COPD, Asthma and Cystic Fibrosis
Zoya Minasyan, RN- MSN-Edu
COPD: Pathophysiology
• Defining features
–Irreversible airflow limitations during
forced exhalation due to loss of elastic
recoil
–Airflow obstruction due to mucous
hypersecretion, mucosal edema, and
bronchospasm
COPD: Pathophysiology
• Supporting structures of lungs are destroyed.
– Air goes in easily, but remains in the lungs.
– Bronchioles tend to collapse.
– Causes barrel-chest look
• Pulmonary vascular changes
– Blood vessels thicken.
– Surface area for diffusion of O2 decreases.
• Common characteristics
– Mucous hypersecretion
– Dysfunction of cilia
– Hyperinflation of lungs
– Gas exchange abnormalities
COPD: Description
• Includes
– Chronic bronchitis
– Emphysema (in which the air sacs are dilated or enlarged
and lack flexibility, so that breathing is impaired)
• Risk factors
– Cigarette smoking
– Occupational chemicals and dust
– Air pollution
– Infection
– Heredity
– Aging
COPD: Cigarette Smoking
• Airway obstruction develops in 15% of smokers.
• 80% to 90% of COPD deaths are related to tobacco smoking.
• Effects of nicotine
• Stimulates sympathetic nervous system
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Increases HR
Causes peripheral vasoconstriction
Increases BP and cardiac workload
↓ Amount of functional hemoglobin
↑ Platelet aggregation
Problems with CAD
Increased production of mucus
Lost or decreased ciliary activity
COPD: Cigarette Smoking
• Carbon monoxide
– ↓ O2 carrying capacity
• ↑ Heart rate
• Passive smoking (second-hand smoke)
– ↓ Pulmonary function
– ↑ Risk of lung cancer
COPD
• Occupational & Environmental
– COPD can develop with intense or prolonged
exposure to
• Dusts, vapors, irritants, or fumes
• High levels of air pollution
• Fumes from heating or cooking in poorly ventilated
areas
• Infection
– Recurring infections impair normal defense
mechanisms.
COPD
• Aging
– Some degree of emphysema is common because
of physiologic changes of aging lung tissue.
• Heredity
– -Antitrypsin (AAT) deficiency
• Genetic risk factor for COPD
• Accounts for 3% of COPD
COPD: Clinical Manifestations
• Develops slowly
• Diagnosis is considered with
– Cough
– Sputum production
– Dyspnea
– Exposure to risk factors
• Dyspnea usually prompts medical attention.
COPD: Clinical Manifestations
• Causes chest breathing
– Use of accessory and intercostal muscles
– fatigue
• Physical examination findings
– Prolonged expiratory phase
– Wheezes
– Decreased breath sounds
• Bluish-red color of skin
– cyanosis
COPD
Complications
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Cor pulmonale
Exacerbations of COPD
Acute respiratory failure
Peptic ulcer disease
Depression/anxiety
COPD: Cor Pulmonale
• Hypertrophy of right side of heart
– Result of pulmonary hypertension (the pressures
on the right side of the heart must increase to
push blood into the lungs).
– Eventually causes right-sided heart failure
• Dyspnea
• Distended neck veins
• Hepatomegaly with upper quadrant tenderness
• Peripheral edema
• Weight gain
COPD: Exacerbations
• to make an already bad or problematic
situation worse
• Signaled by change in usual
– Dyspnea
– Cough
– Sputum
• Primary causes
– Infection
– Air pollution
COPD: Acute Respiratory Failure
• Caused by
– Exacerbations
– Cor pulmonale
– Discontinuing bronchodilator or corticosteroid
medication
– Overuse of sedatives and opioids
– Surgery or severe, painful illness involving chest or
abdomen
COPD
Depression/Anxiety
• Approximately 50% of COPD patients
experience depression.
• If patient become anxious because of
dyspnea, teach pursed lip breathing.
COPD: Diagnostic Studies
• Diagnosis confirmed by pulmonary function tests
– Chest x-rays, spirometry, history, and physical examination.
• ABG typical findings
– Low PaO2
– ↑ PaCO2
– ↓ pH
– ↑ Bicarbonate level found in late stages of COPD
• 6-Minute walk test to determine O2 desaturation in the blood
with exercise
• ECG can show signs of right ventricular failure.
COPD: Collaborative Care
• Primary goals of care
– Prevent progression.
– Relieve symptoms.
– Prevent/treat complications.
– Promote patient participation.
– Prevent/treat exacerbations.
– Improve quality of life and reduce mortality risk.
– Irritants should be evaluated and avoided.
– Smoking cessation
Examples: the nurse should teach the patient to avoid aerosol hair sprays and smoke-filled
rooms.
– The most common antibiotics given for outpatients are macrolides (e.g., azithromycin
[Zithromax]), doxycycline, and cephalosporins (e.g., cefpodoxime [Vantin]).
COPD: Collaborative Care
• Drug therapy
– O2 therapy is used to
• Reduce work of breathing
• Reduce workload on the heart
– Bronchodilators
• Relax smooth muscle in the airway
• Improve ventilation of the lungs
• ↓ Dyspnea
• Inhaled route is preferred.
– β2-Adrenergic agonists(e.g., fluticasone/salmeterol [Advair])
Oxygen-Conserving Cannula
Low-Flow DeliveryDevices: Nasal Cannula.
Low-Flow Delivery Devices: Simple Face Mask.
Low-Flow Delivery Devices: Partial and
Non-Rebreathing Masks.
Fig. 29-11 A
Oxygen-Conserving Cannula
High-Flow Delivery Devices:
Tracheostomy Collar.
Low-Flow Delivery Devices:
Oxygen-Conserving Cannula.
High-Flow Delivery
Devices: Venturi Mask.
Fig. 29-11 A
COPD: Collaborative Care
• 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.
• Humidification
– Used because O2 has a drying effect on the mucosa
– Supplied by nebulizers, vapotherm, and bubble-through humidifiers
• Complications of oxygen therapy
– Combustion
– O2 toxicity
– Absorption atelectasis
– Infection
COPD: Collaborative Care
• Respiratory and physical therapy
– Breathing retraining
– Effective coughing
– Chest physiotherapy
• Percussion
• Vibration
COPD: Collaborative Care
• Breathing retraining
– Decreases dyspnea, improves oxygenation, and
slows respiratory rate
• Pursed lip breathing
• Prolongs exhalation and prevents bronchiolar collapse
and air trapping
– Effective coughing
• Main goals
– Facilitate removal of secretions.
COPD: Collaborative Care
• Percussion
– Hands in a cuplike position to create an air pocket
– Air-cushion impact facilitates movement of thick mucus. A thin towel
should be placed over the area to be percussed, or the patient may
choose to wear a T-shirt or hospital gown.
COPD: Collaborative Care
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Nutritional therapy
– Weight loss and malnutrition are common.
• Pressure on diaphragm from a full stomach causes dyspnea.
• Difficulty breathing while eating leads to inadequate consumption.
• To decrease dyspnea and conserve energy
– Rest at least 30 minutes before eating.
– Use bronchodilator.
– Eat five to six small meals.
– Cold foods may cause less fullness than hot foods.
• Avoid
– Foods that require a great deal of chewing
– Exercises and treatments 1 hour before and after eating
– Gas-forming foods
High-calorie, high-protein diet is recommended.
Fluids (intake of 3 L/day) should be taken between meals.
Nursing Management: Nursing Assessment
• Obtain complete health history and conduct a
complete physical assessment.
– See Table 29-24 in textbook for COPD-specific
information.
Nursing Management: Nursing Diagnoses
• Ineffective airway clearance
• Impaired gas exchange
• Imbalanced nutrition: Less than body
requirements
• Risk for infection
• Insomnia
Nursing Management: Planning
• Goals
– Prevention of disease progression
– Ability to perform ADLs
– Relief from symptoms
– No complications related to COPD
– Knowledge and ability to implement long-term
regimen
– Overall improved quality of life
Nursing Management
Nursing Implementation
• Health promotion
– Abstain from or stop smoking.
– Avoid or control exposure to occupational and
environmental pollutants and irritants.
– Early detection of small-airway disease
– Early diagnosis and treatment of respiratory tract
infection
– Awareness of family history of COPD and AAT
deficiency
Nursing Management: Nursing Implementation
• Activity considerations
– Modify ADLs to conserve energy.
– Walk 15 to 20 minutes a day at least 3 times a week with
gradual increases.
– Adequate rest.
• Sleep
– Can be difficult because of coughing
– Nasal saline sprays, decongestants, or nasal steroid
inhalers can help.
• Psychosocial considerations
– Healthy coping is difficult.
– May feel guilt, depression, anxiety, social isolation, denial,
and dependence
Nursing Management: Evaluation
• Expected outcomes
– Normal breath sounds
– Effective coughing
– Return of PaO2 to normal range for patient
– Improved mental status
– Maintenance of normal body weight
– Normal serum protein levels
– Feeling of being rested
– Improvement in sleep pattern
– Awareness of need to seek medical attention
– Behaviors minimizing risk of infection
– No infection
Question
When reviewing the arterial blood gases of a patient with COPD,
the nurse identifies late stage COPD with which of the following
results?
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1. pH 7.26, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3
30 mEq/L
2. pH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO3
18 mEq/L
3. pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO3
25 mEq/L
4. pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO3
35 mEq/L
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Asthma – Definition
• Chronic inflammatory disorder of airways
– Causes airway hyper-responsiveness leading to
wheezing, breathlessness, chest tightness, and
cough.
Pathophysiology
• Primary response is chronic inflammation
from exposure to allergens or irritants.
– Leading to airway hyperresponsiveness and acute
airflow limitations
– Inflammatory mediators cause early-phase
response.
– Vascular congestion
– Edema formation
– Production of thick, tenacious mucus
– Thickening of airway walls
Pathophysiology
• Late-phase response
– Occurs within 4 to 10 hours after initial attack
– Can be more severe than early phase and can last
for 24 hours or longer
– If airway inflammation is not treated or does not
resolve, it may lead to irreversible lung damage.
Early Phase Response of Asthma
Triggered by Allergen
Allergic asthma is triggered when an allergen cross-links IgE receptors on mast cells, which are then
activated to release histamine and other inflammatory mediators (early-phase response). A late-phase
response may occur due to further inflammation.
Triggers of Asthma
Allergens
 May be seasonal or year round depending on
exposure to allergen
– House dust mites
– Cockroaches
– Furry animals
– Fungi
– Molds
Triggers of Asthma
• Air Pollutants: Can trigger asthma attacks
– Cigarette or wood smoke
– Vehicle exhaust
– Elevated ozone levels
– Sulfur dioxide
• Exercise: Induced or exacerbated after exercise
– Pronounced with exposure to cold air
• Breathing through a scarf or mask may ↓
likelihood of symptoms
Triggers of Asthma
• Respiratory Infection:
– ↑ inflammation hyper-responsiveness of the tracheo-bronchial
system
• Nose and Sinus Problems: Allergic rhinitis and nasal polyps
– Large polyps are removed
– Sinus problems are usually related to inflammation of the mucous
membranes
• Emotional Stress:
– Attacks can trigger panic and anxiety.
– Extent of effect is unknown.
• Occupational Factors:
– Exposure to diverse agents
• Arrive at work well, but experience a gradual decline
Triggers of Asthma: Drugs and Food
Additives
Sensitivity to aspirin and NSAIDs
• Wheezing develops in about 2 hours.
• β-Adrenergic blockers (e.g., metoprolol [Toprol]) or
topical eyedrops (e.g., timolol [Timoptic]) may trigger
asthma as the result of bronchospasm.
• Food allergies may cause asthma symptoms.
– Avoidance diets
Clinical Manifestations
• Unpredictable and variable
– Recurrent episodes of wheezing, breathlessness, cough, and tight
chest
– May be abrupt or gradual
– Lasts minutes to hours
• Expiration may be prolonged.
– Inspiration-expiration ratio of 1:2 to 1:3 or 1:4
– Bronchospasm, edema, and mucus in bronchioles narrow the airways.
– Air takes longer to move out.
• Cough variant asthma
– Cough is only symptom.
– Bronchospasm is not severe enough to cause airflow obstruction.
Clinical Manifestations
• Difficulty with air movement can create a feeling of
suffocation.
– Patient may feel increasingly anxious.
• An acute attack usually reveals signs of hypoxemia.
– Restlessness
– ↑ anxiety
– Inappropriate behavior
– ↑ pulse and blood pressure
– Pulsus paradoxus (drop in systolic BP during
inspiratory cycle >10 mm Hg)
Complications
• Severe acute attack
– Respiratory rate >30/min
– Pulse >120/min
• Life-threatening asthma
 Too dyspneic to speak
 Perspiring profusely
 Drowsy/confused
 Require hospital care and often admitted to ICU
Diagnostic Studies
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Detailed history and physical exam
Pulmonary function tests
Chest x-ray
ABGs
Oximetry
Allergy testing
Blood levels of eosinophils
Sputum culture and sensitivity
Collaborative Care
 Severe exacerbations
– IV corticosteroids are administered every 4 to 6 hours,
then are given orally.
• The length of oral prednisone treatment for both
severe and life-threatening asthma after discharge is
usually about 10 days.
– Continuous monitoring of patient is critical.
– IV magnesium sulfate is given as a bronchodilator.
– Supplemental O2 is given by mask or nasal cannula for 90%
O2 saturation.
• Arterial catheter may be used to facilitate frequent ABG
monitoring.
– IV fluids are given because of insensible loss of fluids.
Drug Therapy
• Three types of antiinflammatory drugs
– Corticosteroids
– Leukotriene modifiers
– Monoclonal antibody to IgE
Drug Therapy
• Corticosteroids (e.g., beclomethasone,
budesonide(Pulmicort))
– Suppress inflammatory response
– Inhaled form is used in long-term control.
– Systemic form to control exacerbations and
manage persistent asthma
– 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
Spacer
Example of an Aero Chamber spacer used with a metered-dose inhaler.
Drug Therapy
• Leukotriene modifiers or inhibitors (e.g.,
zafirlukast, montelukast, zileuton)
– Block action of leukotrienes—potent
bronchoconstrictors
– Have both bronchodilator and antiinflammatory
effects
– Not indicated for acute attacks
– Used for prophylactic and maintenance therapy
Drug Therapy
• Anti-IgE (e.g., Xolair)
– ↓ circulating free IgE levels
– Prevents IgE from attaching to mast cells,
preventing release of chemical mediators
– Subcutaneous administration every 2 to 4 weeks
Drug Therapy
• Three types of bronchodilators
– β2-Adrenergic agonists
– Methylxanthines
– Anticholinergics
Drug Therapy
• β-Adrenergic agonists (e.g., albuterol,
metaproterenol)
• Known as rescue medications.
– Effective for relieving acute bronchospasm
– Onset of action in minutes and duration of 4 to 8
hours
– Prevent release of inflammatory mediators from
mast cells
– Not for long-term use
Drug Therapy
• Methylxanthines (e.g., theophylline)
– Less effective long-term bronchodilator
– Alleviates early phase of attacks but has little
effect on bronchial hyperresponsiveness
– Narrow margin of safety
– The main problem with theophylline is the
relatively high incidence of interaction with other
drugs and the occurrence of side effects.
Drug Therapy
• Anticholinergic drugs (e.g., ipratropium)
– Block action of acetylcholine
– Usually used in combination with a bronchodilator
– Most common side effect is dry mouth.
DPI (dry powder inhaler)
Nursing Management: Nursing Implementation
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Acute intervention
– Monitor respiratory and cardiovascular systems:
• Lung sounds
• Respiratory rate
• Pulse
• BP
An important goal of nursing is to ↓ the patient’s sense of panic.
– Stay with patient.
– Encourage slow breathing using pursed lips for prolonged expiration.
– Position comfortably.
Ambulatory and home care
– Must learn about medications and develop self-management strategies
– Patient and health care professional must monitor responsiveness to
medication.
– Patient must understand importance of continuing medication when
symptoms are not present.
Nursing Management
Nursing Implementation
• Important patient teaching
– Seek medical attention for bronchospasm or when
severe side effects occur.
– Maintain good nutrition.
– Exercise within limits of tolerance.
Cystic Fibrosis
• Autosomal recessive, multisystem disease of
– Lungs
– Pancreas
– Sweat glands
• Abnormally thick mucus can lead to chronic diffusive,
obstructive pulmonary disorder.
• CF results from mutations in a gene located on chromosome
7.
– Alters ionic transport of sodium and chloride in the sweat
Cystic Fibrosis
Etiology and Pathophysiology
• Most common organisms cultured are
– Staphylococcus aureus
– Haemophilus influenzae
– Burkholderia cepacia
– Pseudomonas aeruginosa
Cystic Fibrosis: Etiology and Pathophysiology
• Death usually results from loss of pulmonary
function.
• Exocrine function of pancreas is altered or may be
lost completely.
– Enzymes trypsinogen, lipase, and amylase do not
reach the intestine to digest ingested nutrients.
• Fat, protein, and fat-soluble vitamins are
malabsorbed.
– Results in steatorrhea (an excess of fat in the
stool)
– Protein malabsorption results in failure to grow
and gain weight.
Cystic Fibrosis: Clinical Manifestations
• Early manifestations
– Failure to grow
– Clubbing
– Persistent cough with mucous production
– Tachypnea
– Large, frequent bowel movements
– Clinical manifestations are consistent among
family members.
Cystic Fibrosis : Clinical Manifestations
• First symptom in adult is usually frequent
cough.
– Becomes viscous and purulent
– Produces greenish-colored sputum
• As disease progresses
– Exacerbations of ↑ cough
– Weight loss
– ↑ Sputum
– ↓ In pulmonary function
Cystic Fibrosis
Clinical Manifestations
• Exacerbations become more frequent, and
recovery of lost lung is less complete.
• Ultimately results in respiratory failure
• Distal intestinal obstruction causes
– Right lower quadrant pain
– Loss of appetite
– Emesis
– Palpable mass
Cystic Fibrosis: Complications
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Pneumothorax is common
Hemoptysis (can be life-threatening)
Digital clubbing
Bone disease
Liver disease
Late complications
– Respiratory failure
– Cor pulmonale
Cystic Fibrosis: Diagnostic Studies
• Sweat chloride test with pilocarpine
iontophoresis method
– Pilocarpine carried by electric current is used to
stimulate sweat production.
– Values >60 mEq/L for both sodium and chloride
suggest CF.
Cystic Fibrosis
Diagnostic Studies
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Genetic test
Chest x-ray
Pulmonary function tests
Fecal analysis for fat
Duodenoscopy for quantitative determination
of pancreatic enzymes
Cystic Fibrosis
Collaborative Care
• Provide adequate nutrition.
• Manage pulmonary problems
(e.g., relieving airway obstruction).
• Aerosol and nebulization treatments of
medications to liquefy mucus and to facilitate
coughing
Nursing Management
Nursing Assessment
 Health history
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Respiratory infections, cough with sputum
Family history
Dietary intolerances, weight loss
Large, frequent bowel movements
Decreased activity tolerance, dyspnea
Abdominal pain
Anxiety, depression
Cyanosis, salty skin
Runny nose
Diminished breath sounds
Hemoptysis
Use of accessory muscles
Tachycardia
Foul, fatty stools
Abdominal distention
Abnormal ABGs
X-ray
Nursing Management
Nursing Implementation
 Help patient assume responsibility for career and goals.
 Discuss altered sexuality.
 Provide relief of bronchoconstriction, airway obstruction, and
airflow limitation.
 Antibiotics,
O2 therapy, and corticosteroids
 Adequate nutrition
 Postural drainage with percussion and vibration
 Aerosol-nebulization therapy
 Controlled coughing techniques
 Deep-breathing exercises
 Progressive exercise conditioning