Presentation 2

CARDIOVASCULAR SYSTEM
THE CARDIOVASCULAR SYSTEM

HEART
- Is a four chambered hollow muscular organ, size
of a fist, weighs between 7-15 ounces (200-425
grams)
- Each day the average heart beats 100,000 times,
pumping about 2,000 gallons of blood (7,571 L)
- The heart is located in the LEFT side of the
mediastinum
- Consists of Three layers - epicardium, myocardium
and endocardium
• 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
Epicardium
Myocardium
Endocardium
• 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 heart also has

four chambers -
• two atria and two
ventricles
- Left atrium and the
right atrium
- ventricle and the Left
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 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%)
2. Left coronary artery- branches into the

Left Anterior Descending Coronary (LAD)
Artery 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
Coronary
Sinus
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 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
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 Heart Rate
• Parasympathetic system (Vagus) DECREASES
Heart Rate
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 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 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
Cardiac Assessment
Laboratory Test Rationale

• 1. To assist in diagnosing MI
• 2. To identify abnormalities
• 3. To assess inflammation
Laboratory Test Rationale

• 4. To determine baseline value
• 5. To monitor serum level of
medications
• 6. To assess the effects of
medications
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
CARDIAC Proteins and

enzymes
CK- MB ( creatine kinase)
Normal value is 0-7 U/L
Lactic Dehydrogenase (LDH)
Elevates in MI in 24 hours,
peaks in 48-72 hours
Lactic Dehydrogenase (LDH)
Normal value is 70-200 IU/L
Myoglobin
Rises within 1-3 hours
Peaks in 4-12 hours
Returns to normal in a day
Myoglobin
Not used alone
Muscular and RENAL disease can
have elevated myoglobin
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
Troponin I and T
• REMEMBER to AVOID IM
injections before obtaining
blood sample!
• Early and late diagnosis can
be made!
SERUM LIPIDS
• Lipid profile measures the
serum cholesterol,
triglycerides and lipoprotein
levels
• Cholesterol= 200 mg/dL
• Triglycerides- 40- 150 mg/dL
SERUM LIPIDS
• LDH- 130 mg/dL
• HDL- 30-70- mg/dL
• NPO post midnight (usually
12 hours)
ELECTROCARDIOGRAM (ECG)
• A non-invasive procedure that
evaluates the electrical activity
of the heart
• Electrodes and wires are
attached to the patient
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
Holter Monitoring
• Instruct the client to resume
normal activities and maintain
a diary of activities and any
symptoms that may develop
ECHOCARDIOGRAM
• Non-invasive test that studies
the structural and functional
changes of the heart with the
use of ultrasound
• No special preparation is needed
Stress Test
• A non-invasive test that studies
the heart during activity and
detects and evaluates CAD
• Exercise test, pharmacologic
test and emotional test
Stress Test
• Treadmill testing is the most
commonly used stress test
• Used to determine CAD, Chest
pain causes, drug effects and
dysrhythmias in exercise
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
• 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
Pharmacological stress test

• Use of dipyridamole
• Maximally dilates coronary
artery
• Side-effect: flushing of face
Pharmacological stress test

• Pre-test: 4 hours fasting,
avoid alcohol, caffeine
• Post test: report symptoms
of chest pain
• CARDIAC catheterization
• Insertion of a catheter into the
heart and surrounding vessels
• Determines the structure and
performance of the heart valves
and surrounding vessels
• CARDIAC catheterization
• Used to diagnose CAD,
assess coronary atery
patency and determine
extent of atherosclerosis
• Pretest: Ensure Consent,

assess for allergy to seafood
and iodine, NPO, document
weight and height, baseline
VS, blood tests and document
the peripheral pulses
• Pretest: Fast for 8-12

hours, teachings,
medications to allay
anxiety
• 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
• 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
• 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
CVP
• The CVP is the pressure within
the SVC
• Reflects the pressure under
which blood is returned to the
SVC and right atrium
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
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
1. Assess the cardio-pulmonary

status
VS, BP, Cardiac assessment
2. Enhance cardiac output
– Establish IV line to administer
fluids
3. Promote gas exchange

– Administer O2
– Position client in SEMI-Fowler’s
– Encourage coughing and deep
breathing exercises
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
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
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
2. Unstable angina
–Occurs unpredictably during
exertion and emotion,
severity increases with time
and pain may not be
relieved by rest and drug
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
ETIOLOGY and Risk factors
• 1. CAD
• 2. Coronary vasospasm
• 3. Coronary artery occlusion by
embolus and thrombus
• 4. Conditions that decrease
perfusion- hemorrhage, shock
Risk factors
• 1. Hypercholesterolemia
• 2. Smoking
• 3. Hypertension
• 4. Obesity
• 5. Stress
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
ASSESSMENT findings
1. CHEST PAIN
• Chest pain is described as severe,
persistent, crushing substernal
discomfort
• Radiates to the neck, arm, jaw and
back
ASSESSMENT findings
1. CHEST PAIN
• Occurs without cause, primarily early
morning
• NOT relieved by rest or nitroglycerin
• Lasts 30 minutes or longer
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
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
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
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
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
Myocardial Infarction
• 2. ACE
– Prevents formation of angiotensin II
– Limits the area of infarction
MI
• 3. Thrombolytics
– Streptokinase, Alteplase
– Dissolve clots in the coronary artery
allowing blood to flow
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
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
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
• 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
2. Increase patient tolerance
• Schedule activities with rest periods
in between
CARDIOMYOPATHIES
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
• Etiologic factors
• 1. Bacteria- Organism depends
on several factors
• 2. Fungi
Risk factors
• 1. Prosthetic valves
• 2. Congenital malformation
• 3. Cardiomyopathy
• 4. IV drug users
• 5. Valvular dysfunctions
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
Assessment findings
• 1. Intermittent HIGH fever
• 2. anorexia, weight loss
• 3. cough, back pain and joint
pain
• 4. splinter hemorrhages under
nails
• Assessment findings
• 5. Osler’s nodes- painful
nodules on fingerpads
• 6. Roth’s spots- pale
hemorrhages in the retina
• 7. Heart murmurs
• 8. Heart failure
• Prevention
• Antibiotic prophylaxis if
patient is undergoing
procedures like dental
extractions, bronchoscopy,
surgery, etc.
• LABORATORY EXAM
• Blood Cultures to determine
the exact organism
Nursing management
• 1. regular monitoring of
temperature, heart sounds
• 2. manage infection
• 3. long-term antibiotic
therapy
Medical management
• 1. Pharmacotherapy
• IV antibiotic for 2-6 weeks
• Antifungal agents are given –
amphotericin B
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
• 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
Class 2
• SLIGHT limitation of ADLs
• NO symptom at rest
• Symptom with INCREASED activity
• Basilar crackles and S3
Class 3
• Markedly limitation on ADLs
• Comfortable at rest BUT
symptoms present in LESS than
ordinary activity
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
• 3. Administer medications-
usually cardiac glycosides are
given- DIGOXIN or DIGITOXIN,
Diuretics, vasodilators and
hypolipidemics are prescribed
CHF
• 4. Provide a LOW sodium diet.
Limit fluid intake as necessary
• 5. Provide adequate rest periods
to prevent fatigue
CHF
• 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
ACUTE STAGE
• 4. Provide a LOW fat and LOW
sodium diet
• 5. Provide potassium supplements
• 6. Instruct about fluid restriction
CHF
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
• 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
• 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
• 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
• 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
1. Atherosclerosis
2. Infection= syphilis
3. Connective tissue disorder
4. 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
1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. 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
DISEASE
• Risk factors for Peripheral Arterial
occlusive disease
• Non-Modifiable
• 1. Age
• 2. gender
• 3. family predisposition
DISEASE
• Risk factors for Peripheral Arterial
occlusive disease
Modifiable
• 1. Smoking
• 2. HPN
• 3. Obesity
• 5. DM
• 6. Stress
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
DISEASE
• 1. INTERMITTENT CLAUDICATION-
the hallmark of PAOD
• This pain is RELIEVED by REST
• This commonly affects the muscle
group below the arterial occlusion
DISEASE
• Assessment Findings
• 2. Progressive pain on the extremity
as the disease advances
• 3. Sensation of cold and numbness
of the extremities
DISEASE
• 4. Skin is pale when elevated and
cyanotic/ruddy when placed on a
dependent position
• 5. Muscle atrophy, leg ulceration and
gangrene
DISEASE
• Diagnostic Findings
• 1. Unequal pulses between the
extremities
• 2. Duplex ultrasonography
• 3. Doppler flow studies
PAOD
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
DISEASE
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
DISEASE
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
DISEASE
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
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
• 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
1. Assist in the medical and surgical
management
• Bypass graft
• amputation
2. Strongly advise to AVOID smoking
3. Manage complications appropriately
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
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
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
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
• 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
–Tortuous superficial veins on
the legs
–Leg pain and Heaviness
–Dependent edema
VARICOSE VEINS
• Laboratory findings
–Venography
–Duplex scan pletysmography
VARICOSE VEINS
–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
• 3. Provide high-fiber foods to
prevent constipation
• 4. Teach simple exercise to
promote venous return
VARICOSE VEINS
• 5. Caution patient to avoid
knee-length stockings and
constrictive clothings
VARICOSE VEINS
• 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
• Predisposing factors
–Prolonged immobility
–Varicosities
–Traumatic procedures
• Complication
–PULMONARY
thromboembolism
• Leg tenderness
• Leg pain and edema
• Positive HOMAN’s SIGN
• Venography
• Duplex scan
–Antiplatelets
–Anticoagulants
–Vein stripping and grafting
–Anti-embolic stockings
• 1. Provide measures to avoid
prolonged immobility
–Repositioning Q2
–Provide passive ROM
–Early ambulation
• 2. Provide skin care to prevent
the complication of leg ulcers
• 3. Provide anti-embolic
stockings
• 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
• A condition 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
–Etiologic Factors
–1. Bleeding- the most common
cause
–2. Mal-absorption
–3. Malnutrition
–4. Alcoholism
• Pathophysiology
–The body stores of iron
decrease, leading to
depletion of hemoglobin
synthesis

• Pathophysiology
–The oxygen carrying capacity
of hemoglobin is reduced
tissue hypoxia
• 1. Pallor of the skin and mucous
membrane
• 2. Weakness and fatigue
• 3. General malaise
• 4. Pica

• 5. Brittle nails
• 6. Smooth and sore tongue
• 7. Angular cheilosis
• 1. CBC- Low levels of Hct, Hgb and
RBC count
• 2. low serum iron, low ferritin
• 3. Bone marrow aspiration- MOST
definitive

• 1. Hematinics
• 2. Blood transfusion
Iron Deficiency Anemia
Nursing Management
• 1. Provide iron rich-foods
– Organ meats (liver)
– Beans
– Leafy green vegetables
– Raisins and molasses
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
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
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
• A condition 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
• 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
• 1. Bone marrow
transplantation
• 2. Immunosupressant drugs
• 3. Rarely, steroids
• 4. Blood transfusion
APLASTIC ANEMIA
• 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
• Folic Acid deficiency
• Causative factors
• 1. Alcoholism
• 2. Mal-absorption
• 3. Diet deficient in uncooked
vegetables
• 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
• Vitamin B12 deficiency
• Causative factors
• 1. Strict vegetarian diet
• 2. Gastrointestinal malabsorption
• 3. Crohn's disease
• 4. gastrectomy
• 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
• 1. weakness
• 2. fatigue
• 3. listless
• 4. neurologic manifestations are present
only in Vit. B12 deficiency
• Pernicious Anemia
– Beefy, red, swollen tongue
– Mild diarrhea
– Extreme pallor
– Paresthesias in the extremities
• 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
• 1. Vitamin supplementation
– Folic acid 1 mg daily
• 2. Diet supplementation
– Vegetarians should have vitamin intake
• 3. Lifetime monthly injection of IM Vit
B12
• 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
• A severe chronic incurable

hemolytic anemia that
results from heritance of the
sickle hemoglobin gene.
• Causative factor
–Genetic inheritance of the
sickle gene- HbS gene
• Pathophysiology
• Decreased O2, Cold,
Vasoconstriction can
precipitate sickling process
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
• 1. jaundice
• 2. enlarged skull and facial
bones
• 3. tachycardia, murmurs and
cardiomegaly
• Primary sites of thrombotic
occlusion: spleen, lungs and
CNS
• Chest pain, dyspnea
• 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
Medical Management
• 1. Bone marrow transplant
• 2. Hydroxyurea
–Increases the HbF
• 3. Long term RBC trnasfusion
Nursing Management
• 1. manage the pain
–Support and elevate acutely
inflamed joint
–Relaxation techniques
–analgesics
Nursing Management
• 2. Prevent and manage
infection
–Monitor status of patient
–Initiate prompt antibiotic
therapy
Nursing Management
• 3. Promote coping skills
–Provide accurate information
–Allow patient to verbalize her
concerns about medication,
prognosis and future pregnancy
Nursing Management
• 4. Monitor and prevent potential
complications
–Provide always adequate
hydration
–Avoid cold, temperature that may
cause vasoconstriction
Nursing Management
• 4. Monitor and prevent
potential complications
–Leg ulcer
• Aseptic technique
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
• Causative factor
–unknown
Polycythemia
• Pathophysiology
–The stem cells grow uncontrollably
–The bone marrow becomes
HYPERcellular and all the blood
cells are increased in number
Polycythemia
• Pathophysiology
–The spleen resumes its function of
hematopoiesis and enlarges
–Blood becomes thick and viscous
causing sluggish circulation
Polycythemia
• Pathophysiology
–Overtime, the bone marrow
becomes fibrotic
Polycythemia
–1. Skin is ruddy
–2. Splenomegaly
–3. headache
–4. dizziness, blurred vision
–5. Angina, dyspnea and
thrombophlebitis
Polycythemia
–1. CBC- shows elevated RBC mass
–2. Normal oxygen saturation
–3 Elevated WBC and Platelets
Polycythemia
• Complications
–1. Increased risk for
thrombophlebitis, CVA and MI
–2. Bleeding due to dysfunctional
blood cells
Polycythemia
–1. To reduce the high blood cell
mass- PHLEBOTOMY
–2. Allopurinol
–3. Dipyridamole
–4. Chemotherapy to suppress bone
marrow
Polycythemia
– 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
• CHRONIC myelocytic leukemia

• CHRONIC lymphocytic 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
• ACUTE LEUKEMIA
– Pallor
– Fatigue
– Dyspnea
– Hemorrhages
– Organomegaly
– Headache
– vomiting
Leukemia
• 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
1. Chemotherapy
2. 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

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CARDIOVASCULAR SYSTEM

THE CARDIOVASCULAR SYSTEM

• The layer that covers

• The heart also has

The heart chambers are guarded by

2. Left coronary artery- branches into the

Laboratory Test Rationale

Laboratory Test Rationale

CARDIAC Proteins and

Pharmacological stress test

Pharmacological stress test

• Pretest: Ensure Consent,

• Pretest: Fast for 8-12

1. Assess the cardio-pulmonary

3. Promote gas exchange

8. Minimize patient anxiety

• CAD results from the focal

• Chest pain resulting

Three Common Types of ANGINA

• Death of myocardial tissue in

4. Provide adequate rest periods

NURSING INTERVENTIONS AFTER ACUTE

• Infection of the heart valves

• This condition restricts ventricular

• Fusiform= when the entire segment becomes

Dissecting aneurysm tear in the intima and

• THESE are dilated veins

• A condition in which the

• Iron Deficiency Anemia

• Iron Deficiency Anemia

• Iron Deficiency Anemia

• Iron Deficiency Anemia

• A severe chronic incurable

• CHRONIC myelocytic leukemia

• 3. Provide pain relief

• 4. Provide information as to therapy- chemo

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