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ADVANCED MEDICAL-SURGICAL NURSING I
CASE SCENARIO
NURSING CARE OF CLIENTS WITH RESPIRATORY PROBLEMS
Prepared by: John Henry O. Valencia, RN, RM
Master of Arts in Nursing Student
M.C. a 65-year-old man is admitted to your medical unit for exacerbation of his emphysema
(COPD). He has a history of atopic asthma during his childhood and hypertension which has been well
controlled by Enalopril for the last six years. He presents as a poorly nourished man who is
experiencing difficulty breathing. He complains of coughing spells productive of thick yellow sputum.
M.C. seems irritable and anxious when he tells you that he has been a two-pack-a-day smoker for 38
years. He tells you he has been sleeping poorly and lately feels very tired most of the time even when
he has not done any physical activity. His VS are 162/84, 124, 36, 102 F, SaO2 88%. His admitting
diagnosis is chronic emphysema with an acute exacerbation.
His admitting orders are as follows:
Diet as tolerated
Out of bed with assistance
O2 at 2L/nc
IV Plain NSSS 1L at 50 ml/hr
Sputum C & S
ABGs in AM
CBC with WBC differential
CXR followed by Pulmonary Function test in AM
ECG

Page 1 of 21

1. What are the significant data that you have gathered? What other relevant questions do you
need to ask M.C.?
2. What physical assessment findings do you expect to find? What specific changes in the
respiratory system do you expect to find indicative of emphysema?
3. What is the most common cause of emphysema? Based on this information, what question will
you ask about his health behaviors? What do you believe are the major cause/s of M.Cs
emphysema?
4. Are M.C.s VS and SaO2 appropriate? If not, explain why.
5. Is your patient with chronic hypoxia? Is he compensating for his chronic hypoxia?
6. Why is the O2 inhalation at 2LPM inspite of the SaO2 at 88%? How do we explain the hypoxic
drive in a pt. with emphysema? What important considerations do you have to remember
regarding O2 administration in a pt. with COPD like M.C.?
7. Make an integrated pathophysiologic flowchart of MCs disease condition.
8. Given M.C.s history and your knowledge of pathophysiologic processes, explain the
pathophysiologic basis of the assessment findings in M.C?
9. What are the possible complications of Emphysema and their manifestations?
10. Make a tabular comparison of the pathogenesis and pathophysiologic changes of
Emphysema, Bronchitis and asthma.
11. Based on the assessment findings, identify five priority problems that M.C. may be
experiencing.
The laboratory sends the ff. report several hours after admission: RBC 3.8thou/cmm, WBC13,000 thou/cmm, Hgb 12g/dL, ABGs: pH- 7.28, pO2 80 mmHg, pCO2 65 mmHg, HCO3 22.
12. Interpret the above results. How do the results relate to the pathophysiologic changes of
emphysema?
13. With the ABG result, can you say that M.C. is in respiratory failure or respiratory insufficiency?
Explain the scientific basis of your answer.
14. What are the major hallmarks of respiratory failure? What do you believe are the principal
causes of this problem in M.C.?Explain your answer.
Five days after admission, M.C.s condition has remarkably improved. The MD wants all
medications continued and has shifted the antibiotics to oral preparations.
15. What made the MD say MCs condition has improved? Give the assessment findings that
supports the MDs observation.
16. Summary of journal readings (3) related to the case. Use the table below.
Directions:
1. This scenario is to be accomplished individually and to be submitted on Tuesday,Sept 16,
2014
This must be typewritten in A4 bond paper using Arial Narrow font 11.
Late submission will have demerit rating. Please comply!
2. Discussion of the case will be done on Tuesday. Please come prepared for the discussion

3. Grading rubric is attached. Kindly attach a copy of this on the paper you will submit

ISTIONKO/USTGS/2014

Answers:
1. What are the significant data that you have gathered? What other relevant questions do
you need to ask M.C.?
Patient has a significant History of Chronic smoking (two-pack-a-day smoker for 38 years).
Patient also has a history of atopic asthma and hypertension but well controlled by Enalopril.
Patient was poorly nourished and experiencing DOB. Cough producing yellow-thick sputum.
Relevant Questions that we may asked:
Shortness of breath:

When were you first short of breath (at exercise or at rest)?

How often are you short of breath?

How long have you been short of breath? Is it getting worse?

How far can you walk, and how many steps can you climb before having to stop
because of shortness of breath?

Coughing:

How often and when do you cough?

How long have you been coughing? Is it getting worse?

Do you cough up mucus (sputum)? What color is it?

Have you ever coughed up blood?

Social History:

Childhood respiratory illnesses.

Family history of respiratory disease.

Other medical conditions you may have and their treatment.

How your condition is affecting your quality of life: missed work, disrupted routines,
and depression, for example.

The name and dose of all of the medicines you take, including any inhalers you use.

What type of family and social support you have.

How long have you had cough, shortness of breath, or wheeze?
Have you seen many doctors for it? What are you now doing to treat it?
How many days did you miss from work last year because of the lung problem?
Were you in the hospital for it? How long and how many times last year?
Describe your usual good day.
Do you have more good days than bad days in a week? What are you able to do when
you are feeling youre very best?
Who do you live with?

What recreation do you prefer?

What have you learned to do that helps you to live with it?
Does it ever embarrass you to have lung trouble?

Health history:
Does the patient have a family history of COPD or other chronic respiratory diseases?
How long has the patient had respiratory difficulty?
What is the pattern of symptom development?
Does exertion increase dyspnea? What type of exertion?
What are the limits of the patients tolerance for exercise?
At what times during the day does the patient complain most of fatigue and shortness of
breath?
Which eating and sleeping habits have been affected?
What is the impact of respiratory disease on quality of life?
What does the patient know about his disease?
Does patient has exacerbations or previous hospitalizations for respiratory problems?
Are comorbidities present?
How appropriate are current medical treatment?
2. What physical assessment findings do you expect to find? What specific changes in the
respiratory system do you expect to find indicative of emphysema?
Assessment findings include:
increased anterior-posterior diameter, or "barrel chest"
use of accessory muscles to assist breathing
tripod position
INSPECTION
shortness of breath common, especially on exertion
tachypnea
tactile fremitus decreased
PALPATION
Chest expansion decreased.
hyperresonant
PERCUSSION
decreased vesicular breath sounds
may have prolonged expiration
AUSCULTATION
muffled heart sounds from over distention of lungs
usually no adventitious sounds; occasional wheeze
3. What is the most common cause of emphysema? Based on this information, what
question will you ask about his health behaviors? What do you believe are the major
cause/s of M.Cs emphysema?

SMOKING IS A MAJOR CAUSE OF EMPHYSEMA

In the vast majority of people, smoking is the cause of emphysema.Exactly how smoki
ng destroys the air sac linings in the lungs isn'tknown. However, population studies show that s
mokers are about sixtimes more likely to develop emphysema than nonsmokers.
Estimates vary, but more than 24 million people in the U.S. likely have emphysema or
another form of COPD, and probably many of them don't know it. Emphysema and chronic
bronchitis are the third-leading cause of death in the U.S.

Interestingly, most heavy smokers do not develop emphysema. Why some smokers
get emphysema and others do not is unknown. All heavy smokers experience other negative
health effects of smoking, though.

ALPHA-1 ANTITRYPSIN DEFICIENCY

Besides smoking, the other major known cause of emphysema is alpha-1 antitrypsin
deficiency. However, this is a minor cause compared to smoking.
Alpha-1 antitrypsin (AAT) is a natural protein circulating in human blood. Its main
function is to keep white blood cells from damaging normal tissues. White blood cells contain
destructive substances they use to fight infections.
Some people -- perhaps 100,000 in the U.S. -- have a genetic condition that makes
them deficient in alpha-1 antitrypsin. Deficient levels of the AAT protein in the blood allow
normal white blood cells to continuously damage lung tissue. If people with AAT deficiency
smoke, the damage is even worse.
Over years, most people with severe AAT deficiency develop emphysema. It's not
known how many people have emphysema caused by AAT deficiency. Experts estimate that
about 2% to 3% of people with emphysema have AAT deficiency.
Emphysema in AAT-deficient patients has the same symptoms as emphysema
caused by smoking. However, people with AAT deficiency often develop emphysema at a
younger age. Liver problems may also occur in people with emphysema from AAT deficiency.

SECONDHAND SMOKE AND OTHER POTENTIAL CAUSES

Secondhand smoke may contribute to emphysema. Exposure to environmental
cigarette smoke is known to damage the lungs. Several studies suggest that people exposed
to high amounts of secondhand smoke are probably at higher risk for emphysema.
Air pollution is also believed to contribute to emphysema, although how much is
unknown. Most people are exposed to pollution, and emphysema takes years to develop,
making this effect hard to study.

In the ABOVE scenario, MCs condition was caused by his long exposure to cigarette.

4. Are M.C.s VS and SaO2 appropriate? If not, explain why.

Patients Vital signs are: 162/84mmHg, 124bpm, 36pm, 102 F, SaO2 88%.

Patients VS are all abnormal indicating that the patient was in exacerbation of his condition,
while his SaO2 is somewhat high this is due to bodys compensatory mechanism.

5. Is your patient with chronic hypoxia? Is he compensating for his chronic hypoxia?

Patient is evidently experiencing chronic hypoxia. Yes, patient is compensating as evidenced

by increased HR and increased RR.

TOBACCO SMOKE
Inflammation of the airway epithelium
Infiltration of inflammatory cells and cytokines
(neutrophils, macrophages, lymphocytes, leukotrienes and interleukins)

Increased protease activity with breakdown of elastin in connective tissues of the lungs
(Elastases, Cathepsins, etc.)

Destruction of alveolar septa and loss of elastic recoil of bronchial walls

EMPHYSEMA
Air Trapping

Over Distended Lungs

Loss of surface area for gas exchange

Total Lung Capacity and

Residual Volume

Insufficient alveolar ventilation

Alveolocapillary distribution
abnormality

Hyperexpansion of chest
Hypercapnia and
Hypoxemia

Barrel Chest

CHRONIC HYPOXIA
Central Chemoreceptors
(Ventrolateral Medullary Surface)

Peripheral Chemoreceptor
(Carotid and Aortic Bodies)

Chemoreceptor Relflexes

Use of Accessory muscles

Release of Epinephrine and

Norepinephrine

Increased Rate and

Depth of Breathing
Splenic Contraction
Hyperpnea
Respiratory Rate
(36 bpm)
Physical Activity

Release of stored RBC

in blood from the
spleen

Cardiac Stroke Volume

Heart Rate
(124 bpm)

Vasoconstriction

Basal Metabolic Rate

Blood Pressure
(162 / 84 mmHg)

Temperature
(38.9oC / 102oF)

Erythropoiesis
Erythrocytosis

ALL OF THESE changes in the Vital Signs are result of bodies

COMPENSATORY MECHANISM to hypoxia

6. Why is the O2 inhalation at 2LPM in spite of the SaO2 at 88%? How do we explain the
hypoxic drive in a pt. with emphysema? What important considerations do you have to
remember regarding O2 administration in a pt. with COPD like M.C.?
First things first. It is important to understand that Hypoxic Drive does exist, it is not a myth,
but the Hypoxic Drive Theory is a myth. So let me differentiate the two:
o

Hypoxic Drive: This is when a persons body relies on low levels of O2 to signal them
to breathe faster. A person without COPD normally relies on high levels of CO2 to
signal them to increase their breathing rate.
Hypoxic Drive Theory: When you give a person with COPD high concentrations of
O2, say 100% O2, it will cause their hypoxic drive (their need to breathe) to shut off
and they may stop breathing, go into respiratory failure, and die because of too much
oxygen.

According to Dr. John Hoyt in his article Debunking Myths of Chronic Obstructive Lung
Disease:
It is true that administration of oxygen to a patient with an exacerbated chronic obstructive lung
disease and acute respiratory failure may lead to an increased CO2. It is true that
the hypercarbia may become severe and be associated with cardiorespiratory arrest. The
problem is with interpreting the cause of the events

Both emphysema and chronic bronchitis patients may develop a hypoxic drive to breathe.
Healthy people get their drive to breathe from the amount of carbon dioxide in the blood.
Patients who have emphysema or chronic bronchitis build up consistently high levels of carbon
dioxide. Because of this, the body looks to the levels of oxygen, rather than carbon dioxide, to
determine the need to breathe. If oxygen levels are low, they breathe faster to get more oxygen.
Giving oxygen to a patient with hypoxic drive can be a problem. After oxygen is administered,
its level in the blood increases. In the patient with a true hypoxic drive, increased levels of
oxygen may signal the body to slow down or even stop breathing.
When you give a COPD patient O2, there are several ways in which it can increase CO2
according to Jeff Whitnacks The Death of Hypoxic Drive Theory:

Haldane Effect: Describes the property of Hbg. The idea to this is that if Hbg is carrying a lot
of O2 (oxygenated blood) then it has a lower capacity to carry CO2. It works in reverse too: if
Hbg is carrying very few O2 (deoxygenated blood) then it can take on more CO2.

Hypoxic Pulmonary Vasoconstriction (HPV): This occurs when the alveoli in the lungs are
poorly ventilated and causes the pulmonary arteries to constrict in order to divert more blood to
the oxygen starved alveoli to better ventilate it. However, if we give 100% O2 to the pt, it fools
our body, and this constriction does not happen, and CO2 will continue to build and be trapped
in the alveoli. This causes a V/Q mismatch and increase physiological dead space in some
patients (New, 2006).

The Most Important Mechanism

So we now know that Haldane Effect and HPV, which leads to V/Q mismatch and increase
in physiological dead space, plays a role in increasing CO2 within a COPD pt. But how big of
a role does it play? Well, according to Irven H Young:
worsening ventilation-perfusion mismatching and an accompanying increase in dead space
ventilation contribute about 50% of the increase in carbon dioxide levels.
Understanding these effects are important because it shifts our focus of the possible
exacerbation of respiratory failure in COPD patients from giving oxygen to CO2 being trapped.
We all know that if we dont get O2, we become hypoxic and we die. However, hypercapnia
develops at a slower rate than hypoxaemia (New. 2006). As Dr. Busko wonderfully
summarizes,
Hypoxia kills, hypercapnia happens.
So what does this all mean? It means we should give COPD pts high concentrations of O2
because they need it, but we should do something about the CO2 build up. We need to help
them blow off the CO2. We can do this by mechanical ventilation (Busko).
TOBACCO SMOKE
Inflammation of the airway epithelium
Infiltration of inflammatory cells and cytokines
(neutrophils, macrophages, lymphocytes, leukotrienes and interleukins)

Increased protease activity with breakdown of elastin in connective tissues of the lungs
(Elastases, Cathepsins, etc.)

Destruction of alveolar septa and loss of elastic recoil of bronchial walls

EMPHYSEMA
Loss of surface area for gas exchange
Alveolocapillary distribution abnormality
Co2 in the blood
Hypoxia / Hypercapnia
Chemoreceptor Reflex
(Central and Peripheral)
Activation of
Hypoxic Drive
HALDANE
EFFECT

HYPOXIC PULMONARY
VASOCONSTRICTION

Carbonic
Anhydrase

CO2 Diffuses to
RBC

Sympathetic Nervous
system stimulation

Carbonic acid

Release of Epinephrine and

Norepinephrine

Carbinohaemoglobin
Diffusion rate of CO2 from
the tissue
Deoxyhaemoglobin
Uptake of CO2 by the
RBC
Acidity

Respiratory center
trigered

Release of H+

CONTINOUS BREATHING

H+ binds to HCO3+
Creating Carbonic Water

Pulmonary Artery vasoconstriction

Blood goes to the O2 rich alveoli

Improved V/Q Ratio

ARTERIAL OXYGENATION
(SaO2 of 88 %)
Patient should be on a low level of O2 support to
continuously trigger this HYPOXIC DRIVES to
maintain oxygenation
Haldane Effect and Hypoxic Pulmonary
Vasoconstriction are both part of the Hypoxic
Drive

General points about oxygen therapy in chronic obstructive pulmonary disease:

The respiratory drive is normally largely initiated by PaCO 2 but in chronic obstructive
pulmonary disease (COPD) hypoxia can be a strong driving force and so if the hypoxia is
corrected then the respiratory drive will be reduced. There will also be a loss of physiological
hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross
alveolar hypoventilation.
Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can
have distinct benefits in the long-term.
Chronic hypoxaemia causes slowly progressive pulmonary with the development of right
ventricular hypertrophy and possible cor pulmonale with secondary polycythaemia.
Secondary polycythaemia increases blood viscosity and hence resistance to flow. There is also
sludging and a tendency to thrombosis.

7. Make an integrated pathophysiologic flowchart of MCs disease condition.

8. Given M.C.s history and your knowledge of pathophysiologic processes, explain the pathophysiologic basis of the assessment findings in M.C?
Note:
Numbers seven and eight will be discussed together by the below schematic diagram of the pathophysiologic basis of Emphysema and its manifestations.
TOBACCO SMOKING
Legend:
BOLD words: Present signs and symptoms
BLUE words: Laboratory and diagnostic tests
Green Words: Treatment
Red Words: Potential complications

Oxidative Toxins
Initiates immune and inflammatory response
Release of inflammatory Mediators from ALVEOLAR Macrophages
(IL-6, IL-1, IL-8 and TNF-; Metaloproteases)

Interleukins and TNF-

Metaloprotease

Recruit Neutrophils to the site

Damage to the surrounding tissue

(CHEMOTAXIS)
Secretes PROTEASES
(Elastases and Cathepsins)

Damage to the elastic fibres surrounding the alveoli and

terminal bronchioles

Recruits T-Lymphocytes

Collagen deposition

T-Cell Mediated Apoptosis

Fibrosis formation

Cells will have an unprogrammed

cell death

Irreversible enlargement of the air spaces

distal to the terminal bronchiole
Destruction of alveolar walls and septa and
loss of elastic recoil of bronchial walls
(EMPHYSEMA)
Page 11 of 21

Loss of fibrous and muscle tissue

Breakdown of Alveolar Elasticity
Dyspnea on
Exertion

Reduced pulmonary elastic recoil

Pulmonary
Function Test

Persistent inflammatory
response

End-expiratory (Residual) lung volume

Hyper resonance on Chest

Percussion

Bronchodilators

Dynamic Hyperinflation

Hyperactivity of
epithelial cells

Hyperactivity of
bronchi

Thick yellow
sputum
production

Bronchoconstriction
Air space adjacent to pleurae
(Blebs)

Over Inflated Lungs

Air Trapping
Hyperexpansion of
chest

Loss of Respiratory
Membrane
Ratio of Air to Lung
Tissue

Work of breathing

Reconfiguration of the
Low Flat Diaphragm
Widened retrospinal clear
Ventilation Perfusion Mismatch Airflow Limitation
Rib cage
(<7 anteriorly and <10
space
(V/Q Ratio of < 0.8 or <4/5)
posteriorly)
Ruptured Bullae
CTT
Horizontal
Barrel Chest
Ribcage
(AP / Transverse ratio: >1:2)
Spontaneous Pneumothorax
Hypercapnia / Hypoxemia

Diffusion Defects

Use of accessory
muscles

Number of Pulmonary
capillaries

Labored
Breathing

Right Ventricular Hypertrophy

(Cor Pulmonale)
Electrocardiography

Hypoxia

Chest X-Ray
Inability of the alveoli to recoil normally
after expanding

Pulmonary resistance
Tactile fremetus on
Palpation
Pulmonary
hypertension

Chest X-Ray

Large spaces within lung

parenchyma (Bullae)

Crackles

Pursed lip
Breathing

Appetite
Weight Loss
Hyperinflation of
alveoli

Glycogenesis

Gluconeogenesis

Energy Stores

Muscle Wasting

Fatigue
Diaphragmatic
function

Expectorants

Increased rate and

depth of breathing

Release of cathecolamines
and cortisol

Wheezing

Coughing Spells

Chemoreceptor reflexes

Impaired Glucose delivery

and use

Alveolar collapse on
expiration

Sputum C&S

Cough Reflex
triggered

Respiratory
Acidosis

Hyperpnea
Increased respiratory
Rate
ABG
Analysis

Page 12 of 21

Release of Epinephrine and

Norepinephrine

Basal Metabolic Rate

Splenic Contraction

Temperature
Erythropoeisis

CBC

Vasoconstriction

Cardiac Stroke Volume

Blood Pressure

Release of RBC from spleen into the

bloodstream

Heart Rate

Erythrocytosis

9. What are the possible complications of Emphysema and their manifestations?

I.

ACUTE EXACERBATIONS
Acute exacerbations are episodes that occur when airways suddenly become
obstructed and symptoms worsen. Such events are associated with inflammation in the
airways and are generally triggered by an infection in the airway or throughout the body.
Other factors that can trigger serious lung events:

Certain medications

Exposure to irritants in the air

Seasonal changes

Acute exacerbations include the following symptoms:

Increased volume of sputum
Sputum that is thicker and darker
Worsened shortness of breath that causes the patient to breathe faster and
harder. This is the most common and distressing acute symptom.
Acute exacerbations occur, on average, between two and three times a year in
patients with moderate-to-severe Emphysema. In about 80% of the cases, they are triggered
by infections. Smokers have more episodes than nonsmokers.

II.

REDUCED QUALITY OF LIFE AND MOOD

Nearly half of patients with Emphysema report a limitation in daily activities. They
have trouble walking up stairs or carrying even small packages. Breathing becomes hard work.
More than half of patients with Emphysema have insomnia. Such impairment in quality of life
can negatively affect mood.
Almost half of patients with Emphysema have anxiety, depression, or another
psychiatric disorder, compared with 31% of people in the general population. Women with
COPD are more susceptible to psychological problems than men. If patients with Emphysema
become anxious or depressed, they may have a poorer outlook than those without these
emotional problems. COPD patients with moderate-to-severe depression face a greater 3-year
mortality rate than those who experience less depression. Low oxygen levels also can impair
mental function and short-term memory. Psychological interventions may be particularly helpful
for people with COPD.

Page 13 of 21

III.

MALNOURISHMENT
People with Emphysema often lack good nutrition. Patients with chronic bronchitis
tend to be obese. Patients with emphysema tend to be underweight. Loss of weight and
muscle mass is associated with a poor outcome in Emphysema. Good nutrition improves the
ability to exercise, which in turn builds muscle strength and lung function. Obese patients with
Emphysema who lose weight sleep better.

IV.

HEART DISEASE
Over time, Emphysema causes low levels of oxygen (hypoxia) and high levels of
carbon dioxide (hypercapnia) in the body. In order to boost oxygen delivery, the body
compensates in a number of ways:

Blood vessels in the lung constrict to force blood and oxygen through the
circulatory system. This leads to high blood pressure in the lungs (pulmonary
hypertension).
More red blood cells are produced to increase the blood's oxygen-carrying
capacity.
The heart rate increases to pump more blood.
The rate of breathing increases.

Eventually these activities can lead to very serious and even life-threatening
conditions:

V.

Abnormally high blood pressure in the lungs can cause a complication called cor
pulmonale, in which the right ventricle of the heart enlarges, eventually leading to
heart failure.
Patients with prolonged and severe hypoxia and hypercapnia are at risk for acute
respiratory failure, which can cause heart rhythm abnormalities or other lifethreatening conditions.

OTHER SERIOUS MEDICAL PROBLEMS ASSOCIATED WITH COPD

The smoking that causes COPD is associated with high risks of pneumonia, lung
cancer, stroke, and heart attack. Tobacco smoke contains more than 400 substances, many of
which are oxidants, metals (such as lead, cadmium, and aluminum), and carcinogens. Nicotine
itself may not damage tissues, but it is the chemical that addicts the smoker to tobacco.

Sleep Disturbance. About half of all people with severe COPD experience sleep disorders
such as sleep-related hypoxia or insomnia. Nocturnal hypoxia, a lack of oxygen during sleep,
occurs when breathing is shallowest during rapid-eye-movement (REM) sleep. It may be due
to suppression of the cough reflex and a build-up of mucus. Nocturnal hypoxia is treated with
overnight oxygen therapy. As COPD worsens, many patients have trouble falling or staying
asleep. COPD patients should not use sleep medications. Nighttime oxygen or a change in
COPD medications from beta-agonists to anticholinergics can sometimes help restore restful
sleep.

Osteoporosis. Osteoporosis is a significant problem in patients with COPD. Many conditions

associated with COPD, including smoking, vitamin D deficiency, sedentary lifestyle, and the
use of corticosteroid medications put people at risk for bone density loss and osteoporosis.

Gastroesophageal Reflux (GERD). More than half of patients with severe COPD have
GERD, a condition in which stomach acids back up from the stomach into the esophagus.
However, many COPD patients don't report experiencing GERD symptoms such as heartburn.

10. Make a tabular comparison of the pathogenesis and pathophysiologic changes of

Emphysema, Bronchitis and asthma.
ASTHMA
Age at onset
Smoking history
Cough at Exacerbation
Sputum production
Allergy
Airway Inflammation
Main portion

At Any Age (usually <40

years)
Possible
Usually between 2 to 6am
Infrequent
Common

COPD
CHRONIC BRONCHITIS

EMPHYSEMA

Usually >40 Years

Usually >10 packs per year
Gradual Increase
Common
Possible
Infrequent

Large Airways
Basement membrane
Thickening

Small Airways (Bronchi)

Bronchial Biopsies

Th-2 dominant T Cells

Th-1 dominant T Cells

Reversibility (Peak
Flow Results)

Normalize with time

May improve but not

normalize

Non Reversible

common

Uncommon

Possible (Alpha1
Antitrypsin deficiency)

Normal
Resonant to hyper
resonant

Normal

Decreased

Resonant

Hyper Resonant

Normal to decreased
breath sound; wheezes

Decreased intensity of
breath sounds, usually
with prolonged expiration

Pathophysiology

Family History
Clinical Manifestations
Tactile Fremitus
Percussion
Auscultation
Productive Cough
Dyspnea
Wheezing
Barrel Chest
Prolonged Expiration
Cyanosis
Chronic Hypoventilation
Polycythemia
Cor Pulmonale

Wheezes
None
Common
Continuous
None
Not Present
Common
Hyperventilation
Uncommon
Uncommon

Fibrosis of Bronchi

Classic sign
Late in course

Intermittent
Occasionally
Always present
Common
Common
Common
Common

Small Airways (Alveoli)

Destruction of alveolar
wall
Neutrophils and
Proteases

Late in course with

infection

Common
Minimal
Classic
Always present
Uncommon
Late in Course
Late in Course
Late in Course

Release of Epinephrine and

11. Based on the assessment findings, identify five priority problems that M.C. may Norepinephrine
be
experiencing.
Priorities are:
a. Achieving Airway Clearance
b. Improving Breathing Patterns
c. Improving Activity Tolerance
d. Monitoring and Managing potential complications
e. Continuous assessment of the patient

Nursing Care Priorities:

f.

Impaired Gas exchange and airway clearance due to chronic inhalation of toxins
GOAL: Improvement in gas exchange

g. Impaired gas Exchange related to ventilation-perfusion inequality

GOAL: Improvement in gas exchange
h. Ineffective airway clearance related to bronchoconstriction, increased mucous
production ineffective cough, bronchopulmonary infections and other complications
GOAL: Achievement of airway clearance
i.

Ineffective breathing pattern related to shortness of breath, mucus, bronchoconstriction

and airway irritants
GOAL: Improvement in breathing pattern

j.

Activity intolerance due to fatigue, hypoxemia and ineffective breathing patterns

GOAL: Improvement in activity tolerance

The laboratory sends the ff. report several hours after admission: RBC 3.8thou/cmm, WBC13,000 thou/cmm, Hgb 12g/dL, ABGs: pH- 7.28, pO2 80 mmHg, pCO2 65 mmHg, HCO3 22.

12. Interpret the above results. How do the results relate to the pathophysiologic changes of
emphysema?

RBC: 3, 800, 000 cells/L (Normal Value: 4.7 to 6.1 million/ L)

Hgb: 12 g/dL (Normal Value: 13.5 17.5 g/dL)

Anemia of chronic illness is typically a normocytic anemia and is most commonly observed
in patients with concurrent infectious, and inflammatory or neoplastic diseases. COPD fulfills
the criteria of a chronic, inflammatory, multisystemic disease leading to the expectation
of anemia.
Anemia in COPD is an immune disorder that has been reported in numerous diseases with
an inflammatory component. Inflammatory cytokines have various effects that play a key role in
the pathogenesis of this form of anemia and ultimately interfere with the normal mechanisms of
erythropoiesis. The following possible mechanisms have been proposed:
1. Dysregulation of iron homeostasis caused by the accumulation and retention of iron
within cells of the reticuloendothelial system giving rise to a consequent decrease in available
iron for use by progenitor cells. The administration of IL-1 and TNF- has been shown to lead
to the development of hypoferremia in experimental animals.
2. Impaired proliferation of erythroid precursors. The most potent inhibitor is interferon- ,
although the free radicals generated by oxidative stress also have this effect. This
phenomenon can result in an increase in the apoptosis of these cells or a decrease in the
expression of EPO in their receptors.

3. Impaired bone marrow response to EPO caused directly by cytokines. IL-1 and TNF-
inhibit the expression of this hormone in vitro. Finally, the activation of these mediators may
stimulate the production of hepcidin, a recently discovered polypeptide synthesized in the liver
that participates in the process of iron absorption and is thought to play a key role in the
development of anemia of chronic disease.
COPD INFLAMMATION
Acute-Phase Reactants
(CRP,LDH, Fibrinogen)

Cytokine release
TNF-, IL-6, IL-8
Inhibition of Erythroid
precursors

Hepcidin

Inteference with the

action of EPO

Macrophage Iron
Sequestration

Inhibition of Iron
Absorption

Inhibition of
Erythropoiesis
RBC production
(3, 800, 000 cells/L)

ANEMIA
(Hgb: 12 g/dL)

ABGs: pH- 7.28, pO2 80 mmHg, pCO2 65 mmHg, HCO3 22.

Patient is experiencing Uncompensated Respiratory Acidosis a classic sign found in
patients with emphysema (see schematic diagram of the clinical manifestations).

Reference:
1.

AUTHOR;
SOURCE
Matthias John,
MD, PhD,
Soeren
Hoernig, MD

Agusti AG, Noguera A, Sauleda J, et al. Systemic effects of chronic obstructive pulmonary
disease. Eur Respir J 2003; 21:347360

TITLE
Anemia
and
Inflamm
ation in
COPD

PROBLEM
Although chronic
obstructive
pulmonary disease
(COPD) is
traditionally
associated with
polycythemia, its
systemic
inflammatory
components can
interfere with
erythropoietin and
result in anemia of
chronic disease.
Researchers
assessed the
frequency of
anemia and its
relation to serum
erythropoietin
(EPO) levels and
severity of the
disease in a group
of COPD patients.

SIGNIFICANCE TO
NURSING

SUMMARY OF FINDINGS

This study documents

The present study is

that anemia occurs relatively

limited by a relative small

frequently in COPD patients

number of patients. For

and is related to the presence

future investigations,

of inflammation. Anemia is an

larger study populations

understudied issue in COPD

are needed. This would

but may be of great importance

allow investigating

in this disease. In our cohort,

whether anemia is related

anemia (with hemoglobin

to the primary disease

concentrations < 12.0 g/dL in

process per se or to

women and < 13.5 g/dL in

secondary systemic

men) was present in as many

manifestations such as

as 13% of all COPD patients.

weight loss, loss of lean

This may be an

tissue mass, hypoxia, or

underestimation of the anemia

systemic inflammation.

prevalence, as we have
excluded patients with anemia
related to bleeding and known
folate or vitamin B12 deficiency.
Furthermore, anemic COPD
patients showed increased
levels of erythropoietin
compared to nonanemic
patients and normal control
subjects.

Anemia in COPD is
understudied. There are
no previous reports on
anemia frequency and
pathophysiology in
COPD. More detailed
investigations on
hematologic and clinical
parameters ( ie ,
prevalence of anemia in

Anemia of chronic illness is

COPD and its gender

typically a normocytic anemia

relatedness, exercise

and is most commonly

capacity, 6-min walk test)

observed in patients with

and prognosis are

concurrent infectious, and

required to provide

inflammatory or neoplastic

indications whether

diseases. COPD fulfills the

anemia is merely a

criteria of a chronic,

marker or a mediator of

inflammatory, multisystemic

pathophysiologic

disease leading to the

processes that may impair

expectation of anemia. While

physical functioning in

anemia in chronic heart failure

COPD. Interventions with

or renal insufficiency has been

erythropoietin and iron

frequently investigated, it is

supplementation would

understudied in COPD.

then seem very promising

The mechanism of anemia

development in COPD might
be similar to that in other
chronic diseases. It has been

in order to improve the

poor health status and
prognosis of patients with
COPD.

shown that mediators of the

immune and inflammatory
response, such as tumor
necrosis factor-, IL-6, and
interferon- are potentially
involved in the development of
anemia in chronic illness. The
increased levels of
inflammatory cytokines lead to
a shortened RBC survival, with
a demand for a slight increase
in RBC production. The bone
marrow cannot adequately
respond to the increased
demand for RBCs. This is
caused by a relative
erythropoietin resistance due
to an impaired ability of RBC
progenitors to respond to
erythropoietin. An impaired
mobilization of
reticuloendothelial iron stores
is an additional
pathophysiologic factor.
Monica J
Fletcher, Birthe
H Dahl

Expandin
g nurse
practice
in COPD:
is it key

The prevalence of
chronic obstructive
pulmonary disease
(COPD), a common

The nursing role in COPD and

essentially in all chronic diseases
is becoming increasingly important
and is characterised by continuity

Nurses represent an
appropriate resource to deliver
care and support to individuals
with COPD throughout the

to
providing
high
quality,
effective
and safe
patient
care?

and preventable
chronic disease, is
on the increase,
and so are the
financial and social
burdens associated
with it. The
management of
COPD is
particularly
challenging, as
patients have
complex health and
social needs
requiring life-long
monitoring and
treatment. In order
to address these
issues and reduce
the burden
imposed by COPD,
the development of
innovative disease
management
models is vital.
Nurses are in a key
position to assume
a leading role in the
management of
COPD since they
frequently
represent the first
point of contact for
patients and are
involved in all
stages of care.
Although evidence
is still limited, an
increasing number
of studies have
suggested that
nurse-led
consultations and
interventions for
the management of
COPD have the
potential to impact
positively on the

of care. Nurses are involved in the

management of COPD at all
stages, from prevention to provision
of end-of-life care within a variety of
settings, both in the community
(including patients own homes and
family practice) and hospitals.
Nurses often play a key role in new
care models based on different
types of telemedicine
support.5,6Nurse-led consultations
and disease management
interventions are important
interventions which enable nurses
to provide, complement, or extend
the care delivered by doctors.
Nurse-led consultations carried out
by experienced nurses frequently
include tasks that traditionally
belong to physicians, such as
physical examination of patients,
diagnosis and, in countries such as
the UK, prescription of medicines.
Nurse-led management
interventions are aimed at helping
patients cope with their condition
and improve their quality of life.
They include patient education,
guided self-management, smoking
cessation, and pulmonary
rehabilitation programmes.

entire course of the disease.

Even though more research is
needed to establish the
effectiveness of nurse-led
interventions and
consultations, there is some
growing evidence to
demonstrate the benefits
provided by these
interventions, particularly in
relation to the hospital-athome and early discharge
schemes, smoking cessation,
and pulmonary rehabilitation
programmes as well as
interventions aimed at
improving self-management
behaviour. Studies have also
shown that nurses are able to
deliver care that is as effective
as that provided by doctors.
However, a paucity of
standardised competencies
and specified training
requirements coupled with a
lack of clinical supervision,
appropriate funding, and
workload pressures among
nurses delivering COPD care
highlight specific areas for
improvement. Nurses need to
strengthen their role to plan
and deliver more strategies to
improve the quality of life of
patients with COPD and
reduce the burden of this
disease in the future. In doing
so, nurses cannot assume an
increased responsibility in
isolation. More coordinated
efforts and better mentorship
and support from colleagues,
along with a formal recognition
of their new role, is needed to
allow nurses to provide highquality, safe, and cost-effective
care and, in that way, to
optimise the use of limited

health and quality

of life of patients.
The role of nurses
in the management
of COPD around
the world could be
significantly
expanded and
strengthened.
Providing adequate
educational
opportunities and
support to nurses,
as well as
addressing funding
issues and system
barriers and
recognising the
importance of the
expanding roles of
nurses, is vital to
the well-being of
patients with longterm medical
conditions such as
COPD and to
society as a whole,
in order to reduce
the burden of this
disease.

healthcare resources
worldwide.