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CARDIOLOGY

NURSING
THE CARDIOVASCULAR SYSTEM

HEART’S NORMAL ANATOMY


The heart is located in the LEFT side of the
mediastinum
Consists of Three layers - epicardium,
myocardium and endocardium
THE CARDIOVASCULAR SYSTEM

The epicardium covers the outer surface of


the heart
The myocardium is the middle muscular
layer of the heart
The endocardium lines the chambers and
the valves
THE CARDIOVASCULAR SYSTEM

The layer that covers the heart is the


PERICARDIUM
There are two parts - parietal and visceral
pericardium
The space between the two pericardial
layers is the pericardial space
THE CARDIOVASCULAR SYSTEM

The heart also has four chambers -


two atria and two ventricles
The Left atrium and the right
atrium
The left ventricle and the right
ventricle
The Cardiovascular System

The heart chambers are guarded by


valves
The atrio-ventricular valves -
tricuspid and bicuspid
The semi-lunar valves - pulmonic and
aortic valves
The Cardiovascular System
The Blood supply of the heart comes from
the Coronary arteries
1. Right coronary artery supplies the
RIGHT atrium and RIGHT ventricle,
inferior portion of the LEFT ventricle,
the POSTERIOR septal wall and the two
nodes - AV (90%) and SA node (55%)
The Cardiovascular System
2. Left coronary artery- branches into the
LAD and the circumflex branch
The LAD supplies blood to the anterior
wall of the LEFT ventricle, the anterior
septum and the Apex of the left ventricle
The CIRCUMFLEX branch supplies the
left atrium and the posterior LEFT
ventricle
The Cardiovascular System
The CONDUCTING SYSTEM OF THE
HEART
Consists of the
1. SA node- the pacemaker
2. AV node- slowest conduction
3. Bundle of His – branches into the Right
and the Left bundle branch
4. Purkinje fibers- fastest conduction
The Cardiovascular System
The Heart sounds
1. S1- due to closure of the AV valves
2. S2- due to the closure of the semi-lunar
valves
3. S3- due to increased ventricular filling
4. S4- due to forceful atrial contraction
The Cardiovascular System
Heart rate
Normal range is 60-100 beats per minute
Tachycardia is greater than 100 bpm
Bradycardia is less than 60 bpm
Sympathetic system INCREASES HR
Parasympathetic system (Vagus)
DECREASES HR
The Cardiovascular System
Blood pressure
Cardiac output X peripheral resistance
Control is neural (central and
peripheral) and hormonal
Baroreceptors in the carotid and aorta
Hormones- ADH, aldosterone,
epinephrine can increase BP; ANF can
decrease BP
The Cardiovascular System
The vascular system consists of the arteries,
veins and capillaries
The arteries are vessels that carry blood
away from the heart to the periphery
The veins are the vessels that carry blood to
the heart
The capillaries are lined with squamos cells,
they connect the veins and arteries
The Cardiovascular System
The lymphatic system also is part of the
vascular system and the function of this
system is to collect the extravasated fluid
from the tissues and returns it to the blood
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

CARDIAC Proteins and


enzymes
CK- MB ( creatine kinase)
Elevates in MI within 4
hours, peaks in 18 hours
and then declines till 3 days
The Cardiovascular System
LABORATORY PROCEDURES

CARDIAC Proteins and


enzymes
CK- MB ( creatine
kinase)
Normal value is 0-7 U/L
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins and
enzymes
Lactic Dehydrogenase (LDH)
Elevates in MI in 24 hours,
peaks in 48-72 hours
Normally LDH1 is greater
than LDH2
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins and
enzymes
Lactic Dehydrogenase (LDH)
MI- LDH2 greater than
LDH1 (flipped LDH pattern)
Normal value is 70-200 IU/L
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins and
enzymes
Myoglobin
Rises within 1-3 hours
Peaks in 4-12 hours
Returns to normal in a day
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins and
enzymes
Myoglobin
Not used alone
Muscular and RENAL disease
can have elevated myoglobin
The Cardiovascular System
LABORATORY PROCEDURES
Troponin I and T
Troponin I is usually utilized for
MI
Elevates within 3-4 hours, peaks
in 4-24 hours and persists for 7
days to 3 weeks!
Normal value for Troponin I is
less than 0.6 ng/mL
The Cardiovascular System
LABORATORY PROCEDURES
Troponin I and T
REMEMBER to AVOID IM
injections before obtaining
blood sample!
Early and late diagnosis can
be made!
The Cardiovascular System
LABORATORY PROCEDURES
SERUM LIPIDS
Lipid profile measures the
serum cholesterol,
triglycerides and lipoprotein
levels
Cholesterol= 200 mg/dL
Triglycerides- 40- 150 mg/dL
The Cardiovascular System
LABORATORY PROCEDURES
SERUM LIPIDS
LDH- 130 mg/dL
HDL- 30-70- mg/dL
NPO post midnight (usually
12 hours)
The Cardiovascular System
LABORATORY PROCEDURES
ELECTROCARDIOGRAM
(ECG)
A non-invasive procedure that
evaluates the electrical activity
of the heart
Electrodes and wires are
attached to the patient
The Cardiovascular System
LABORATORY PROCEDURES
Holter Monitoring
A non-invasive test in
which the client wears a
Holter monitor and an
ECG tracing recorded
continuously over a period
of 24 hours
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

Treadmill testing is the most


commonly used stress test
Used to determine CAD,
Chest pain causes, drug
effects and dysrhythmias in
exercise
The Cardiovascular System
LABORATORY PROCEDURES
Stress Test
Pre-test: consent may be
required, adequate rest ,
eat a light meal or fast for
4 hours and avoid
smoking, alcohol and
caffeine
The Cardiovascular System
LABORATORY PROCEDURES
Post-test: instruct client to
notify the physician if any
chest pain, dizziness or
shortness of breath . Instruct
client to avoid taking a hot
shower for 10-12 hours after
the test
The Cardiovascular System
LABORATORY PROCEDURES
Pharmacological stress test
Use of dipyridamole
Maximally dilates
coronary artery
Side-effect: flushing of
face
The Cardiovascular System
LABORATORY PROCEDURES
Pharmacological stress test
Pre-test: 4 hours fasting,
avoid alcohol, caffeine
Post test: report
symptoms of chest pain
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC catheterization
Insertion of a catheter into
the heart and surrounding
vessels
Determines the structure and
performance of the heart
valves and surrounding
vessels
The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC catheterization
Used to diagnose CAD,
assess coronary atery
patency and determine
extent of atherosclerosis
The Cardiovascular System
LABORATORY PROCEDURES
Pretest: Ensure Consent,
assess for allergy to
seafood and iodine, NPO,
document weight and
height, baseline VS, blood
tests and document the
peripheral pulses
The Cardiovascular System
LABORATORY PROCEDURES

Pretest: Fast for 8-12


hours, teachings,
medications to allay
anxiety
The Cardiovascular System
LABORATORY PROCEDURES
Intra-test: inform patient of
a fluttery feeling as the
catheter passes through the
heart; inform the patient
that a feeling of warmth and
metallic taste may occur
when dye is administered
The Cardiovascular System
LABORATORY PROCEDURES
Post-test: Monitor VS and cardiac
rhythm
Monitor peripheral pulses, color and
warmth and sensation of the
extremity distal to insertion site
Maintain sandbag to the insertion site
if required to maintain pressure
Monitor for bleeding and hematoma
formation
The Cardiovascular System
LABORATORY PROCEDURES
Maintain strict bed rest for 6-12 hours
Client may turn from side to side but bed
should not be elevated more than 30 degrees
and legs always straight
Encourage fluid intake to flush out the dye
Immobilize the arm if the antecubital vein
is used
Monitor for dye allergy
The Cardiovascular System
LABORATORY PROCEDURES
CVP
The CVP is the pressure
within the SVC
Reflects the pressure under
which blood is returned to
the SVC and right atrium
The Cardiovascular System
LABORATORY PROCEDURES
CVP
Normal CVP is 0 to 8 mmHg/ 4-
10 cm H2O
Elevated CVP indicates increase
in blood volume, excessive IVF or
heart/renal failure
Low CVP may indicated
hypovolemia, hemorrhage and
severe vasodilatation
The Cardiovascular System
LABORATORY PROCEDURES
Measuring CVP
1. Position the client supine with bed
elevated at 45 degrees
2. Position the zero point of the CVP
line at the level of the right atrium.
Usually this is at the MAL, 4th ICS
3. Instruct the client to be relaxed
and avoid coughing and straining.
CARDIAC ASSESSMENT
ASSESSMENT
1. Health History
Obtain description of present
illness and the chief
complaint
Chest pain, SOB, Edema, etc.
Assess risk factors
CARDIAC ASSESSMENT
2. Physical examination
Vital signs- BP, PP, MAP
Inspection of the skin
Inspection of the thorax
Palpation of the PMI, pulses
Auscultation of the heart
sounds
CARDIAC ASSESSMENT
3. Laboratory and diagnostic studies
CBC
cardiac catheterization
Lipid profile
arteriography
Cardiac enzymes and proteins
CXR
CVP
EEG
Holter monitoring
Exercise ECG
CARDIAC
IMPLEMENTATION
• Assess the cardio-pulmonary
status
VS, BP, Cardiac assessment
2. Enhance cardiac output
Establish IV line to administer
fluids
CARDIAC
IMPLEMENTATION
3. Promote gas exchange
Administer O2
Position client in SEMI-Fowler’s
Encourage coughing and deep
breathing exercises
CARDIAC
IMPLEMENTATION
4. Increase client activity tolerance
Balance rest and activity periods
Assist in daily activities
5. Promote client comfort
Assess the client’s description of
pain and chest discomfort
Administer medication as
prescribed
CARDIAC
IMPLEMENTATION
6. Promote adequate sleep
7. Prevent infection
Monitor skin integrity of lower
extremities
Assess skin site for edema, redness
and warmth
Monitor for fever
Change position frequently
CARDIAC
IMPLEMENTATION

8. Minimize patient anxiety


Encourage verbalization of
feelings, fears and concerns
Answer client questions.
Provide information about
procedures and medications
CARDIAC DISEASES
Coronary Artery Disease
Myocardial Infarction
Congestive Heart Failure
Infective Endocarditis
Cardiac Tamponade
Cardiogenic Shock
VASCULAR DISEASES
Hypertension
Buerger’s disease
Varicose veins
Deep vein thrombosis
Aneurysm
CAD

CAD results from the focal


narrowing of the large and
medium-sized coronary
arteries due to deposition of
atheromatous plaque in the
vessel wall
CAD
RISK FACTORS
1. Age above 45/55 and Sex- Males and
post-menopausal females
2. Family History
3. Hypertension
4. DM
5. Smoking
6. Obesity
7. Sedentary lifestyle
8. Hyperlipedimia
CAD
RISK FACTORS
Most important MODIFIABLE
factors:
Smoking
Hypertension
Diabetes
Cholesterol abnormalities
CAD
Pathophysiology
Fatty streak formation in the
vascular intima  T-cells and
monocytes ingest lipids in the area
of deposition atheroma
narrowing of the arterial lumen 
reduced coronary blood flow 
myocardial ischemia
CAD
Pathophysiology
There is decreased perfusion of
myocardial tissue and inadequate
myocardial oxygen supply
If 50% of the left coronary arterial
lumen is reduced or 75% of the other
coronary artery, this becomes
significant
Potential for Thrombosis and
embolism
Angina Pectoris

Chest pain resulting


from coronary
atherosclerosis or
myocardial ischemia
Angina Pectoris: Clinical Syndromes
Three Common Types of
ANGINA
1. STABLE ANGINA
The typical angina that
occurs during exertion,
relieved by rest and drugs
and the severity does not
change
Angina Pectoris: Clinical Syndromes
Three Common Types of ANGINA
2. Unstable angina
Occurs unpredictably
during exertion and
emotion, severity increases
with time and pain may not
be relieved by rest and drug
Angina Pectoris: Clinical Syndromes
Three Common Types of ANGINA
3. Variant angina
Prinzmetal angina, results
from coronary artery
VASOSPASMS, may occur
at rest
Angina Pectoris
ASSESSMENT FINDINGS
1. Chest pain- ANGINA
The most characteristic symptom
PAIN is described as mild to
severe retrosternal pain, squeezing,
tightness or burning sensation
Radiates to the jaw and left arm
Angina Pectoris
ASSESSMENT FINDINGS
1. Chest pain- ANGINA
Precipitated by Exercise, Eating
heavy meals, Emotions like
excitement and anxiety and
Extremes of temperature
Relieved by REST and Nitroglycerin
Angina Pectoris
ASSESSMENT FINDINGS
2. Diaphoresis
3. Nausea and vomiting
4. Cold clammy skin
5. Sense of apprehension and
doom
6. Dizziness and syncope
Angina Pectoris
LABORATORY FINDINGS
1. ECG may show normal tracing if
patient is pain-free. Ischemic changes
may show ST depression and T wave
inversion
2. Cardiac catheterization
Provides the MOST DEFINITIVE
source of diagnosis by showing the
presence of the atherosclerotic lesions
Angina Pectoris
NURSING MANAGEMENT
1. Administer prescribed medications
Nitrates- to dilate the coronary arteries
Aspirin- to prevent thrombus
formation
Beta-blockers- to reduce BP and HR
Calcium-channel blockers- to dilate
coronary artery and reduce vasospasm
2. Teach the patient management of anginal
attacks
Advise patient to stop all activities
Put one nitroglycerin tablet under the
tongue
Wait for 5 minutes
If not relieved, take another tablet and
wait for 5 minutes
Another tablet can be taken (third tablet)
If unrelieved after THREE tablets seek
medical attention
Angina Pectoris
3. Obtain a 12-lead ECG
4. Promote myocardial perfusion
Instruct patient to maintain bed rest
Administer O2 @ 3 lpm
Advise to avoid valsalva maneuvers
Provide laxatives or high fiber diet to
lessen constipation
Encourage to avoid increased physical
activities
Angina Pectoris
5. Assist in possible treatment modalities
PTCA- percutaneous transluminal
coronary angioplasty
To compress the plaque against the
vessel wall, increasing the arterial
lumen
CABG- coronary artery bypass graft
To improve the blood flow to the
myocardial tissue
Angina Pectoris
6. Provide information to family
members to minimize anxiety
and promote family
cooperation
7. Assist client to identify risk
factors that can be modified
8. Refer patient to proper
agencies
Myocardial infarction
Death of myocardial tissue
in regions of the heart
with abrupt interruption
of coronary blood supply
Myocardial infarction
ETIOLOGY and Risk factors
1. CAD
2. Coronary vasospasm
3. Coronary artery occlusion by
embolus and thrombus
4. Conditions that decrease
perfusion- hemorrhage, shock
Myocardial infarction
Risk factors
1. Hypercholesterolemia
2. Smoking
3. Hypertension
4. Obesity
5. Stress
6. Sedentary lifestyle
Myocardial infarction
PATHOPHYSIOLOGY
Interrupted coronary blood flow
myocardial ischemia anaerobic
myocardial metabolism for several
hours myocardial death 
depressed cardiac function 
triggers autonomic nervous system
response  further imbalance of
myocardial O2 demand and supply
Myocardial infarction
ASSESSMENT findings
1. CHEST PAIN
Chest pain is described as severe,
persistent, crushing substernal
discomfort
Radiates to the neck, arm, jaw
and back
Myocardial infarction
ASSESSMENT findings
1. CHEST PAIN
Occurs without cause, primarily
early morning
NOT relieved by rest or
nitroglycerin
Lasts 30 minutes or longer
Myocardial infarction
Assessment findings
2. Dyspnea
3. Diaphoresis
4. cold clammy skin
5. N/V
6. restlessness, sense of doom
7. tachycardia or bradycardia
8. hypotension
9. S3 and dysrhythmias
Myocardial infarction
Laboratory findings
1. ECG- the ST segment is ELEVATED.
T wave inversion, presence of Q wave
2. Myocardial enzymes- elevated CK-
MB, LDH and Troponin levels
3. CBC- may show elevated WBC count
4. Test after the acute stage- Exercise
tolerance test, thallium scans, cardiac
catheterization
Myocardial infarction
Nursing Interventions
1. Provide Oxygen at 2 lpm, Semi-fowler’s
2. Administer medications
Morphine to relieve pain
nitrates, thrombolytics, aspirin and
anticoagulants
Stool softener and hypolipidemics
3. Minimize patient anxiety
Provide information as to procedures
and drug therapy
Myocardial infarction

4. Provide adequate rest periods


5. Minimize metabolic demands
Provide soft diet
Provide a low-sodium, low
cholesterol and low fat diet
6. Minimize anxiety
Reassure client and provide
information as needed
Myocardial infarction
7. Assist in treatment modalities
such as PTCA and CABG
8. Monitor for complications of MI-
especially dysrhythmias, since
ventricular tachycardia can
happen in the first few hours after
MI
9. Provide client teaching
MI
Medical Management
1. ANALGESIC
The choice is MORPHINE
It reduces pain and anxiety
Relaxes bronchioles to enhance
oxygenation
MI
Medical Management
2. ACE
Prevents formation of angiotensin
II
Limits the area of infarction
MI
Medical Management
3. Thrombolytics
Streptokinase, Alteplase
Dissolve clots in the coronary
artery allowing blood to flow
Myocardial infarction
NURSING INTERVENTIONS
AFTER ACUTE EPISODE
1. Maintain bed rest for the first
3 days
2. Provide passive ROM
exercises
3. Progress with dangling of the
feet at side of bed
Myocardial infarction
NURSING INTERVENTIONS
AFTER ACUTE EPISODE
4. Proceed with sitting out of
bed, on the chair for 30 minutes
TID
5. Proceed with ambulation in
the room toilet hallway TID
Myocardial infarction
NURSING INTERVENTIONS AFTER
ACUTE EPISODE
Cardiac rehabilitation
To extend and improve quality of life
Physical conditioning
Patients who are able to walk 3-4 mph
are usually ready to resume sexual
activities
CARDIOMYOPATHIES
Heart muscle disease
associated with cardiac
dysfunction
CARDIOMYOPATHIES
1. Dilated Cardiomyopathy
2. Hypertrophic
Cardiomyopathy
3. Restrictive cardiomyopathy
DILATED CARDIOMYOPATHY
ASSOCIATED FACTORS
1. Heavy alcohol intake
2. Pregnancy
3. Viral infection
4. Idiopathic
DILATED CARDIOMYOPATHY
PATHOPHYSIOLOGY
Diminished contractile proteins
poor contraction decreased
blood ejection increased blood
remaining in the ventricle
ventricular stretching and
dilatation.
SYSTOLIC DYSFUNCTION
HYPERTROPHIC
CARDIOMYOPATHY

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

This condition restricts


ventricular filling resulting to
decreased cardiac output
Acute tamponade may happen
when there is a sudden
accumulation of more than 50
ml fluid in the pericardial sac
CARDIAC TAMPONADE
Causative factors
1. Cardiac trauma
2. Complication of Myocardial
infarction
3. Pericarditis
4. Cancer metastasis
CARDIAC TAMPONADE
ASSESSMENT FINDINGS
1. BECK’s Triad- Jugular vein
distention, hypotension and
distant/muffled heart sound
2. Pulsus paradoxus
3. Increased CVP
4. decreased cardiac output
CARDIAC TAMPONADE
ASSESSMENT FINDINGS
5. Syncope
6. anxiety
7. dyspnea
8. Percussion- Flatness across the
anterior chest
CARDIAC TAMPONADE
Laboratory FINDINGS
1. Echocardiogram
2. Chest X-ray
CARDIAC TAMPONADE
NURSING INTERVENTIONS
1. Assist in PERICARDIOCENTESIS
2. Administer IVF
3. Monitor ECG, urine output and BP
4. Monitor for recurrence of
tamponade
Pericardiocentesis
Patient is monitored by ECG
Maintain emergency equipments
Elevate head of bed 45-60 degrees
Monitor for complications-
coronary artery rupture,
dysrhythmias, pleural laceration
and myocardial trauma
HYPERTENSION
A systolic BP greater than 140
mmHg and a diastolic pressure
greater than 90 mmHg over a
sustained period, based on two
or more BP measurements.
HYPERTENSION
Types of Hypertension
1. Primary or ESSENTIAL
Most common type
2. Secondary
Due to other conditions like
Pheochromocytoma, renovascular
hypertension, Cushing’s, Conn’s ,
SIADH
HYPERTENSION

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

Fusiform= when the entire segment


becomes dilated
ANEURYSM
RISK FACTORS
• Atherosclerosis
• Infection= syphilis
• Connective tissue disorder
• Genetic disorder= Marfan’s Syndrome
ANEURYSM
PATHOPHYSIOLOGY
Damage to the intima and media weakness
 outpouching

Dissecting aneurysm tear in the intima and


media with dissection of blood through
the layers
ANEURYSM
ASSESSMENT
• Asymptomatic
• Pulsatile sensation on the abdomen
• Palpable bruit
ANEURYSM
LABORATORY:
• CT scan
• Ultrasound
• X-ray
• Aortography
ANEURYSM
Medical Management:
• Anti-hypertensives
• Synthetic graft
ANEURYSM
Nursing Management:
• Administer medications
• Emphasize the need to avoid increased
abdominal pressure
• No deep abdominal palpation
• Remind patient the need for serial
ultrasound to detect diameter changes
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Refers to arterial insufficiency of
the extremities usually secondary
to peripheral atherosclerosis.
Usually found in males age 50 and
above
The legs are most often affected
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Risk factors for Peripheral
Arterial occlusive disease
Non-Modifiable
1. Age
2. gender
3. family predisposition
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Risk factors for Peripheral Arterial
occlusive disease
Modifiable
1. Smoking
2. HPN
3. Obesity
4. Sedentary lifestyle
5. DM
6. Stress
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
ASSESSMENT FINDINGS
1. INTERMITTENT
CLAUDICATION- the hallmark of
PAOD
This is PAIN described as aching,
cramping or fatiguing discomfort
consistently reproduced with the
same degree of exercise or activity
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
ASSESSMENT FINDINGS
1. INTERMITTENT
CLAUDICATION- the hallmark
of PAOD
This pain is RELIEVED by REST
This commonly affects the muscle
group below the arterial occlusion
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Assessment Findings
2. Progressive pain on the
extremity as the disease advances
3. Sensation of cold and
numbness of the extremities
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Assessment Findings
4. Skin is pale when elevated and
cyanotic/ruddy when placed on a
dependent position
5. Muscle atrophy, leg ulceration
and gangrene
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Diagnostic Findings
1. Unequal pulses between the
extremities
2. Duplex ultrasonography
3. Doppler flow studies
PAOD
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
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Nursing Interventions
1. Maintain Circulation to the
extremity
Evaluate regularly peripheral pulses,
temperature, sensation, motor
function and capillary refill time
Administer post-operative care to
patient who underwent surgery
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Nursing Interventions
2. Monitor and manage complications
Note for bleeding, hematoma,
decreased urine output
Elevate the legs to diminish edema
Encourage exercise of the extremity
while on bed
Teach patient to avoid leg-crossing
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Nursing Interventions
3. Promote Home management
Encourage lifestyle changes
Instruct to AVOID smoking
Instruct to avoid leg crossing
BUERGER’S DISEASE
Thromboangiitis obliterans
A disease characterized by
recurring inflammation of the
medium and small arteries and
veins of the lower extremities
Occurs in MEN ages 20-35
RISK FACTOR: SMOKING!
BUERGER’S DISEASE

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

 3. Provide pain relief

 4. Provide information as to
therapy- chemo and bone
marrow transplantation