Medical Nursing II

LECTURE NOTES FOR BSc NURSING TOP UP GROUP (L300)
CARDIOVASCULAR DISORDERS
SECTION A: BLOOD DISORDERS
ANAEMIAS
IRON-DEFICIENCY ANAEMIA
1. Chronic microcytic, hypochromic anemia caused by either inadequate absorption or

excessive loss of iron
2. Acute or chronic bleeding principal cause in adults (chiefly from trauma, excessive
menses, and GI bleeding)
3. May also be caused by inadequate intake of iron-rich foods or by inadequate absorption
of iron (from chronic diarrhea, malabsorption syndromes, high cereal-product intake with
low animal protein ingestion, partial or complete gastrectomy, pica)
4. Incidence related to geographic location, economic class, age group, and sex
a. More common in developing countries and tropical zones (blood-sucking parasites)
b. Women between ages 15-45 and children affected more frequently, as are the poor
5. In iron-deficiency states, iron stores are depleted first, followed by a reduction in Hgb
formation.
Clinical manifestations of Iron deficiency anaemia
1. Mild cases usually asymptomatic

2. Palpitations, dizziness, and cold sensitivity
3. Brittleness of hair and nails; pallor
4. Dysphagia, stomatitis, and atrophic glossitis
5. Dyspnea, weakness
Laboratory investigations/diagnosis
1. RBCs small (microcytic) and pale (hypochromic)

2. Hgb markedly decreased
3. Hct moderately decreased
4. Serum iron markedly decreased
5. Hemosiderin absent from bone marrow
6. Serum ferritin decreased
7. Reticulocyte count decreased
Nursing interventions for Iron deficiency anaemia
1. Monitor for signs and symptoms of bleeding through hematest of all elimination
including stool, urine, and gastric contents.
2. Provide for adequate rest: plan activities so as not to overtire.
3. Provide a thorough explanation of all diagnostic tests used to determine sources of
possible bleeding (helps allay anxiety and ensure cooperation).
4. Administer iron preparations as ordered.
a. Oral iron preparations: route of choice:

1. Give following meals or a snack.
2. Dilute liquid preparations well and administer using a straw to prevent staining teeth.
3. When possible administer with orange juice as vitamin C (ascorbic acid) enhances iron
absorption.
4. Warn clients that iron preparations will change stool color and consistency (dark and
tarry) and may cause constipation.
b. Parenteral: used in clients intolerant to oral preparations, who are noncompliant
with therapy, or who have continuing blood losses.
1. Use one needle to withdraw and another to administer iron preparations as tissue
staining and irritation are a problem.
2. use the Z-track injection technique to prevent leakage into tissues
3. Do not massage injection site but encourage ambulation as this will enhance
absorption; advise against vigorous exercise and constricting garments.
4. Observe for local signs of complications: pain at the injection site, development of
sterile abscesses, lymphadenitis as well as fever, headache, urticaria, hypotension, or
anaphylactic shock.
2. Provide dietary teaching regarding foods high in iron.
3. Encourage ingestion of roughage and increase fluid intake to prevent constipation if oral
iron preparations are being taken.
PERNICIOUS ANAEMIA
1. Chronic progressive, macrocytic anemia caused by a deficiency of intrinsic factor; the

result is abnormally large erythrocytes and hypochlorhydria (a deficiency of hydrochloric
acid in gastric secretions)
2. Characterized by neurologic and GI symptoms; death usually results if untreated
3. Lack of intrinsic factor is caused by gastric mucosal atrophy (possibly due to heredity,
prolonged iron deficiency, or an autoimmune disorder); can also result in clients who
have had a total gastrectomy if vitamin B12 not administered
4. Usually occurs in men and women over age 50, with an increase in blue-eyed persons of
Scandinavian descent
Pathophysiology of Pernicious Anaemia
1. Intrinsic factor is necessary for the absorption of vitamin B12 into the small intestine.
2. B12 deficiency diminishes DNA synthesis, which results in defective maturation of cells
(particularly rapidly dividing cells such as blood cells and GI tract cells).
3. B12 deficiency can alter structure and function of peripheral nerves, spinal cord, and the
brain.
Medical management
a. Drug therapy
1. Vitamin B12 injections: monthly maintenance

2. Iron preparations (if Hgb level inadequate to meet increased numbers of erythrocytes)
3. Folic acid: reverses anemia and GI symptoms but may intensify neurologic symptoms. It
may be safe if given in small amounts in addition to vitamin B12
b. Transfusion therapy
Clinical manifestations
1. Anemia, weakness, pallor, dyspnea, palpitations, fatigue

2. GI symptoms: sore mouth; smooth, beefy, red tongue; weight loss; dyspepsia;
constipation or diarrhea; jaundice
3. CNS symptoms; tingling, paresthesias of hands and feet, paralysis, depression, psychosis
Laboratory investigations/diagnosis
1. Erythrocyte count decreased

2. Blood smear: oval, macrocytic erythrocytes with a proportionate amount of Hgb
3. Bone marrow:
a. increased megaloblasts (abnormal erythrocytes)

b. few normoblasts or maturing erythrocytes
c. defective leukocyte maturation
2. Bilirubin (indirect): elevated unconjugated fraction
3. Serum LDH elevated
4. Positive Schilling test
a. measures absorption of radioactive vitamin B12 both before and after parenteral
administration of intrinsic factor
b. definitive test for pernicious anemia
c. used to detect lack of intrinsic factor
d. fasting client is given radioactive vitamin B12 by mouth and nonradioactive vitamin B12
IM to saturate tissue binding sites and to permit some excretion of radioactive vitamin
B12 in the urine if it is absorbed
e. 24-48 hour urine collection is obtained; client is encouraged to drink fluids
f. if indicated, second stage Schilling test performed 1 week after first stage. Fasting
client is given radioactive vitamin B12 combined with human intrinsic factor and test is
repeated.
2. Gastric analysis: decreased free hydrochloric acid
3. Large numbers of reticulocytes in the blood following parenteral vitamin B12
administration
Nursing interventions for Pernicious Anaemia
1. Provide a nutritious diet high in iron, protein, and vitamins (fish, meat, milk/milk
products, and eggs).
2. Avoid highly seasoned, coarse, or very hot foods if client has mouth sores.
3. Provide mouth care before and after meals using a soft toothbrush and nonirritating
rinses.
4. Bed rest may be necessary if anemia is severe.
5. Provide safety when ambulating (especially if carrying hot items, etc.)
6. Provide client teaching and discharge planning concerning
a. Dietary instruction
b. Importance of lifelong vitamin B12 therapy
c. Rehabilitation and physical therapy for neurologic deficits, as well as instruction
regarding safety
APLASTIC ANAEMIA
1. Pancytopenia or depression of granulocyte, platelet, and erythrocyte production due

to fatty replacement of the bone marrow
2. Bone marrow destruction may be idiopathic or secondary
3. Secondary aplastic anemia may be caused by:
a. Chemical toxins (e.g., benzene)
b. Drugs (e.g., chloramphenicol, cytotoxic drugs)
c. Radiation
d. Immunologic injury
Clinical manifestations of Aplastic Anaemia
1. Fatigue, dyspnea, pallor

2. Increased susceptibility to infection
3. Bleeding tendencies and hemorrhage
4. Laboratory findings: normocytic anemia, granulocytopenia, thrombocytopenia
5. Bone marrow biopsy: marrow is fatty and contains very few developing cells.
Medical management of Aplastic Anaemia
1. Blood transfusions (see Laboratory/Diagnostic Tests): key to therapy until client's

own marrow begins to produce blood cells
2. Aggressive treatment of infections
3. Bone marrow transplantation
4. Drug therapy
1. Corticosteroids and/or androgens to stimulate bone marrow function

and to increase capillary resistance (effective in children but usually
not in adults)
2. Estrogen and/or progesterone to prevent amenorrhea in female clients
2. Identification and withdrawal of offending agent or drug
Nursing interventions
1. Administer blood transfusions as ordered.

2. Provide nursing care for client with bone marrow transplantation.
3. Administer medications as ordered.
4. Monitor for signs of infection and provide care to minimize risk.
1. Maintain neutropenic precautions.

2. Encourage high-protein, high-vitamin diet to help reduce incidence of
infection.
3. Provide mouth care before and after meals.
2. Monitor for signs of bleeding and provide measures to minimize risk.
1. Use a soft toothbrush and electric razor.
2. Avoid intramuscular injections.
3. Hematest urine and stool.
4. Observe for oozing from gums, petechiae, or ecchymoses.
1. Self-care regimen
2. Identification of offending agent and importance of avoiding it (if
possible) in future
HAEMOLYTIC ANAEMIA
1. General information
1. A category of diseases in which there is an increased rate of RBC destruction.
2. May be congenital or acquired.
1. Congenital: includes hereditary spherocytosis, G6PD deficiency, sickle
cell anemia, thalassemia
2. Acquired: includes transfusion incompatibilities, thrombotic
thrombocytopenic purpura, disseminated intravascular clotting, spur
cell anemia
3. Cause often unknown, but erythrocyte life span is shortened and hemolysis
occurs at a rate that the bone marrow cannot compensate for.
4. The degree of anemia is determined by the lag between erythrocyte hemolysis
and the rate of bone marrow erythropoiesis.
5. Diagnosis is based on laboratory evidence of an increased rate of erythrocyte
destruction and a corresponding compensatory effort by bone marrow to
increase production.
2. Medical management
1. Identify and eliminate (if possible) causative factors

2. Drug therapy
1. Corticosteroids in autoimmune types of anemia

2. Folic acid supplements
2. Blood transfusion therapy
3. Splenectomy (see below)
2. Assessment findings
1. Clinical manifestations vary depending on severity of anemia and the rate of

onset (acute vs chronic)
2. Pallor, scleral icterus, and slight jaundice (chronic)
3. Chills, fever, irritability, precordial spasm, and pain (acute)
4. Abdominal pain and nausea, vomiting, diarrhea, melena
5. Hematuria, marked jaundice, and dyspnea
6. Splenomegaly and symptoms of cholelithiasis, hepatomegaly
7. Laboratory tests
1. Hgb and hct decreased

2. Reticulocyte count elevated (compensatory)
3. Coombs' test (direct): positive if autoimmune features present
4. Bilirubin (indirect): elevated unconjugated fraction
2. Nursing interventions
1. Monitor for signs and symptoms of hypoxia including confusion, cyanosis,

shortness of breath, tachycardia, and palpitations.
2. Note that the presence of jaundice may make assessment of skin color in
hypoxia unreliable.
3. If jaundice and associated pruritus are present, avoid soap during bathing and
use cool or tepid water.
4. Frequent turning and meticulous skin care are important as skin friability is
increased.
5. Teach clients about the nature of the disease and identification of factors that
predispose to episodes of hemolytic crisis.
SICKLE-CELL ANAEMIA
1. General information (see Figure 5.2 below)

1. Most common inherited disorder in US African American population; sickle
cell trait found in 10% of African Americans
2. Autosomal recessive inheritance pattern
3. Individuals who are homozygous for the sickle cell gene have the disease
(more than 80% of their hemoglobin is abnormal [HgbS]).
4. Those who are heterozygous for the gene have sickle cell trait (normal
hemoglobin predominates, may have 25%-50% HgbS). Although sickle cell
trait is not a disease, carriers may exhibit symptoms under periods of severe
anoxia or dehydration.
5. In this disease, the structure of hemoglobin is changed; the sixth rung of the
beta chain changes glutamine for valine.
6. HgbS (abnormal Hgb), which has reduced oxygen-carrying capacity, replaces
all or part of the hemoglobin in the RBCs.
7. When oxygen is released, the shape of the RBCs changes from round and
pliable to crescent shaped, rigid, and inflexible.
8. Local hypoxia and continued sickling lead to plugging of vessels.
9. Sickled RBCs live for 6-20 days instead of 120, causing hemolytic anemia.
10. Usually no symptoms prior to age 6 months; presence of increased level of
fetal hemoglobin tends to inhibit sickling.
11. Death often occurs in early adulthood due to occlusion or infection.
12. Sickle cell crisis
1. Vaso-occlusive (thrombocytic) crisis: most common type
1. crescent-shaped RBCs clump together; agglutination causes
blockage of small blood vessels.
2. blockage causes the blood viscosity to increase, producing
sludging and resulting in further hypoxia and increased
sickling.
2. Splenic sequestration: often seen in toddler/preschooler
1. sickled cells block outflow tract resulting in sudden and

massive collection of sickled cells in spleen.
2. blockage leads to hypovolemia and severe decrease in
hemoglobin and blood pressure, leading to shock.
2. Medical management: sickle cell crisis
1. Drug therapy
1. Urea: interferes with hydrophobic bonds of the HgbS molecules

2. Analgesics/narcotics to control pain
3. Antibiotics to control infection
2. Exchange transfusions
3. Hydration: oral and IV
4. Bed rest
5. Surgery: splenectomy
6.
1. First sign in infancy may be "colic" due to abdominal pain (abdominal infarct)
2. Infants may have dactylitis (hand-foot syndrome): symmetrical painful soft
tissue swelling of hands and feet in absence of trauma (aseptic, self-limiting)
3. Splenomegaly: initially due to hemolysis and phagocytosis; later due to
fibrosis from repeated infarct to spleen
4. Weak bones or spinal defects due to hyperplasia of marrow and osteoporosis
5. Frequent infections, especially with H. influenzae and D. pneumoniae
6. Leg ulcers, especially in adolescents, due to blockage of blood supply to skin
of legs
7. Delayed growth and development, especially delay in sexual development
8. CVA/infarct in the CNS
9. Renal failure: difficulty concentrating urine due to infarcts; enuresis
10. Heart failure due to hemosiderosis
11. Priapism: may result in impotence
12. Pain wherever vaso-occlusive crisis occurs
13. Development of collateral circulation
14. Diagnostic tests
1. Hgb indicates anemia, usually 6-9 g/dl

2. Sickling tests
1. sickle cell test: deoxygenation of a drop of blood on a slide

with a cover slip; takes several hours for results to be read;
false negatives for the trait possible.
2. Sickledex: a drop of blood from a finger stick is mixed with a
solution; mixture turns cloudy in presence of HgbS; results
available within a few minutes; false negatives in anemia
clients or young infants possible.
2. Hgb electrophoresis: diagnostic for the disease and the trait; provides
accurate, fast results.
2. Nursing interventions: sickle cell crisis
1. Keep child well hydrated and oxygenated.

2. Avoid tight clothing that could impair circulation.
3. Keep wounds clean and dry.
4. Provide bed rest to decrease energy expenditure and oxygen use.
5. Correct metabolic acidosis.
1. Analgesics: acetaminophen, meperidine, morphine (avoid aspirin as it

enhances acidosis, which promotes sickling)
2. Avoid anticoagulants (sludging is not due to clotting)
3. Antibiotics
2. Administer blood transfusions as ordered.
3. Keep arms and legs from becoming cold.
4. Decrease emotional stress.
5. Provide good skin care, especially to legs.
6. Test siblings for presence of sickle cell trait/disease.
1. Pre-op teaching for splenectomy if needed

2. Genetic counseling
3. Need to avoid activities that interfere with oxygenation, such as
mountain climbing, flying in unpressurized planes
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
1. Diffuse fibrin deposition within arterioles and capillaries with widespread
coagulation all over the body and subsequent depletion of clotting factors.
2. Hemorrhage from kidneys, brain, adrenals, heart, and other organs.
3. Cause unknown
4. Clients are usually critically ill with an obstetric, surgical, hemolytic, or
neoplastic disease.
5. May be linked with entry of thromboplastic substances into the blood.
6. Pathophysiology
1. Underlying disease (e.g., toxemia of pregnancy, cancer) causes release
of thromboplastic substances that promote the deposition of fibrin
throughout the microcirculation.
2. Microthrombi form in many organs, causing microinfarcts and tissue
necrosis.
3. RBCs are trapped in fibrin strands and are hemolysed.
4. Platelets, prothrombin, and other clotting factors are destroyed, leading
to bleeding.
5. Excessive clotting activates the fibrinolytic system, which inhibits
platelet function, causing further bleeding.
7. Mortality rate is high, usually because underlying disease cannot be corrected.
1. Identification and control of underlying disease is key

2. Blood transfusions: include whole blood, packed RBCs, platelets, plasma,
cryoprecipitates, and volume expanders
3. Heparin administration
1. Somewhat controversial
2. Inhibits thrombin thus preventing further clot formation, allowing
coagulation factors to accumulate
1. Petechiae and ecchymoses on the skin, mucous membranes, heart, lungs, and
other organs
2. Prolonged bleeding from breaks in the skin (e.g., IV or venipuncture sites)
3. Severe and uncontrollable hemorrhage during childbirth or surgical procedures
4. Oliguria and acute renal failure
5. Convulsions, coma, death
6. Laboratory findings
1. PT prolonged
2. PTT usually prolonged
3. Thrombin time usually prolonged
4. Fibrinogen level usually depressed
5. Platelet count usually depressed
6. Fibrin split products elevated
7. Protamine sulfate test strongly positive
8. Factor assays (II, V, VII) depressed
1. Monitor blood loss and attempt to quantify.

2. Observe for signs of additional bleeding or thrombus formation.
3. Monitor appropriate laboratory data.
4. Prevent further injury.
1.Avoid IM injections.
2.Apply pressure to bleeding sites.
3.Turn and position client frequently and gently.
4.Provide frequent nontraumatic mouth care (e.g., soft toothbrush or
gauze sponge).
2. Provide emotional support to client and significant others.
3. Administer blood transfusions and medications as ordered.
4. Teach client the importance of avoiding aspirin or aspirin-containing
compounds.
HAEMOPHILIA
1. A group of bleeding disorders where there is a deficit of one of several factors
in clotting mechanism
2. Sex-linked, inherited disorder; classic form affects males only
3. Types
1. Hemophilia A: factor VIII deficiency (75% of all hemophilia)
2. Hemophilia B (Christmas disease): factor IX deficiency (10%-12% of
all hemophilia)
3. Hemophilia C: factor XI deficiency (autosomal recessive, affects both
sexes)
4. Only the intrinsic system is involved; platelets are not affected, but fibrin clot
does not always form; bleeding from minor cuts may be stopped by platelets.
5. If individual has less than 20%-30% of factor VIII or IX, there is an
impairment of clotting and clot is jelly-like.
6. Bleeding in neck, mouth, and thorax requires immediate professional care.
1. Prolonged bleeding after minor injury
1. At birth after cutting of cord

2. Following circumcision
3. Following IM immunizations
4. Following loss of baby teeth
5. Increased bruising as child learns to crawl and walk
2. Bruising and hematomas but no petechiae
3. Peripheral neuropathies (due to bleeding near peripheral nerves): pain,
paresthesias, muscle atrophy
4. Hemarthrosis
1. Repeated bleeding into a joint results in a swollen and painful joint

with limited mobility
2. May result in contractures and possible degeneration of joint
3. Knees, ankles, elbows, wrists most often affected
2. Diagnostic tests
1. Platelet count normal

2. Prolonged coagulation time: PTT increased
3. Anemia
1. Control acute bleeding episode.
1.Apply ice compress for vasoconstriction.

2.Immobilize area to prevent clots from being dislodged.
3.Elevate affected extremity above heart level.
4.Provide manual pressure or pressure dressing for 15 minutes; do not
keep lifting dressing to check for bleeding status.
5. Maintain calm environment to decrease pulse.
6. Avoid sutures, cauterization, aspirin: all exacerbate bleeding.
7. Administer hemostatic agents as ordered.
1. fibrin foam
2. topical application of adrenalin/epinephrine to promote
vasoconstriction
2. Provide care for hemarthrosis.
1. Immobilize joint and control acute bleeding.

2. Elevate joint in a slightly flexed position.
3. Avoid excessive handling of joint.
4. Administer analgesics as ordered; pain relief will minimize increases
in pulse rate and blood loss.
5. Aspirin should not be given because it inhibits platelet function.
6. Instruct to avoid weight bearing for 48 hours after bleeding episode if
bleeding is in lower extremities.
7. Provide active or passive ROM exercises after bleeding has been
controlled (48 hours), as long as exercises do not cause pain or irritate
trauma site.
2. Administer cryoprecipitate (frozen factor VIII) as ordered.
1. Thaw slowly.
2. Gently rotate bottle; shaking deteriorates antihemophilic factor.
3. Infuse immediately when thawed; factor VIII deteriorates at room
temperature.
1. Prevention of trauma (see Idiopathic Thrombocytopenic Purpura)

1. when mother is carrier: 50% chance with each pregnancy for

sons to have hemophilia, 50% chance with each pregnancy for
daughters to be carriers
2. when father has hemophilia, mother is normal: no chance for
children to have disease, but all daughters will be carriers
2. Availability of support/counseling agencies
LEUKAEMIA
Description
There are two major forms of acute leukemia: lymphocytic leukemia and
nonlymphocytic leukemia. Lymphocytic leukemia involves the lymphocytes (cells that are
derived from the stem cells and circulate among the blood, lymph nodes, and lymphatic
organs) and lymphoid organs; nonlymphocytic leukemia involves hematopoietic stem cells
that differentiate into monocytes, granulocytes, red blood cells (RBCs), and platelets. Up to
90% of acute leukemias are a form of lymphocytic leukemia, acute lymphoblastic leukemia
(ALL), which is characterized by the abnormal growth of lymphocyte precursors called
lymphoblasts. Acute myelogenous leukemia (AML) (also known as acute nonlymphocytic
leukemia, or ANLL) causes the rapid accumulation of megakaryocytes (precursors to
platelets), monocytes, granulocytes, and RBCs. As the disease progresses, the patient may
have central nervous system (CNS) dysfunction with seizures, decreased mental status, or
coma and renal insufficiency. Death occurs when the abnormal cells encroach on vital tissues
and cause complications and organ dysfunction.
Causes
The exact cause of acute leukemia is unknown, but there are several risk factors.
Overexposure to radiation even years before the development of the disease, particularly if
the exposure is prolonged, is a major risk factor. Other risk factors include exposure to
certain chemicals (benzene),medications (alkylating agents used to treat other cancers in
particular), and viruses. Other related factors in children include genetic abnormalities such
as Down syndrome, albinism, and congenital immunodeficiency syndrome. People who have
been treated with chemotherapeutic agents for other forms of cancer have an increased risk
for developing AML. Such cases generally develop within 9 years of chemotherapy.
Signs and Symptoms
 The patient appears acutely ill, short of breath, and pale.

 Children are often febrile.
 When you inspect the lips and mouth, you may note bleeding gums and ulcerated
areas of the mouth and throat.
 On palpation, you may feel lymph node swelling and enlargement of the liver and
spleen.
 When you auscultate the patient’s lungs, you may hear decreased breath sounds,
shallow and rapid respirations, a rapid heart rate, and a systolic ejectionmurmur.
Diagnostic Evaluation
1. CBC and blood smear – peripheral WBC count varies widely from 1,000 to
100,000/mm3 and may include significant numbers of abnormal immature (blast)
cells, anemia may be profound; platelet count may be abnormal and coagulopathies
may exist.
2. Bone marrow aspiration and biopsy – cells also studied for chromosomal
abnormalities (cytogenetics) and immunologic markers to classify type of leukemia
further.
3. Lymph node biopsy – to detect the spread.
4. Lumbar puncture and examination of cerebrospinal fluid for leukemic cells
(especially ALL).
PRIMARY NURSING DIAGNOSIS
 Risk for infection related to decreased primary and secondary responses

 OUTCOMES. Immune status; Knowledge: Infection control; Risk control; Risk
detection;Nutrition status; Treatment behavior: Illness or injury; Hydration;
Knowledge: Infection control
 INTERVENTIONS. Infection control; Infection protection; Surveillance;
Fluid/electrolyte management; Medication management; Temperature regulation
Pharmacologic Interventions
Different types of leukemia are best treated with different kinds of medicine.
 Acute lymphoblastic leukemia (ALL) drugs include prednisone, vincristine,

daunorubicin, L-asparaginase or pegaspargase, methotrexate, and cyclophosphamide.
Imatinib (Gleevec) is sometimes used to treat ALL. Dasatinib (Sprycel) is a newer
drug for treating some ALL that has not improved with other drugs.
 Acute myelogenous leukemia (AML) drugs include daunorubicin, idarubicin, cytosine
arabinoside, and mitoxantrone.10 Gemtuzumab (Mylotarg) may be given to people
whose AML has relapsed. It helps your body destroy cancer cells.
 Acute promyelocytic leukemia (APL) drugs include all-trans-retinoic acid (ATRA)
and chemotherapy with arsenic trioxide, idarubicin, or daunorubicin. ATRA helps
control the risk of life-threatening bleeding from disseminated intravascular
coagulation (DIC). Later treatment can include ATRA with or without methotrexate
and 6-mercaptopurine. Or if a first round of ATRA and chemotherapy does not work,
arsenic trioxide may be used.
 To treat leukemia in the brain or prevent it from spreading to the brain and central
nervous system, methotrexate and cytarabine/cytosine arabinoside are injected into
the spinal canal. This is called intrathecal chemotherapy.
Supportive treatments during cancer treatment include:
 Antibiotics and immunoglobulins help to prevent or fight infections. This is important

when you do not have enough normal white blood cells to fight infections on your
own.
 Transfusions of red blood cells and platelets.
 Epoetin and hematopoietic stimulants help your body make new blood cells.
 Allopurinol to prevent kidney problems and gout.
 Saline or steroid eyedrops for relief during treatment with cytarabine/cytosine
arabinoside.
Medical Management
 The treatment for acute leukemia occurs in four phases: induction, consolidation,
continuation, and treatment of (CNS) leukemia. During the induction phase, the
patient receives an intense course of chemotherapy that is meant to cause a complete
remission of the disease. Complete remission occurs when the patient has less than
5% of the bone marrow cells as blast cells and the peripheral blood counts are normal.
Once remission has been sustained for 1 month, the patient enters the consolidation
phase, during which she or he receives a modified course of chemotherapy to
eradicate any remaining disease. The continuation, or maintenance, phase
may continue for more than a year, during which time the patient receives small doses
of chemotherapy every 3 to 4 weeks. Treatment of CNS leukemia is an essential
component of therapy that has replaced irradiation, which leads to significant CNS
complications, with intensive intrathecal and systemic chemotherapy for most
patients.
 Some patients also need transfusions with blood component therapy to control
infection and prevent bleeding and anemia. Bone marrow transplantation (BMT) is an
option for some patients. Early BMTs were allogenic transplants using stem cells that
had been harvested from bone marrow from siblings or matched from unrelated
relatives. In autologous BMTs in the 1980s, physicians began using frozen cells
harvested from the donor’s own marrow during remission. More recently, a newer
form of transplant has occurred with peripheral blood stem cell transplant (SCT) or
peripheral blood progenitor cell transplant. Multiple pheresis, or removal of cells from
the blood, provides the stem cells from the patient for transplantation. SCT permits
the use of doses of chemotherapy and radiation therapy high enough to destroy the
patient’s bone marrow; after the treatment is completed SCT restores blood-producing
bone marrow stem cells. Radiation treatment is sometimes used to treat leukemic cells
in the brain, spinal cord, or testicles.
Nursing Interventions
Preventing infection:
 Frequently monitor the client for pneumonia, pharyngitis, esophagitis, perianal

cellulitis, urinary tract infection, and cellulitis, which are common in leukemia and
which carry significant morbidity and mortality.
 Monitor for fever, flushed appearance, chills, tachycardia; appearance of white
patches in the mouth; redness, swelling, heat or pain in the eyes, ears, throat, skin,
joints, abdomen, rectal and perineal areas; cough, changes in sputum; skin rash.
 Check results of granulocyte counts. Concentrations less than 500/mm3 put the
patient at serious risk for infection.
 Avoid invasive procedures and trauma to skin or mucous membrane to prevent entry
of microorganisms.
 Use the following rectal precautions to prevent infections: Avoid diarrhea and
constipation, which can irritate the rectal mucosa, avoid the use of rectal
thermometers, and keep perineal are clean.
 Care for the patient in private room with strict handwashing practice.
 Encourage and assist patient with personal hygiene, bathing, and oral care.
 Obtain cultures and administer antimicrobials promptly as directed.
Preventing and Managing bleeding:
 Watch for signs of minor bleeding, such as petechiae, ecchymosis, conjunctival

hemorrhage, epistaxis, bleeding gums, bleeding at puncture sites, vaginal spotting,
heavy menses.
 Be alert for signs of serious bleeding, such as headache with change in
responsiveness, blurred vision, hemoptysis, hematemesis, melena, hypotension,
tachycardia, dizziness.
 Test all urine, stool, emesis for gross and occult blood.
 Monitor platelet counts daily.
 Administer blood components as directed.
 Keep patient on bed rest during bleeding episodes.
Patient Education and Health Maintenance:
 Teach signs and symptoms of infection and advise whom to notify.

 Encourage adequate nutrition to prevent emaciation from chemotherapy.
 Teach avoidance of constipation with increased fluid and fiber, and good perineal
care.
 Teach bleeding precautions.
 Encourage regular dental visits to detect and treat dental infections and disease.
References:
 http://nursingcrib.com/case-study/leukemia-case-study/
 http://www.cancer.gov/dictionary?cdrid=45145
 http://www.cancer.org/cancer/leukemia-
acutelymphocyticallinadults/detailedguide/leukemia-acute-lymphocytic-risk-factors
 Diseases and Disorders a Therapeutic Manual, 2007
BLOOD TRANSFUSION
Whole blood or components of whole blood can be transfused. Blood components include
packed red blood cells (RBCs), plasma, albumin, clotting factors, prothrombin complex,
cryoprecipitate, and platelets. Incompatibility is a major concern when administering blood or
blood products. Blood is typed based on the presence of antigens.
Another consideration is the Rh factor: Blood that contains D antigen makes the Rh factor
positive. Rh positive blood given to an Rh negative person will cause hemolysis.
Transfusion Types
1. Transfusion from blood donors

2. Autologous transfusion: The client’s own blood is collected in anticipation of future
transfusions (elective surgery). This blood is designated for and can be used only by
the client.
3. Intraoperative blood salvage: Blood loss during certain surgeries can be recycled
through a cell-saver machine and transfused intraoperatively or postoperatively
(orthopedic surgeries, CABG).
Indications for Transfusions
1. Excessive blood loss (hemoglobin 6 to 10 g/dL and depending on symptoms) USE

whole blood
2. Anemia (hemoglobin 6 to 10 g/dL and depending on symptoms) USE packed RBCs
3. Chronic renal failure USE packed RBCs
4. Coagulation factor deficiencies such as hemophilia USE fresh frozen plasma
5. (FFP)
6. Thrombocytopenia/platelet dysfunction (platelets < 20,000 or < 80,000 and actively
bleeding) USE platelets
Nursing responsibilities
1. Ensure appropriate venous access for the infusion of blood and blood products.
2. Assess the client’s vital signs prior to, during, and following blood transfusion.
3. Following policies for checking blood products prior to administration, verify client
identity and document interventions.
4. Deliver and monitor flow rate and discontinue blood and blood products.
5. Monitor and document the client’s response to blood transfusion.
6. Administer and discontinue blood (red blood cells) and blood products (for example,
platelets).
7. Perform/assist with relevant laboratory, diagnostic, and therapeutic procedures within
the nursing role, including:
8. Monitoring and taking actions, including client education, to prevent or minimize the
risk of complications.
9. Recognizing signs of potential complications and reporting to the primary care
provider.
10. Recommending changes in the test/procedure as needed based on client
SPECIFIC NURSING INTERVENTIONS FOR TTRANSFUSION
Before the Transfusion
1. Assess laboratory values, such as hemoglobin and hematocrit.

2. Verify order for specific blood product.
3. Obtain blood samples for compatibility determination.
4. Initiate large-bore IV access.
5. Assess for a history of blood-transfusion reactions.
6. Obtain blood products from the blood bank. Inspect the blood for discoloration,
excessive bubbles, or cloudiness.
7. Following specific institution protocol, confirm the client’s identity, blood
compatibility, and expiration time of the blood product with another nurse.
8. Prime the blood administration set with normal saline (NS). Blood products are only
infused with NS. NEVER add medications to blood products.
9. Ascertain whether or not a filter should be used.
10. Obtain baseline vital signs.
11. Begin the transfusion. Use a blood warmer if indicated.
During the Transfusion
1.Remain with the client for the first 15 min of the infusion (reactions occur most often
during first 15 min) and monitor:
a. Vital signs.
b. Rate of infusion.
c. Respiratory status.
d. Sudden increase in anxiety.
e. Breath sounds.
f. Neck-vein distention.
2.Notify the primary care provider immediately for any signs of reaction.
3.Complete the transfusion within a 2 to 4 hr time frame to avoid bacterial growth.
Following the Transfusion
1. Obtain vital signs upon completion of the transfusion.

2. Dispose of the blood-administration set appropriately (biohazard bags).
3. Monitor blood values as prescribed (CBC, hemoglobin, hematocrit).
4. Hemoglobin levels should rise by approximately 1 g/dL with each unit transfused.
5. Complete paperwork and file in the appropriate places.
6. Document the client’s response.
7. Stop the transfusion immediately if a reaction is suspected.
8. Initiate a saline infusion. The saline infusion should be initiated with a separate line,
so as not to give more blood from the transfusion tubing.
9. Save the blood bag with the remaining blood and the blood tubing for testing.
COMPLICATIONS OF TRANSFUSION
1. Transfusion reaction
2. Circulatory overload
3. Sepsis
4. Septic shock
SECTION B: DISORDERS OF BLOOD VESSLES
Thromboangiitis Obliterans (Buerger's Disease)
1. Acute, inflammatory disorder affecting medium/smaller arteries and veins of
the lower extremities. Occurs as focal, obstructive process; results in occlusion
of a vessel with subsequent development of collateral circulation.
2. Most often affects men ages 25-40
3. Disease is idiopathic; high incidence among smokers.
2. Medical management: see Arteriosclerosis Obliterans, above; only really effective
treatment is cessation of smoking.
1. Intermittent claudication, sensitivity to cold (skin of extremity may at first be

white, changing to blue, then red)
2. Decreased or absent peripheral pulses (posterior tibial and dorsalis pedis),
trophic changes, ulceration and gangrene (advanced)
3. Diagnostic tests: same as in Arteriosclerosis Obliterans except no elevation in
serum triglycerides
1. Prepare client for surgery.

1. Drug regimen (vasodilators, anticoagulants, analgesics) to include
names, dosages, frequency, and side effects
2. Need to avoid trauma to the affected extremity
3. Need to maintain warmth, especially in cold weather
4. Importance of stopping smoking.
Arteriosclerosis Obliterans
1. A chronic occlusive arterial disease that may affect the abdominal aorta or the
lower extremities. The obstruction to blood flow with resultant ischemia
usually affects the femoral, popliteal, aortal, and iliac arteries.
2. Occurs most often in men ages 50-60
3. Caused by atherosclerosis
4. Risk factors: cigarette smoking, hyperlipidemia, hypertension, diabetes
mellitus
1. Drug therapy
1. Vasodilators: papaverine, isoxsuprine HCl (Vasodilan), nylidrin HCl
(Arlidin), nicotinyl alcohol (Roniacol), cyclandelate (Cyclospasmol),
tolazoline HCl (Priscoline) to improve arterial circulation;
effectiveness questionable
2. Analgesics to relieve ischemic pain
3. Anticoagulants to prevent thrombus formation
4. Lipid-reducing drug: cholestyramine (Questran), colestipol HCl
(Cholestid), dextrothyroxine sodium (Choloxin), clofibrate (Atromid-
S), gemfibrozil (Lopid), niacin, lovastatin (Mevacor) (see Unit 2)
2. Surgery: bypass grafting, endarterectomy, balloon catheter dilation; lumbar
sympathectomy (to increase blood flow), amputation may be necessary
1. Pain, both intermittent claudication and rest pain, numbness or tingling of the
toes
2. Pallor after 1-2 minutes of elevating feet, and dependent hyperemia/rubor;
diminished or absent dorsalis pedis, posterior tibial and femoral pulses; trophic
changes; shiny, taut skin with hair loss on lower legs
3. Diagnostic tests
1. Oscillometry may reveal decrease in pulse volume

2. Doppler ultrasound reveals decreased blood flow through affected
vessels
3. Angiography reveals location and extent of obstructive process
2. Elevated serum triglycerides; sodium
1. Encourage slow, progressive physical activity (out of bed at least 3-4

times/day, walking 2 times/day).
3. Assist with Buerger-Allen exercises q.i.d.
1. Client lies with legs elevated above heart for 2-3 minutes
2. Client sits on edge of bed with legs and feet dependent and exercises
feet and toes--upward and downward, inward and outward--for 3
minutes
3. Client lies flat with legs at heart level for 5 minutes
2. Assess for sensory function and trophic changes.
3. Protect client from injury.
1. Restricted kcal, low-saturated-fat diet; include family (see Related

Links: Special Diets)
2. Importance of continuing with established exercise program
3. Measures to reduce stress (relaxation techniques, biofeedback)
4. Importance of avoiding smoking, constrictive clothing, standing in any
position for a long time, injury
5. Importance of foot care, immediately taking care of cuts, wounds,
injuries
2. Prepare client for surgery if necessary.
IDIOPATHIC THROMBOCYTOPENIC PURPURA
1. Increased destruction of platelets with resultant platelet count of less than
100,000/mm3 characterized by petechiae and ecchymoses of the skin
2. Exact cause unknown; may be an autoimmune mechanism; onset sudden,
often preceded by a viral illness
3. The spleen is the site for destruction of platelets; spleen is not enlarged
1. Drug therapy: steroids and immunosuppressive agents

2. Platelet transfusion
3. Surgery: splenectomy
1. Petechiae: spider-web appearance of bleeding under skin due to small size of

platelets
2. Ecchymosis
3. Blood in any body secretions, bleeding from mucous membranes, nosebleeds
4. Diagnostic tests: platelet count decreases, anemia
1. Control bleeding
1. Administer platelet transfusions as ordered.
2. Apply pressure to bleeding sites as needed.
3. Position bleeding part above heart level if possible.
2. Prevent bruising.
3. Provide support to client and be sensitive to change in body image.
4. Protect from infection.
5. Measure normal circumference of extremities for baseline.
6. Administer medications orally, rectally, or IV, rather than IM; if administering
immunizations, give subcutaneously (SC) and hold pressure on site for 5
minutes.
7. Administer analgesics (acetaminophen) as ordered; avoid aspirin.
8. Provide care for the client with a splenectomy (see Splenectomy, in Unit 4).
1. Pad crib and playpen, use rugs wherever possible.

2. Provide soft toys.
3. Sew pads in knees and elbows of clothing.
4. Provide protective headgear during toddlerhood.
5. Use soft Toothettes instead of bristle toothbrushes.
6. Keep weight to low normal to decrease extra stress on joints.
7. Use stool softeners to prevent straining.
8. Avoid contact sports; suggest swimming, biking, golf, pool.
VARICOSE VEINS
1. Dilated veins that occur most often in the lower extremities and trunk. As the
vessel dilates, the valves become stretched and incompetent with resultant
venous pooling/edema
2. Most common between ages 30 and 50
3. Predisposing factor: congenital weakness of the veins, thrombophlebitis,
pregnancy, obesity, heart disease
2. Medical management: vein ligation (involves ligating the saphenous vein where it
joins the femoral vein and stripping the saphenous vein system from groin to ankle)
1. Pain after prolonged standing (relieved by elevation)

2. Swollen, dilated, tortuous skin veins
3. Diagnostic tests
1. Trendelenburg test: varicose veins distend very quickly (less than 35
seconds)
2. Doppler ultrasound: decreased or no blood flow heard after calf or
thigh compression
1. Elevate legs above heart level.

2. Measure circumference of ankle and calf daily.
3. Apply knee-length elastic stockings.
4. Provide adequate rest.
5. Prepare client for vein ligation, if necessary.
1. Provide routine pre-op care.

2. In addition to routine post-op care
1. keep affected extremity elevated above the level of the heart to
prevent edema.
2. apply elastic bandages and stockings, which should be removed
every 8 hours for short periods and reapplied.
3. assist out of bed within 24 hours, ensuring that elastic stockings
are applied.
4. assess for increased bleeding, particularly in the groin area.
2. Provide client teaching and discharge planning: same as for thrombophlebitis
(see Thrombophlebitis).
THROMBOPHLEBITIS
1. Inflammation of the vessel wall with formation of a clot (thrombus); may
affect superficial or deep veins.
2. Most frequent veins affected are the saphenous, femoral, and popliteal.
3. Can result in damage to the surrounding tissues, ischemia, and necrosis.
4. Risk factors: obesity, CHF, prolonged immobility, MI, pregnancy, oral
contraceptives, trauma, sepsis, cigarette smoking, dehydration, severe
anemias, venous cannulation, complication of surgery
1. Anticoagulant therapy
1. Heparin
1. blocks conversion of prothrombin to thrombin and reduces
formation or extension of thrombus
2. side effects: spontaneous bleeding, injection site reactions,
ecchymoses, tissue irritation and sloughing, reversible transient
alopecia, cyanosis, pain in arms or legs, thrombocytopenia
2. Warfarin (coumadin)
1. blocks prothrombin synthesis by interfering with vitamin K

synthesis
2. side effects
1. GI: anorexia, nausea and vomiting, diarrhea, stomatitis
2. hypersensitivity: dermatitis, urticaria, pruritus, fever
3. other: transient hair loss, burning sensation of feet,
bleeding complications
2. Surgery
1. Vein ligation and stripping (see Thrombophlebitis)

2. Venous thrombectomy: removal of a clot in the iliofemoral region
3. Plication of the inferior vena cava: insertion of an umbrella-like
prosthesis into the lumen of the vena cava to filter incoming clots
1. Pain in the affected extremity

2. Superficial vein: tenderness, redness, induration along course of the vein
3. Deep vein: swelling, venous distension of limb, tenderness over involved vein,
positive Homan's sign, cyanosis
4. Elevated WBC and ESR
5. Diagnostic tests
1. Venography (phlebography): increased uptake of radioactive material

2. Doppler ultrasonography: impairment of blood flow ahead of thrombus
3. Venous pressure measurements: high in affected limb until collateral
circulation is developed
1. Provide bed rest, elevating involved extremity to increase venous return and
decrease edema.
2. Apply continuous warm, moist soaks to decrease lymphatic congestion.
3. Administer anticoagulants as ordered
1. Heparin
1. monitor PTT; dosage should be adjusted to keep PTT between

1.5-2.5 times normal control level.
2. use infusion pump to administer IV heparin.
3. ensure proper injection technique.
1. use 26- or 27-gauge syringe with 1/2-5/8-in needle,

inject into fatty layer of abdomen above iliac crest.
2. avoid injecting within 2 inches of umbilicus.
3. insert needle at 90° to skin.
4. do not withdraw plunger to assess blood return.
5. apply gentle pressure after removal of needle, avoid
massage.
2. assess for increased bleeding tendencies (hematuria;
hematemesis; bleeding gums; petechiae of soft palate,
conjunctiva, retina; ecchymoses, epistaxis, bloody sputum,
melena) and instruct patient to observe for and report these.
3. have antidote (protamine sulfate) available.
4. instruct client to avoid aspirin, antihistamines, and cough
preparations containing glyceryl guaiacolate, and to obtain
physician's permission before using other OTC drugs.
2. Warfarin (Coumadin)
1. assess PT daily; dosage should be adjusted to maintain PT at

1.5-2.5 times normal control level; INR of 2.
2. obtain careful medication history (there are many drug-drug
interactions).
3. advise client to withhold dose and notify physician immediately
if bleeding or signs of bleeding occur (see Heparin, above).
4. instruct client to use a soft toothbrush and to floss gently.
5. have antidote (vitamin K) available.
6. alert client to factors that may affect the anticoagulant response
(high-fat diet or sudden increases in vitamin K-rich foods).
7. instruct client to wear Medic-Alert bracelet.
2. Assess vital signs every 4 hours.
3. Monitor for chest pain or shortness of breath (possible pulmonary embolism).
4. Measure thighs, calves, ankles, and instep every morning.
1. Need to avoid standing, sitting for long periods; constrictive clothing;
crossing legs at the knees; smoking; oral contraceptives
2. Importance of adequate hydration to prevent hypercoagulability
3. Use of elastic stockings when ambulatory
4. Importance of planned rest periods with elevation of the feet
5. Drug regimen
6. Plan for exercise/activity
1. begin with dorsiflexion of the feet while sitting or lying down

2. swim several times weekly
3. gradually increase walking distance
2. Importance of weight reduction if obese
PULMONARY EMBOLISM
1. Most pulmonary emboli arise as detached portions of venous thrombi formed
in the deep veins of the legs, right side of the heart, or pelvic area.
2. Distribution of emboli is related to blood flow; emboli involve the lower lobes
of the lung because of higher blood flow.
3. Embolic obstruction to blood flow increases venous pressure in the pulmonary
artery and pulmonary hypertension.
4. Risk factors: venous thrombosis, immobility, pre- and post-op states, trauma,
pregnancy, CHF, use of oral contraceptives, obesity
1. Drug therapy
1. Anticoagulants (see Thrombophlebitis)
2. Thrombolytics: streptokinase or urokinase
3. Dextran 70 to decrease blood viscosity and aggregation of blood cells
4. Narcotics for pain relief
5. Vasopressors (in the presence of shock)
2. Surgery: embolectomy (surgical removal of an embolus from the pulmonary
arteries)
1. Chest pain (pleuritic), severe dyspnea, feeling of impending doom

2. Tachypnea, tachycardia, anxiety, hemoptysis, shock symptoms (if massive)
3. Decreased pCO2; increased pH (due to hyperventilation)
4. Increased temperature
5. Intensified pulmonic S2; rales or crackles
6. Diagnostic tests
1. Pulmonary angiography: reveals location/extent of embolism

2. Lung scan reveals adequacy/ inadequacy of pulmonary circulation
1. Administer medications as ordered; monitor effects and side effects.

2. Administer oxygen therapy to correct hypoxemia.
3. Assist with turning, coughing, deep breathing, and passive ROM exercises.
4. Provide adequate hydration to prevent hypercoagulability.
5. Offer support/reassurance to client/family.
6. Elevate head of bed to relieve dyspnea
7. Provide client teaching and discharge planning: same as for thrombophlebitis.
HYPERTENSION
1. According to the World Health Organization, hypertension is a persistent
elevation of the systolic blood pressure above 140 mm Hg and of the diastolic
above 90 mm Hg.
2. Types
1. Essential (primary, idiopathic): marked by loss of elastic tissue and
arteriosclerotic changes in the aorta and larger vessels coupled with
decreased caliber of the arterioles
2. Benign: a moderate rise in blood pressure marked by a gradual onset
and prolonged course
3. Malignant: characterized by a rapid onset and short dramatic course
with a diastolic blood pressure of more than 150 mm Hg
4. Secondary: elevation of the blood pressure as a result of another
disease such as renal parenchymal disease, Cushing's disease,
pheochromocytoma, primary aldosteronism, coarctation of the aorta
3. Essential hypertension usually occurs between ages 35 and 50; more common
in men over 35, women over 45; African-American men affected twice as
often as white men/women
4. Risk factors for essential hypertension include positive family history, obesity,
stress, cigarette smoking, hypercholesteremia, increased sodium intake
1. Diet and weight reduction (restricted sodium, kcal, cholesterol)

2. Life-style changes: alcohol moderation, exercise regimen, cessation of
smoking
3. Antihypertensive drug therapy (see Table 2.17, in Unit 2)
1. Pain similar to anginal pain; pain in calves of legs after ambulation or exercise
(intermittent claudication); severe occipital headaches, particularly in the
morning; polyuria; nocturia; fatigue; dizziness; epistaxis; dyspnea on exertion
2. Blood pressure consistently above 140/90, retinal hemorrhages and exudates,
edema of extremities (indicative of right-sided heart failure)
3. Rise in systolic blood pressure from supine to standing position (indicative of
essential hypertension)
4. Diagnostic tests; elevated serum uric acid, sodium, cholesterol levels
1. Record baseline blood pressure in three positions (lying, sitting, standing) and
in both arms.
2. Continuously assess blood pressure and report any variables that relate to
changes in blood pressure (positioning, restlessness).
3. Administer antihypertensive agents as ordered; monitor closely and assess for
side effects.
4. Monitor intake and hourly outputs.
1. Risk factor identification and development/implementation of methods

to modify them
2. Restricted sodium, kcal, cholesterol diet; include family in teaching
(see Related Links: Special Diets)
3. Antihypertensive drug regimen (include family); see Table 2.17, in
Unit 2
1. names, actions, dosages, and side effects of prescribed
medications
2. take drugs at regular times and avoid omission of any doses
3. never abruptly discontinue the drug therapy
4. supplement diet with potassium-rich foods if taking potassium-
wasting diuretics
5. avoid hot baths, alcohol, or strenuous exercise within 3 hours of
taking medications that cause vasodilation
4. Development of a graduated exercise program
5. Importance of routine follow-up care
Hypertension
 Hypertension, or high blood pressure (BP), 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).
 Contributing factors to the development of hypertension include cardiovascular risk
factors combined with socioeconomic conditions and ethnic differences.
 Hypertension is generally an asymptomatic condition. Individuals who remain
undiagnosed and untreated for hypertension present the greatest challenge and
opportunity for health care providers.
 Is the most important modifiable risk factor for stroke.
o High blood pressure increases the risk of ischemic heart disease by 3-4 fold
o The incidence of stroke increases approximately 8 fold in persons with
definite hypertension
o It has been estimated that 40% of cases of acute MI or stroke are attributable
to hypertension
Etiology of Hypertension
 Primary (essential or idiopathic) hypertension: elevated BP without an identified

cause; accounts for 90% to 95% of all cases of hypertension.
 Secondary hypertension: elevated BP with a specific cause; accounts for 5% to 10%
of hypertension in adults.
Pathophysiology
PATHOPHYSIOLOGY OF PRIMARY HYPERTENSION
 The hemodynamic hallmark of hypertension is persistently increased SVR.

 Water and sodium retention: A high-sodium intake may activate a number of
pressor mechanisms and cause water retention.
 Altered renin-angiotensin mechanism: High plasma renin activity (PRA) results in
the increased conversion of angiotensinogen to angiotensin I causing arteriolar
constriction, vascular hypertrophy, and aldosterone secretion.
 Stress and increased SNS activity: Arterial pressure is influenced by factors such as
anger, fear, and pain. Physiologic responses to stress, which are normally protective,
may persist to a pathologic degree, resulting in prolonged increase in SNS activity.
Increased SNS stimulation produces increased vasoconstriction, increased HR, and
increased renin release.
 Insulin resistance and hyperinsulinemia: Abnormalities of glucose, insulin, and
lipoprotein metabolism are common in primary hypertension. Additional pressor
effects of insulin include vascular hypertrophy and increased renal sodium
reabsorption.
 Endothelial cell dysfunction: Some hypertensive people have a reduced vasodilator
response to nitric oxide. Nitric oxide, an endothelium-derived relaxing factor (EDRF),
helps maintain low arterial tone at rest, inhibits growth of the smooth muscle layer,
and inhibits platelet aggregation. Endothelin produces pronounced and prolonged
vasoconstriction.
Clinical Manifestations of Hypertension
 Often called the “silent killer” because it is frequently asymptomatic until it becomes
severe and target organ disease occurs.
 Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney
(nephrosclerosis), and eyes (retinal damage).
 Hypertension is a major risk factor for coronary artery disease (CAD).
 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.
 Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels,
leading to the development of peripheral vascular disease, aortic aneurysm, and aortic
dissection.
 Intermittent claudication (ischemic muscle pain precipitated by activity and relieved
with rest) is a classic symptom of peripheral vascular disease involving the arteries.
 Hypertension is one of the leading causes of end-stage renal disease, especially
among African Americans. The earliest manifestation of renal dysfunction is usually
nocturia.
 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.
Classification of Hypertension: WHO/ISH*
Category Systolic Diastolic

Optimal < 120 <80
Normal <130 <85
High Normal 130-139 85-89
Grade 1 (mild hypertension) 140-159 90-99

- Subgroup: borderline 140-149 90-94
Grade 2 (moderate hypertension) 160-179 100-109
Grade 3 (severe Hypertension) ≥ 180 ≥110
Isolated Systolic Hypertension (ISH) ≥140 <90

- Subgroup (borderline) 140-149 <90
World Health Organization –ISH International Society of Hypertension
National Institutes of Health Classification
Category Systolic Diastolic
Optimal < 120 <80
Pre-hypertensive 120-139 80-89
Hypertensive ≥140 ≥90
Stage 1 140-159 90-99
Stage 2 ≥160 ≥100

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.
 Measurement of serum electrolytes, especially potassium levels, is done to detect
hyperaldosteronism, a cause of secondary hypertension.
 Blood glucose levels assist in the diagnosis of diabetes mellitus.
 Lipid profile provides information about additional risk factors that predispose to
atherosclerosis and cardiovascular disease.
 ECG and echocardiography provide information about the cardiac status.
Nursing and Collaborative Management
 Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm
Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and
less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney
disease).
 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 Restriction of alcohol
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.
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.
o Hypertensive emergency develops over hours to days and is defined as BP that
is severely elevated (more than 180/120 mm Hg) with evidence of acute target
organ damage.
o Hypertensive emergencies can precipitate encephalopathy, intracranial or
subarachnoid hemorrhage, acute left ventricular failure with pulmonary
edema, MI, renal failure, dissecting aortic aneurysm, and retinopathy.
o Hypertensive emergencies require hospitalization, intravenous (IV)
administration of antihypertensive drugs, and intensive care monitoring.
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).
SECTION C: CARDIAC PROBLEMS
PACEMAKERS
1. A pacemaker is an electronic device that provides repetitive electrical
stimulation to the heart muscle to control the heart rate.
2. Artificial pacing system consists of a battery-powered generator and a pacing
wire that delivers the stimulus to the heart.
2. Indications for use
1. Adams-Stokes attack
2. Acute MI with Mobitz II AV block
3. Third-degree AV block with slow ventricular rate
4. Right bundle branch block
5. New left bundle branch block
6. Symptomatic sinus bradycardia
7. Sick sinus syndrome
8. Arrhythmias (during or after cardiac surgery)
9. Drug-resistant tachyarrhythmia
2. Modes of pacing
1. Fixed rate: pacemaker fires electrical stimuli at preset rate, regardless of the
client's rate and rhythm.
2. Demand: pacemaker produces electrical stimuli only when the client's own
heart rate drops below the preset rate per minute on the generator.
2. Types of pacemakers
1. Temporary
1. Used in emergency situations and performed via an endocardial
(transvenous) or transthoracic approach to the myocardium.
2. Performed at bedside or using fluoroscopy.
2. Permanent
1. Endocardial or transvenous procedure involves passing endocardial
lead into right ventricle with subcutaneous implantation of pulse
generator into right or left subclavian areas. Usually done under local
anesthesia.
2. Epicardial or myocardial method involves passing the electrode
transthoracically to the myocardium where it is sutured in place. The
pulse generator is implanted into the abdominal wall.
1. Assess pacemaker function
1. Monitor heart rate, noting deviations from the preset rate.

2. Observe the presence of pacemaker spikes on ECG tracing or cardiac
monitor; spike before P wave with atrial pacemaker; spike before QRS
complex with ventricular pacemaker
3. Assess for signs of pacemaker malfunction, such as weakness, fainting,
dizziness, or hypotension.
2. Maintain the integrity of the system
1. Ensure that catheter terminals are attached securely to the pulse

generator (temporary pacemaker)
2. Attach pulse generator to client securely to prevent accidental
dislodgment (temporary pacemaker)
2. Provide safety and comfort
1. Provide safe environment by properly grounding all equipment in the

room.
2. Monitor electrolyte level periodically, particularly potassium.
2. Prevent infection
1. Assess vital signs, particularly temperature changes.

2. Assess catheter insertion site daily for signs of infection.
3. Maintain sterile dressing over catheter insertion site.
1. Fundamental concepts of cardiac physiology

2. Daily pulse check for one minute
3. Need to report immediately any sudden slowing or increase in pulse rate
4. Importance of adhering to weekly monitoring schedule during first month after
implantation and when battery depletion is anticipated (depending on type of
battery)
5. Wear loose-fitting clothing around the area of the pacemaker for comfort
6. Notify physician of any pain or redness over incision site
7. Avoid trauma to area of pulse generator
8. Avoid heavy contact sports
9. Carry an identification card/bracelet that indicates physician's name, type and
model number of pacemaker, manufacturer's name, pacemaker rate
10. Display identification card and request scanning by hand scanner when going
through weapons detector at airport
11. Remember that periodic hospitalization is necessary for battery
changes/pacemaker unit replacement
PULMONARY EDEMA
1. A medical emergency that usually results from left-sided heart failure. The
capillary pressure within the lungs becomes so great that fluid pours from the
blood into the alveoli, bronchi, and bronchioles. Death occurs by suffocation if
this condition is untreated.
2. Caused by left-sided heart failure, rapid administration of IV fluids.
1. Oxygen therapy
2. Endotracheal/nasotracheal intubation (possible)
3. Drug therapy
1. Morphine sulfate to induce vasodilation and decrease anxiety; 5 mg
IV, administer slowly
2. Digitalis to improve cardiac output
3. Diuretics (furosemide [Lasix] is drug of choice) to relieve fluid
retention
4. Aminophylline to relieve bronchospasm and increase cardiac output;
250-500 mg IV, administer slowly
5. Vasodilators (nitroglycerin, isosorbide dinitrate) to dilate the vessels,
thereby reducing amount of blood returned to the heart
4. Rotating tourniquets or phlebotomy
1. Dyspnea
2. Cough with large amounts of blood-tinged sputum
3. Tachycardia, pallor, wheezing, rales or crackles, diaphoresis
4. Restlessness, fear/anxiety
5. Jugular vein distension
6. Decreased pO2, increased pCO2, elevated CVP
1. Assist with intubation (if necessary) and monitor mechanical ventilation.

2. Administer oxygen by mask in high concentrations (40%-60%) if not
intubated.
3. Place client in semi-Fowler's position or over bedside table to ease dyspnea.
5. Apply and monitor rotating tourniquets.
1. Occlude vessels of each limb for no more than 45 minutes at a time.

2. Rotate in a clockwise fashion every 15 minutes.
3. Assess continuously for presence of arterial pulses.
4. Observe skin for signs of irritation.
5. When discontinuing, remove 1 tourniquet every 15 minutes to avoid
rapid influx of fluid to the heart.
2. Assist with phlebotomy (removal of 300-500 ml of blood from a peripheral
vein) if performed.
3. CVP/hemodynamic monitoring.
1. Prescribed medications, including name, purpose, schedule, dosage,

and side effects
2. Dietary restrictions: low sodium, low cholesterol
3. Importance of adhering to planned rest periods with gradual
progressive increase in activities
4. Daily weights
5. Need to report the following symptoms to physician immediately:
dyspnea, persistent productive cough, pedal edema, restlessness
CPR
1. General information: process of externally supporting the circulation and respiration

of a person who has had a cardiac arrest
2. Nursing interventions: unwitnessed cardiac arrest
1. Assess LOC.
1. Shake victim's shoulder and shout.
2. If no response, summon help.
2. Position victim supine on a firm surface.
3. Open airway.
1. Use head tilt, chin lift maneuver.

2. Place ear over nose and mouth.
1. look to see if chest is moving.
2. listen for escape of air.
3. feel for movement of air against face.
3. If no respiration, proceed to #4.
2. Ventilate twice, allowing for deflation between breaths.
3. Assess circulation: palpate for carotid pulse; if not present, proceed to #6.
4. Initiate external cardiac compressions
1. Proper placement of hands: lower half of the sternum

2. Depth of compressions: 1 1/2-2 inches for adults
3. One rescuer: 15 compressions (at rate of 80-100 per minute) with 2
ventilations
4. Two rescuers: 5 compressions (at rate of 80-100 per minute) with 1
ventilation
CARDIAC ARREST
1. General information: sudden, unexpected cessation of breathing and adequate

circulation of blood by the heart
1. Cardiopulmonary resuscitation (CPR); see below
2. Drug therapy
1. Lidocaine, procainamide, verapamil
2. Dopamine (Intropin), isoproterenol (Isuprel), norepinephrine
(Levophed): see also Drugs Used to Treat Shock, Table 4.9
3. Epinephrine to enhance myocardial automaticity, excitability,
conductivity, and contractility
4. Atropine sulfate to reduce vagus nerve's control over the heart, thus
increasing the heart rate
5. Sodium bicarbonate: administered during first few moments of a
cardiac arrest to correct respiratory and metabolic acidosis
6. Calcium chloride: calcium ions help the heart beat more effectively by
enhancing the myocardium's contractile force
3. Defibrillation (electrical countershock)
3. Assessment findings: unresponsiveness, cessation of respiration, pallor, cyanosis,
absence of heart sounds/blood pressure/palpable pulses, dilation of pupils, ventricular
fibrillation (if client on a monitor)
4. Nursing interventions: monitored arrest caused by ventricular fibrillation
1. Begin precordial thump and, if successful, administer lidocaine.

2. If unsuccessful, defibrillation.
3. If defibrillation unsuccessful, initiate CPR immediately.
4. Assist with administration of and monitor effects of additional emergency
drugs.
PERICARDITIS
1. An inflammation of the visceral and parietal pericardium
2. Caused by a bacterial, viral, or fungal infection; collagen diseases; trauma;
acute MI; neoplasms; uremia; radiation therapy; drugs (procainamide,
hydralazine, doxorubicin HCl [Adriamycin])
1. Determination and elimination/control of underlying cause

2. Drug therapy
1. Medication for pain relief
2. Corticosteroids, salicylates (aspirin), and indomethacin (Indocin) to
reduce inflammation
3. Specific antibiotic therapy against the causative organism may be
indicated.
1. Chest pain with deep inspiration (relieved by sitting up), cough, hemoptysis,
malaise
2. Tachycardia, fever, pleural friction rub, cyanosis or pallor, accentuated
component of S2, pulsus paradoxus, jugular vein distension
3. Elevated WBC and ESR, normal or elevated AST (SGOT)
4. Diagnostic tests
1. Chest x-ray may show increased heart size if effusion occurs

2. ECG changes: ST elevation (precordial leads and 2- or 3-limb heads),
T wave inversion
1. Ensure comfort: bed rest with semi- or high-Fowler's position.

2. Monitor hemodynamic parameters carefully.
3. Administer medications as ordered and monitor effects.
1. Signs and symptoms of pericarditis indicative of a recurrence (chest

pain that is intensified by inspiration and position changes, fever,
cough)
2. Medication regimen including name, purpose, dosage, frequency, side
effects.
ENDOCARDITIS
1. Inflammation of the endocardium; platelets and fibrin deposit on the mitral
and/or aortic valves causing deformity, insufficiency, or stenosis.
2. Caused by bacterial infection: commonly S. aureus, S. viridans, B-hemolytic
streptococcus, gonococcus
3. Precipitating factors: rheumatic heart disease, open-heart surgery procedures,
GU/Ob-Gyn instrumentation/surgery, dental extractions, invasive monitoring,
septic thrombophlebitis
1. Drug therapy
1. Antibiotics specific to sensitivity of organism cultured
2. Penicillin G and streptomycin if organism not known
3. Antipyretics
2. Cardiac surgery to replace affected valve
1. Fever, malaise, fatigue, dyspnea and cough (if extensive valvular damage),
acute upper quadrant pain (if splenic involvement), joint pain
2. Petechiae, murmurs, edema (if extensive valvular damage), splenomegaly,
hemiplegia and confusion (if cerebral infarction), hematuria (if renal
infarction)
3. Elevated WBC and ESR, decreased Hgb and Hct
4. Diagnostic tests: positive blood culture for causative organism
1. Administer antibiotics as ordered to control the infectious process.

2. Control temperature elevation by administration of antipyretics.
3. Assess for vascular complications (see Thrombophlebitis, and Pulmonary
Embolism).
1. Types of procedures/treatments (e.g., tooth extractions, GU

instrumentation) that increase the chances of recurrences
2. Antibiotic therapy, including name, purpose, dose, frequency, side
effects
3. Signs and symptoms of recurrent endocarditis (persistent fever, fatigue,
chills, anorexia, joint pain)
4. Avoidance of individuals with known infections.
CARDIAC TAMPONADE
1. An accumulation of fluid/blood in the pericardium that prevents adequate
ventricular filling; without emergency treatment client will die in shock.
2. Caused by blunt or penetrating chest trauma, malignant pericardial effusion;
can be a complication of cardiac surgery
2. Medical management: emergency treatment of choice is pericardiocentesis (insertion
of a needle into the pericardial sac to aspirate fluid/blood and relieve the pressure on
the heart)
1. Chest pain
2. Hypotension, distended neck veins, tachycardia, muffled or distant heart
sounds, paradoxical pulse, pericardial friction rub
3. Elevated CVP, decreased Hgb and Hct if massive hemorrhage
4. Diagnostic test: chest x-ray reveals enlarged heart and widened mediastinum.
1. Administer oxygen therapy

2. Monitor CVP/IVs closely
3. Assist with pericardiocentesis.
1. Monitor ECG, blood pressure, and pulse.
2. Assess aspirated fluid for color, consistency.
3. Send specimen to lab immediately.
CORONARY ARTERY DISEASE

Description
 Is characterized by the accumulation of plaque within coronary arteries, which

progressively enlarge, thicken and calcify. This causes critical narrowing of the
coronary artery lumen (75% occlusion), resulting in a decrease in coronary blood flow
and an inadequate supply of oxygen to the heart muscle.
 Ischemia may be silent (asymptomatic but evidenced by ST depression of 1 mm or
more on electrocardiogram (ECG) or may be manifested by angina pectoris (chest
pain).
 Risk factor for Coronary Artery Disease include dyslipidemia, smoking, hypertension,
male gender (women are protected until menopause), aging, non-white race, family
history, obesity, sedimentary lifestyle, diabetes mellitus, metabolic syndrome,
elevated homocysteine, and stress.
 Acute coronary syndrome is a complication of CAD due to lack of oxygen to the
myocardium. Mnaifestations include unstable angina, non ST-segment elevation
infarction, and ST-segment elevation infarction.
 Other causes of angina include coronary artery spasm, aortic stenosis,
cardiomyopathy, severe anemia, and thyrotoxicosis.
Risk Factors
Modifiable

 Cigarette smoking
 Elevated blood pressure
 High blood cholesterol (hyperlipidemia)
 Hyperglycemia (diabetes mellitus)
 Obesity
 Physical inactivity
 Use of oral contraceptives
 Infection (e.g., gingivitis): possibly associated
 Behavior patterns ( stress, aggressiveness, hostility)
 Geography: higher incidence in industrialize regions
Non-modifiable
 Positive family history ( first degree relative with cardiovascular disease at age 55 or
less for males at age 65 or less for female
 Age ( more than 45 yrs. for men, more than 55 yrs for women)
 Gender ( occurs 3 times more often in men than in women)
 Race: higher incidence in Africans Americans than in Caucasian.
Assessment
Chest pain is provoked by exertion or stress and is relieved by nitroglycerin and rest.
1. Character. Substernal chest pain, pressure, heaviness, or discomfort. Other sensations

include a squeezing, aching, burning, choking, strangling, or cramping pain.
2. Severity. Pain maybe mild or severe and typically present with a gradual buildup of
discomfort and subsequent gradual fading away.
3. Location. Behind middle or upper third of sternum; the patient will generally will
make a fist over the site of pain (positive Levine sign; indicates diffuse deep visceral
pain), rather than point to it with fingers.
4. Radiation. Usually radiates to neck, jaw, shoulders, arms, hands, and posterior
intrascapular area. Pain occurs more commonly on the left side than the right; may
produce numbness or weakness in arms, wrist, or hands.
5. Duration. Usually last 2 to 10 minutes after stopping activity; nitroglycerin relieves
pain within 1 minute.
6. Precipitating factors. Physical activity, exposure to hot or cold weather, eating a
heavy meal, and sexual intercourse increase the workload of the heart and, therefore,
increase oxygen demand.
7. Associated manifestation. Diaphoresis, nausea, indigestion, dyspnea, tachycardia, and
increase in blood pressure.
8. Signs of unstable angina:
 A change in frequency, duration, and intensity of stable angina symptoms.

 Angina pain last longer than 10 minutes, is unrelieved by rest or sublingual
nitroglycerin, and mimics signs and symptoms of impending myocardial infarction.
1. Resting ECG may show left ventricular hypertrophy, ST-T changes, arrhythmias, and
possible Q waves.
2. Exercise stress testing with or without perfusion studies shows ischemia.
3. Cardiac catheterization shows blocked vessels.
4. Position emission tomography may show small perfusion defects.
5. Radionuclide ventriculography shows wall motion abnormalities and ejection
fraction.
6. Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein,
lipoprotein A, homocysteine, and triglycerides may be abnormal.
7. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies.
Primary Nursing Diagnosis
 Altered tissue perfusion (myocardial) related to narrowing of the coronary artery(ies)

associated with atherosclerosis, spasm, and/or thrombosis
Other Diagnoses that may occur in Nursing Care Plans For CAD
 Acute pain
 Risk for decreased cardiac output
 Anxiety
 Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care,
and discharge needs
Medical Management
The goals of medical management are to decrease the oxygen demands of the myocardium
and to increase the oxygen supply through pharmacological therapy and risk factor control
Surgical Interventions
1. Percutaneous transluminal coronary angioplasty or intracoronary atherectomy, or

placement of intracoronarystent.
2. Coronary artery bypass grafting.
3. Transmyocardial revascularization.
Pharmacologic Intervention
1. Antianginal medications (nitrates, beta-adrenergic blockers, calcium channel blockers,

and angiotensin converting enzyme inhibitors) to promote a favorable balance of
oxygen supply and demand.
2. Antilipid medications to decrease blood cholesterol and tricglyceride levels in patients
with elevated levels.
3. Antiplatelet agents to inhibit thrombus formation.
4. Folic acid and B complex vitamins to reduce homocysteine levels.
Nursing Intervention
1. Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an
anginal attack.
2. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor
for arrhythmias and ST elevation.
3. Place patient in comfortable position and administer oxygen, if prescribed, to enhance
myocardial oxygen supply.
4. Identify specific activities patient may engage in that are below the level at which
anginal pain occurs.
5. Reinforce the importance of notifying nursing staff whenever angina pain is
experienced.
6. Encourage supine position for dizziness caused by antianginals.
7. Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic
blocker and calcium channel blocker therapy. These drug must be tapered to prevent a
“rebound phenomenon”; tachycardia, increase in chest pain, and hypertension.
8. Explain to the patient the importance of anxiety reduction to assist to control angina.
9. Teach the patient relaxation techniques.
10. Review specific factors that affect CAD development and progression; highlight those
risk factors that can be modified and controlled to reduce the risk.
Documentation Guidelines
 Episodes of angina describing character, location, and severity of pain; precipitating

or mitigating factors; interventions; and evaluation
 Patient teaching about disease process and planned treatments, including medication
regimen
 Perioperative hemodynamic response: Pulmonary and systemic arterial pressures,
presence of pulses, capillary refill, urine output
 Pulmonary assessment: Breath sounds, ventilator settings, response to mechanical
ventilation, secretions
 Complications: Bleeding, blood gas alterations, fluid volume deficit, hypotension,
dysrhythmias, hypothermia
 Coping: Patient and family
 Mediastinal drainage and autotransfusion
Discharge and Home Healthcare Guidelines
 PREVENTION. Review the risk factor and lifestyle modifications that are
acceptable to the patient and her or his family members.
 MEDICATIONS. Be certain that the patient and appropriate family members
understand all medications, including the correct dosage, route, action, and adverse
effects.
 PERIOPERATIVE
o Care of Incision. Often the incision heals with no home healthcare, but the
patient needs to know the signs of infection.
o Activity Restrictions. The activity recommendations will depend on the type
and extent of the patient’s underlying condition.
Sources:
ADAM for images
Marilyn Sawyer Sommers, RN, PhD, FAAN , Susan A. Johnson, RN, PhD, Theresa A.
Beery, PhD, RN , DISEASES AND DISORDERS A Nursing Therapeutics Manual, 2007 3rd
ed
Nursing crib.com
Handbook for Brunner & Suddarth’s, Textbook of Medical-SurgicalNursing, 11th ed
ANGINA PECTORIS
Description
1. Angina is chest pain resulting from myocardial ischemia caused by inadequate

myocardial blood and oxygen supply.
2. Angina is caused by an imbalance between oxygen supply and demand.
3. Causes include obstruction of coronary blood flow because of atherosclerosis,
coronary artery spasm, and conditions increasing myocardial oxygen consumption.
4. The goal of treatment is to provide relief of an acute attack, correct the imbalance
between myocardial oxygen supply and demand, and prevent the progression of the
disease ad further attacks to reduce the risk of MI.
Patterns of angina
1. Stable angina
 Stable angina also called exertional angina.

 Stable angina occurs with activities that involve exertion or emotional stress and is
relieved with rest or nitroglycerin.
 Stable angina usually has a stable pattern of onset, duration, severity, and relieving
factors.
2. Unstable angina
 Unstable angina also is called preinfarction angina.

 Unstable angina occurs with an unpredictable degree of exertion or emotion and
increases in occurrence, duration, and severity over time.
 Pain may not be relieved with nitroglycerin.
3. Variant angina
 Variant angina also is called Prinzmetal’s or vasospastic angina.

 Variant angina results from coronary artery spasm.
 Variant angina may occur at rest.
 Attacks may be associated with ST segment elevation noted on the electrocardiogram.
4. Intractable angina is a chronic, incapacitating angina that is unresponsive to
interventions.
5. Preinfarction angina
 Preinfarction angina is associated with acute coronary insufficiency.

 Preinfarction angina lasts longer than 15 minutes.
 Preinfarction angina is a symptom of worsening cardiac ischemia.
6. Postinfarction angina occurs after an MI, when residual ischemia may cause episodes of
angina.
Risk Factors
 Atherosclerosis
 Hypertension
 Diabetes Mellitus
 Thromboangitis Obliterans
 Polycythemia Vera
 Aortic Regurgitation
Assessment
1. Pain
a. Pain can develop slowly or quickly.
b. Pain usually is described as mild or moderate.
c. Substernal, crushing, squeezing, pain may occur.
d. Pain may radiate to the shoulders, arms, jaw, neck, and back.
e. Pain usually lasts less than 5 minutes, however, pain can last up to 15 to 20 minutes.
f. Pain is relieved by nitroglycerin or rest.
2. Dyspnea
3. Pallor
4. Sweating
5. Palpitations and tachycardia
6. Dizziness and faintness
7. Hypertension
8. Digestive disturbances
1. Electrocardiogram: Readings are normal during rest, with ST depression or elevation

and/or T wave inversion during an episode of pain.
2. Stress test: Chest pain or changes in the electrocardiogram or vital signs during testing
may indicate ischemia.
3. Cardiac enzymes and troponins: Findings are normal in angina.
4. Cardiac catheterization: Catheterization provides a definitive diagnosis by providing
information about the patency of the coronary arteries.

and associated with atherosclerosis, spasm, or thrombosis
Other Diagnoses that may occur in Nursing Care Plans For Angina
 Acute pain
 Risk for decreased cardiac output
 Anxiety
 Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care,
and discharge needs
Medical Management
The goals of medical management are to decrease the oxygen demands of the myocardium
and to increase the oxygen supply through pharmacologic therapy and risk factor control.
Surgical Management
Frequently, therapy includes a combination of medicine and surgery. Surgically, the goals of
management include revascularization of the blood supply to the myocardium.
 Coronary artery bypass surgery or minimally invasive direct coronary artery bypass
(MIDCAB)
 Percutaneous transluminal coronary angioplasty (PTCA) or percutaneous transluminal
myocardial revascularization (PTMR)
 Application of intracoronary stents and atherectomy to enhance blood flow
 Lasers to vaporize plaques
 Percutaneous coronary endarterectomy to extract obstruction.
 Nitrates, the mainstay of therapy (nitroglycerin)

 Beta-adrenergic blockers (metoprolol [Toprol])
 Calcium ion antagonists and calcium-channel blockers (amlodipine [Norvase] and
diltiazem [Cardizem])
 Antiplatelet and anticoagulant medications (aspirin, clopidogrel (Plavix], ticlopidine
[Ticlid], or heparin)
 Oxygen therapy
Immediate management
1. Assess pain.
2. Provide bed rest.
3. Administer oxygen at 3 L/min by nasal cannula as prescribed.
4. Administer nitroglycerin as prescribed to dilate the coronary arteries, reduce the
oxygen requirements of the myocardium and relieve the chest pain.
5. Obtain a 12-Lead electrocardiogram.
6. Provide continuous cardiac monitoring.
Following acute episode:
1. Instruct the client regarding the purpose of diagnostic medical and surgical procedures
and the preprocedure and postprocedure expectations.
2. Assist the client to identify angina precipitating events.
3. Instruct the client to stop activity and rest if chest pain occurs and to take
nitroglycerin as prescribed.
4. Instruct the client to seek medical attention if pain persists.
5. Instruct the client regarding prescribed medications.
6. Provide diet instructions o the client, stressing that dietary changes are not temporary
and must be maintained or life.
7. Assist the client to identify risk factors that can be modified.
8. Assist the client to set goals that will promote changes in lifestyle to reduce the
impact of risk factors.
9. Assist the client to identify barriers to compliance with therapeutic plan and to
identify methods to overcome barriers.
10. Provide community resources to the client regarding exercise, smoking reduction, and
stress reduction.
 Description of pain: Onset (sudden, gradual), character (aching, sharp, burning,

pressure), precipitating factors, associated symptoms (anxiety, dyspnea, diaphoresis,
dizziness, nausea, cyanosis, pallor), duration, and alleviating factors of the anginal
episode
 Response to prescribed medications
 Reaction to bedrest or limitation in activity
 PREVENTION. Teach the patient factors that may precipitate anginal episodes and
the appropriate measures to control episodes. Teach the patient the modifiable
cardiovascular risk factors and ways to reduce them. Manage risk factors, including
hypertension, diabetes mellitus, obesity, and hyperlipidemia.
 ACTIVITY. Each person has a different level of activity that will aggravate anginal
symptoms. Most patients with stable angina can avoid symptoms during daily
activities by reducing the speed of any activity.
 MEDICATIONS. Be sure the patient understands all medications, including the
dose, route, action, and adverse effects. If the patient’s physician prescribes
sublingual nitroglycerin (NTG), instruct the patient to lie in semi-Fowler position and
take up to three tablets 5 minutes apart to relieve chest discomfort. Instruct the patient
that if relief is not obtained after ingestion of the three tablets, he or she should seek
medical attention immediately. Remind the patient to check the expiration date on the
NTG tablets and to replace the bottle, once it is opened, every 3 to 5 months.
 COMPLICATIONS. Teach the patient the importance of not denying or ignoring
angina episodes and of reporting them to the healthcare provider immediately.
Sources:
ed
Handbook for Brunner & Suddarth’s, Textbook of Medical-SurgicalNursing, 11th ed
MI
Description
 Refers to a dynamic process by which one or more regions of the heart muscle
experience a severe and prolonged decrease in oxygen supply because of insufficient
coronary blood flow. The affected muscle tissue subsequently becomes necrotic.
 Onset of Myocardial Infarction may be sudden or gradual, and the process takes 3 to 6
hours to run its course.
 It is the most serious manifestation of acute coronary syndrome, a complication of
coronary artery disease (CAD).
 Approximately 90% of Myocardial Infarction are precipitated by acute coronary
thrombosis (partial or total) secondary to severe CAD (greater than 70% narrowing of
the artery).
 Other causative factors include coronary artery spasm, coronary artery embolism,
infectious diseases causing arterial inflammation, hypoxia, anemia, and severe
exertion or stress on the heart in the presence of significant coronary artery disease.
Risk Factors
Modifiable
 Infarctions may occur for a variety of reasons, but coronary thrombosis of a coronary
artery narrowed with plaque is the most common cause.
 Other causes include spasms of the coronary arteries; blockage of the coronary
arteries by embolism of thrombi, fatty plaques, air, or calcium; and disparity between
myocardial oxygen demand and coronary arterial supply.
 Multiple risk factors have been identified for coronary artery disease and MI.
 Modifiable risk factors include cigarette smoking, which causes arterial
vasoconstriction and increases plaque formation. A diet high in saturated fats,
cholesterol, sugar, salt, and total calories increases the risk for MIs. Elevated serum
cholesterol and low-density lipoprotein levels increase the chance for atherosclerosis.
Hypertension and obesity increase the workload of the heart, and diabetes mellitus
decreases the circulation to the heart muscle.
 Hostility and stress may also increase sympathetic nervous system activity and pose
risk.
 A sedentary lifestyle diminishes collateral circulation and decreases the strength of
the cardiac muscle.
 Medications can also prevent risks.
 Oral contraceptives may enhance thrombus formation, cocaine use can cause coronary
artery spasm, and anabolic steroid use can accelerate atherosclerosis.
Non-Modifiable
 Some factors—such as age, family history, and gender—cannot be modified.

 Aging increases the atherosclerotic process, family history may increase the risk by
both genetic and environmental influences, and males are more prone to MIs than are
premenopausal women.
 Premenopausal women have the benefit of protective estrogens and a lower
hematocrit, although heart disease is on the rise in this population, possibly because of
an increased rate of smoking in women. Once women become postmenopausal, their
risk for MI increases, as it also does for men over age 50.
Assessment
1. Chest pain
o Character: variable, but often diffuse, steady substernal chest pain. Other
sensations include a crushing and squeezing feeling in the chest. Other
sensations include a crushing and squeezing feeling in the chest.
o Severity: pain may be severe; not relieved by rest or sublingual vasodilator
therapy, requires opioids.
o Location: variable, but often pain resides behind upper or middle third of
sternum.
o Radiation: pain may radiate to the arms (commonly the left), and to the
shoulders, neck, back, or jaw.
o Duration: pain continues for more than 15 minutes.
2. Associated manifestations include anxiety, diaphoresis, cool clammy skin, facial
pallor, hypertension or hypotension, bradycardia or tachycardia, premature ventricular
or atrial beats, palpitations, dyspnea, disorientation, confusion, restlessness, fainting,
marked weakness, nausea, vomiting, and hiccups.
3. Atypical symptoms of MI include epigastric or abdominal distress, dull aching or
tingling sensations, shortness of breath, and extreme fatigue (more frequent in
women).
4. Risk factors for MI include male gender, age over 45 for men, age over 55 for men,
smoking; high blood cholesterol levels, hypertension, family history of premature
CAD, diabetes and obesity.

associated with atherosclerosis, spasm, or thrombosis
1. Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2
to 12 hours, but may take 72 to 96 hours.
o ST-segment depression and T-wave inversion indicate a pattern of ischemia;
ST elevation indicates an injury pattern.
o Q waves indicate tissue necrosis and are permanent.
2. Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and
myoglobulin may be elevated.
3. More specific creatinine phosphokinase isoenzyme CK-MB will be elevated.
4. Triponin T and I are myocardial proteins that increase in the serum about 3 to 4 hours
after an MI, peak in 4 to 24 hours, and are detectable for upto 2 weeks; the test is easy
to run, can help diagnose an MI up to 2 weeks earlier, and only unstable angina causes
a false positive.
5. White blood cell count and sedimentation rate may be elevated.
6. Radionuclide imaging, positron emission tomography, and echocardiography may be
done to evaluate heart muscle.
Medical Management
The goals of medical management are to minimize myocardial damage, preserve myocardial
function, and prevent complications such as lethal dysrrhythmias and cardiogenic shock.
 Oxygen administration is initiated at the onset of chest pain.

 Reperfusion via emergency use of thrombolytic medications or percutaneous coronary
interventions (PCI).
 Coronary artery bypass or minimally invasive direct coronary bypass (MIDCAB).
Medications
 Analgesic
1. For relief of pain. This is a priority. Pain may cause shock.
2. Morphine Sulfate. Lidocaine or Nitroglycerine administered intravenously.
 Thrombolytic Therapy:
1. To disitegrate blood clot by activating the fibrinolytic processes.
2. Streptokinase, urokinase and tissue plasminogen activator (TPA) are currently
used.
3. Adminstration is most crucial between 3 to 6 hours after the initial infarction
has occurred.
4. Detect for occult bleeding during and after thrombolytic therapy
5. Assess neurologic status changes which may indicate G.I. bleeding or cardiac
tamponade.
 Anticoagulant and antiplatelet medications are administered after thrombolytic
therapy to maintain arterial patency.
 Other medications: Beta-adrenergic blockings agents; diazepam (Valium)
1. Pain control drugs to reduce catecholamine-induced oxygen demand to injured heart

muscle.
o Opiate analgesics: Morphine
o Vasodilators: Nitroglycerin
o Anxiolytics: Benzodiazepines
2. Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation
and reduce the size of the infarction.
3. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic
therapy.
4. Reperfusion arrhythmias may follow successful therapy.
5. Beta-adrenergic blockers, to improve oxygen supply and demand, decrease
sympathetic stimulation to the heart, promote blood flow in the small vessels of the
heart, and provide antiarrhythmic effects.
6. Calcium channel blockers, to improve oxygen supply and demand.
1. Monitor continuous ECG to watch for life threatening arrhythmias (common within
24 hours after infarctions) and evolution of the MI (changes in ST segments and T
waves). Be alert for any type of premature ventricular beats- these may herald
ventricular fibrillation or ventricular tachycardia.
2. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs.
Also monitor blood pressure continuously when giving nitroglycerin I.V.
3. Handle the patient carefully while providing care, starting I.V. infusion, obtaining
baseline vital signs, and attaching electrodes for continuous ECG monitoring.
4. Reassure the patient that pain relief is a priority, and administer analgesics promptly.
Place the patient in supine position during administration to minimize hypotension.
5. Emphasize the importance of reporting any chest pain, discomfort, or epigastric
distress without delay.
6. Explain equipment, procedures, and need for frequent assessment to the patient and
significant others to reduce anxiety associated with facility environment.
7. Promote rest with early gradual increase in mobilization to prevent deconditioning,
which occurs during bed rest.
8. Take measures to prevent bleeding if patient is thrombolitic therapy
9. Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation,
hallucinations, diminished pain tolerance, and aggressiveness.
10. Tell the patient that sexual relations may be resumed on advise of health care
provider, usually after exercise tolerance is assessed.
 Response to vasodilators and pain medications

 Physical findings of cardiac functions: Vital signs, heart sounds, breath sounds, urine
output, peripheral pulses, level of consciousness
 Psychosocial response to treatment and diagnosis
 Presence of complications: Bleeding tendencies, respiratory distress, unrelieved chest
pain, constipation
 Be sure the patient understands all the medications, including the dosage, route,
action, and adverse effects. Instruct the patient to keep the nitroglycerin bottle sealed
and away from heat.
 The medication may lose its potency after the bottle has been opened for 6 months. If
the patient does not feel a sensation when the tablet is put under the tongue or does
not get a headache, the pills may have lost their potency.
 Explain the need to treat recurrent chest pain or MI discomfort with sublingual
nitroglycerin every 5 minutes for three doses. If the pain persists for 20 minutes, teach
the patient to seek medical attention. If the patient has severe pain or becomes short of
breath with chest pain, teach the patient to take nitroglycerin and seek medical
attention right away. Explore mechanisms to implement diet control, an exercise
program, and smoking cessation if appropriate.
Sources:
Nursingcrib.com
ADAM for images
UDAN, Medical Surgical Nursing
Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing ,11th ed
HEART FAILURE
Description
1. Congestive Heart Failure or CHF is a severe circulatory congestion due to decreased
myocardial contractility, which results in the heart’s inability to pump sufficient blood
to meet the body’s needs.
2. About 80% of CHF cases occur before 1 year of age
Etiology
1. The primary cause of CHF in the first 3 years of life is CHD.

2. Other causes in children include:
o Other myocardial disorders, such as cardiomyopathies, arrhythmias, and
hypertension
o Pulmonary embolism or chronic lung disease
o Severe hemorrhage or anemia
o Adverse effects of anesthesia or surgery
o Adverse effects of transfusions or infusions
o Increased body demands resulting from conditions such as fever, infection and
arteriovenous fistula
o Adverse effects of drugs, such as doxorubicin
o Severe physical or emotional stress
o Excessive sodium intake
3. In general, causes can be classified according to the following:
o Volume overload may cause the right ventricle to hypertrophy to compensate
for added volume.
o Pressure overload usually results from an obstructive lesion, such as COA
o Decrease contractility can result from problems such as sever anemia,
asphyxia, heart block and acidemia.
o High cardiac output demands occur when the body’s need for oxygen exceeds
the heart’s output s seen in sepsis and hyperthyroidism.
Pathophysiology
 Right ventricular failure occurs when the right ventricle is unable to pump blood into
the pulmonary circulation. Less blood is oxygenated and pressure increases in the
right atrium and systemic venous circulation, which results in edema of the
extremities.
 Left ventricular failure occurs when the left ventricle in unable to pump blood into
systemic circulation. Pressure increases in the left atrium and pulmonary veins; then
the lungs become congested with blood, causing elevated pulmonary pressure and
pulmonary edema.
 To compensate, the cardiac muscle hypertrophies eventually resulting in decreased
ventricular compliance. Decreased compliance requires higher filling pressure to
produce the same stroke volume. Increased muscle mass impedes oxygenation of the
heart muscle, which leads to decreased contraction force and heart failure.
 As cardiac output fails, stretch receptors and baroreceptors stimulate the sympathetic
nervous system, releasing catecholamines that increase the force and rate of
myocardial contraction.
 This causes increased systemic resistance, increased venous return, and reduced blood
flow to the limbs, viscera and kidneys.
 Sweating results from sympathetic cholinergic fibers, there is extra work for the heart
muscle, and there is less systemic blood flow.
 The renal system responds by releasing renin-angiotensin, which sets off a chain of
events – vasoconstriction, leading to increased aldosterone release, causing sodium
and water retention and, in turn, increasing preload. Finally, sodium and water
retention becomes excessive, resulting in signs of systemic venous congestion and
fluid overload.
Assessment
1. Right ventricular failure

o Signs of right ventricular failure are evident in the systemic circulation
o Pitting, dependent edema in the feet, legs, sacrum, back, and buttocks
o Ascites from portal hypertension
o Tenderness of right upper quadrant, organomegaly
o Distended neck veins
o Pulsus alternans (regular alteration of weak and strong beats noted in the
pulse)
o Abdominal pain, bloating
o Anorexia, nausea
o Fatigue
o Weight gain
o Nocturnal diuresis
2. Left ventricular failure
o Signs of left ventricular failure are evident in the pulmonary system
o Cough, which may become productive with frothy sputum
o Dyspnea on exertion
o Orthopnea
o Paroxysmal nocturnal dyspnea
o Presence of crackles on auscultation
o Tachycardia
o Pulsus alternans
o Fatigue
o Pallor
o Cyanosis
o Confusion and disorientation
o Signs of cerebral anoxia
3. Acute pulmonary edema
o Severe dyspnea and orthopnea
o Pallor
o Tachycardia
o Expectoration of large amounts of blood-tinged, frothy sputum
o Wheezing and crackles on auscultation
o Bubbling respirations
o Acute anxiety, apprehension, restlessness
o Profuse sweating
o Cold, clammy skin
o Cyanosis
o Nasal flaring
o Use of accessory breathing muscles
o Tachypnea
o Hypocapnia, evidenced by muscle cramps, weakness, dizziness, and
paresthesias
1. Chest radiography reveals cardiomegaly and pulmonary congestion

2. CBC reveals dilution hyponatremia, hypochloremia, and hyperkalemia
3. ECG reveals ventricular hypertrophy
 Decreased CO related to an ineffective ventricular pump
Medical Management
 Initial management of the patient with HF depends on severity of HF, seriousness of
symptoms, etiology, presence of other illnesses, and precipitating factors. Medication
management is paramount in patients with HF. The general principles for
management are treatment of any precipitating causes, control of fluid and sodium
retention, increasing myocardial contractility, decreasing cardiac workload, and
reducing pulmonary and systemic venous congestion. The physician may also
prescribe fluid and sodium restriction in an attempt to reduce volume and thereby
reduce preload.
Surgical Management
 Coronary bypass surgery, PTCA, other innovative therapies as indicated (e.g,

mechanical assist devices , transplantation)
Alone or in combination: vasodilator therapy (angiotensin-converting enzyme (ACE)

inhibitors), angiotensin II receptor blockers (ARBs), select beta-blockers, calcium channel
blockers, diuretic therapy, cardiac glycosides (digitalis), and others
 Dobutamine, milrinone, anticoagulants, beta-blockers, as indicated

 Possibly antihypertensives or antianginal medications and anticoagulants
1. Monitor for signs of respiratory distress

o Provide pulmonary hygiene as needed
o Administer oxygen as prescribed
o Keep the head of the bed elevated
o Monitor ABG values.
2. Monitor for signs of altered cardiac output, including
o Pulmonary edema
o Arrhythmias, including extreme tachycardia and bradycardia
o Characteristic ECG and heart sound changes
3. Evaluate fluid status
o Maintain strict fluid intake and output measurements
o Monitor daily weights
o Assess for edema and severe diaphoresis
o Monitor electrolyte values and hematocrit level
o Maintain strict fluid restrictions as prescribed
4. Administer prescribed medications which may include:
o Antiarrhythmias to increase cardiac performance
o Diuretics, to reduce venous and systemic congestion
o Iron and folic acid supplements to improve nutritional status.
5. Prevent Infection
6. Reduce cardiac demands
o Keep the child warm
o Schedule nursing interventions to allow for rest
o Do not allow an infant to feed for more than 45 minutes at a time
o Provide gavage feedings if the infant becomes fatigued before ingesting an
adequate amount
7. Promote adequate nutrition. Maintain a high-calorie, low-sodium as prescribed.
8. Promote optimal growth and development
9. As appropriate, refer the family to a community health nurse for follow up care after
discharge.
 Physical findings indicative of HF:Mental confusion,pale,cyanotic,clammy

skin,presence of jugular vein distension and HJR,ascites,edema,pulmonary crackles or
wheezes,adventitious heart sounds
 Fluid intake and output,daily weights
 Response to medications such as diuretics,nitrates,dopamine,dobutamine,and oxygen
 Psychosocial response to illness
 PREVENTION. To prevent exacerbations, teach the patient and family to monitor

for an increase in shortness of breath or edema. Tell the patient to restrict fluid intake
to 2 to 2.5 L per day and restrict sodium intake as prescribed. Teach the patient to
monitor daily weights and report weight gain of more than 4 pounds in 2 days.
 MEDICATIONS. Be sure the patient and family understand all medications,
including effect, dosage, route, adverse effects, and the need for routine laboratory
monitoring for drugs such as digoxin.
 COMPLICATIONS OF HF. Tell the patient to call for emergency assistance for
acute shortness of breath or chest discomfort that is not alleviated with rest.
Sources:
ed
Lippincott’s Review Series – Pediatric Nursing
Handbook for Brunner & Suddarth’s ,Textbook of Medical-Surgical Nursing, 11th ed
ECG
Definition
Electrocardiography is the most commonly used test for evaluating cardiac status,
graphically records the electrical current (electrical potential) generated by the heart. This
current radiates from the heart in all directions and, on reaching the skin, is measured by
electrodes connected to an amplier and strip chart recorder. The standard resting ECG uses
five electrodes to measure the electrical potential from 12 different leads; the standard limb
leads (I,II,III), the augmented limb leads (aVf, aVL, and aVr), and the precordial, or chest,
leads (V1 through V6).
ECG tracings normally consist of three identifiable waveforms: the P wave, the QRS
complex, and the T wave. The P wave depicts atrial depolarization; the QRS complex,
ventricular depolarization; and the T wave, ventricular repolarization.
Computerized ECG machines use small electrode tabs that peel off a sheet and adhere to the
patient’s skin. The entire ECG tracing is displayed on a screen so abnormalities can be
corrected before printing; then it’s printed on one sheet of paper. Electrode tabs can remain
on the patient’s chest, arms, and legs to provide continuous lead placement for serial ECG
studies.
Purpose
 To help identify primary conduction abnormalities, cardiac arrhythmias, cardiac

hypertrophy, pericarditis, electrolyte imbalances, myocardial ischemia, and the site
and extent of myocardial infarction.
 To monitor recovery from an MI.
 To evaluate the effectiveness of cardiac medication.
 To assess pacemaker performance
 To determine effectiveness of thrombolytic therapy and the resolution of ST-segment
depression or elevation and T-wave changes.
Procedure
Patient Preparation for Electrocardiography (ECG)
1. Explain to the patient the need to lie still, relax, and breathe normally during the
procedure.
2. Note current cardiac drug therapy on the test request form as well as any other
pertinent clinical information, such as chest pain or pacemaker.
3. Explain that the test is painless and takes 5 to 10 minutes.
Implementation
1. Place the patient in a supine or semi-Fowler’s position.

2. Expose the chest, ankles, and wrists.
3. Place electrodes on the inner aspect of the wrists, on the medical aspect of the lower
legs, and on the chest.
4. After all electrodes are in place, connect the lead wires.
5. Press the START button and input any required information.
6. Make sure that all leads are represented in the tracing. If not, determine which
electrode has come loose, reattach it, and restart the tracing.
7. All recording and other nearby electrical equipment should be properly grounded.
8. Make sure that the electrodes are firmly attached.
1. Disconnect the equipment, remove the electrodes, and remove the gel with a moist
cloth towel.
2. If the patient is having recurrent chest pain or if serial ECG’s are ordered, leave the
electrode patches in place.
Interpretations
Normal Results
1. P wave that doesn’t exceed 2.5 mm (0.25 mV) in height or last longer than 0.12
second.
2. PR interval (includes the P wave plus the PR segment) persisting for 0.12 to 0.2
second for heart rates above 60 beats/min.
3. QT interval that varies with the heart rate and lasts 0.4 to 0.52 second for heart rates
above 60 beats/min.
4. Voltage of the R wave leads V1 through V6 that doesn’t exceed 27 mm.
5. Total QRS complex lasting 0.06 to 0.1 second.
Abnormal Results
1. Myocardial infarction (MI), right or left ventricular hypertrophy, arrhythmias, right or

left bundle-branch block, ischemia, conduction defects or pericarditis, and electrolyte
abnormalities.
2. Abnormal wave forms during angina episodes or during exercise.
Precautions
 The recording equipment and other nearby electrical equipment should be properly
grounded to prevent electrical interference.
 Double-check color codes and lead markings to be sure connectors march.
 Make sure that the electrodes are firmly attached, and reattached them if loose skin
contact is suspended. Don’t use cables that are broken, frayed, or bare.
Interfering Factors
 Improper lead placement.
Complications
 Skin sensitivity to the electrodes.
image by: ealthcentral.com
Cardiac Catheterization
Definition
Cardiac catheterization involves passing a catheter into the right or left side of the heart.
Catheterization can determine blood pressure and blood flow in the chambers of the heart,
permits blood sample collection, and record films of the heart’s ventricles (contrast
ventriculography) or arteries (coronary arteriography or angiography).
Catheterization of the heart’s left side assesses the patency of the coronary arteries, mitral
and aortic valve function, and left ventricular function. Catheterization of the heart’s right
side assesses tricuspid and pulmonic valve function and pulmonary artery pressures.
Purpose of Cardiac Catheterization
 To evaluate valvular insufficiency or stenosis, septal defects, congenital anomalies,

myocardial function, myocardial blood supply, and cardiac wall motion.
 To aid in diagnosing left ventricular enlargement, aortic root enlargement, ventricular
aneurysms, and intracardiac shunts.
Procedure
Patient Preparation
1. Explain the procedure to the patient

2. Tell him to restrict fluids for at least 6 hours before the test.
3. Inform him that the test takes 1 to 2 hours.
4. Tell him that he may receive a mild sedative but will remain conscious during the
procedure.
5. Have the patient to void just before the procedure.
6. Check the patient history for hypersensitivity to shellfish, iodine, or contrast media
used in other diagnostic tests. Discontinue any anticoagulant therapy as ordered.
Implementation
1. The patient is placed supine on padded table and his heart rate and rhythm,
respiratory status, and blood pressure are monitored throughout the procedure.
2. An I.V. line is started, if not already in place, and a local anesthetic is injected at the
insertion site.
3. A small incision is made into the artery or vein, depending on whether the test is for
the left or right.
4. The catheter is passed through the sheath into the vessel and guided using
fluoroscopy.
5. In the right-sided catheterization, the catheter is inserted into the antecubital or
femoral vein and advanced through the vena cava into the right side of the heart and
into the pulmonary artery.
6. If left-sided heart catheterization, the catheter is inserted into the brachial or femoral
artery and advanced retrograde through the aorta into the coronary artery ostium and
left ventricle.
7. When the catheter is in place, contrast medium is injected to make visible the cardiac
vessels and structures.
8. Nitroglycerin is given to eliminate catheter-induced spasm or watch its effect on the
coronary arteries.
9. After the catheter is removed, direct pressure is applied to the incision site until
bleeding stops, and a sterile dressing is applied.
1. Monitor the patient’s heart rate and rhythm, respiratory and pulse rates, and blood
pressure frequently.
2. Monitor the patient’s vital signs every 15 minutes for 2 hours after the procedure,
every 30 minutes for the next 2 hours, and then every hour for 2 hours.
3. If no hematoma or other problems arise, begin monitoring every 4 hours. If vital signs
are unstable, check every 5 minutes and notify the practitioner.
4. Observe the insertion site for a hematoma or blood loss. Additional compression may
be necessary to control bleeding.
5. Check the patient’s color, skin temperature, and peripheral pulse below the puncture
site.
6. Enforce bed rest for 8 hours. If the femoral route was used for catheter insertion, keep
the patient’s leg extended for 6 to 8 hours.
7. If medications were withheld before the test, check with the practiotner about
resuming their administration.
8. Administer prescribed analgesics.
9. Make sure a posttest ECG is scheduled to check for possible myocardial damage.
Interpretation
Normal Results
 No abnormalities of heart valves, chamber size, pressures, configuration, wall motion,

or thickness, and blood flow.
 Coronary arteries have a smooth and regular outline.
Abnormal Results
 Coronary artery narrowing greater than 70% suggests significant coronary artery
disease.
 Narrowing of the left main coronary artery and occlusion or narrowing high in the left
anterior descending artery suggests the need for revascularization surgery.
 Impaired wall motion suggests myocardial incompetence.
 A pressure gradient indicates valvular heart disease.
 Retrograde flow of the contrast medium across a valve during systole indicates
valvular incompetence.
Precautions
 Coagulopathy, impaired renal function, and debilitation usually contraindicate
catheterization of both sides of the heart. Unless a temporary pacemaker is inserted to
counteract induced ventricular asystole, left bundle-branch block contraindicates
catheterization of the right side of the heart.
 If the patient has valvular heart disease, prophylactic antimicrobial therapy may be
indicated to guard against subacute bacterial endocarditis.
Complications
 Ineffective endocarditis in a patient with vulvular heart disease.

 Myocardial infarction, arrhythmias, cardiac tamponade, pulmonary edema,
hematoma, blood loss, adverse reaction to contrast media, and vasovagal response.
RESPIRATORY DISORDERS
RELEVANT ANATOMY AND PHYSIOLOGY

Overview
Cells in the body require oxygen to survive. Vital functions of the body are carried out as the
body is continuously supplied with oxygen. Without the respiratory system exchange of gases
in the alveoli will not be made possible and systemic distribution of oxygen will not be made
possible. The transportation of oxygen in the different parts of the body is accomplished by
the blood of the cardiovascular system. However, it is the respiratory system that carries in
oxygen to the body and transports oxygen from the tissue cells to the blood. Thus,
cardiovascular system and respiratory system works hand in hand with each other. A problem
in the cardiovascular system would affect the other and vice versa.
Functional Anatomy of the Respiratory System

Nose
The nose is the only external part of the respiratory system and is the part where the air
passes through. During inhalation and exhalation, air enters the nose by passing through the
external nares or nostrils. Nasal cavity is found inside the nose and is divided by a nasal
septum. The receptors for the sense of smell, olfactory receptors are found in the mucosa of
the slit-like superior part of the nasal cavity which is located beneath the ethmoid bone.
Respiratory mucosa lines the rest of the nasal cavity and rests on a rich network of thin-
walled veins that warms the air passing by.
Important information about nose is the presence of the sticky mucus that is produced by the
mucosa’s gland. This important characteristic moistens the air and traps the incoming
bacteria and other foreign debris passing through the nasal cavity. Cells of the nasal mucosa
are ciliated and it creates a gentle current that moves the contaminated mucus posteriorly
towards the throat, where it is swallowed and digested by stomach juices.
In cases where the temperature of the environment is cold, the cilia become sluggish. Thus,
more mucus are allowed to accumulate in the nasal cavity and to dribble outward through the
nostrils. This is the main reason why a “runny nose” is noted during a cold day.
Conchae – these are three mucosa-covered projections or lobes that greatly increase the
surface area of the mucosa exposed to the air. Aside from that, conchae increase the air
turbulence in the nasal cavity.
Palate – a partition that separates the nasal cavity from the oral cavity. Anteriorly, the palate
that is supported by a bone called the hard palate and the one which is unsupported is the soft
palate.
Paranasal Sinuses – these are structures surrounding the casal cavity and are located in the
frontal, sphenoid, ethmoid and maxillary bones.
Pharynx
The pharynx is a 13 cm long muscular tube that is commonly called the throat. This muscular
passageway serves as a common food and air pathway. This structure is continuous with the
nasal cavity anteriorly via the internal nares.
Parts of pharynx:
1. Nasopharynx – the superior portion of the pharynx. The pharyngotympanic tubes that
drain the middle ear open in this area. This is the main reason why children who have
otitis media may follow a sore throat or other tyoes of pharyngeal infections since the
two mucosae of these regions are continuous.
2. Oropharynx – middle part
3. Laryngopharynx – part of pharynx that enters the larynx.
When food enters the oral cavity, it travels to the oropharynx and laryngopharynx. However,
instead of entering the larynx, the food is directed into the esophagus and not to the larynx.
Tonsils – clusters of lymphatic tissues found in the pharynx.
Types of Tonsils:
1. Palatine tonsils – tonsils found at the end of the soft palate.

2. Pharyngeal tonsils – lymphatic tissues located high in the nasopharynx. This is also
called adenoid.
3. Lingual tonsils – located at the base of the tongue.
Larynx
The larynx is the one that routes the air and food into their proper channels. Also termed as
the voice box, it plays an important role in speech. This structure is located inferior to the
pharynx and is formed by:
1. Eight rigid hyaline cartilages

2. Spoon-shaped flap of elastic cartilage, which is called the epiglottis.
Thyroid cartilage – this is the largest hyaline cartilage that protrudes anteriorly in males and
is referred to as the Adam’s apple.
Epiglottis – this is a flap of tissue that serves as a guardian of the airways as it protects the
superior portion of the larynx. The epiglottis does not restrict passage of air into the lower
respiratory passages when a person is not swallowing. However, when a person swallows
food, the epiglottis tips and forms a lid or blocks the opening of the larynx so that food will
not be directed to the lower respiratory passages. The food will be then routed to the
esophagus and in cases where it enters the larynx, a cough reflex is triggered to expel the
substance and prevent it from continuing into the lungs. This protective reflex does not work
when a person is unconscious that is why it is not allowed to offer or administer fluids to an
unconscious client.
Vocal folds – a pair of folds which is also called the true vocal cords that vibrate when air is
expelled.
Glottis – the slit-like passageway between the vocal folds.
Trachea
Also called the windpipe, the trachea is about 10 to 12 cm long or about 4 incheas and travels
dwon from the larynx to the fifth thoracic vertebra. This structure is reinforced with C-shaped
rings of hyaline cartilage and these rings are very important for the following purposes:
1. The open parts of the rings abut the esophagus that allows the structure to expand
anteriorly when a person swallows a large size of food.
2. The solid portions of the C-rings are supporting the walls of the trachea to keep it
patent or open even though pressure changes during breathing.
The trachea is lined with ciliated mucosa that primarily serves for this purpose: To propel
mucus loaded with dust particles and other debris away from the lungs towards the throat
where it can either be swallowed or spat out.
Main Bronchi
The main bronchi, both the right and the left, are both formed by tracheal divisions. There is a
slight difference between the right and left main bronchi. The right one is wider, shorter and
straighter than the left. This is the most common site for an inhaled foreign object to become
lodged. When air reaches the bronchi, it is already warmed, cleansed of most impurities and
well humidified.
Lungs
The lungs are fairly large organs that occupy the most of the thoracic cavity. The most central
part of the thoracic cavity, the mediastinum, is not occupied by the lungs as this area houses
the heart.
Apex – the narrow superior portion of each lung and is located just below the clavicle
Base – the resting area of the lung. This is a broad lung area that rests on the diaphragm.
Divisions of the Lungs
The lungs are divided into lobes by the presence of fissures. The left lung has two lobes while
the right lung has three.
Pleural Layers
Visceral pleura – also termed as the pulmonary pleura and covers each surface of the lings.
Parietal pleura – covers the walls of the thoracic cavity.
Pleural fluid – a slippery serous secretion that allows the lungs to slide along over the thorax
wall during breathing movements and causes the two pleural layers to cling together.
Bronchioles – smallest air-conducting passageways.
Bronchial tree or respiratory tree – a network formed due to the branching and rebranching of
the respiratory passageways within the lungs.
Alveoli – air sacs. This is the only area where exchange of gases takes place. Millions of
clustered alveoli resembles bunches of grapes and these structures make up the bulk of the
lungs.
Respiratory Zone – this part includes the respiratory bronchioles, alveolar ducts, alveolar
sacs, alveoli.
Physiology of Respiration
The respiratory primarily supplies oxygen to the body and disposes of carbon dioxide through
exhalation. Four events chronologically occur, for respiration to take place.
1. Pulmonary ventilation – this process is commonly termed as breathing. With
pulmonary ventilation, air must move out into and out of the lungs so that the alveoli
of the lungs are continuously drained and filled with air.
2. External respiration – this is the exchange of gases or the loading of oxygen and the
unloading of carbon dioxide between the pulmonary blood and alveoli.
3. Respiratory gas transport – this is the process where the oxygen and carbon dioxide is
transported to the and from the lungs and tissue cells of the body through the
bloodstream.
4. Internal respiration – in internal respiration the exchange of gases is taking place
between the blood and tissue cells.
Mechanics of Breathing
Breathing, also called pulmonary ventilation is a mechanical process that completely depends
on the volume changes occurring in the thoracic cavity. Thus, a when volume changes
pressure also changes, and this would lead to the flow of gases equalizing with the pressure.
Inspiration – also called inhalation. This is the act of allowing air to enter the body. Air is
flowing into the lungs with this process. Inspiratory muscles are involved with inspiration
which includes:
1. The diaphragm
2. External intercostals
These muscles contract when air is flowing in and thoracic cavity increases. When the
diaphragm contracts it slides inferiorly and is depressed. As a result the thoracic cavity
increases. The contraction of the external intercostal muscles lifts the rib cage and thrusts the
sternum forward. This increases the anteroposterior and lateral dimensions of the thorax.
Expiration – also called expiration. It the process of breathing out air as it leaves the lungs.
This process causes the gases to flow out to equalize the pressure inside and outside the
lungs. Under normal circumstances, the process of expiration is effortless.
Laryngotracheobronchitis
1. Viral infection of the larynx that may extend into trachea and bronchi
2. Most common cause for stridor in febrile child
3. Parainfluenza viruses most common cause
4. Infection causes endothelial insult, increased mucous production, edema, low

grade fever
5. Affects children less than five years of age
6. Onset more gradual than with croup, takes longer to resolve; usually develops
over several days with upper respiratory infection
7. Usually treated on outpatient basis; indications for admission include

dehydration and respiratory compromise
1. Drug therapy
1. Aerosolized racemic epinephrine
2. Antibiotics only if secondary bacterial infection present
3. Steroids: still controversial
2. Oxygen therapy: low concentrations to relieve mild hypoxia (concentrations

greater than 30% may mask signs of obstruction and should not be used)
3. Oral or nasotracheal intubation for moderate hypoxia
4. IV fluids to maintain hydration
1. Fever, coryza, inspiratory stridor, barking cough, tachycardia, tachypnea,

retractions
2. May have difficulty taking fluids
3. WBC normal
1. Instruct parents to take child into steamy bathroom for acute distress.
2. Keep child calm.
3. After distress subsides, use cool mist vaporizer in bedroom.
4. Child can vomit large amounts of mucus after the episode; reassure parents
that this is normal.
5. For hospitalized child
1. Monitor vital signs, I&O, skin color, and respiratory effort.
2. Maintain hydration.
3. Provide care for the intubated child.

4. Plan care to disturb the child as little as possible.
5. Avoid direct examination of the epiglottis as it may precipitate spasm

and obstruction.
Epiglottitis
1. Life-threatening bacterial infection of epiglottis and surrounding structures
2. Primary organism: H. influenzae, type B
3. Often preceded by upper respiratory infection
4. Rapid progression of swelling causes reduction in airway diameter; may lead

to sudden respiratory arrest
5. Affects children ages 3-7 years
1. Fever, tachycardia, inspiratory stridor, labored respirations with retractions,

sore throat, dysphagia, drooling
2. Irritability, restlessness, anxious-looking
3. Position: sitting upright, head forward and jaw thrust out
4. Diagnostic tests
1. WBC increased
2. Lateral neck x-ray reveals characteristic findings
1. Provide mist tent with oxygen.
2. Administer IV antibiotics as ordered.
3. Provide tracheostomy or endotracheal tube care (see The Respiratory System -

Traceostomy Care, in Unit 4); note the following
1. Restlessness, fatigue, dyspnea, cyanosis, pallor, tachycardia,

tachypnea, diminished breath sounds, adventitious lung sounds.
2. Need for suctioning to remove secretions; note amount, color,
consistency.
2. Reassure child through touch, sound, and physically being present.
3. Involve parents in all aspects of care.
4. Avoid direct examination of the epiglottis as it may precipitate spasm and

obstruction.
5. Remember this is extremely frightening experience for child and parents;

explain procedures and findings; reinforce explanations of physician.
Pleural Effusion
1. Collection of fluid in the pleural space
2. A symptom, not a disease; may be produced by numerous conditions
3. Classification
1. Transudative: accumulation of protein-poor, cell-poor fluid
2. Suppurative (empyema): accumulation of pus
4. May be found in clients with liver/kidney disease, pneumonia, tuberculosis,

lung abscess, bronchial carcinoma, leukemia, trauma, pulmonary edema,
systemic infection, disseminated lupus erythematosus, polyarteritis nodosa
1. Identification and treatment of the underlying cause
2. Thoracentesis
3. Drug therapy
1. Antibiotics: either systemic or inserted directly into pleural space
2. Fibrinolytic enzymes: trypsin, streptokinase-streptodornase to decrease

thickness of pus and dissolve fibrin clots
2. Closed chest drainage
3. Surgery: open drainage
1. Dyspnea, dullness over affected area upon percussion, absent or decreased
breath sounds over affected area, pleural pain, dry cough, pleural friction rub
2. Pallor, fatigue, fever, and night sweats (with empyema)
3. Diagnostic tests
1. Chest x-ray positive if greater than 250 ml pleural fluid
2. Pleural biopsy may reveal bronchogenic carcinoma
3. Thoracentesis may contain blood if cause is cancer, pulmonary

infarction, or tuberculosis; positive for specific organism in empyema
2. Nursing interventions: vary depending on etiology
1. Assist with repeated thoracentesis.
2. Administer narcotics/sedatives as ordered to decrease pain.
3. Assist with instillation of medication into pleural space (reposition client every
15 minutes to distribute the drug within the pleurae).
4. Place client in high-Fowler's position to promote ventilation.
Tuesday, May 20, 2008 | Labels: respiratory disorder | 0 Comments
Atelectasis
1. Collapse of part or all of a lung due to bronchial obstruction
2. May be caused by intrabronchial obstruction (secretions, tumors,

bronchospasm, foreign bodies); extrabronchial compression (tumors, enlarged
lymph nodes); or endobronchial disease (bronchogenic carcinoma,
inflammatory structures)
1. Signs and symptoms may be absent depending upon degree of collapse and
rapidity with which bronchial obstruction occurs
2. Dyspnea, decreased breath sounds on affected side, decreased respiratory

excursion, dullness to flatness upon percussion over affected area
3. Cyanosis, tachycardia, tachypnea, elevated temperature, weakness, pain over

affected area
4. Diagnostic tests
1. Bronchoscopy: may or may not reveal an obstruction
2. Chest x-ray shows diminished size of affected lung and lack of

radiance over atelectic area
3. pO2 decreased
2. Nursing interventions (prevention of atelectasis in hospitalized clients is an important

nursing responsibility)
1. Turn and reposition every 1-2 hours while client is bedridden or obtunded.
2. Encourage mobility (if permitted).
3. Promote liquification and removal of secretions.
4. Avoid administration of large doses of sedatives and opiates that depress

respiration and cough reflex.
5. Prevent abdominal distension.
6. Administer prophylactic antibiotics as ordered to prevent respiratory infection.
Pneumothorax/Hemothorax
1. Partial or complete collapse of the lung due to an accumulation of air or fluid

in the pleural space
2. Types
1. Spontaneous pneumothorax: the most common type of closed

pneumothorax; air accumulates within the pleural space without an
obvious cause. Rupture of a small bleb on the visceral pleura most
frequently produces this type of pneumothorax.
2. Open pneumothorax: air enters the pleural space through an opening in

the chest wall; usually caused by stabbing or gunshot wound.
3. Tension pneumothorax: air enters the pleural space with each

inspiration but cannot escape; causes increased intrathoracic pressure
and shifting of the mediastinal contents to the unaffected side
(mediastinal shift).
4. Hemothorax: accumulation of blood in the pleural space; frequently

found with an open pneumothorax resulting in a hemopneumothorax.
1. Sudden sharp pain in the chest, dyspnea, diminished or absent breath sounds
on affected side, decreased respiratory excursion on affected side,
hyperresonance on percussion, decreased vocal fremitus, tracheal shift to the
opposite side (tension pneumothorax accompanied by mediastinal shift)
2. Weak, rapid pulse; anxiety; diaphoresis
3. Diagnostic tests
1. Chest x-ray reveals area and degree of pneumothorax
2. pCO2 elevated
3. pO2, pH decreased
1. Provide nursing care for the client with an endotracheal tube: suction
secretions, vomitus, blood from nose, mouth, throat, or via endotracheal tube;
monitor mechanical ventilation.
2. Restore/promote adequate respiratory function.
1. Assist with thoracentesis and provide appropriate nursing care.
2. Assist with insertion of a chest tube to water-seal drainage and provide

appropriate nursing care.
3. Continuously evaluate respiratory patterns and report any changes.
2. Provide relief/control of pain.
1. Administer narcotics/analgesics/sedatives as ordered and monitor

effects.
2. Position client in high-Fowler's position.
Flail Chest
1. Fracture of several ribs and resultant instability of the affected chest wall.
2. Chest wall is no longer able to provide the bony structure necessary to

maintain adequate ventilation; consequently, the flail portion and underlying
tissue move paradoxically (in opposition) to the rest of the chest cage and
lungs.
3. The flail portion is sucked in on inspiration and bulges out on expiration.

4. Result is hypoxia, hypercarbia, and increased retained secretions.
5. Caused by trauma (sternal rib fracture with possible costochondral

separations).
1. Internal stabilization with a volume-cycled ventilator
2. Drug therapy (narcotics, sedatives)
1. Severe dyspnea; rapid, shallow, grunty breathing; paradoxical chest motion
2. Cyanosis, possible neck vein distension, tachycardia, hypotension
3. Diagnostic tests
1. pO2 decreased
2. pCO2 elevated
3. pH decreased
1. Maintain an open airway: suction secretions/blood from nose, throat, mouth,

and via endotracheal tube; note changes in amount, color, characteristics.
2. Monitor mechanical ventilation.
3. Encourage turning, coughing, and deep breathing.
4. Monitor for signs of shock.
Histoplasmosis
1. General information: a systemic fungal disease caused by inhalation of dust

contaminated by Histoplasma capsulatum which is transmitted through bird manure.
2. Medical management: antifungal agent Amphotericin B
1. Very toxic: toxicity includes anorexia, chills, fever, headache, and renal failure
2. Acetaminophen, Benadryl, and steroids given with Amphotericin B to prevent

reactions
1. Symptoms similar to tuberculosis or pneumonia

1. Cough
2. Fever
3. Joint pain
4. Malaise
2. Sometimes asymptomatic
3. Diagnostic tests
1. Chest x-ray (often appears similar to tuberculosis)
2. Histoplasmin skin test (read the same as PPD)
1. Monitor respiratory status
2. Administer medications as ordered; observe for severe side effects of

Amphotericin B: fever (acetaminophen given prophylactically), anaphylactic
reaction (Benadryl and steroids given prophylactically), abnormal renal
function with hypokalemia and azotemia.
Chronic Obstructive Pulmonary Disease (COPD)

Refers to respiratory conditions that produce obstruction of air flow; includes emphysema,
bronchitis, bronchiectasis, and asthma.
Pulmonary Emphysema
1. Enlargement and destruction of the alveolar, bronchial, and bronchiolar tissue
with resultant loss of recoil, air trapping, thoracic overdistension, sputum
accumulation, and loss of diaphragmatic muscle tone
2. These changes cause a state of carbon dioxide retention, hypoxia, and
respiratory acidosis.
3. Caused by cigarette smoking, infection, inhaled irritants, heredity, allergic
factors, aging
1. Anorexia, fatigue, weight loss

2. Feeling of breathlessness, cough, sputum production, flaring of the nostrils,
use of accessory muscles of respiration, increased rate and depth of breathing,
dyspnea
3. Decreased respiratory excursion, resonance to hyperresonance, decreased
breath sounds with prolonged expiration, normal or decreased fremitus
4. Diagnostic tests: pCO2 elevated or normal; pO2 normal or slightly decreased

1. Bronchiodilators: aminophylline, isoproterenol (Isuprel), terbutaline
(Brethine), metaproterenol (Alupent), theophylline, isoetharine
(Bronkosol); used in treatment of bronchospasm
2. Antimicrobials: tetracycline, ampicillin to treat bacterial infections
3. Corticosteroids: prednisone
2. Facilitate removal of secretions. at least
1. Ensure fluid intake of 3 liters/day.

2. Provide (and teach client) chest physical therapy, coughing and deep
breathing, and use of hand nebulizers.
3. Suction as needed.
4. Provide oral hygiene after expectoration of sputum.
2. Improve ventilation.
1. Position client in semi- or high-Fowler's.

2. Instruct client to use diaphragmatic muscle to breathe.
3. Encourage productive coughing after all treatments (splint abdomen to
help produce more expulsive cough).
4. Employ pursed-lip breathing techniques (prolonged, slow relaxed
expiration against pursed lips).
1. Prevention of recurrent infections

1. avoid crowds and individuals with known infection.
2. adhere to high-protein, high-carbohydrate, increased vitamin C
diet.
3. receive immunizations for influenza and pneumonia.
4. report changes in characteristics and color of sputum
immediately.
5. report worsening of symptoms (increased tightness of chest,
fatigue, increased dyspnea).
2. Control of environment
1. use home humidifier at 30%-50% humidity.

2. wear scarf over nose and mouth in cold weather to prevent
bronchospasm.
3. avoid smoking and others who smoke.
4. avoid abrupt changes in temperature.
2. Avoidance of inhaled irritants
1. stay indoors if pollution levels are high.

2. use air conditioner with high-efficiency particulate air filter to
remove particles from air.
2. Increasing activity tolerance
1. start with mild exercises, such as walking, and gradually

increase amount and duration.
2. use breathing techniques (pursed lip, diaphragmatic) during
activities/exercises to control breathing.
3. have oxygen available as needed to assist with activities.
4. plan activities that require low amounts of energy.
5. plan rest periods before and after activities.
Bronchitis
1. Excessive production of mucus in the bronchi with accompanying persistent
cough.
2. Characteristic changes include hypertrophy/hyperplasia of the mucus-secreting
glands in the bronchi, decreased ciliary activity, chronic inflammation, and
narrowing of the small airways.
3. Caused by the same factors that cause emphysema.
2. Medical management: drug therapy includes bronchodilators, antimicrobials,
expectorants (e.g., Robitussin)
1. Productive (copious) cough, dyspnea on exertion, use of accessory muscles of

respiration, scattered rales and rhonchi
2. Feeling of epigastric fullness, slight cyanosis, distended neck veins, ankle
edema
3. Diagnostic tests: increased pCO2, decreased pO2
2. Nursing interventions: same as for emphysema
Bronchiectasis
1. Permanent abnormal dilation of the bronchi with destruction of muscular and
elastic structure of the bronchial wall
2. Caused by bacterial infection; recurrent lower respiratory tract infections;
congenital defects (altered bronchial structures); lung tumors; thick, tenacious
secretions
2. Medical management: same as for emphysema.
1. Chronic cough with production of mucopurulent sputum, hemoptysis,

exertional dyspnea, wheezing
2. Anorexia, fatigue, weight loss
3. Diagnostic tests
1. Bronchoscopy reveals sources and sites of secretions
2. Possible elevation of WBC
2. Nursing interventions: same as for emphysema
ASTHMA
Definition
 Asthma is a chronic inflammatory disease of the airways characterized by hyper-

responsiveness, mucosal edema, and mucus production.
 This inflammation ultimately leads to recurrent episodes of asthma symptoms: cough,
chest tightness, wheezing, and dyspnea.
 Patients with asthma may experience symptom-free periods alternating with acute
exacerbations that last from minutes to hours or days.
 Asthma, the most common chronic disease of childhood, can begin at any age.
Causes
The main triggers for asthma are allergies, viral infections, autonomic nervous system
imbalances that can cause an increase in parasympathetic stimulation, medications,
psychological factors, and exercise. Of asthmatic conditions in patients under 30 years old,
70% are caused by allergies. Three major indoor allergens are dust mites, cockroaches, and
cats. In older patients,the cause is almost always nonallergic types of irritants such as smog.
Heredity plays a part in about one-third of the cases.
Pathophysiology of asthma
1. An asthma attack may occur spontaneously or in response to a trigger. Either way, the
attack progresses in the following manner:
 There is an initial release of inflammatory mediators from bronchial mast cells,

epithelial cells, and macrophages, followed by activation of other inflammatory cells
 Alteration of autonomic neural control of airway tone and epithelial integrity occur
and the increased responsiveness in airways smooth muscle results in clinical
manifestations (e.g. wheezing and dyspnea)
2. Three events contribute to clinical manifestations
 Bronchial spasm
 Inflammation and edema of the mucosa
 Production of thick mucus, which results in increased airway resistance, premature
closure of airways, hyperinflation, increased work of breathing, and impaired gas
exchange
3. If not treated promptly, status asthmaticus – an acute, severe, prolonged asthma attack that
is unresponsive to the usual treatment – may occur, requiring hospitalization.
Classification
1. Extrinsic Asthma – called Atopic/allergic asthma. An “allergen” or an “antigen” is a

foreign particle which enters the body. Our immune system over-reacts to these often
harmless items, forming “antibodies” which are normally used to attack viruses or bacteria.
Mast cells release these antibodies as well as other chemicals to defend the body.
Common irritants:
 Cockroach particles
 Cat hair and saliva
 Dog hair and saliva
 House dust mites
 Mold or yeast spores
 Metabisulfite, used as a preservative in many beverages and some foods
 Pollen
2. Intrinsic asthma – called non-allergic asthma, is not allergy-related, in fact it is caused

by anything except an allergy. It may be caused by inhalation of chemicals such as cigarette
smoke or cleaning agents, taking aspirin, a chest infection, stress, laughter, exercise, cold air,
food preservatives or a myriad of other factors.
 Smoke
 Exercise
 Gas, wood, coal, and kerosene heating units
 Natural gas, propane, or kerosene used as cooking fuel
 Fumes
 Smog
 Viral respiratory infections
 Wood smoke
 Weather changes
Clinical Manifestations
 Most common symptoms of asthma are cough (with or without mucus production),
dyspnea, and wheezing (first on expiration, then possibly during inspiration as well).
 Asthma attacks frequently occur at night or in the early morning.
 An asthma exacerbation is frequently preceded by increasing symptoms over days,
but it may begin abruptly.
 Chest tightness and dyspnea occur.
 Expiration requires effort and becomes prolonged.
 As exacerbation progresses, central cyanosis secondary to severe hypoxia may occur.
 Additional symptoms, such as diaphoresis, tachycardia, and a widened pulse pressure,
may occur.
 Exercise-induced asthma: maximal symptoms during exercise, absence of nocturnal
symptoms, and sometimes only a description of a “choking” sensation during
exercise.
 A severe, continuous reaction, status asthmaticus, may occur. It is life-threatening.
 Eczema, rashes, and temporary edema are allergic reactions that may be noted with
asthma.
Ineffective airway clearance related to obstruction from narrowed lumen and thick mucus
OUTCOMES. Respiratory status: Gas exchange; Respiratory status: Ventilation; Symptom

control behavior; Treatment behavior: Illness or injury; Comfort level
INTERVENTIONS. Airway management; Anxiety reduction; Oxygen therapy; Airway
suctioning;Airway insertion and stabilization; Cough enhancement; Mechanical ventilation;
Positioning;Respiratory monitoring
Assessment and Diagnostic Methods
 Family, environment, and occupational history is essential.

 During acute episodes, sputum and blood test, pulse oximetry, ABGs, hypocapnia and
respiratory alkalosis, and pulmonary function (forced expiratory volume [FEV] and
forced vital capacity [FVC] decreased) tests are performed.
 Spirometry will detect:
a. Decreased for expiratory volume (FEV)

b. Decreased peak expiratory flow rate (PEFR)
c. Diminished forced vital capacity (FVC)
d. Diminished inspiratory capacity (IC)
Steps of Clinical and Diagnostic as per National Asthma Education and Prevention
Program
Mild Intermittent Asthma
 Symptoms ? 2 times per week

 Brief exacerbations
 Nighttime symptoms ? 2 times a month
 Asymptomatic and normal PEF (peak expiratory flow) between exacerbations
 PEF or FEV, (forced expiratory volume in 1 second) ? 80% of predicted value
 PEF variability < 20%
Mild Persistent Asthma
 Symptoms > 2 times/week, but less than once a day

 Exacerbations may affect activity
 Nighttimes symptoms > 2 times a month
 PEF/FEV ? 80% of predicted value
 PEF variability 20%-30%
Moderate Persistent Asthma

 Daily Symptoms
 Daily use of inhaled short-acting ?2 - agonists
 Exacerbations affect activity
 Exacerbations ? 2 times a week
 Exacerbations may last days
 Nighttime symptoms > once a week
 PEF/FEV > 60%-<80% of predicted value
 PEF variability > 30%
Severe Persistent Asthma
 Continual symptoms
 Frequent exacerbations
 Frequent nighttime symptoms
 Limited physical activity
 PEF or FEV ? 60% of predicted value
 PEF variability > 30 %
Medical Management
Pharmacologic Therapy
There are two classes of medications—long-acting control and quick-relief medications—as

well as combination products.
 Short-acting beta2-adrenergic agonists

 Anticholinergics
 Corticosteroids: metered-dose inhaler (MDI)
 Leukotriene modifiers inhibitors/antileukotrienes
 Methylxanthines
Nursing Management of asthma
The immediate nursing care of patients with asthma depends on the severity of symptoms.
The patient and family are often frightened and anxious because of the patient’s
dyspnea. Therefore, a calm approach is an important aspect of care.
 Assess the patient’s respiratory status by monitoring the severity of symptoms, breath

sounds, peak flow, pulse oximetry, and vital signs.
 Obtain a history of allergic reactions to medications before administering
medications.
 Identify medications the patient is currently taking.
 Administer medications as prescribed and monitor the patient’s responses to those
medications; medications may include an antibiotic if the patient has an underlying
respiratory infection.
 Administer fluids if the patient is dehydrated.
 Assist with intubation procedure, if required.
Teaching Points
 Teach patient and family about asthma (chronic inflammatory), purpose and action of
medications, triggers to avoid and how to do so, and proper inhalation technique.
 Instruct patient and family about peak-flow monitoring.
 Teach patient how to implement an action plan and how and when to seek assistance.
 Obtain current educational materials for the patient based on the patient’s diagnosis,
causative factors, educational level, and cultural background.
Continuing Care
 Emphasize adherence to prescribed therapy, preventive measures, and need for

followup appointments.
 Refer for home health nurse as indicated.
 Home visit to assess for allergens may be indicated (with recurrent exacerbations).
 Refer patient to community support groups.
 Remind patients and families about the importance of health promotion strategies and
recommended health screening.
 Respiratory status: Patency of airway, auscultation of the lungs, presence or absence

of adventitious breath sounds, respiratory rate and depth
 Response to medications, oxygen therapy, hydration, bedrest
 Presence of complications: Respiratory failure, ruptured bleb that may result in a
pneumothorax
CHRONIC BRONCHITIS
Description
 Is an inflammation of the lower airways characterized by excessive secretion of

mucus, hypertrophy of mucous glands, and recurring infection, progressing to
narrowing and obstruction of airflow.
Causes/ Risk Factors
 The primary cause of chronic bronchitis is smoking or exposure to some type of

respiratory irritant. Established risk factors include a history of smoking, occupational
exposures, air pollution,reduced lung function, and heredity. Children of parents who
smoke are at higher risk for pulmonary infections that may lead to bronchitis.
Pathophysiology
Assessment
1. Signs and symptoms of chronic bronchitis (insidious onset):

o Productive cough lasting at least 3 months during a year for 2 successive
years.
o Thick, gelatinous sputum (greater amounts produced during superimposed
infections).
o Dyspnea and wheezing as disease progresses.
1. Pulmonary function tests, to demonstrate airflow obstruction-reduced forced

expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity ratio; increased
residual volume to total lung capacity (TLC) ration, possibly increased TLC.
2. Chest X-rays to detect hyperinflation, flattened diaphragm, increased retrosternal
space, decreased vascular markings, possible bullae (all in late stages).
3. Arterial blood gases, to detect decreased arterial oxygen pressure (PaO2), pH, and
increased arterial carbon dioxide pressure (Paco2).
4. Sputum smears and cultures to identify pathogens.
 Impaired gas exchange related to obstructed airways
Therapeutic Intervention / Medical Management
1. Smoking cessation to stop the progression and preserve lung capacity.

2. Low-flow oxygen to correct severe hypoxemia in a controlled manner and minimize
carbon dioxide retention.
3. Home oxygen therapy, especially at night to prevent turnal oxygen desaturation.
4. Pulmonary rehabilitation to reduce symptoms that limit activity.
5. Chest physical therapy, including postural drainage and breathing retraining.
6. Lung transplant in severe cases of alpha1-antitrypsin deficiency.
1. Bronchodilators to reduce dyspnea and control bronchospasm delivered by metered-

dose inhaler, other handheld devices, or nebulization.
2. Inhaled corticosteriods may be useful for some with severe airflow limitation and
frequent exacerbations.
3. Corticosteroids by mouth or I.V. in acute exacerbations.
4. Antimicrobials to control secondary bacterial infections in the bronchial tree, thus
clearing the airways.
5. Alpha1-antitrypsin replacement delivered by I.V. infusion.
1. Monitor for adverse effects of bronchodilators-tremulousness, tachycardia, cardiac

arrhythmias, central nervous system stimulation, hypertension.
2. Monitor oxygen saturation at rest and with activity.
3. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation
usually reduces pulmonary irritation, sputum production, and cough. Keep the
patient’s room as dust-free as possible.
4. Use postural drainage positions to help clear secretions responsible for airway
obstruction.
5. Teach controlled coughing.
6. Encourage high level of fluid intake (8 to 10 glasses; 2 to 2.5 L daily) within level of
cardiac reserve.
7. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum.
Add moisture (humidifier, vaporizer) to indoor air.
8. Avoid dairy products if these increase sputum production.
9. Encourage the patient to assume comfortable position to decrease dyspnea.
10. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and
depth of respiration and improve respiratory muscle coordination.
11. Discuss and demonstrates relaxation exercises to reduce stress, tension, and anxiety.
12. Encourage frequent small meals if the patient is dyspneic; en a small increase in
abdominal contents may press on diaphragm and impede breathing.
13. Offer liquid nutritional supplements to improve caloric intake and counteract weight
loss.
14. Avoid foods producing abdominal discomfort.
15. Encourage use of portable oxygen system for ambulation for patients with hypoxemia
and marked disability.
16. Encourage the patient in energy conservation techniques.
 Respiratory status of the patient: Respiratory rate, breath sounds, use of oxygen, color
of nail beds and lips; note any respiratory distress
 Response to activity: Degree of shortness of breath with any exertion,degree of
fatigue
 Comfort, body temperature
 Response to medications, oxygen,and breathing treatments
 Need for assistance with activities of daily living
 Response to diet and increased caloric intake, daily weights
1. Medications. Be sure that the patient understands all medications, including the
dosage, route, action, and adverse effects. Patients on aminophylline should have
blood levels drawn as ordered by the physician. Before being discharged from the
hospital, the patient should demonstrate the proper use of metered-dose inhalers.
2. Complications. Instruct patients to notify their primary healthcare provider of any
change in the color or consistency of their secretions. Green-colored secretions may
indicate the presence of a respiratory infection. Patients should also report
consistent, prolonged periods of dyspnea that are unrelieved by medications.
3. Follow-up. Consider that patients with severe disease may need assistance with
activities of daily living after discharge. Note any referrals to social services. Send
patients home with a diet, provided by the dietitian and reinforced by the nurse, which
provides a high-caloric intake. Encourage the patient to cover the face with a scarf if
he or she goes out-of-doors in the winter. If the patient continues to smoke,provide the
name of a smoking cessation program or a support group. Encourage the patient to
avoid irritants in the air.
Sources:
ADAM for Images
Nursingcrib.com
ed
Bronchiolitis
1. Pulmonary viral infection characterized by wheezing
2. Usually caused by respiratory syncytial virus
3. Virus invades epithelial cells of nasopharynx and spreads to lower respiratory
tract, causing increased mucus production, decreased diameter of bronchi,
hyperinflation, and possible atelectasis
4. Affects infants ages 2-8 months
5. Increased incidence of asthma as child grows older
2. Medical management: IV epinephrine (if provides relief, follow with epinephrine
suspension [Sus-Phrine], which is longer acting, then theophylline); if no response to
epinephrine, all treatment is supportive
1. Difficulty feeding, fever

2. Cough, coryza
3. Wheezing, prolonged expiratory phase, tachypnea, nasal flaring, retractions
(intercostal more pronounced than supraclavicular retractions)
4. Diagnostic tests
1. WBC normal
2. X-ray reveals hyperaeration
1. Provide high-humidity environment, with oxygen in some cases (instruct

parents to take child into steamy bathroom if at home).
2. Offer small, frequent feedings; clear fluids if trouble with secretions.
3. Provide adequate rest.
4. Administer antipyretics as ordered to control fever.
PNEUMONIA
Description
1. Pneumonia is an infection of the pulmonary tissue, including the interstitial spaces,

the alveoli, and the bronchioles.
2. The edema associated with inflammation stiffens the lung, decreases lung compliance
and vital capacity, and causes hypoxemia.
3. Pneumonia can be community acquired or hospital acquired.
4. The chest x-ray film shows diffuse patches throughout the lungs or consolidation in a
lobe.
5. A sputum culture identifies the organism.
6. The white blood cells and the erythrocyte sedimentation rate are elevated.
Causes
 Primary pneumonia is caused by the patient’s inhaling or aspirating a pathogen such

as bacteria or a virus. Bacterial pneumonia, often caused by staphylococcus,
streptococcus, or klebsiella, usually occurs when the lungs’ defense mechanisms are
impaired by such factors as suppressed cough reflex, decreased cilia action, decreased
activity of phagocytic cells, and the accumulation of secretions. Viral pneumonia
occurs when a virus attacks bronchiolar epithelial cells and causes interstitial
inflammation and desquamation, which eventually spread to the alveoli.
 Secondary pneumonia ensues from lung damage that was caused by the spread of
bacteria from an infection elsewhere in the body or by a noxious chemical. Aspiration
pneumonia is caused by the patient’s inhaling foreign matter such as food or vomitus
into the bronchi. Factors associated with aspiration pneumonia include old age,
impaired gag reflex, surgical procedures, debilitating disease, and decreased level of
consciousness.
 Community-acquired pneumonia is caused by bacteria that are divided into two

groups: typical and atypical. Organisms that cause typical pneumonia include
Streptococcus pneumonia (pneumococcus) and Haemophilus and Staphylococcus
species. Organisms that cause atypical pneumonia include Legionella, Mycoplasma,
and Chlamydia species.
Pathophysiology
Risk factors
 Cigarette smoking
 Recent viral respiratory infection (common cold, laryngitis, influenza)
 Difficulty swallowing (due to stroke, dementia, Parkinson's disease, or other
neurological conditions)
 Chronic lung disease (COPD, bronchiectasis, cystic fibrosis)
 Cerebral palsy
 Other serious illnesses, such as heart disease, liver cirrhosis, or diabetes mellitus
 Living in a nursing facility
 Impaired consciousness (loss of brain function due to dementia, stroke, or other
neurologic conditions)
 Recent surgery or trauma
 Immune system problem
Assessment
1. Chills
2. Elevated temperature
3. Pleuritic pain
4. Rhonchi and wheezes
5. Use of accessory muscles for breathing
6. Cyanosis
7. Mental status changes
8. Sputum production
Complications
 Respiratory failure, which requires a breathing machine or ventilator

 Empyema or lung abscesses. These are infrequent, but serious, complications of
pneumonia. They occur when pockets of pus form inside or around the lung. These
may sometimes need to be drained with surgery.
 Sepsis, a condition in which there is uncontrolled swelling (inflammation) in the
body, which may lead to organ failure
 Acute respiratory distress syndrome (ARDS), a severe form of respiratory failure
 Ineffective airway clearance related to increased production of secretions and

increased viscosity
 Sputum cultures and sensitivities reveals presence of infecting organisms. Cultures
identify organism; sensitivity testing identifies how resistant or sensitive the bacteria
are to antibiotics.
 Chest x-ray reveals areas of increased density, (can be a lung segment, lobe, one lung,
or both lungs). Findings reflect areas of infection and consolidation.
Medical Management
1. Antibiotics are prescribed based on Gram stain results and antibiotic guidelines
(resistance patterns, risk factors, etiology must be considered). Combination therapy
may be used.
2. Supportive treatment includes hydration, antipyretics, antihistamines, or nasal
decongestants.
3. Best rest is recommended until infection shows signs of clearing.
4. Oxygen therapy is given for hypoxemia.
5. Respiratory support includes endotracheal intubation, high inspiratory oxygen
concentrations, and mechanical ventilation.
6. Treatment of atelectasis, pleural effusion, shock, respiratory failure, superinfection is
instituted, if needed.
7. For groups of high risk for community-acquired pneumonia, pneumococcal
vaccination is advised.
Antibiotics
 Initial antibiotic: macrolides including erythromycin, azithromycin, roxithromycin

and clarithyromycin. Macrolides provide coverage for likely organisms in
community-acquired bacterial pneumonia.
 Other antibiotics: Penicillin G for streptococcal pneumonia; nafcillin or oxacillin for
staphylococcal pneumonia; aminoglycoside or a cephalosporin for klebsiella
pneumonia; penicillin G or clindamycin for aspiration pneumonia .Alternatives:
amoxicillin and clavulanate (Augmentin); doxycycline; trimethoprim and
sulfamethoxazole (Bactrim DS, Septra); levofloxacin (Levaquin)
1. Administer oxygen as prescribed.

2. Monitor respiratory status.
3. Monitor for labored respirations, cyanosis, and cold and clammy skin.
4. Encourage coughing and deep breathing and use of incentive spirometer.
5. Position client in semi-Fowler position to facilitate breathing and lung expansion.
6. Change client’s position frequently and ambulate as tolerated to mobilize secretions
7. Provide CPT
8. Perform nasotracheal suctioning if the client is unable to clear secreations.
9. Monitor pulse oximetry.
10. Monitor and record color, consistency, and amount of sputum.
11. Provide a high-calorie, high protein diet with small frequent meals.
12. Encourage fluids up to 3 L a day to thin secretions unless contraindicated.
13. Provide a balance of rest and activity, increasing activity gradually.
14. Administer antibiotics as prescribed.
15. Administer antipyretics, bronchodilators, cough suppressants, mucolytic agents, and
expectorants as prescribed.
16. Prevent the spread of infection by hand washing and the proper disposal of secretions.
 Physical findings of chest assessment: Respiratory rate and depth, auscultation

findings, chest tightness or pain, vital signs
 Assessment of degree of hypoxemia: Lips and mucous membrane color, oxygen
saturation by pulse oximetry
 Response to deep-breathing and coughing exercises, color and amount of sputum
 Response to medications: Body temperature, clearing of secretions
 Be sure the patient understands all medications, including dosage, route, action, and
adverse effects.
 The patient and family or significant other need to understand the importance of
avoiding fatigue by limiting activity and taking frequent rests.
 Advise small, frequent meals to maintain adequate nutrition.
 Fluid intake should be maintained at approximately 3000 mL/day so that the
secretions remain thin.
 Teach the patient to maintain pulmonary hygiene measures of coughing, deep
breathing, and incentive spirometry at home.
 Provide information about how to stop smoking.
PULMONARY TUBERCULOSIS
1. Bacterial infectious disease caused by M. tuberculosis and spread via airborne
droplets when infected persons cough, sneeze, or laugh
2. Once inhaled, the organisms implant themselves in the lung and begin
dividing slowly, causing inflammation, development of the primary tubercle,
and eventual caseation and fibrosis.
3. Infection spreads via the lymph and circulatory systems.
4. Half of the cases occur in inner-city neighborhoods, and incidence is highest
in areas with a large population of native Americans. Nonwhites affected four
times more often than whites. Men affected more often than women. The
greatest number of cases occur in persons age 65 and over. Socially and
economically disadvantaged, alcoholic, and malnourished individuals affected
more often.
5. The causative agent, M. tuberculosis, is an acid-fast bacillus spread via droplet
nuclei from infected persons.
1. Cough (yellow mucoid sputum), dyspnea, hemoptysis, rales or crackles

2. Anorexia, malaise, weight loss, afternoon low-grade fever, pallor, pain,
fatigue, night sweats
3. Diagnostic tests
1. Chest x-ray indicates presence and extent of disease process but cannot
differentiate active from inactive form
2. Skin test (PPD) positive; area of induration 10 mm or more in diameter
after 48 hours
3. Sputum positive for acid-fast bacillus (three samples is diagnostic for
disease)
4. Culture positive
5. WBC and ESR increased
1. Administer medications as ordered (see Table 2.23).

2. Prevent transmission.
1. Strict isolation not required if client/significant others adhere to special

respiratory precautions for tuberculosis.
2. Client should be in a well-ventilated private room, with the door kept
closed at all times.
3. All visitors and staff should wear masks when in contact with the client
and should discard the used masks before leaving the room; client
should wear a mask when leaving the room for tests.
4. All specimens should be labelled "AFB precautions."
5. Handwashing is required after direct contact with the client or
contaminated articles.
2. Promote adequate nutrition.
1. Make ongoing assessments of client's appetite and do kcal counts for 3

days; consult dietitian for diet guidelines.
2. Offer small, frequent feedings and nutritional supplements; assist client
with menu selection stressing balanced nutrition.
3. Weigh client at least twice a week.
4. Encourage activity as tolerated to increase appetite.
2. Prevent social isolation.
1. Impart a comfortable, confident attitude when caring for the client.

2. Explain the nature of the disease to the client, significant others, and
visitors in simple terms.
3. Stress that visits are important, but isolation precautions must be
followed.
2. Vary the client's routine to prevent boredom.
3. Discuss the client's feelings and assess for boredom, depression, anxiety,
fatigue, or apathy; provide support and encourage expression of concerns.
1. Medication regimen: prepare a sheet with each drug name, dosage,

time due, and major side effects; stress importance of following
medication schedule for prescribed period of time (usually 9 months);
include significant others
2. Transmission prevention: client should cover mouth when coughing,
expectorate into a tissue and place it in a paper bag; client should also
wash hands after coughing or sneezing; stress importance of plenty of
fresh air; include significant others
3. Importance of notifying physician at the first sign of persistent cough,
fever, or hemoptysis (may indicate recurrence)
4. Need for follow-up care including physical exam, sputum cultures, and
chest x-rays
5. Availability of community health services
6. Importance of high-protein, high-carbohydrate diet with inclusion of
supplemental vitamins
CYSTIC FIBROSIS
Description
 Is an autosomal recessive disorder affecting the exocrine glands, in which their

secretions become abnormally viscous and liable to obstruct glandular ducts.
 It primarily affects pulmonary and GI function.
 The average life expectancy for the cystic fibrosis patient is currently age 30 to 40.
Death may occur because of respiratory infection and failure.
 Other complications include esophageal varices, diabetes, chronic sinusitis,
pancreatitis, rectal polyps, intussusceptions, growth retardation, and infertility.
The responsible gene,the CF transmembrane conductance regulator (CFTR),is mapped to

chromosome 7 (see Genetic Considerations). The underlying defect of this autosomal
recessive condition involves a defective protein that interferes with chloride transport, which,
in turn, makes the body’s secretions very thick and tenacious. The ducts of the exocrine
glands subsequently become obstructed.
Assessment
 Usually present before age 6 months but severity varies and may present later.
 Meconium ileus is found in neonate.
 Usually present with respiratory symptoms, chronic cough, and wheezing.
 Parents may report salty taste when skin is kissed.
 Recurrent pulmonary infections.
 Failure to gain weight or grow in the presence of a good appetite.
 Frequent, bulky, and foul smelling stools (steatorrhea), excessive flatus, pancreatitis
and obstructive jaundice may occur.
 Protuberant abdomen, pot belly, wasted buttocks.
 Bleeding disorders.
 Clubbing of fingers in older child.
 Increased anteroposterior chest diameter (barrel chest).
 Decreased exertional endurance.
 Hyperglycemia, glucosuria with polyuria, and weight loss.
 Sterility in males.
1. Sweat chloride test measures sodium and chloride level in sweat.

o Chloride level of more than 60 mEq/L is virtually diagnostic.
o Chloride level of 40 to 60 mEq/L is borderline and should be repeated.
2. Duodenal secretions: low trypsin concentration is virtually diagnostic.
3. Stool analysis:
o Reduced trypsin and chymotrypsin levels-used for initial screening for cystic
fibrosis.
o Increased stool fat concentration.
o BMC ( Boehringer-Mannheim Corp.) meconium strip test for stool includes
lactose and protein content; used for screening.
4. Chest X-ray may be normal initially; later shows increased areas of infection,
overinflation, bronchial thickening and plugging, atelectasis, and fibrosis.
5. Pulmonary function studies (after age 4) show decreased vital capacity and flow rates
and increased residual volume or increased total lung capacity.
6. Diagnosis is made when a positive sweat test is seen in conjunction with one or more
of the following:
o Positive family history of cystic fibrosis.
o Typical chronic obstructive lung disease.
o Documented exocrine pancreatic insufficiency.
7. Genetic screening may be done for affected families.
 Ineffective airway clearance related to excess tenacious mucus
Treatment for lung problems includes:
 Antibiotics to prevent and treat lung and sinus infections. They may be taken by
mouth, or given in the veins or by breathing treatments. People with cystic fibrosis
may take antibiotics only when needed, or all the time. Doses are usually higher than
normal.
 Inhaled medicines to help open the airways
 DNAse enzyme replacement therapy to thin mucus and make it easier to cough up
 Flu vaccine and pneumococcal polysaccharide vaccine (PPV) yearly (ask your health
care provider)
 Lung transplant is an option in some cases
 Oxygen therapy may be needed as lung disease gets worse
Treatment for bowel and nutritional problems may include:
 A special diet high in protein and calories for older children and adults (see: Cystic
fibrosis nutrional considerations)
 Pancreatic enzymes to help absorb fats and protein
 Vitamin supplements, especially vitamins A, D, E, and K
 Your doctor can suggest other treatments if you have very hard stools
1. Antimicrobial therapy as indicated for pulmonary infection.

o Oral or I.V. antibiotics as required.
o Inhaled antibiotics, such as gentamicin or tobramycin, may be used for severe
lung disease or colonization of organisms.
2. Bronchodilators to increase airway size and assist in mucus clearance.
3. Pulmozyme recombinant human DNase (an enzyme) administered via nebulization to
decrease viscosity of secretions.
4. Pancreatic enzyme supplements with each feeding.
o Favored preparation is pancrelipase.
o Occasionally, antacid is helpful to improve tolerance of enzymes.
o Favorable response to enzymes is based on tolerance of fatty foods, decreased
stool frequency, absence of steatorrhea, improved appetite, and lack of
abdominal pain.
5. Gene therapy, in which recombinant DNA containing a corrected gene sequence is
introduced into the diseased lung tissue by nebulization, is in clinical trials.
 Monitor weight at least weekly to assess effectiveness of nutritional interventions.

 Monitor respiratory status and sputum production, to evaluate response to respiratory
care measures.
 To promote airway clearance, employ intermittent aerosol therapy three to four times
per day when the child is symptomatic.
 Perform chest physical therapy three to four times per day after aerosol therapy.
 Help the child to relax to cough more easily after postural drainage.
 Suction the infant or young child when necessary, if not able to cough.
 Teach the child breathing exercises using pursed lips to increase duration of
exhalation.
 Provide good skin care and position changes to prevent skin breakdown in
malnourished child.
 Provide frequent mouth care to reduce chances of infection because mucus is present.
 Restrict contact with people with respiratory infection.
 Encourage diet composed of foods high in calories and protein and moderate to high
in fat because absorption of food is incomplete.
 Administer fat-soluble vitamins, as prescribed, to counteract malabsorption.
 Increase salt intake during hot weather, fever, or excessive exercise to prevent sodium
depletion and cardiovascular compromise.
 To prevent vomiting, allow ample time for feeding because of irritability if not feeling
well and coughing.
 Encourage regular exercise and activity to foster sense of accomplishments and
independence and improve pulmonary function.
 Provide opportunities for parents to learn all aspects of care for the child.
 Teach the parents about dietary regimen and special need for calories, fat, and
vitamins.
 Discuss need for salt replacement, especially on hot summer days or when fever,
vomiting, and diarrhea occur.
 Physical response: Pulmonary assessment; color, odor, character of mucus; cardiac

and GI assessment; pulse oximetry
 Nutritional data:Weight,use of enzymes,adherence to supplemental feedings
 Emotional response: Patient’s feelings about dealing with a chronic illness, patient’s
body image,parents’coping ability,siblings’response
Teach the patient and family how to prevent future episodes of pneumonia through
CPT,expectoration of sputum, and avoidance of peers with common colds and
nasopharyngitis. Explain that medications need to be taken at the time of each meal,
especially pancreatic enzymes and supplemental vitamins. Teach the parents protocols for
home IV care, as needed. Teach parents when to contact the physician:when temperature is
elevated over 100.5°F, sputum has color to it, or the child complains of increased lung
congestion or abdominal pain. Also educate parents on the need to keep routine follow-up
appointments for medication,laboratory, and general checkups. Teach the patient or parents
proper insulin administration and the appropriate signs and symptoms of high and low
glucose levels.
1. Disorder characterized by dysfunction of the exocrine glands (mucus-
producing glands of the respiratory tract, GI tract, pancreas, sweat glands,
salivary glands)
2. Transmitted as an autosomal recessive trait
3. Incidence: 1 in 1500-2000 live births
4. Most common lethal genetic disease among Caucasians in U.S. and Europe
5. No test to detect carriers
6. Prenatal diagnosis of CF is not reliable
7. Secretions from mucous glands are thick, causing obstruction and fibrosis of
tissue
8. Sweat and saliva have characteristic high levels of sodium chloride
9. Affected organs
1. Pancreas: 85% of CF clients have pancreatic involvement
1. obstruction of pancreatic ducts and eventual fibrosis and
atrophy of the pancreas leads to little or no release of enzymes
(lipase [fats], amylase [starch], and trypsin [protein])
2. absence of enzymes causes malabsorption of fats and proteins
3. unabsorbed food fractions excreted in the stool produce
steatorrhea
4. loss of nutrients and inability to absorb fat-soluble vitamins
causes failure to thrive
2. Respiratory tract: 99.9% of CF clients have respiratory involvement
1. increased production of secretions causes increased obstruction

of airway, air trapping, and atelectasis
2. pulmonary congestion leads to cor pulmonale
3. eventually death occurs by drowning in own secretions
2. Reproductive system
1. males are sterile

2. females can conceive, but increased mucus in vaginal tract
makes conception more difficult
3. pregnancy causes increased stress on respiratory system of
mother
2. Liver: one-third of clients have cirrhosis/portal hypertension
2. The disease is ultimately fatal; average age at death is 20 years; 95% of deaths
are from abnormal mucus secretion and fibrosis in the lungs
1. Pancreatic involvement: aimed at promoting absorption of nutrients
1. Diet modification
1. infant: predigested formula

2. older children: may require high-calorie, high-protein, or
low/limited-fat diet, but many CF clients tolerate normal diet
2. Pancreatic enzyme supplementation: enzyme capsules, tablets, or
powders (Pancrease, Cotazym, Viokase) given with meals and snacks
2. Respiratory involvement: goals are to maintain airway patency and to prevent
lung infection
1. Chest physiotherapy
2. Antibiotics for infection
2. Assessment findings: symptoms vary greatly in severity and extent
1. Pancreatic involvement
1. Growth failure; failure to thrive
2. Stools are foul smelling, large, frequent, foamy, fatty (steatorrhea),
contain undigested food
3. Meconium ileus (meconium gets stuck in bowel due to lack of
enzymes) in newborns
4. Rectal prolapse is possible due to greasy stools
5. Voracious appetite
6. Characteristic protruding abdomen with atrophy of extremities and
buttocks
7. Symptoms associated with deficiencies in the fat-soluble vitamins
8. Anemia
9. Diagnostic tests
1. trypsin decreased to absent in aspiration of duodenal contents

2. fecal fat in stool specimen increased
2. Respiratory involvement
1. Signs of respiratory distress

2. Barrel chest due to air trapping
3. Clubbing of digits
4. Decreased exercise tolerance due to distress
5. Frequent productive cough
6. Frequent pseudomonas infections
7. Diagnostic tests
1. chest x-ray reveals atelectasis, infiltrations, emphysemic

changes
2. pulmonary function studies abnormal
3. ABGs show respiratory acidosis
2. Electrolyte involvement
1. Hyponatremia/heat exhaustion in hot weather

2. Salty taste to sweat
3. Diagnostic tests
1. pilocarpine iontophoresis sweat test: indicates 2-5 times normal

amount of sodium and chloride in the sweat
2. fecal fat elevated
3. fecal trypsin absent or decreased
1. Pancreatic involvement
1. Administer pancreatic enzymes with meals as ordered: do not mix

enzymes until ready to use them; best to mix in applesauce.
2. Provide a high-calorie, high-carbohydrate (no empty-calorie foods),
high-protein, normal-fat diet.
3. Provide a double dose of multivitamins per day, especially fat-soluble
vitamins (A, D, E, K), in water-soluble form.
4. If low-fat diet required, MCT (medium-chain triglycerides) oil may be
used.
2. Respiratory involvement
1. Administer antibiotics as ordered (all antibiotics for pseudomonas are

given IV; doses may be above recommended levels (for virulent
organisms)
2. Administer expectorants, mucolytics (rarely used) as ordered.
3. Avoid cough suppressants and antihistamines.
4. Encourage breathing exercises.
5. Provide percussion and postural drainage 4 times a day.
6. Provide aerosol treatments as needed; hand-held nebulizers, mask,
intermittent positive pressure breathing (IPPB), mist tent.
2. Electrolyte involvement
1. Add salt to all meals, especially in summer.

2. Give salty snacks (pretzels).
2. Provide appropriate long-term support to child and family.
2. Promotion of child's independence
3. Avoidance of cigarette smoking in the house
4. Availability of support groups/community agencies
5. Alternative school education during extended hospitalization/home
recovery
Aspiration of a Foreign Object
1. Relatively common airway problem.
2. Severity depends on object (e.g., pins, coins, nuts, buttons, parts of toys)
aspirated and the degree of obstruction.
3. Depending on object aspirated, symptoms will increase over hours or weeks.
4. The curious toddler is most frequently affected.
5. If object does not pass trachea immediately, respiratory distress will be
evident.
6. If object moves beyond tracheal region, it will pass into one of the main stem
bronchi; symptoms will be vague, insidious.
7. Causes 400 deaths per year in children under age 4.
1. Objects in upper airway require immediate removal.

2. Lower airway obstruction is less urgent (bronchoscopy or laryngoscopy).
1. Sudden onset of coughing, dyspnea, wheezing, stridor, apnea (upper airway)

2. Persistent or recurrent pneumonia, persistent croupy cough or wheeze
3. Object not always visible on x-ray
4. Secondary infection
1. Perform Heimlich maneuver if indicated.

2. Reassure the scared toddler.
3. After removal, place child in high-humidity environment and treat secondary
infection if applicable.
4. Counsel parents regarding age-appropriate behavior and safety precautions.
PLEURAL EFFUSION
Definition
It is a collection of fluid in the pleural space of the lungs. Fluid normally resides in the
pleural space and acts as a lubricant for the pleural membranes to slide across one another
when we breathe. Fluid is constantly being added and reabsorbed by capillaries and lymph
vessels in the pleura. When this recycling process is interrupted, a pleural effusion can result.
Causes
Physicians determine the cause of the effusion based on the type of fluid that is accumulating.
 Transudative (watery fluid) effusions: Heart failure, pulmonary embolism, cirrhosis,
post open heart surgery, trauma
 Exudative (protein-rich fluid) effusions: Pneumonia , cancers, pulmonary embolism,
kidney disease, inflammatory diseases
Pleural fluid may be bloody (hemorrhagic), chylous (thick and white), rich in cholesterol, or
purulent.
Signs and symptoms
(Small effusions may not present with symptoms and may only be found via chest X-ray.
Larger effusions can cause symptoms such as:)
 Decreased lung expansion
 Dyspnea
 Dry, non-productive cough
 Tactile fremitus
 Orthopnea
 Tachycardia
Diagnostic Procedures
 Chest x-ray
 CT scan of the chest
 Ultrasound of the chest
 Thoracentesis
 Pleural fluid analysis via thoracentesis
Medical Management
 Thoracentesis
 Pleurectomy- consists of surgically stripping the parietal pleura from the visceral
pleura. This produces and inflammatory reaction that causes adhesion formation
between the two layers as they heal.
 Pleurodesis- involves the instillation of a sclerosing agent (talc, doxycycline, or
tetracycline) into the pleural space via a thoracotomy tube. These agents cause the pleura
to sclerose together.
Nursing interventions for pleural effusions
1. Identify and treat the underlying cause

2. Monitor breath sounds
3. Place the client in a high Fowler’s position
4. Encourage coughing and deep breathing
5. Prepare the client for thoracentesis
6. If pleural effusion is recurrent, prepare the client for pleurectomy or pleurodesis as
prescribed

References
 Black, Joyce M. and Hawks, Jane H. Medical-Surgical Nursing. Clinical
Management for Positive Outcomes. Pp 1872-1873
 http://my.clevelandclinic.org/disorders/pleural_effusion/ts_overview.aspx
 Silvestri, Linda Ann. Comprehensive Review for the NCLEX-RN Examination. 4th
Ed. Pp 811-826

Pneumothorax
Description
1. Pneumothorax is the accumulation of atmospheric air in the pleural space,
which results in a rise in intrathoracic pressure and reduced vital capacity.
2. The loss of negative intrapleural pressure results in collapse of the lung.

3. A spontaneous pneumothorax occurs with the rupture of a bleb.
4. An open pneumothorax occurs when an opening through the chest wall
allows the entrance of positive atmospheric pressure into the pleural space.
5. Diagnosis of pneumothorax is made by chest x-ray film.
Causes
The cause of a closed or primary spontaneous penumothorax is the rupture
of a bleb (vesicle) on the surface of the visceral pleura. Secondary
spontaneous pneumothorax can result from chronic obstructive pulmonary
disease (COPD), which is related to hyperinflation or air trapping, or from
the effects of cancer, which can result in the weakening of lung tissue or
erosion into the pleural space by the tumor. Blunt chest trauma and
penetrating chest trauma are the primary causes of traumatic and tension
pneumothorax. Other possible causes include therapeutic procedures such
as thoracotomy, thoracentesis, and insertion of a central line.
Assessment
1. Absent breath sounds on affected side
2. Cyanosis
3. Decreased chest expansion unilaterally
4. Dyspnea
5. Hypotension
6. Sharp chest pain
7. Subcutaneous emphysema as evidenced by crepitus on palpation
8. Sucking sound with open chest wound
9. Tachycardia
10. Tachypnea
11. Tracheal deviation to the unaffected side with tension pneumothorax
Complications
 Another collapsed lung in the future
 Shock
 Impaired gas exchange related to decreased oxygen diffusion capacity
 Chest x-ray reveals lung collapse with air between chest wall and visceral
pleura. Lungs are not filled with air but rather are collapsed.
 Other Tests: Complete blood count, plasma alcohol level, arterial blood
gases, rib x-rays, computed tomography (CT) scan.
Medical Management
 The priority is to maintain airway, breathing, and circulation. The most
important interventions focus on reinflating the lung by evacuating the pleural
air. Patients with a primary spontaneous pneumothorax that is small with
minimal symptoms may have spontaneous sealing and lung reexpansion.
 For patients with jeopardized gas exchange, chest tube insertion may be
necessary to achieve lung re-expansion.
 Maintain a closed chest drainage system; be sure to tape all connections, and
secure the tube carefully at the insertion site with adhesive bandages. Regulate
suction according to the chest tube system directions; generally, suction does
not exceed 20 to 25 cm H2O negative pressure.
 Monitor a chest tube unit for any kinks or bubbling, which could indicate an
air leak, but do not clamp a chest tube without a physician’s order because
clamping may lead to tension pneumothorax.
 Stabilize the chest tube so that it does not drag or pull against the patient or
against the drainage system. Maintain aseptic technique, changing the chest
tube insertion site dressing and monitoring the site for signs and symptoms of
infection such as redness, swelling, warmth, and drainage.
 Oxygen therapy and mechanical ventilation are prescribed as needed.
Surgical interventions include removing the penetrating object, exploratory
thoracotomy if necessary, thoracentesis, and thoracotomy for patients with two
or more episodes of spontaneous pneumothorax or patients with pneumothorax
that does not resolve within 1 week.
Pharmacologic Highlights
No routine pharmacologic measures will treat pneumothorax, but the
patient may need antibiotics, local anesthesia agents for procedures, and
analgesics, depending on the extent and nature of the injury. Analgesia is
administered for pain once the patient’s pulmonary status has stabilized.
1. Apply a dressing over an open chest wound.
2. Administer oxygen as prescribed.
3. Position the client in high fowler’s position.
4. Prepare for chest tube placement until the lung has expanded fully.
5. Monitor chest tube drainage system.
6. Monitor for subcutaneous emphysema.
 Physical findings: Breath sounds, vital signs, level of consciousness, urinary
output, skin temperature, amount and color of chest tube drainage, dyspnea,
cyanosis, nasal flaring, altered chest expansion, tracheal deviation, absence of
breath sounds
 Response to pain: Location, description, duration, response to interventions
 Response to treatment: Chest tube insertion—type and amount of drainage,
presence of air leak, presence or absence of crepitus, amount of suction,
presence of clots, response to fluid resuscitation; response to surgical
management
 Complications: Infection (fever, wound drainage); inadequate gas exchange
(restlessness, dropping SaO2); tension pneumothorax
 Review all follow-up appointments, which often involve chest x-rays,
arterial blood gas analysis, and a physical exam. If the injury was alcohol-
related, explore the patient’s drinking pattern.
 Refer for counseling, if necessary. Teach the patient when to notify the
physician of complications (infection, an unhealed wound, and anxiety) and to
report any sudden chest pain or difficulty breathing.
DIGESTIVE SYSTEM DISORDERS
HEPATITIS
Description
 Is a viral infection of the liver associated with a broad spectrum of clinical

manifestations from asymptomatic infection through icteric hepatitis to hepatic
necrosis.
Five forms of viral hepatits
Type A Hepatitis (HAV), (infectious hepatitis)
 Is caused by an RNA virus of the enterovirus family.

 It spreads primarily by fecal-oral route, usually through the ingestion of infected food
or liquids.
 It may also spread from person-to-person contact and, rarely, by blood transfusion.
 Type A hepatitis occurs worldwide, especially in areas with overcrowding and poor
sanitation.
Type B Hepatitis (HBW), (serum hepatitis)
 Is caused by a double-shelled virus containing DNA.

 It spreads primarily through blood (percutaneous and permucosal route).
 It can also spread by way of saliva, breast feeding, or sexual activity (blood, semen,
saliva, or vaginal secretions.
 Male homosexuals are at high risk for infection.
 After acute infection, 10% of patients progress on to carrier status or develop chronic
hepatitis.
 HBV is the main cause of cirrhosis and hepatocellular carcinoma.
Type C Hepatitis (HCV),( non-A, non-B hepatitis or posttransfusion hepatitis)
 Formerly called non-A, non-B hepatitis, usually spreads through blood or blood
product transfusion, usually from asymptomatic blood donors.
 It may also be transmitted through unsterile piercing or tattooing tools or dyes.
 It commonly affects I.V. drug users and renal dialysis patients and personnel.
 HCV is the most common form of postransfusion hepatitis.
Type D Hepatitis (HDV),(delta agent hepatitis)
 Also known as Delta hepatitis.

 Is caused by a defective RNA virus that requires the presence of hepatitis B-
specifically, hepatitis B surface antigen (HBsAg) – to replicate.
 HDV occurs along with HBV or may superinfect a chronic HBV carrier, and cannot
outlast a hepatitis B infection.
 It occurs primarily in I.V. drug abusers or those who have had multiple blood
transfusions, but the highest incidence is in the Mediterranean, Middle East, and
South America.
Type E Hepatitis (HEV),(enterically transmitted or epidemic non-A, non-B)
 Is caused by a nonenveloped, single-strand RNA virus.

 It transmitted by the fecal-oral route but is hard to detect because it is inconsistently
shed in the feces.
 Its occurence is primarily in India, Africa, Asia, or Central America.
Fulminant Hepatitis
 Is a rare but severe complication of hepatitis, which may require liver transplantation.
Stages of Viral Hepatitis
1. Preicteric Stage- The first stage of hepatitis preceding the apperance of jaundice.
2. Icteric Stage- The second stage of Hepatitis, which includes the apperance of
jaundice and associated symptoms such as elevated bilirubin levels, dark or tea-
colored urine, and clay-colored stools
3. Posticteric Stage- The convalescent stage in which the jaundice decreases and the
color of the urine and stool return to normal.
 Hepatitis can be caused by bacteria,by hepatotoxic agents (drugs,alcohol,industrial

chemicals), or most commonly,by a virus.
Pathophysiology
Assessment
Type A hepatitis
 Incubation period, 3 to 5 weeks.

 Prodromal symptoms: fatigue, anorexia, malaise, headache, low-grade fever, nausea,
vomiting. Highly contagious at this time, usually 2 weeks before onset of jaundice.
 Icteric phase: jaundice, tea-colored urine, clay0colored stools, right upper quadrant
pain and tenderness.
 Symptoms often milder in children.
Type B hepatitis
 Incubation period, 2 to 3 months.
 Prodronal symptoms (insidious onset): fatigue, anorexia, transient fever, abdominal
discomfort, nausea, vomiting, headache.
 May also have myalgias, photophobia, arthritis, angioedema, urticaria, maculopapular
rash, vasculitis.
 Icteric phase occurs 1 week to 2 months after onset of symptoms.
Type C hepatitis
 Incubation period, 6 weeks to several months.

 Similar to HBV but less severe.
Type D hepatitis
 Unclear incubation period.

 Similar to HBV but more severe.
Applicable to all type:
 Obtain a patient history. Ask about I.V. drug use, blood transfusions, contact with
infected persons (including sexual activity), travel to endemic areas, and ingestion of
possible contaminated food or water to help determine cause of hepatitis.
1. All forms of hepatitis; elevated serum transferase levels (aspartate aminotransferase,

lanine aminotransferase); may have abnormal clotting tests.
2. HAV: radioimmunoassay detects immunoglobulin M (IgM) antibodies to hepatitis A
virus in the acute phase.
3. HBV: radioimmunoassays detect hepatitis B surface antigen (HBsAg), antibody to
hepatitis B core antigen (anti-HBc), anti-HBsAg in various stages of hepatitis B
infection.
4. HCV: hepatitis C antibody may not be detected for 3 to 6 months after onset of illness
(used for screening); polymerase chain reaction testing evaluates viral activity.
5. HDV: anti-delta antibodies in the presence of HBsAg, or detection of IgM in acute
disease and IgG in chronic disease.
6. Hepatitis E antigen (with HCV ruled out).
7. If indicated, prepare the patient for liver biopsy to detect chronic active disease, track
progression, and evaluate response to therapy.
 Altered nutrition:Less than body requirements related to decreased oral intake,

nausea, vomiting,and anorexia
 Vitamin K injected subcutaneously (S.C.) if prothrombin time is prolonged.
 I.V. fluid and electrolyte replacements as indicated.
 Antiemetic for nausea.
 Long-term interferon therapy in combination with oral ribavirin may produce
remission inHCV patients. Peginterferon alfa-2b is a long-acting preparation given
S.C., once per week, and ribavirin is taken twice daily.
 Antiviral treatment is being investigated for HBV.
1. Monitor hydration through intake and output.

2. Monitor prothrombin time and for signs of bleeding.
3. Encourage the patient to eat meals in a sitting position to reduce pressure on the liver.
4. Encourage pleasing meals in an environment with minimal noxious stimuli (odors,
noise, and interruptions).
5. Teach self-administration of antiemetics as prescribed.
6. Encourage rest during symptomatic phase, according to level of fatigue.
7. Encourage diversional activities when recovery and convalescence are prolonged.
8. Encourage gradual resumption of activities and mild exercise during convalescent
period.
9. Stress importance of proper public and home sanitation and proper preparation and
dispensation of foods.
10. Encourage specific protection for close contacts.
11. Explain precautions about transmission and prevention of transmission to others to the
patient and family.
12. Warn the patient to avoid trauma that may cause bruising.
13. Stress the need to follow precautions with blood and secretions until the patient is
deemed free of HBsAg.
14. Emphasize that most hepatitis is self-limiting, but follow up is needed for liver
function tests.
 Findings of physical exam and ongoing assessments: Nausea, vomiting, anorexia,

diarrhea, color of stools and urine, daily weights, vital signs, jaundice, pruritus,
edema, ascites, pain, level of consciousness
 Response to medical and nursing interventions:Medications,comfort
measures,diet,hydration
 Pain:Location, duration,precipitating factors,response to interventions
 Provide instruction on the prevention of the spread of hepatitis to others. With

hepatitis A, do the following for 1 to 2 weeks after the onset of jaundice. Use strict
hand washing after bowel movements and before meals. Have separate toilet facilities
if possible (if not,clean the seat with bleach after each use). Wash linens,towels,and
undergarments separately from other items in hot,soapy water. Do not donate blood or
work in food services until such work is cleared by a physician.
 With hepatitis B,C,or D,do the following,as directed by a physician,until antigen-
antibody tests are negative. Maintain strict hand washing after urination and
defecation. Do not share personal items (toothbrush, razor,washcloth). Use disposable
eating utensils or wash utensils separately in hot, soapy water. Do not share food or
eating utensils. Do not share needles, and dispose of them properly after a single use.
Avoid intimate sexual contact; when sex can be resumed, use a condom and avoid
intercourse during menstruation. Do not donate blood. Instruct the patient to inform
household members and sexual partners of the fact that she or he has developed
hepatitis and to encourage them to notify a primary healthcare provider immediately
to assess the risk of the disease.
 To prevent complications, teach the patient to avoid alcohol for 6 months to 1 year,
avoid illicit drugs and toxic chemicals, and take acetaminophen only when necessary
and not beyond the recommended dosage. Note that in viral hepatitis, the patient has
immunity only to the type of hepatitis he or she has had.
1. Widespread inflammation of the liver tissue with liver cell damage due to
hepatic cell degeneration and necrosis; proliferation and enlargement of the
Kupffer cells; inflammation of the periportal areas (may cause interruption of
bile flow)
2. Hepatitis A
1. Incubation period: 15-45 days
2. Transmitted by fecal/oral route: often occurs in crowded living
conditions; with poor personal hygiene; or from contaminated food,
milk, water, or shellfish
3. Hepatitis B

2. Transmitted by blood and body fluids (saliva, semen, vaginal
secretions): often from contaminated needles among IV drug abusers;
intimate/sexual contact
2. Hepatitis C

2. Transmitted by parenteral route: through blood and blood products,
needles, syringes
1. Preicteric stage
1. Anorexia, nausea and vomiting, fatigue, constipation or diarrhea,

weight loss
2. Right upper quadrant discomfort, hepatomegaly, splenomegaly,
lymphadenopathy
2. Icteric stage
1. Fatigue, weight loss, light-colored stools, dark urine

2. Continued hepatomegaly with tenderness, lymphadenopathy,
splenomegaly
3. Jaundice, pruritus
2. Posticteric stage
1. Fatigue, but an increased sense of well-being

2. Hepatomegaly gradually decreasing
2. Diagnostic tests
1. All three types of hepatitis

1. SGPT (ALT), SGOT (AST), alkaline phosphatase, bilirubin,
ESR: all increased (preicteric)
2. leukocytes, lymphocytes, neutrophils: all decreased (pericteric)
3. prolonged PT
2. Hepatitis A
1. hepatitis A virus (HAV) in stool before onset of disease

2. anti-HAV (IgG) appears soon after onset of jaundice; peaks in
1-2 months and persists indefinitely
3. anti-HAV (IgM): positive in acute infection; lasts 4-6 weeks
2. Hepatitis B
1. HBsAg (surface antigen): positive, develops 4-12 weeks after

infection
2. anti-HBsAG: negative in 80% of cases
3. anti-HBc: associated with infectivity, develops 2-16 weeks
after infection
4. HBeAg: associated with infectivity and disappears before
jaundice
5. anti-HBe: present in carriers, represents low infectivity
2. Hepatitis C: no specific serologic tests
1. Promote adequate nutrition.
1. Administer antiemetics as ordered, 30 minutes before meals to

decrease occurrence of nausea and vomiting.
2. Provide small, frequent meals of a high-carbohydrate, moderate- to
high-protein, high-vitamin, high-calorie diet.
3. Avoid very hot or very cold foods.
2. Ensure rest/relaxation: plan schedule for rest and activity periods, organize
nursing care to minimize interruption.
3. Monitor/relieve pruritus (see Cirrhosis of the Liver).
4. Administer corticosteroids as ordered.
5. Institute isolation procedures as required; pay special attention to good hand-
washing technique and adequate sanitation.
6. In hepatitis A administer immune serum globulin (ISG) early to exposed
individuals as ordered.
7. In hepatitis B
1. Screen blood donors for HBsAg.
2. Use disposable needles and syringes.
3. Instruct client/others to avoid sexual intercourse while disease is
active.
4. Administer ISG to exposed individuals as ordered.
5. Administer hepatitis B immunoglobulin (HBIG) as ordered to provide
temporary and passive immunity to exposed individuals.
6. To produce active immunity, administer hepatitis B vaccine to those
individuals at high risk.
2. In non-A, non-B: use disposable needles and syringes; ensure adequate
sanitation.
1. Importance of avoiding alcohol

2. Avoidance of persons with known infections
3. Balance of activity and rest periods
4. Importance of not donating blood
5. Dietary modifications
6. Recognition and reporting of signs of inadequate convalescence:
anorexia, jaundice, increasing liver tenderness/discomfort
7. Techniques/importance of good personal hygiene
CIRRHOSIS
Description
 Is a chronic disease that causes cell destruction and fibrosis (scarring) of hepatic
tissue.
 Fibrosis alters normal liver structure and vasculature, impairing blood and lymph flow
and resulting in hepatic insufficiency and hypertension in the portal vein.
 Complications include hyponatremia, water retention, bleeding esophageal varices,
coagulopathy, spontaneous bacterial peritonitis, and hepatic encephalopathy.
Three major forms:
1. Laennec’s (alcohol induced) Cirrhosis

o Fibrosis occurs mainly around central veins and portal areas.
o This is the most common form of cirrhosis and results from chronic
alcoholism and malnutrition.
2. Postnecrotic (micronodular) Cirrhosis
o Consist of broad bands of scar tissue and results from previous acute viral
hepatitis or drug-induced massive hepatic necrosis.
3. Biliary Cirrhosis
o Consist of Scarring of bile ducts and lobes of the liver and results from chronic
biliary obstruction and infection (cholangitis), and is much rarer than the
preceding forms.
 Cirrhosis of the liver is a chronic disease that causes cell destruction and fibrosis
(scarring) of hepatic tissues. Fibrosis alters normal liver structure and vasculature,
impairing blood and lymph flow and resulting in hepatic insufficiency and
hypertension in the portal vein. Complications include hyponatremia, water retention,
bleeding esophageal varices, coagulopathy, spontaneous bacterial peritonitis, and
hepatic encephalopathy.
 Cirrhosis is known in three major forms. In Laennec’s (alcohol-induced)

cirrhosis, fibrosis occurs mainly around central veins and portal areas. This is the
most common form of cirrhosis and results from chronic alcoholism and malnutrition.
Postnecrotic (micronodular) cirrhosis consist of broad bands of scar tissue and results
from previous acute viral hepatitis or drug-induced massive hepatic necrosis. Biliary
cirrhosis consists of scarring of bile ducts and lobes of the liver and results from
chronic biliary obstruction and infection (cholangitis), and is much rarer than the
preceding forms.
Pathophysiology
Assessment
1. Early complaints including fatigue, anorexia, edema of the ankles in the evening,
epistaxis, bleeding gums, and weight loss.
2. In later disease:
o Chronic dyspepsia, constipation and diarrhea.
o Esophageal varices; dilated cutaneous veins around umbilicus (caput medusa);
internal hemorrhoids, ascites, splenomegaly.
o Fatigue, weakness, and wasting caused by anemia and poor nutrition.
o Deterioration of mental function.
o Estrogen-androgen imbalance causing spider angioma and palmar erythema;
menstrual irregularities in women; testicular and prostatic atrophy,
gynecomastia, loss of libido, and impotence in men.
o Bleeding tendencies and hemorrhage.
3. Enlarged, nodular liver.
1. Elevated serum liver enzyme levels, reduced serum albumin.

2. Liver biopsy detects cell destruction and fibrosis of hepatic disease.
3. Liver scan shows abnormal thickening and a liver mass.
4. CT scan determines the size of the liver and its irregular nodular surface.
5. Esophagoscopy determines the presence of esophageal varices.
6. Percutaneous transhepatic cholangiography differentiates extrahepatic from
intrahepatic obstructive jaundice.
7. Paracentesis examines ascitic fluid for cell, protein, and bacteria counts.
 Fluid volume excess related to retention
Medical management is based on presenting symptoms.
 Treatment includes antacids, vitamins, balanced diet, and nutritional supplements;

potassium-sparing diuretics (for ascites); avoidance of alcohol.
 Colchicine may increase the length of survval in patients with mild to moderate
cirrhosis.
Surgical Intervention
1. Transjugular intrahepatic portosystemic shunt may be performed in patients

whose ascites prove resistant. This percutaneous procedure creates a shunt from the
portal to systemic cisculation to reduce portal pressure and relieve ascites.
2. Orthotopic liver transplantation may be necessary.
Transjugular intrahepatic portosystemic shunt
 Provide asymptomatic relief measures such as pain medications and antiemetics.

 Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic that
inhibits the action of aldosteroe on the kidneys.
 I.V albumin to maintain osmotic pressure and reduce ascites.
 Administration of lactulose or neomycin through a nasogastric tube or retention
enema to reduce ammonia levels during periods of hepatic encephalopathy.
 Observe stools and emesis for color, consistency, and amount, and test each one for
occult blood.
 Monitor fluid intake and output and serum electrolyte levels to prevent dehydration
and hypokalemia, which may precipitate hepatic encephalopathy.
 Maintain some periods of rest with legs elevated to mobilize edema and ascites.
Alternate rest periods with ambulation.
 Encourage and assist with gradually increasing periods of exercise.
 Encourage the patient to eat high-calorie, moderate protein meals and supplementary
feedings. Suggest small, frequent feedings.
 Encourage oral hygiene before meals.
 Administer or teach self-administration of medications for nausea, vomiting, diarrhea
or constipation.
 Encourage frequent skin care, bathing with soap, and massage with emollient lotions.
 Keep the patient’s finger nails short to prevent scratching from pruritus.
 Keep the patient quiet and limit activity if signs of bleeding are evident.
 Encourage the patient to eat foods high vitamin C content.
 Use small gauge needles for injections and maintain pressure over injection site until
bleeding stops.
 Protect from sepsis through good handwashing and prompt recognition and
management of infection.
 Pad side rails and provide careful nursing surveillance to ensure the patient’s safety.
 Stress the importance of giving up alcohol completely.
 Involve the person closest to the patient, because recovery usually is not easy and
relapses are common.
 Physical findings:Bleeding,abdominal enlargement,weight gain or loss,fluid intake

and output,easy respirations,breath sounds,heart sounds,level of
consciousness,gastrointestinal status (nausea,vomiting,anorexia, diarrhea),color of
skin and sclera
 Laboratory results:White blood cell count, hemoglobin and hematocrit, albumin,
serum electrolytes,ALT,AST
 Nutrition:Tolerance of diet,appetite,ability to maintain body weight
 Response to treatment:Medications,surgery,pericentesis
 ALCOHOL ABUSE TREATMENT. Emphasize to the patient with alcoholic liver

cirrhosis that continued alcohol use exacerbates the disease. Stress that alcoholic liver
disease in its early stages is reversible when the patient abstains from alcohol.
Encourage family involvement in alcohol abuse treatment. Assist the patient in
obtaining counseling or support for her or his alcoholism.
 FOLLOW-UP. Encourage the patient to seek frequent medical follow-up. Visits
from a community health nurse to monitor the patient’s progress and to help with any
questions or problems at home are also helpful.
 SUPPORT GROUPS. Refer the patient to an alcohol support group or liver
transplant support group.
HEPATIC CARCINOMAS
 General information
1. Primary cancer of the liver is extremely rare, but it is a common site for metastasis
because of liver's large blood supply and portal drainage. Primary cancers of the
colon, rectum, stomach, pancreas, esophagus, breast, lung, and melanomas frequently
metastasize to the liver.
2. Enlargement, hemorrhage, and necrosis are common occurrences; primary liver
tumors often metastasize to the lung.
3. Higher incidence in men.
4. Prognosis poor; disease well advanced before clinical signs evident.
 Medical management
1. Chemotherapy and radiotherapy (palliative) to decrease tumor size and pain

2. Resection of liver segment or lobe if tumor is localized
 Assessment findings
1. Weakness, anorexia, nausea and vomiting, weight loss, slight increase in temperature
2. Right upper quadrant discomfort/ tenderness, hepatomegaly, blood-tinged ascites,
friction rub over liver, peripheral edema, jaundice
3. Diagnostic tests: same as cirrhosis of the liver (see Cirrhosis of the Liver) plus
1. Blood sugar decreased
2. Alpha fetoprotein increased
3. Abdominal x-ray, liver scan, liver biopsy all positive
 Nursing interventions: same as for cirrhosis of the liver plus
1. Provide emotional support for client/significant others regarding poor prognosis.

2. Provide care of the client receiving radiation therapy or chemotherapy.
3. Provide care of client with abdominal surgery plus
1. Preoperative
1. Perform bowel prep to decrease ammonium intoxication.
2. Administer vitamin K to decrease risk of bleeding.
2. Postoperative
1. Administer 10% glucose for first 48 hours to avoid rapid blood sugar
drop.
2. Monitor for hyper/hypoglycemia.
3. Assess for bleeding (hemorrhage is most threatening complication).
4. Assess for signs of hepatic encephalopathy
HEPATIC ENCEPHALOPATHY
1. Frequent terminal complication in liver disease
2. Diseased liver is unable to convert ammonia to urea, so that large quantities
remain in the systemic circulation and cross the blood/brain barrier, producing
neurologic toxic symptoms.
3. Caused by cirrhosis, GI hemorrhage, hyperbilirubinemia, transfusions
(particularly with stored blood), thiazide diuretics, uremia, dehydration
1. Early in course of disease: changes in mental functioning (irritability);

insomnia, slowed affect; slow slurred speech; impaired judgment; slight
tremor; Babinski's reflex, hyperactive reflexes
2. Progressive disease: asterixis, disorientation, apraxia, tremors, fetor hepaticus,
facial grimacing
3. Late in disease: coma, absent reflexes
4. Diagnostic tests
1. Serum ammonia levels increased (particularly later)
2. PT prolonged
3. Hgb and hct decreased
1. Conduct ongoing neurologic assessment and report deteriorations.

2. Restrict protein in diet; provide high carbohydrate intake and vitamin K
supplements.
3. Administer enemas, cathartics, intestinal antibiotics, and lactulose as ordered
to reduce ammonia levels.
4. Protect client from injury: keep side rails up; provide eye care with use of
artificial tears/eye patch.
5. Avoid administration of drugs detoxified in liver (phenothiazines, gold
compounds, methyldopa, acetaminophen).
6. Maintain client on bed rest to decrease metabolic demands on liver.
ESOPHAGEAL VARICES
1. Dilation of the veins of the esophagus, caused by portal hypertension from
resistance to normal venous drainage of the liver into the portal vein
2. Causes blood to be shunted to the esophagogastric veins, resulting in
distension, hypertrophy, and increased fragility.
3. Caused by portal hypertension, which may be secondary to cirrhosis of the
liver (alcohol abuse), swallowing poorly masticated food, increased intra-
abdominal pressure
1. Iced normal saline lavage

2. Transfusions with fresh whole blood
3. Vitamin K therapy
4. Sengstaken-Blakemore tube: a three-lumen tube used to control bleeding by
applying pressure on the cardiac portion of the stomach and against bleeding
esophageal varices. One lumen serves as NG suction, a second lumen is used
to inflate the gastric balloon, the third to inflate the esophageal balloon.
5. Intra-arterial or IV vasopressin
6. Injection sclerotherapy
7. Surgery for portal hypertension (decompresses esophageal varices and helps to
maintain optimal portal perfusion)
1. Ligation of esophageal and gastric veins to stop acute bleeding
2. Portacaval shunt: end-to-side or side-to-side anastomosis of the portal
vein to the inferior vena cava
3. Splenorenal shunt: end-to-side or side-to-side anastomosis of the
splenic vein to the left renal vein
4. Mesocaval shunt: end-to-side or use of a graft to anastomose the
inferior vena cava to the side of the superior mesenteric vein
1. Anorexia, nausea and vomiting, hematemesis, fatigue, weakness

2. Splenomegaly, increased splenic dullness, ascites, caput medusae, peripheral
edema, bruits
3. Diagnostic tests
1. PT prolonged
2. Hematest of vomitus positive
3. Serum albumin, RBC, Hgb, and hct decreased
4. LDH, SGOT (AST), SGPT (ALT), BUN, increased
1. Monitor/provide care for client with Sengstaken-Blakemore tube.
1. Facilitate placement of the tube: check and lubricate tip and elevate
head of bed.
2. Prevent dislodgment of the tube by placing client in semi-Fowler's
position; maintain traction by securing the tube to a piece of sponge or
foam rubber placed on the nose.
3. Keep scissors at bedside at all times.
4. Monitor respiratory status; assess for signs of distress and if respiratory
distress occurs cut the tubing to deflate the balloons and remove tubing
immediately.
5. Label each lumen to avoid confusion; maintain prescribed amount of
pressure on esophageal balloon and deflate balloon as ordered to avoid
necrosis.
6. Observe nares for skin breakdown and provide mouth and nasal care
every 1-2 hours (encourage client to expectorate secretions, suction
gently if unable).
2. Promote comfort: place client in semi-Fowler's position (if not in shock);
provide mouth care.
3. Monitor for further bleeding and for signs and symptoms of shock; hematest
all secretions.
4. Administer vasopressin as ordered and monitor effects.
5. Provide routine pre- and post-op care if the client has portasystemic or
portacaval shunt.
1. Minimizing esophageal irritation (avoidance of salicylates, alcohol; use

of antacids as needed; importance of chewing food thoroughly)
2. Avoidance of increased abdominal, thoracic, and portal pressure
3. Recognition and reporting of signs of hemorrhage
Ascites
1. Accumulation of free fluid in the abdominal cavity
2. Most frequently caused by cirrhotic liver damage, which produces
hypoalbuminemia, increased portal venous pressure, and hyperaldosteronism
3. May also be caused by CHF
1. Supportive: modify diet, bed rest, salt-poor albumin

2. Diuretic therapy (see Antihypertensive Drugs, Table 2.17, in Unit 2)
3. Surgery
1. Paracentesis: insertion of a needle into the peritoneal cavity through
the abdomen to remove abnormally large amounts of peritoneal fluid.
1. peritoneal fluid assessed for cell count, specific gravity,
protein, and microorganisms.
2. used in clients with acute respiratory or abdominal distress
secondary to ascites.
2. LeVeen shunt (peritoneal-venous shunt): used in chronic,
unmanageable ascites
1. permits continuous reinfusion of ascitic fluid back into the

venous system through a silicone catheter with a one-way
pressure-sensitive valve.
2. one end of the catheter is implanted into the peritoneal cavity
and is channeled through the subcutaneous tissue to the
superior vena cava, where the other end of the catheter is
implanted; the valve opens when pressure in the peritoneal
cavity is 3-5 cm of water higher than in superior vena cava,
thereby allowing ascitic fluid to flow into the venous system.
1. Anorexia, nausea and vomiting, fatigue, weakness, changes in mental

functioning
2. Positive fluid wave and shifting dullness on percussion, flat or protruding
umbilicus, abdominal distension/tautness with striae and prominent veins,
abdominal pain
3. Peripheral edema, shortness of breath
4. Diagnostic tests
1. Potassium and serum albumin decreased

2. PT prolonged
3. LDH, SGOT (AST), SGPT (ALT), BUN, sodium increased
1. Monitor nutritional status/provide adequate nutrition with modified diet.
1. Restrict sodium to 200-500 mg/day.

2. Restrict fluids to 1000-1500 ml/day.
3. Promote high-calorie foods/snacks.
2. Monitor/prevent increasing edema.
1. Administer diuretics as ordered and monitor for effects.

2. Measure I&O.
3. Monitor peripheral pulses.
4. Measure abdominal girth.
5. Inspect/palpate extremities, sacrum.
6. Administer salt-poor albumin to replace vascular volume.
2. Monitor/promote skin integrity.
1. Reposition frequently.
2. Apply lotions to stretched areas.
3. Assess for redness, breakdown.
2. Promote comfort: place client in mid- to high-Fowler's and reposition
frequently.
3. Provide nursing care for the client undergoing paracentesis.
1. Confirm that client has signed a consent form.

2. Instruct client to empty bladder before the procedure to prevent
inadvertent puncture of the bladder during insertion of trocar.
3. Inform client that a local anesthetic will be provided to decrease pain.
4. Place in sitting position to facilitate the flow of fluid by gravity.
5. Measure abdominal girth and weight before and after the procedure.
6. Record color, amount, and consistency of fluid withdrawn and client
tolerance during procedure.
7. Assess insertion site for leakage.
2. Provide routine pre- and post-op care for the client with LeVeen shunt.
Definition
Cholelithiasis
 Refers to formation of calculi (e.g. gallstones) in the gallbladder.
Cholecystitis
 Is acute or chronic inflammation of the gallbladder.
 Acute cholecystits – may be calculous (with gallstones) or acalculous (with

gallstones).
 Chronic cholecystitis – may follow acute cholecystitis, although it often

occurs independently. It is usually associated with gallstone formation.
Risk Factors
Cholelithiasis
Results from changes in bile components or bile stasis, associated with:
 Infection
 Cirrhosis
 Pancreatitis
 Celiac disease
 Diabetes mellitus
 Pregnancy
 Hormonal contraceptive use
Cholecystitis
 Obstruction of the cystic duct by an impacted gallstone
 Tissue damage due to trauma, massive burns, or surgery
 Gram-negative septicemia
 Multiple blood transfusion
 Prolonged fasting
 Hypertension
 Overuse of opioid analgesics
Pathophysiology
Cholelithiasis
Calculi usually from solid constituents of bile; the three major types are:
 Cholesterol gallstones – the most common type, thought to form in supersaturated bile
 Pigment gallstones – formed mainly of unconjugated pigments in bile precipitate
 Mixed types – with characteristics of pigment and cholesterol stones.
Gallstones can obstruct the cystic duct, causing cholecystitsi, or the common bile duct, which
is called choledocholithiasis.
Cholecystitis
 In acute and chronic cholecystitis, inflammation causes the gallbladder wall to

become thickened and edematous and causes the cystic lumen to increase in diameter.
 If inflammation spreads to the common bile duct, obstruction of bile drainage can lead
to jaundice. Other possible complications include: (Empyema i.e. pus-filled
gallbladder, perforation, emphysematous cholecystitis)
Assessment/Clinical Manifestations/Signs And Symptoms

Cholelithiasis (up to ½ of persons with gallstones are asymptomatic; however possible
clinical manifestations include the following)
 Episodic (commonly after a high-fat meal), cramping pain in the right upper
abdominal quadrant or the epigastrium, possibly radiating to the back near the right
scapular tip (i.e. biliary colic)
 Nausea and vomiting
 Fat intolerance
 Fever and leukocystosis
 Signs and symptoms of jaundice
Acute Cholecystitis
 Biliary colic
 Tenderness and rigidity in the right upper quadrant elicited on palpation (i.e.
Murphy’s sign)
 Fever
 Nausea and vomiting
 Fat intolerance
 Signs and symptoms of jaundice
Chronic Cholecystitis
 Pain, which is less severe than in the acute form
 Fever, which is less severe than in the acute form
 Fat intolerance
 Heartburn
 Flatulence
Laboratory and diagnostic study findings
Cholelithiasis
 Biliary ultrasonography (i.e. cholecystosonography) can detect gallstones in most

cases.
Cholecystitis
 White blood cell count reveals leukocytosis

 Serum alkaline phosphatase is elevated
 Ultrasonography detects gallstone
 Endoscopic retrograde cholangiopancreatography may reveal inflamed common bile

ducts, gallbladder, and gallstones.
 Percutaneous transheptic cholangiography can identify gallstones within the bile

ducts.
Medical Management
Teach the client about planned treatments.
 Chenodeoxycholic acid is administered to dissolve gallstones. It is effective in

dissolving about 60% of radiolucent gallstones. Pigment gallstones cannot be
dissolves and must be excised.
 Nonsurgical removal, such as lithotripsy or extracorpeal shock wave therapy, may be

implemented.
Surgical treatment may be ordered.
Laparoscopic cholecytectomy (usually outpatient surgery) is performed through a small

incision made through the abdominal wall in the umbilicus.
 Assess incision sites for infection. Instruct the client to notify the health care provider
if loss of appetite, vomiting, pain, abdominal distention, or fever occur.
 Advise the client that he will need assistance at home for 2 to 3 days.
Cholecystectomy is removal of the gallbladder after ligation of the cystic duct and artery.
Inform the client that a T-tube will be inserted to drain blood; serosanguineous fluids, and
bile and that the T-tube must be taped below the incision
Choledochostomy is an incision into the common bile duct for calculi removal.
Cholecystomy is the surgical opening of the gallbladder for removal of stones, bile, or pus,
after which a drainage tube is placed.
Nursing Diagnosis
 Acute pain secondary to biliary obstruction
 Ineffective coping related to nausea
 Deficient knowledge related to diagnosis
 Impaired gas exchange related to high abdominal surgical incision.

 Impaired skin integrity related to altered biliary drainage after surgical incision.
 Imbalanced nutrition related to inadequate bile secretion.
Nursing Management
Provide nursing interventions during an acute gallbladder attack.
 Intervene to relive pain; give prescribed analgesics
 Promote adequate rest
 Administer IV fluids, monitor intake and output
 Monitor nasogastric tube and suctioning
 Administer antibiotics if prescribed.
Provide adequate nutrition.
 Assess nutritional status. Encourage a high-protein, high-carbohydrate, low-fat diet.
Cholecystitis/Cholelithiasis
1. Cholecystitis: acute or chronic inflammation of the gallbladder, most

commonly associated with gallstones. Inflammation occurs within the walls of
the gallbladder and creates a thickening accompanied by edema.
Consequently, there is impaired circulation, ischemia, and eventual necrosis.
2. Cholelithiasis: formation of gallstones, cholesterol stones most common

variety
3. Most often occurs in women after age 40, in postmenopausal women on
estrogen therapy, in women taking oral contraceptives, and in the obese;
Caucasians and Native Americans are also more commonly affected.
4. Stone formation may be caused by genetic defect of bile composition,

gallbladder/bile stasis, infection.
5. Acute cholecystitis usually follows stone impaction, adhesions; neoplasms

may also be implicated.
1. Supportive treatment: NPO with NG intubation and IV fluids
2. Diet modification with administration of fat-soluble vitamins
3. Drug therapy
1. Narcotic analgesics (Demerol is drug of choice) for pain. Morphine

sulfate is contraindicated because it causes spasms of the sphincter of
Oddi.
2. Anticholinergics (atropine) for pain. (Anticholinergics relax smooth

muscle and open bile ducts.)
3. Antiemetics
4. Surgery: cholecystectomy / choledochostomy
1. Epigastric or right upper quadrant pain, precipitated by a heavy meal or

occurring at night
2. Intolerance for fatty foods (nausea, vomiting, sensation of fullness)
3. Pruritus, easy bruising, jaundice, dark amber urine, steatorrhea
4. Diagnostic tests
1. Direct bilirubin transaminase, alkaline phosphatase, WBC, amylase,

lipase: all increased
2. Oral cholecystogram (gallbladder series): positive for gallstone
1. Administer pain medications as ordered and monitor for effects.
2. Administer IV fluids as ordered.

3. Provide small, frequent meals of modified diet (if oral intake allowed).
4. Provide care to relieve pruritus.
5. Provide care for the client with a cholecystectomy or choledochostomy.
Cholecystectomy/Choledochostomy
1. Cholecystectomy: removal of the gallbladder with insertion of a T-tube into

the common bile duct if common bile duct exploration is performed
2. Choledochostomy: opening of common duct, removal of stone, and insertion

of a T-tube
3. Cholecystectomy performed via laparoscopy for uncomplicated cases when

client has not had previous abdominal surgery
2. Nursing interventions: routine preoperative care
3. Nursing interventions: postoperative
1. Provide routine post-op care.
2. Position client in semi-Fowler's or side-lying positions; reposition frequently.
3. Splint incision when turning, coughing, and deep breathing.
4. Maintain/monitor functioning of T-tube.
1. Ensure that T-tube is connected to closed gravity drainage.
2. Avoid kinks, clamping, or pulling of the tube.
3. Measure and record drainage every shift.
4. Expect 300-500 ml bile-colored drainage first 24 hours, then 200 ml/24

hours for 3-4 days.
5. Monitor color of urine and stools (stools will be light colored if bile is
flowing through T-tube but normal color should reappear as drainage
diminishes).
6. Assess for signs of peritonitis.
7. Assess skin around T-tube; cleanse frequently and keep dry.

1. Adherence to dietary restrictions
2. Resumption of ADL (avoid heavy lifting for at least 6 weeks; resume

sexual activity as desired unless ordered otherwise by physician);
clients having laparoscopy cholecystectomy usually resume normal
activity within two weeks.
3. Recognition and reporting of signs of complications (fever, jaundice,

pain, dark urine, pale stools, pruritus)
Appendicitis
General information
Inflammation of the appendix that prevents mucus from passing into the cecum; if untreated,
ischemia, gangrene, rupture, and peritonitis occur. Most common in school-age children. May
be caused by mechanical obstruction (fecaliths, intestinal parasites) or anatomic defect; may
be related to decreased fiber in the diet
Assessment findings
6. Diffuse pain, localizes in lower right quadrant
7. Nausea/vomiting
8. Guarding of abdomen, rebound tenderness, walks stooped over
9. Decreased bowel sounds
10. Fever
11. Diagnostic tests
1. WBC increased
2. Elevated acetone in urine
6. Administer antibiotics/antipyretics as ordered
7. Prevent perforation of the appendix; do not give enemas or cathartics or use

heating pad
8. In addition to routine pre-op care for appendectomy
1. Give support to parents if seeking treatment was delayed.
2. Explain necessity of obtaining lab work prior to surgery.

2. In addition to routine post-op care
1. Monitor NG tube (usually with low suction).
2. Monitor Penrose drains.
3. Position in semi-Fowler's or lying on right side to facilitate drainage.
4. Administer antibiotics as ordered.
APPENDECTOMY
Definition
 The excision of the appendix usually performed to remove an acutely inflamed organ.
 Many surgeons perform an appendectomy as a prophylactic procedure when operating

in the abdomen for other reasons. This procedure is then referred to as an incidental
appendectomy.
Position
 Supine, with arms extended on armboards
Incision Site
 McBurney (muscle splitting) incision.
Packs/ Drapes
 Laparotomy pack
 Four folded towels
Instrumentation
 Major Lap tray or minor tray
 Internal stapling device

Supplies/ Equipment
 Basin set
 Blades
 Needle counter
 Penrose drain
 Culture tubes
 Solutions
 Sutures
 Internal stapling instruments
 Medication
Procedure
1. An incision is made in the right lower abdomen, either transversely oblique

(McBurney) or vertically (for a primary appendectomy).
2. The surgeon’s assistant retracts the wound edges with a Richardson or similar
retractor.
3. The appendix is identifies and its vascular supply ligated.
4. The surgeon grasps the appendix with a Babcock clamp, and delivers it into the
wound site.
5. The tip of the appendix may then be grasped with a Kelly clamp to hold it up, and a
moist Lap sponge is placed around the base of the appendix (stump) to prevent
contamination of bowel contents, in case any spill out occurs during the procedure.
6. The surgeon isolates the appendix from its attachments to the bowel (mesoappendix)
using a Metzenbaum scissors.
7. Taking small bits of tissue along the appendix, the mesoappendix is double-clamped,
and ligated with free ties.
8. The base of the appendix is grasped with a straight Kelly clamp, and the appendix is
removed.
9. The stump may be inverted into the cecum, using a purse-string suture on a fine
needle, cauterize with chemicals, or simply left alone after ligation.
10. Another technique is to devascularize the appendix and invert the entire appendix into
the cecum.
11. The appendix, knife, needle holder, and any clamps or scissors that have come in
contact with the appendix are delivered in a basin in the circulating nurse.
12. The wound is irrigated with warm saline, and is closed in layers, except when an
abscess has occurred, as with acute appendicitis.
13. A drain may be placed into the abscess cavity, exiting through the incision or a stab
wound.
14. An alternative technique may be use the internal stapling device, by placing the
stapling instrument around the tissue at the appendiocecum junction.
15. By using the technique, the possibility of contamination from spillage is greatly
reduced.
Perioperative Nursing Consideration
1. Instruments used for amputation of the appendix are to be isolated in a basin.
2. If ruptured, the case must be considered contaminated, and the surgeon may elect to
use antibiotic irrigation prior to closure of the abdomen with an insertion of a drain.
3. There may be no skin closure of the wound if the appendix has rupture.
PUD
GERD
Definition
 Gastroesophageal reflux disease (GERD) is excessive reflux of hydrochloric acid into

the esophagus.
Risk Factors
 Incompetent lower esophageal sphincter (LES), pyloric stenosis or a motility disorder.

Pathophysiology
 A weak or incompetent LES allows backward movement of gastric contents into the
esophagus; decreased esophageal peristalsis and salivary function impair clearance of the
refluxed acid, resulting in mucosal injury to the esophagus.
image by : myhealth.alberta.ca
Assessment/Clinical Manifestations/Signs and Symptoms
 Pyrosis (i.e. burning sensation in the esophagus)

 Regurgitation of sour-tasting secretions
 Dysphagia (i.e. difficulty swallowing) and odynophagia ( i.e pain on swallowing)
 Symptoms mimicking those of a heart attack
Nursing Management
Teach the client to avoid factors that increase lower esophageal irritation.
 Eat a low-fat, high-fiber diet

 Avoid irritants, such as spicy or acidic foods, alcohol, caffeine, and tobacco, because
they increase gastric acid production.
 Avoid food or drink 2 hours before bedtime or lying down after eating
 Elevate the head of the bed on 6” to 8” bocks
 Lose weight if necessary
If symptoms persist, prepare the client for surgical repair, which includes a
funduplication (i.e. wrapping a portion of the gastric fundus around the sphincter area
of the esophagus)
Administer medications, which may include antacids, histamine-receptor antagonists,

and proton-pump inhibitors.
CLEFT LIP/PALATE
Definiton
Cleft palate repair – is surgical repair of congentinal defects in the palate
Causes of defects
1. Lack of embryonic development elements of the prepalate (face, lips, premaxilla and
incisors)
2. Palate (hard or soft palate, uvula and additional maxillary teeth
Complications
 Nursing or feeding defects
 Speech defects
 Respiratory defects
Time of surgery preferred:
 Before the 2 years old

Procedure
 General anesthesia induction.

 Insertion of endotracheal tube
 Local anesthesia with epinephrine is injected to prevent homeostasis
 Repair of a complete unilateral (prepalatal and palatal) defect incisions are made of
the soft palate
 Development of layers of oral mucosa, muscle and nasal mucosa
 Suture replacement are placed on the hard palate
 Optimal bone grafts are done
 Two layers are sutured muscle layers and oral mucosa
Nursing Considerations in preparing the patient
 The patient must be restrained properly since the table may be in reverse
Trendelenburg position
 Keep the patient’s temperature well regulated since the patient’s body surface area is
small
 Assist the surgeon in extending the head of the bed during the procedure
 Always observe aseptic technique during the surgery
 Minimize skin exposure as much as possible during the surgery
Nursing Considerations after the procedure
 Place comfortably the patient on his or her sides

 Use restraints on elbow level to prevent ample movement of the child
 Hydrate the child using cups instead of bottles, as well as to clean suture lines
 Support proper positioning by holding the child while feeding sessions to prevent
aspiration.
Hemorrhoids LAN
 Hemorrhoids are vascular masses that protrude into the lumen of the
lower rectum or perianal area.
 They result when increased intra-abdominal pressure causes
engorgement in the vascular tissue lining the anal canal.
 Loosening of vessels from surrounding connective tissue occurs with
protrusion or prolapse into the anal canal.
 There are two main types of hemorrhoids: external hemorrhoids
appear outside the external sphincter, and internal hemorrhoids appear
above the internal sphincter.
 When blood within the hemorrhoids becomes clotted because of
obstruction, the hemorrhoids are referred to as being thrombosed.
 Predisposing factors include pregnancy, prolonged sitting or
standing, straining stool, chronic constipation or diarrhea, anal
infection, rectal surgery or episiotomy, genetic predisposition,
alcoholism, portal hypertension (cirrhosis), coughing, sneezing, or
vomiting, loss of muscle tone attributable to old age, and anal
intercourse.
 Complications include hemorrhage, anemia, incontinence of stool,
and strangulation.
 Hemorrhoids are the most common of a variety of anorectal
disorders.
Causes/Risk Factors
Modifiable
 Some factors that are associated with hemorrhoids are occupations
that require prolonged sitting or standing; heart failure; anorectal
infections; anal intercourse; alcoholism; pregnancy; colorectal cancer;
and hepatic disease such as cirrhosis, amoebic abscesses, or hepatitis.
 Straining because of constipation, diarrhea, coughing, sneezing, or
vomiting and loss of muscle tone because of aging, rectal surgery, or
episiotomy can also cause hemorrhoids.
Assessment
1. Pain (more so with external hemorrhoids), sensation of incomplete
fecal evacuation, constipation, and anal itching. Sudden rectal pain may
occur if external hemorrhoids are thrombosed.
2. Bleeding may occur during defecation; bright red blood on stool
caused by injury of mucosa covering hemorrhoid.
3. Visible and palpable masses at anal area.
1. External examination with anoscope or proctoscope shows single or
multiple hemorrhoids.
2. Barium edema or colonoscopy rules out more serious colonic lesions
causing rectal bleeding such as polyps.
 Pain (acute or chronic) related to rectal swelling and prolapse
1. High-fiber diet to keep stools soft.
2. Warm sitz baths to ease pain and combat swelling.
3. Reduction of prolapsed external hemorrhoid manually.
Surgical Interventions:
1. Injection of sclerosing solutions to produce scar tissue and decrease
prolapse is an office procedure.
2. Cryodestruction (freezing) of hemorrhoids is an office procedure.
3. Surgery may be indicated in presence of prolonged bleeding,
disabling pain, intolerable itching, and general unrelieved discomfort.
1. Stool softeners to keep stools soft and relieve symptoms.
2. Topical creams, suppositories or other preparation such as Anusol,
Preparation H, and witch-hazel compresses to reduce itching and
provide comfort.
3. Oral analgesics may be needed.
1. After thrombosis or surgery, assist with frequent repositioning using
pillow support for comfort.
2. Provide analgesics, warm sitz baths, or warm compresses to reduce
pain and inflammation.
3. Apply witch-hazel dressing to perianal area or anal creams or
suppositories, if ordered, to relieve discomfort.
4. Observe anal area postoperatively for drainage and bleeding.
5. Administer stool softener or laxative to assist with bowel movements
soon after surgery, to reduce risk of stricture.
6. Teach anal hygiene and measures to control moisture to prevent
itching.
7. Encourage the patient to exercise regularly, follow a high fiber diet,
and have an adequate fluid intake (8 to 10 glasses per day) to avoid
straining and constipation, which predisposes to hemorrhoid formation.
8. Discourage regular use of laxatives; firm, soft stools dilate the anal
canal and decrease stricture formation after surgery.
9. Tell patient to expect a foul-smelling discharge for 7 to 10 days after
cryodestruction.
10. Determine the patient’s normal bowel habits and identify
predisposing factors to educate patient about preventing recurrence of
symptoms.
1. Physical findings:Rectal examination,urinary retention,bleeding,and
mucous drainage
2. Wound healing:Drainage,color,swelling
3. Pain management:Pain (location,duration,frequency),response to
interventions
4. Postoperative bowel movements:Tolerance for first bowel movement
Teach the patient the importance of a high-fiber diet, increased fluid intake,
mild exercise, and regular bowel movements. Be sure the patient schedules
a follow-up visit to the physician. Teach the patient which analgesic
applications for local pain may be used. If the patient has had surgery,
teach her or him to recognize signs of urinary retention, such as bladder
distension and hemorrhage,and to contact the physician at their
appearance.
Sources:
Nursingcrib.com
Marilyn Sawyer Sommers, RN, PhD, FAAN , Susan A. Johnson, RN, PhD, Theresa
A. Beery, PhD, RN , DISEASES AND DISORDERS A Nursing
Therapeutics Manual, 2007 3rd ed
Hemorrhoidectomy
Definition
 Excision of painful distended veins of the anus and rectum.
 Hemorrhoids are classified as internal or external, depending on their
location. Hemorrhoids are generally associated with local anal
problems such as anal ulcers and fistulas, or they may accompany
pregnancy. Anesthesia may be regional, local, or general.
Position
 Lithotomy, modified lateral (Sims), or jack knife.
Skin Preparation
 The buttocks is taped apart with wide adhesive tape on each side of
the anus, attaching the other end to the table frame. Only a minimal
prep is usually performed.
Packs/ Drapes
 Laparotomy pack (jackknife or lateral sims position)
 Lithotomy pack (lithotomy position)
Instrumentation
 Minor tray
 Rectal tray with dilators and rectractor
 Sigmoidoscopy instrument (optional)
Supplies/ Equipment
 Stirrups
 Pillows or roll for positioning
 Suction
 Blades – (1) #10, (1) #15
 Minor basin set
 Needle counter
 Hemostatic agent
 Lubricant
 Pressure dressing
 Laser (optional)
Procedure Overview
 Before beginning the surgical procedure, a sigmoidoscopy may be
performed, followed by gentle dilation of the rectum.
 The hemorrhoid is grasped with a Penington, Allis, or Kocher clamp.
 The proximal portion of the hemorrhoid is excised by scalpel, cautery,
or laser. Is the anus is stemotic, the distal internal sphincter may be
incised.
 A mucous membrane flap and/ or skin flaps may be used to cover
the denuded areas.
 Bleeders are controlled with ligature ties (3-0 Dexon/ chromic) or by
cautery.
 Care is taken not to excise too much skin, anoderm, or mucous
membrane and to avoid injury to the sphincter mechanism.
Perioperative Nursing Considerations
 Be prepared to perform a sigmoidoscopy prior to the procedure.
 When electrosurgical unit is used, apply the ground pad after the
patient has been placed in the lithotomy position.
 Protect the skin under the adhesive tape with tincture of benzoin.
 Should laser be used, all safety precautions must be in place prior to
the patient’s entry into the procedure room.
IMMUNE DISORDERS
Acquired Immune Deficiency Syndrome (AIDS)
1. Characterized by severe deficits in cellular immune function; manifested

clinically by opportunistic infections and/or unusual neoplasms
2. Etiologic factors
1. Results from infection with human immunodeficiency virus (HIV), a

retrovirus that preferentially infects helper T-lymphocytes (T4cells)
2. Transmissible through sexual contact, contaminated blood or blood

products, and from infected woman to child in utero or possibly
through breast-feeding
3. HIV is present in an infected person's blood, semen, and other body

fluids
3. Epidemiology is similar to that of hepatitis B; increased incidence in

populations in which sexual promiscuity is common and in IV drug abusers
1. No effective cure for AIDS at present; several categories of antiretroviral

drugs now available
1. Nucleoside Analogues: Didanosine (Videx) (ddl), Lamivudine (3TC)

(Epivir), Stavudine (d4T) (Zerit), Zidovudine (AZT) (Retrovir)
2. Nucleoside Analogues: Didanosine (Videx) (ddl), Lamivudine (3TC)

(Epivir), Stavudine (d4T) (Zerit), Zidovudine (AZT) (Retrovir)
3. Non Nucleoside Analogues: Delavirdine (DLV) (Rescriptor),

Nevirapine (NVP) (Viramune)
4. Protease Inhibitors: Indinavir (Crixivan), Nelfinavir (Viracept),

Ritonavir (Norvir), Saquinavir (Invirase)
2. Primary goal of treatment is to treat opportunistic infections and cancers that

develop and provide supportive care for the effects of the disease, e.g.,
diarrhea, malnutrition, mental changes, etc.
3. Drugs used to treat PCP include
1. PO or IV trimethoprim-sulfamethoxazole (Bactrim, Septra); side

effects include rash, leukopenia, fever
2. IM or IV pentamidine (Pentam 300); side effects include

hepatotoxicity, nephrotoxicity, blood sugar imbalances, abscess or
necroses at IM injection site, hypotension
2. Assessment findings (see Table 4.18)
1. Fatigue, weakness, anorexia, weight loss, diarrhea, pallor, fever, night sweats
2. Shortness of breath, dyspnea, cough, chest pain, and progressive hypoxemia

secondary to infection (pneumonia)
3. Progressive weight loss secondary to anorexia, nausea, vomiting, diarrhea, and

a general wasting syndrome; fatigue, malaise
4. Temperature elevations (persistent or intermittent); night sweats
5. Neurologic dysfunction secondary to acute meningitis, progressive dementia,

encephalopathy, encephalitis
6. Presence of opportunistic infection, for example
1. Pneumocystis carinii pneumonia
2. Herpes simplex, cytomegalovirus, and Epstein-Barr viruses
3. Candidiasis: oral or esophageal
4. Mycobacterium-avium complex
2. Neoplasms
1. Kaposi's sarcoma
2. CNS lymphoma
3. Burkitt's lymphoma
4. Diffuse undifferentiated non-Hodgkin's lymphoma
2. Laboratory findings: diagnosis based on clinical criteria and positive HIV

antibody test--ELISA (enzyme-linked immunosorbent assay) confirmed by
Western blot assay. Other lab findings may include
1. Leukopenia with profound lymphopenia
2. Anemia
3. Thrombocytopenia
4. Decreased circulatory T4 lymphocyte cells
5. Low T4:T8 lymphocyte ratio
1. Administer medications as ordered for concomitant disease; monitor for signs

of medication toxicity.
2. Monitor respiratory status; provide care as appropriate for respiratory

problems, e.g., pneumonia.
3. Assess neurological status; reorient client as needed; provide safety measures

for the confused/disoriented client.
4. Assess for signs and symptoms of fluid and electrolyte imbalances; monitor
lab studies; ensure adequate hydration.
5. Monitor client's nutritional intake; provide supplements, total parenteral

nutrition, etc., as ordered.
6. Assess skin daily (especially perianal area) for signs of breakdown; keep skin
clean and dry; turn q4 hours while in bed.
7. Inspect oral cavity daily for ulcerations, signs of infection; instruct client to
rinse mouth with normal saline and hydrogen peroxide or normal saline and
sodium bicarbonate rinses.
8. Observe for signs and symptoms of infection; report immediately if any occur.
9. If severe leukopenia develops, institute neutropenic precautions
1. Prevent trauma to skin and mucous membranes, e.g., avoid enemas,

rectal temperatures; minimize all parenteral infections
2. Do not place client in a room with clients having infections
3. Screen visitors for colds, infections, etc.
4. Do not allow fresh fruits, vegetables, or plants in client's room.
5. Mask client when leaving room for walks, x-rays, etc.
2. Institute blood and body fluid precautions (see Nursing Responsibilities in

Prevention of Spread of Infection)
3. Provide emotional support for client/significant others; help to decrease sense

of isolation
1. Importance of observing for signs of infections and notifying physician

immediately if any occur
2. Ways to reduce chance of infection
1. Clean kitchen and bathroom surfaces regularly with

disinfectants.
2. Avoid direct contact with pet's litter boxes or stool, bird cage
droppings, and water in fish tanks.
3. Avoid contact with people with infections, e.g., cold, flu.
4. Importance of balancing activity with rest.
5. Need to eat a well-balanced diet with plenty of fluids.
3. Prevention of disease transmission
1. Use safer sex practices, e.g., condoms for sexual intercourse.
2. Do not donate blood, semen, organs.
3. Do not share razors, toothbrushes, or other items that may draw

blood.
4. Inform all physicians, dentists, sexual partners of diagnosis.
2. Resources include Public Health Service, National Gay Task Force,

American Red Cross, local support groups
TABLE 4.18 Classification System for HIV Infection
A B C
CD4 + T-cell categories Asymptomatic, acute Symptomatic, not AIDS-
HIV or PGL (A) or (C) indicator
conditions conditions
(1) 500/uL A1 B1 C1
(2) 200-499/uL A2 B2 C2
(3) <200/ul A3 B3 C3
Clinical Category A Clinical Category B Clinical Category C

1 or more of the following, * Candidiasis (oral or * Candidiasis of bronchi,
confirmed HIV infection, and vaginal), frequent or trachea, or lungs
without conditions in B and C poorly resistant to * Cervical cancer, invasive
* Asymptomatic HIV therapy * Coccidiomycosis
infection * Cervical * Cryptosporidiosis
* Persistent Generalized dysplasia/cervical * Cytomegalovirus
Lymphadenopathy (PGL) carcinoma in situ * Encephalopathy
* Acute (primary) HIV * Fever or diarrhea * Herpes simplex: chronic ulcer
infection with accompanying exceeding 1 month - exceeding 1 month duration
illness or history of acute HIV * Hairy leukoplakia, oral * Histoplasmosis
infection * Herpes zoster, * Kaposi's sarcoma
involving 2 episodes or * Lymphoma
more than one * Mycobacterium - avium
dermatome complex
* ITP * Mycobacterium tuberculosis
* PID * Pneumocystis carinii
* Peripheral neuropathy pneumonia
* Salmonella
* Toxoplasmosis of brain
* Wasting syndrome due to
HIV
Adopted from Centers for Disease Control, U.S. Dept. of Health and Human Services,
1993 revised classification system for HIV infections and expanded surveilance case
definition for AIDS among adolescents and adults.
Multiple Myeloma
1. A neoplastic condition characterized by the abnormal proliferation of plasma

cells in the bone marrow, causing the development of single or multiple
tumors composed of abnormal plasma cells. Disease disseminates into lymph
nodes, liver, spleen, and kidneys and causes bone destruction throughout the
body.
2. Cause unknown, but environmental factors thought to be involved
3. Disease occurs after age 40; affects men twice as often as women
4. Pathophysiology
1. Bone demineralization and destruction with osteoporosis and a
negative calcium balance
2. Disruption of erythrocyte, leukocyte, and thrombocyte production
1. Drug therapy
1. Analgesics for bone pain
2. Chemotherapy (melphalan [Alkeran] and cyclophosphamide

[Cytoxan]) to reduce tumor mass; may intensify the pancytopenia to
which these clients are prone; requires careful monitoring of laboratory
studies
3. Antibiotics to treat infections
4. Gammaglobulin for infection prophylaxis
5. Corticosteroids and mithramycin for severe hypercalcemia
2. Radiation therapy to reduce tumor mass and for palliation of bone pain
3. Transfusion therapy
1. Headache and bone pain increasing with activity
2. Pathologic fractures
3. Skeletal deformities of sternum and ribs
4. Loss of height (spinal column shortening)
5. Osteoporosis
6. Renal calculi
7. Anemia, hemorrhagic tendencies, and increased susceptibility to infection
8. Hypercalcemia
9. Renal dysfunction secondary to obstruction of convoluted tubules by

coagulated protein particles
10. Neurologic dysfunction: spinal cord compression and paraplegia
11. Laboratory tests

1. Radiologic: diffuse bone lesions, widespread demineralization,
osteoporosis, osteolytic lesions of skull
2. Bone marrow; many immature plasma cells; depletion of other cell

types
3. CBC: reduced Hgb, WBC, and platelet counts
4. Serum globulins elevated
5. Bence-Jones protein: positive (abnormal globulin that appears in the

urine of clients with multiple myeloma and other bone tumors)
1. Provide comfort measures to help alleviate bone pain.
2. Encourage ambulation to slow demineralization process.
3. Promote safety as clients are prone to pathologic and other fractures.
4. Encourage fluids: 3000-4000 ml/day to counteract calcium overload and to

prevent protein from precipitating in the renal tubules.
5. Provide nursing care for clients with bleeding tendencies and susceptibility to
infection.
6. Provide a supportive atmosphere to enhance communication and reduce

anxiety.
1. Crucial importance of long-term hydration to prevent urolithiasis and

renal obstruction
2. Safety measures vital to decrease the risk of injury
3. Avoidance of crowds or sources of infection if leukopenic
Polycythemia Vera
1. An increase in both the number of circulating erythrocytes and the

concentration of Hgb within the blood
2. Three forms: polycythemia vera, secondary polycythemia, and relative
polycythemia
3. Classified as a myeloproliferative disorder (bone marrow overgrowth)
4. Cause unknown, but thought to be a form of malignancy similar to leukemia
5. Usually develops in middle age, common in Jewish men
6. Pathophysiology
1. A pronounced increase in the production of erythrocytes accompanied

by an increase in the production of myelocytes (leukocytes within bone
marrow) and thrombocytes.
2. The consequences of this overproduction are an increase in blood

viscosity, an increase in total blood volume (2-3 times greater than
normal), and severe congestion of all tissues and organs with blood.
1. Ruddy complexion and duskiness of mucosa secondary to capillary congestion

in the skin and mucous membranes
2. Hypertension associated with vertigo, headache, and "fullness" in the head

secondary to increased blood volume
3. Symptoms of CHF secondary to overwork of the heart
4. Thrombus formation: CVA, MI, gangrene of the extremities, DVT, and

pulmonary embolism can occur
5. Bleeding and hemorrhage secondary to congestion and overdistension of

capillaries and venules
6. Hepatomegaly and splenomegaly
7. Peptic ulcer secondary to increased gastric secretions
8. Gout secondary to increased uric acid released by nucleoprotein breakdown
9. Laboratory tests
1. CBC: increase in all mature cell forms (erythrocytes, leukocytes, and

platelets)
2. Hct: increased
3. Bone marrow: increase in immature cell forms
4. Bilirubin (indirect): increase in unconjugated fraction

5. Liver enzymes may be increased
6. Uric acid increased
7. Hematuria and melena possible
1. Monitor for signs and symptoms of bleeding complications.
2. Force fluids and record I&O.
3. Prevent development of DVT.
4. Monitor for signs and symptoms of CHF.
5. Provide care for the client having a phlebotomy.
6. Prevent/provide care for bleeding or infection complications.
1. Radioactive phosphorus (32P): reduction of erythrocyte production,

produces a remission of 6 months to 2 years
2. Nitrogen mustard, busulfan (Myleran), chlorambucil,

cyclophosphamide to effect myelosuppression
3. Antigout and peptic ulcer drugs as needed.
1. Decrease in activity tolerance, need to space activity with periods of

rest
2. Phlebotomy regimens: outpatient frequency is determined by hct;

importance of long-term therapy
3. High fluid intake
4. Avoidance of iron-rich foods to avoid counteracting the therapeutic

effects of phlebotomy
5. Recognition and reporting of bleeding
6. Need to avoid persons with infections, especially in leukopenic clients.
Leukemia
1. Most common form of childhood cancer

2. Peak incidence is 3 to 5 years of age
3. Proliferation of abnormal white blood cells that do not mature beyond the blast
phase
4. In the bone marrow, blast cells crowd out healthy white blood cells, red blood
cells, and platelets, leading to bone marrow depression
5. Blast cells also infiltrate other organs, most commonly the liver, spleen,
kidneys, and lymph tissue
6. Symptoms reflect bone marrow failure and associated involvement of other

organs
7. Types of leukemia, based on course of disease and cell morphology
1. Acute lymphocytic leukemia (ALL)
1. 80-85% of childhood leukemia
2. malignant change in the lymphocyte or its precursors
3. acute onset
4. 95% chance of obtaining remission with treatment
5. 75% chance of surviving 5 years or more
6. prognostic indicators include: initial white blood count (less

than 10,000/mm3), child's age (2-9 years), histologic type, sex
2. Acute nonlymphocytic leukemia (ANLL)
1. includes granulocytic and monocytic types
2. 60-80% will obtain remission with treatment
3. 30-40% cure rate
4. prognostic indicators less clearly defined
1. Diagnosis: blood studies, bone marrow biopsy
2. Treatment stages
1. Induction: intense and potentially life threatening
2. CNS prophylaxis: to prevent central nervous system disease.

Combination of radiation and intrathecal chemotherapy.
3. Maintenance: chemotherapy for 2 to 3 years.
1. Anemia (due to decreased production of RBCs), weakness, pallor, dyspnea
2. Bleeding (due to decreased platelet production), petechiae, spontaneous

bleeding, ecchymoses
3. Infection (due to decreased WBC production), fever, malaise
4. Enlarged lymph nodes
5. Enlarged spleen and liver
6. Abdominal pain with weight loss and anorexia
7. Bone pain due to expansion of marrow
1. Provide care for the child receiving chemotherapy and radiation therapy.
2. Provide support for child/family; needs will change as treatment progresses.
3. Support child during painful procedures (frequent bone marrow aspirations,

lumbar punctures, venipunctures needed).
1. Use distraction, guided imagery.
2. Allow child to retain as much control as possible.
3. Administer sedation prior to procedure as ordered.
Hodgkin's Lymphoma
1. Malignant neoplasm of lymphoid tissue, usually originating in localized group

of lymph nodes; a proliferation of lymphocytes
2. Metastasizes first to adjacent lymph nodes
3. Cause unknown
4. Most prevalent in adolescents; accounts for 5% of all malignancies
5. Prognosis now greatly improved for these children; influenced by stage of

disease and histologic type
6. Long-term treatment effects include increased incidence of second
malignancies, especially leukemia and infertility
1. Diagnosis: extensive testing to determine stage, which dictates treatment

modality
1. Lymphangiogram determines involvement of all lymph nodes (reliable

in 90% of clients); is helpful in determining radiation fields
2. Staging via laparotomy and biopsy
1. stage I: single lymph node involved; usually in neck; 90%-98%

survival
2. stage II: involvement of 2 or more lymph nodes on same side of

diaphragm; 70%-80% survival
3. stage III: involvement of nodes on both sides of diaphragm;

50% survival
4. stage IV: metastasis to other organs
3. Laparotomy and splenectomy
4. Lymph node biopsy to identify presence of Reed-Sternberg cells and

for histologic classification
2. Radiation: used alone for localized disease
3. Chemotherapy: used in conjunction with radiation therapy for advanced

disease
1. Major presenting symptom is enlarged nodes in lower cervical region; nodes

are nontender, firm, and movable
2. Recurrent, intermittent fever
3. Night sweats
4. Weight loss, malaise, lethargy
5. Pruritus
6. Diagnostic test: presence of Reed-Sternberg cells
1. Provide care for child receiving radiation therapy.
2. Administer chemotherapy as ordered and monitor/alleviate side effects.
3. Protect client from infection, especially if splenectomy performed.
4. Provide support for child/parents; specific needs of adolescent client must be

considered.
Non-Hodgkin's Lymphoma
1. Tumor originating in lymphatic tissue
2. Significantly different from Hodgkin's lymphoma
1. Control of primary tumor is difficult
2. Disease is diffuse, cell type undifferentiated
3. Tumor disseminates early
4. Includes wide range of disease entities: lymphosarcoma, reticulum cell

sarcoma, Burkitt's lymphoma
3. Primary sites include GI tract, ovaries, testes, bone, CNS, liver, breast,
subcutaneous tissues
4. Affects all age groups.
1. Chemotherapy: multiagent regimens including cyclophosphamide (Cytoxan),

vincristine, prednisone, procarbazine, doxorubicin, bleomycin
2. Radiation therapy: primary treatment in localized disease
3. Surgery for diagnosis and clinical staging
1. Depend on anatomic site and extent of involvement
2. Rapid onset and progression
3. Many have advanced disease at diagnosis
2. Nursing interventions: provide care for child receiving chemotherapy, radiation

therapy, and surgery.

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LECTURE NOTES FOR BSc NURSING TOP UP GROUP (L300)

SECTION A: BLOOD DISORDERS

1. Chronic microcytic, hypochromic anemia caused by either inadequate absorption or

Clinical manifestations of Iron deficiency anaemia

1. Mild cases usually asymptomatic

1. RBCs small (microcytic) and pale (hypochromic)

Nursing interventions for Iron deficiency anaemia

a. Oral iron preparations: route of choice:

1. Chronic progressive, macrocytic anemia caused by a deficiency of intrinsic factor; the

Pathophysiology of Pernicious Anaemia

1. Vitamin B12 injections: monthly maintenance

1. Anemia, weakness, pallor, dyspnea, palpitations, fatigue

1. Erythrocyte count decreased

a. increased megaloblasts (abnormal erythrocytes)

Nursing interventions for Pernicious Anaemia

1. Pancytopenia or depression of granulocyte, platelet, and erythrocyte production due

Clinical manifestations of Aplastic Anaemia

1. Fatigue, dyspnea, pallor

Medical management of Aplastic Anaemia

1. Blood transfusions (see Laboratory/Diagnostic Tests): key to therapy until client's

1. Corticosteroids and/or androgens to stimulate bone marrow function

1. Administer blood transfusions as ordered.

1. Maintain neutropenic precautions.

1. Identify and eliminate (if possible) causative factors

1. Corticosteroids in autoimmune types of anemia

1. Clinical manifestations vary depending on severity of anemia and the rate of

1. Hgb and hct decreased

1. Monitor for signs and symptoms of hypoxia including confusion, cyanosis,

1. General information (see Figure 5.2 below)

1. sickled cells block outflow tract resulting in sudden and

1. Urea: interferes with hydrophobic bonds of the HgbS molecules

1. Hgb indicates anemia, usually 6-9 g/dl

1. sickle cell test: deoxygenation of a drop of blood on a slide

1. Keep child well hydrated and oxygenated.

1. Analgesics: acetaminophen, meperidine, morphine (avoid aspirin as it

1. Pre-op teaching for splenectomy if needed

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

1. Identification and control of underlying disease is key

1. Monitor blood loss and attempt to quantify.

1. Prolonged bleeding after minor injury

1. At birth after cutting of cord

1. Repeated bleeding into a joint results in a swollen and painful joint

1. Platelet count normal

1. Control acute bleeding episode.

1.Apply ice compress for vasoconstriction.

1. Immobilize joint and control acute bleeding.

1. Prevention of trauma (see Idiopathic Thrombocytopenic Purpura)

1. when mother is carrier: 50% chance with each pregnancy for

Signs and Symptoms

 The patient appears acutely ill, short of breath, and pale.

PRIMARY NURSING DIAGNOSIS

 Risk for infection related to decreased primary and secondary responses

 Acute lymphoblastic leukemia (ALL) drugs include prednisone, vincristine,

Supportive treatments during cancer treatment include:

 Antibiotics and immunoglobulins help to prevent or fight infections. This is important

 Frequently monitor the client for pneumonia, pharyngitis, esophagitis, perianal

Preventing and Managing bleeding:

 Watch for signs of minor bleeding, such as petechiae, ecchymosis, conjunctival

Patient Education and Health Maintenance:

 Teach signs and symptoms of infection and advise whom to notify.

1. Transfusion from blood donors

Indications for Transfusions

1. Excessive blood loss (hemoglobin 6 to 10 g/dL and depending on symptoms) USE

Before the Transfusion