“
COPD/Bronchitis
Lauren Lowe, Tami Pohorenec
Just breathe………….
”
Chronic Obstructive Pulmonary Disease (COPD)
Bronchitis
 COPD is a progressive, preventable and non-reversible disorder with
systemic manifestations characterized by air flow limitation, inflammation of
the airways, cough and mucous production (Maclay, Rabinovic, & Macnee, 2009, p.533)
 It is progressive in nature and worsens over time. COPD can be treated but
not cured (Rabe et al., 2007 p.53)
 Chronic Bronchitis and Emphysema are subsets of COPD. Chronic Bronchitis
is inflammation of the airways in the lungs accompanied with
mucous/sputum production, lasting most days for more than 3 months of
the year and is recurrent at least two years in a row (Kim & Criner, 2013, p.228)
 Chronic Bronchitis is associated with increased morbidity and mortality due
to decline in lung function (Kim & Criner, 2013, p. 228)
Pathophysiology
 With COPD Inflammation and mucous cause airway narrowing which limits
airflow (Rabe et al., 2007, p.534)
 With emphysema parenchymal tissue is destroyed- especially in long term
smokers (Rabe et al., 2007, p.534)
 Cigarette smoking, exposure to noxious gases, causes narrowing of central
and peripheral airways. Inflammation and irritation leads to increased
mucous production and changes to the pulmonary vasculature (“COPD”,
n.d., p.2)
 T cells- TH1, TH2 and TH17 are associated with mucous metaplasia which is
mucous production in response to inflammatory signals. Smoking,
environmental toxins, bacterial and viral illnesses stimulate these cells and
mucous production. People with COPD/Bronchitis have trouble clearing
these secretions because of poor ciliary function, distal airway congestion,
fibrosis, ineffective cough, weak respiratory muscles and low peak
expiratory flow ( Kim & Criner, 2013, p.229)
 There is an increase in inflammatory response and stress in the lungs of people
with COPD leading to an increase in circulating antibodies, stimulation of the T
cells activating protein kinases which in turn leads to inflammation and mucous
production (Maclay et al., 2008, p. 535
 Cannabis and tobacco exposure (direct and indirect), air pollution, A1antitrypsin deficiency, occupational exposure ( like fireman and smoke,
carpenters and dust) viral infections, bacterial infections like severe
pneumonias/respiratory infections at a young age lead to impaired gas
exchange as well as obstructed airways and destruction of the parenchyma (
“5 miniute consult”,n.d., p.1)
 A1-antitrypsin deficiency is a rare inherited genetic disorder leading to
increased inflammation (Maclay, et al., 2008 p.535)
 Weak elastic recoil of the lungs, narrowed airways, increased mucous
production a1-antitrypsin disorders, cigarette use, all lead to COPD (Dunphy,
2011)
 Alpha 1 antitrypsin is responsible for neutralizing a substance called neutrophil
elastase which prevents inflammatory lung tissue damage. If this enzyme is
lacking,damage to lung tissue occurs and neutrophils produce increased
mucous. This rare genetic condition affects smokers and non smokers equally
(“COPD”, n.d.)
(U.S. National Library of Medicine, 2014)
Incidence
 Emphysema is a major cause of disability in the United States. Males are affected more than Femalesthough that is starting to equalize due to both genders engaging in tobacco use. Emphysema is typically
seen in individuals older than 40 (Hensley & Hollier, 2011)
 1.7 million people have Emphysema (Hensley & Hollier, 2011)
 <1% have a1 antitrypsin deficiency, the remaining have alveolar destruction of unknown etiology (Hensley &
Hollier, 2011)
 COPD has a high morbidity and mortality rate resulting in high direct and indirect costs
(Gupta et al., 2013 ,p. 229)
 More than 5% of adults are affected, it is the 12th leading cause of morbidity and 4th leading cause of
death in the U.S. and globally. COPD is most common in those over age 65 with a 41% increase in the
number of cases in the U.S. since 1985 (“COPD”, n.d., p.2)
 Chronic Bronchitis is common in the general population but is even more common in those with COPD.
14.2 million people have COPD, 12.5 million have chronic bronchitis with the average mean age of the
patient being over age 50 (Hensley & Hollier, 2011)
 Morbidity is less early in the disease face and increases as the disease progresses, as age increases and
when accompanied by comorbid conditions (Rabe et al. , 2007, p.535)

“A diagnosis of COPD should be considered in those with dyspnea, chronic cough, sputum production and a
history of exposure/disease risks (Rabe et al., 2007, p. 537)
Screening and Risk Factors
 Those exposed to environmental factors such as noxious fumes, cooking over
open fires, firefighters, those working with asbestos, construction workers with
dust exposure, inhalant exposure, cigarette smokers and those exposed to
second hand smoke should be screened for COPD especially if they have a
cough, dyspnea and sputum production (Gupta et al., 2013)
 Advanced age, genetic factors such as a1- antitrypsin deficencies that lead to
emphysema, being of lower socioeconomic status increase risk factors for
COPD (“COPD”, n.d., p.2)
 Men and women are now at equal risk. (Rabe et al., 2007)
 A history of severe childhood respiratory infections in childhood and a low birth
weight are associated with a higher risk of COPD as does Pneumonias in early
life (Rabe et al., 2007)
 Chronic poorly controlled respiratory allergies also increases risk for COPD
(Hensley & Hollier, 2011)
Clinical Findings
 Cough is a symptom that leads many to seek healthcare evaluation and I s a symptom of COPD
(Dunphy, 2011,p. 331)
 Chronic Bronchitis is the most common type of COPD and is defined as cough lasting more than 3
months of the year for two or more years (Dunphy, 2011, p. 332)
 Chronic cough, sputum production, shortness of breath acute and chronic occurring at rest and
with activity (Dunphy, 2011, p. 334)
 Barrel chest, poor air movement, wheezing, crackles, hypoxia, tachypnea, distended neck veins,
lower extremity edema, fatigue, headache, cyanosis, clubbing, hepatosplenomegaly and
heptojugular reflux are common findings in COPD (“COPD”,n.d., 2011, p.1)
 Symptoms typically begin in the 6th decade of life, cough is worse in the A.M., increased sputum,
dyspnea, increased respiratory rate, prolonged expiratory phase, right sided heart failure and
secondary polycythemia are noted in COPD (Hensley & Hollier, 2011, p. 576)
(Muniz, 2014)
Differentials
 Some of the differential diagnoses to consider include
-asthma
-Lung CA
-CHF
-Acute Viral Illness
-Bronchiectasis
-Normal aging of the lungs
-Tuberculosis
-Sleep Apnea
-Bronchiolitis
- Chronic Pulmonary Embolism
-Upper airway disorders
-Reactive airway disorder
-Chronic sinusitis
-Mesothelioma
-GERD
-Asbestosis
-ACE inhibitor use
- Cystic fibrosis (rule out in young adults)
(“COPD”, n.d., p. 4) (“5 minute consult”, n.d., p.1) (Hensley & Hollier, 2011) (Dunphy, 2011, p.334) (Gupta et. al., 2013 p. 229)
Social Environmental
- Tobacco use/ Cigarette smoking is leading cause of bronchitis/COPD (“Bronchitis”, 2014)
- IV drug use (cocaine, meth, Heroin) causes damage to the pulmonary vasculature from
The insoluble fibers in the drug from the fillers used such as talc, cornstarch etc.(“COPD”, n.d., p.1)
- As discussed before those with exposure to cigarette smoking active and secondary, noxious
fumes, gases, smoke/fire, asbestos ( Kim & Criner, 2013, p.228)
-COPD is costly. The direct costs in the U.S. in 2006 was 18 billion and the indirect costs was 14 billion
(Rabe et al., 2007, p. 536)
Labs and Diagnostics
Acute Bronchitis
-Generally diagnosed clinically based on history, symptomology/physical exam
-PFTs can be helpful in recurrent bronchitis to r/o asthma (Evensen, 2010, pp.607-613)
-Chest x-ray- will be normal with acute bronchitis can r/o
pneumonia/complications
-Sputum Culture/Sensitivity if Chest X-ray is abnormal
-Influenza testing
(Domino et al., 2014)
Image (WebMD, 2010)
Labs and Diagnostics
COPD
- Pulmonary Function Tests/Spirometry: not during an acute exacerbation, shows
little response with bronchodilators.
COPD Staging - Mild: FEV1>80%, Moderate: FEV1 50-80%,
Severe: FEV1 30-50% Very Severe: FEV1<30% (Domino et al., 2014)
-Oximetry- low
C X-ray- Hyperinflation
ABGs- PaCO2 >50 mmHg and/or PaO2 of <60 mmHg (Sharifaba & Parsons, 2014)
-Chronic Bronchitis: Bacteria colonization airways, increased secretory cells,
thickened small airways, mucous plug
-Emphysema- Bronchi usually with no secretions, alveoli enlargement, entire lung
affected
CBC- elevated HCT, increased WBC
Sleep Study- nocturnal hypoxemia (Domino et al., 2014)
Acute Bronchitis Treatment
Pharmacological
-Antipyretics: ibuprofen, asa, apap
-Antibiotics: if pathogen is present/significant comorbidities: *antibiotics not usually
recommended most cases viral* Amoxicillin or Azithrimycin shown to be most
effective. Doxycycline is Mycoplsma suspected, Quinolone for elderly with comorbidities.
-Systemic Steroids: treat if severe bronchospasm, Prednisone- short course
-Inhaled Beta Agonist: for cough with bronchospasm, Albuterol
-Cough Suppressants (not with COPD pts): guaifensiin, dextromethorphan
Non-Pharmacological
-Smoking cessation, avoid second hand smoke
-Steam/Vaporizers
-Increase Fluids and Rest
(Domino et al., 2014)
COPD
Treatment
Pharmacological
First Line Tx:
Short Acting Beta Agonist- as needed for rescue inhaler, Albuterol
Anticholinergics- titropripium (Spiriva), use one inhalation per day
(and/or) Long-Acting Beta Agonists- Salmeterol (Serevent) use one inhalation per
day/Combination- Ipatropium & Albuterol (Combivent) (Domino et al., 2014)
Second Line tx:
Inhaled Corticosteroids-try if moderate-severe
Combination LABA + inhaled Corticosteroid- Fluticasone/Salmeteral (Advair)
Systemic Corticosteroids- prednisone, not recommended for long term monotherapy
Sympathomimetic- Theophylline, can give up to 400mg/day, monitor levels (Evensen, 2010, pp.607-613)
Adjuncts:
Home Oxygen- if trending oximetry is less than or equal to 88%, 2-3L NC (Fitzgerald, 2010, p.101)
Mucolytic Agents can help with secretions, Guaifenesin
Antibiotics- Bactrim DS, doxycycline, Augmentin- decrease inflammation in acute
exacerbation/severe infection
Non-Pharmacological
-Smoking cessation
-Hydration
-Influenza/Pneumonia Vaccines
-Pulmonary Rehabilitation
-High protein diet
Complications
Acute Bronchitis: Pneumonia, acute respiratory failure, hemoptysis, chronic
cough, asthma exacerbation in pts with asthma
-Treated outpatient unless elderly, complications of underlying comorbidities
-Inpatient Criteria- severe bronchospasm, hypoxia, underlying lung dx,
dehydration
COPD- Malnutrition, infections, polycythemia, ARF, pneumothorax, arrhythmias, cor
pulmonale, pulmonary HTN, poor sleep quality
-Outpatient tx unless hypoxemia or hypercarbia, underlying comorbidities
-Inpatient – Give 02, short acting bronchodilators, antibiotics, and systemic steroids
recommended, If AFR-possible mechanical ventilation needed
(Domino et al., 2014)
Follow Up
 Acute Bronchitis:
-Cough may persist for several weeks, usually self-limited with complete
resolution within 6 weeks (Domino et al., 2014)
-If smoker, continue reinforcing cessation
-Metered-dose Inhaler technique education (Hueston, 2014)
 COPD:
-
F/U with chest x ray if pneumonia caused exacerbation
-
Recommended pulmonary rehab to improve respiratory muscles
-
See severe COPD patients monthly, stable pts can be see q 6 months
-
If using oxygen at home, monitor O2 sats frequently, ABGs yearly or with
condition change, PFTs every 3 years
-
When on stable dose of Theophylline- check level q 6-12mos
(Domino et al., 2014)
Counseling and Education
 Acute Bronchitis
Increase fluids to 3 to 4 Liters/day
Cough may linger for weeks
Smoking Cessation (Domino et al., 2014)
 COPDHigh protein diet, this can improve hypercarbia
Avoid traveling at high altitudes
Educate proper inhaler use, technique, not using LABA for rescue
Advance directive conversation
Educate on getting pneumonia and flu vaccinations
Regular Physical Activity can decrease exacerbations (Domino et al., 2014)
Education on tapering systemic corticosteroids
Respiratory Hygiene: avoiding pollution, smoking, allergens, people with
respiratory infections (Evensen, 2010, pp.607-613)
Consultation and Referral
 Acute Bronchitis:
-If recurrent in children, consider asthma(Domino et al., 2014)
-Refer for complications (Pneumonia/ARF), existing COPD, Cough >3 months
(Hueston, 2014)
 COPD:
-Refer if frequently hospitalized, one severe exacerbation, less than 40 years old, weight loss
or rapid disease progression
-Surgical- lung reduction or transplantation in individualized cases (Domino et al., 2014)
-Pumlonary Rehabilitation Program- Exercise, Strength Training, Medication/Disease
Education (Sharifaba & Parsons, 2014)
Patient Resources:
COPD Foundation
American Lung Association
Multiple Choice Questions with
Answers and Rationales
1.
When should a chest x ray be obtained in a patient with COPD?
a) Every year to monitor lung capacity
b) When trying to r/o pneumonia during an exacerbation
c) After a pt complains of shortness of breath after climbing stairs
Answer B Rationale Chest x rays can r/o pneumonia in suspecting
patients, but should not be used as a part of a routine yearly work up or
for normal expected symptoms such as shortness of breath with exertion.
2. A patient is having an acute bronchospasm, the nurse practitioner
informs the best medication to use first is Advair
A)True
B)False
Answer F, Rationale- Long acting beta agonists should not be
used as first line treatment of bronchospasm, a short acting beta
agonist should be used as a rescue inhaler.
3. The diagnosis COPD includes all but which conditions?
a)Chronic bronchitis
b)Emphysema
c)Acute Bronchitis
d)Refractory Asthma
Answer C, Rationale- Acute bronchitis is not considered COPD it
is usually resolved within 6 weeks without permanent symptoms,
refractory asthma is nonreversible and is included along with
emphysema nad chronic bronchitis in the umbrella of COPD.
4. Which medication is indicated for a patient with COPD at any
stage of severity?
a) Theophylline
b) Advair
c) Serevent
d) Albuterol
Answer: A, Rationale- Short acting beta agonists are indicated for
all COPD patients by the GOLD COPD guidelines.
5. A 50 year old male has a mild COPD exacerbation, what
treatment would be the most appropriate first choice?
a)Rifampin
b)Short acting beta agonist and anticholinergic
c)Doxycyline
d) Z-Pack
Answer- B, Rationale- Using Short acting beta agonists or using a
combination of anticholinergics and short acting beta agonists is the
first step of outpatient therapy. Antibiotics are useful in reducing
mortality in moderate to severe COPD patients.
6. The leading risk factor in developing COPD is
a) coal mining
b) smoking
c) Having seasonal allergies
Answer B, Rational, smoking is the number one leading
risk factor in developing COPD
7. Acute Bronchitis is usually bacterial in origin so
antibiotics should be given to every patient
a)True
b)False
Answer False, Rational, The leading causes of acute bronchitis are
rhinovirus, RSV, adenovirus, influenza, and parainfluenza. Bacteria is
a rare cause.
8. A patient diagnosed with acute bronchitis calls your office and
says she has not stopped coughing for three weeks, your best
response would be?
a) You should get to the ED right away
b) The cough should last for about 4 months, so get used to it.
c) That is normal, a cough can persist up to 6-8 weeks. If it is
interfering with your daily activities or causing shortness of breath, a
cough suppressant and inhaler can help.
Answer C, Rationale-Most patients with acute bronchitis have a
cough for greater than two weeks and less than 4 weeks, but it can
last up to 6-8 weeks.
9. The most common characteristic prominent in early chronic
bronchitis is
a) excessive mucous production
b) alveolar stenosis
c) bronchodilation
Answer A, rationale- People with chronic bronchitis have a cough with
excessive mucus production most days for 3 months a year for 2 consecutive
years.
10) Theophylline is not used frequently due to
A) its narrow therapeutic index
B) need continuous for drug level monitoring
C) it has been shown have only marginal therapeutic effects on patients
d) all of the above
Answer D, Rationale, Theophylline has a mild anti-inflammatory
effect and causes some bronchodilation, but needs to be
monitored closely d/t its narrow therapeutic window.
References
Domino, F. J., Baldor, R. A., Golding, J., & Grimes, J. A. (Eds.). (2014). The 5-minute clinical
consult (22nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Evensen, A. (2010). Management of copd exacerbations. American Family Physician. 81(5),
607-613.
Fitzgerald, M. (2010). Nurse practitioner certification examination and practice preparation.
(3rd Ed.) Philadelphia, PA: F.A. Davis Company.
Hueston, W. (2014). Acute bronchitis. Epocrates Online. Retrieved September 27, 2014 from
https://online.epocrates.com/noFrame/showPage?method=diseases&MonographId=135&
ActiveSectionId=11
Sharifaba, M., & Parsons, J. (2014). COPD. Epocrates Online. Retrieved September 27, 2014
from
https://online.epocrates.com/noFrame/showPage?method=diseases&MonographId=7&A
ctiveSectionId=11
WebMD. (2010). Lung disease and respiratory health. Retrieved September 27, 2014 from
http://www.webmd.com/lung/acute-bronchitis
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
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