COPD:
Prevention, Identification &
Management
Dr. Kenya V. Beard Ed.D. CNE GNP-BC NP-C ACNP-BC
K Beard & Associates, LLC President
Hunter College, Assistant Professor
KBeard@hunter.cuny.edu
Objectives
Discuss the role of the nurse in caring for
clients with COPD
Compare and Contrast Emphysema and
Chronic Bronchitis
COPD
4th Leading cause of death in the Untied States
COPD mortality rate has increased over the
last 30 years
Malnutrition- Found in up to 1/3rd of individuals
with COPD
 Adversely affects exercise tolerance, surfactant
production, protein synthesis, and it increases
morbidity and mrotality.
Role of Pulmonary System:
Ventilation
 Gases must move into and out of the lungs
 Ventilatory rate measures how many times gas is
inhaled and exhaled over one minute
 Minute volume aka minute ventilation represents
the ventilatory rate x tidal volume (volume of air
per breath)
 Why is CO2 elimination necessary?
 How does the health care professional determine
whether ventilation is adequate?
Pulmonary System
 Bring oxygen to alveoli, diffuse oxygen into and
carbon dioxide out of blood
 Alveoli- Functional unit of the respiratory system
 Gas Exchange Airways
 Respiratory bronchioles
 Alveolar ducts
 Alveoli (primary gas-exchange unit)
 Alveolar Capillary Membrane
Alveoli Facts
 Adult lungs contain about 300 million alveoli
 Alveoli type 1 cells for structure and type II cells for
surfactant
 Surfactant is needed to prevent lung collapse
 helps alveoli expand during inhalation
 reduces surface tension at end-expiration
 Pulmonary capillaries surround the alveoli
 Alveolar macrophages ingest foreign matter
Pulmonary Capillaries
 Pulmonary Artery (Receives blood from right
ventricle)
 Pulmonary Vein (Blood sent to left atrium)
 Pulmonary Capillaries
 Wall has an endothelial layer & thin basement
membrane
 Capillary basement membrane can fuse with
alveolar membrane
Alveolocapillary membrane
 Site for gas exchange
 Made up of alveolar and capillary basement
membrane (& both endothelium and interstitial
space)
 Very fragile (blood or plasma could leak into
alveolar space)
 Gas exchange is impaired if any disorder thickens
the membrane
Chronic Obstructive Pulmonary Disease
 Disease state characterized by the presence of
irreversible airflow limitation due to chronic
bronchitis or emphysema
(American Thoracic Society)
 A preventable and treatable disease that’s usually
progressive and associated with a chronic
inflammatory response. It is not fully reversible.
(Global Initiative for Chronic Obstructive Lung Disease,
2011)
What’s the biggest risk factor for
COPD?
1.
2.
3.
4.
Poor ventilation in the home
Tobacco smoke
Car exhaust fumes
Occupational exposure
Risk Factors
 Tobacco smoke (includes environmental tobacco
smoke)
 Indoor air pollution (biomass fuel used in poorly
vented dwellings)
 Occupational dusts and chemicals (irritants, fumes
or vapors)
 Outdoor air pollution (contributes to burden but
small effect in causing COPD)
Consider COPD whenever a
patient has
Chronic mucous production
History of exposure to risk factors
A chronic cough
Dyspnea
CHAD should be Screened
COPD Diagnosis
 Spirometry test
 Results must indicate
 Post-bronchodilator FEV1/FVC <0.70 (confirms
that a persistent airflow limitation exists)
Spirometry
 Forced vital capacity (FVC) – the amount of air that is
exhaled from full inhalation to full exhalation (shows us
the respiratory muscle strength and ventilatory reserve)
 Forced expiratory volume in the first second (FEV1) –
the amount of air that is blown out as hard and fast as
possible in the first second of the forced exhalation
following full inhalation (is effort dependent)
 FEV1/FVC shows us airflow obstruction.
 Peak expiratory flow (PEF) – fastest airflow rate that’s
achieved at any time during exhalation
In order to establish a diagnosis of
COPD the patient would
1. Need to have a chronic cough for at least
3 months
2. Need to have an arterial blood gas done
3. Need to have a spirometry test performed
4. Need to have an abnormal ventilatory
rate
Chronic Bronchitis
The presence of chronic cough
 Hypersecretion of sputum production
Exists for at least 3 months over 2 consecutive
years
Not always associated with airflow limitation
Increased incidence in smokers
Major health problem for adults
Chronic Bronchitis: Step by Step
Irritants increase mucus production (thick and tenacious)
Increase in mucus glands and goblet cells
Bacteria enjoy sticky coating (allows them to embed and
reproduce rapidly)
Streptococcus pneumoniae, Haemophilus influenzae
Impaired ciliary function
Bronchial walls thicken
Permanent narrowing of airways
Airways collapse in early expiration
Gas trapping in distal parts of the lung
Tidal volume decreases, hypoventilation and hypercapnia
Chronic Bronchitis:
Clinical Manifestations
Decrease in exercise tolerance (exercise
induced hypoxemia)
Wheezing
SOB
May have a smoker’s cough
Decreased FEV1
Increase occurrence of pulmonary infections
Emphysema
Permanent enlargement of gas exchange
airways (respiratory bronchioles, alveolar
ducts and alveoli = acinus)
Alveolar wall destruction (Loss of elastic
recoil)
One of the many structural abnormalities
that could exist in a patient with COPD
Emphysema: Alpha Antitrypsin
Alpha antitrypsin deficiency (enzyme that
inhibits the action of proteolytic enzymes. In
the lungs these proteolytic enzymes can
destroy lung tissue if unchecked.
Individuals with this deficiency who smoke have
a greater risk for developing emphysema than
those who don’t have the deficiency
Emphysema: Step by Step
 Secondary emphysema usually initiated by cigarette smoke
(toxins cause airway epithelial inflammation)
 Inflammatory cells infiltrate epithelium
 Cytokines released which increase protease activity
 (elastases, cathepsins and matrix metalloproteases)
 Elastin within the septa is broken down by proteases
 Septal destruction eliminates parts of the pulmonary
capillary bed and reduces elastic recoil of airways
 VQ mismatching and hypoxemia results
 Air trapping results in chest hyperexpansion & increase work
of breathing
Emphysema: Clinical
Manifestations
 Dyspnea on exertion
 Could progress to dyspnea at rest
 Little coughing and sputum produces
 Patients are usually thin
 Tachypnea with prolonged expiration (May note pursed
lip breathing)
 Accessory muscles used
 AP diameter greater than transverse diameter
 Percussion note changes to hyperresonant
What happens as a result of the
loss in airway elastic recoil?
1. It becomes difficult for the patient to exhale and
patients need more energy to exhale
2. Volume of air exhaled passively decreases so
residual volume increases
3. Alveoli become hyperinflated and bullae (large
air spaces in the lung parenchyma) develop
4. All of the above
Respiratory Assessment
History & Physical Exam
Ask the patient if they smoke or if they’ve experienced
any chest pain, shortness of breath (dypsnea),
wheezing, cough, hemoptysis) If so get the DeTAILS
(duration, type, associated factors, influencing
factors, location and severity)
Note the following
Inspect: note chest shape (AP diameter >)
Palpate: fremitus decreased with COPD
Percuss: hyperresonance
Auscultate: adventitious sounds (wheezing or ronchi)
Nursing Diagnosis
 Impaired Gas Exchange r/t alveolar-capillary
membrane changes, decreased size of airway, or
hypersecretion of mucus, ventilatory muscle fatigue
 Ineffective Breathing Pattern r/t airway obstruction or
decrease in energy
 Ineffective Airway Clearance r/t fatigue, ineffective
cough or hypersecretion of mucus.
 Imbalanced Nutrition: Less than Body Requirements r/t
anorexia or fatigue
 Activity Intolerance r/t fatigue, difficulty breathing, O2
imbalance
Goal
Relieve symptoms
Improve exercise tolerance
Prevent disease progression
Prevent exacerbations
Reduce mortality
Determining Severity of COPD
Symptoms- use questionnaires like the COPD
Assessment Test
Degree of airflow limitation- Use the GOLD Criteria
for mild, moderate, severe, very severe (FEV1 >
80% predicted, 50-50, 50-30, less than 30)
Risk of exacerbations- increases with increased
airflow limitation & hx of previously treated events
Comorbidities- osteoporosis, anxiety, skeletal
muscle dysfunction, lung ca
How is COPD Managed?
Quit smoking and encourage tobacco-control policies
Emphasize primary and secondary prevention
Increase physical activity
Bronchodilators (prn or regular basis)
Inhaled corticosteroids (FEV1 < 60% predicted)
Influenza vaccine recommended annually
Pneumococcal vaccine recommended for pts over 65
Mucolytic Agents may be helpful
Management
 Oxygen Therapy
 Indicated for severe hypoxemia in order to prevent
Cor Pulmonale (PaO2 , 55 mmHg) or O2 sat <88
 Must be administered carefully if pt has CO2
retention along with severe hypoxemia
central chemoreceptors are no longer the primary
breathing stimulus. Peripheral chemoreceptors are in
charge and they are sensitive to PaO2 changes. If
PaO2 exceeds 60mmHg the stimulus to breathe will
decrease and the PaCO2 will increase- apnea results.
What happens if an adequate
oxygenation level can’t be achieved
without causing respiratory
depression?
1.
2.
3.
4.
Patient goes on a ventilator
Patient is referred to hospice
Patient is given morphine sulfate
Patient is given a respiratory stimulant
Which of the following statements
by a client with COPD suggests
that teaching has been effective?
1. “I will get a pneumococcal vaccine every year”
2. “I will perform sedentary activities to prevent
disease exacerbation”
3. “I will notify my health care provider if I notice
that I’m more short of breath”
4. “I will try to take slow shallow breaths when
performing breathing exercises”
References
 Global Initiative for Chronic Obstructive Lung Disease.
(2011). Global Strategies for diagnosis, management and
prevention of COPD. Retrieved from
http://www.goldcopd.org/uploads/users/files/GOLD_Pocket_
May2512.pdf
 McCance, K. L., Huether S. E., Brashers, V. LO. & Rote, N.
S. (2010). Pathophysiology: The biologic basis for disease in
adults and children. 6th ed. Missouri: Mosby Elsevier.