimen is collected and measured for radioactivity. All urine must be
collected. Patients with renal disease may require longer periods of collection.
iv. If very little has been excreted, the test is repeated several days later (the “second stage”) with a
capsule of oral intrinsic factor added to the oral Vitamin B12.
v. If the patient has pernicious anemia, this time much more radioactivity will be found in the 24-
hours urine specimen.
• Hemolytic anemias
• 1. The RBC is destroyed at abnormally high rates.
• 2. The activity of the bone marrow increases to compensate for the shortened survival time of the RBC.
• 3. Products of red cell breakdown increase with hemolysis.
• 4. Jaundice results when the liver is unable to clear the blood of the pigment resulting from breakdown of
hemoglobin from destroyed red cells.
• 5. Bone marrow hypertrophies and occupies a larger than normal share of the inner structure of bones.
• Sickle Cell Anemia
• Sickle cell disease is a severe, chronic, hemolytic anemia occurring in persons who are homozygous for
the sickle gene. The clinical course is characterized by episodes of pain due to the occlusion of small
blood vessels by sickled blood cells. Persons heterozygous for the sickling gene are said to possess
sickle cell trait, which is associated with a benign clinical course.
• Etiology:
• 1. Genetically determined, inherited disease
• 2. Each person inherits 1 gene from each parent, which governs the synthesis of hemoglobin.
• Transmission of Sickle Cell Disease
Probability of abnormal Hemoglobin in Offspring
Genotype Parents Normal Trait Disease
1 Parents with trait 50% 50% 0
Both parents with trait, 25% 50% 25%
1parent with trait; 1 parent with
disease 0 50% 50%
Both parents with disease 0 0 100%
• Incidence:
• 1. Found almost entirely in American Blacks and persons of Spanish-American Ancestry
• 2. Approximately 8% of Black Americans have sickle cell trait.
• 3. Approximately 1 of every 600 Black infants born in the US has sickle cell anemia.
• Altered Physiology
• 1. Each hemoglobin molecule consists of 4 molecules of heme folded into 1 molecule of globin.
• 2. Each globin molecule consists of 2 alpha chains and 2 beta chains.
• 3. The amino acid sequence on the beta chain is altered in sickle cell hemoglobin. Valine is substituted for
glutamic acid in the 6th position.
• 4. Sickle cell hemoglobin aggregates into elongated crystals under conditions of low oxygen
concentration.
• 5. This distorts the membrane of the RBC causing it to assume a crescent or sickle shape. The cells
easily become entangled and enmeshed leading to increase blood viscosity.
• 6. Sickled red cells are fragile and are rapidly destroyed in the circulation.
• 7. Anemia results when the rate of destruction of red cells is greater than the rate of production.
• Prognosis:
• 1. Variable; improving with new forms of treatment.
• 2. Greatest risk of death is in children under 5 years of age.
• 3. Crises usually become less frequent and severe, as child becomes older.
• Preventive measures
• 1. Every black child admitted to the hospital should be tested for sickle cell anemia.
• 2. Parents at risk should be counseled regarding the genetic aspects of sickle cell anemia.
• 3. All siblings of any child who admitted to the hospital with sickle cell anemia should be tested for the
disease.
• Clinical manifestations:
• A. Symptoms
• 1. Children are rarely symptomatic until late in the first year of life
• 2. Clinical manifestation is sporadic.
• a. The child may be asymptomatic for several months.
• b. Periods of crisis occur at variable intervals.
• c. Precipitating factors of crisis include:
• (1) Dehydration
• (2) Infection
• (3) Trauma
• (4) Strenuous physical exertion
• (5) Extreme fatigue
• (6) Cold exposure
• (7) Hypoxia
• 3. Signs of crisis
• a. Loss of appetite
• b. Paleness
• c. Weakness
• d. Fever
• e. Pain in abdomen, back, joints, and/or extremities
• f. Swelling of joints, hands, or feet (“hand-foot syndrome”)
• g. Irritability
• Jaundice
• B. Thrombocytic Crisis (Most common form of crisis)
• 1. Small blood vessels are occluded by the sickle-shaped cells, causing distal ischemia and infarction.
• 2. Extremities
• 2a. Bony destruction
• 2b.Periosteal reaction
• 2c. Ulcers
• 3. Spleen – abdominal pain
• 4. Cerebral occlusion
• 4a. Strokes
• 4b. Hemiplegia
• 4c. Blindness
• 5. Pulmonary infarction, thromboses
• 6. Cardiac decompensation
• 7. Impaired liver function
• 8. Convulsions, cerebral infarction
• 9. Retinal damage, blindness
• C. Sequestrian Crisis
• 1. Large amounts of blood become pooled in the liver and spleen.
• 2. Spleen becomes massively enlarged.
• 3. Signs of circulatory collapse develop rapidly.
• 4. Frequent cause of death in infants with sickle cell disease.
• D. Aplastic Crisis – Bone marrow ceases production of red blood cells
• E. Chronic Symptoms
• 1. Jaundice
• 2. Gallstones
• 3. Progressive impairment of kidney function.
• 4. Fibrotic spleen
• 5. High susceptibility to salmonella, osteomyelitis, and pneumococcal septicemia.
• 6. Growth failure
• 7. Delayed puberty
• 8. Decreased life span.
• β -Thalassemia
• Beta-thalassemia or Thalassemia Major or Cooley’s refers to an inherited group of blood disorders
characterized by a reduction or absence of the beta globulin chain in hemoglobin synthesis. Homozygous
β-thalassemia is the most severe of the β-thalssemia syndromes and is also known as thalassemia major
or Cooley’s anemia.
• Etiology:
• 1. Genetically determined, inherited disease.
• 2. Autosomal-recessive pattern of interitance. Two types of β-thalassemia genes produce different
severities of the disease.
• Altered Physiology
• 1. Insufficient beta globulin synthesis allows large amount of unstable alpha chains to accumulate.
• 2. The precipitates of alpha chains that form cause red cells to be rigid and easily destroyed, leading to
severe anemia and resultant chronic hypoxia.
• 3. Erythroid activity is markedly increased in an attempt to overcome the increased rate of destruction,
resulting in enormous expansion of bone marrow.
• 4. Rapid destruction of defective RBC, decreased production of hemoglobin, and increased absorption of
dietary iron due to the body’s response to anemia result in an excess supply of available iron.
• 5. In response to the low level of adult hemoglobin, large concentration of fetal hemoglobin, which does
not contain beta chains, are produced.
• Prognosis
• 1. No known cure
• 2. Unable to predict which severely afflicted children will follow a more favorable course.
• 3. Often fatal in late childhood or early adolescence.
• Preventive Measures:
• 1. Parents of a child with thalassemia should be tested for the trait, and referred for genetic counseling.
• 2. Prenatal diagnosis is possible through fetal blood sampling early enough to allow the opportunity to
terminate the pregnancy.
• Management:
• 1. Frequent and regular blood transfusions to maintain hemoglobin levels above 9-10 gm./dl
• 1a. Washed, packed red cells are usually used to minimize the possibility of transfusion
reactions.
• 1b. The frequency and amount of transfusions depend on the size of the child, with older
children often reaching a peak requirement of 500ml of packed cells every 2-3 weeks.
• 2. Iron chelation therapy to reduce the toxic effects of excess iron.
• 3. Supportive management of complications.
• Clinical Manifestations:
• 1. Onset is usually insidious, with symptoms noted toward the end of the first year of life.
• 2. Symptoms are primarily related to the progressive anemia, expansion of the marrow cavities of the
bone and the development of hemesiderosis (excess iron storage in various body tissues).
• 3. Early symptoms often include progressive pallor, poor feeding, and protuberant abdomen due to
hepatospleenomegaly.
• 4. Further signs of progressive anemia include headache, bone pain, exercise intolerance, and
listlessness.
• Complications:
• 1. Spleenomegaly
• 2. Growth and endocrine Complications
• 3. Skeletal complications
• 4. Cardiac complications
• 5. Liver enlargement
• 6. Gallbladder disease
• 7. Megaloblastic anemia
• 8. Skin and leg ulcers
• Diagnostic Evaluation:
• 1. Hemoglobin level – decreased
• 2. Red cells indices – microcytocis and hypochromia
• 3. Peripheral blood smear –
• 4. Reticulocyte count – low, usually less than 10%
• 5. Hemoglobin electrophoresis
• Aplastic Anemia
• Anemia from bone marrow aplasia (failure) is characterized by deficiency in all the cellular elements of the
blood.
• Aplastic Anemia is a stem cell disorder characterized by bone marrow failure with pancytopenia
(deficiency in all cellular elements of the blood).
• Causes:
• 1. Idiopathic (50% of all cases).
• 2. Chemical toxins
• 3. Idiosyncratic response to drugs.
• 4. Virus, especially hepatitis.
• 5. Congenital (Fanconi’s anemia)
• Note: Secondary bone marrow aplasia is a predictable marrow suppression induced by antineoplastic
agents and radiation therapy or bone marrow transplantation.
• Etiology and Risk factors:
• Acquired Aplastic anemia may result from either an autoimmune mechanism or a direct injury by
myelotoxins. Three groups of myelotoxins are:
• 1. Agents that always cause marrow damage when received in insufficiently large doses, such as radiant
energy (x-rays, radium, and radioactives, alkylating agents, and antimetabolites used to treat malignant
tumors. Radiation causes the bone marrow to stop producing blood cells by inhibiting mitosis, or cell
division, and antimetabolites used in cancer therapy block the synthesis of purines or nucleic acids.
• 2. Agents that occasionally cause marrow failure, such as chloramphenicol (Chloromycetin, the drug most
commonly linked with aplastic anemia), sulfonamides, quinacrine, phenylbutazone, the anticonvulsants
phenytoin and mephenytoin, and gold compounds.
• 3. Agents that have been linked with aplastic anemia in only a few cases, such as streptomycin,
tripelennamine, DDT, meprobamate, hair and aniline dyes, and carbon tetrachloride.
Clinical Course:
• 1. The clinical course is variable, and the overall mortality rate is high; patients with severe pancytopenia
with totally aplastic marrow have a poor prognosis.
• 2. Patients with aplastic anemia are at serious risk of infection, hemorrhage, and other complications of
chronic anemia.
• Treatment:
• 1. Search for cause / prevention of toxic exposure
• 2. Bone marrow transplant (treatment of choice for patients with severe aplastic anemia who have
matched donors.
• 3. Androgens (oxymetholone or testosterone enanthate) – controversial.
• 4. Immunosupressive treatment (splenectomy; cyclophosphamide).
• 5. Immunologic therapy (antithymocyte globulin [ATG])
• Clinical Manifestations:
• 1. Abnormal bleeding – resulting from thrombocytopenia
• a. Bleeding from gums, nose, gastrointestinal and genitourinary tracts.
• b. Purpora; petechia; ecchymoses.
• 2. Anemia – resulting from depression of hemoglobin; symptoms pronounced because of rapidity of blood
cell change.
• a. Pallor; weakness
• b. Exertional dyspnea, palpitations
• 3. Infections with high fever – resulting from granulocytopenia.
• a. Pharyngitis and oropharyngeal mucositis.
• b. Sepsis via gastrointestinal tract or genitourinary tract.
Diagnostic Evaluation:
• 1. Peripheral blood smear shows pancytopenia.
• 2. Potential for infection related to lack of circulating granulocytes.
• 3. Potential for hemorrhge related to thrombocytopenia.
2. Clotting Disorders
a. Vascular Purpuras:
• The term purpura refers to extravasation (escape) of blood into the skin and mucous membranes.
Purpuric lesions may occur spontaneously as an isolated phenomenon or as an accompaniment of
obvious disease.
• Types of Purpura
• 1. Petechiae – small pinpoint hemorrhages under the skin.
• 2. Ecchymoses – escape of blood into tissues; producing a large bruise.
• 3. Petechiae and echymosses may occur as the result of vascular rupture, permitting the leakage of blood
into the subcutaneous tissue of the mucous membranes.
• 4. Symptomatic or secondary purpura – certain types of blood stream infections (e.g., meningococcemia
and infective endocarditis) exhibit this phenomenon because of damage to the vascular walls by the
infectious agent or by immune complexes.
• 5. Severe arterial hypertension – may cause the patient to bruise easily; valsalva maneuver may cause
petechiae.
• 6. Anaphylactoid purpura – generally regarded as an allergic disorder in which there are various skin
lesions (purpuric and otherwise) and episodes of arthritis, abdominal pain, hematuria, gastrointestinal
hemorrhage, and fever.
• A. Attacks last several weeks and recur for years.
• B. Steroid therapy is often effective.
• 7. Familial hemorrhagic telangiectasia – a hereditary disorder manifested by an abnormal tendency to
bleed and bruise.
• A. Precise nature of defect is obscure.
• B. Condition does not respond to any proved method of treatment.
• 8. Toxic Purpura – a condition observed after exposure to certain drugs and poisons.
• 9. Vitamin C deficiency – a vascular purpura.
• 10. Senile purpura.
• 11. Rheumatic and collagen – vascualr diseases – associated with palpable purpura caused deposition of
immune complexes in blood vessels of the skin.
• 12. Steroid purpura – associated with loss of capillary integrity.
b. Hemophilia
Hemophilia is an inherited, congenital blood dyscrasia, which is characterized by a disturbance of blood
clotting factors. It appears in males but is transmitted by females.
Three major types of Hemophilia:
1. Hemophilia A (Classic hemophilia)
2. Hemophilia B (Christmas disease)
3. von Willebrand’s disease
• Etiology:
• 1. Hereditary (about 80% of patients)
• Sex-linked, recessive trait
• Altered Physiology:
• 1. Hemophilia results from the absence or malfunction of any one of the blood clotting factors from the
plasma.
• 2. These blood clooting factors are necessary for the formation of prothrombin activator, which acts as a
catalyst in the conversion of prothrombin to thrombin.
• A. The rate of formation of thrombin from prothrombin is almost directly proportional to the
amount of prothrombin activator available.
• B. The rapidity of the clotting process is proportional to the amount of thrombin formed.
• 3. The most common types of hemophilia and the clotting factors involved in the chart below:
Type of Hemophilia Clotting Factor
Hemiphilia A (Classic Hemophilia) Factor VIII (antihemophilic globulin)
Hemophilia B (Christmas disease) Factor IX (Plasma thromboplastin component)
Hemophiliac C Factor XI (Plasma thromboplastin antecedent)
Clinical (Manifestations) Signs and Symptoms:
1. Easily bruised which results to slow persistent bleeding
2. Prolonged bleeding from the mucous membranes of the nose and mouth or from lacerations.
3. Spontaneous soft-tissue hematomas
4. Hemorrhages into the joints – especially elbows, knees, and ankles (Hemarthrosis).
a. Causes pain, swelling, limitation of movement.
b. Repeated hemorrhages may produce degenerative changes with osteoporosis and muscle athrophy.
5. Spontaneous hematuria
6. Gastrointestinal bleeding
Complications:
• 1. Airway obstruction due to hemorrhage into the neck and pharynx
• 2. Intestinal obstruction due to bleeding into intestinal walls or peritoneum.
• 3. Compression of nerves with paralysis due to hemorrhaging into deep tissues.
• 4. Intracranial bleeding
• 5. Secondary complications associated with therapy – liver disease, immunologic problems, thrombotic
complications.
• Diagnostic Evaluation:
• 1. Routine bleeding and clotting tests – often normal
• 2. Partial thromboplastin time (PTT) – prolonged
• 3. Prothrombin consumption – decreased
• 4. Thromboplastin generation – increased
• 5. Specific assays for clotting factors – abnormal
c. Immune Thrombocytopenic Purpura. Is a group of bleeding disorders due to immune destruction of
platelets. Antiplatelet antibodies are produced for unknown reasons, so that the platelet life span is
markedly shortend. Antibody-coated platelets are removed from the circulation by reticuloendothelial cells
of the spleen and liver.
• Clinical Manifestations:
• 1. History of Easy bruising
• 2. Bleeding – mild to severe (Thrombocytopenia not usually accompanied by bleeding unless the platelet
count falls accompanied by bleeding unless the platelet count falls below 20,000/mm3)
• a. Skin lesions – small red hemorrhages; do not blanch on pressure.
• b. Purpuric lesions may occur in vital organ (brain).
• c. Bleeding may occur from nose, mouth, genitourinary tract.
• Laboratory Manifestations:
• 1. Platelets may be absent or only slightly decreased in number; abnormalities may be seen in platelet
size or morphologic appearance.
• 2. Increased levels of immunoglobulins (IgG) or complement components on the platelet surface.
• 3. Bone marrow examination – bone marrow megakaryocytes are increased in numbers.
d. Idiopathic Thrombocytopenic Purpura (ITP) is an autoimmune bleeding disorder characterized by the
development of autoimmune bodies to one’s own platelets, the binding of autoantibodies to antigens, and
the destruction of platelets in the spleen and, to lesser extent, in the liver.
Normally, Platelets survive 8 t0 10 days within the circulation.
In ITP, platelet survival is as brief as 1 to 3 days or less.
• Clinical manifestations:
• 1. Petechia
• 2. Ecchymosis
• 3. Epistaxis
• 4. Bleeding from the gums
• 5. Easy bruising
• 6. In women may have extremely heavy menses or bleeding between periods.
• Diagnostic Findings that confirm the presence of ITP include:
• 1. A platelet count below 100,000/mm3
• 2. Prolonged bleeding time with normal coagulation time (all coagulation factors are present and normal)
• 3. Increased capillary fragility, as demonstrated by the tourniquet test.
• 4. Positive platelet antibody screening
• 5. Bone marrow aspirate containing normal or increased numbers of megakaryocytes.
• Complications of ITP include:
• 1. Cerebral hemorrhage, which proves fatal in 1% to 5% of clients with ITP,
• 2. Severe hemorrhages from the nose, GI tract, and urinary system,
• 3. Bleeding into the diaphragm, which can result in pulmonary complications; and
• 4. Nerve pain, extremity anesthesia, or paralysis resulting from the pressure of hematomas on nerves or
brain tissues.
• Medical management:
• Treatment of choice is steroids to inhibit the macrophage ingestion of the antibody-coated platelets.
Plasmapheresis is sometimes used as short-term therapy until the steroid therapy takes effect. If the
client is actively bleeding or requires surgery, IV gamma globulin can be used to increase the platelet
count.
• Spleenectomy is also recommended if the client has not have sustained remission.
• The effectiveness of spleenectomy is believed to be related to the removal of the site of premature
destruction of the antibody-sensitized platelets.
• Danazol (Danocrine) has been also used with success in some clients.
• Immunosuppressive therapy used in refractory cases includes vincristine, vinblastine (Velban),
azathioprine (Imuran), and cyclophosphamide.
e. Thrombocytopenia is a decrease in the circulating platelet count, which may result in bleeding or
hemorrhage.
• Altered Physiology and Causes:
• 1. Decreased platelet production (infiltrative diseases of bone marrow, leukemia, myelosuppressive
therapy, other tumors, myelofibrosis, radiation therapy, drug effect, aplastic anemia, etc).
• 2. Increased platelet destruction (infection, immune thrombocytopenic purpura, disseminated intrvascular
coagulation, drug-induced, etc).
• 3. Abnormal distributions or sequestration – hypersplenism.
• 4. Loss of platelets from body, (extracorporeal circulation, dilution due to blood loss and multiple blood
transfusions).
• Clinical manifestations:
• When the platelet count drops below 20,000/mm3:
• 1. Petechiae occur spontaneously.
• 2. Ecchymoses occurs at the sites of minor trauma (venipuncture, bruises).
• 3. Hematomas occur at sites of more significant trauma (surgical wounds).
• 4. Bleeding from mucosal surfaces, nose, GI, and genitourinary (GU) tracts, respiratory tract, and CNS
may occur.
• 5. Menorrhagia is common (excessive menstrual bleeding).
• 6. Excessive dental after dental extractions is seen.
1. Neoplastic growth
• a. Acute leukemias
• b. Prostatic cancer
• c. Bronchogenic cancer
• d. Giant cavernous hemangioma
• 2. Obstetric conditions
• a. Abruptio placenta
• b. Retained dead fetus
• c. Amniotic fluid embolism
• Clinical Manifestations:
• The onset of DIC is usually acute and develops within days to hours after an initial assault to the body
system such as shock. Subacute DIC may not be apparent initially but may become fulminant as the
clinical course progresses. Chronic cases of DIC characteristically develop in clients with cancer or in
women carrying a dead fetus.
• Manifestations may be mild or extremely severe. They include
• 1. Purpura, petechia, and ecchymosis on the skin, mucous membranes, heart lining and
lungs;
• 2. Prlonged bleeding from venipuncture;
• 3. Severe, uncontrolled hemorrhage during surgery or childbirth;
• 4. Oliguria and acute renal failure;
• 5. Ischimia of the peripheral tissue leads to coolness and mottling of the extremities.
• 6. Convulsion and coma.
• The prognosis for clients with DIC varies.
• The condition may be self-limiting.
• On the other hand, hemorrhage, organ damage (especially acute respiratory distress syndrome), or even
death may occur within a few days or even a few hours if associated with gram-negative sepsis.
• In severe cases, the mortality rate reaches to 80%.
• Diagnostic Findings:
• Prolonged prothrombin time and activated partial thromboplastin time.
• Very low (and failing) platelet count (<100,000/mm3),
• Low plasma levels of coagulation inhibitors.
• Prolonged clotting time
• Medical management:
• To treat DIC successfully, clinicians must:
• 1. Correct the basic problem (such as infection, delivery of a fetus, surgery, or irradiation for cancer),
• 2. Reverse the pathologic clotting,
• 3. Control bleeding and shock
• 4. Detect occult bleeding
• 5. Measure blood loss,
• 6. Administer blood products and medication as prescribed, and
• 7. Observe for and report transfusion reactions and medication side effects.
• Manifestations of thrombosis are treated with IV heparin, which interrupts the clotting cascade by blocking
thrombi.
• The use of heparin is controversial and is reserved for clients with thrombosis seen in acute renal failure
to skin ischemia.
• Low dose doses are given, such as 300 to 500 units per hour by continuous infusion.
• Washed packed RBCs are administered to replace blood volume lost through hemorrhage without
administering anticoagulant substances.
• Cryoprecipitate is given for depletion of factors V and VIII.
• Administration of Antithrombin III (in fresh frozen plasma) shortens the course of the disorder and
reduces the complications of DIC.
• When bleeding cannot be controlled with heparin, aminocaproic acid (Amicar) is given.
• Nursing Management:
• Assess all body systems for the effects of DIC, including:
• 1. Integumentary bleeding or oozing of blood from venipuncture sites or mucosal surfaces and wounds,
pallor, petechiae.
• 2. Respiratory tachypnea, hemoptysis, orthopnea, and basilar rales,
• 3. Cardiovascular tachycardia and hypotension
• 4. GI abdominal distention, guaiac-positive stools or gastric contents;
• 5. Genitourinary hematuria and oliguria
• 6. Neurologic vision changes, dizziness, headache, changes in mental status, and irritability.
3. Bone marrow Transplantation (BMT) since 1970s, BMT has progressed from a treatment of last resort
to a viable therapeutic modality for a variety of hematologic, malignant, and nonmalignant disorders.
• Indications (Bone marrow transplant may be considered as a treatment for clients with the following:
• 1. Aplastic anemia;
• 2. Malignant disorders, specifically myelodysplastic syndromes, leukemia, lymphoma, multiple myeloma,
neuroblastoma, and selected solid tumors.
• 3. Nonmalignant hematologic disorders, such as Fanconi’s anemia, thalassemia, and sickle cell anemia.
• 4. Immunodeficiency disorders, such as severe combined immunodeficiency disease and Wiskott-Aldrich
syndrome.
• Sources of Bone Marrow:
• There are three types of Bone marrow donors:
• 1. Allogeneic bone marrow is obtained from a relative or unrelated donor having a close HLA (Human
Leukocyte antigen) type. This was the most common type of marrow transplant but it carried the highest
rate of morbidity and mortality because of complications of incompatibility such as GVHD (graft-versus-
host disease).
• 2. Syngeneic Bone Marrow is donated by an identical twin. Although syngeneic marrow is perfect HLA
match, which eliminates the risks of marrow rejection, the incidence of leukemic relapse is higher than
when an allogeneic donor is used because GVDH is considered to have an antileukemic effect.
• 3. Autologous Bone marrow is removed from the intended recipient during the remission phase to allow
another course of ablative therapy to be given if a relapse occurs. This relapse may be due to
contamination of the harvested bone marrow by malignant cells or to failure of pretransplant
chemotherapy to eradicate completely the tumor cells from the body.
• Siblings have a 1 in 4 chance of having identical sets of HLA antigens.
• Nonrelated clients have less than a 1 in 5000 chance of having identical HLA types.
Allogeneic donor preparation: an extensive work-up is performed for ensuring compatibility and the mental
and physical well being of the prospective donors. Evaluation includes:
• 1. Histocompatibility testing
• 2. Medical history
• 3. Physical examination
• 4. Chest film
• 5. ECG
• 6. Laboratory evaluation (CBC, chemistry profile, viral testing, rapid plasma regain test, ABO and Rh
blood typing, coagulation studies),
• 7. Psychological testing (may include psychiatric consultation).
• Bone marrow harvest, needs an informed consent, including potential donor complications, (pain, fever,
hematoma). Because of the potential for significant blood loss during the harvesting process, syngeneic
and allogeneic donors are required to donate autologous blood for reinfusion before the procedure.
• Newborns currently are being used as potential donors through the use of their cord blood, which is rich
in stem cells. Newborns cord blood are being frozen for future use.
• Marrow collection:
• When collecting marrow, the client or donor is given general or spinal anesthesia in the operating room.
The marrow is obtained in 2- to – 5 ml aliquots from the marrow spaces of the posterior and, occasionally,
anterior iliac crest and sternum. Numerous skin punctures may be required; the aspiration needle is
redirected to various marrow spaces without being withdrawn. A total of 400 to 800 ml of marrow usually
is obtained. The blood is placed in heparinized tissue culture media and filtered for removal of fat and
bone particles. Marrow can be infused immediately or frozen in a solution containing dimethyl sulfoxide
(DMSO), which preserves stem cells in the frozen state.
• Peripheral Stem Cell Collection
• Peripheral stem (progenitor) cells are harvested by Apheresis or Leukapheresis, a process that
removes blood through a large-bore catheter and runs it through a machine that removes the stem cells
before running the blood to the client. Because stem cells concentration is much lower in peripheral blood
compared with bone marrow, a process to increase the concentration in the peripheral blood must be
initiated first. To increase the number of circulating stem cells, a stimulus, such as a Colony Stimulating
Factor (CSF),interleukins (ILs), fusion molecules (made from a combination of a CSF and IL-3), or some
chemotherapeutic agents, may be given to the donor before the stem cell harvest. As mentioned earlier,
the umbilical cord of newborns also is rich in stem cells.
• Once the stem cells are harvested, they are preserved in the manner as bone marrow. The engraftment
of stem cells occurs at approximately the same rate as or slightly fastere than with marrow
transplantation.
ALLOGENEIC TRANSPLANT:
• Recipient Preparation:
• The physical and psychological evaluation of the recipient is similar to that of the donor. Additional testing
may be required to stage existing disease accurately. The recipient must undergo a preparative regimen
before transplantation. Such a regimen serves three purposes:
• 1. Malignant cells are destroyed.
• 2. The immune system is inactivated, which reduces the risk of GVHD in allogeneic transplant clients.
• 3. The marrow cavities are emptied to provide space for implantation of the transfused stem cells.
• Common protocols combine total body irradiation and high doses of a single chemotherapeutic agent
(cyclophosphamide is one of the most common agents used) or fractionated/high doses of multiple
agents. A multilumen central venous catheter is inserted to provide suitable access for marrow infusion as
well as for antibiotics, blood products, hyperalimentation, and frequent blood sampling.
Bone Marrow Infusion:
• The infusion of the marrow is commonly anticlimactic after the client has undergone the rigorous
preparatory chemotherapy and radiation therapy (often referred to as the Conditioning regimen). The
marrow usually is administered immediately after the conditioning regimen is complete. Marrow is
administered from a large blood infusion bag by a multilumen catheter, using an infusion pump, or small
volumes may be prefiltered and given by IV push by a physician.
• The BMT client remains pancytopenic until the transplanted stem cells make their way to the medullary
cavities, where subsequent growth and reconstitution of the marrow are confirmed. Indications of
successful engraftment are an increase in platelets and RBCs in peripheral blood count. This change may
occur 14 days after marrow infusion. Each day that recovery is delayed places the client at added risk.
Graft rejection is evident if the bone marrow fails to produce peripheral blood cells after several weeks.
• Nursing Mangement of BMT clients follows the plan of care for any completely immunosuppressed
client. Clients receiving allogeneic transplant must be observed closely for manifestations of GVHD.
Potential immediate adverse reactions are allergic (urticaria, chills, fever), volume overload, and
pulmonary complications secondary to fat emboli. Renal damage may occur from too many erythrocytes.
The period immediately after transplant is crucial. Multisystem failure related to ablative therapy is
common, as are immune reactions caused by the transplanted cells.
• The most common and disastrous complication of allogeneic BMT is GVHD, which may occur 7 to
30 days after infusion of viable lymphocytes. The donor T lymphocytes form an immunologic reaction
against the host cells. The clients at highest risk for development of GVHD are those who have had
allogeneic BMT. But moderate risk is noted to clients with HLA-identical donors.
ANEMIA, APLASTIC
bone marrow hypoplasia or aplasia resulting in pancytopenia (decreased WBC, RBC and
platelets)
Aplastic anemia is a normocytic-normochromic anemia that results from a loss of blood cell precursors,
causing hypoplasia of bone marrow, RBCs, WBCs, and platelets. Symptoms result from severe anemia,
thrombocytopenia (petechiae, bleeding), or leukopenia (infections). Diagnosis requires demonstration of
peripheral pancytopenia and the absence of cell precursors in bone marrow. Treatment is equine
antithymocyte globulin and cyclosporine. Erythropoietin, granulocyte-macrophage colony-stimulating factor,
and bone marrow transplantation may also be useful.
The term aplastic anemia commonly implies a panhypoplasia of the marrow
with associated leukopenia and thrombocytopenia. In contrast, pure RBC
aplasia is restricted to the erythroid cell line. Although both disorders are
uncommon, aplastic anemia is more common.
Etiology
True aplastic anemia (most common in adolescents and young adults) is idiopathic in about ½ of cases. Recognized causes are
chemicals (eg, benzene, inorganic arsenic), radiation, and drugs (eg, antineoplastic drugs, antibiotics, NSAIDs, anticonvulsants,
acetazolamide (Diamox), , gold salts, penicillamine (Cuprimine), , quinacrine) . The mechanism is unknown, but selective
(perhaps genetic) hypersensitivity appears to be the basis.
Fanconi's anemia is a very rare, familial form of aplastic anemia with bone abnormalities, microcephaly, hypogonadism, and
brown pigmentation of skin. It occurs in children with abnormal chromosomes. Fanconi's anemia is often inapparent until some
illness (especially an acute infection or inflammatory disorder) supervenes, causing peripheral cytopenias. With clearing of the
supervening illness, peripheral values return to normal despite reduced marrow mass.
Pure RBC aplasia may be acute and reversible. Acute erythroblastopenia is a brief disappearance of RBC precursors from the
marrow during various acute viral illnesses (particularly human parvovirus infection), especially in children. The anemia lasts
longer than the acute infection. Chronic pure RBC aplasia has been associated with hemolytic disorders, thymomas, and
autoimmune mechanisms and, less often, with drugs (eg, tranquilizers, anticonvulsants), toxins (organic phosphates), riboflavin
deficiency, and chronic lymphocytic leukemia. A rare congenital form, Diamond-Blackfan anemia, usually occurs during infancy
but has also been reported in adulthood. Diamond-Blackfan anemia is associated with bony abnormalities of the thumbs or digits
and short stature.
Severe thrombocytopenia may cause petechiae, ecchymosis, and bleeding from the gums, into the conjunctivae, or other
tissues. Agranulocytosis commonly causes life-threatening infections. Splenomegaly is absent unless induced by transfusion
hemosiderosis. Symptoms of pure RBC aplasia are generally milder and relate to the degree of the anemia or to the underlying
disorder.
Diagnosis
• CBC
Aplastic anemia is suspected in patients, particularly young patients, with pancytopenia (eg, WBC < 1500/μL, platelets <
50,000/μL). Pure RBC aplasia (including Diamond-Blackfan anemia) is suspected in patients with bony abnormalities and
normocytic anemia but normal WBC and platelet counts. If either diagnosis is suspected, bone marrow examination is done.
In aplastic anemia, RBCs are normochromic-normocytic (sometimes marginally macrocytic). The WBC count reduction occurs
chiefly in the granulocytes. Platelets are often far below 50,000/μL. Reticulocytes are decreased or absent. Serum iron is
elevated. The bone marrow is acellular. In pure RBC aplasia, normocytic anemia, reticulocytopenia, and elevated serum iron are
present, but with normal WBC and platelet counts. Bone marrow cellularity and maturation may be normal except for absence of
erythroid precursors.
Treatment
• Equine antithymocyte globulin, corticosteroids, and cyclosporine (Sandimmune)
• Sometimes cytokines
Hematopoietic cell transplantation may help younger patients (particularly patients < 30) but requires an identical twin or an HLA-
compatible sibling. At diagnosis, siblings are evaluated for HLA compatibility. Because transfusions pose a risk to subsequent
transplantation, blood products are used only when essential.
Pure RBC aplasia has been successfully managed with immunosuppressants ( prednisone), or cyclophosphamide
(Cytoxan).especially when an autoimmune mechanism is suspected. Because patients with thymoma-associated pure RBC
aplasia improve after thymectomy, CT is used to seek the presence of such a lesion, and surgery is considered.
Signs and symptoms of folic acid deficiency anemia gradually produces clinical features
similar to other megaloblastic anemias, but without neurologic manifistations of B12
deficiency. Symptoms include the following:
• progressive fatigue
• shortness of breath
• heart palpitations
• weakness
• glossitis (inflammation of the tongue)
• nausea
• anorexia
• headache
• fainting
• irritability
• forgetfulness
• pallor
• slight jaundice
Conventional treatment consists primarily of folic acid supplements (about 400 mg. three times daily)
and, more importantly, the elimination of contributing causes. Oral administrations of folate preparations
are 1 to 5 mg daily. Prophylactic doses are given in pregnancy or those considering getting pregnant.
Parenteral administration of folic acid can relieve acute symptoms within 48 hours. Blood transfusions
are given to treat severe cardiac or respiratory distress as a result of severe deficiency.
IM; Fatigue
Lab. Data: Decreased folate levels
Nsg. Dx: Activity intolerance
Interventions:
Teach the patient to increase sources of folic acid in the diet like: green vegetables (asparagus,
broccoli and spinach), yeast, liver, organ meats and fresh fruits.
Avoid overcooking of vegetables.
Teach the patient regarding oral folic acid replacement.
Iron deficiency is the most common cause of anemia and usually results from blood loss. Symptoms are usually nonspecific.
RBCs tend to be microcytic and hypochromic, and iron stores are low as shown by low serum ferritin and low serum iron levels
with high serum total iron binding capacity. If the diagnosis is made, occult blood loss is suspected. Treatment involves iron
replacement and treatment of the cause of blood loss.
Pathophysiology
Iron is distributed in active metabolic and storage pools. Total body iron is about 3.5 g in healthy men and 2.5 g in women; the
difference relates to women's smaller body size, lower androgen levels, and dearth of stored iron because of iron loss with
menses and pregnancy. The distribution of body iron in an average man is Hb, 2100 mg; ferritin, 700 mg (in cells and plasma);
hemosiderin, 300 mg (in cells); myoglobin, 200 mg; tissue (heme and nonheme) enzymes, 150 mg; and transport-iron
compartment, 3 mg.
Iron absorption: Iron is absorbed in the duodenum and upper jejunum. Absorption of iron is determined by the type of iron
molecule and by what other substances are ingested. Iron absorption is best when food contains heme iron (meat). Dietary
nonheme iron must be reduced to the ferrous state and released from food binders by gastric secretions. Nonheme iron
absorption is reduced by other food items (eg, vegetable fiber phytates and polyphenols; tea tannates, including
phosphoproteins; bran) and certain antibiotics (eg, tetracycline SOME TRADE NAMES
ACHROMYCIN V
TETRACYN
TETREX
Click for Drug Monograph
). Ascorbic acid is the only common food element known to increase nonheme iron absorption.
The average American diet, which contains 6 mg of elemental iron/kcal of food, is adequate for iron homeostasis. Of about 15
mg/day of dietary iron, adults absorb only 1 mg, which is the approximate amount lost daily by cell desquamation from the skin
and intestines. In iron depletion, absorption increases, although the exact signaling mechanism is not known; however,
absorption rarely increases to > 6 mg/day unless supplemental iron is added. Children have a greater need for iron and appear to
absorb more to meet this need.
Iron transport and usage: Iron from intestinal mucosal cells is transferred to transferrin, an iron-transport protein synthesized in
the liver; transferrin can transport iron from cells (intestinal, macrophages) to specific receptors on erythroblasts, placental cells,
and liver cells. For heme synthesis, transferrin transports iron to the erythroblast mitochondria, which insert the iron into
protoporphyrin for it to become heme. Transferrin (plasma half-life, 8 days) is extruded for reutilization. Synthesis of transferrin
increases with iron deficiency but decreases with any type of chronic disease.
Iron storage and recycling: Iron not used for erythropoiesis is transferred by transferrin, an iron transporting protein, to the
storage pool which has 2 forms, ferritin and hemosiderin.The most important is ferritin (a heterogeneous group of proteins
surrounding an iron core), which is a soluble and active storage fraction located in the liver (in hepatocytes), bone marrow, and
spleen (in macrophages); in RBCs; and in serum. Iron stored in ferritin is readily available for any body requirement. Circulating
(serum) ferritin level parallels the size of the body stores (1 ng/mL=8 mg of iron in the storage pool).The 2nd storage pool of iron
is in hemosiderin, which is relatively insoluble and is stored primarily in the liver (in Kupffer cells) and in the marrow (in
macrophages).
Because iron absorption is so limited, the body recycles and conserves iron. Transferrin grasps and recycles available iron from
aging RBCs undergoing phagocytosis by mononuclear phagocytes. This mechanism provides about 97% of the daily iron needed
(about 25 mg of iron). With aging, iron stores tend to increase because iron elimination is slow.
Iron deficiency: Deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing progressive depletion
of bone marrow iron stores. As stores decrease, absorption of dietary iron increases in compensation. During later stages,
deficiency impairs RBC synthesis, ultimately causing anemia.
Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.
Etiology
Because iron is poorly absorbed, dietary iron barely meets the daily requirement for most people. Even so, people who eat a
typical Western diet are unlikely to become iron deficient solely as a result of dietary deficiency. However, even modest losses,
increased requirements, or decreased intake readily produces iron deficiency.
Blood loss is almost always the cause. In men, the most frequent cause is chronic occult bleeding, usually from the GI tract.In
premenopausal women, cumulative menstrual blood loss (mean, 0.5 mg iron/day) is a common cause. Another possible cause of
blood loss in men and women is chronic intravascular hemolysis (see Anemias Caused by Hemolysis) if the amount of iron
released during hemolysis exceeds the haptoglobin-binding capacity.Vitamin C deficiency can contribute to iron deficiency
anemia by producing capillary fragility, hemolysis, and bleeding.
Increased iron requirement may contribute to iron deficiency. From birth to age 2 and during adolescence, when rapid growth
requires a large iron intake, dietary iron often is inadequate. During pregnancy, the fetal iron requirement increases the maternal
iron requirement (mean, 0.5 to 0.8 mg/day—see Pregnancy Complicated by Disease: Anemia in Pregnancy) despite the absence
of menses. Lactation also increases the iron requirement (mean, 0.4 mg/day).
Decreased iron absorption can result from gastrectomy and upper small-bowel malabsorption syndromes. Rarely, absorption is
decreased by dietary deprivation from undernutrition.
In addition to the usual manifestations of anemia, some uncommon symptoms occur in severe iron deficiency. Patients may have
pica, an abnormal craving to eat substances (eg, ice, dirt, paint). Other symptoms of severe deficiency include glossitis, cheilosis,
concave nails (koilonychia), and, rarely, dysphagia caused by a postcricoid esophageal web (Plummer-Vinson syndrome).
Diagnosis
• CBC, serum iron, iron-binding capacity, and serum ferritin
• Rarely, bone marrow examination
Iron deficiency anemia is suspected in patients with chronic blood loss or microcytic anemia, particularly if pica is present. In such
patients, CBC, serum iron and iron-binding capacity, and serum ferritin are obtained.
Iron and iron-binding capacity (or transferrin) are usually both measured, because their relationship is important. Various tests
exist; the range of normal values relates to the test used.In general, normal serum iron is 75 to 150 μg/dL (13 to 27 μmol/L) for
men and 60 to 140 μg/dL (11 to 25 μmol/L) for women; total iron-binding capacity is 250 to 450 μg/dL (45 to 81 μmol/L). Serum
iron level is low in iron deficiency and in many chronic diseases and is elevated in hemolytic disorders and in iron-overload
syndromes (see Iron Overload). Patients taking oral iron may have normal serum iron despite a deficiency; in such
circumstances, a valid test requires cessation of iron therapy for 24 to 48 h. The iron-binding capacity increases in iron
deficiency. Serum transferrin receptor levels reflect the amount of RBC precursors available for active proliferation; levels are
sensitive and specific. The range of normal is 3.0 to 8.5 μg/mL. Levels increase in early iron deficiency and with increased
erythropoiesis.
Serum ferritin levels closely correlate with total body iron stores. The range of normal in most laboratories is 30 to 300 ng/mL,
and the mean is 88 in men and 49 in women. Low levels (< 12 ng/mL) are specific for iron deficiency. However, ferritin is an
acute-phase reactant, and levels increase in inflammatory and neoplastic disorders, so ferritin may also be elevated in cases of
liver injury (eg, hepatitis) and in some tumors (especially acute leukemia, Hodgkin lymphoma, and GI tract tumors). The most
sensitive and specific criterion for iron-deficient erythropoiesis, however, is absent marrow stores of iron, although a bone marrow
examination is rarely needed.
Stages of iron deficiency: Laboratory test results help stage iron deficiency anemia.
Stage 1 is characterized by decreased bone marrow iron stores; Hb and serum iron remain normal, but serum ferritin level falls to
< 20 ng/mL. The compensatory increase in iron absorption causes an increase in iron-binding capacity (transferrin level).
During stage 2, erythropoiesis is impaired. Although the transferrin level is increased, the serum iron level decreases; transferrin
saturation decreases. Erythropoiesis is impaired when serum iron falls to < 50 μg/dL (< 9 μmol/L) and transferrin saturation to <
16%. The serum ferritin receptor level rises (> 8.5 mg/L).
During stage 3, anemia with normal-appearing RBCs and indices develops.
During stage 5, iron deficiency affects tissues, resulting in symptoms and signs.
Diagnosis of iron deficiency anemia prompts consideration of its cause, usually bleeding. Patients with obvious blood loss (eg,
women with menorrhagia) may require no further testing. Men and postmenopausal women without obvious blood loss should
undergo evaluation of the GI tract, because anemia may be the only indication of an occult GI cancer. Rarely, chronic epistaxis or
GU bleeding is underestimated by the patient and requires evaluation in patients with normal GI study results.
Other microcytic anemias: Iron deficiency anemia must be differentiated from other microcytic anemias (see Table 1: Anemias
Caused by Deficient Erythropoiesis: Differential Diagnosis of Microcytic Anemia Due to Decreased RBC Production ). If tests
exclude iron deficiency in patients with microcytic anemia, then anemia of chronic disease, structural Hb abnormalities (eg,
hemoglobinopathies), and congenital RBC membrane abnormalities are considered. Clinical features, Hb studies (eg, Hb
electrophoresis and HbA2), and genetic testing (eg, α-thalassemia) may help distinguish these entities.
Treatment
• Oral supplemental iron
• Rarely, parenteral iron
Iron therapy without pursuit of the cause is poor practice; the bleeding site should be sought even in cases of mild anemia.
Iron can be provided by various iron salts (eg, ferrous sulfate SOME TRADE NAMES
FEOSOL
FER-GEN-SOL
FER-IN-SOL
Click for Drug Monograph
, gluconate, fumarate) or saccharated iron po 30 min before meals (food or antacids may reduce absorption). A typical initial dose
is 60 mg of elemental iron (eg, as 325 mg of ferrous sulfate SOME TRADE NAMES
FEOSOL
FER-GEN-SOL
FER-IN-SOL
Click for Drug Monograph
) given 1 or 2 times/day. Larger doses are largely unabsorbed but increase adverse effects, especially constipation. Ascorbic acid
either as a pill (500 mg) or as orange juice when taken with iron enhances iron absorption without increasing gastric distress.
Parenteral iron causes the same therapeutic response as oral iron but can cause adverse effects, such as anaphylactoid
reactions, serum sickness, thrombophlebitis, and pain. It is reserved for patients who do not tolerate or who will not take oral iron
or for patients who steadily lose large amounts of blood because of capillary or vascular disorders (eg, hereditary hemorrhagic
telangiectasia). The dose of parenteral iron is determined by a hematologist. Oral or parenteral iron therapy should continue for ≥
6 mo after correction of Hb levels to replenish tissue stores.
The response to treatment is assessed by serial Hb measurements until normal RBC values are achieved. Hb rises little for 2 wk
but then rises 0.7 to 1 g/wk until near normal, at which time rate of increase tapers. Anemia should be corrected within 2 mo. A
subnormal response suggests continued hemorrhage, underlying infection or cancer, insufficient iron intake, or, very rarely,
malabsorption of oral iron.
IM: Easy fatigability; poor sucking (infants) chubby but pale babies (milk babies)
Lab. Data: Decreased Hgb and Hct; microcytic, hypochromic RBC’s.
Nsg. Dx: Activity Intolerance
Interventions:
Instruct the patient to have frequent rest periods.
Increase iron in the diet (organ meat, egg yolk)
Milk is a poor source of iron. Administer oral iron supplement as ordered.
ANEMIA, PERNICIOUS
Other names:
Macrocytic achylic anemia; Congenital pernicious anemia; Juvenile pernicious anemia; Vitamin B12
deficiency (malabsorption)
Definition Return to top
Pernicious anemia is a decrease in red blood cells that occurs when the body cannot properly absorb vitamin
B12 from the gastrointestinal tract. Vitamin B12 is necessary for the formation of red blood cells.
Pernicious anemia is a type of megaloblastic anemia.
See also: Anemia
Causes Return to top
Pernicious anemia is caused by a lack of intrinsic factor. Intrinsic factor is a protein produced by the stomach
that helps the body absorb vitamin B12. When stomach does not have enough intrinsic factor, it cannot
properly absorb the vitamin. Nerve and blood cells need vitamin B12 to function properly.
Very rarely, infants and children are born without the ability to produce enough intrinsic factor. Congenital
(born with) pernicious anemia is inherited as an autosomal recessive disorder (you need the defective gene
from each parent to get it). Most often, however, pernicious anemia and other forms of megaloblastic anemia
in children result from other causes of vitamin B12 deficiency or other vitamin deficiencies.
Other causes of low levels of intrinsic factor (and thus of pernicious anemia) include atrophic gastric mucosa,
autoimmunity against gastric parietal cells, and autoimmunity against intrinsic factor.
The onset of the disease is slow and may take decades. Although the congenital form occurs in children,
pernicious anemia usually does not appear before age 30. The average age at diagnosis is 60.
Risk factors include:
• Certain drugs, including colchicine, neomycin, and para amino salicylic acid used for tuberculosis
treatment
• Gastrointestinal disease (stomach removal surgery, celiac disease, Crohn's disease)
• Infection (intestinal parasites, bacterial overgrowth)
• Metabolic disorders (methylmalonic aciduria, homocystinuria)
• Nutritional problems (strict vegetarians without B12 supplementation, poor diet in infant, or poor
nutrition during pregnancy)
• Shortness of breath
• Fatigue
• Pallor
• Rapid heart rate
• Loss of appetite
• Diarrhea
• Tingling and numbness of hands and feet
• Sore mouth
• Unsteady gait, especially in the dark
• Tongue problems
• Impaired sense of smell
• Bleeding gums
• Positive Babinski's reflex
• Loss of deep tendon reflexes
• Personality changes, "megaloblastic madness"
Exams and Tests Return to top
Tests that may used to diagnose or monitor pernicious anemia include:
This disease may also alter the results of the following tests:
• Bilirubin
• Cholesterol test
• Gastrin
• Leukocyte alkaline phosphatase
• Peripheral smear
• TIBC
Vitamin B12 deficiency affects the appearance of all epithelial cells, therefore an untreated woman may have
a false positive pap smear.
Treatment Return to top
Monthly vitamin B12 injections are prescribed to correct the vitamin B12 deficiency. This therapy corrects the
anemia and may correct the neurological complications if taken soon enough.
Some doctors recommend that elderly patients with gastric atrophy take vitamin B12 supplements by mouth
in addition to monthly injections.
There is also a preparation of vitamin B12 that may be given through the nose).
A well-balanced diet is essential to provide other elements for healthy blood cell development, such as folic
acid, iron, and vitamin C.
Outlook (Prognosis) Return to top
The outcome is usually excellent with treatment.
Possible Complications Return to top
People with pernicious anemia may have gastric polyps and get gastric cancer and gastric carcinoid tumors
twice as often than the normal population.
Persistent neurological defects may be present if treatment is delayed.
reduced Vitamin B12 absorption due to the absence of the intrinsic factor, usually related to
gastrectomy and atrophy of the gastric mucosa.
increased platelet aggregation and coagulation factor consumption occur. DIC that evolves slowly (over weeks or months) causes primarily venous
thrombotic and embolic manifestations; DIC that evolves rapidly (over hours or days) causes primarily bleeding. Severe, rapidly evolving DIC is diagnosed
by demonstrating thrombocytopenia, an elevated PTT and PT, increased levels of serum fibrin degradation products, and a decreasing plasma fibrinogen
level. Treatment includes correction of the underlying cause and replacement of platelets, coagulation factors (in fresh frozen plasma), and fibrinogen (in
cryoprecipitate) to control severe bleeding. Heparin is used as therapy (or prophylaxis) in patients with slowly evolving DIC who have (or are at risk for)
venous thromboembolism.
Etiology and Pathophysiology
DIC usually results from exposure of tissue factor to blood, initiating the coagulation cascade (see Fig. 2: Hemostasis: Fibrinolytic pathway. ). DIC occurs
• Complications of obstetrics—eg, abruptio placentae, saline-induced therapeutic abortion, retained dead fetus or products of conception, or
amniotic fluid embolism. Placental tissue with tissue factor activity enters or is exposed to the maternal circulation.
• Infection, particularly with gram-negative organisms. Gram-negative endotoxin causes generation of tissue factor activity in phagocytic,
endothelial, and tissue cells.
• Malignancy, particularly mucin-secreting adenocarcinomas of the pancreas and prostate and acute promyelocytic leukemia, in which tumor cells
expose or release tissue factor activity.
• Shock from any cause that produces ischemic tissue injury and tissue factor exposure.
Less common causes of DIC include severe tissue damage from head trauma, burns, frostbite, or gunshot wounds; complications of prostate surgery that
allow prostatic material with tissue factor activity (along with plasminogen activators) to enter the circulation; venomous snake bites in which enzymes enter
the circulation that activate one or several coagulation factors and generate thrombin or directly convert fibrinogen to fibrin; profound intravascular hemolysis;
and aortic aneurysms or cavernous hemangiomas (Kasabach-Merritt syndrome) associated with vessel wall damage and areas of blood stasis.
Slowly evolving DIC primarily causes venous thromboembolic manifestations (eg, deep venous thrombosis, pulmonary embolism), although occasionally
cardiac valve vegetations occur; abnormal bleeding is uncommon. In contrast, in severe, rapidly evolving DIC, thrombocytopenia and depletion of plasma
clotting factors and fibrinogen cause bleeding. Bleeding into organs, along with microvascular thromboses, may cause hemorrhagic tissue necrosis in
multiple organs.
In severe, rapidly evolving DIC, skin puncture sites (eg, IV or arterial punctures) bleed persistently, ecchymoses form at sites of parenteral injections, and
serious GI bleeding may occur. Delayed dissolution of fibrin polymers by fibrinolysis may result in the mechanical disruption of RBCs and mild intravascular
hemolysis (see Thrombocytopenia and Platelet Dysfunction: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)).
Occasionally, microvascular thrombosis and hemorrhagic necrosis produce dysfunction and failure in multiple organs.
Diagnosis
DIC is suspected in patients with unexplained bleeding or venous thromboembolism, especially if a predisposing condition exists. If DIC is suspected, platelet
count, PT, PTT, plasma fibrinogen level, and plasma D-dimer (an indication of in vivo fibrin deposition and degradation) are obtained.
Slowly evolving DIC produces mild thrombocytopenia, a normal to minimally prolonged PT (results are typically reported as INR) and PTT, a normal or
moderately reduced fibrinogen level, and an increased plasma D-dimer level. Because a variety of illnesses stimulate increased synthesis of fibrinogen as an
acute-phase reactant, a declining fibrinogen level on 2 consecutive measurements can help make the diagnosis of DIC.
Severe, rapidly evolving DIC results in more severe thrombocytopenia, more prolonged PT and PTT, rapidly declining plasma fibrinogen concentrations, and
A factor VIII level can sometimes be helpful if severe, acute DIC must be differentiated from massive hepatic necrosis, which can produce similar
abnormalities in coagulation studies. The factor VIII level is elevated in hepatic necrosis, because factor VIII is made in hepatocytes and released as they are
destroyed; factor VIII is reduced in DIC because of the thrombin-induced generation of activated protein C, which proteolyses factor VIII.
Treatment
Immediate correction of the underlying cause is the priority (eg, broad-spectrum antibiotic treatment of suspected gram-negative sepsis, evacuation of the
uterus in abruptio placentae). If treatment is effective, DIC should subside quickly. If bleeding is severe, adjunctive replacement therapy is indicated,
consisting of platelet concentrates to correct thrombocytopenia; cryoprecipitate to replace fibrinogen and factor VIII; and fresh frozen plasma to increase
levels of other clotting factors and natural anticoagulants (antithrombin, proteins C and S). The effects of infusion of concentrates of antithrombin or activated
usually is not indicated in DIC. An exception is in women with a retained dead fetus and evolving DIC with a progressive decrease in platelets, fibrinogen,
is administered for several days to control DIC, increase fibrinogen and platelets, and decrease excessive coagulation factor consumption before uterine
evacuation.
widespread coagulation all over the body resulting to subsequent depletion of clotting factors.
CM: Petechiae and ecchymosis on the skin, mucous membrane, heart, lungs and other organs.
Lab. Data: Prolonged PT and PTT
Nsg. Dx: Risk for injury
Interventions:
Monitor for signs of bleeding
Administer heparin as ordered.
Heparin inhibits thrombin thus preventing further clot formation and allowing coagulation factors to
accumulate.
Administer blood transfusion as ordered.
Instruct the patient to avoid aspirin or aspirin containing compounds.
CM: Fever
Lab. Data: Elevated ESR
Nsg. Dx: Altered Cardiac Output
Interventions:
Record daily weight
Evaluate JVD – this signifies the development of CHF.
Instruct the patient to take antibiotics before dental procedures that can cuse bleeding.
Avoid sharing of needles.
Teach the women in child bearing years the risks of using IUDs, or birth control (source of
infection).
• Rheumatic heart disease is a chronic condition resulting from rheumatic fever that
is characterized by scarring and deformity of the heart valves.
• About 40% of ARF episodes are marked by carditis, meaning that all layers of the
heart are involved, and this is referred to as rheumatic pancarditis.
o Rheumatic endocarditis is found primarily in the valves. Vegetation forms and
valve leaflets may fuse and become thickened or even calcified, resulting in
stenosis or regurgitation.
o Myocardial involvement is characterized by Aschoff’s bodies.
o Rheumatic pericarditis affects the pericardium, which becomes thickened and
covered with a fibrinous exudate, and often involves pericardial effusion.
o The lesions of rheumatic fever are systemic, especially involving the
connective tissue, as well as the joints, skin, and CNS.
• The overall goals for a patient with rheumatic fever include (1) normal or baseline
heart function, (2) resumption of daily activities without joint pain, and (3)
verbalization of the ability to manage the disease.
• The expected outcomes for the patient with rheumatic fever and heart disease
include (1) ability to perform ADLs with minimal fatigue and pain, (2) adherence to
treatment regimen, and (3) expression of confidence in managing disease.
damage to the heart valves resulting to regurgitation, obstruction, narrowing or stenosis.
CM:
Hemarthrosis, usually in the elbows, ankles and knees.
Increased pain means bleeding continues.
Lab. Data:
Prolonged PTT
Normal PT
Nsg. Dx:
Altered Tissue Perfusion
Fluid Volume Deficit
Pain
Interventions:
Avoid ASPIRIN
Control bleeding by utilizing RICE Principle.
Avoid contact sports and rectal temperature monitoring.
Administer missing coagulation factors as ordered. Stop transfusion if hives, headache, tingling,
chills, flushing or fever develops.
Administer short course of corticosteroids to relieve inflammation.
Refer to PT to prevent contractures and orthotics to prevent joint injury. Gentle, passive exercise 48
hours after the acute phase can be implemented for less severe hemarthrosis.
Airway obstruction may occur due to bleeding in the neck and pharynx.