cardio med-surg nursing
TRANSCRIPT
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Nursing Board Review
Cardiovascular System
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The Cardiovascular System
Normal Anatomy
The heart is located in the LEFT side of the
mediastinumConsists of Three layers- epicardium,
myocardium and endocardium
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The Cardiovascular System
The epicardium covers the outer surface of
the heart
The myocardium is the middle muscularlayer of the heart
The endocardium lines the chambers and
the valves
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The Cardiovascular System
The layer that covers the heart is the
PERICARDIUM
There are two parts- parietal and visceralpericardium
The space between the two pericardial
layers is the pericardial space
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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
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The Cardiovascular System
The Blood supply of the heart comes from
the Coronary arteries
1. Right coronary artery supplies theRIGHT atrium and RIGHT ventricle,
inferior portion of the LEFT ventricle,
the POSTERIOR septal wall and the two
nodes- AV (90%) and SA node (55%)
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The Cardiovascular System
2. Left coronary artery- branches into the
LAD and the circumflex branch
The LAD supplies blood to the anteriorwall of the LEFT ventricle, the anterior
septum and the Apex of the left ventricle
The CIRCUMFLEX branch supplies theleft atrium and the posterior LEFT
ventricle
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The Cardiovascular System
The CONDUCTING SYSTEM OF THEHEART
Consists of the
1. SA node- the pacemaker
2. AV node- slowest conduction
3. Bundle of His – branches into the Rightand the Left bundle branch
4. Purkinje fibers- fastest conduction
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The Heart sounds
1. S1- due to closure of the AV valves
2. S2- due to the closure of the semi-lunarvalves
3. S3- due to increased ventricular filling
4. S4- due to forceful atrial contraction
The Cardiovascular System
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The Cardiovascular System
Heart rate
Normal range is 60-100 beats per minute
Tachycardia is greater than 100 bpmBradycardia is less than 60 bpm
Sympathetic system INCREASES HR
Parasympathetic system (Vagus)
DECREASES HR
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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
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The Cardiovascular System
The vascular system consists of the arteries,veins and capillaries
The arteries are vessels that carry bloodaway from the heart to the periphery
The veins are the vessels that carry blood tothe heart
The capillaries are lined with squamos cells,they connect the veins and arteries
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The Cardiovascular System
The lymphatic system also is part of the
vascular system and the function of this
system is to collect the extravasated fluidfrom the tissues and returns it to the blood
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The Cardiovascular System
Cardiac Assessment
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The Cardiovascular System
Laboratory Test Rationale
1. To assist in diagnosing MI2. To identify abnormalities
3. To assess inflammation
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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
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
CK- MB ( creatine kinase)
Elevates in MI within 4
hours, peaks in 18 hoursand then declines till 3 days
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
CK- MB ( creatinekinase)
Normal value is 0-7 U/L
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
Lactic Dehydrogenase (LDH)
Elevates in MI in 24 hours,
peaks in 48-72 hoursNormally LDH1 is greater
than LDH2
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
Lactic Dehydrogenase (LDH)
MI- LDH2 greater than
LDH1 (flipped LDH pattern)Normal value is 70-200 IU/L
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
Myoglobin
Rises within 1-3 hours
Peaks in 4-12 hoursReturns to normal in a day
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC Proteins andenzymes
Myoglobin
Not used alone
Muscular and RENAL diseasecan have elevated myoglobin
Th C di l S t
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The Cardiovascular System
LABORATORY PROCEDURES
Troponin I and TTroponin 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
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The Cardiovascular System
LABORATORY PROCEDURES
Troponin I and T
REMEMBER to AVOIDIM injections before
obtaining blood sample!
Early and late diagnosis can
be made!
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The Cardiovascular System
LABORATORY PROCEDURES
SERUM LIPIDS
Lipid profile measures the
serum cholesterol,triglycerides and lipoprotein
levelsCholesterol= 200 mg/dL
Triglycerides- 40- 150 mg/dL
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The Cardiovascular System
LABORATORY PROCEDURES
SERUM LIPIDS
LDH- 130 mg/dLHDL- 30-70- mg/dL
NPO post midnight (usually12 hours)
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The Cardiovascular System
LABORATORY PROCEDURES
Holter Monitoring
A non-invasive test in
which the client wears aHolter monitor and an
ECG tracing recordedcontinuously over a periodof 24 hours
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The Cardiovascular System
LABORATORY PROCEDURES
Holter Monitoring
Instruct the client to resumenormal activities and maintain
a diary of activities and anysymptoms that may develop
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The Cardiovascular System
LABORATORY PROCEDURES
ECHOCARDIOGRAM
Non-invasive test that studies
the structural and functionalchanges of the heart with the
use of ultrasoundNo special preparation isneeded
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The Cardiovascular System
LABORATORY PROCEDURES
Stress Test
A non-invasive test thatstudies the heart duringactivity and detects and
evaluates CADExercise test, pharmacologictest and emotional test
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The Cardiovascular System
LABORATORY PROCEDURES
Stress Test
Pre-test: consent may berequired, adequate rest ,eat a light meal or fast for
4 hours and avoidsmoking, alcohol and
caffeine
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The Cardiovascular System
LABORATORY PROCEDURES
Post-test: instruct client tonotify the physician if any
chest pain, dizziness orshortness of breath . Instruct
client to avoid taking a hotshower for 10-12 hours afterthe test
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The Cardiovascular System
LABORATORY PROCEDURES
Pharmacological stress test
Use of dipyridamoleMaximally dilatescoronary artery
Side-effect: flushing of face
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The Cardiovascular System
LABORATORY PROCEDURES
Post-test: instruct client tonotify the physician if any
chest pain, dizziness orshortness of breath . Instruct
client to avoid taking a hotshower for 10-12 hours afterthe test
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The Cardiovascular System
LABORATORY PROCEDURES
Pharmacological stress test
Pre-test: 4 hours fasting,avoid alcohol, caffeine
Post test: reportsymptoms of chest pain
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC catheterization
Insertion of a catheter into
the heart and surroundingvessels
Determines the structure andperformance of the heartvalves and surrounding
vessels
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The Cardiovascular System
LABORATORY PROCEDURES
CARDIAC catheterization
Used to diagnose CAD,
assess coronary atery
patency and determine
extent of atherosclerosis
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The Cardiovascular System
LABORATORY PROCEDURES
Pretest: Ensure Consent,assess for allergy to
seafood and iodine, NPO,document weight and
height, baseline VS, bloodtests and document theperipheral pulses
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The Cardiovascular System
LABORATORY PROCEDURES
Pretest: Fast for 8-12
hours, teachings,medications to allay
anxiety
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The Cardiovascular System
LABORATORY PROCEDURES
Intra-test: inform patient of a fluttery feeling as the
catheter passes through theheart; inform the patient
that a feeling of warmth andmetallic taste may occurwhen dye is administered
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The Cardiovascular System
LABORATORY PROCEDURES
Post-test: Monitor VS and cardiacrhythm
Monitor peripheral pulses, color andwarmth and sensation of theextremity distal to insertion site
Maintain sandbag to the insertion siteif required to maintain pressure
Monitor for bleeding and hematomaformation
h C di l S
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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 veinis used
Monitor for dye allergy
Th C di l S
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The Cardiovascular System
LABORATORY PROCEDURES
CVP
The CVP is the pressurewithin the SVC
Reflects the pressure under
which blood is returned tothe SVC and right atrium
Th C di l S
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The Cardiovascular System
LABORATORY PROCEDURES
CVP
Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O
Elevated CVP indicates increasein blood volume, excessive IVF or
heart/renal failureLow CVP may indicatedhypovolemia, hemorrhage and
severe vasodilatation
Th C di l S
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The Cardiovascular System
LABORATORY PROCEDURES
Measuring CVP
1. Position the client supine with bed
elevated at 45 degrees2. Position the zero point of the CVPline at the level of the right atrium.
Usually this is at the MAL, 4 th
ICS3. Instruct the client to be relaxedand avoid coughing and straining.
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CARDIAC ASSESSMENT
ASSESSMENT
1. Health History
Obtain description of presentillness and the chief complaint
Chest pain, SOB, Edema, etc.
Assess risk factors
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CARDIAC ASSESSMENT
2. Physical examinationVital signs- BP, PP, MAP
Inspection of the skinInspection of the thorax
Palpation of the PMI, pulses
Auscultation of the heartsounds
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CARDIAC ASSESSMENT3. Laboratory and diagnostic studies
CBC
cardiac catheterization
Lipid profilearteriography
Cardiac enzymes and proteins
CXR
CVP
EEG
Holter monitoring
Exercise ECG
CARDIAC
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CARDIAC
IMPLEMENTATION
1. Assess the cardio-pulmonary
status
VS, BP, Cardiac assessment
2. Enhance cardiac output
Establish IV line to administerfluids
CARDIAC
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CARDIAC
IMPLEMENTATION
3. Promote gas exchange
Administer O2
Position client in SEMI-Fowler’s
Encourage coughing and deep
breathing exercises
CARDIAC
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CARDIAC
IMPLEMENTATION
4. Increase client activity tolerance
Balance rest and activity periods
Assist in daily activities5. Promote client comfort
Assess the client’s description of
pain and chest discomfortAdminister medication asprescribed
CARDIAC
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CARDIAC
IMPLEMENTATION
6. Promote adequate sleep
7. Prevent infection
Monitor skin integrity of lowerextremities
Assess skin site for edema, redness
and warmthMonitor for fever
Change position frequently
CARDIAC
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CARDIAC
IMPLEMENTATION
8. Minimize patient anxiety
Encourage verbalization of feelings, fears and concerns
Answer client questions.Provide information aboutprocedures and medications
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CARDIAC DISEASES
Coronary Artery Disease
Myocardial Infarction
Congestive Heart FailureInfective Endocarditis
Cardiac TamponadeCardiogenic Shock
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VASCULAR DISEASES
Hypertension
Buerger’s disease
Varicose veins
Deep vein thrombosis
Aneurysm
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CAD
CAD results from the focal
narrowing of the large andmedium-sized coronary
arteries due to deposition of atheromatous plaque in the
vessel wall
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CADRISK FACTORS
1. Age above 45/55 and Sex- Males andpost-menopausal females
2. Family History
3. Hypertension
4. DM
5. Smoking
6. Obesity
7. Sedentary lifestyle
8. Hyperlipedimia
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CADRISK FACTORS
Most important MODIFIABLE
factors:
Smoking
Hypertension
DiabetesCholesterol abnormalities
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CAD
Pathophysiology
Fatty streak formation in the
vascular intima T-cells andmonocytes ingest lipids in the area
of deposition atheroma
narrowing of the arterial lumen reduced coronary blood flow
myocardial ischemia
CAD
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CAD
Pathophysiology
There is decreased perfusion of myocardial tissue and inadequatemyocardial oxygen supply
If 50% of the left coronary arteriallumen is reduced or 75% of the othercoronary artery, this becomes
significantPotential for Thrombosis andembolism
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Angina Pectoris
Chest pain resulting
from coronaryatherosclerosis or
myocardial ischemia
A i P t i Cli i l S d
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Angina Pectoris: Clinical Syndromes
Three Common Types of ANGINA
1. STABLE ANGINA
The typical angina thatoccurs during exertion,relieved by rest and drugs
and the severity does not change
A i P t i Cli i l S d
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Angina Pectoris: Clinical Syndromes
Three Common Types of ANGINA
2. Unstable angina
Occurs unpredictably
during exertion andemotion, severity increaseswith time and pain may not
be relieved by rest and drug
A i P t i Cli i l S d
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Angina Pectoris: Clinical Syndromes
Three Common Types of ANGINA
3. Variant angina
Prinzmetal angina, results
from coronary arteryVASOSPASMS, may occur at rest
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Angina Pectoris
ASSESSMENT FINDINGS
1. Chest pain- ANGINA
The most characteristic symptomPAIN is described as mild tosevere retrosternal pain, squeezing,
tightness or burning sensation Radiates to the jaw and left arm
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Angina Pectoris
ASSESSMENT FINDINGS
1. Chest pain- ANGINA
Precipitated by Exercise, Eatingheavy meals, Emotions like
excitement and anxiety and
Extremes of temperature
Relieved by REST and Nitroglycerin
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Angina Pectoris
ASSESSMENT FINDINGS
2. Diaphoresis
3. Nausea and vomiting4. Cold clammy skin
5. Sense of apprehension anddoom
6. Dizziness and syncope
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Angina Pectoris
LABORATORY FINDINGS
1. ECG may show normal tracing if patient is pain-free. Ischemic changes
may show ST depression and T waveinversion
2. Cardiac catheterization
Provides the MOST DEFINITIVEsource of diagnosis by showing thepresence of the atherosclerotic lesions
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Angina Pectoris
NURSING MANAGEMENT
1. Administer prescribed medications
Nitrates- to dilate the coronary arteriesAspirin- to prevent thrombusformation
Beta-blockers- to reduce BP and HRCalcium-channel blockers- to dilatecoronary artery and reduce vasospasm
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2. Teach the patient management of anginalattacks
Advise patient to stop all activities
Put one nitroglycerin tablet under thetongue
Wait for 5 minutes
If not relieved, take another tablet and waitfor 5 minutes
Another tablet can be taken (third tablet)
If unrelieved after THREE tablets seekmedical attention
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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 tolessen constipation
Encourage to avoid increased physicalactivities
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Angina Pectoris
5. Assist in possible treatment modalities
PTCA- percutaneous transluminalcoronary angioplasty
To compress the plaque against thevessel wall, increasing the arteriallumen
CABG- coronary artery bypass graft
To improve the blood flow to themyocardial tissue
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Angina Pectoris
6. Provide information to familymembers to minimize anxiety
and promote familycooperation
7. Assist client to identify riskfactors that can be modified
8. Refer patient to proper
agencies
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Myocardial infarction
Death of myocardial
tissue in regions of the
heart with abrupt
interruption of coronary
blood supply
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Myocardial infarction
ETIOLOGY and Risk factors
1. CAD
2. Coronary vasospasm3. Coronary artery occlusion byembolus and thrombus
4. Conditions that decreaseperfusion- hemorrhage, shock
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Myocardial infarction
Risk factors
1. Hypercholesterolemia
2. Smoking3. Hypertension
4. Obesity
5. Stress
6. Sedentary lifestyle
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Myocardial infarction
PATHOPHYSIOLOGY
Interrupted coronary blood flow
myocardial ischemia anaerobicmyocardial metabolism for severalhours myocardial death depressed cardiac function
triggers autonomic nervous systemresponse further imbalance of myocardial O2 demand and supply
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Myocardial infarction
ASSESSMENT findings
1. CHEST PAIN
Chest pain is described as severe,persistent, crushing substernaldiscomfort
Radiates to the neck, arm, jawand back
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Myocardial infarction
ASSESSMENT findings
1. CHEST PAIN
Occurs without cause, primarilyearly morning
NOT relieved by rest or
nitroglycerin
Lasts 30 minutes or longer
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Myocardial infarction
Assessment findings
2. Dyspnea
3. Diaphoresis
4. cold clammy skin
5. N/V
6. restlessness, sense of doom7. tachycardia or bradycardia
8. hypotension
9. S3 and dysrhythmias
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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- Exercisetolerance test, thallium scans, cardiaccatheterization
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Myocardial infarction
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Myocardial infarctionNursing Interventions
1. Provide Oxygen at 2 lpm, Semi-fowler’s
2. Administer medications
Morphine to relieve pain
nitrates, thrombolytics, aspirin andanticoagulants
Stool softener and hypolipidemics
3. Minimize patient anxiety
Provide information as to proceduresand drug therapy
Myocardial infarction
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Myocardial infarction
4. Provide adequate rest periods
5. Minimize metabolic demands
Provide soft dietProvide a low-sodium, low
cholesterol and low fat diet
6. Minimize anxiety
Reassure client and provide
information as needed
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Myocardial infarction
7. Assist in treatment modalitiessuch as PTCA and CABG
8. Monitor for complications of MI-especially dysrhythmias, sinceventricular tachycardia can
happen in the first few hours afterMI
9. Provide client teaching
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MI
Medical Management
1. ANALGESIC
The choice is MORPHINE
It reduces pain and anxiety
Relaxes bronchioles to enhanceoxygenation
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MI
Medical Management
2. ACE
Prevents formation of angiotensin
II
Limits the area of infarction
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MI
Medical Management
3. Thrombolytics
Streptokinase, Alteplase
Dissolve clots in the coronary
artery allowing blood to flow
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Myocardial infarction
NURSING INTERVENTIONSAFTER ACUTE EPISODE
1. Maintain bed rest for the first3 days
2. Provide passive ROM
exercises3. Progress with dangling of thefeet at side of bed
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Myocardial infarction
NURSING INTERVENTIONSAFTER ACUTE EPISODE
4. Proceed with sitting out of bed, on the chair for 30 minutesTID
5. Proceed with ambulation inthe room toilet hallway TID
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Myocardial infarction
NURSING INTERVENTIONS AFTERACUTE 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
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CARDIOMYOPATHIES
Heart muscle disease
associated with cardiac
dysfunction
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CARDIOMYOPATHIES
1. Dilated Cardiomyopathy
2. Hypertrophic
Cardiomyopathy
3. Restrictive cardiomyopathy
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DILATED CARDIOMYOPATHY
ASSOCIATED FACTORS
1. Heavy alcohol intake
2. Pregnancy
3. Viral infection
4. Idiopathic
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DILATED CARDIOMYOPATHY
PATHOPHYSIOLOGY
Diminished contractile proteins
poor contraction decreasedblood ejection increased bloodremaining in the ventricle
ventricular stretching anddilatation.
SYSTOLIC DYSFUNCTION
HYPERTROPHIC
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CARDIOMYOPATHY
Associated factors:
1. Genetic2. Idiopathic
HYPERTROPHIC
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CARDIOMYOPATHY
Pathophysiology
Increased size of myocardium
reduced ventricular volume increased resistance to
ventricular filling diastolic
dysfunction
RESTRICTIVE
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CARDIOMYOPATHY
Associated factors
1. Infiltrative diseases like
AMYLOIDOSIS
2. Idiopathic
RESTRICTIVE
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CARDIOMYOPATHY
Pathophysiology
Rigid ventricular wall
impaired stretch and diastolic
filling decreased output
Diastolic dysfunction
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CARDIOMYOPATHIES
Assessment findings1. PND
2. Orthopnea
3. Edema
4. Chest pain
5. Palpitations6. dizziness
7. Syncope with exertion
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CARDIOMYOPATHIES
Laboratory Findings
1. CXR- may reveal
cardiomegaly2. ECHOCARDIOGRAM
3. ECG
4. Myocardial Biopsy
CA O O A S
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CARDIOMYOPATHIES
Medical Management
1. Surgery
2. pacemaker insertion
3. Pharmacological drugs for
symptom relief
CARDIOMYOPATHIES
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CARDIOMYOPATHIES
Nursing Management
1.Improve cardiac output
Adequate rest
Oxygen therapy
Low sodium diet
CARDIOMYOPATHIES
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CARDIOMYOPATHIES
Nursing Management
2. Increase patient tolerance
Schedule activities with rest
periods in between
CARDIOMYOPATHIES
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CARDIOMYOPATHIES
Nursing Management
3. Reduce patient anxiety
SupportOffer information abouttransplantations
Support family in anticipatorygrieving
I f i d di i
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Infective endocarditis
Infection of the heart
valves and the endothelial
surface of the heart
Can be acute or chronic
I f i d di i
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Infective endocarditis
Etiologic factors
1. Bacteria- Organism
depends on several factors
2. Fungi
I f i d di i
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Infective endocarditis
Risk factors
1. Prosthetic valves
2. Congenital malformation3. Cardiomyopathy
4. IV drug users5. Valvular dysfunctions
I f i d di i
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Infective endocarditis
PathophysiologyDirect invasion of microbes microbes adhere to damagedvalve surface and proliferate damage attracts plateletscausing clot formation erosionof valvular leaflets andvegetation can embolize
I f ti d diti
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Infective endocarditis
Assessment findings1. Intermittent fever
2. anorexia, weight loss3. cough, back pain and jointpain
4. splinter hemorrhages undernails
I f ti d diti
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Infective endocarditis
Assessment findings
5. Osler’s nodes- painful
nodules on fingerpads6. Roth’s spots- pale
hemorrhages in the retina
I f ti d diti
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Infective endocarditis
Assessment findings
7. Heart murmurs
8. Heart failure
I f ti d diti
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Infective endocarditis
Prevention
Antibiotic prophylaxis if
patient is undergoingprocedures like dental
extractions, bronchoscopy,surgery, etc.
I f ti d diti
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Infective endocarditis
LABORATORY EXAM
Blood Cultures to determine
the exact organism
I f ti d diti
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Infective endocarditis
Nursing management
1. regular monitoring of
temperature, heart sounds2. manage infection
3. long-term antibiotictherapy
I f ti d diti
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Infective endocarditis
Medical management
1. Pharmacotherapy
IV antibiotic for 2-6 weeks
Antifungal agents are given –
amphotericin B
Infective endocarditis
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Infective endocarditis
Medical management
2. Surgery
Valvular replacement
CHF
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CHF
A syndrome of congestion of both pulmonary and systemic
circulation caused byinadequate cardiac functionand inadequate cardiac
output to meet the metabolicdemands of tissues
CHF
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CHF
Inability of the heart to pumpsufficiently
The heart is unable to maintainadequate circulation to meet themetabolic needs of the body
Classified according to the majorventricular dysfunction- Left orRight
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CHF
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CHFEtiology of CHF
1. CAD
2. Valvular heart diseases
3. Hypertension4. MI
5. Cardiomyopathy
6. Lung diseases7. Post-partum
8. Pericarditis and cardiac tamponade
New York Heart Association
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New York Heart Association
Class 1
Ordinary physical activity does
NOT cause chest pain andfatigue
No pulmonary congestion
Asymptomatic
NO limitation of ADLs
New York Heart Association
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New York Heart Association
Class 2
SLIGHT limitation of ADLs
NO symptom at restSymptom with INCREASEDactivity
Basilar crackles and S3
New York Heart Association
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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
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New York Heart Association
Class 4
SYMPTOMS are present at
rest
CHF
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CHF
PATHOPHYSIOLOGY
LEFT Ventricular pump
failure back up of bloodinto the pulmonary veins increased pulmonarycapillary pressure pulmonary congestion
CHF
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CHF
PATHOPHYSIOLOGY
LEFT ventricular failure
decreased cardiac output decreased perfusion to thebrain, kidney and othertissues oliguria, dizziness
CHF
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CHF
PATHOPHYSIOLOGY
RIGHT ventricular failure
blood pooling in thevenous circulation increased hydrostaticpressure peripheraledema
CHF
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CHF
PATHOPHYSIOLOGY
RIGHT ventricular
failure blood pooling
venous congestion in the
kidney, liver and GIT
LEFT SIDED CHF
ASSESSMENT FINDINGS
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ASSESSMENT FINDINGS
1. Dyspnea on exertion
2. PND
3. Orthopnea
4. Pulmonary crackles/rales
5. cough with Pinkish, frothysputum
6. Tachycardia
LEFT SIDED CHF
ASSESSMENT FINDINGS
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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
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ASSESSMENT FINDINGS
1. Peripheral dependent, pittingedema
2. Weight gain3. Distended neck vein
4. hepatomegaly
5. Ascites
RIGHT SIDED CHF
ASSESSMENT FINDINGS
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ASSESSMENT FINDINGS
6. Body weakness
7. Anorexia, nausea8. Pulsus alternans
CHF
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CHF
LABORATORY FINDINGS1. CXR may reveal
cardiomegaly2. ECG may identify Cardiachypertrophy
3. Echocardiogram may showhypokinetic heart
CHF
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CHF
LABORATORY FINDINGS
4. ABG and Pulse oximetry may
show decreased O2 saturation
5. PCWP is increased in LEFT
sided CHF and CVP is increasedin RIGHT sided CHF
CHF
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CHF
NURSING INTERVENTIONS
1. Assess patient's cardio-
pulmonary status
2. Assess VS, CVP and PCWP.
Weigh patient daily to monitorfluid retention
CHF
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CHF
NURSING INTERVENTIONS
3. Administer medications-
usually cardiac glycosides aregiven- DIGOXIN or
DIGITOXIN, Diuretics,vasodilators and
hypolipidemics are prescribed
CHF
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CHF
NURSING INTERVENTIONS
4. Provide a LOW sodium
diet. Limit fluid intake asnecessary
5. Provide adequate restperiods to prevent fatigue
CHF
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CHF
NURSING INTERVENTIONS
6. Position on semi-fowler’s
to fowler’s for adequate chestexpansion
7. Prevent complications of immobility
CHF
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CHF
NURSING INTERVENTION AFTERTHE ACUTE STAGE
1. Provide opportunities for
verbalization of feelings2. Instruct the patient about themedication regimen- digitalis,
vasodilators and diuretics3. Instruct to avoid OTC drugs,Stimulants, smoking and alcohol
CHF
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CHF
NURSING INTERVENTIONAFTER THE ACUTE STAGE
4. Provide a LOW fat and LOWsodium diet
5. Provide potassium
supplements6. Instruct about fluid restriction
CHF
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CHF
NURSING INTERVENTIONAFTER THE ACUTE STAGE
7. Provide adequate rest periodsand schedule activities
8. Monitor daily weight and
report signs of fluid retention
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
Heart fails to pump adequatelyresulting to a decreased cardiac outputand decreased tissue perfusion
ETIOLOGY1. Massive MI
2. Severe CHF
3. Cardiomyopathy4. Cardiac trauma
5. Cardiac tamponade
CARDIOGENIC SHOCK
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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
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CARDIOGENIC SHOCK
LABORATORY FINDINGS
Increased CVP
Normal is 4-10 cmH2O
CARDIOGENIC SHOCK
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C OG N C S OC
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
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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 andnitrates
CARDIAC TAMPONADE
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A condition where the heart
is unable to pump blood due
to accumulation of fluid inthe pericardial sac
(pericardial effusion)
CARDIAC TAMPONADE
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This condition restrictsventricular filling resulting to
decreased cardiac outputAcute tamponade may happenwhen there is a sudden
accumulation of more than 50ml fluid in the pericardial sac
CARDIAC TAMPONADE
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Causative factors
1. Cardiac trauma
2. Complication of Myocardialinfarction
3. Pericarditis4. Cancer metastasis
CARDIAC TAMPONADE
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ASSESSMENT FINDINGS
1. BECK’s Triad- Jugular vein
distention, hypotension anddistant/muffled heart sound
2. Pulsus paradoxus
3. Increased CVP
4. decreased cardiac output
CARDIAC TAMPONADE
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ASSESSMENT FINDINGS
5. Syncope
6. anxiety7. dyspnea
8. Percussion- Flatness across theanterior chest
CARDIAC TAMPONADE
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Laboratory FINDINGS
1. Echocardiogram
2. Chest X-ray
CARDIAC TAMPONADE
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NURSING INTERVENTIONS
1. Assist in PERICARDIOCENTESIS
2. Administer IVF
3. Monitor ECG, urine output and BP
4. Monitor for recurrence of tamponade
Pericardiocentesis
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Patient is monitored by ECG
Maintain emergency equipments
Elevate head of bed 45-60 degreesMonitor for complications-
coronary artery rupture,
dysrhythmias, pleural laceration
and myocardial trauma
HYPERTENSION
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A systolic BP greater than 140
mmHg and a diastolic
pressure greater than 90mmHg over a sustained
period, based on two or more
BP measurements.
HYPERTENSION
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Types of Hypertension
1. Primary or ESSENTIAL
Most common type2. Secondary
Due to other conditions like
Pheochromocytoma, renovascularhypertension, Cushing’s, Conn’s ,
SIADH
HYPERTENSION
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CLASSIFICATION OF
HYPERTENSION by JNC-
VII
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HYPERTENSION
PATHOPHYSIOLOGY
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PATHOPHYSIOLOGY
Multi-factorial etiology
BP= CO (SV X HR) x TPR
Any increase in the aboveparameters will increase BP
1. Increased sympathetic activity2. Increased absorption of Sodium,
and water in the kidney
HYPERTENSION
PATHOPHYSIOLOGY
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PATHOPHYSIOLOGY
Multifactorial etiology
BP= CO (SV X HR) x TPR
Any increase in the above parameterswill increase BP
3. Increased activity of the RAAS
4. Increased vasoconstriction of theperipheral vessels
5. insulin resistance
HYPERTENSION
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ASSESSMENT FINDINGS
1. Headache
2. Visual changes
3. chest pain
4. dizziness5. N/V
HYPERTENSION
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Risk factors for CardiovascularProblems in Hypertensive patients
Major Risk factors
1. Smoking2. Hyperlipidemia
3. DM
4. Age older than 605. Gender- Male and post menopausal W
6. Family History
HYPERTENSION
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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
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MEDICAL
MANAGEMENT
1. Lifestyle modification
2. Drug therapy
3. Diet therapy
HYPERTENSION
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MEDICAL MANAGEMENTDrug therapy
Diuretics
Beta blockersCalcium channel blockers
ACE inhibitors
A2 Receptor blockersVasodilators
HYPERTENSION
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NURSING INTERVENTIONS1. Provide health teaching topatient
Teach about the disease process
Elaborate on lifestyle changes
Assist in meal planning to loseweight
HYPERTENSION
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NURSING INTERVENTIONS1. Provide health teaching to thepatient
Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day
Limit alcohol intake to 30 ml/dayRegular aerobic exercise
Advise to completely Stop smoking
HYPERTENSION
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Nursing Interventions2. Provide information about anti-hypertensive drugs
Instruct proper compliance and notabrupt cessation of drugs even if ptbecomes asymptomatic/ improvedcondition
Instruct to avoid over-the-counterdrugs that may interfere with thecurrent medication
HYPERTENSION
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Nursing Intervention
3. Promote Home care management
Instruct regular monitoring of BPInvolve family members in care
Instruct regular follow-up
4. Manage hypertensive emergency
and urgency properly
Vascular Diseases
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ANEURYSM
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Dilation involving an artery formed at aweak point in the vessel wall
ANEURYSM
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Saccular= when one side of the vessel isaffected
Fusiform= when the entire segment
becomes dilated
ANEURYSM
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RISK FACTORS
1. Atherosclerosis
2. Infection= syphilis
3. Connective tissue disorder
4. Genetic disorder= Marfan’s Syndrome
ANEURYSM
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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
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ASSESSMENT
1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. Palpable bruit
ANEURYSM
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LABORATORY:
• CT scan
• Ultrasound
• X-ray
• Aortography
ANEURYSM
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Medical Management:
• Anti-hypertensives
• Synthetic graft
ANEURYSM
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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
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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
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Risk factors for PeripheralArterial occlusive disease
Non-Modifiable1. Age
2. gender
3. family predisposition
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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Risk factors for Peripheral Arterialocclusive disease
Modifiable
1. Smoking2. HPN
3. Obesity
4. Sedentary lifestyle
5. DM
6. Stress
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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ASSESSMENT FINDINGS1. INTERMITTENT CLAUDICATION- the hallmark of
PAOD
This is PAIN described as aching,cramping or fatiguing discomfortconsistently reproduced with thesame degree of exercise or activity
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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ASSESSMENT FINDINGS1. INTERMITTENTCLAUDICATION- the hallmarkof PAOD
This pain is RELIEVED by REST
This commonly affects the musclegroup below the arterial occlusion
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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Assessment Findings2. Progressive pain on theextremity as the disease advances
3. Sensation of cold andnumbness of the extremities
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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Assessment Findings4. Skin is pale when elevated andcyanotic/ruddy when placed on adependent position
5. Muscle atrophy, leg ulceration
and gangrene
PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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Diagnostic Findings
1. Unequal pulses between the
extremities2. Duplex ultrasonography
3. Doppler flow studies
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PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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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
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PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
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Nursing Interventions
3. Promote Home management
Encourage lifestyle changes
Instruct to AVOID smoking
Instruct to avoid leg crossing
BUERGER’S DISEASE
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Thromboangiitis obliterans
A disease characterized by
recurring inflammation of themedium and small arteries and
veins of the lower extremities
Occurs in MEN ages 20-35RISK FACTOR: SMOKING!
BUERGER’S DISEASE
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PATHOPHYSIOLOGY
Cause is UNKNOWNProbably an Autoimmune disease
Inflammation of the arteries
thrombus formation occlusion of
the vessels
BUERGER’S DISEASE
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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
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ASSESSMENT FINDINGS
3. Intense RUBOR (reddish-blue
discoloration), progresses toCYANOSIS as disease advances
4. Paresthesia
BUERGER’S DISEASE
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Diagnostic Studies
1. Duplex ultrasonography
2. Contrast angiography
BUERGER’S DISEASE
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Nursing Interventions
1. Assist in the medical and surgical
management
Bypass graft
amputation
2. Strongly advise to AVOID smoking3. Manage complications appropriately
BUERGER’S DISEASE
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Nursing InterventionsPost-operative care: after amputation
Elevate stump for the FIRST 24 HOURS
to minimize edema and promote venousreturn
Place patient on PRONE position after 24
hoursAssess skin for bleeding and hematoma
Wrap the extremity with elastic bandage
RAYNAUD’S DISEASE
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A form of intermittent arteriolarVASOCONSTRICTION that resultsin coldness, pain and pallor of the
fingertips or toes
Cause : UNKNOWN
Most commonly affects WOMEN, 16-40 years old
RAYNAUD’S DISEASE
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ASSESSMENT FINDINGS1. Raynaud’s phenomenon
A localized episode of vasoconstriction of the smallarteries of the hands and feet
that causes color andtemperature changes
RAYNAUD’S DISEASE
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W-B-RPallor- due to vasoconstriction,then
Blue- due to pooling of Deoxygenated blood
Red- due to exaggeratedreflow/hyperemia
RAYNAUD’S DISEASE
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ASSESSMENT FINDINGS2. tingling sensation
3. Burning pain on the hands andfeet
RAYNAUD’S DISEASE
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Medical management
Drug therapy with the use of
CALCIUM channel blockersTo prevent vasospasms
RAYNAUD’S DISEASE
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Nursing Interventions1. instruct patient to avoid situationsthat may be stressful
2. instruct to avoid exposure to coldand remain indoors when the climateis cold
3. instruct to avoid all kinds of nicotine4. instruct about safety. Carefulhandling of sharp objects
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Venous diseases
VARICOSE VEINS
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THESE are dilated veinsusually in the lower
extremities
VARICOSE VEINS
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Predisposing FactorsPregnancy
Prolonged standing or sitting
Constipation (forhemorrhoids)
Incompetent venous valves
VARICOSE VEINS
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Pathophysiology
Factors venous stasis
increased hydrostaticpressure edema
VARICOSE VEINS
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Assessment findings
Tortuous superficial veins
on the legs
Leg pain and Heaviness
Dependent edema
VARICOSE VEINS
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Laboratory findings
Venography
Duplex scan
pletysmography
VARICOSE VEINS
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Medical management
Pharmacological therapy
Leg vein stripping
Anti-embolic stockings
VARICOSE VEINS
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Nursing management
1. Advise patient to elevate
the legs
2. Caution patient to avoid
prolonged standing or sitting
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VARICOSE VEINS
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Nursing management
5. Caution patient to
avoid knee-length
stockings and constrictive
clothings
VARICOSE VEINS
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Nursing management6. Apply anti-embolic
stockings as directed7. Avoid massage on the
affected area
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DVT- Deep Vein Thrombosis
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Predisposing factors
Prolonged immobility
Varicosities
Traumatic procedures
DVT- Deep Vein Thrombosis
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Complication
PULMONARYthromboembolism
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DVT- Deep Vein Thrombosis
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Laboratory findings
Venography
Duplex scan
DVT- Deep Vein Thrombosis
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Medical management
Antiplatelets
Anticoagulants
Vein stripping and
grafting
Anti-embolic stockings
DVT- Deep Vein Thrombosis
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Nursing management
1. Provide measures to avoid
prolonged immobilityRepositioning Q2
Provide passive ROM
Early ambulation
DVT- Deep Vein Thrombosis
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Nursing management
2. Provide skin care to
prevent the complication of leg ulcers
3. Provide anti-embolicstockings
DVT- Deep Vein Thrombosis
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Nursing management
4. Administer anticoagulants
as prescribed5. Monitor for signs of
pulmonary embolism
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Blood disorders
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AnemiaNutritional anemia
Hemolytic anemia Aplastic anemia
Sickle cell anemia
ANEMIA
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A condition in whichthe hemoglobin
concentration islower than normal
ANEMIA
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Three broad categories1. Loss of RBC- occurs with
bleeding
2. Decreased RBC production
3. Increased RBC destruction
Hypoproliferative Anemia
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Iron Deficiency Anemia –Results when the
dietary intake of ironis inadequate to
produce hemoglobin
Hypoproliferative Anemia
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Iron Deficiency Anemia –Etiologic Factors –1. Bleeding- the most
common cause –2. Mal-absorption –3. Malnutrition
–4. Alcoholism
Hypoproliferative Anemia
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Iron Deficiency AnemiaPathophysiology
–The body stores of irondecrease, leading todepletion of hemoglobinsynthesis
Hypoproliferative Anemia
fi i i
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Iron Deficiency AnemiaPathophysiology
–The oxygen carryingcapacity of hemoglobin
is reduced tissuehypoxia
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Hypoproliferative Anemia
fi i i
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Iron Deficiency Anemia Assessment Findings
5. Brittle nails6. Smooth and sore
tongue7. Angular cheilosis
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Hypoproliferative Anemia
I D fi i A i
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Iron Deficiency AnemiaMedical management
1. Hematinics
2. Blood transfusion
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Hypoproliferative Anemia
Nursing Management
2 Ad i i t i
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2. Administer ironOral preparations- liquid It stains teeth
Drink it with a strawStool may turn blackish- dark in
color
Advise to eat high-fiber diet tocounteract constipation
Hypoproliferative Anemia
Nursing Management
2 Ad i i t i
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2. Administer iron IM preparation Administer DEEP IM using the Z-
track method Avoid vigorous rubbingCan cause local pain and staining
APLASTIC ANEMIA
A diti
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A conditioncharacterized by
decreased number of RBC as well as WBC
and platelets
APLASTIC ANEMIA
CAUSATIVE FACTORS
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CAUSATIVE FACTORS1. Environmental toxins-
pesticides, benzene
2. Certain drugs-Chemotherapeutic agents,chloramphenicol,phenothiazines, Sulfonamides
3. Heavy metals4. Radiation
APLASTIC ANEMIA
P th h i l
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PathophysiologyToxins cause a direct bonemarrow depression acellualrbone marrow decreasedproduction of blood elements
APLASTIC ANEMIA
ASSESSMENT FINDINGS
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ASSESSMENT FINDINGS1. fatigue2. pallor
3. dyspnea4. bruising5. splenomegaly6. retinal hemorrhages
APLASTIC ANEMIA
LABORATORY FINDINGS
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LABORATORY FINDINGS1. CBC- decreased blood cell
numbers
2. Bone marrow aspirationconfirms the anemia-hypoplastic or acellularmarrow replaced by fats
APLASTIC ANEMIA
M di l M t
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Medical Management1. Bone marrowtransplantation2. Immunosupressantdrugs3. Rarely, steroids4. Blood transfusion
APLASTIC ANEMIA
N i t
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Nursing management1. Assess for signs of bleeding and infection2. Instruct to avoidexposure to offending
agents
Megaloblastic Anemias
A i h t i d b
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Anemias characterized byabnormally large RBCsecondary to impairedDNA synthesis due todeficiency of Folic acid
and/or vitamin B12
Megaloblastic Anemias
Folic Acid deficienc
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Folic Acid deficiencyCausative factors
1. Alcoholism2. Mal-absorption
3. Diet deficient inuncooked vegetables
Megaloblastic Anemias
Pathophysiology of Folic acid
deficiency
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deficiencyDecreased folic acid impaired
DNA synthesis in the bone
marrow impaired RBCdevelopment, impaired nuclearmaturation but CYTOplasmicmaturation continues largesize
Megaloblastic Anemias
Vitamin B12 deficiency
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Vitamin B12 deficiencyCausative factors
1. Strict vegetarian diet
2. Gastrointestinalmalabsorption
3. Crohn's disease
4. gastrectomy
Megaloblastic Anemias
Vitamin B12 deficiency
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Vitamin B12 deficiency
Pernicious Anemia
Due to the absence of intrinsicfactor secreted by the parietalcells
Intrinsic factor binds with Vit.B12 to promote absorption
Megaloblastic Anemias
Assessment findings
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Assessment findings1. weakness
2. fatigue
3. listless
4. neurologic manifestations are
present only in Vit. B12deficiency
Megaloblastic Anemias
Assessment findings
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Assessment findingsPernicious Anemia
–Beefy, red, swollen tongue
–Mild diarrhea
–Extreme pallor
–Paresthesias in the extremities
Megaloblastic Anemias
Laboratory findings
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Laboratory findings1. Peripheral blood smear- shows
giant RBCs, WBCs with giant
hypersegmented nuclei2. Very high MCV
3. Schilling’s test
4. Intrinsic factor antibody test
Megaloblastic Anemias
Medical Management
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Medical Management1. 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
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Nursing Management1. Monitor patient
2. Provide assistance in
ambulation3. Oral care for tongue sore
4. Explain the need for lifetimeIM injection of vit B12
Hemolytic Anemia: Sickle Cell
A severe chronic
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A severe chronicincurable hemolytic
anemia that resultsfrom heritance of the
sickle hemoglobingene.
Hemolytic Anemia: Sickle Cell
Causative factor
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Causative factor –Genetic inheritance of
the sickle gene- HbS gene
Hemolytic Anemia: Sickle Cell
Pathophysiology
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PathophysiologyDecreased O2, Cold,
Vasoconstriction canprecipitate sickling
process
Hemolytic Anemia: Sickle Cell
Pathophysiology
Factors cause defective
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Factors cause defectivehemoglobin to acquire arigid, crystal-like C-shaped
configuration Sickled RBCswill adhere to endothelium pile up and plug the vessels ischemia results pain,swelling and fever
Hemolytic Anemia: Sickle Cell
Assessment Findings
1 j di
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1. jaundice
2. enlarged skull andfacial bones
3. tachycardia, murmursand cardiomegaly
Hemolytic Anemia: Sickle Cell
Assessment Findings
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Assessment FindingsPrimary sites of
thrombotic occlusion:spleen, lungs and CNS
Chest pain, dyspnea
Hemolytic Anemia: Sickle Cell
Assessment Findings
1 Sickle cell crises
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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 inthe CXR
Hemolytic Anemia: Sickle Cell
Medical Management
1 B
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1. Bone marrowtransplant
2. Hydroxyurea
–Increases the HbF
3. Long term RBCtrnasfusion
Hemolytic Anemia: Sickle Cell
Nursing Management
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Nursing Management1. manage the pain
–Support and elevateacutely inflamed joint
–
Relaxation techniques –analgesics
Hemolytic Anemia: Sickle Cell
Nursing Management
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Nursing Management2. Prevent and manage
infection –Monitor status of patient
–Initiate prompt antibiotictherapy
Hemolytic Anemia: Sickle Cell
Nursing Management
3 Promote coping skills
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3. Promote coping skills
–Provide accurate
information – Allow patient to verbalize
her concerns aboutmedication, prognosis andfuture pregnancy
Hemolytic Anemia: Sickle Cell
Nursing Management
4 Monitor and prevent
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4. Monitor and preventpotential complications
–Provide always adequatehydration
–
Avoid cold, temperaturethat may causevasoconstriction
Hemolytic Anemia: Sickle Cell
Nursing Management
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Nursing Management4. Monitor and prevent
potential complications –Leg ulcer
Aseptic technique
Hemolytic Anemia: Sickle Cell
Nursing Management
4 Monitor and prevent
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4. Monitor and preventpotential complications
–PriapismSudden painful erection
Instruct patient to emptybladder, then take a warmbath
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Polycythemia
POLYCYTHEMIA VERA
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POLYCYTHEMIA VERA –Primary Polycythemia
–
A proliferative disorder inwhich the myeloid stemcells become uncontrolled
Polycythemia
POLYCYTHEMIA VERA
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POLYCYTHEMIA VERACausative factor
–unknown
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
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Pathophysiology –The stem cells grow
uncontrollably –The bone marrow becomes
HYPERcellular and all theblood cells are increased innumber
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
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Pathophysiology
–The spleen resumes its
function of hematopoiesisand enlarges
–
Blood becomes thick andviscous causing sluggishcirculation
Polycythemia
POLYCYTHEMIA VERA
Pathophysiology
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Pathophysiology
–Overtime, the bone marrow
becomes fibrotic
PolycythemiaPOLYCYTHEMIA VERA
Assessment findings
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Assessment findings –1. Skin is ruddy
–2. Splenomegaly
–3. headache
–
4. dizziness, blurred vision –5. Angina, dyspnea and
thrombophlebitis
PolycythemiaPOLYCYTHEMIA VERA
Laboratory findings
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Laboratory findings –1. CBC- shows elevated RBC
mass –2. Normal oxygen saturation
–3 Elevated WBC andPlatelets
PolycythemiaPOLYCYTHEMIA VERA
Complications
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Complications –1. Increased risk for
thrombophlebitis, CVA andMI
–2. Bleeding due to
dysfunctional blood cells
PolycythemiaPOLYCYTHEMIA VERA
Medical Management
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Medical Management –1. To reduce the high blood
cell mass- PHLEBOTOMY –2. Allopurinol
–3. Dipyridamole
–4. Chemotherapy tosuppress bone marrow
Polycythemia Nursing Management
–1. Primary role of the nurse is
EDUCATOR
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–2. Regularly asses for thedevelopment of complications
–3. Assist in weekly phlebotomy
–4. Advise to avoid alcohol andaspirin
–5. Advise tepid sponge bath or coolwater to manage pruritus
Leukemia
Malignant disorders of blood
forming cells characterized byUNCONTROLLED lif ti
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forming cells characterized byUNCONTROLLED proliferationof WHITE BLOOD CELLS in
the bone marrow- replacingmarrow elements . The WBCcan also proliferate in theliver, spleen and lymphnodes.
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Leukemia
The leukemias are namedalso according to the
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The leukemias are namedalso according to thematuration of cells
ACUTE –The cells are primarily
immature
CHRONIC
–The cells are primarily mature
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Leukemia
ETIOLOGIC FACTORSUNKNOWM
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ETIOLOGIC FACTORS –UNKNOWM
–Probably exposure to radiation
–Chemical agents
–Infectious agents
–Genetic
Leukemia
–PATHOPHYSIOLOGY of ACUTELeukemia
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Leukemia
Uncontrolled proliferation of
immature cells suppressesbone marrow function severeanemia, thrombocytopenia and
granulocytopenia
Leukemia
–PATHOPHYSIOLOGY of CHRONIC Leukemia
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CHRONIC Leukemia
Uncontrolled proliferation of
DIFFERENTIATED cells slowsuppression of bone marrowfunction milder symptoms
Leukemia
ASSESSMENT FINDINGS
ACUTE LEUKEMIA
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– Pallor
– Fatigue
–Dyspnea
– Hemorrhages
– Organomegaly
–Headache
– vomiting
Leukemia
ASSESSMENT FINDINGS
CHRONIC LEUKEMIA
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CHRONIC LEUKEMIA
–Less severe symptoms
–organomegaly
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Leukemia
Medical Management
1 Chemotherapy
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1. Chemotherapy
2. Bone marrow transplantation
Leukemia
Nursing Management
1 Manage AND prevent infection
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1. Manage AND prevent infection
– Monitor temperature
– Assess for signs of infection
– Be alert if the neutrophil countdrops below 1,000 cells/mm3
Leukemia
Nursing Management
2. Maintain skin integrity
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g y
3. Provide pain relief
4. Provide information as to therapy-chemo and bone marrowtransplantation
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