COPD

Case Study

Submitted by:

Maria Pia Faith Q. Reasonda, RN

I.

Introduction
Chronic obstructive pulmonary disease (COPD) is a disease state characterized by

airflow limitation that is not fully reversible. This newest definition COPD, provided by the
Global Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that
better explains this disorder and its signs and symptoms(GOLD, World Health Organization
[WHO] & National Heart, Lung and Blood Institute [NHLBI], 2004). Although previous
definitions have include emphysema and chronic bronchitis under the umbrella classification
of COPD, this was often confusing because most patient with COPD present with over
lapping signs and symptoms of these two distinct disease processes.
COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic
bronchitis) or any combination of these disorders. Other diseases as cystic fibrosis,
bronchiectasis, and asthma that were previously classified as types of chronic obstructive lung
disease are now classified as chronic pulmonary disorders. However, asthma is now considered
as a separate disorder and is classified as an abnormal airway condition characterized primarily
by reversible inflammation. COPD can co-exist with asthma. Both of these diseases have the
same major symptoms; however, symptoms are generally more variable in asthma than
in COPD.
Currently, COPD is the fourth leading cause of mortality and the 12th leading cause of
disability. However, by the year 2020 it is estimated that COPD will be the third leading cause
of death and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People
with COPD commonly become symptomatic during the middle adult years, and the incidence
of the disease increases with age.
II.

Anatomy and Physiology

The respiratory system consists of all the organs involved in breathing. These include the

nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very
important things: it brings oxygen into our bodies, which we need for our cells to live and

function properly; and it helps us get rid of carbon dioxide, which is a waste product of cellular
function. The nose, pharynx, larynx, trachea and bronchi all work like a system of pipes through
which the air is funneled down into our lungs. There, in very small air sacs called alveoli,
oxygen is brought into the bloodstream and carbon dioxide is pushed from the blood out into the
air. When something goes wrong with part of the respiratory system, such as an infection like
pneumonia, chronic obstructive pulmonary diseases, it makes it harder for us to get the oxygen
we need and to get rid of the waste product carbon dioxide. Common respiratory symptoms
include breathlessness, cough, and chest pain.

The Upper Airway and Trachea

When you breathe in, air enters your body through your nose or mouth. From there, it
travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe)
before entering your lungs. All these structures act to funnel fresh air down from the outside
world into your body. The upper airway is important because it must always stay open for you
to be able to breathe. It also helps to moisten and warm the air before it reaches your lungs.
The Lungs
Structure

The lungs are paired, cone-shaped organs which take up most of the space in our chests,
along with the heart. Their role is to take oxygen into the body, which we need for our cells to
live and function properly, and to help us get rid of carbon dioxide, which is a waste product.
We each have two lungs, a left lung and a right lung. These are divided up into lobes, or big
sections of tissue separated by fissures or dividers. The right lung has three lobes but the left
lung has only two, because the heart takes up some of the space in the left side of our chest. The
lungs can also be divided up into even smaller portions, called bronchopulmonary segments.
These are pyramidal-shaped areas which are also separated from each other by
membranes. There are about 10 of them in each lung. Each segment receives its own blood
supply and air supply.

COPD VERSUS HEALTHY LUNG

How they work

Air enters your lungs through a system of pipes called the bronchi. These pipes start from
the bottom of the trachea as the left and right bronchi and branch many times throughout the
lungs, until they eventually form little thin-walled air sacs or bubbles, known as the alveoli. The
alveoli are where the important work of gas exchange takes place between the air and your
blood. Covering each alveolus is a whole network of little blood vessel called capillaries, which

are very small branches of the pulmonary arteries. It is important that the air in the alveoli and
the blood in the capillaries are very close together, so that oxygen and carbon dioxide can move
(or diffuse) between them. So, when you breathe in, air comes down the trachea and through the
bronchi into the alveoli. This fresh air has lots of oxygen in it, and some of this oxygen will
travel across the walls of the alveoli into your bloodstream. Traveling in the opposite direction
is carbon dioxide, which crosses from the blood in the capillaries into the air in the alveoli and
is then breathed out. In this way, you bring in to your body the oxygen that you need to live, and
get rid of the waste product carbon dioxide.

Blood Supply
The lungs are very vascular organs, meaning they receive a very large blood supply. This
is because the pulmonary arteries, which supply the lungs, come directly from the right side of
your heart. They carry blood which is low in oxygen and high in carbon dioxide into your lungs
so that the carbon dioxide can be blown off, and more oxygen can be absorbed into the
bloodstream. The newly oxygen-rich blood then travels back through the paired pulmonary
veins into the left side of your heart. From there, it is pumped all around your body to supply
oxygen to cells and organs.
The Work of Breathing
The Pleurae
The lungs are covered by smooth membranes that we call pleurae. The pleurae have two
layers, a visceral layer which sticks closely to the outside surface of your lungs, and a

parietal layer which lines the inside of your chest wall (ribcage). The pleurae are important
because they help you breathe in and out smoothly, without any friction. They also make sure
that when your ribcage expands on breathing in, your lungs expand as well to fill the extra
space.
The Diaphragm and Intercostal Muscles
When you breathe in (inspiration), your muscles need to work to fill your lungs with air.
The diaphragm, a large, sheet-like muscle which stretches across your chest under the ribcage,
does much of this work. At rest, it is shaped like a dome curving up into your chest. When you
breathe in, the diaphragm contracts and flattens out, expanding the space in your chest and
drawing air into your lungs. Other muscles, including the muscles between your ribs (the
intercostal muscles) also help by moving your ribcage in and out. Breathing out (expiration)
does not normally require your muscles to work. This is because your lungs are very elastic, and
when your muscles relax at the end of inspiration your lungs simply recoil back into their
resting position, pushing the air out as they go.
The Respiratory System and Ageing
The normal process of ageing is associated with a number of changes in both the
structure and function of the respiratory system. These include:
A. Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaning
that there is less area for gases to be exchanged across. This change is sometimes referred
to as senile emphysema.
B. The compliance (or springiness) of the chest wall decreases, so that it takes more effort to
breathe in and out.
C. The strength of the respiratory muscles (the diaphragm and intercostal muscles)
decreases. This change is closely connected to the general health of the person.
All of these changes mean that an older person might have more difficulty coping with
increased stress on their respiratory system, such as with an infection like pneumonia, than a
younger person would.
PREDISPOSING FACTORS

Risk factors for COPD include environmental exposures and host factors. The most
important risk factor for COPD is cigarette smoking. Other risk factors are pipe, cigar, and
other types of tobacco smoking. In addition, passive smoking contributes to respiratory
symptoms and COPD. Smoking depresses the activity of scavenger cells and affects the
respiratory tracts ciliary cleansing mechanism, which keeps breathing passages free of inhaled
irritants, bacteria, and other foreign matter. When smoking damages this cleansing mechanism,
airflow is obstructed and air becomes trapped behind the obstruction. The alveoli greatly
distend, diminished lung capacity. Smoking also irritates the goblet cells and mucus glands,
causing an increased accumulation of mucus, which in turn produces more irritation, infection,
and damage to the lung. In addition, carbon monoxide (a by product of smoking) combines with
hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin
cannot carry oxygen efficiently.
A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that
protects the lung parenchyma from injury. This deficiency predisposes young people to rapid
development of lobular emphysema, even if they do not smoke. Genetically susceptible people
are sensitive to environmental factors (eg. Smoking, air pollution, infectious agents, allergens)
and eventually developed chronic obstructive symptoms. Carriers of this genetic defect must be
identified so that they can modify environmental risk factors to delay or prevent overt
symptoms of disease

III.

Epidemiology
According to the World Health Organization, COPD is the fourth leading cause of death

in the world, with approximately 2.75 million deaths per annum, or 4.8% of deaths. COPD
affects twice as many males as females but this difference will diminish, given the fact that
more and more females throughout the world have taken up smoking in the past few years in
developed countries, and that nonsmoking females are exposed to biomass combustion products
in developing countries. However, the studies based on spirometric measurements are somewhat
skewed.
Active smoking is the main risk factor for COPD. The risk attributable to active smoking
in COPD is thought to vary from 40% to 70% according to the country. Active smoking by
females during pregnancy will also alter fetal lung development and be responsible for asthma
in predisposed children. Among children whose parents have a low respiratory function (last
quintile), 37% will have a comparatively low respiratory function. Conversely, among children
whose parents have a normal or high respiratory function, 41% will have a normal function. At
present, only a severe deficit in 1-antitrypsin, responsible for the PiZZ phenotype, is a proven
genetic causal factor.
COPD is a disorder that includes various phenotypes, the continuum of which remains
under debate. The major challenge in the coming years will be to prevent onset of smoking
along with early detection of the disease in the general population.
IV. Pathophysiology (see separate paper)
V. Personal Profile
Name: OC
Sex: Female
Address: Quezon city
Age: 77 y/o
Nationality: Filipino
Religion: Roman catholic
Dialect: Tagalog
Date of Admission: 6/29/16
Chief Complaint: Difficulty of breathing
Admitting Diagnosis: ARF secondary to Pneumonia, COPD, BAIAE
8

Final Diagnosis:
VI. Assessment

PSYCHOSOCIAL
SIGNIFICANT OTHERS: Son and Daughter in law
COPING MECHANISMS: Flight.
RELIGION: Roman Catholic
PRIMARY LANGUAGE: Tagalog
OCCUPATION: n/a

LEVEL OF CONSCIOUSNESS:
ORIENTATION: Oriented to time, date and place.
MEMORY: Intact
SPEECH: n/a (Patient on Mech Vent)
NONVERBAL BEHAVIOR: Patient uses pen and paper for communication.

REST AND ACTIVITY

CURRENT ACTIVITY LEVEL: currently confined in bed due to mechanical
ventilator, with 2 point restraints as precautionary measures for possible self extubation.
ADLs: According to patient, she spends most of her time doing cross stitch or travelling
out of the country
SLEEP: 7-8 hours a day
POSTURE: n/a
GAIT: n/a
MOTOR:

FINE: good

GROSS: good
RANGE OF MOTION:

MUSCLE STRENGTH:

Right Leg: 5/5

Left Leg: 5/5

Right arm: 5/5

Left arm: 5/5

PAIN: 0/10
SAFE ENVIRONMENT
ALLERGIC REACTIONS ON:

MEDICATION: n/a

FOOD: seafood, chicken, egg, nuts

TEMPERATURE:

RATE: 37.5deg

ROUTE: Tympanic

OXYGENATION:
AIRWAY CLEARANCE: noted thick yellowish sputum upon suctioning
RESPIRATIONS:
RATE: 21cpm
LUNG SOUNDS: noted wheezes and crackles on both lungs
COLOR:
SKIN: fair
Nails: pinkish
LIPS: (-) cyanotic
CAPILLARY REFILL: 1-2 seconds
BLOOD PRESSURE: 128/86mmHg
NUTRITION
HOSPITAL DIET: NPO for possible extubation
IVF: D5lr 1L to run for 8 hours while on NPO
HEIGHT: 153 cm
WEIGHT: 80 kg
BMI: 31.2

Classification: Obese class 1

VII. History of Present Illness
4 days PTA patient has productive cough, nasal congestion and self medicated with
Lagundi. No noted difficulty of breathing and no chest pain.
2 days PTA, cough and cold presented accompanied by intermittent fever temporarily relieved by
Biogesic and Bioflu.
4 hours PTA, after moving her bowels she noted difficulty of breathing. No oxygen support was
given. Patient did nebulize with Salbutamol however, patient still experiences severe dyspnea
prompted her daughters to bring her to ER.
VIII. History of Past Illness
Patient is diagnosed with asthma 25 years ago and despite the condition, she was a
smoker for 30 years already consuming 1 pack per day and not compliant to her asthma
maintenance for the her reason that her face is getting fat. She also had Coronary Angiography
last August 2014 when she was rushed to TMC-ER due to chest pain and difficulty of breathing;
results showed single vessel coronary artery disease, 20-30% stenosis at mid-segment and 7080% ostial stenosis at the septal perforator branch. This prompted her to have regular check up
with Dr. H, a cardiologist.
IX. History of family Illness

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 Father had asthma.

Eldest daughter died from breast cancer at age of 41.
X. Course In The Ward
4 days PTA patient has productive cough, nasal congestion and self medicated with
Lagundi. No noted difficulty of breathing and no chest pain.
2 days PTA, cough and cold presented accompanied by intermittent fever
temporarily relieved by Biogesic and Bioflu.
4 hours PTA, after moving her bowels she noted difficulty of breathing. No oxygen
support was given. Patient did nebulize with Salbutamol however, patient still
experiences severe dyspnea prompted her daughters to bring her to ER.
Admissi
on:
6/29/16
9:30 PM

Patient is drowsy, has tight air entry, audible crackles noted, with thick
yellowish phlegm and distended neck veins. O2sat = 95% at 6LPM/min
oxygen. Furosemide 40mg/IV, Atrovent 1 nebule, Hydrocotisone
100mg/IV given still no improvement. ABG = Respiratory acidosis (pH =
7.0)
Start Piperacillin Tazobactam (Piptaz) 4.5g IV now then every 8
hours
Hydrocortisone (Solucortef) 100mg IV every 8 hours
Dr. R ordered intubation with mechanical ventilation settings to AC mode
Fi02 = 100%, BUR = 16, PEEP = 5,PF = 60, TV = 400

10:30
PM

11PM

6/30/16

Chest x-ray done after intubation to check ET level.

ABG done 1 hour after intubation
Folley catheter inserted
NGT inserted
ETA GS/CS done
Head of bed elevated at 45deg
Admit to ICU
ABG results in:
pH = 7.086
pCO2 = 83.2
HCO3 = 5.2
O2sat = 97.3
fiO2 decreased to 80%
Patient is agitated
Precedex drip started 200mcg/2ml to make 50 ml PNSS, started
at .2mcg/kg/hr. (max dose of 0.7mcg/kg/hr) to maintain riker score
of 4.
Hypotension noted 90/50mmHg. Referred back to Dr. H. Hypotension due

11

Day 2
12 AM

12:15
AM

to post-intubation.
Nebivolol and Olmesartan put on hold.
PNSS 300 ml fast drip
Feeding started Nutren 1,600 kcal 1:1 dilution divided into 6 equal
feedings with 30 ml flush pre and post feeding.
ABG results in:
pH = 7.330
pCO2 = 41.3
HCO3 = 22
O2sat = 99.9
Decrease fiO2 to 40%

12:30
AM

BP: 70/40
PNSS 300ml fast drip

1:15 AM

Wheezing noted on both lungs

Mech Vent settings changed to CPAP mode PSV = 18, PEEP = 5,
fiO2 = 35%
Regular suctioning done
Add Azithromycin 500mg IV every 8 hours to start at unit
BP: 95/60
HR: 77
O2sat: 99%
PNSS 500ml fast drip
Atorvastatin increased to 40mg/tab once a day

2 AM

Patient transferred to ICU.

Budesonide started 500mg nebulization every 12 hrs
Mech vent shifted to AC mode fiO2 = 35%, IP = 15, IT = 0.75, BUR
= 10, PEEP = 5, FT = 1
NPO for now due to possible extubation
Hold precede at 6am
Shift to CPAP mode at 6am, PS = 18, PEEP = 5, fiO2 = 35%

7 AM

CPAP mode.

7:10 AM

PS decreased to 5
Observe for 1 hour
Noted thick yellowish secretions per ET. Ronchi and bilateral crackles
noted. PS increased to 10. Deferred exubation for now. IVF shifted to
D5LR x 125ml/hour while on NPO. Start feeding at 1pm.

3 PM

NPO at 5am tomorrow morning. Increase PS to 14.

12

11 PM

Patient has less secretion per ET. Not dyspneic, no subjective complaints,
awake and follows commands.
Decrease PS to 10 now then decrease PS by 1 every hour targeting
PS of 5 by 5am.

07/01/1
6
Day 2
8 AM

Patient extubated, NGT and folley catheter removed. Monitor patient for
respiratory distress. Hook patient to oxygen support via nasal cannula at
2LPM. May continue feeding in small amounts. If ok with all APs may
transfer to regular room.

10 AM

Last dose of Azithromycin tomorrow

5 PM

Patient was transferred to regular room 15th floor

XI. Drug Study

Generic name: Hydrocortisone
Brand name: Solu-cortef
Classification: Corticosteroids
Action: Glucocorticoid; elicits mild mineralocorticoid activity and moderate anti-inflammatory
effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing
migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, and reversing capillary
permeability
Indication: status asthmaticus
Contraindication:
Allergy to any component of the drug
Fungal infections
Immunosuppression
Renal insufficiency
Adverse effects:
GI: diarrhea, pancreatitis
INTEG: rash, pruritus, oral candidiasis
Hypotension
Fluid retention
Cardiac arrhythmias
Increase CBG
Nursing consideration:
Do not give live vaccines with immunosuppressive doses of hydrocortisone.
Give daily before 9am to mimic normal peak diurnal corticosteroid levels.
Space multiple doses evenly throughout the day.
Do not give IM injections if patient has thrombocytopenic purpura.
Monitor blood sugar levels
Accurate input and output monitoring
Observe patient for signs of infection
13

Generic name: Ipratopium + Salbutamol Nebule

Brand name: Combivent
Classification: Anticholinergic (parasympatholytic) agent;
Action: Inhibits vagally mediated reflexes by antagonizing acetylcholine action; prevents
increase in intracellular calcium concentration caused by interaction of acetylcholine with
muscarinic receptors on bronchial smooth muscle
Indication: Bronchodilator formaintenance therapy of bronchospasm.
Contraindication: hypersensitivity to atropine or its derivatives
Adverse effects:
CNS: dizziness, blurred vision
GI: nausea, dry mouth
Respi: dyspnea, broncho spasms, horseness
CV: palpitations, chest pain
Nursing consideration:
Monitor the patients vital signs, noting hypotension and an irregular or abnormal pulse.
Maintain a quiet, comfortable environment to minimize anxiety and perhaps decrease
palpitations.
Teach the patient pursed-lip breathing, diaphragmatic breathing, and chest splinting
Generic name: Furosemide
Brand name: Lasix
Classification: Loop Diuretic
Action: Inhibits the reabsorption of sodium chloride from the ascending limb of the loop of
Henle, leading to a sodium-rich diuresis.
Indication: Edema associated with Congestive heart failure (CHF), Hypertension
Contraindication: allergy to furosemide, sulfonamides. Use cautiously with diabetes
mellitus/with metabolic disorders.
Adverse effects:
CNS: dizziness, fever, vertigo, tinnitus
CV: arrhythmias, orthostatic hypotension
GI: nausea, vomiting, constipation
GU: frequent urination, nocturia
Nursing consideration:
Check BP before giving the medication
Monitor sodium and potassium serum electrolytes.
Give early in the day so that increased urination will not disturb sleep.
Accurate input and output monitoring
Generic name: Piperacillin Tazobactam
Brand name: Piptaz
Classification: Antiinfective; Beta-lactamantibiotic; Anti-pseudomonal penicillin

14

Action: Antipseudomonal penicillin plus beta-lactamase inhibitor, inhibits biosynthesis of cell

wall mucopeptide synthesis by binding to 1 or more of the penicillin-binding proteins and is
effective during active-multiplication stage.
Indication: nosocomial pneumonia
Contraindication:
Hypersensitivity to penicillins, cephalosphorins, or other drugs.
Safety in children< 12 years old
Pregnancy and lactation
Persons with thromobocytopenia, renal insufficiency and seizure
Adverse effects:
CNS: headache
GI: diarrhea
INTEG: rash, pruritus, jaundice, oral candidiasis
Intertistial nephritis
Cardiac arrythmias
Nursing consideration:
Obtain history of hypersensitivity topenicillins, cephalosphorins, or other drugs prior to
administration.
Obtain specimen for culture and sensitivity prior to first dose of the drug.
Start drug pending results. Periodic CBC with differential, platelet count,
Hgb & Hgt, and serum electrolytes.
Monitor for hypersensitivity response.
discontinue drug and notify physician if allergic response noted.
Monitor for hemorrhagic manifestations because high dose may induce coagulation
abnormalities.
Instruct family/significant others to report significant, unexplained diarrhea.
Monitor vital signs because of cardiac arrhythmias, hypertension and fever as adverse
reactions.
Generic name: Azithromycin
Brand name: Zithromax
Classification: Macrolide antibiotic, Pregnancy Category B
Action: Binds to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of
peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest; does not
affect nucleic acid synthesis.
Indication: Treatment of LRIs: Acute bacterial exacerbations of COPD due
to H. influenzae, Moraxella catarrhalis, S. pneumoniae; community-acquired pneumonia due
to S. pneumoniae, H. influenzae
Contraindication:
Hypersensitivity to azithromycin, erythromycin, or any macrolide antibiotic.
Use cautiously with gonorrhea or syphilis, pseudomembranous colitis, hepatic or renal
impairment.
Pregnancy and lactation
Adverse effects:
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CNS: Dizziness, headache, vertigo, somnolence, fatigue

GI: Diarrhea, abdominal pain, nausea and vomiting
Other: Superinfections, angioedema, rash, photosensitivity, vaginitis
Nursing consideration:
Take the full course prescribed. Do not take with antacids. Take with food if GI upset
occurs.
You may experience these side effects: Stomach cramping, discomfort, diarrhea; fatigue,
headache (medication may help); additional infections in the mouth or vagina (consult
with health care provider for treatment).
Report severe or watery diarrhea, severe nausea or vomiting, rash or itching, mouth sores,
vaginal sores.
Administer on an empty stomach 1 hour before or 23 hr after meals. Food affects the
absorption of this drug.

XII. Laboratory Diagnosis

ABG @ ER
pH = 7.086
paCO2 = 83.2
PaO2 = 133.4
HCO3 = 25.2
O2sat= 92.3%
Interpretation: Uncompensated Respiratoy Acidosis

Hemoglobin
Hematocrit
Platelet Count
WBC

Result

Normal ranges

Interpretation

134 g/l
0.44
293
22.5/L

120-160 g/l
F 37.0-47.0
140-440 x 10 g/L
4.3-10.0 x 10 g/L

N
N
N
Infection

Presence of slight toxic granules in some neutrophils

Lactate(6/29/16)
3.79
0.50-2.20
high
inadequate amount of oxygen in cells and tissues (hypoxia).
HS Troponin-I(6/30/16)

2,938
< or = 15.6 pg/ml
Indicates some degree of damage to the heart.

high

B-type Natriuretic
482.20
<100 pg/ml
high
Peptide(6/30/16)
Level of BNP in the blood increases when heart failure symptoms worsen.

16

Blood CS 2 sites (6/30/16)

No growth after 24 hours of incubation

XII. Nursing Care Plan

ASSESSMENT

DIAGNOSIS

PLANNING

INTERVENTIONS

EVALUATION

S/O
Thick
yellowish
sputum upon
suctioning
Elevated temp
38.0deg
Increased
WBC &
neutrophils

Infection r/t
chronic
respiratory disease
process evidenced
by thick
secretions &
increased
neutrophil count

Patient will have

no futher s/sx
of respiratory
infection after
antibiotic
treatment as
evidence by WBC
normalize,
afebrile temps,
and nonmucopurulent
sputum

Monitored for signs

of infection

Patient showed no
further signs and
symptoms
of infection during
stay in hospital.

Administered
antibiotics as
ordered
Suctioned secretions
every hour and as
needed.
Monitored patient
and kept O2sat
normal
Kept patient
thermoregulated
Oral care done
Turning every 2
hours done

ASSESSMENT

DIAGNOSIS

PLANNING

INTERVENTIONS

EVALUATION

S/O
Thick
yellowish
sputum
ABG result
showed
Uncompensate
d Respiratory
Acidosis

Ineffective airway
clearance r/t thick
secretions in
bronchi and
obstructed airway
as evidence by
hypoxemia and
dypsnea

Pt will
demonstrate
improved
ventilation and
adequate
oxygenation with
in normal
parameters as
evidenced by
blood gas levels
before extubation

Monitored RR,
depth, and effort,
use of accessory
muscles, and
abnormal breathing
patterns.

Patient not
dyspneic, less
secretions noted
after every
suctioning, O2sats
remained at 9798%

Pt will maintain
clear lung fields

17

Auscultated breath
sounds for presence
of crackles, wheezes
may signify airway
obstruction, leading
to or exacerbating
existing hypoxia.

Patient not in
distress within
course of
intubation.

and remain free of

signs of
respiratory
distress
throughout
hospital stay

Observe sputum,
noting
characteristics
Monitored pts
behavior and mental
status for onset of
restlessness,
agitation, confusion,
and extreme
lethargy.
Changes in behavior
and mental status
can be early signs of
impaired gas
exchange
Monitored O2sats,
connect patient to
continuous pulse
oximeter.
Observed for
cyanosis of the skin;
especially note color
of the tongue and
oral mucous
membranes.

ASSESSMENT

DIAGNOSIS

PLANNING

INTERVENTIONS

EVALUATION

S/O
Thick
yellowish
sputum
ABG result
showed
Uncompensate
d Respiratory
Acidosis

Impaired Gas
Exchange

Patient will be
able to maintain
adequate gas
exchange as
evidenced by
stable blood gas
values and normal
respiration

ABG done 1 hour

after intubation

ABG 1 hour post

intubation = O2sat
= 99.9%

Monitored
mechanical
ventilator settings
Hooked patient to
continuous pulse
oximeter and
monitore O2sat
Raised head of bed
to 30-40deg
Kept patient calm
Suctioned secretions

18

No further signs of
desaturation and
dyspnea

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