ADULT NURSING 1 – CHRONIC
CHEST DISORDERS
Incidence
The economic burden of COPD extends beyond direct medical
costs. Hospital admissions for COPD patients cost more
annually than for patients without COPD. These patients are
also 60% more likely to call in sick and 2.6 times more likely
to incur short-term disability compared to those without COPD.
Chronic Obstructive Pulmonary Disease
(COPD)
COPD is a preventable and treatable, slowly progressive
respiratory disease characterized by airflow obstruction
involving the airways, pulmonary parenchyma, or both. Its
incidence increases with age, and it often presents with
overlapping signs and symptoms of emphysema and chronic
bronchitis
- 88-93%
- Sit the patient up:
Smoking, genetic factors, exposure to toxic
.
Pathophysiology

Airflow limitation is progressive and linked to
an abnormal inflammatory response to harmful particles or
gases.

There is an increase in goblet cells.

Chronic inflammation leads to tissue damage.

Scar tissue in the airways causes narrowing.

Scar tissue in the parenchyma reduces elastic recoil
(decreases compliance).

Scar tissue in the pulmonary vasculature thickens the
vessel lining and causes smooth muscle hypertrophy,
potentially leading to pulmonary hypertension.
Emphysema
Emphysema is defined by the abnormal distention of air
spaces beyond the terminal bronchioles, accompanied by the
destruction of the walls of over-distended alveoli.

This leads to a decreased alveolar surface area,
increasing "dead space" and impairing oxygen diffusion,
resulting in hypoxemia.

Increased pulmonary artery pressure can cause right-sided
heart failure (cor pulmonale), leading to blood backup in
the venous system.
Main Types of Emphysema

Panlobular: Destruction of the respiratory bronchioles,
alveolar ducts, and alveoli, resulting in enlarged air
spaces. Expiration becomes an active process.

Centrilobar: Pathologic changes occur in the center of
the secondary lobules, leading to ventilation-perfusion
derangement, hypoxemia, hypercapnia, and polycythemia
(abnormally high number of RBCs in the blood).
Risk Factors

Exposure to tobacco smoke: Accounts for an estimated 80%90% of cases.

Passive smoking (second-hand smoke).

Increased age.

Occupational exposure: Dust, chemicals.

Indoor and outdoor air pollution.

Genetic abnormalities: Such as alpha1-antitrypsin
deficiency, which is an enzyme inhibitor that normally
counteracts lung tissue destruction by certain enzymes.
Clinical Manifestations

Chronic cough

Sputum production

Dyspnea

Weight loss
Grades of COPD

Grade I (Mild): Forced Expiratory Volume in 1 second
(FEV1) ≥80% predicted.

Grade II (Moderate): FEV1 50%-79% predicted.

Grade III (Severe): FEV1 30%-49% predicted.

Grade IV (Very Severe): FEV1 <30% predicted.
Assessment

Health history

Inspection and examination findings

Review of diagnostic tests (Arterial Blood Gases - ABGs,
Chest X-ray - CXR, screening)

Spirometry: Used to evaluate airflow obstruction and
assess reversibility.
Factors Determining Clinical Course and Survival

History of cigarette smoking

Exposure to second-hand smoke

Age

Rate of decline of FEV1

Hypoxemia

Pulmonary artery pressure

Resting heart rate

Weight loss

Reversibility of airflow obstruction

Comorbidities
Specific Considerations for the Patient with COPD
Receiving Oxygen Therapy

Oxygen therapy can be administered as long-term
continuous therapy, during exercise, or to prevent acute
dyspnea during an exacerbation.

The primary goal is to increase the baseline resting
partial pressure of arterial oxygen (PaO2) to at least 60
mm Hg at sea level, corresponding to an arterial oxygen
saturation (SaO2) of 90%.

For patients with exercise-induced hypoxemia, oxygen
supplementation during exercise may improve dyspnea but
will not reduce breathlessness in daily life.
Medical Management

Risk reduction

Pharmacological management:
o
Bronchodilators:

Beta-Adrenergic agents: Salbutamol (shortacting), Serevent Diskus (long-acting).

Anticholinergic agents: Ipratropium Bromide.

Combined: Combivent.
o
Inhaled Corticosteroids: Such as Symbicort or
combinations like salmeterol/fluticasone.
o
Alpha1-antitrypsin augmentation therapy.
o
Antibiotic agents.
o
Mucolytic agents.
o
Antitussive agents.
o
Vasodilators - medicines that widen (relax) blood vessels so
blood can flow more easily. This: Lowers blood pressure, improves
blood flow, and reduces the heart’s workload
o
Opioids - strong pain-relief medicines that work on the brain and
spinal cord to reduce the feeling of pain.
o
Vaccines: To prevent exacerbations by preventing
respiratory infections.
Management of Exacerbations
An exacerbation is an event in the natural course of COPD
characterized by acute changes (worsening) in respiratory
symptoms beyond normal day-to-day variations, needing a change
in medication.

Primary causes: Viral infections.

Treatment: Finding and treating the specific cause.
Surgical Management

Bullectomy

Lung volume reduction surgery

Lung transplant
Pulmonary Rehabilitation
Primary goals include:
1. Reducing symptoms.
2. Improving quality of life.
3. Increasing physical and emotional participation in
everyday activities.
Benefits include:

Improvement of exercise capacity.

Reduction in the perceived intensity of breathlessness.

Improvement in health-related quality of life.

Reduction in the number and duration of hospitalizations.

Reduction in anxiety and depression associated with COPD.
Nursing Management/Implementation

Assess the client.

Achieve airway clearance (Chest Physiotherapy - CPT,
postural drainage, High-Frequency Chest Wall Oscillation
- HFCWO).

Improve breathing patterns (pursed-lip breathing,
diaphragmatic breathing, breathing retraining).

Improve activity tolerance.

Monitor and manage potential complications (infections,
respiratory failure, atelectasis, pneumothorax, pulmonary
hypertension).

Educate the client about self-care.

Nutrition management.

Encourage effective coping.

Palliative care.

Promote home, community-based, and transitional care.
Emphysema
Emphysema is defined as the abnormal distention of air spaces
beyond the terminal bronchioles, accompanied by the
destruction of the walls of over-distended alveoli 10.
Pathophysiology and Consequences

Decreased Alveolar Surface Area: The destruction of
alveolar walls leads to a reduction in the surface area
available for gas exchange.

Increased "Dead Space": This refers to lung areas that
are ventilated but not perfused, or areas where gas
exchange is impaired. The increased dead space
contributes to inefficient breathing.

Impaired Oxygen Diffusion: With less surface area and
compromised diffusion pathways, the transfer of oxygen
from the lungs into the bloodstream is hindered.

Hypoxemia: The impaired oxygen diffusion directly results
in lower oxygen levels in the blood (hypoxemia).

Cor Pulmonale: Chronic hypoxemia and increased resistance
in the pulmonary arteries can lead to elevated pulmonary
artery pressure. This increased pressure strains the
right side of the heart, potentially causing right-sided
heart failure, a condition known as cor pulmonale. Blood
can then back up into the venous system, leading to
systemic venous congestion 10.
Bronchiectasis
Bronchiectasis is a chronic, irreversible dilation of the
bronchi and bronchioles resulting from the destruction of
muscles and elastic connective tissue.

It is caused by recurrent respiratory infections, Cystic
Fibrosis (CF), rheumatic and other systemic diseases,
primary ciliary dysfunction, tuberculosis, or immune
deficiency disorders.

It predominantly affects the lower lobes of the lungs.
Pathophysiology
The inflammatory process associated with pulmonary infections
damages the bronchial walls, leading to a loss of supporting
structure. This results in thick sputum that obstructs the
bronchi. The bronchial walls become permanently distended and
distorted, impairing mucociliary clearance. The retention of
secretions and subsequent obstruction ultimately cause the
collapse of alveoli distal to the obstruction (atelectasis).
Inflammatory scarring or fibrosis replaces functioning lung
tissue.
Clinical Manifestations

Chronic cough

Copious production of purulent sputum

Hemoptysis (coughing up blood)

Clubbing of the fingers

Repeated episodes of pulmonary infection
Diagnostic
Bronchiectasis can be challenging to diagnose as symptoms may
mimic chronic bronchitis. A prolonged history of productive,
chronic cough with sputum consistently negative for tubercle
bacilli is a key indicator. The diagnosis is definitively
established by a CT scan, which reveals bronchial dilation.
High-resolution CT scanning allows for earlier diagnosis.
Medical Management
Treatment objectives focus on promoting bronchial drainage,
clearing excessive secretions, and preventing or controlling
infection and inflammation.

Postural drainage

Chest physiotherapy

Smoking cessation

Antimicrobial therapy

Nebulized mucolytics

Bronchodilators

Surgery
Nursing Management
The nursing focus is on alleviating symptoms and clearing
pulmonary secretions.

Patient teaching includes:
o
Postural drainage techniques.
o
Avoiding exposure to irritants.
o
Conserving energy.
o
Nutritional guidance.
Asthma
Asthma is a chronic inflammatory disease of the
airways characterized by airway hyperresponsiveness, mucosal
edema, and mucus production 34. This inflammation leads to
symptoms such as cough, chest tightness, wheezing, and
dyspnea.
Pathophysiology
Asthma involves reversible, diffuse airway
inflammation leading to long-term airway narrowing. This
narrowing is exacerbated by several airway changes:

Bronchoconstriction

Airway edema

Airway hyperresponsiveness

Airway remodeling
The interplay of these factors dictates the clinical
manifestations.
Clinical Manifestations
The three most common symptoms are cough, dyspnea, and
wheezing. In some cases, cough may be the sole symptom. Asthma
attacks often occur at night or in the early morning,
potentially due to circadian variations affecting airway
receptor thresholds.
Prevention

Patients with recurrent asthma should undergo testing to
identify precipitating substances. Common triggers
include dust, dust mites, roaches, certain fabrics, pets,
horses, detergents, soaps, certain foods, molds, and
pollens. Seasonal attacks may indicate pollen as a strong
suspect.

Patients are instructed to avoid causative agentswhenever
possible. Knowledge and identification of triggers are
crucial for effective asthma care.

Occupational asthma is induced by workplace exposures
(dusts, vapors, fumes) and may occur with or without a
pre-existing asthma diagnosis.
Management

Prevention of risk factors.

Pharmacologic therapy:
o
Bronchodilators: Short-acting beta-2 adrenergic
agonists and anticholinergics.
o
Corticosteroids: Patients should rinse their mouths
after using inhaled forms.
o
Leukotriene inhibitors: Such as Montelukast.
o
Phosphodiesterase inhibitors: Such as Roflumilast.
o
Immunomodulators: Such as Omalizumab.
The nurse assesses the patient's respiratory status by
monitoring symptom severity, breath sounds, peak flow, pulse
oximetry, and vital signs.
Peak Flow Monitoring
Peak flow monitoring uses color-coded zones to guide
management:

Green Zone: 80%-100% of personal best – indicates good
control.

Yellow Zone: 60%-80% of personal best – indicates
caution; asthma may be worsening.

Red Zone: <60% of personal best – indicates a medical
alert; requires immediate action.
Pathophysiology of Severe Bronchospasm

Inflammation and Constriction: Inflammation of the
bronchial mucosa, along with constriction of the
bronchiolar smooth muscle and thickened secretions, leads
to a decrease in the diameter of the bronchioles.

Asphyxia: Severe bronchospasm can result in asphyxia.

Hypoxemia and Acidosis: Ventilation-perfusion imbalances
arise, leading to hypoxemia and subsequent respiratory
acidosis.
Clinical Manifestations of Severe
Bronchospasm

Labored breathing

Engorged neck veins

Prolonged exhalation

Wheezing (may disappear as obstruction worsens,
indicating respiratory failure) 46
Management of Severe Bronchospasm

Assessment and diagnostic findings

Bronchodilators

Corticosteroids

Oxygen therapy

Intravenous fluids

Magnesium sulfate (a calcium antagonist)

Intubation

Bronchial Thermoplasty 47
Cystic Fibrosis
Cystic Fibrosis: Incidence and Genetics

Prevalence: Cystic Fibrosis (CF) is the most common fatal
autosomal recessive disease among Caucasians. It is less
common in Hispanic, Asian, and African Americans 49.

Inheritance: An individual must inherit a defective copy
of the CF gene from each parent to have CF 49.

Diagnosis: Approximately 1000 new cases of CF are
diagnosed annually, with over 75% of patients diagnosed
by 2 years of age (Cystic Fibrosis Foundation [CFF],
2019a) 49.
Cystic Fibrosis: Pathophysiology

CFTR Protein Dysfunction: CF is caused by mutations or
dysfunction in the cystic fibrosis transmembrane
conductance regulator (CFTR) protein, which is
responsible for transporting chloride ions across
epithelial cell membranes 50.

Consequences of Gene Mutations: Gene mutations disrupt
ion transport, leading to CF. This condition is
characterized by thick, viscous secretions in the lungs,
pancreas, liver, intestine, and reproductive tract.
Additionally, there is an increased salt content in sweat
gland secretions 50.
Cystic Fibrosis: Clinical Manifestations

Pulmonary Symptoms: Manifestations include a productive
cough, wheezing, hyperinflation of lung fields on chest
X-ray, and pulmonary function test results indicative of
obstructive airway disease 51.

Chronic Inflammation and Infection: Impaired mucus
clearance leads to chronic respiratory inflammation and
infection 51.

Bacterial Colonization: Airways are typically colonized
with pathogenic bacteria early in life. Common organisms
include S. aureus and H. influenzae during early
childhood 51.
Cystic Fibrosis: Medical Management
CF management requires both acute and chronic therapies. Key
components include:

Multimodal Antibiotic Regimens: For infections.

Airway Clearance Measures:
o
Mucolytics (e.g., dornase alfa, inhaled hypertonic
saline) 52.
o
Pulmonary techniques to promote mucus expectoration.
o
Chest Physical Therapy (CPT) and High-Frequency
Chest Wall Oscillation (HFCWO).

Bronchodilators: To open airways.

CFTR Modulators: Medications targeting the underlying
CFTR defect.

Nutritional Support: Including oral pancreatic enzyme
supplements.

Exercise: Important for overall health and lung function.
Cystic Fibrosis: Nursing Management
Nursing care focuses on helping patients manage pulmonary
symptoms and prevent complications. Key interventions include:

Promoting Secretion Removal: Implementing strategies for
effective mucus clearance.

CPT: Including postural drainage, chest percussion, and
vibration.

Breathing Exercises: Teaching patients and families these
techniques from an early age.

Risk Factor Reduction: Educating patients on minimizing
exposure to crowds or individuals with known infections
to reduce respiratory infection risk.

Early Symptom Recognition: Teaching patients the early
signs and symptoms of respiratory infection and disease
progression that warrant notification of a primary
healthcare provider.