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Perfusion Part 1

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Perfusion
Learning Outcomes

At the end of the lecture the student will:

Identify risk factors for developing selected perfusion disorders.

Articulate the recommended screening practices, laboratory and
diagnostic studies for selected perfusion disorders.

Discuss clinical manifestations of selected disorders of perfusion.

Plan and prioritize nursing interventions for a patient with an alteration in
perfusion.

Develop a teaching plan, utilizing current research, for a patient with an
alteration in perfusion.

Apply principles of pharmacologic management to the care of patients
with an alteration in perfusion.

Discuss management of care for patients receiving transfusion therapy.
Exemplars

Peripheral Vascular Disease
 Arteriosclerosis
& Atherosclerosis
 Hypertension

Cardiovascular Disease
 Stable
Angina
 Chronic

Heart Failure
Hematologic diseases
 Anemia
 Leukemia
Perfusion

Central Perfusion: a normal physiologic process that
requires the heart to generate sufficient cardiac output
to transport blood through patent blood vessels for
distribution in the tissues throughout the body.

Tissue perfusion refers to the flow of blood through
target tissues. The blood flows through arteries and
capillaries, delivering nutrients and oxygen to cells, and
removing cellular waste products.
Normal Physiological Process
Central Perfusion
Cardiac Output
Preload
Stroke
Volume
HR
Afterload
Contractility
Impaired Central Perfusion


Impairment of central perfusion occurs when
cardiac output is inadequate.

Conduction or valve problems

Disease of the heart muscle

Increased SVR (afterload)-HTN, Aortic stenosis

Decreased SVR (afterload)-hemorrhage
Reduced cardiac output results in a reduction of
oxygenated blood reaching the body tissues
(systemic effect).

If untreated, leads to ischemia, cell injury and cell death

If severe, associated with shock
Impaired Tissue Perfusion


Impaired tissue perfusion occurs when there
is reduced blood flow to the target tissues
through the arteries and capillaries.

Poor central perfusion

Blockage of the vessel leading to target organ or tissue

Excessive edema interferes with cellular oxygen
exchange
Results of impaired tissue perfusion is
impaired blood flow to target tissue

Ischemia, irreversible cell injury and necrosis (cell
death)
Risk Factors Associated with
Impaired Perfusion

Increased age

Male

Genetics

Congenital Heart Defects

Cardiovascular Disease

Peripheral Vascular Disease
Impaired Perfusion
Risk Factors
Non-Modifiable
Modifiable

Age

Smoking

Sex

Obesity

Genetics

Hyperlipidemia

Ethnicity

HTN

DM

Sedentary lifestyle
Hypertension
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11
Hypertension
Modifiable risk factor to prevent CVD
 As BP increases, so does the risk of:







MI
Heart failure
Stroke
Renal disease
Retinopathy
Affects ~46% adults in United States

Heart disease associated with HTN leads to
23.7% of deaths in United States
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12
Hypertension

Promoting health equity

All ethnicities: Three factors for decreased
prevalence


Born outside United States; do not speak English; limited time
living in United States
Blacks

Highest prevalence; more resistant HTN; develop at younger age;
female greater than male; more nocturnal nondipping BP; more
end-organ damage; highest death rate

Less response to renin inhibiting meds; better control with calcium
channel blockers and diuretics

Increased risk of angioedema with ACE inhibitors
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13
Hypertension

Promoting health equity


Hispanics

Less likely to receive treatment

Lower rate of: awareness, treatment, and control
Gender differences

Men—more common before middle age

Women

increased 2-3x with oral contraceptives

Preeclampsia—possible early sign

More common after menopause; harder to control with older
women
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14
Normal Regulation of
Blood Pressure

Blood pressure (BP)—force exerted by
blood against walls of blood vessels

Involves both systemic factors and peripheral vascular
effects

Important to maintain tissue perfusion during activity and
rest.

Function of cardiac output (CO) and systemic vascular
resistance (SVR)

CO = SV × HR
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15
Gu
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16
Audience Response Question
The nurse determines that the patient has stage 2
hypertension when the patient’s average blood pressure is:
(Select all that apply.)
a.
150/96 mm Hg.
b.
155/88 mm Hg.
c.
172/92 mm Hg.
d.
160/110 mm Hg.
e.
182/106 mm Hg.
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17
Etiology of Hypertension

Primary hypertension

Also called essential or idiopathic HTN

Elevated BP of unknown cause

90% to 95% of all cases

Many contributing factors
 Altered
endothelial function, increased
SNS activity, increased Na+ intake,
overproduction of Na+ retaining
hormones, overweight, diabetes,
tobacco, excess alcohol
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18
Etiology of Hypertension

Secondary hypertension

Elevated BP with a specific cause; sudden development

5% to 10% of adult cases

Clinical findings relate to underlying cause (See Table 32-3 in the textbook)
 Cirrhosis;
aortic problems; drug-related; endocrine,
neurologic, or renal problems; pregnancy-induced,
or sleep apnea

Treatment aimed at removing or treating cause
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19
Risk Factors for Primary
Hypertension

Age

Family history

Alcohol use

Obesity

Tobacco use

Ethnicity

Diabetes

Sedentary lifestyle

Elevated serum lipids

Socioeconomic status

Excess dietary sodium

Stress

Gender
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20
Audience Response Question
While performing blood pressure screening at a
health fair, the nurse counsels which person as
having the greatest risk for developing
hypertension?
a. A 56-year-old man whose father died at age
62 from a stroke
b. A 30-year-old female advertising agent who
is unmarried and lives alone
c. A 68-year-old man who uses herbal remedies
to treat his enlarged prostate gland
d. A 43-year-old man who travels extensively
with his job and exercises only on weekends
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21
Hypertension
Clinical Manifestations

“Silent killer”—asymptomatic until
severe and target organ disease occurs

Symptoms of severe hypertension

Fatigue

Dizziness

Palpitations

Angina

Dyspnea
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22
Hypertension
Complications

Target organ diseases occur most
frequently in:

Heart
 Coronary
 Left
ventricular hypertrophy (Fig. 32-4)
 Heart

artery disease; atherosclerosis
failure
Brain—cerebrovascular disease
 TIA/Stroke;
atherosclerosis
 Hypertensive
encephalopathy; changes in
autoregulation
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23
Left ventricular hypertrophy (A)
Normal thickness (B) (Fig. 32-4)
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24
Hypertension
Complications

Peripheral vascular disease
 Atherosclerosis
leads to PVD, aortic
aneurysm, aortic dissection
 Intermittent claudication

Kidney
 Nephrosclerosis
disease (CKD)

Eyes—retinal damage
 Blurry

leads to chronic kidney
or loss of vision; retinal hemorrhage
Damaged retinal vessels indicate concurrent damage to vessels
in heart, brain, and kidneys.
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25
Hypertension
Diagnostic Studies
Measurement of BP
Labs to:
1)
identify or rule out secondary HTN
2)
evaluate target organ disease
3)
determine CV risk
4)
establish baselines before starting therapy (Table 32-5)
Renal function, U/A, BMP, CBC, serum lipid profile, uric acid, ECG,
ophthalmic exam
Other; Echo, LFTs, TSH

Ambulatory blood pressure monitoring (ABPM); avoids “white coat”
HTN
 Noninvasive, fully automated system that measures BP at
preset intervals over 12 to 24-hour period. Teach patient to hold
arm still while device reads BP and keep diary of activities
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26
Hypertension
Interprofessional Care

Overall goals (Table 32-5)

Achieve and maintain goal BP

Reduce CV risk factors and target organ disease

Lifestyle modifications

AHA Life’s Simple 7:
(1) Manage BP,
(2) Control cholesterol,
(3) Reduce blood sugar,
(4) Get active,
(5) Eat better,
(6) Lose weight,
(7) Stop smoking
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27
Hypertension
Lifestyle Modifications

Weight Reduction

Dash Diet

Low Sodium Dietary Intake

Moderation of Alcohol Intake

Physical activity

Avoid tobacco products

Management of risk factors
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28
Causes of Secondary HTN
 Neurological
 Increased
 Sleep
Disorders
ICP
apnea
 Vascular:
 Coarctation
of aorta
 Pregnancy
 Medications
 Renal
Disease
Hypertension: Drug Therapy

High Blood Pressure Clinical Practice
Guidelines—antihypertensive
recommendations




Age > 65, SBP > 130 mmHg, ambulatory in
community setting: Goal SBP < 130 mmHg
Age > 65, SBP >130 mmHg, care facility or
multiple comorbidities or limited life
expectancy: Goal—patient/team decision
Age> 18 with HTN, known CVD or other risk
factors: Goal—130/80
All others without CVD or other risk factors:
Goal BP <130/80
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30
Hypertension: Drug Therapy

Two primary actions:

Decrease circulating blood volume

Reduce SVR

See: Tables 32-6, 32-7, and 32-8 and Fig. 32-5
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31
Sympathetic Nervous System
Receptors Affecting BP
Receptor
Location
Response When Activated
α1
Vascular smooth muscle
Vasoconstriction
Heart
Increased contractility (positive inotropic
effect)
Presynaptic nerve terminals
Inhibition of norepinephrine release
Vascular smooth muscle
Vasoconstriction
Heart
Increased contractility (positive inotropic
effect)
Increased heart rate (positive chronotropic
effect)
Increased conduction (positive dromotropic
effect)
Juxtaglomerular cells of the kidney
Increased renin secretion
β2
Smooth muscle of blood vessels in heart
(e.g., coronary arteries), lungs (e.g.,
bronchi), and skeletal muscle
Vasodilation
Dopamine receptors
Primarily renal blood vessels
Vasodilation
α2
β1
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32
Drug Therapy (Fig. 32-5)
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33
Hypertension: Drug
therapy

Beta Blockers

Cardioselective: Blocks β1-adrenergic receptors, reduces
BP by blocking β-adrenergic effects, decreases CO and
reduce sympathetic vasoconstrictor tone, decreases renin
secretion by kidneys (Metoprolol)

Non-Cardioselective: Blocks β1- and β2-adrenergic
receptors, reduces BP by blocking β1- and β2-adrenergic
effects (Propranolol)
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34
Hypertension: Drug therapy
Adrenergic inhibiting agents—Decrease SNS
stimulation; work centrally on vasomotor
center and peripherally to inhibit NE release
or block adrenergic receptors on blood vessels
(Prazosin)
 ACE Inhibitors—prevent conversion of
angiotensin I to angiotensin II; reduce
vasoconstriction and sodium and water
retention (Lisinopril)
 A-II receptor blockers—prevent angiotensin II
from binding to receptors in blood vessel
walls (Losartan)

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35
Hypertension: Drug Therapy
Calcium channel blockers (CCB)—increase Na+
excretion and cause arteriolar vasodilation by
preventing the movement of extracellular Ca+
into cells (Amlodipine)
 Direct vasodilators—relax vascular smooth
muscle and reduce SVR (Nitroglycerine)
 Diuretics—reduce plasma volume by increased
sodium and water excretion and reduce
vascular response to catecholamines (Loop:
Furosemide; Potassium Sparing:
Spironolactone; Thiazide:
Hydrochlorothiazide)

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36
Hypertension: Drug Therapy


Patient with HTN—nonpharmacologic
treatment + 1 first line pharmacologic
drug
Patient with stage 2 HTN—
nonpharmacologic therapy + 2
antihypertensives from two different
classifications

If a drug is not tolerated, then another classification will be
used

Monthly follow-up visits until at goal BP; then 3 to 6 months

Stage 2 HTN or comorbidities—more frequent
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37
Hypertension: Drug Therapy
Patient and caregiver education—*report all
side effects; different medication may be
tried if severe or undesirable; need to
continue adherence to therapy
 Common side effects





Orthostatic hypotension—feel dizzy or faint
when change position
Sexual problems—reduced libido or erectile
dysfunction
Dry mouth—sugarless gum or candy
Frequent voiding—take diuretic early in the
day to avoid getting up at night
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38
Chronic Stable Angina
Chronic Stable Angina (CSA)

Temporary imbalance
between coronary artery’s
ability to supply oxygen
and cardiac muscle’s
demand for oxygen
Ischemia limited in
duration
 Frequent, familiar
 Subsides with rest

Assessment of Chest pain
(P) Provocative

What makes the symptom(s) better or worse?
(Q) Quality

Describe the symptom(s).
(R) Region or Radiation

Where in the body does the symptom occur? Is there radiation
or extension of the symptom(s) to another area of the body?
(S) Severity

On a scale of 1-10 how bad is the symptom(s)?
(T) Timing

Does it occur in association with something else (e.g. eating,
exertion, movement?)
Chronic Stable Angina
Treatment
Home

Rest

SL Nitroglyercin


Repeat every 5 minutes
X3
If pain persists call 911
Acute setting

EKG within 10min. of
onset

Monitor

Frequent VS

O2 2-4L via nc if Spo2
<94%

NTG SL every 5 min X3
Nitroglycerin


Sublingual

Tablet or spray for angina

Given every 5 minutes X 3

If pain not relieved notify MD/911
IV gtt for acute MI

patient must have continuous cardiac monitoring, ICU
level of care

Potent vasodilator

VS every 3-5 minutes
Heart Failure

Inability of heart to work effectively as a pump

Major types:

Left-sided

Right-sided
Etiology of Heart Failure

Any interference with mechanisms
regulating cardiac output (CO)

Primary causes


Conditions that directly damage the heart
Precipitating causes

Conditions that increase workload of the heart
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47
Risk Factors

Primary risk factors

Hypertension
 Modifiable
risk factor
 If
aggressively treated and managed,
incidence of HF can be reduced by 50%


CAD
Co-morbidities contribute to
development of HF
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48
Left-Sided Heart Failure

Inability of the left ventricle to pump enough blood

Pooling of blood in the left ventricle and atrium

Eventually backing up into the pulmonary vasculature
causing congestion

Cardiac output
Typical Causes Left-sided
Heart Failure
Hypertension
Coronary
Artery Disease
Left Ventricular Myocardial
Infarction
Valvular Disease
Aortic and Mitral valve
stenosis/insufficiency
Other Common Causes of HF
Cause
Mechanism
Anemia
↓ O2-carrying capacity of the blood stimulating ↑ in CO to meet tissue demands,
leading to increase in cardiac workload and increase in size of LV
Bacterial endocarditis
Infection: ↑ metabolic demands and O2 requirements
Valvular dysfunction: causes stenosis or regurgitation
Dysrhythmias
May ↓ CO and ↑ workload and O2 requirements of myocardial tissue
Hypervolemia
↑ Preload causing volume overload on the RV
Hypothyroidism
Indirectly predisposes to ↑ atherosclerosis. Severe hypothyroidism decreases
myocardial contractility.
Infection
↑ O2 demand of tissues, stimulating ↑ CO
Nutritional deficiencies
May ↓ cardiac function by ↑ myocardial muscle mass and myocardial contractility
Obstructive sleep apnea
Frequent nighttime apnea results in ↑ afterload, intermittent hypoxia, and ↑
sympathetic nervous system activity.
Paget’s disease
↑ Workload of the heart by ↑ vascular bed in the skeletal muscle
Pulmonary embolism
↑ Pulmonary pressure resulting from obstruction leads to pulmonary HTN, ↓ CO.
Thyrotoxicosis
Changes the tissue metabolic rate, ↑ HR and workload of the heart
Left-Sided Heart Failure
Clinical Manifestations
Decreased Cardiac output
Weakness
Fatigue
Dizziness/ lightheaded
Restless/anxious
 Acute confusion
 Dysuria/Oliguria




Pulmonary
congestion
Dyspnea
Cough
Pulmonary crackles
Low SpO2
 Pink frothy sputum
 Third heart sound (S3)




Right ventricle cannot empty completely
 Increased volume and pressure in venous system and peripheral edema
 Causes:




Left ventricular failure
Right ventricular MI
Pulmonary hypertension
Pulmonary
COPD
ARDS
emboli
Right-sided Heart Failure
Clinical manifestations








Jugular vein distention (JVD)
Increased abdominal girth
Dependent edema
Hepatomegaly
Hepatojugular reflux
Ascites
Weight gain
Fatigue
Compensatory Mechanisms

Sympathetic nervous system stimulation

Increase in HR, BP = increase in CO
increased preload

Vasoconstriction
increased afterload

RAAS activation



Reduced blood flow to the kidneys
Sodium and H2O retention
Chemical responses

BNP-Brain-type natriuretic peptide



Normal <100pg/ml
Pituitary-ADH in response to low CO
Myocardial hypertrophy

Myocardial muscle wall thickening
Classification
Patient Assessment


History

Heart disease

MI

Rheumatic fever

HTN

Smoke
Weight gain

Current medications

Activity tolerance

Diet

Sleep
Assessment

Subjective data

Past health history

Drugs

Functional Health Patterns

Sleep/Rest

Elimination

Cognitive/Perceptual
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61
Assessment

Objective ata

Skin color and temperature

Edema

Respiratory rate and sounds

Frothy, blood-tinged sputum

Heart rate and sounds

Abdominal distention

Changes in LOC
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62
Assessment of Heart Failure
Laboratory

Electrolytes

Hemoglobin and hematocrit

B-type natriuretic peptide (BNP)

Urinalysis (proteinuria/high specific gravity)

ABGs
Assessment of Heart Failure

Imaging

CXR

Echocardiography

ECG

Pulmonary artery
catheter
Pulmonary Edema
http://www.heartf
ailure.org/heartfailure/lungs/
Goals of Therapy

Symptom relief

Optimizing volume status

Supporting oxygenation and ventilation

Identifying and addressing causes

Avoiding complications

Teaching related to exacerbations
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66
Improving Gas Exchange

Promoting oxygenation and gas exchange

Ventilation assistance

Monitor respiratory rate every 1-4 hr

Auscultate breath sounds every 4-8 hr

Position in high Fowler’s if patient dyspneic

Maintain oxygen saturation of 90%
Interventions that Reduce Preload

Nutrition therapy



Sodium restriction <2400mg/daily
Fluid restriction 2L/daily
Drug therapy

Diuretics



Loop, Thiazide, and K sparing
Furosemide, HCTZ, Spironolactone
Venous vasodilators

Nitrates,


IV, PO
Morphine
Drug Therapy

Diuretics

Decrease volume overload (preload)
 Loop

diuretics—Furosemide
Vasodilators

Reduce circulating blood volume and improve coronary
artery circulation
 IV
nitroglycerin
 IV
sodium nitroprusside
 IV
nesiritide
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69
Drug Therapy


Morphine

Reduces preload and afterload

Relieves dyspnea and anxiety
Positive inotropes

β-agonists (dopamine, dobutamine, norepinephrine
[Levophed])

Phosphodiesterase inhibitors (milrinone)

Digitalis
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70
Medications to Reduce Afterload

ACE inhibitors


Captopril, Lisinopril, Enalapril
Angiotensin Receptor Blockers-ARB

Losartan, Valsartan, Olmesartan
Drugs that Affect Contractility
Inotropic drugs



Positive
Negative
Other + Inotropes

Dobutamine

Milrinone
Digoxin





Cardiac glycoside
Positive Inotrope
Negative Chronotrope
Side effects:


h/a, weakness, drowsiness
Yellow halo ★

Beta- blockers

Metoprolol, Carvedilol

Not for use in acute heart failure

Negative Inotrope

Negative Chronotrope
Indications for Worsening or
Recurrent Heart Failure

Rapid weight gain

Decrease in exercise tolerance

Excessive awakening at night to urinate

Development of dyspnea/angina at rest

Increased edema in feet, ankles, hands
Patient Teaching

Signs and symptoms of worsening HF

Telehealth and device remote monitoring technology

Therapeutic interventions can be implemented to avoid
re-hospitalization
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74
Patient Teaching/Expected
Outcomes



Drug therapy
Exercise Training/Cardiac Rehab
Health Promotion

Influenza & Pneumococcal Vaccines

Pallative Care

Expected outcomes for patient with HF




Maintain adequate O2/CO2 exchange to meet O2 needs of the body
Maintain adequate blood pumped by heart to maintain metabolic
demands
Reduction or absence of edema and stable baseline weight
Achieve a realistic program of activity that balances with energy
conserving activities
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75
Coronary Artery
Disease
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76
Coronary Artery Disease
(CAD)

Occurs when there is decrease in
perfusion to the myocardium
 Arteriosclerosis
 Atherosclerosis

Leads to:
 Ischemia
 Infarction
Risk Factors for CAD

Non Modifiable Risk Factors

Age

Gender

Ethnicity

Genetics
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78
Risk Factors

Major modifiable risk factors

High serum lipids (Table 31-6)

Cholesterol >200 mg/dL

High-density lipoproteins (HDL) < 40 mg/dL


Low-density lipoproteins (LDL) > 130 mg/dL


High LDLs increase atherosclerosis and CAD
Fasting triglycerides >150 mg/dL


High HDLs prevent lipid accumulation in
arteries
High levels increase risk for CAD
http://www.cvriskcalculator.com
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79
Risk Factors

Major modifiable risk factors

Hypertension (HTN)

Normal BP <120/<80 mm Hg

Elevated BP 120 to 129/<80 mm Hg

Stage 1 HTN 130 to 139/80 to 89 mm Hg

Stage 2 HTN >140/>90 mm Hg

Lifestyle changes for elevated BP and HTN; treat stage 1 or 2
HTN with drugs (Table 32-5)

Elevated BP—endothelial injury leads to left ventricular
hypertrophy and reduced stroke volume
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80
Risk Factors

Major modifiable risk factors

Tobacco use
 Nicotine:
Increased catecholamine results
in increased HR and BP, peripheral
vasoconstriction
 Increased LDL, decreased HDL, increased
oxygen radicals—vessel inflammation and
thrombosis
 Increased carbon monoxide—reduces O2
carrying capacity of Hgb

Second-hand smoke - Increased CAD 25% to 30%

Tobacco cessation
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81
Risk Factors

Major modifiable risk factors

Physical inactivity
 Lack
of regular exercise
 30 to 60 minutes brisk walking 5 days/week

Obesity
 BMI
> 30 kg/m2
 Waist circumference > 40” men; 35”
women
 Increased LDLs, triglycerides; HTN; insulin
resistance
 Apple figure > CAD than pear figure
Copyright © 2020 by Elsevier, Inc. All rights reserved.
82
Risk Factors

Contributing modifiable risk factors

Diabetes—2-4 × CAD
 Increased
endothelial dysfunction
 Altered
lipid metabolism, increased
cholesterol and triglycerides

Metabolic syndrome
 Multiple
risk factors related to insulin
resistance including central obesity,
HTN, abnormal serum lipids, and high
fasting blood glucose (Table 40-2)
Copyright © 2020 by Elsevier, Inc. All rights reserved.
83
Risk Factors

Contributing modifiable risk factors

Psychologic states
 Type A
personality
 Acute
and chronic stress, depression,
anxiety, hostility and anger, lack of social
support results in increased SNS stimulation
results in increased catecholamines results
in endothelial injury, increased HR,
increased force of myocardial contraction
results in increased O2 demand
 Altered
coagulation
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84
Risk Factors

Contributing modifiable risk factors

Increased homocysteine level
 Breakdown
of essential amino acid
methionine (protein)
 Damage
endothelium, promote plaque
buildup, enhance clotting

Substance use
 Cocaine
and methamphetamine results
in coronary artery spasm resulting in
chest pain and MI
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85
Audience Response Question (1 of
2)
Two risk factors for coronary artery disease that increase
the workload of the heart and increase myocardial oxygen
demand are:
a.
obesity and smokeless tobacco use.
b.
hypertension and cigarette smoking.
c.
elevated serum lipids and diabetes.
d.
physical inactivity and elevated homocysteine levels.
Copyright © 2020 by Elsevier, Inc. All rights reserved.
86
Audience Response Question (1 of
2)
Which patient is most at risk for developing coronary artery disease?
a.
A patient with hypertension who smokes
b.
An overweight patient who uses smokeless tobacco
c.
A patient with diabetes who uses methamphetamines
d.
A sedentary patient with elevated homocysteine levels
Copyright © 2020 by Elsevier, Inc. All rights reserved.
87
Interprofessional and
Nursing Care
Health promotion

Identifying high-risk persons

Health history, including family history

Presence of cardiovascular symptoms

Lifestyle patterns

Psychosocial history

Employment history

Values and beliefs about health and illness; education and
literacy
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88
Interprofessional and
Nursing Care

Managing high-risk persons

Prevention: control modifiable risk factors

Encourage lifestyle changes

Education

Clarify personal values

Set realistic goals
Copyright © 2020 by Elsevier, Inc. All rights reserved.
89
Interprofessional and
Nursing Care

Physical activity

FITT formula:

Frequency, Intensity, Type and Time

30 minutes most days plus weight training 2 days/wk

Regular physical activity helps with:
 Weight
reduction
 Reduction
 Increase
of systolic BP
in HDL cholesterol
Copyright © 2020 by Elsevier, Inc. All rights reserved.
90
Interprofessional and
Nursing Care

Nutritional Therapy

See: Tables 33-4, and 33-5

Reduced Saturated fats and cholesterol

Increased Complex carbohydrates and fiber

Reduced Red meat, egg yolks, and whole milk

Increased Omega-3 fatty acids
Copyright © 2020 by Elsevier, Inc. All rights reserved.
91
Audience Response Question
The nurse determines that teaching about
implementing dietary changes to decrease the risk of
CAD has been effective when the patient says,
a. “I should not eat any red meat such as beef, pork,
or lamb.”
b. “I should have some type of fish at least 3 times
a week.”
c. “Most of my fat intake should be from olive oil or
the oils in nuts.”
d. “If I reduce the fat in my diet to about 5% of my
calories, I will be much healthier.”
Copyright © 2020 by Elsevier, Inc. All rights reserved.
92
Interprofessional and
Nursing Care

Lipid-lowering drug therapy

Lipid profile screening

Statin therapy recommended:
 Patients
 LDL
with known CVD
cholesterol > 190 mg/dL
 Age
40 to 75 with diabetes and LDL 70
to 189 mg/dL
 Age
40 to 75 with LDL 70 to 189 mg/dL
and 10-year risk for CVD at least 7.5%
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93
Interprofessional and
Nursing Care
HMG-CoA Reductase Inhibitors (Statins)
atorvastatin (Lipitor)
fluvastatin (Lescol XL)
lovastatinpitavastatin (Livalo)
pravastatin (Pravachol)
rosuvastatin (Crestor)
simvastatin (Zocor)
Copyright © 2020 by Elsevier, Inc. All rights reserved.
94
Gerontologic Considerations:
CAD

Increased incidence and mortality
associated with CAD in older adults

Strategies to reduce risk and treat CAD
are effective


Treat: hypertension and increased lipids

Smoking cessation, increased physical activity
Most likely to change when
hospitalized or have chest pain
Copyright © 2020 by Elsevier, Inc. All rights reserved.
95
Peripheral Artery
Disease
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96
Peripheral Artery Disease (PAD)

Involves thickening of the artery walls and
progressive narrowing of arteries of upper
and lower extremities

Symptomatic age 60 to 80; earlier with diabetes

In United States, 8.5 million have PAD



 prevalence with blacks
Strongly related to other cardiovascular
disease (CVD) and risk factors
Higher risk of mortality, CVD mortality,
major coronary events and stroke
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97
Etiology and Pathophysiology

Atherosclerosis is leading cause in majority of cases

Gradual thickening of the intima and media due to
cholesterol and lipid deposits

Exact cause unknown; inflammation and endothelial injury
play a major role; See Fig. 33-1 (next slide)
Copyright © 2020 by Elsevier, Inc. All rights reserved.
98
Fig. 33-1 Pathogenesis of
Atherosclerosis
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99
Etiology and Pathophysiology

Risk factors:

Tobacco use

Atherosclerosis

Diabetes

HTN

High cholesterol

Age greater than 60

See Gender Differences Box

Multiple risk factors increase the risk of PAD

Atherosclerosis often affects coronary, carotid, and lower
extremity arteries

Symptoms occur when arteries are 60% to 75% blocked
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100
PAD of Lower Extremities
Fig. 37-1 Common Sites of Atherosclerotic
Lesions
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101
Clinical Manifestations

Classic symptom of PAD—intermittent
claudication

Ischemic muscle pain that is caused by a constant level of
exercise
 Build
up of lactic acid from anaerobic
metabolism

Resolves within 10 minutes or less with rest

Reproducible
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102
Clinical Manifestations

Paresthesia

Numbness or tingling in the toes or feet from nerve tissue
ischemia

Neuropathy causes severe shooting or burning pain

Produces loss of pressure and deep pain sensations from
reduced blood flow

Injuries often go unnoticed by patient
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103
Clinical Manifestations

Reduced blood flow to limb:

Thin, shiny, and taut skin

Loss of hair on the lower legs

Diminished or absent pedal, popliteal, or femoral pulses

Pallor of foot with leg elevation

Reactive hyperemia of foot with dependent position
Copyright © 2020 by Elsevier, Inc. All rights reserved.
104
Clinical Manifestations

Pain at rest

Progressive disease

Occurs in feet or toes

Aggravated by limb elevation

Occurs from insufficient blood flow to distal tissues

Occurs more often at night

Pain relief by gravity
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105
Complications
Prolonged ischemia leads to:

Atrophy of skin and underlying muscles

Delayed healing

Wound infection

Tissue necrosis

Arterial ulcers over bony prominences

See: Table 37-1
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106
Complications

Most serious: Nonhealing arterial
ulcers and gangrene


Collateral circulation may prevent gangrene
May result in amputation

If adequate blood flow is not restored and if severe
infection occurs

Indicated with uncontrolled pain and spreading infection
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107
Diagnostic Studies (Table 372)

Doppler ultrasound


Duplex imaging


Bidirectional, color Doppler
Ankle-brachial index (ABI) (Table 37-3)


Segmental blood pressure
Done using a hand-held Doppler
Angiography and magnetic resonance
angiography (Table 31-7)
Copyright © 2020 by Elsevier, Inc. All rights reserved.
108
Interprofessional Care
Risk Factor Modification

Goal: reduce CVD risk factors

BP control (reduce sodium; DASH diet)

Tobacco cessation (Tables 10-3 to 10-6)

Hemoglobin A1C <7.0% for diabetics

Aggressive treatment of hyperlipidemia—diet and statins
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109
Interprofessional Care
Drug Therapy

ACE inhibitors—reduce PAD symptoms

Ramipril (Altace)
 Decreases
cardiovascular morbidity
 Decreases
mortality
 Increases
peripheral blood flow
 Increases
ABI
 Increases
Walking distance
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110
Interprofessional Care
Drug Therapy

Antiplatelet agents

Aspirin

Clopidogrel (Plavix)

See Drug Alert
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111
Interprofessional Care
Drug Therapy

Drugs prescribed for treatment of
intermittent claudication

Cilostazol (Pletal)—See Drug Alert
 Inhibits
platelet aggregation
 Increased

vasodilation
Pentoxifylline (Trental)
 Improves
flexibility of RBCs and WBCs
 Decreases
fibrinogen concentration,
platelet adhesiveness, and blood
viscosity
Copyright © 2020 by Elsevier, Inc. All rights reserved.
112
Interprofessional Care
Exercise Therapy

Walking is most effective exercise for
individuals with claudication

30 to 45 minutes daily, 3 times/wk

Women have faster decline and
mobility loss than men

Daily exercise increases survival rates
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113
Interprofessional Care
Nutritional Therapy

BMI <25 kg/m2

Waist circumference is less than 40 in for men and less
than 35 in for women

3% to 5% weight loss yields reduced triglycerides,
glucose, A1C, and decreased risk of type 2 diabetes

Recommend reduced calories and salt for obese or
overweight persons
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114
Nursing Management
Planning

Overall goals for patient with PAD

Adequate tissue perfusion

Relief of pain

Increased exercise tolerance

Intact, healthy skin on extremities

Increased knowledge of disease and treatment plan
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115
Nursing Management
Nursing Implementation

Health promotion

Acute care

Ambulatory care
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116
Nursing Management
Evaluation

Adequate peripheral tissue perfusion

Increased activity tolerance

Effective pain management

Knowledge of disease and treatment plan
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117
Acute Arterial
Ischemic
Disorders
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118
Acute Arterial Ischemic
Disorders

Etiology and pathophysiology

Sudden interruption in arterial blood supply to a tissue,
organ, or extremity. If untreated, can result in tissue
death

Causes: embolism, thrombosis, or trauma
Copyright © 2020 by Elsevier, Inc. All rights reserved.
119
Clinical Manifestations

6 P’s

Pain

Pallor

Pulselessness

Paresthesia

Paralysis (late sign)

Poikilothermia
 Immediate
intervention needed to
avoid ischemia, necrosis, and gangrene
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120
Venous Thrombosis

Formation of a thrombus (clot) with
vein inflammation

Most common venous disorder

Superficial vein thrombosis

Deep vein thrombosis (DVT)


See Table 37-7 for comparison
Venous thromboembolism (VTE)

DVT to pulmonary embolism (PE)
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121
Venous Thrombosis: Etiology


Virchow’s triad (Fig. 37-9)

Venous stasis

Damage to endothelium

Hypercoagulability of blood
Risk factors for VTE: Table 37-8
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122
Fig. 37-9
Pathophysiology of VTE
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123
VTE


Deep veins of arms or legs, pelvis, vena
cava, and pulmonary system
Manifestations (Table 37-7)

Lower extremity
 Unilateral
edema
 Pain, tenderness with palpation
 Dilated superficial veins
 Full sensation in thigh or calf
 Paresthesias
 Red, warm
Fever greater than 100.4° F (38° C)
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124
VTE

Manifestations (Table 37-7)

Inferior vena cava
 Legs

edematous and cyanotic
Superior vena cava
 Similar
symptoms of arms, neck, back
and face


Some patients are asymptomatic
Diagnosis:

Assessment, D-dimer and/or ultrasound
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125
VTE: Complications
 Most
serious:
 PE
 Chronic
thromboembolic pulmonary
hypertension
 Postthrombotic
 Phlegmasia
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syndrome (PTS)
cerulea dolens
126
VTE Diagnostic Studies

Diagnostic studies (Table 37-9)

Blood: ACT, aPTT, INR, bleeding time, Hgb, Hct, platelet
count, D-dimer, fibrin monomer complex

Noninvasive venous: venous compression ultrasound,
duplex ultrasound

Invasive venous: CT venography, MR venography, contrast
venography
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127
VTE: Interprofessional Care

Prevention and prophylaxis

VTE prophylaxis is a core measure of high-quality health
care in high-risk hospitalized patients developed by The
Joint Commission (TJC) and the National Quality Forum.

TJC recommends all hospitals have a VTE prevention
policy for all adult patients
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128
VTE: Interprofessional Care

Early and aggressive mobilization

Bed rest—reposition every 2 hours

Flex and extend feet, knees and hips every 2 to 4 hours
while awake

OOB to chair

Walk 4 to 6 times/day
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129
VTE: Interprofessional Care

Graduated compression stockings

Thromboembolic deterrent (TED)

Often used with anticoagulation

Fit and wear correctly:
 Toe
hole under toes, heel patch over
heel; thigh gusset on inner thigh
 No
wrinkles; don’t roll down, cut, or
alter

Not recommended if VTE already exists
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130
VTE: Interprofessional Care

Intermittent pneumatic compression
devices (IPCs) - increased venous
return

External pressure from electric pump inflates sleeves or
boots to compress calf or thigh and/or foot and ankle

Use with graduated compression stockings

Fit and apply correctly; wear continuously except for
bathing, skin assessment, and ambulation

Do not use with active VTE; risk of PE
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131
VTE: Drug Therapy

Drug therapy: anticoagulants

Three classifications (Table 37-10)
 Vitamin
K antagonists (VKA)
 Thrombin
inhibitors (direct and
indirect)
 Factor
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Xa inhibitors
132
Covered in Pharm

Vitamin K antagonists: Warfarin

Inhibits Vitamin K-dependent coagulation factors II, VII, IX,
and X and anticoagulant proteins C and S

For long-term or extended
anticoagulation
 Takes
48 to 72 to be effective; often
overlap with parenteral anticoagulant
for 5 days
 Monitor
INR (Table 37-11)
 Antidote:
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Vitamin K
133
Covered in Pharm

Warfarin (continued)

Do not give with antiplatelet drugs or NSAIDS

Many interactions: See Complementary and Alternative
Therapies Box

Avoid vitamin K in diet; alters INR
 Green

leafy vegetables
Genetic variants may alter response
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134
Covered in Pharm

Thrombin inhibitors

Indirect: UH (heparin) and LMWH
 Affects
intrinsic plasma antithrombin
coagulation pathway; inhibits thrombin
mediated conversion of fibrinogen to
fibrin (Fig. 29-4)
 Prophylaxis—subcutaneously
 Existing
VTE—continuous IV; monitor
aPTT (Table 37-11)
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135
Covered in Pharm


Heparin (continued)

Serious side effect: heparin-induced thrombocytopenia
(HIT)

Long-term side effect: osteoporosis
LMWH—enoxaparin

More predictable, longer half-life, fewer bleeding
complications

Antidote: protamine
Copyright © 2020 by Elsevier, Inc. All rights reserved.
136
Covered in Pharm

Direct thrombin inhibitors (Table 37-10)


Hirudin derivative—bivalirudin (Angiomax)

Binds with thrombin and inhibits function

Continuous IV infusion
Synthetic (Argatroban)—


Hinders thrombin
Both:

Indications: patients with or at risk for HIT having a
percutaneous coronary intervention

Monitor aPTT or ACT (Table 37-11)

No antidote
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137
Covered in Pharm

Direct thrombin inhibitors (Table 37-10)

Dabigatran (Pradaxa)—oral
 Indications:
VTE prevention after elective
joint replacement, for stroke prevention in
nonvalvular atrial fibrillation, and as a
treatment for VTE
 Antidote:
idarucizumab
 Advantages

over warfarin
Rapid onset, no monitoring, few drugfood interactions, decreased risk of
bleeding, predictable response
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138
Covered in Pharm

Factor Xa Inhibitors (Table 37-10)

Inhibit factor Xa; rapid anticoagulation
 VTE
prophylaxis and treatment
 Fondaparinux (Arixtra)—Subcutaneous

Contraindicated with severe renal disease
 Rivaroxaba
(Xarelto), apixaban (Eliquis),
edoxaban (Savaysa)—oral
 Monitoring not required but can use anti-Xa
assays (Table 37-11)
 Andexant Alfa—reverses rivaroxaban and
apixaban
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139
Covered in Pharm

Anticoagulant therapy for VTE
prophylaxis

Hospitalized patient not bleeding
 UH,
LMWH, or fondaparinux

Low risk VTE—no prophylaxis

Moderate risk—UH or LMWH
 General,

GYN or urologic surgery
High risk—UH or LMWH
 Trauma,
abdominal or pelvic surgery for
cancer, or orthopedic surgery
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140
Covered in Pharm

Anticoagulant therapy for VTE
treatment

Initial: LMWH, UH, or oral Factor XA or VKA

INR—maintain 2.0 to 3.0 (VKA therapy)

Continue 3 or more months

Co-morbidities, complex issues, or vary large VTE—
hospitalization
 IV
UH initially
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141
Covered in Pharm

Thrombolytic therapy for VTE
treatment

Thrombolytic drug (tPA or urokinase) administered via
catheter to dissolve clots, reduce acute symptoms,
improve deep venous flow, reduce valvular reflux, and 
PTS

Indication: patients with low risk of bleeding and acute,
extensive, symptomatic, proximal VTE

Must have systemic anticoagulation before, during, and
after thrombolysis
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142
VTE: Interprofessional Care

Surgical and interventional radiology
therapies

Surgical options:
 Open
venous thrombectomy—incision
into vein to remove clot
 Inferior
vena cava interruption
devices—filters placed via right femoral
or internal jugular veins (Fig. 37-11) to
trap clots without impeding blood flow
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143
Fig. 37-11 Inferior Vena Cava Interruption
Device

Recommended for acute PE
or proximal VTE of leg with
active bleeding, or if
anticoagulation
contraindicated or
ineffective

Complications: air
embolism, improper
placement, filter
migration, perforation of
vena cava with
retroperitoneal bleeding,
clogged filter
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144
VTE: Interprofessional Care

Percutaneous endovascular interventional
radiology procedures
 Options:
Mechanical thrombectomy,
pharmacomechanical devices, postthrombus extraction, angioplasty,
and/or stenting
 Can be used with catheter-directed
thrombolytic therapy
 Nursing
care: Maintain catheter
systems, monitor for bleeding,
embolization, and impaired perfusion;
and teach VTE prevention
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145
Nursing Management: VTE

Nursing assessment (Table 37-12)

Subjective data
 Important
health information
Past history
 Medications
 Surgery or other treatments

 Functional
health patterns
Health-perception–Health management
 Activity–exercise
 Cognitive–perceptual

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146
Nursing Management: VTE

Nursing assessment (Table 37-12)

Objective data
 General
 Integumentary
 Cardiovascular
 Possible
Copyright © 2020 by Elsevier, Inc. All rights reserved.
diagnostic findings
147
Nursing Management: VTE

Nursing diagnoses
 Acute
pain
 Impaired
 Risk
Planning/goals:
 The
patient will have:
tissue
 Pain
mobility
 Increased
integrity
 Impaired

for bleeding
relief
 Decreased
edema
knowledge
of disease and
treatment plan
 No
skin ulceration
 No
bleeding
complications
 No
Copyright © 2020 by Elsevier, Inc. All rights reserved.
evidence of PE
148
Nursing Management: VTE

Nursing implementation: Acute care

Focus on prevention of thrombi and reduction of
inflammation
 See
Nursing Management: Caring for
the Patient with VTE; all healthcare
team members have important roles

Review any interfering factors with anticoagulation
therapy (see Complementary and Alternative Therapies
Box)

Monitor anticoagulation and significant lab studies; titrate
drug doses and administer reversal agents as needed
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149
Nursing Management: VTE

Nursing implementation: Acute care

Monitor and reduce the risk of bleeding See: Table 37-13
(Assessment, Injections, Patient Care)
See: Drug Alert: Anticoagulant Therapy

Acute VTE—initial bed rest

Early ambulation

Teach importance of physical activity
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150
Nursing Management: VTE

Ambulatory care

Discharge teaching (Table 37-14)
 VTE

risk factors
Smoking, hormone therapy, travel,
prolonged sitting, signs/symptoms of PE
 Drug
doses, actions, side effects and
routine blood tests; wear medic-alert ID
Avoid falls and trauma
 Apply pressure to bleeding sites for 10-15
minutes
 No ASA or NSAIDs; limit alcohol

Copyright © 2020 by Elsevier, Inc. All rights reserved.
151
Nursing Management: VTE

Discharge teaching (continued)


Dietary and Exercise Instructions

Vitamin K and warfarin

Obtain and maintain desired weight
Guidelines for follow-up

Report/call EMS:
Copyright © 2020 by Elsevier, Inc. All rights reserved.

Bleeding (urine, stool, vomit, nose, gums, skin)

Severe headache, stomach pain, chest pain,
palpitations, dyspnea, mental status changes

Inform all HCP and dentist of anticoagulation
152
Nursing Management: VTE

Evaluation

Expected outcomes:
 Minimal
 Intact
to no pain
skin
 Increased
knowledge of disorder and
treatment plan
 No
signs of hemorrhage or occult
bleeding
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153
Chronic Venous Insufficiency
(CVI) and Venous Leg Ulcers

CVI—abnormalities of venous system
include edema, skin changes, and venous
leg ulcers

Etiology and Pathophysiology

Ambulatory venous hypertension
 Serous
fluid and RBC leak results in edema
and chronic inflammatory changes
 Hemosiderin—brown
 Skin
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skin discoloration
is hard, thick, and contracted
154
Chronic Venous Insufficiency
(CVI) and Venous Leg Ulcers

Clinical Manifestations and
Complications

Lower leg—brown, leathery and edematous

Eczema with itching and scratching (Table 37-1)

Venous ulcers (Fig. 37-13)
 Pain
especially with dependent position
 Risk
of infection
Copyright © 2020 by Elsevier, Inc. All rights reserved.
155
Fig. 37-13 Venous Leg Ulcer
Copyright © 2020 by Elsevier, Inc. All rights reserved.
156
Chronic Venous Insufficiency
(CVI) and Venous Leg Ulcers

Interprofessional and nursing care


Compression for healing and prevention of
recurrence

Stockings, bandages, IPCs, wraps

Teach proper fit and application

Assess for PAD prior to compression
Activity guidelines and limb positioning

Avoid prolonged sitting or standing

Elevate legs above heart

Daily walking

Avoid trauma

Daily foot and leg care
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157
Chronic Venous Insufficiency
(CVI) and Venous Leg Ulcers

Interprofessional and nursing care

Wound care and dressings—moist environment

Nutrition—adequate protein, vitamins A and C, zinc
 Diabetics—normal

blood glucose levels
Monitor for infection
 Debridement,
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excision, antibiotics
158
Chronic Venous Insufficiency
(CVI) and Venous Leg Ulcers

Interprofessional and nursing care

Drug therapy—pentoxifylline or micronized flavonoid
fraction

Other: skin replacement (e.g., grafts)

Daily moisturizing
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159
Tissue Perfusion
Hematologic
N 1020 Fall 2020
Memorize this slide!

RBCs = oxygen

WBCs = infection & inflammation (leuko-)

Platelets = clotting

-cytosis = too many
 leukocytosis,

(erythro-)
(thrombo-)
thrombocytosis
-penia = too few
 leukopenia,
thrombocytopenia
Assessment of Hematologic
System

Objective Data

Head to Toe Physical examination
Abnormalities that require f/u:

Pallor

Red tongue or mouth ulcers

DOE, tachypnea

Weak pulses

Hematuria

Bone tenderness

Palpable spleen or liver

Numbness/tingling

Lymph node enlargement
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Anemia

A deficiency in the

number of erythrocytes (RBCs), quantity
or quality of hemoglobin (Hgb) & volume
of packed RBCs (hematocrit)

The amount of oxygen delivered to
body tissues is also diminished

Not a specific disease

Manifestation of a pathologic process
Copyright © 2020 by Elsevier, Inc. All rights reserved.
163
Causes of Anemia
164
Anemia

Classified according to
 Morphology
 Cellular
 RBC
characteristic
size and color
 Etiology
 Cause
 Clinical
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condition causing anemia
165
Anemia
Clinical Manifestations

Caused by body’s response to tissue
hypoxia (i.e. decreased perfusion)
 Manifestations
vary based on how fast
anemia has evolved, its severity, and
any coexisting disease


Hgb levels are often used to determine
severity of anemia
Fatigue is the #1 most common
symptom
Copyright © 2020 by Elsevier, Inc. All rights reserved.
166
166
Anemia
Integumentary Manifestations


Pallor
 Decreased
Hemoglobin
 Decreased
blood flow to the skin
Jaundice
 Increased
concentration of serum
bilirubin

Pruritus
 Increased
serum and skin bile salt
concentrations
Copyright © 2020 by Elsevier, Inc. All rights reserved.
167
Anemia
Cardiopulmonary Manifestations

Result from heart and lungs trying to provide
adequate O2 to tissues
 Results
in increased heart rate &
respiratory rate

Cardiac output maintained by increasing
heart rate and stroke volume

Low Hgb can result in a “demand MI”
Copyright © 2020 by Elsevier, Inc. All rights reserved.
168
Anemia
Clinical Manifestations

Respiratory


Dyspnea on exertion
Neurologic
 Fatigue
 Headache
 Paresthesias
 Gait
of hands and feet
and balance disorders
Anemia
Nursing Assessment

Subjective data
 Important
 Past
health information
health history
 Medications
 Surgery
or other treatments
 Dietary
history
 Functional
Copyright © 2020 by Elsevier, Inc. All rights reserved.
health patterns
170
Anemia
Nursing Assessment

Objective data
 General
 Integumentary
 Respiratory
 Cardiovascular
 GI
 Neurologic
 Diagnostic
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findings
171
Anemia
Nursing Interventions

Patients with fatigue
 Alternate
rest and activity
 Prioritize
activities
 Accommodate
 Maximize
 Aid
energy levels
O2 supply for vital functions
to minimize risk of injury from falls
 Monitor
cardiorespiratory response
 Evaluate
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nutritional needs
172
Anemia
Gerontologic Considerations

Anemia is not normal
 More
common in the 70s and beyond
 Often

related to an underlying cause
Signs and symptoms may be
overlooked
 Other
 May
health issues
be mistaken for normal aging
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173
Anemia
Decreased Erythrocyte
Production

RBC production (erythropoiesis) is in
equilibrium with RBC destruction/ loss

Balance ensures that adequate number of
RBCs is always available

Three changes in erythropoiesis may
decrease RBC production:

Decreased Hgb synthesis Defective DNA
synthesis in RBCs

Diminished availability of erythrocyte
precursors
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174
Iron-Deficiency Anemia
Etiology

Most common nutritional disorder

Etiology
 Inadequate
dietary intake
 Pregnant/nursing
women, adolescents
 Malabsorption
 Blood
loss
 Menstruating
women, GI bleending
175
Iron-Deficiency Anemia
Etiology

Blood loss
 Major
cause of iron deficiency in adults
 Chronic blood loss most commonly
through GI and GU systems
 Bleeding often not apparent
 May take time to identify
 Postmenopausal bleeding, chronic
kidney disease, and dialysis may
contribute
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176
Iron-Deficiency Anemia
Clinical Manifestations

General manifestations of anemia
 Pallor
is most common
 Glossitis
is second
 Inflammation
 Cheilitis
is also found
 Inflammation
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of tongue
of lips
177
Iron-Deficiency Anemia
Diagnostic Studies

Laboratory findings
↓
RBC, Hgb, Ferritin, Serum Iron
 RBC
↑
are microcytic (small)
TIBC (Transferrin)

Stool occult blood test

Endoscopy and colonoscopy

Bone marrow biopsy
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178
Iron-Deficiency Anemia
Collaborative Management

Goal


Treat underlying problem causing loss, reduced
intake or poor absorption of iron
Replace iron

Nutritional therapy
 Lean
beef, turkey, pork & chicken, fish, legumes,
dark green leafy vegetables, beans, enriched
breads & cereals

Iron supplements

Transfusion of packed RBCs
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179
Iron-Deficiency Anemia
Drug Therapy

Indications


Treatment of iron deficiency anemias and may
be used as adjunctive therapy in pts receiving
Epoetin Alfa
Pharmacokinetics

Absorbed in small intestines

Transported in the blood bound to transferrin

Small amounts are lost daily in the sweat,
urine, sloughing of skin and mucosal cell and
sloughing of intestinal cells.
180
Iron-Deficiency Anemia
Drug Therapy

Oral iron (ferrous sulfate, ferrous glucontate)

Best absorbed in an acidic environment
 Take
@ 1 hr before meals
 Take
with Vit. C to be properly absorbed
 Do
not take at same time as Calcium

Undiluted liquid iron may stain teeth

Side effects
 Heartburn,
nausea, constipation, diarrhea
 Discoloration
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of stools (dark green to black)
181
Iron-Deficiency Anemia
Collaborative Management

Parenteral iron
Indicated for malabsorption, oral iron intolerance,
 need for iron beyond normal limits, poor patient
compliance
 Can be given IM or IV, IM may stain skin, use Z-track
 Reassess Hgb and RBC count to evaluate response to therapy
 Emphasize adherence to dietary and drug therapy



Need to take supplement for 2 to 3 months after
Hgb returns to normal
Monitor for liver problems with lifelong therapy
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182
Megaloblastic Anemias

Group of disorders
 Caused
by impaired DNA synthesis
 Presence

of large RBCs (megaloblasts)
Majority result from deficiency in
 Cobalamin
 Folic
(vitamin B12)
acid
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183

Vitamin B12 anemia

Deficiency in vitamin B12
(cobalamin)

Strict vegetarians

Malabsorption

Lack of intrinsic factor-this
type of anemia is called
Pernicious Anemia.

Weakness

Fatigue

Bone marrow and blood
changes look like folic acid
anemia


Folic acid anemia

Deficiency in folic
acid intake

Chronic alcoholism/
Repeated pregnancies

Weakness

Fatigue

Bone marrow and blood
changes look like vitamin
B12 anemia
Neuro dysfunctions
Megaloblastic Anemias
RBCs will be larger
than normal.
Cobalamin Vit B12 Deficiency
Etiology

Most commonly caused by pernicious anemia

Caused by absence of intrinsic factor (IF)


IF: Protein secreted by parietal cells of gastric
mucosa, needed for cobalamin absorption
Can also occur:






Surgery or chronic diseases of the GI tract
Excess alcohol or hot tea ingestion
Smoking
Long-term users of H2 histamine receptor
blockers and proton pump inhibitors
Strict vegetarians
Familial predisposition
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185
Cobalamin Vit B12 Deficiency
Clinical Manifestations

General manifestations of anemia develop
slowly due to tissue hypoxia

GI problems:
 Sore,
red, beefy, and shiny tongue
(glossitis) anorexia, nausea, vomiting,
and abdominal pain

Neuromuscular problems:
 Weakness,
paresthesias of feet and
hands, decreased vibratory and position
senses, ataxia, muscle weakness, and
impaired thought processes
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186
Glossitis-smooth beefy red tongue
and paresthesias are common
symptoms of B12 deficiency
anemia.
187
Megoblastic Anemias
Diagnostic Studies

CBC

Vitamin B12 level

MMA (methylmalonic acid)

Homecysteine level

RBC Folate level

Intrinsic factor assay

Bone Marrow staining
Copyright © 2020 by Elsevier, Inc. All rights reserved.
188
Cobalamin Vit B12 Deficiency
Collaborative Management

Medical Management:


Nutritional therapy



Vit B12 injection (hydroxocobalamin) or intranasal
(cyanocobalamin)
Milk, eggs, fish, enriched grains, dairy products
Early detection and treatment
Ensure safety



Diminished sensations to heat and pain from neurologic
impairment
Protect from falling, burns, and trauma
Physical therapy may be needed
Copyright © 2020 by Elsevier, Inc. All rights reserved.
189
Folic Acid Deficiency
Etiology

Folic acid is needed for DNA synthesis

RBC formation and maturation

Manifestations are similar to those of
cobalamin deficiency without neurological

Common causes:
 Dietary
deficiency, Malabsorption
syndromes, Drugs, Increased
requirement , Alcohol use and
anorexia, Loss during hemodialysis
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190
Folic Acid Deficiency
Collaborative Management

Serum folate level is low

Normal is 5 to 25 ng/mL (11 to 57 nmol/L)

Serum cobalamin level is normal

Treated with replacement therapy


Usual dose is 1 mg/day by mouth
Nutrition therapy

Green leafy vegetables, enriched grain
products & breakfast cereals, orange
juice, peanuts, avacado
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191
Before a transfusion…

IV Access-
Blood cannot be “piggybacked” or infused with any other solutions except
for normal saline (0.9% NS). Separate IV access may be needed if other
iv infusions cannot be stopped (TPN, Vasopressors, insulin etc.). A large
bore IV (bigger than a 22g for adults in most facilities) is required for
blood so the cells aren’t destroyed by being squeezed through a small tube.
Each facility has its own policy.

A type and crossmatch (patient blood sample)-
must be sent to the lab so the blood to be transfused can be
tested for compatibility with the patient.

Other baseline labs-
CBC, electrolytes and coagulation studies may be sent for
baseline data. Usually a cbc result is the reason a transfusion is
ordered.
Before a transfusion…

Assess your patient-
We’re adding fluid. A baseline assessment should include fluid status
i.e. a good cardiovascular assessment should be performed first.
BASELINE VITAL SIGNS. MD should be made aware if patient is febrile.

Premedication
In many facilities patients are premedicated with acetaminophen and
diphenhydramine first.

Patient teaching
Assess knowledge of procedure. Instruct the patient to immediately report any
changes-chills, itching, feeling of warmth, difficulty breathing, pain in the back,
the abdomen, the chest, or at the IV site once the transfusion has begun.

IF possible-ask your patient to void or empty their catheter drainage before
starting the transfusion
•All blood or blood components
not used within 30 minutes must
be stored in a monitored
refrigerator that has been
approved by the blood bank.

Do not allow Blood
Products to stand at
room temperature
longer than 30
minutes before
administration.
•Transfusions should be
completed within 4 hours and
before the expiration date/time of
the blood component.
Blood Transfusion Procedure

The following elements MUST be double-checked with a
second RN or MD prior to administration of the blood or
blood products

Patient name

Patient medical record number

Donor unit identification

Blood type (ABO group)

Rh type

Donor unit expiration dates and when applicable time

Presence of antibodies and/or agglutinins

Product type
Copyright © 2020 by Elsevier, Inc. All rights reserved.
You cannot delegate
Blood Transfusions to UAP
195
Blood Transfusion Procedure

Verify that there is a written order from a physician for blood or
blood components

Verify that there is a signed consent with the patient’s name and
medical record number documented

Complete a baseline physical assessment of the patient as a basis to
assess changes during and after the transfusion

Insure the IV line has an appropriate catheter size and is patent

Adjust infusion rate of transfusion according to the patient’s need,
providers orders and agency policy

Assess patient for signs of transfusion reaction

Delegate UAP to take vital signs as directed

Evaluate for therapeutic effect of blood product (improvement in
CBC, increased BP, decreased bleeding)

Monitor for signs of circulatory overload (i.e. SOB) if the transfusion
is given rapidly
Copyright © 2020 by Elsevier, Inc. All rights reserved.
196
Type & Crossmatch Blood
198
Blood Compatibilities for
Transfusions
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199
Rhesus (“Rh”) Factor

Copyright © 2020 by Elsevier, Inc. All rights reserved.
Read your book! This
will become important
when you take
Maternity
200
Transfusion Procedure

Spike bag of 0.9% sodium chloride (NS) with one of the
Y-tubing spikes, hang bag on IV pole and prime IV tubing

Gently invert the blood component bag several times to
suspend cells (to mix thoroughly before infusion)

Spike blood component bag with the other Y-tubing
connection. Ensure the drip chamber is half-full and the
filter is covered to prevent damage to blood cells

Clean the IV port per institution policy, then attach the
Y-tubing to the patient’s IV site. Open the roller clamp
on the blood. A gentle squeeze on the filter helps start
the flow of blood
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201
Transfusion Procedure

Infuse slowly for the first 15 minutes while observing the
patient for reactions. This step allows for assessment to
make sure the patient is not in need of rapid, life-sustaining
interventions. Most serious reactions occur during this time

After 15 minutes, reassess vital signs and adjust the flow rate
to the desired speed, if no signs of a transfusion reactions
are noted. Infusion time for RBCs should not exceed 4 hours.
The longer the RBCs are left at room temperature, the
greater the danger of bacterial proliferation and RBC
hemolysis.

Continue the assessment of the patient (always include vital
signs) throughout the transfusion as needed, according to the
patient’s condition, the number of units being administered
and the facility policy.
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202
Signs and Symptoms of
Transfusion Reactions

Fever (Temp increase of >
1Cor 2F) with or without
chills

Skin changes, including
flushing, uticaria localized or
generalized edema

Shaking chills (rigors) with or
without fever

Nausea, with or without
vomiting

Pain at infusion site or in the
chest, abdomen or flanks,
muscle aches

Bradycardia or tachycardia

Pruritis, diaphoresis, cyanosis
or pallor

Blood pressure changes,
usually acute, either
hypertension or hypotension

Respiratory distress,
including dyspnea,
tachypnea, hypoxemia,
shortness of breath,
wheezing, cough or rales
Copyright © 2020 by Elsevier, Inc. All rights reserved.
Basically, if there is ANY CHANGE from baseline
assessment…Sometimes it’s as simple as an itchy face or flushing…
When in doubt, stop the transfusion and ask for assistance.
203
204
Management of a Transfusion
Reaction

Immediately STOP the transfusion once a reaction has been
suspected or identified.

Maintain IV access with normal saline using new primed tubing.

Call the patient’s physician STAT! and notify the blood bank.

Recheck the identifying tags and numbers

Immediately take the patient’s vital signs. Monitor VS and
urine output

Treat patient’s symptoms per the physician’s orders.

Return the blood bag and tubing to the blood bank for
examination

Collect required blood and urine specimens based on policy

Document on transfusion reaction form and patient medical
record
Copyright © 2020 by Elsevier, Inc. All rights reserved.
205
Blood Transfusion
General Principles

No medications or solutions (except normal saline)
should be added to or transfused concurrently with
blood components

If the integrity of any component is questioned on visual
inspection, the unit should be returned to the blood
bank of further evaluation

Lactated Ringer’s solution or other electrolyte solutions
containing calcium should never be administered
concurrently with a blood component mixed with an
anticoagulant containing citrate, because calcium binds
to citrate
Copyright © 2020 by Elsevier, Inc. All rights reserved.
206
Blood Transfusion
Documentation

Per organizational policy

Component infused and amount

Unit number and expiration date

ABO & Rh type of component and patient

Length of infusion time

Unexpected outcomes or transfusion reactions

Physician notifications of transfusion reactions

Signature of both RNs double checking
Copyright © 2020 by Elsevier, Inc. All rights reserved.
207
Leukemia

A group of cancers affecting the blood
and blood-forming tissues of

Bone marrow

Lymph system

Spleen

Occurs in all age-groups

Overproduction of WBCs

Accumulation of dysfunctional cells due to loss
of regulation in cell division
Copyright © 2020 by Elsevier, Inc. All rights reserved.
208
208
Leukemia
Etiology and Pathophysiology

No single cause

Combination of genetic and environmental
influences
 Oncogenes,
or abnormal genes, can
cause many types of cancers
 Chemical
agents, chemotherapeutic
agents, viruses, radiation, and
immunologic deficiencies have been
associated with development of
leukemia
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Pathophysiology of Leukemia
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Leukemia
Classification

Acute vs Chronic

Cell maturity and nature of disease onset
Acute: Clonal proliferation of immature
hematopoietic cells
 Chronic: More mature forms of WBC and
onset is more gradual


Based on type of WBC




Acute lymphocytic leukemia (ALL)
Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML)
Chronic lymphocytic leukemia (CLL)
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ACUTE MYELOGENOUS LEUKEMIA
ACUTE LYMPHOCYTIC LEUKEMIA
All age groups impacted; peak > 60 y.o.
Children: peak 4 y.o., rare after 15 y.o.
Prognosis highly variable -- the younger the patient, the better
the prognosis
Prognosis: 5 year survival 80% for children but 40% for
adults
“Undifferentiated” form: worse prognosis
Bone/abdominal, CNS pain
Neutropenia: fever, weakness, bleeding
Chemo: corticosteroids and vinca alkaloids
Chemo: aggressive induction therapy
Bone marrow transplant
Bone marrow transplant
CHRONIC MYELOGENOUS LEUKEMIA
CHRONIC LYMPHOCYTIC LEUKEMIA
Rare: < 20 y.o.; median age 55-60 y.o.
Most common form; 2/3 > 60 y.o.
Prognosis: 3-5 years while chronic, only months once it
becomes acute
Prognosis: 2 (late) – 14 (early) years
Three stages: chronic, transformation, accelerated (blast)
crisis
Painful enlarged lymph nodes
“B” symptoms: night sweats, weight loss, fever
Malaise, anorexia, weight loss possible
Chemo: monoclonal antibodies
Gleevec, Interferon, hydroxyurea
Infections: antibiotics, immunoglobulin
Bone marrow transplant
Leukemia

Manifestations

Bruises, petechiae,
pallor

Open lesions,
bleeding gums

Anorexia, wt. loss

Enlarged liver and
spleen

Tachycardia,
palpitations

Orthostatic
hypotension

D.O.E., fatigue,
headache, fever,

Bone or joint pain
and swelling,
hematuria
Leukemia from a conceptual view:
You will have problems with both
PERFUSION and PROTECTION. The
patient suffers from symptoms of
pancytopenia. The overproduction
non-working WBCs will take over,
meaning the patient has no ability
to PROTECT themselves (either
from infection or bleeding) and
reduced RBCs which means
decreased PERFUSION. Hence, the
manifestations on the left.
Leukemia
Clinical Manifestations

Inadequate marrow elements
predispose patient to

Anemia

Thrombocytopenia

Decreased number and function of WBCs
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Leukemia
Collaborative Care

Initial goal is to attain remission

Complete, partial, or molecular
 Prognosis
is directly related to ability
to maintain a remission
 Prognosis
becomes more unfavorable
with each relapse

Chemotherapy is the mainstay of treatment
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Leukemia
Chemotherapy Regimens

Combination chemotherapy

Mainstay of treatment

Three purposes
 Decrease
drug resistance
 Decrease
drug toxicity by using
multiple drugs
 Interrupt
cell growth at multiple points
in cell cycle
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Leukemia
Other Treatments

Corticosteroids

Radiation therapy


Total body radiation in preparation for bone marrow
transplantation

Organ- or field-specific such as liver or spleen
Immunotherapy and targeted therapy
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Leukemia
Hematopoietic Stem Cell
Transplant

Goal of HSCT



Eliminate all leukemic cells using combinations of
chemotherapy with or without total body irradiation
Eradicates patient’s hematopoietic stem cells
Replaced with those of an HLA-matched

Sibling

HLA-half-matched relative

Volunteer donor (allogenic)

Identical twin (syngeneic)
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Nursing Management
Planning

Overall goals

Understand and adhere to treatment plan

Have minimal side effects and complications of
disease and treatment

Establish realistic hope and goals, feeling
supported during periods of treatment,
relapse, and remission
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Nursing Management
Acute Care

Many physical and psychologic needs

Diagnosis evokes great fear

Equated with death

Family needs help adjusting to stress of sick
role

May be viewed as hopeless, horrible
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Nursing Management
Acute Care

Important nursing interventions

Maximizing patient’s physical functioning

Teaching patients that acute side effects of
treatment are usually temporary

Encouraging patients to discuss quality of life
issues
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Leukemia – Case Study
What should be included in this
teaching?

Your patient has been diagnosed with
leukemia after presenting to the office
with frequent bruising, bleeding gums,
fatigue and fevers. You are to teach the
patient about bleeding precautions,
managing fatigue and protecting himself
from infections
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