Professional Documents
Culture Documents
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
Iron Deficiency Anemia
–Results when the dietary
intake of iron is
inadequate to produce
hemoglobin
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
synthesis
Hypoproliferative Anemia
IronDeficiency Anemia
Pathophysiology
–The oxygen carrying capacity
of hemoglobin is reduced
tissue hypoxia
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 absorption
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, swelling and
fever
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
–Support
acutely inflamed joint
Relaxation techniques
–Relaxation
analgesics
–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
–Provide
Allow patient to verbalize her
–Allow
concerns about medication,
prognosis and future
pregnancy
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
–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 circulation
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 thrombophlebitis
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 suppress bone
marrow
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 liver, spleen and lymph nodes.
Leukemia
The leukemias 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 mature or
diferentiated
Leukemia
ACUTE myelocytic leukemia
ACUTE lymphocytic leukemia