Obstructive Pulmonary Diseases

Chapter 28
Obstructive Pulmonary Diseases
Copyright © 2020 by Elsevier, Inc. All rights reserved.

Asthma
Copyright © 2020 by Elsevier, Inc. All rights reserved. 2

 Asthma
• 38% higher in blacks than whites
• Hispanics, especially from Puerto Rico have higher rates of asthma
and age-adjusted death rates than all other racial and ethnic groups
• Black females have the highest mortality rates from asthma

Asthma Definition
 Heterogeneous disease characterized by a combination of
bronchial hyperresponsiveness with reversible expiratory
airflow limitation
 Signs and symptoms may vary
 Clinical course can be unpredictable

Significance
 Affects about 20.4 million adult Americans
 1.7 million ED visits/year
 Incidence increasing but mortality decreasing
 Gender differences
 More men affected before puberty; more women in adulthood
 Women more likely to be hospitalized
 Higher mortality in women

Risk Factors for Asthma and
Triggers of Asthma Attacks
See Table 28-1
 Related to patient (e.g., genetic factors)
 Related to environment (e.g., pollen)

Triggers of Asthma
Nose and Sinus Problems
 History of allergic rhinitis common
 Treatment improves symptoms
 Acute and chronic sinusitis might make asthma worse
 Inflammation of mucous membranes can precipitate an
asthma attack; need to treat
 Large polyps need to be removed

Triggers of Asthma
Respiratory Tract Infections
 Major precipitating factor of an acute asthma attack
 Acute infection—reduced airway diameter and increased
airway hyperresponsiveness
 Viral-induced changes may exacerbate asthma

Triggers of Asthma
Allergens
 Role in development of asthma unclear
 Cockroaches
 Animal dander
 Dust mites
 Fungi
 Pollen
 Molds

Triggers of Asthma
Cigarette Smoke
 Smokers with asthma have:
 Faster decline in lung function
 Increased severity
 More visits to HCP
 Decreased response to treatment
 CDC estimates 21% of patients with asthma smoke

Triggers of Asthma
Air Pollutants
 Can trigger asthma attacks—role unclear
 Wood smoke
 Vehicle exhaust
 Concentrated pollution
• Heavily populated areas
• More industry
• Climate conditions

Triggers of Asthma
Occupational Factors
 Occupational asthma—most common job-related
respiratory disorder
 Exposure to diverse irritating agents
• Include: wood dusts, laundry detergents, metal salts, chemicals,
paints, solvents, and plastics
 May take months or years of exposure
 Arrive at work well, but experience a gradual decline

Triggers of Asthma
Exercise
 Exercise-induced asthma (EIA) or exercise-induced
bronchospasm (EIB) is induced or exacerbated during
physical exertion
 Airway obstruction occurs with changes to mucosa from
hyperventilation, cooling or rewarming air, and capillary
leakage
 EIA: pronounced during activity
 EIB: occurs after vigorous exercise

Triggers of Asthma
Drugs and Food Additives (1 of 2)
 Asthma triad: nasal polyps, asthma, and sensitivity to
aspirin and NSAIDs
 Wheezing develops in about 2 hours, also see rhinorrhea,
congestion, tearing, and angioedema
 Salicylic acid and NSAIDs—must avoid
• Found in many OTC drugs, foods, beverages, and flavorings

Triggers of Asthma
Drugs and Food Additives (2 of 2)
 β-Adrenergic blockers—bronchospasm
 ACE inhibitors—cough
 Sulfite-containing preservatives
 Eyedrops, IV corticosteroids, inhaled bronchodilators
 Fruits, beer, wine, and salad bars (prevent oxidation)
 Tartrazine (yellow dye no.5)

Triggers of Asthma
Gastroesophageal Reflux Disease
 GERD more common in persons with asthma
 Reflux may trigger bronchoconstriction as well as cause
aspiration
 Asthma medications may worsen GERD symptoms (2-
agonists relax lower esophageal sphincter)
 Treating GERD may reduce nocturnal asthma

Risk Factors and Triggers
 Genetics-inherited component is complex
 Atopy—genetic predisposition to develop IgE-mediated
response to common allergens is a major risk factor
 Immune response–hygiene hypothesis
 Baby’s immune system must be conditioned to function
properly; exposure to microbes

Triggers of Asthma
Emotional Stress
 Asthma is not psychosomatic
 Psychologic factors/stress can worsen symptoms
 Extreme behavioral expressions leads to hyperventilation and
hypocapnia leads to airway narrowing (bronchoconstriction)
 Attacks can trigger panic, stress, and anxiety

Case Study (1 of 26)
 A.D., a 30-year-old woman, comes to the emergency
department with severe wheezing, dyspnea, and
anxiety.
 She recently had a cold that did not resolve.
 She is upset that her children had just brought home a
stray cat.
 She does not know if she is allergic to the cat.

Pathophysiology (1 of 5)
 Main pathophysiologic process is inflammation
 Exposure to allergens or irritants triggers the inflammatory
cascade involving a variety of inflammatory cells
 Inflammation leads to bronchoconstriction,
hyperresponsiveness, and edema of airways leads to limited
airflow

Fig. 28-1 Pathophysiology of Asthma

 Early-phase response—30 to 60 minutes after exposure to
allergen or irritant
 Mast cells release inflammatory mediators when an allergen
cross-links IgE receptors
 Mediators include: leukotrienes, histamine, cytokines,
prostaglandins, and nitric oxide

Fig. 28-2 Early Phase Response of
Asthma Triggered by Allergen

 Inflammatory mediators effect:
 Blood vessels—vasodilation and increased capillary
permeability (runny nose)
 Nerve cells (itching)
 Smooth muscle cells (bronchial spasms and narrowed
airway)
 Goblet cells—mucus production

Fig. 28-3 Factors Causing Obstruction

 Late-phase response
 Airway inflammation occurs within 4 to 6 hours after initial
attack due to influx and activation of more inflammatory cells
• Occurs in about 50% of patients
• Symptoms can be more severe than early phase and can last
for 24 hours or longer
 Corticosteroids are used to treat inflammation

 A.D. has been in the emergency department for 2
hours.
 She is now breathing a little easier and wants to go
home.

 Remodeling
 Structural changes in bronchial wall from chronic
inflammation
• Changes include: fibrosis, smooth muscle hypertrophy, mucus
hypersecretion, angiogenesis
• Progressive loss of lung function not fully reversible results in
persistent asthma

Clinical Manifestations (1 of 5)
 Characteristic manifestations: wheezing, cough, dyspnea,
and chest tightness
 Hyperinflation and prolonged expiration due to air trapping in
narrowed airways
 Acute attack—wheezing is most common
 Initially expiration, then with progression, both inspiration and
expiration

 Wheezing—unreliable to gauge severity of attack (must
move air to make the sound)
 Mild attack—may have loud wheezing
 Severe attack—wheezing with forced expiration or no
wheezing at all

 Decreased or absent breath sounds may occur with
exhaustion or inability to have enough muscle force for
breathing
 “Silent chest”—ominous sign
 Severe airway obstruction or impending respiratory failure;
may be life-threatening (See Safety Alert)

 Hyperventilation—increased lung volume from trapped air
and limited airflow
 Abnormal alveolar perfusion and ventilation
 Hypoxemic, decreased PaCO2, increased pH
 Respiratory alkalosis results in respiratory acidosis as patient
tires; sign of respiratory failure

 Cough variant asthma
 Cough is only symptom
 Bronchospasm is not severe enough to cause airflow
obstruction
 May be nonproductive or productive with thick, tenacious
secretions

 A.D. continues with wheezing.
 Her anxiety increases.
 What other signs of hypoxemia would you assess for?

Asthma Classifications (1 of 2)
 Classifications
 Intermittent
 Mild persistent
 Moderate persistent
 Severe persistent
 Impairment criteria:
 Frequency of symptoms
 Nighttime awakenings
 SABA use for symptoms
 Interference with normal activity
 Lung function: FEV1,FVC
 Risk of exacerbation

Asthma Classifications (2 of 2)
 Severity is used to guide treatment decisions initially, then
addresses level of control
 All patients should have an asthma action plan for acute
attacks and to prevent future attacks
 Patient education and adherence is emphasized

 A.D. is diagnosed with intermittent asthma.
 It is probably exacerbated by an allergic response to
the cat.
 What other assessment findings would you anticipate?

Complications
 Asthma attacks are variable and unpredictable
 Mild to life-threatening
 Last few minutes to hours
 Between attacks, often asymptomatic
 Compromised pulmonary function to debilitation
 Complications may include: pneumonia, tension
pneumothorax, status asthmaticus or acute respiratory failure

Status Asthmaticus (1 of 2)
 Extreme acute asthma attack characterized by hypoxia,
hypercapnia, and acute respiratory failure; life-threatening
 Also see: chest tightness, increased shortness of breath, and
sudden inability to speak
 Without treatment leads to hypotension, bradycardia, and
respiratory/cardiac arrest
 Bronchodilators and corticosteroids not effective

Status Asthmaticus (2 of 2)
 Emergency treatment:
 Intubation and mechanical ventilation
 Hemodynamic monitoring
 Analgesia and sedation
 IV magnesium sulfate

 You perform a detailed assessment on A.D.
 She reports that she is a beautician.
 She smokes about ½ pack of cigarettes/day.

Diagnostic Studies (1 of 2)
 Detailed history and physical exam
 Peak expiratory flow rate (PEFR)
 Peak flow meter
 Predict attack or monitor severity
 Spirometry—lung volumes and capacities
 Stop bronchodilators 6 to 12 hours prior
 Reversibility of obstruction following bronchodilator is
important for diagnosis

 Fraction of exhaled nitric oxide (FENO)
 Increased levels with eosinophilic-induced inflammation
 Serum eosinophils and IgE—increased levels with atopy
 Allergy testing
 Oximetry; ABGs
 Chest x-ray—rule out other disorders
 Sputum culture and sensitivity
 Rule out bacterial infection

Interprofessional Care (1 of 5)
 Goal of treatment is to achieve and maintain control; return
to best possible level of daily functioning
 Medication guidelines based on steps
• Symptoms worse—step up medications
• Symptoms controlled—step down medications

Fig. 28-4 Drug Therapy
Stepwise Approach

 Mild to moderate attacks—symptoms
 No more than 2x/week
 Minimal interference in ADLs
 Alert, oriented, speaks in sentences
 May have some chest tightness and dyspnea
 Increased use of asthma meds
 O2 saturation > 90% on room air
 PEFR > 50% predicted or personal best

 Mild to moderate attack—treatment
 *Inhaled bronchodilators and oral corticosteroids
 Monitor VS
 Monitor as outpatient unless not responding to treatment or
another contributing factor
 Follow-up with HCP

 Severe attack—symptoms
 Alert and oriented but focused on breathing
• Frightened; agitated if hypoxemic
 Tachycardia, tachypnea (>30 breaths/min)
 Accessory muscle use; sits forward
 Wheezing
 PEFR < 50% predicted or personal best
 Recurring symptoms interfere with ADLs

 Severe attack—treatment
 ED  hospital admission
 Supplemental O2 and oximetry
• PaO2 > 60 mmHg or SaO2 > 93%
 Monitor PEFR, ABGs, VS
 Bronchodilators and oral corticosteroids
 Silent chest—immediately notify HCP

 A.D. has intermittent asthma.
 Based on this diagnosis, she will be treated at Step
One.
 She was treated in the E.D. with a nebulizer treatment.

Audience Response Question (1 of 2)
A patient is admitted to the emergency department with a
severe exacerbation of asthma. Which finding is of most
concern to the nurse?
a. Unable to speak and sweating profusely
b. PaO2 of 80 mm Hg and PaCO2 of 50 mm Hg
c. Presence of inspiratory and expiratory wheezing
d. Peak expiratory flow rate at 60% of personal best

Answer: A
Unable to speak and sweating profusely

Drug Therapy (1 of 14)
 Quick relief or rescue medications—treat acute attacks
 Bronchodilators:
 Short-acting inhaled 2-adrenergic agonists (SABAs)—all
patients should have this
 Inhaled anticholinergics; often used with SABA
 Antiinflammatory Drugs
 IV corticosteroids

 Long-term control medications—achieve and maintain control
 Bronchodilators:
 Long-acting inhaled or oral 2-adrenergic agonists (LABAs)
 Methylxanthines
 Anticholinergics
 Antiiflammatory Drugs
 Oral or inhaled corticosteroids (ICS)
 Leukotriene modifiers
 Anti-IgE

 Short-acting β-Adrenergic agonists (SABAs)
 Example: albuterol
 Stimulate 2 receptors in bronchioles to produce
bronchodilation
 Most effective for relieving acute bronchospasm with acute
attack
 Onset: minutes and duration: 4 to 8 hours

 Short-acting β2-adrenergic agonists
 Prevent release of inflammatory mediators from mast cells
• Take before exercise to prevent attack
 Too frequent use results in tremors, anxiety, tachycardia,
palpitations, and nausea
 Not for long-term use
 See: Drug Alert

 Long-acting β2-Adrenergic Agonist Drugs
 Examples: Salmeterol (Serevent), formoterol (Foradil)
 Added to daily ICSs; combination ICS and LABA available
 Used once every 12 hours; decreases the need for SABAs
 Never used for acute attack

 Methylxanthines
 Example: theophylline
 Less effective long-term bronchodilator
• Used only as alternative
• Many drug interactions and side effects
 Action: unknown
 Narrow margin of safety—monitor blood levels
• Toxicity: nausea, vomiting, seizures, insomnia

 Anticholinergic drugs
 Promote bronchodilation by preventing muscles around
bronchi from tightening
 Less effective than SABAs for asthma
• Used more with COPD
 Not used in routine management; except for severe acute
asthma attacks

 Three classes of antiinflammatory drugs
 Corticosteroids
 Leukotriene modifiers
 Monoclonal antibodies
• Anti-IgE
• Anti-Interleukin 5

 Corticosteroids—reduce bronchial hyperresponsiveness,
block late-phase response, and inhibit migrations of
inflammatory cells
 Most effective long-term control drug
 Examples: beclomethasone, budesonide

 Oral corticosteroids—use 1 to 2 weeks for maximum
effect for severe chronic asthma
 Inhaled corticosteroids (ICS)—effects in 24 hours; used
in long-term control on a fixed schedule
• Little systemic absorption except for high dose (easy
bruising, reduced bone density)

 1 month after discharge A.D. returns to the ED with an
acute exacerbation of her asthma.
 IV corticosteroids are given in the ED.
 An inhaled corticosteroid is prescribed for daily use.

 Corticosteroids—local side effects
 Oropharyngeal candidiasis, hoarseness, and a dry cough are
local side effects of inhaled drug
 Can be reduced using a spacer or by gargling after each use

 Leukotriene modifying agents (LTMAs)
 Examples: zafirlukast, montelukast, zileuton; administered
orally
 Interfere with synthesis or block the action of leukotrienes;
produce both bronchodilator and antiiflammatory effects
 Take for prophylaxis and maintenance; not for acute attacks

 Anti-IgE (monoclonal antibody)
 Example: omalizumab
 Reduced circulating IgE levels
 Prevents IgE from attaching to mast cells, preventing release
of chemical mediators
 Subcutaneous administration every 2 to 4 weeks for
moderate-severe asthma
 Risk of anaphylaxis

 Anti-Interleukin 5 (monoclonal antibody)
 Examples: mepolizumab and reslizumab
 Inhibits interleukin 5 (IL-5) to inhibit the production and
survival of eosinophils
 Used with severe asthma attacks despite current asthma
medications

Nonprescription Combination Drugs
 Bronchodilator (ephedrine) and expectorant (guaifenesin)
 OTC —many side effects; should avoid
 Epinephrine and ephedrine inhalers
 Stimulate CV and CNS—potentially dangerous
 Ephedrine can be used to produce methamphetamine
 Reformulated with phenylephrine

Inhalation Devices for Drug Delivery
 Many asthma drugs are given by inhalation
 Faster action
 Fewer systemic side effects
 Devices used to inhale medications:
• Metered dose inhalers (MDI)
• Dry powdered inhaler (DPI)
• Nebulizers

Inhalers (1 of 2)
 MDI—small, hand-held, pressurized devices
 Deliver dose with activation; 1 to 2 puffs
• Propellant —hydrofluoroalkane (HFA)
 Can be used with spacer or holding chamber to:
• Reduce oropharyngeal medication deposition
• Increase delivery to lungs
• Reduce problems with hand-breath coordination
 See Fig. 28-6

Fig. 28-6 Spacer with MDI

Inhalers (2 of 2)
 Teach correct technique and care
 Taking several MDIs leads to confusion
• Provide education
 Potential for overuse
• Bronchodilator use of greater than 2 canisters/month should
prompt visit to HCP; may need antiiflammatory

Fig. 28-7 Inhaler Use

 A.D. is being discharged from the ED after her
exacerbation.
 She has had difficulty with administration of her MDI.
 A DPI is ordered.

Dry Powdered Inhaler (DPI)
 DPI (dry powder inhaler)
 Powdered medication; breath activated
 Advantages over MDIs:
• Less manual dexterity and inhalation coordination
• No spacer needed
 Disadvantages:
• Low FEV1—inadequate inspiration
• Not all common meds available as DPI
• Powder may clump

Fig. 28-8 Example of a DPI

Nebulizers
 Machine converts drug solutions into a fine mist for
inhalation via face mask or mouthpiece; easy to use
 Requires air compressor or O2 generator
 Provide education for technique and care

Patient Teaching Related to
 Correct administration of drugs
 Name, purpose, dosage, method of administration, and when
to use
 Printed instructions
 Response to drug therapy; keep diary/log
 Symptoms improving or need help (HCP)
 Side effects and actions if occur
 How to clean and care for devices

Patient Teaching Related to
 Identify factors that affect correct use
 Age, dexterity, psychologic state, affordability, convenience,
administration time and preference
 Financial resource: www.needymeds.org
 Importance of adhering to management plan
 Continue long-term therapy even when asymptomatic;
explain why

Nursing Assessment (1 of 2)
 Subjective data (consider degree of distress)
 Important health information
• Past health history
• Medications
 Functional health patterns
• Health-perception–health management
• Activity–exercise
• Sleep–rest
• Coping–stress

 Objective data
 General
 Integumentary
 Respiratory
 Cardiovascular
 Possible diagnostic findings

Nursing Diagnoses
 Impaired breathing
 Activity intolerance
 Anxiety
 Lack of knowledge
 See eNursing Care Plan 28-1 on the Evolve website

Planning
 Overall goals
 Have minimal symptoms during the day and night
 Maintain acceptable activity levels (including exercise)
 Maintain greater than 80% of personal best PEFR
 Few or no adverse effects of therapy
 Adequate knowledge to carry out plan

Nursing Implementation (1 of 11)
 Health promotion
 Teach patient to identify and avoid known triggers and
irritants
• Avoid allergens
• Use scarves or masks for cold air
• Avoid aspirin and NSAIDs; read OTC labels
 Prompt diagnosis and treatment of upper respiratory
infections and sinusitis

 Weight loss
 Fluid intake of 2 to 3 L every day
 Good nutrition
 Adequate rest
 Exercise; pretreatment plan if needed

 Acute care
 Goal: maximize the patient’s ability to safely manage acute
asthma using an asthma action plan
 Plan is based on asthma symptoms and PEFR and when and
what change is needed to gain control

 Asthma action plan
 Green zone
 Doing well
• No symptoms
• Participate in usual activities
• Peak flow results
 Usually greater than 80% of personal best
• Remain on medications

 Asthma action plan
 Yellow zone
• Asthma is getting worse
• Symptomatic
• Able to do some activities but not all
• PEFR
 50% to 79% of personal best

 Asthma action plan
 Red zone
• Medical alert!
• Symptomatic and medications are not helping
• Cannot do usual activities
• PEFR
 50% or less of personal best
• Call doctor now; call ambulance or get to hospital

 Acute care
 Monitor respiratory and cardiovascular systems
• Lung sounds
 Wheezing may get louder as airflow increases
• Heart rate and rhythm, respiratory rate and work of breathing,
and BP
• Pulse oximetry, peak expiratory flow rates, and ABGs
• Give drugs as ordered
• Evaluate response to therapy; may take several days

 An important goal of nursing is to decrease patient’s
anxiety and sense of panic
 Position comfortably (semi to high-Fowler’s)
 Use “talking down” to keep calm
• Coach to use pursed-lip breathing (Table 28-12)
 Stay with patient
 After attack subsides, allow rest
• When appropriate, complete H and P if unable to obtain earlier

 Ambulatory care
 Patient/Caregiver Teaching—drug therapy and monitoring for
control of symptoms
• Review asthma action plan
• Daily PEFR
• Green, yellow, and red zone meaning and management
• Step up/step down medications

 A.D.’s husband is with her in the ED and preparing to
take her home after discharge.
 They both express concern about exacerbations and
knowing when to come in for help.

 Ambulatory care (continued)
 Include caregiver with patient teaching
 Other:
 Maintain good nutrition
 Exercise within limits of tolerance
 Uninterrupted sleep is important
 Home monitoring (See Informatics in Practice)

 Consider socioeconomic status, access to health care, and
cultural beliefs
 Provide educational resources in patient’s language
 Relaxation therapies (See Chapter 6)
 For example, yoga, meditation, breathing and relaxation
techniques
 Asthma support groups

Evaluation
 Expected outcomes
 Maintain patent airway with removal of secretions
 Have normal breath sounds an respiratory rate
 Report decreased anxiety with increased control of breathing
 Demonstrate correct use of medications
 Express confidence in ability to manage asthma

Chronic Obstructive Pulmonary
Disease (COPD)

 COPD
 See Cultural and Ethnic Health Disparities
• Whites have highest incidence despite higher rates of smoking
among other ethnic groups
• Hispanics have lower death rates related to COPD than other
ethnic groups
 16 million in United States have COPD
 Third leading cause of death; > 120,000/year

COPD (1 of 3)
 Gender differences
 More common in men
 Men have poorer response to O2 therapy
 COPD is increasing in women due to smoking and increased
susceptibility
 More women die from COPD
 Women have lower quality of life, more exacerbations and
increased dyspnea

COPD (2 of 3)
 Preventable, treatable, often progressive disease
characterized by persistent airflow limitation
 Chronic inflammatory response in airways and lungs,
primarily caused by cigarette smoking and other noxious
particles or gases
 Exacerbations and other coexisting illness contribute to
severity of the disease

COPD (3 of 3)
 The definition of COPD no longer includes chronic
bronchitis and emphysema
 Chronic bronchitis—the presence of cough and sputum
production for at least 3 months in each of 2 consecutive
years
 Emphysema—destruction of alveoli without fibrosis

COPD
Risk Factors
 Cigarette smoking
 Clinically significant airway obstruction develops in 20% of
smokers
 COPD should be considered in any person who is over 40
with a smoking history of 10 or more pack-years

COPD
Cigarette Smoking (1 of 2)
 Effects on respiratory tract
 Hyperplasia of cells
• Goblet cell—increased production of mucus
• Reduced airway diameter
 Lost or decreased ciliary activity
 Abnormal distal dilation and destruction of alveolar walls
 Chronic, enhanced inflammation results in remodeling

COPD
Cigarette Smoking (2 of 2)
 Oxidative stress
 Passive smoking (environmental tobacco smoke [ETS] or
secondhand smoke)
 Decreased pulmonary function
 Increased respiratory symptoms
 Increased risk of lung and nasal sinus cancer

COPD
Risk Factors (1 of 5)
 Infection
 Severe, recurring respiratory infections in childhood
 HIV
 Tuberculosis

COPD
 Asthma
 Considerable pathologic and functional overlap between
asthma and COPD
 Older adults may have components of both diseases
• Asthma-COPD overlap syndrome

COPD
 Air pollution
 Urban areas
 Coal and biomass fuels—cooking and indoor heating
 Mechanism unclear
 Occupational dusts and chemicals
 Dusts, vapors, irritants, or fumes

COPD
 Aging
 Unclear if aging results in COPD or occurs due to cumulative
effects of exposures during life
 Normal aging changes similar to COPD
• Loss of elastic recoil, decreased compliance
• Changes in thoracic and rib cage
• Decreased functional alveoli and surface area for gas exchange

COPD
 Genetics
 1 genetic factor identified
 1-Antitrypsin deficiency (AATD)
 Autosomal recessive disorder; 3% of COPD
 ATT protects lungs from proteases during inflammation;
deficiency results in premature bullous emphysema;
accelerated by smoking
 See Genetics in Clinical Practice

 G.S., a 77-year-old man, comes to the hospital
reporting of shortness of breath, morning cough, and
swelling in his lower extremities.
 He has difficulty breathing when he walks short
distances, such as to the bathroom.

COPD
 Characterized by chronic inflammation of airways, lung
parenchyma, and pulmonary blood vessels
 Defining feature: airflow limitation not fully reversible
during forced exhalation due to:
• Loss of elastic recoil
• Airflow obstruction due to mucous hypersecretion,
mucosal edema, and bronchospasm

COPD
 Disease progression marked by worsening:
 Abnormalities in airflow limitation
 Air trapping
 Gas exchange
 Severe disease:
 Pulmonary hypertension
 Systemic manifestations
 Impaired or destroyed lung tissue exists alongside normal
tissue

COPD
Fig. 28-10 Pathophysiology

COPD
 Primary process is inflammation
 Inhalation of noxious particles and gases results in
inflammation which results in damage to lung tissue and
impaired normal defense mechanisms and repair processes
 Predominate inflammatory cells are neutrophils,
macrophages, and lymphocytes
 Oxidants contribute to structural destruction

COPD
 Main characteristic of COPD is the inability to expire air
 Main site of airflow limitation is the smaller airways
• Peripheral airways are obstructed and trap air during expiration
results in increased residual volume which results in barrel -
shaped chest
• Patient becomes dyspneic and has limited exercise capacity as
they try to inhale against overinflated lungs

COPD
 As air trapping increases, alveolar walls are destroyed
resulting in formation of bullae and blebs
 Bullae and blebs have no surrounding capillary bed resulting
in ventilation-perfusion (V/Q) mismatch resulting in
hypoxemia and hypercapnia (especially with severe disease
and in late stages)

COPD
Fig. 28-11 Pathophysiology

COPD
 Excess mucus production and cough
 Increased mucus-secreting goblet cells
 Enlarged submucosal glands
 Dysfunction of cilia
 Stimulation from inflammatory mediators
 Not all patients with COPD have sputum production

COPD
 COPD is a systemic disease as a result of chronic
inflammation
 Cardiovascular diseases are common
 Other: osteoporosis, diabetes, metabolic syndrome

COPD
 Pulmonary vascular changes
 Vasoconstriction of small pulmonary arteries due to hypoxia
 Vascular smooth muscle of pulmonary arteries thicken with
advanced disease
 Pressure in pulmonary circulation increases
 Results in pulmonary hypertension resulting in right
ventricular hypertrophy which results in right heart failure

COPD Classification
 Diagnosis of COPD
 FEV1/FVC ratio of < 70%
 Severity of obstruction—postbronchodilator FEV1 results
• GOLD 1 Mild
• GOLD 2 Moderate
• GOLD 3 Severe
• GOLD 4 Very severe
• (Global initiative for Chronic Obstructive Lung Disease)

 G.S. states that he sleeps in a recliner to make it
easier to breathe.
 He feels his shoes are tight at the end of the day.
 He is placed on oxygen at 2 L/min via nasal cannula.

 Develops slowly
 Diagnosis is considered with:
 Chronic cough (intermittent—first symptom)
 Sputum production
 Dyspnea; occurs with exertion and progressive
 Exposure to risk factors
 Distinguish from asthma—Table 28-4

 Chest heaviness, can’t take a deep breath, gasping,
increased effort to breathe, and air hunger
 Symptoms often ignored; patients change behaviors to avoid
dyspnea
 Dyspnea usually prompts medical attention
 Occurs with exertion in early stages
 Present at rest with advanced disease

 Chest breather (versus abdominal)
 Use of accessory and intercostal muscles
 Inefficient breathing
 Wheezing and chest tightness
 Fatigue
 Weight loss and anorexia

 Prolonged expiratory phase
 Decreased breath sounds, wheezing
 Barrel chest
 Tripod position
 Pursed-lip breathing
 Peripheral edema (ankles)—right HF

 Hypoxemia PaO2 < 60 mmHg; SaO2< 88 %
 Hypercapnia PaCO2 > 45 mmHg
 Increased production of red blood cells
 Hemoglobin concentrations may reach 20 g/dL (200 g/L) or
more
 Bluish-red color of skin—polycythemia and cyanosis

Complications (1 of 6)
 Pulmonary hypertension
 Pulmonary vessel vasoconstriction due to alveolar hypoxia
 Increased pulmonary vascular resistance
 Polycythemia from chronic hypoxia results in increased
viscosity

 Cor pulmonale (right-sided heart failure)
 Late manifestation
 Pulmonary HTN results in increased right ventricle pressure
 Dyspnea most common
 Other: S3 and S4, murmurs, distended neck veins,
hepatomegaly, peripheral edema, weight gain

Pathophysiology of Cor Pulmonale

 Cor pulmonale (right-sided heart failure)
 Chest x-ray: large pulmonary vessels
 Echocardiogram: Right side heart enlargement
 Increased BNP level
 Treatment
 Long-term O2 therapy
 Diuretics
 Anticoagulation

 Acute exacerbations
 Worsening of respiratory symptoms
• Increased dyspnea, increased sputum volume, increased
sputum purulence
• Malaise, insomnia, fatigue, depression, confusion, decreased
exercise tolerance, wheezing, fever
 Common cause: bacterial or viral infections
 Increase in frequency with disease progression

 Treatment as inpatient or outpatient depends on severity;
medical history, current symptoms, hemodynamic stability,
O2 requirements, work of breathing, ABG’s and coexisting
disease
 Treatments:
 SABAs and oral corticosteroids
• Other: anticholinergic, antibiotics, diuretics
 Oxygen
• Noninvasive preferred

 Acute exacerbations
 Patient education
• Manifestations of exacerbations
 Acute respiratory failure
 May occur if wait too long to see HCP with exacerbations

 History and physical exam
 Spirometry—confirms diagnosis
 FEV1/FVC ratio <70%
 Chest x-ray
 Serum 1-antitrypsin levels
 6-minute walk test
 Pulse ox <88% at rest—qualify for supplemental O2

 COPD assessment test (CAT)
 www.catestonline.org
 Clinical COPD Questionnaire (CCQ)
 www.ccq.nl
 ABGs
 ECG, Echo, MUGA scan
 Sputum culture and sensitivity

 G.S. is exhibiting symptoms of mild to moderate
COPD.
 He states he has smoked a pack of cigarettes/day for
30 years.
 His history includes heart disease and GERD.

 G.S. shares that he has experienced “attacks” like this
in the past year, but this one was a bit worse.
 He states that he and his wife had visited their

daughter and her 3 kids who were sick with colds.

 G.S.’s ABGs show a slight decrease in PaO2 and
increased PaCO2, and his chest x-ray shows flattening
of his diaphragm.
 O2 saturation is 88%.

 His FEV1/FVC is 65%
 He states he is having difficulty completing ADLs

without frequent rest periods.

 Most treated as outpatients
 Hospitalized for complications
• Acute exacerbations
• Acute respiratory failure
 Evaluate for exposure to environmental or occupational
irritants
 Influenza virus vaccine—annually
 Pneumococcal vaccine

 Smoking cessation
 Most important reducing risk of developing COPD or the
progression
 Accelerated decline in pulmonary function slows to almost
nonsmoking levels

 Drug therapy
 Bronchodilators
• Relax smooth muscle in the airway
• Improve ventilation of the lungs
• Decreased dyspnea and increased FEV1
• Inhaled route is preferred
• Include: β2-Adrenergic agonists, anticholinergics,
methylxanthines

 Drug therapy
 Moderate stage: FEV1 < 60%
• Inhaled long-acting anticholinergic (LABA)
• Inhaled corticosteroids (ICS)
 Severe COPD and chronic bronchitis
• Rofumilast (Daliresp)—antiinflammatory drug

 G.S. is given a short-acting bronchodilator via
nebulizer.
 He will also be given a SABA inhaler and an ICS for
home use.
 He is started on azithromycin (Zithromax).

 Surgical therapy
 Lung volume reduction surgery (LVRS)
• Removes diseased tissue so healthy tissue works better
 Bronchoscopic lung volume reduction surgery
• Place 1 way valve in airways to diseased lung leads to collapse
• Pneumothorax is common complication

 Surgical therapy
 Bullectomy
• Removal of one or more bullae to decrease work of breathing
 Lung transplantation
• Single or double
Not all patients are surgical candidates

 COPD therapies
 Oxygen therapy
 O2 therapy is used to treat hypoxemia
• Keep O2 saturation > 90% during rest, sleep, and exertion, or
PaO2 > 60 mm Hg
• Individualized
• Improves survival

 Methods of administration
 O2 delivery systems are high- or low-flow
 Low-flow is most common
 Low-flow is mixed with room air, and delivery is less precise
than high-flow
 High-flow fixed concentration
• Venturi mask

 Humidification and Nebulization
 Used because O2 has a drying effect on the mucosa and
secretions
 Use sterile distilled water
 Supplied bubble-through humidifiers

 Complications of oxygen therapy
 Combustion—no smoking or open flames
 CO2 narcosis—CO2 no longer stimulus to breathe
• Hypoxic drive; administer O2 carefully
 O2 toxicity—prolonged high O2
• Severe inflammation
 Infection—humidity supports bacterial growth
• Pseudomonas aeruginosa
• Disposable equipment

 Oxygen therapy at home
 Short-term O2 therapy—up to 30 days
• May need upon discharge from hospital
 Long-term O2 Therapy (LTOT)
• Use O2 15 or more hours/day
• Need central source at home; portable system

Fig. 28-13 Portable Liquid Oxygen
System

 Long-term O2 therapy (LTOT) at home
 Respiratory therapist comes to home to set up and provide
education
• Decreasing risk of infection
• Safety issues
 Patients are encouraged to remain active and travel

 Respiratory care
 Breathing retraining
• Pursed-lip breathing
 Prolongs expiration to reduce bronchial collapse and air trapping
• Diaphragmatic breathing
 Use of diaphragm instead of accessory muscles to achieve
maximum inhalation and slow respiratory rate

 Airway clearance techniques
• Often used with other treatments (bronchodilator)
• Loosen mucus to clear with coughing
 Effective coughing or huff coughing
• Conserves energy, reduces fatigue, and facilitate removal of
secretions

 Chest physiotherapy (CPT) indicated for
 Excessive, difficult-to-clear bronchial secretions
• Postural drainage, percussion, and vibration
 Complications
• Fractured ribs, bruising, hypoxemia, discomfort

 Postural drainage
 Position patient so gravity assists in draining secretions from
lung segments to bronchi and trachea where they can be
coughed up
 Done 2 to 4 times/day (or every 4 hours)
 Contraindications:
• Traumatic brain injury, chest trauma, hemoptysis, heart disease,
PE, or unstable condition

 Percussion
• Hands in a cuplike position to create an air pocket; not on
bare skin
• Air-cushion impact facilitates movement of thick mucus
• If it is performed correctly, a hollow sound should be heard

Fig. 28-14 Cupped-Hand Position

 Vibration
• Tense hand and arm muscles to creating vibration on
exhalation
• Facilitates movement of secretions to larger airways
• Commercial mechanical vibrators available

 Airway clearance devices
 Use positive expiratory pressure (PEP) to mobilize
secretions; more tolerable than CPT
• Flutter
• Acapella
• TheraPEP

Fig. 28-15
Acapella Airway Clearance Device

 High-frequency chest wall oscillation
• Inflatable vest connected to high-frequency pulse generator
that vibrates the chest
• Dislodges and mobilizes mucus, moves toward larger airways
• Patient can use on their own
• Portable

 G.S. is going to be discharged to home.
 He is given an Acapella device to assist him with
expulsion of mucus.
 His wife is present, and you begin to teach them about
home care.
Copyright © 2017, Elsevier Inc. All Rights Reserved.

 Nutritional therapy
 Malnutrition in COPD patients is multifactorial
• Increased inflammatory mediators
• Increased metabolic rate
• Lack of appetite
 Advanced stages—weight loss is a predicator of poor
prognosis

• To decrease dyspnea and conserve energy
• Rest at least 30 minutes before eating
• Avoid exercise for 1 hour before and after eating
• Use bronchodilator before meals

• Supplemental O2 may be helpful
• High-calorie, high-protein, moderate carbohydrates, and
moderate fats diet is recommended
• Eat 5 to 6 small meals to avoid bloating and early satiety

• Avoid:
• Foods that require a great deal of chewing
• Exercises and treatments 1 hour before and after eating
• Gas-forming foods

Gerontologic Considerations (1 of 2)
 Reduced lean body mass and decreased respiratory
muscle strength, increased dyspnea, and lower exercise
tolerance leads to higher incidence of acute
exacerbations
 Smoking cessation important
 Often have other comorbidities
• Increased complications, stress, and drug interactions

Gerontologic Considerations (2 of 2)
 Adherence may be an issue
 Cognitive impairment: memory
 Complex medication regimens
 Physical issues: arthritis, vision, side effects of meds (ICS)
 Quality of life issues
 Psychologic and emotional support
 Palliative care and hospice—later stages

 Subjective data
• Medications
• Health-perception–health management
• Nutritional–metabolic
• Activity–exercise

• Elimination
• Sleep–rest
• Cognitive–perceptual
• Coping–stress

 Objective data
 General
 Integumentary
 Respiratory
 Cardiovascular
 Gastrointestinal
 Musculoskeletal
 Possible diagnostic findings

 G.S. appears fatigued and has difficulty answering the
many questions he is asked.
 His wife expresses concern that he has not been
sleeping well.

Nursing Diagnoses
 Impaired breathing
 Activity intolerance
 Impaired nutritional status
 Difficulty coping

Planning
 Goals
 Relief from symptoms
 Ability to perform ADLs an improved exercise tolerance
 No complications related to COPD
 Knowledge and ability to implement a long-term treatment
plan
 Overall improved quality of life

 What areas could be addressed with G.S. in regard to
health promotion?
 How can his wife and family help?
Copyright © 2017, Elsevier Inc. All Rights Reserved.

• Abstain from or stop smoking.
• Early diagnosis and treatment of respiratory tract infections;
avoidance measures
• Avoid or control exposure to occupational and environmental
pollutants and irritants.
• Influenza and pneumococcal vaccines

• Awareness of family history of COPD and AAT deficiency
• Genetic counseling

 Acute care
 Hospitalization required for acute exacerbations or
complications:
• Pneumonia, cor pulmonale, or acute respiratory failure
 Degree and severity of underlying respiratory problem
should be assessed

 G.S. comes into the clinic in one week for follow-up.
 He is breathing much easier and states that he is able
to perform ADLs with less distress.
 He and his wife ask about how to prevent further
breathing difficulties.

 Ambulatory care
 Patient/caregiver teaching
• Pulmonary rehabilitation
• Activity considerations
• Sexual activity
• Sleep
• Psychosocial considerations

 Pulmonary rehabilitation (PR) is designed to reduce
symptoms and improve quality of life
 Includes exercise training, smoking cessation, nutrition
counseling, and education
 Alternate: internet programs

 Activity considerations
 Exercise training leads to energy conservation
• In upper extremities, it may improve muscle function and reduce
dyspnea
 Modify ADLs to conserve energy
• Hair care, shaving, showering
• O2 during activities of hygiene

 Activity considerations
 Walk 15 to 20 minutes a day at least 3 times a week with
gradual increases
• Adequate rest should be allowed
 Exercise-induced dyspnea should return to baseline within 5
minutes after exercise

 Psychosocial considerations
• Healthy coping with lifestyle changes is a challenge
• May feel denial, anger, frustration, loneliness, and guilt (if
smoking was the cause), depression, anxiety
• Provide support and education
• Support groups
• Counselors, cognitive and behavioral therapy
• Medications

 Sexuality and sexual activity
• Plan when breathing is best
• Use slow, pursed lip breathing
• Refrain after eating or drinking alcohol
• Choose less stressful positions
• Use O2 if prescribed

 Sleep
• Adequate sleep is extremely important
• O2 saturations may drop during sleep
• Hypercapnia leads to frequent awakenings
 Interfering factors:
• Current tobacco use, depression, anxiety, meds, congestion,
coughing or wheezing, sleep apnea

COPD
End-of-Life Considerations
 Symptoms can be managed, but COPD cannot be
cured
 End-of-life issues and advanced directives are
important topics for discussion
 Palliative care, end-of-life, and hospice care are
important in advanced COPD

Evaluation
 Expected outcomes
 Maintain patent airway by effective coughing
 Have an effective rate, rhythm, and depth of respirations
 Have clear breath sounds
 Return to pre-exacerbation baseline respiratory function
 PaCO2 and PaO2 return to levels normal for patient

The nurse reviews the arterial blood gases of a patient. Which

result would indicate the patient has later stage COPD?
a. pH 7.32, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3− 30 mEq/L
b. pH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO3− 18 mEq/L
c. pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO3− 25 mEq/L
d. pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO3− 35 mEq/L

Answer: A
pH 7.32, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3− 30
mEq/L

Cystic Fibrosis

Cystic Fibrosis (1 of 3)
 Autosomal recessive, multisystem disease with altered
transport of sodium and chloride ions in and out of
epithelial cells of epithelial cells. Primarily affects:
 Lungs
 Pancreas and biliary tract
 Reproductive tract

 Whites have the highest incidence
• In United States 1 in 3000 white births
• One in 20 to 25 whites are carriers of the gene
 Uncommon among blacks ( 1 in 15,000),
Hispanics (1 in 9,200), and Asian Americans
(1 in 30,000)

 First signs and symptoms usually occur in children;
some patients are not diagnosed until adulthood
 Median life span is more than 37.5 years
 Blood-based DNA testing is available
 Prenatal testing may also be done for known carriers
 In United States, all newborns are screened at birth

Etiology and Pathophysiology (1 of 12)
 The CF gene is found on chromosome 7
 CFTR gene provides the instructions for making the
protein that controls the channel that transports sodium
and chloride
 The mutation of the gene CFTR change the protein to
block the transport channels.
 The secretions from the affected organs are low in
sodium chloride and water.
• Many mutations of the gene have been identified

Fig. 28-16
Etiology and Pathophysiology

 Obstruction of ducts of lungs, pancreas, and intestines is
caused by thick, sticky secretions
 Mucus fills (plugs up) glands in these organs causing scarring
and ultimately organ failure
 Patients with CF have high concentrations of sodium and
chloride in their sweat

 Hallmark of CF is the effect on the airways
 Upper respiratory tract manifestations include:
 Chronic sinusitis
 Nasal polyposis

 In the lower respiratory tract, the disease affects the small
airways then progresses to the larger airways
 Mucus becomes dehydrated and tenacious
 Cilia motility is decreased
 Thick secretions obstruct bronchioles, leading to scarring, air
trapping, and hyperinflation

 CF is characterized by persistent, chronic airway infection
 Most common organisms cultured are
• *Pseudomonas aeruginosa
• Staphylococcus aureus
• Haemophilus influenzae
 Less common but more serious
• Burkholderia cepacia

 Chronic infection results in
 Antibiotic resistance
 Pulmonary inflammation, narrowed airways, and decreased
function
 Inflammatory mediators results in progression

 Initially: chronic bronchiolitis and bronchiectasis
 Progression: pulmonary vascular remodeling occurs
because of local hypoxia and arteriolar vasoconstriction
 Leads to pulmonary hypertension, enlarged arteries and cor
pulmonale in later phases

Fig. 28-17
Pathologic changes in bronchiectasis

 Blebs and large cysts in lungs are severe manifestations of
destruction
 Complications include:
 Hemoptysis (which can be fatal)
 Pneumothorax

 Pancreatic insufficiency is caused by mucus plugs in
pancreatic ducts results in atrophy
 Exocrine function of pancreas is altered or may be lost
completely
 Insufficient production of enzymes lipase, amylase, and
proteases do not allow for absorption of nutrients

(10 of 12)
 Malabsorption of fat, protein, and fat-soluble vitamins
manifest as:
 Steatorrhea
• Frequent bulky, foul-smelling stools
 Failure to grow and gain weight
• Low body mass index (BMI)
 Osteopenia and osteoporosis

(11 of 12)
 CF-related diabetes mellitus (CFRD) is related to
underdevelopment of islet cells in utero and later
destruction of islet cells
 See type 1 and type 2 characteristics

(12 of 12)
 Many also have GI problems
 GERD, gallstones, and pancreatitis
 Liver enzymes elevated results in cirrhosis
 Portal hypertension
 DIOS (distal intestinal obstruction syndrome)
• Thick, dehydrated stool and mucus cause intermittent
obstruction at ileocecal valve
• RLQ pain, palpable mass, decreased appetite, nausea,
vomiting

 K.W., a 28-year-old man with cystic fibrosis, visits a
clinic for his annual physical exam.
 He is married and in good overall health.
 He has a cough with scant wheezes auscultated.

 Median age of diagnosis 6 to 8 months
 2/3 diagnosed in first year of life
 Early manifestations that suggest CF:
 Meconium ileus in the newborn
 Acute or persistent respiratory symptoms
 Failure to thrive or malnutrition
 Steatorrhea
 Family history

 Without treatment, patient develops:
 Large, protuberant abdomen
 Emaciated appearance of extremities
 Bronchiectasis
 Delayed puberty
• Females: menstrual irregularities, amenorrhea, difficulty
conceiving; most are able to conceive
• Males: vas deferens doesn’t develop; with technology, able to
father a child

 Atypical presentation in adults
 Diabetes or infertility
 Commonly see: frequent cough
• Becomes persistent
• Produces sputum
 Viscous and purulent
 Yellow or greenish-colored
 Most common bacteria—Pseudomonas

 Recurrent respiratory problems may be indicative of CF
 Exacerbations increase in frequency
• Increased cough and sputum
• Weight loss
• Decreased respiratory function
• Eventually results in respiratory failure

 K.W. states that he and his wife are thinking of starting
a family.
 He asks what the chances are of transmission of cystic
fibrosis to his children.

Complications
 CFRD
 Bone disease
 Sinus disease
 Liver disease
 Pneumothorax
 Hemoptysis (can be life-threatening if massive)
 Digital clubbing
 Late complications
 Respiratory failure
 Cor pulmonale

Diagnostic Studies
 Clinical presentation, family history, lab and genetic testing
 Gold standard: *sweat chloride test with pilocarpine
iontophoresis method
 Pilocarpine carried by electric current is used to stimulate
sweat production (in both arms)
 Sweat is collected and analyzed
 Sweat chloride values >60 mmol/L are considered positive for
CF

 His primary care provider refers K.W. to new CF care
center in his city.
 K.W. asks what this center will provide for him.

 Cystic fibrosis foundation
 CF care centers
• Improved length and quality of life
• Best care, treatment, and support
 Team
• Physician, nurse/nurse practitioner, respiratory therapist,
physical therapist, social worker, dietician

 Treatment focuses on relieving airway obstruction and
controlling infection
 Treatment includes: aerosol and nebulization treatments of
medications to dilate the airways and liquefy mucus and to
facilitate clearance
 Inhaled dornase alpha (Pulmozyme)
 Inhaled hypertonic saline (7%)
 Bronchodilators (e.g., β2-adrenergic agonists)

 Airway clearance techniques
 CPT
 High-frequency chest wall oscillation systems
 Specialized expiratory techniques
• PEP devices
• Breathing exercises
• Pursed-lip breathing
• Huff coughing

 Lung infections
 Early intervention with antibiotics
 Long courses of antibiotics are usual treatment (10 days to 3
weeks) or chronic suppression therapy
 Drugs are abnormally metabolized and quickly excreted—
may need prolonged high-dose therapy

 Antibiotic therapy
 If resources available, IV therapy at home with two different
antibiotics with different mechanisms of action
 Oxygen therapy—cor pulmonale or hypoxemia
 Mild exacerbations—oral agents
 Pseudomonas—aerosolized tobramycin

 Pneumothorax—chest tube drainage
 If recurrent, pleural sclerosis, stripping or abrasion
 Massive hemoptysis -bronchial artery embolization
 Lung transplant

 Pancreatic insufficiency management
 Replacement of pancreatic enzymes and supplements
 Adequate fat, calorie, and vitamins (A, D, E, K)
 Caloric supplements
 Added dietary salt
 Insulin if hyperglycemia develops

 Partial or complete DIOS
 Medical management
• Options: probiotics, mucolytics, stimulant laxatives, lactulose,
polyethylene glycol
 Surgery if medical not successful

 CFTR genotyping for CFTR modulator therapy
 Ivacaftor (Kalydeco) and Ivacaftor/lumacaftor are used to
treat patients who have a mutation in a specific CFTR gene

Nursing Management (1 of 7)
Nursing assessment
 Subjective data
• Medications

 Functional health patterns
 Health-perception–health maintenance
 Nutrition–metabolic
 Elimination
 Activity–exercise
 Cognitive–perceptual
 Sexuality–reproductive
 Coping–stress tolerance

 Objective data
 General
 Integumentary
 Eyes
 Respiratory
 Cardiovascular
 Gastrointestinal
 Possible Diagnostic Findings

 What questions would you want to ask K.W. about his
health in the past year?
 The past month?

 K.W. states that he has some difficulty with increased
cough and sputum in the morning.
 He has difficulty coughing up sputum due to its
thickness.

 Nursing diagnoses
 Impaired airway clearance
 Impaired respiratory system function
 Impaired nutritional status
 Difficulty coping

Planning
 Overall goals:
 Adequate airway clearance
 Absence of respiratory infection
 Adequate nutritional support to maintain appropriate BMI

 Goals (continued)
 Ability to perform ADLs
 Recognition and treatment of complications related to CF
 Active participation in planning and implementing an
achievable treatment plan

Nursing implementation
 Acute care
 Relief of bronchoconstriction, airway obstruction, and airflow
limitations
• Aggressive CPT, antibiotics, O2 therapy, and corticosteroids
 Adequate nutrition

 K.W. states that he and his wife want to begin an
exercise program.
 He asks what type of exercise might be best and if he
needs to consider anything special related to his CF.

Interprofessional Care
 Aerobic exercise can be effective in clearing airways
 Increased nutritional demands of exercise
 Observe for dehydration
 Increase fluid intake and replace salt losses

Nursing implementation
 Help patient assume responsibility for care and life goals
 Discuss altered sexuality
 Delayed development
 Marriage and childbearing
 Genetic counseling
 Shortened life span

 Crises, life transitions, and resources
 Employment
 Motivation
 Coping
 Dependence
 Sharing diagnosis with others
 Emotional needs; depression
 Financial needs

Bronchiectasis

Bronchiectasis (1 of 2)
 Etiology and pathophysiology
 Permanent, abnormal dilation of medium-sized bronchi due to
inflammatory changes
• Destruction of elastic and muscular structures of the bronchial
wall
• Cyclical process of inflammation results in damage which
results in remodeling
• Colonization of microorganisms (Pseudomonas) results in
weakening of walls and pockets of infection

Bronchiectasis (2 of 2)

 Bronchial wall injury:
 Damages mucociliary mechanism, results in accumulation of
mucus and bacteria
 Bacteria attracts neutrophils which increased inflammation
and edema
 Reduced mucus clearance and decreased expiratory flow

 Causes
 CF in children
 Bacterial lung infections in adults
 Airway obstruction
 Systemic diseases
• Inflammatory bowel disease
• Rheumatoid arthritis
• Immune disorders

Clinical Manifestations
 Cough with persistent production of thick, tenacious,
purulent sputum
 Hemoptysis
 Other: pleuritic chest pain, dyspnea, wheezing,
clubbing, weight loss, anemia, adventitious breath
sounds

Diagnostic Studies
 *CT scan
 Chest x-rays
 Spirometry
 Sputum
 CBC
 AAT

Interprofessional and
 Treatment Goals:
 Treat flare-ups and prevent decline in lung function
 Antibiotics
 Patient education to take as prescribed
 Bronchodilators
 SABA, LABA, anticholinergics
 Corticosteroids

 Promote drainage and removal of mucus
 Airway clearance techniques
• CPT
• Hydration of respiratory tract
 Patient education
 Manifestations to report to HCP
• Increased sputum, increased dyspnea, fever, chills, chest pain,
hemoptysis (moderate to large amount)

 Acute care
 Hemoptysis
• Elevate HOB; side-lying position with bleeding side down
• Monitor VS and respiratory status
 Hydration—2 to 3 L/day unless contraindicated
 Rest
 Nutrition
 Surgical resection or lung transplant

Obstructive Pulmonary Diseases

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Chapter 28

Obstructive Pulmonary Diseases

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 Related to environment (e.g., pollen)

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