Management of Patients With
Chronic Pulmonary Disease
Chronic Obstructive Pulmonary Disease
and Associated Respiratory Diseases
COPD is a slowly progressive respiratory disease of
airflow obstruction
o Emphysema, chronic bronchitis
o Preventable and treatable but not fully reversible
o Involving the airways, pulmonary parenchyma, or
both
o Cannot get air out
Other
o Cystic fibrosis, bronchiectasis, asthma
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Pathophysiology of COPD
Airflow limitation is progressive, with abnormal
inflammatory response to noxious particles or gases
Chronic inflammation damages tissue
Scar tissue in airways results in narrowing
Scar tissue in the parenchyma decreases elastic recoil
(compliance)
Scar tissue in pulmonary vasculature causes thickened
vessel lining and hypertrophy of smooth muscle
(pulmonary hypertension)
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Risk Factors
Exposure to tobacco smoke accounts for an estimated
80% to 90% of cases
Passive smoking (i.e., secondhand smoke)
Increased age
Occupational exposure—dust, chemicals Indoor and
outdoor air pollution
Genetic abnormalities
o deficiency of alpha1-antitrypsin
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Chronic Bronchitis
Cough and sputum production for at least 3 months in
each of 2 consecutive years
Ciliary function is reduced, bronchial walls thicken,
bronchial airways narrow, and mucous may plug airways
Alveoli become damaged, fibrosed, and alveolar
macrophage function diminishes
The patient is more susceptible to respiratory infections
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Pathophysiology of Chronic Bronchitis
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Emphysema
Abnormal distention of air spaces beyond the terminal
bronchioles with destruction of the walls of the alveoli
Decreased alveolar surface area increases in “dead
space,” impaired oxygen diffusion
Hypoxemia results
Increased pulmonary artery pressure may cause rightsided heart failure (cor pulmonale)
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Clinical Manifestations of COPD
Three primary symptoms
o Chronic cough
o Sputum production
o Dyspnea
Diminished breath sounds, wheezes, crackles
Accessory muscle use
Weight loss due to dyspnea
“Barrel chest”
ABGs ➡ high PCO2 and low pH
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Normal Chest versus Barrel-Shaped Chest
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Typical Posture of a Person With COPD
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Assessment and Diagnosis of COPD
Health history, refer to Chart 20-2
Pulmonary function tests
Spirometry
Arterial blood gas
Chest x-ray
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Complications of COPD
Respiratory insufficiency and failure
Pneumonia
Chronic atelectasis
Pneumothorax
Cor pulmonale
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Medical Management
Promote smoking cessation
Reducing risk factors
Managing exacerbations
Providing supplemental oxygen therapy
Pneumococcal vaccine
Influenza vaccine
Pulmonary rehabilitation
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Oxygen Therapy
Oxygen via nasal cannula up to 2 lpm…why is this?
o Poor gas exchange leads to hypoxia and hypercapnia
o Chronic hypercapnia ➡ drive to breathe
Maintain SpO2 88-92%
What will happen with too much oxygen administration?
o Reduce drive to breathe
o Hypercapneic respiratory failure ➡ narcosis
Bipap or intubation to reverse hypercapneic respiratory
failure.
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Medications to Treat COPD
Bronchodilators, MDIs
o Beta-adrenergic agonists
o Muscarinic antagonists (anticholinergics)
o Combination agents
Corticosteroids
Antibiotics
Mucolytics
Antitussives
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Patient Education
Pursed lip breathing
Small frequent meals
Increase fluids
Smoking cessation
Oxygen safety at home
Avoid triggers and allergens
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Bronchiectasis
Bronchiectasis is a chronic, irreversible dilation of the
bronchi and bronchioles
Caused by:
o Airway obstruction, pulmonary infections
o Diffuse airway injury
o Genetic disorders
o Abnormal host defenses
o Idiopathic causes
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Bronchiectasis: Clinical Manifestations
and Medical Management
Chronic cough
Purulent sputum in copious amounts
Clubbing of the fingers
Postural drainage
Chest physiotherapy
Smoking cessation
Antimicrobial therapy
Bronchodilators and mucolytics
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Bronchiectasis: Nursing Management
Focus is on alleviating symptoms and clearing pulmonary
secretions
Patient teaching
o Smoking cessation
o Postural drainage
o Early signs and symptoms of respiratory infections
o Conserving energy
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Asthma
Chronic inflammatory disease of the airways that causes
hyperresponsiveness, mucosal edema, and mucus
production
Inflammation leads to cough, chest tightness, wheezing,
and dyspnea (Fig. 20-10)
Asthma is largely reversible; spontaneously or with
treatment
Allergy is the strongest predisposing factor
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Clinical Manifestations
Cough, dyspnea, wheezing
Exacerbations
o Cough, productive or not
o Generalized wheezing
o Chest tightness and dyspnea
o Diaphoresis
o Tachycardia
o Hypoxemia and central cyanosis
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Medications Management for Asthma
Stepwise, refer to Figure 24-7
Quick-relief medications
o Beta2-adrenergic agonists
o Anticholinergics
Long-acting medications
o Corticosteroids
o Long-acting beta2-adrenergic agonists
o Leukotriene modifiers
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Patient Teaching
How to identify and avoid triggers
Proper inhalation techniques
How to perform peak flow monitoring
How to implement an action plan
When and how to seek assistance
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Cystic Fibrosis
Most common autosomal recessive disease among the
Caucasian population
Genetic screening to detect carriers
Genetic counseling for couples at risk
Genetic mutation changes chloride transport which leads
to thick, viscous secretions in the lungs, pancreas, liver,
intestines, and reproductive tract
Respiratory infections are the leading cause of morbidity
and mortality
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Medical Management of CF
Chronic: control of infections; antibiotics
Acute: aggressive therapy involves airway clearance and
antibiotics based on results of sputum cultures
Anti-inflammatory agents
Corticosteroids; inhaled, oral, IV during exacerbations
Inhaled bronchodilators
Oral pancreatic enzyme supplementation with meals
Cystic fibrosis transmembrane conductance regulator
(CFTR) modulators are a new class of drugs and help to
improve function of the defective CFTR protein
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Nursing Management of CF
Strategies that promote removal of pulmonary secretions
o CPT and breathing exercises
Remind patient to reduce risk factors for resp infection
Adequate fluid and electrolyte intake
Palliative care
Discuss end-of-life issues and concerns
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