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NURSING
THE CARDIOVASCULAR SYSTEM
Cardiac Assessment
The Cardiovascular System
Laboratory Test Rationale
1. To assist in diagnosing MI
2. To identify abnormalities
3. To assess inflammation
The Cardiovascular System
Laboratory Test Rationale
4. To determine baseline value
5. To monitor serum level of
medications
6. To assess the effects of
medications
The Cardiovascular System
LABORATORY PROCEDURES
Holter Monitoring
Instruct the client to resume
normal activities and maintain
a diary of activities and any
symptoms that may develop
The Cardiovascular System
LABORATORY PROCEDURES
ECHOCARDIOGRAM
Non-invasive test that studies
the structural and functional
changes of the heart with the
use of ultrasound
No special preparation is
needed
The Cardiovascular System
LABORATORY PROCEDURES
Stress Test
A non-invasive test that
studies the heart during
activity and detects and
evaluates CAD
Exercise test, pharmacologic
test and emotional test
The Cardiovascular System
LABORATORY PROCEDURES
Stress Test
Associated factors:
1. Genetic
2. Idiopathic
HYPERTROPHIC
CARDIOMYOPATHY
Pathophysiology
Increased size of myocardium
reduced ventricular volume
increased resistance to
ventricular filling diastolic
dysfunction
RESTRICTIVE
CARDIOMYOPATHY
Associated factors
1. Infiltrative diseases like
AMYLOIDOSIS
2. Idiopathic
RESTRICTIVE
CARDIOMYOPATHY
Pathophysiology
Rigid ventricular wall
impaired stretch and diastolic
filling decreased output
Diastolic dysfunction
CARDIOMYOPATHIES
Assessment findings
1. PND
2. Orthopnea
3. Edema
4. Chest pain
5. Palpitations
6. dizziness
7. Syncope with exertion
CARDIOMYOPATHIES
Laboratory Findings
1. CXR- may reveal
cardiomegaly
2. ECHOCARDIOGRAM
3. ECG
4. Myocardial Biopsy
CARDIOMYOPATHIES
Medical Management
1. Surgery
2. pacemaker insertion
3. Pharmacological drugs for
symptom relief
CARDIOMYOPATHIES
Nursing Management
1.Improve cardiac output
Adequate rest
Oxygen therapy
Low sodium diet
CARDIOMYOPATHIES
Nursing Management
2. Increase patient tolerance
Schedule activities with rest
periods in between
CARDIOMYOPATHIES
Nursing Management
3. Reduce patient anxiety
Support
Offer information about
transplantations
Support family in anticipatory
grieving
Infective endocarditis
Infection of the heart
valves and the endothelial
surface of the heart
Can be acute or chronic
Infective endocarditis
Etiologic factors
1. Bacteria- Organism
depends on several factors
2. Fungi
Infective endocarditis
Risk factors
1. Prosthetic valves
2. Congenital malformation
3. Cardiomyopathy
4. IV drug users
5. Valvular dysfunctions
Infective endocarditis
Pathophysiology
Direct invasion of microbes
microbes adhere to damaged
valve surface and proliferate
damage attracts platelets
causing clot formation
erosion of valvular leaflets and
vegetation can embolize
Infective endocarditis
Assessment findings
1. Intermittent HIGH fever
2. anorexia, weight loss
3. cough, back pain and joint
pain
4. splinter hemorrhages under
nails
Infective endocarditis
Assessment findings
5. Osler’s nodes- painful
nodules on fingerpads
6. Roth’s spots- pale
hemorrhages in the retina
Infective endocarditis
Assessment findings
7. Heart murmurs
8. Heart failure
Infective endocarditis
Prevention
Antibiotic prophylaxis if
patient is undergoing
procedures like dental
extractions, bronchoscopy,
surgery, etc.
Infective endocarditis
LABORATORY EXAM
Blood Cultures to determine
the exact organism
Infective endocarditis
Nursing management
1. regular monitoring of
temperature, heart sounds
2. manage infection
3. long-term antibiotic
therapy
Infective endocarditis
Medical management
1. Pharmacotherapy
IV antibiotic for 2-6 weeks
Antifungal agents are given –
amphotericin B
Infective endocarditis
Medical management
2. Surgery
Valvular replacement
CHF
A syndrome of congestion of
both pulmonary and systemic
circulation caused by
inadequate cardiac function
and inadequate cardiac
output to meet the metabolic
demands of tissues
CHF
Inability of the heart to pump
sufficiently
The heart is unable to maintain
adequate circulation to meet the
metabolic needs of the body
Classified according to the major
ventricular dysfunction- Left or
Right
CHF
Etiology of CHF
1. CAD
2. Valvular heart diseases
3. Hypertension
4. MI
5. Cardiomyopathy
6. Lung diseases
7. Post-partum
8. Pericarditis and cardiac tamponade
New York Heart Association
Class 1
Ordinary physical activity does
NOT cause chest pain and
fatigue
No pulmonary congestion
Asymptomatic
NO limitation of ADLs
New York Heart Association
Class 2
SLIGHT limitation of ADLs
NO symptom at rest
Symptom with INCREASED
activity
Basilar crackles and S3
New York Heart Association
Class 3
Markedly limitation on ADLs
Comfortable at rest BUT
symptoms present in LESS
than ordinary activity
New York Heart Association
Class 4
SYMPTOMS are present at
rest
CHF
PATHOPHYSIOLOGY
LEFT Ventricular pump
failure back up of blood
into the pulmonary veins
increased pulmonary
capillary pressure
pulmonary congestion
CHF
PATHOPHYSIOLOGY
LEFT ventricular failure
decreased cardiac output
decreased perfusion to the
brain, kidney and other
tissues oliguria, dizziness
CHF
PATHOPHYSIOLOGY
RIGHT ventricular failure
blood pooling in the
venous circulation
increased hydrostatic
pressure peripheral
edema
CHF
PATHOPHYSIOLOGY
RIGHT ventricular failure
blood pooling venous
congestion in the kidney,
liver and GIT
LEFT SIDED CHF
ASSESSMENT FINDINGS
1. Dyspnea on exertion
2. PND
3. Orthopnea
4. Pulmonary crackles/rales
5. cough with Pinkish, frothy
sputum
6. Tachycardia
LEFT SIDED CHF
ASSESSMENT FINDINGS
7. Cool extremities
8. Cyanosis
9. decreased peripheral pulses
10. Fatigue
11. Oliguria
12. signs of cerebral anoxia
RIGHT SIDED CHF
ASSESSMENT FINDINGS
1. Peripheral dependent, pitting
edema
2. Weight gain
3. Distended neck vein
4. hepatomegaly
5. Ascites
RIGHT SIDED CHF
ASSESSMENT FINDINGS
6. Body weakness
7. Anorexia, nausea
8. Pulsus alternans
CHF
LABORATORY FINDINGS
1. CXR may reveal
cardiomegaly
2. ECG may identify Cardiac
hypertrophy
3. Echocardiogram may show
hypokinetic heart
CHF
LABORATORY FINDINGS
4. ABG and Pulse oximetry may
show decreased O2 saturation
5. PCWP is increased in LEFT
sided CHF and CVP is increased
in RIGHT sided CHF
CHF
NURSING INTERVENTIONS
1. Assess patient's cardio-
pulmonary status
2. Assess VS, CVP and PCWP.
Weigh patient daily to monitor
fluid retention
CHF
NURSING INTERVENTIONS
3. Administer medications-
usually cardiac glycosides are
given- DIGOXIN or
DIGITOXIN, Diuretics,
vasodilators and
hypolipidemics are prescribed
CHF
NURSING INTERVENTIONS
4. Provide a LOW sodium
diet. Limit fluid intake as
necessary
5. Provide adequate rest
periods to prevent fatigue
CHF
NURSING INTERVENTIONS
6. Position on semi-fowler’s
to fowler’s for adequate chest
expansion
7. Prevent complications of
immobility
CHF
NURSING INTERVENTION AFTER
THE ACUTE STAGE
1. Provide opportunities for
verbalization of feelings
2. Instruct the patient about the
medication regimen- digitalis,
vasodilators and diuretics
3. Instruct to avoid OTC drugs,
Stimulants, smoking and alcohol
CHF
NURSING INTERVENTION
AFTER THE ACUTE STAGE
4. Provide a LOW fat and LOW
sodium diet
5. Provide potassium
supplements
6. Instruct about fluid restriction
CHF
NURSING INTERVENTION
AFTER THE ACUTE STAGE
7. Provide adequate rest periods
and schedule activities
8. Monitor daily weight and
report signs of fluid retention
CARDIOGENIC SHOCK
Heart fails to pump adequately
resulting to a decreased cardiac output
and decreased tissue perfusion
ETIOLOGY
1. Massive MI
2. Severe CHF
3. Cardiomyopathy
4. Cardiac trauma
5. Cardiac tamponade
CARDIOGENIC SHOCK
ASSESSMENT FINDINGS
1. HYPOTENSION
2. oliguria (less than 30 ml/hour)
3. tachycardia
4. narrow pulse pressure
5. weak peripheral pulses
6. cold clammy skin
7. changes in sensorium/LOC
8. pulmonary congestion
CARDIOGENIC SHOCK
LABORATORY FINDINGS
Increased CVP
Normal is 4-10 cmH2O
CARDIOGENIC SHOCK
NURSING INTERVENTIONS
1. Place patient in a modified
Trendelenburg (shock ) position
2. Administer IVF, vasopressors and
inotropics such as DOPAMINE and
DOBUTAMINE
3. Administer O2
4. Morphine is administered to decreased
pulmonary congestion and to relieve pain
CARDIOGENIC SHOCK
5. Assist in intubation, mechanical
ventilation, PTCA, CABG, insertion
of Swan-Ganz cath and IABP
6. Monitor urinary output, BP and
pulses
7. cautiously administer diuretics and
nitrates
CARDIAC TAMPONADE
A condition where the heart
is unable to pump blood due
to accumulation of fluid in
the pericardial sac
(pericardial effusion)
CARDIAC TAMPONADE
CLASSIFICATION OF
HYPERTENSION by JNC-
VII
HYPERTENSION
PATHOPHYSIOLOGY
Multi-factorial etiology
BP= CO (SV X HR) x TPR
Any increase in the above
parameters will increase BP
1. Increased sympathetic activity
2. Increased absorption of Sodium,
and water in the kidney
HYPERTENSION
PATHOPHYSIOLOGY
Multifactorial etiology
BP= CO (SV X HR) x TPR
Any increase in the above parameters
will increase BP
3. Increased activity of the RAAS
4. Increased vasoconstriction of the
peripheral vessels
5. insulin resistance
HYPERTENSION
ASSESSMENT FINDINGS
1. Headache
2. Visual changes
3. chest pain
4. dizziness
5. N/V
HYPERTENSION
Risk factors for Cardiovascular
Problems in Hypertensive patients
Major Risk factors
1. Smoking
2. Hyperlipidemia
3. DM
4. Age older than 60
5. Gender- Male and post menopausal W
6. Family History
HYPERTENSION
DIAGNOSTIC STUDIES
1. Health history and PE
2. Routine laboratory- urinalysis,
ECG, lipid profile, BUN, serum
creatinine , FBS
3. Other lab- CXR, creatinine
clearance, 24-huour urine protein
HYPERTENSION
MEDICAL MANAGEMENT
1. Lifestyle modification
2. Drug therapy
3. Diet therapy
HYPERTENSION
MEDICAL MANAGEMENT
Drug therapy
Diuretics
Beta blockers
Calcium channel blockers
ACE inhibitors
A2 Receptor blockers
Vasodilators
HYPERTENSION
NURSING INTERVENTIONS
1. Provide health teaching to
patient
Teach about the disease process
Elaborate on lifestyle changes
Assist in meal planning to lose
weight
HYPERTENSION
NURSING INTERVENTIONS
1. Provide health teaching to the
patient
Provide list of LOW fat , LOW
sodium diet of less than 2-3 grams
of Na/day
Limit alcohol intake to 30 ml/day
Regular aerobic exercise
Advise to completely Stop smoking
HYPERTENSION
Nursing Interventions
2. Provide information about anti-
hypertensive drugs
Instruct proper compliance and not
abrupt cessation of drugs even if pt
becomes asymptomatic/ improved
condition
Instruct to avoid over-the-counter
drugs that may interfere with the
current medication
HYPERTENSION
Nursing Intervention
3. Promote Home care management
Instruct regular monitoring of BP
Involve family members in care
Instruct regular follow-up
4. Manage hypertensive emergency
and urgency properly
Vascular Diseases
ANEURYSM
Dilation involving an artery formed at a
weak point in the vessel wall
ANEURYSM
Saccular= when one side of the vessel is
affected
PATHOPHYSIOLOGY
Cause is UNKNOWN
Probably an Autoimmune disease
Inflammation of the arteries
thrombus formation occlusion
of the vessels
BUERGER’S DISEASE
ASSESSMENT FINDINGS
1. Leg PAIN
Foot cramps in the arch (instep
claudication) after exercise
Relieved by rest
Aggravated by smoking, emotional
disturbance and cold chilling
2. Digital rest pain not changed by activity
or rest
BUERGER’S DISEASE
ASSESSMENT FINDINGS
3. Intense RUBOR (reddish-blue
discoloration), progresses to
CYANOSIS as disease advances
4. Paresthesia
BUERGER’S DISEASE
Diagnostic Studies
1. Duplex ultrasonography
2. Contrast angiography
BUERGER’S DISEASE
Nursing Interventions
1. Assist in the medical and surgical
management
Bypass graft
amputation
2. Strongly advise to AVOID smoking
3. Manage complications appropriately
Medical Management
1. Drug therapy
Pentoxyfylline (Trental) reduces blood
viscosity and improves supply of O2
blood to muscles
Cilostazol (Pletaal) inhibits platelet
aggregation and increases
vasodilatation
2. Surgery- Bypass graft and
anastomoses
BUERGER’S DISEASE
Nursing Interventions
Post-operative care: after amputation
Elevate stump for the FIRST 24 HOURS
to minimize edema and promote venous
return
Place patient on PRONE position after 24
hours
Assess skin for bleeding and hematoma
Wrap the extremity with elastic bandage
RAYNAUD’S DISEASE
A form of intermittent arteriolar
VASOCONSTRICTION that results
in coldness, pain and pallor of the
fingertips or toes
Cause : UNKNOWN
Most commonly affects WOMEN, 16-
40 years old
RAYNAUD’S DISEASE
ASSESSMENT FINDINGS
1. Raynaud’s phenomenon
A localized episode of
vasoconstriction of the small
arteries of the hands and feet
that causes color and
temperature changes
RAYNAUD’S DISEASE
W-B-R
Pallor- due to vasoconstriction,
then
Blue- due to pooling of
Deoxygenated blood
Red- due to exaggerated
reflow/hyperemia
RAYNAUD’S DISEASE
ASSESSMENT FINDINGS
2. tingling sensation
3. Burning pain on the hands and
feet
RAYNAUD’S DISEASE
Medical management
Drug therapy with the use of
CALCIUM channel blockers
To prevent vasospasms
RAYNAUD’S DISEASE
Nursing Interventions
1. instruct patient to avoid situations
that may be stressful
2. instruct to avoid exposure to cold
and remain indoors when the climate is
cold
3. instruct to avoid all kinds of nicotine
4. instruct about safety. Careful
handling of sharp objects
Venous diseases
VARICOSE VEINS
THESE are dilated veins
usually in the lower
extremities
VARICOSE VEINS
Predisposing Factors
Pregnancy
Prolonged standing or sitting
Constipation (for
hemorrhoids)
Incompetent venous valves
VARICOSE VEINS
Pathophysiology
Factors venous stasis
increased hydrostatic
pressure edema
VARICOSE VEINS
Assessment findings
Tortuous superficial veins
on the legs
Leg pain and Heaviness
Dependent edema
VARICOSE VEINS
Laboratory findings
Venography
Duplex scan
pletysmography
VARICOSE VEINS
Medical management
Pharmacological therapy
Leg vein stripping
Anti-embolic stockings
VARICOSE VEINS
Nursing management
1. Advise patient to elevate
the legs
2. Caution patient to avoid
prolonged standing or sitting
VARICOSE VEINS
Nursing management
3. Provide high-fiber foods
to prevent constipation
4. Teach simple exercise to
promote venous return
VARICOSE VEINS
Nursing management
5. Caution patient to avoid
knee-length stockings and
constrictive clothings
VARICOSE VEINS
Nursing management
6. Apply anti-embolic
stockings as directed
7. Avoid massage on the
affected area
DVT- Deep Vein Thrombosis
Inflammation of the deep
veins of the lower extremities
and the pelvic veins
The inflammation results to
formation of blood clots in
the area
DVT- Deep Vein Thrombosis
Predisposing factors
Prolonged immobility
Varicosities
Traumatic procedures
DVT- Deep Vein Thrombosis
Complication
PULMONARY
thromboembolism
DVT- Deep Vein Thrombosis
Assessment findings
Leg tenderness
Leg pain and edema
Positive HOMAN’s SIGN
DVT- Deep Vein Thrombosis
Laboratory findings
Venography
Duplex scan
DVT- Deep Vein Thrombosis
Medical management
Antiplatelets
Anticoagulants
Vein stripping and grafting
Anti-embolic stockings
DVT- Deep Vein Thrombosis
Nursing management
1. Provide measures to avoid
prolonged immobility
Repositioning Q2
Provide passive ROM
Early ambulation
DVT- Deep Vein Thrombosis
Nursing management
2. Provide skin care to
prevent the complication of
leg ulcers
3. Provide anti-embolic
stockings
DVT- Deep Vein Thrombosis
Nursing management
4. Administer anticoagulants
as prescribed
5. Monitor for signs of
pulmonary embolism
Blood disorders
Anemia
Nutritional anemia
Hemolytic anemia
Aplastic anemia
Sickle cell anemia
ANEMIA
Acondition in
which the
hemoglobin
concentration is
lower than normal
ANEMIA
Three broad categories
1. Loss of RBC- occurs
with bleeding
2. Decreased RBC
production
3. Increased RBC
destruction
Hypoproliferative Anemia
IronDeficiency
Anemia
–Results when the
dietary intake of
iron is inadequate
to produce
Hypoproliferative Anemia
Iron Deficiency Anemia
– Etiologic Factors
– 1. Bleeding- the most
common cause
– 2. Mal-absorption
– 3. Malnutrition
– 4. Alcoholism
Hypoproliferative Anemia
IronDeficiency
Anemia
Pathophysiology
–The body stores of
iron decrease,
leading to depletion
of hemoglobin
Hypoproliferative Anemia
IronDeficiency
Anemia
Pathophysiology
–The oxygen carrying
capacity of
hemoglobin is
Hypoproliferative Anemia
Iron Deficiency Anemia
Assessment Findings
1. Pallor of the skin and
mucous membrane
2. Weakness and fatigue
3. General malaise
4. Pica
Hypoproliferative Anemia
Iron Deficiency Anemia
Assessment Findings
5. Brittle nails
6. Smooth and sore
tongue
7. Angular cheilosis
Hypoproliferative Anemia
Iron Deficiency Anemia
Laboratory findings
1. CBC- Low levels of Hct,
Hgb and RBC count
2. low serum iron, low
ferritin
3. Bone marrow
aspiration- MOST
definitive
Hypoproliferative Anemia
Iron Deficiency
Anemia
Medical
management
1. Hematinics
2. Blood transfusion
Hypoproliferative Anemia
Iron Deficiency Anemia
Nursing Management
1. Provide iron rich-foods
– Organ meats (liver)
– Beans
– Leafy green vegetables
– Raisins and molasses
Hypoproliferative Anemia
Nursing Management
2. Administer iron
Oral preparations tablets- Fe
fumarate, sulfate and
gluconate
Advise to take iron ONE hour
before meals
Take it with vitamin C
Continue taking it for several
months
Hypoproliferative Anemia
Nursing Management
2. Administer iron
Oral preparations- liquid
It stains teeth
Drink it with a straw
Stool may turn blackish- dark
in color
Advise to eat high-fiber diet to
counteract constipation
Hypoproliferative Anemia
Nursing Management
2. Administer iron
IM preparation
Administer DEEP IM using the
Z-track method
Avoid vigorous rubbing
Can cause local pain and
staining
APLASTIC ANEMIA
Acondition
characterized by
decreased number
of RBC as well as
WBC and platelets
APLASTIC ANEMIA
CAUSATIVE FACTORS
1. Environmental toxins-
pesticides, benzene
2. Certain drugs-
Chemotherapeutic agents,
chloramphenicol,
phenothiazines,
Sulfonamides
3. Heavy metals
4. Radiation
APLASTIC ANEMIA
Pathophysiology
Toxins cause a direct bone
marrow depression
acellualr bone marrow
decreased production of
blood elements
APLASTIC ANEMIA
ASSESSMENT FINDINGS
1. fatigue
2. pallor
3. dyspnea
4. bruising
5. splenomegaly
6. retinal hemorrhages
APLASTIC ANEMIA
LABORATORY FINDINGS
1. CBC- decreased blood
cell numbers
2. Bone marrow
aspiration confirms the
anemia- hypoplastic or
acellular marrow
replaced by fats
APLASTIC ANEMIA
Medical Management
1. Bone marrow
transplantation
2. Immunosupressant
drugs
3. Rarely, steroids
4. Blood transfusion
APLASTIC ANEMIA
Nursing management
1. Assess for signs of
bleeding and
infection
2. Instruct to avoid
exposure to offending
agents
Megaloblastic Anemias
Anemias characterized
by abnormally large
RBC secondary to
impaired DNA
synthesis due to
deficiency of Folic acid
and/or vitamin B12
Megaloblastic Anemias
Folic Acid deficiency
Causative factors
1. Alcoholism
2. Mal-absorption
3. Diet deficient in
uncooked vegetables
Megaloblastic Anemias
Pathophysiology of Folic
acid deficiency
Decreased folic acid
impaired DNA synthesis in
the bone marrow
impaired RBC development,
impaired nuclear
maturation but
CYTOplasmic maturation
continues large size
Megaloblastic Anemias
Vitamin B12 deficiency
Causative factors
1. Strict vegetarian diet
2. Gastrointestinal
malabsorption
3. Crohn's disease
4. gastrectomy
Megaloblastic Anemias
Vitamin B12 deficiency
Pernicious Anemia
Due to the absence of
intrinsic factor secreted by
the parietal cells
Intrinsic factor binds with
Vit. B12 to promote
Megaloblastic Anemias
Assessment findings
1. weakness
2. fatigue
3. listless
4. neurologic manifestations
are present only in Vit. B12
deficiency
Megaloblastic Anemias
Assessment findings
Pernicious Anemia
– Beefy, red, swollen tongue
– Mild diarrhea
– Extreme pallor
– Paresthesias in the extremities
Megaloblastic Anemias
Laboratory findings
1. Peripheral blood smear-
shows giant RBCs, WBCs with
giant hypersegmented nuclei
2. Very high MCV
3. Schilling’s test
4. Intrinsic factor antibody
test
Megaloblastic Anemias
Medical Management
1. Vitamin supplementation
– Folic acid 1 mg daily
2. Diet supplementation
– Vegetarians should have
vitamin intake
3.Lifetime monthly injection
of IM Vit B12
Megaloblastic Anemias
Nursing Management
1. Monitor patient
2. Provide assistance in
ambulation
3. Oral care for tongue sore
4. Explain the need for
lifetime IM injection of vit
B12
Hemolytic Anemia: Sickle
Cell
Asevere chronic
incurable hemolytic
anemia that results
from heritance of the
sickle hemoglobin
gene.
Hemolytic Anemia: Sickle
Cell
Causative factor
–Genetic inheritance
of the sickle gene-
HbS gene
Hemolytic Anemia: Sickle
Cell
Pathophysiology
Decreased O2, Cold,
Vasoconstriction can
precipitate sickling
process
Hemolytic Anemia: Sickle
Cell
Pathophysiology
Factors cause defective
hemoglobin to acquire a
rigid, crystal-like C-
shaped configuration
Sickled RBCs will adhere
to endothelium pile up
and plug the vessels
ischemia results pain,
Hemolytic Anemia: Sickle
Cell
Assessment Findings
1. jaundice
2. enlarged skull and
facial bones
3. tachycardia,
murmurs and
cardiomegaly
Hemolytic Anemia: Sickle
Cell
Assessment Findings
Primary sites of
thrombotic occlusion:
spleen, lungs and
CNS
Chest pain, dyspnea
Hemolytic Anemia: Sickle
Cell
Assessment Findings
1. Sickle cell crises
– Results from tissue hypoxia
and necrosis
2. Acute chest syndrome
– Manifested by a rapidly
falling hemoglobin level,
tachycardia, fever and
chest infiltrates in the CXR
Hemolytic Anemia: Sickle
Cell
Medical Management
1. Bone marrow
transplant
2. Hydroxyurea
–Increases the HbF
3.Long term RBC
trnasfusion
Hemolytic Anemia: Sickle
Cell
Nursing Management
1. manage the pain
–Support and elevate
acutely inflamed joint
–Relaxation techniques
–analgesics
Hemolytic Anemia: Sickle
Cell
Nursing Management
2. Prevent and
manage infection
–Monitor status of
patient
–Initiate prompt
antibiotic therapy
Hemolytic Anemia: Sickle
Cell
Nursing Management
3. Promote coping skills
– Provide accurate
information
– Allow patient to
verbalize her concerns
about medication,
prognosis and future
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and prevent
potential complications
– Provide always adequate
hydration
– Avoid cold, temperature
that may cause
vasoconstriction
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and
prevent potential
complications
–Leg ulcer
Aseptic technique
Hemolytic Anemia: Sickle
Cell
Nursing Management
4. Monitor and prevent
potential complications
– Priapism
Sudden painful erection
Instruct patient to empty
bladder, then take a warm
bath
Polycythemia
Refers to an INCREASE
volume of RBCs
The hematocrit is
ELEVATED to more than
55%
Clasified as Primary or
Secondary
Polycythemia
POLYCYTHEMIA VERA
– Primary Polycythemia
– A proliferative disorder
in which the myeloid
stem cells become
uncontrolled
Polycythemia
POLYCYTHEMIA VERA
Causative factor
– unknown
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– The stem cells grow
uncontrollably
– The bone marrow
becomes HYPERcellular
and all the blood cells
are increased in number
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– The spleen resumes its
function of
hematopoiesis and
enlarges
– Blood becomes thick and
viscous causing sluggish
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
– Overtime, the bone
marrow becomes fibrotic
Polycythemia
POLYCYTHEMIA VERA
Assessment findings
– 1. Skin is ruddy
– 2. Splenomegaly
– 3. headache
– 4. dizziness, blurred
vision
– 5. Angina, dyspnea and
Polycythemia
POLYCYTHEMIA VERA
Laboratory findings
– 1. CBC- shows elevated
RBC mass
– 2. Normal oxygen
saturation
– 3 Elevated WBC and
Platelets
Polycythemia
POLYCYTHEMIA VERA
Complications
– 1. Increased risk for
thrombophlebitis, CVA
and MI
– 2. Bleeding due to
dysfunctional blood cells
Polycythemia
POLYCYTHEMIA VERA
Medical Management
– 1. To reduce the high
blood cell mass-
PHLEBOTOMY
– 2. Allopurinol
– 3. Dipyridamole
– 4. Chemotherapy to
Polycythemia
Nursing Management
– 1. Primary role of the nurse is
EDUCATOR
– 2. Regularly asses for the
development of complications
– 3. Assist in weekly phlebotomy
– 4. Advise to avoid alcohol and
aspirin
– 5. Advise tepid sponge bath or
cool water to manage pruritus
Leukemia
Malignant disorders of
blood forming cells
characterized by
UNCONTROLLED
proliferation of WHITE
BLOOD CELLS in the bone
marrow- replacing marrow
elements . The WBC can
also proliferate in the
Leukemia
Theleukemias are named
after the specific lines of
blood cells afffected
primarily
– Myeloid
– Lymphoid
– Monocytic
Leukemia
The leukemias are named
also according to the
maturation of cells
ACUTE
– The cells are primarily
immature
CHRONIC
– The cells are primarily
Leukemia
ACUTE myelocytic
leukemia
ACUTE lymphocytic
leukemia
CHRONIC myelocytic
leukemia
Leukemia
ETIOLOGIC FACTORS
– UNKNOWM
– Probably exposure to
radiation
– Chemical agents
– Infectious agents
– Genetic
Leukemia
– PATHOPHYSIOLOGY of
ACUTE Leukemia
Uncontrolled proliferation of
immature cells
suppresses bone marrow
function severe anemia,
thrombocytopenia and
granulocytopenia
Leukemia
– PATHOPHYSIOLOGY of
CHRONIC Leukemia
Uncontrolled proliferation of
DIFFERENTIATED cells
slow suppression of bone
marrow function milder
symptoms
Leukemia
ASSESSMENT FINDINGS
ACUTE LEUKEMIA
– Pallor
– Fatigue
– Dyspnea
– Hemorrhages
– Organomegaly
– Headache
– vomiting
Leukemia
ASSESSMENT FINDINGS
CHRONIC LEUKEMIA
– Less severe symptoms
– organomegaly
Leukemia
LABORATORY FINDINGS
Peripheral WBC count varies
widely
Bone marrow aspiration
biopsy reveals a large
percentage of immature cells-
BLASTS
Erythrocytes and platelets are
decreased
Leukemia
Medical Management
2. Chemotherapy
3. Bone marrow transplantation
Leukemia
Nursing Management
1. Manage AND prevent
infection
– Monitor temperature
– Assess for signs of infection
– Be alert if the neutrophil count
drops below 1,000 cells/mm3
Leukemia
Nursing Management
2. Maintain skin integrity
4. Provide information as to
therapy- chemo and bone
marrow transplantation