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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:
How far can you walk, and how many steps can you climb before having to stop
because of shortness of breath?
Coughing:
Social History:
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 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?
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.
In the ABOVE scenario, MCs condition was caused by his long exposure to cigarette.
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?
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.)
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
Vasoconstriction
Blood Pressure
(162 / 84 mmHg)
Temperature
(38.9oC / 102oF)
Erythropoiesis
Erythrocytosis
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).
Increased protease activity with breakdown of elastin in connective tissues of the lungs
(Elastases, Cathepsins, etc.)
HYPOXIC PULMONARY
VASOCONSTRICTION
Carbonic
Anhydrase
CO2 Diffuses to
RBC
Sympathetic Nervous
system stimulation
Carbonic acid
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
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.
Oxidative Toxins
Initiates immune and inflammatory response
Release of inflammatory Mediators from ALVEOLAR Macrophages
(IL-6, IL-1, IL-8 and TNF-; Metaloproteases)
Metaloprotease
(CHEMOTAXIS)
Secretes PROTEASES
(Elastases and Cathepsins)
Recruits T-Lymphocytes
Collagen deposition
Fibrosis formation
Persistent inflammatory
response
Bronchodilators
Dynamic Hyperinflation
Hyperactivity of
epithelial cells
Hyperactivity of
bronchi
Thick yellow
sputum
production
Bronchoconstriction
Air space adjacent to pleurae
(Blebs)
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
Hypoxia
Chest X-Ray
Inability of the alveoli to recoil normally
after expanding
Pulmonary resistance
Tactile fremetus on
Palpation
Pulmonary
hypertension
Chest X-Ray
Crackles
Pursed lip
Breathing
Appetite
Weight Loss
Hyperinflation of
alveoli
Glycogenesis
Gluconeogenesis
Energy Stores
Muscle Wasting
Fatigue
Diaphragmatic
function
Expectorants
Release of cathecolamines
and cortisol
Wheezing
Coughing Spells
Chemoreceptor reflexes
Alveolar collapse on
expiration
Sputum C&S
Cough Reflex
triggered
Respiratory
Acidosis
Hyperpnea
Increased respiratory
Rate
ABG
Analysis
Page 12 of 21
Splenic Contraction
Temperature
Erythropoeisis
CBC
Vasoconstriction
Blood Pressure
Heart Rate
Erythrocytosis
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
Seasonal changes
II.
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.
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.
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.
COPD
CHRONIC BRONCHITIS
EMPHYSEMA
Large Airways
Basement membrane
Thickening
Bronchial Biopsies
Reversibility (Peak
Flow Results)
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
Common
Minimal
Classic
Always present
Uncommon
Late in Course
Late in Course
Late in Course
Impaired Gas exchange and airway clearance due to chronic inhalation of toxins
GOAL: Improvement in gas exchange
j.
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?
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
Macrophage Iron
Sequestration
Inhibition of Iron
Absorption
Inhibition of
Erythropoiesis
RBC production
(3, 800, 000 cells/L)
ANEMIA
(Hgb: 12 g/dL)
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
future investigations,
of inflammation. Anemia is an
allow investigating
process per se or to
secondary systemic
manifestations such as
This may be an
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
relatedness, exercise
required to provide
inflammatory or neoplastic
indications whether
anemia is merely a
criteria of a chronic,
marker or a mediator of
inflammatory, multisystemic
pathophysiologic
physical functioning in
frequently investigated, it is
supplementation would
understudied in COPD.
Expandin
g nurse
practice
in COPD:
is it key
The prevalence of
chronic obstructive
pulmonary disease
(COPD), a common
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
healthcare resources
worldwide.