COPD, asthma.pdf

11/15/2022
By Getu M( Bsc, Msc)
1
Chronic Obstructive Pulmonary Disease

Objectives
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At the end of the session the students will able to:
 Describe COPD
 Describe patho-physiology of chronic bronchitis and
emphysema
 List clinical features of chronic bronchitis and emphysema
 Identify managements of chronic bronchitis and emphysema
 Develop nursing process for the patients with chronic
bronchitis and emphysema

Chronic Obstructive Pulmonary Disease
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 It is defined as a disease state characterized by persistent respiratory
symptoms and airflow obstruction
 COPD includes emphysema, an anatomically defined condition
characterized by destruction of the lung alveoli with air space
enlargement;
 Chronic bronchitis, a clinically defined condition with chronic cough
and phlegm; and/or small airway disease, a condition in which small
bronchioles are narrowed and reduced in number

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 The classic definition of COPD requires:
 The presence of chronic airflow obstruction,
 Determined by spirometry,
 That usually occurs in the setting of noxious
environmental exposures—most commonly products
of combustion,
 cigarette smoking in the United States, and
 biomass fuels in some other countries

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 Respiratory symptoms and other features of COPD can occur
in subjects who do not meet a definition of COPD based only
on airflow obstruction determined by spirometric population
thresholds of normality.
 Investigators in the COPDGene study recently proposed a
multidimensional approach to COPD diagnosis, which is based
on domains of environmental exposures, respiratory symptoms,
imaging abnormalities, and physiologic abnormalities.

Pathophysiology
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 Pathologic changes in chronic obstructive pulmonary
disease (COPD) occur in the large (central) airways, the
small (peripheral) bronchioles, and the lung parenchyma.
 Most cases of COPD are the result of exposure to
noxious stimuli, most often cigarette smoke.
 The normal inflammatory response is amplified in persons
prone to COPD development.
 The pathogenic mechanisms are not clear but are most
likely diverse.
 Increased numbers of activated polymorphonuclear
leukocytes and macrophages release elastases in a manner
that cannot be counteracted effectively by antiproteases,
resulting in lung destruction.

Cont.….
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 The primary offender has been found to be human
leukocyte elastase, with synergistic roles suggested for
proteinase-3 and macrophage-derived matrix
metalloproteinases (MMPs), cysteine proteinases, and a
plasminogen activator.
 Additionally, increased oxidative stress caused by free
radicals in cigarette smoke, the oxidants released by
phagocytes, and polymorphonuclear leukocytes all may lead
to apoptosis or necrosis of exposed cells.
 Accelerated aging and autoimmune mechanisms have also
been proposed as having roles in the pathogenesis of COPD.

Cont.….
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 Cigarette smoke causes neutrophil influx, which is
required for the secretion of MMPs; this suggests,
therefore, that neutrophils and macrophages are required
for the development of emphysema.
 Studies have also shown that in addition to macrophages,
T lymphocytes, particularly CD8+, play an important role
in the pathogenesis of smoking-induced airflow limitation

Pathogenesis of emphysema
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Etiology
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Cigarette smoking
 The primary cause of COPD is exposure to tobacco smoke.
Overall, tobacco smoking accounts for as much as 90% of
COPD risk.
 Cigarette smoking induces macrophages to release
neutrophil chemotactic factors and elastases, which lead to
tissue destruction.
 Clinically significant COPD develops in 15% of cigarette
smokers, although this number is believed to be an
underestimate.
 Age of initiation of smoking, total pack-years, and current
smoking status predict COPD mortality.

Cont.….
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Airway hyperresponsiveness
 Airway hyper-responsiveness (ie, Dutch hypothesis)
stipulates that patients who have nonspecific airway
hyper-reactivity and who smoke are at increased risk of
developing COPD with an accelerated decline in lung
function.

Cont.….
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Environmental factors
 COPD does occur in individuals who have never smoked.
 Although the role of air pollution in the etiology of COPD is
unclear, the effect is small when compared with that of cigarette
smoking.
 In developing countries, the use of biomass fuels with indoor
cooking and heating is likely to be a major contributor to the
worldwide prevalence of COPD.
 Long-term exposure to traffic-related air pollution may be a
factor in COPD in patients with diabetes and asthma.

Cont.….
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Alpha1-antitrypsin deficiency
 Alpha1-antitrypsin (AAT) is a glycoprotein member of the
serine protease inhibitor family that is synthesized in the
liver and is secreted into the bloodstream.
 The main purpose of this 394-amino-acid, single-chain
protein is to neutralize neutrophil elastase in the lung
interstitium and to protect the lung parenchyma from
elastolytic breakdown.
 Severe AAT deficiency predisposes to unopposed elastolysis
with the clinical sequela of an early onset of panacinar
emphysema.

Cont.….
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Intravenous drug use
 Emphysema occurs in approximately 2% of persons who
use intravenous (IV) drugs.
 This is attributed to pulmonary vascular damage that
results from the insoluble filler (eg, cornstarch, cotton
fibers, cellulose, talc) contained in methadone or
methylphenidate.

Cont.….
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Immunodeficiency syndromes
 Human immunodeficiency virus (HIV) infection has been
found to be an independent risk factor for COPD, even after
controlling for confounding variables such as smoking, IV
drug use, race, and age.
 Apical and cortical bullous lung damage occurs in patients
who have autoimmune deficiency syndrome and Pneumocystis
carinii infection.

Epidemiology
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 The exact prevalence of COPD worldwide is largely unknown, but
estimates have varied from 7-19%.
 Globally, there are an estimated 250 million individuals with COPD.
 The Burden of Obstructive Lung Disease (BOLD) study found a global
prevalence of 10.1%.
 Men were found to have a pooled prevalence of 11.8% and women
8.5%.
 The numbers vary in different regions of the world.
 Cape Town, South Africa, has the highest prevalence, affecting 22.2% of
men and 16.7% of women.

Diagnoses of COPD
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Hx (main symptoms + smoking, occupational,
environmental exposure),
Physical exam
Chest-X-ray- hyperlucency (emphysema) and hyperinflation
(Increased lung volumes and flattening of the diaphragm
suggest)
Spirometric dx (Lung function test): to establish dx
 Failure to improves significantly in airflow reduction with administration
of bronchodilators (FEV1/FVC < 0.7 - persistent airflow limitation)

Cont.….
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ABG analysis ( PaCo2, decrease PaO2)
 Normal in moderate disease
 Later: hypercapnia and respiratory acidosis
Sputum culture
CBC
 Increase RBC
 Leukocytes

Cont.….
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 The formal diagnosis of COPD is made with spirometry.
 when the ratio of forced expiratory volume in 1 second over
forced vital capacity (FEV1/FVC) is less than 70% of that
predicted for a matched control, it is diagnostic for a
significant obstructive defect.

Cont.….
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Criteria for assessing the severity of airflow obstruction
(based on the percent predicted post-bronchodilator FEV1)
are as follows:
 Stage I (mild): FEV1 80% or greater of predicted
 Stage II (moderate): FEV1 50-79% of predicted
 Stage III (severe): FEV1 30-49% of predicted
 Stage IV (very severe): FEV1 less than 30% of predicted or
FEV1 less than 50% and chronic respiratory failure

GOLD criteria
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Signs and symptoms
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 Patients typically present with a combination of signs and
symptoms of chronic bronchitis, emphysema, and reactive
airway disease.
Symptoms include the following:
 Cough, usually worse in the mornings and productive of a
small amount of colorless sputum
 Breathlessness:The most significant symptom, but usually
does not occur until the sixth decade of life
 Wheezing: May occur in some patients, particularly during
exertion and exacerbations

Findings in severe disease include the following:
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 Tachypnea and respiratory distress with simple activities
 Use of accessory respiratory muscles and paradoxical
indrawing of lower intercostal spaces (Hoover sign)
 Cyanosis
 Elevated jugular venous pulse (JVP)
 Peripheral edema

Thoracic examination reveals the following:
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 Hyperinflation (barrel chest)
 Wheezing – Frequently heard on forced and unforced
expiration
 Diffusely decreased breath sounds
 Hyperresonance on percussion
 Prolonged expiration
 Coarse crackles beginning with inspiration in some case

Certain characteristics allow differentiation between
disease that is predominantly chronic bronchitis and
that which is predominantly emphysema
Chronic bronchitis Emphysema
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 Patients may be obese
 Frequent cough and
expectoration are typical
 Use of accessory muscles of
respiration is common
 Coarse rhonchi and wheezing
may be heard on auscultation
 Patients may have signs of
right heart failure (i.e. cor
pulmonale), such as edema
and cyanosis
 Patients may be very thin with a
barrel chest
 Patients typically have little or no
cough or expectoration
 Breathing may be assisted by
pursed lips and use of accessory
respiratory muscles; patients may
adopt the tripod sitting position
 The chest may be hyperresonant,
and wheezing may be heard
 Heart sounds are very distant

Chronic bronchitis
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Presence of recurrent or chronic productive cough for a
minimum of 3 months for 2 consecutive years.
Risk factors
 Bronchial irritants (e.g. cigarette smoke, exposure to
pollution)
 Genetic predisposition (alpha-1 antitrypsin deficiency)
 Respiratory infections

Chronic Bronchitis: Pathophysiology
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Chronic inflammation
Hypertrophy & hyperplasia of bronchial glands that secrete
mucus
Increase number of goblet cells
Cilia are destroyed
Bronchial smooth muscle hyper reactivity

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Narrowing of airway
 airflow resistance
 work of breathing
Hypoventilation & CO2 retention  hypoxemia &
hypercapnea

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Bronchial walls thickened, bronchial lumen narrowed, and
mucus may plug in the airway.
Alveoli become damaged and fibrosed,
Altered function of the alveolar macrophages
The patient becomes more susceptible to respiratory
infection.

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Mucus plug
Normal lumen

Chronic Bronchitis cont’d…
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Clinical manifestations
In early stages
Clients may not recognize symptoms
Symptoms progress slowly
May not be diagnosed until severe episode occurs
 Productive cough (copious)
 Cyanosis
 Dyspnea
 Tachypnea
 Wheezing

Emphysema
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 Is a pathologic term that describes an abnormal distention
of the airspaces beyond the terminal bronchioles and
destruction of the walls of the alveoli.
 Main types of emphysema, based on the changes taking
place in the lung
Panlobular (panacinar) type of emphysema, there is
destruction of the respiratory bronchiole, alveolar duct, and
alveolus.
Centrilobular (centroacinar) form, pathologic changes take
place mainly in the center of the secondary lobule,
preserving the peripheral portions of the acinus.

Emphysema….
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Emphysema….
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 Clinical manifestation
 Early stages
 Barell chest
 Central cyanosis
 Finger clubbing
 Dyspnea
Wheezing
Chronic fatigue
Difficult in sleeping
Hypoxia
Polycythemia
Cough & sputum production

Emphysema….
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 Later stages
 Hypercapnea
 Purse-lip breathing
 Use of accessory muscles to breathe
 Underweight
No appetite & increase breathing workload

Emphysema…..
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Emphysema
Use accessory muscle Pursed lips breathing
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Treatment of COPD
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 Treatment
Objectives
- Relieve symptoms and improve exercise tolerance
- Prevent disease progression
- Prevent and treat complications
- Prevent and treat exacerbations
- Reduce mortality
Non pharmacologic
- Stop smoking
- Decrease indoor and outdoor air exposure to airway
irritants and polluted air
- Pulmonary rehabilitation

Cont.….
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 Pharmacologic
Management of acute exacerbations
Chronic therapy
Step up the treatment based on the severity of COPD
I. Mild COPD
– Rapid-acting bronchodilator when needed
II. Moderate COPD
– Add regular treatment with one or more long-acting
bronchodilators
– Add pulmonary rehabilitation (including exercise training)
III. Severe COPD
– Add medium- to high-dose inhaled steroids
IV.Very severe COPD-
– Long-term oxygen if chronic respiratory failure
– Consider surgical referral

Cont.….
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Inhaled ß2 agonist
 Salbutamol, MDI, 200mcg 6 hourly as needed using a spacer.
PLUS
 Inhaled corticosteroids and long acting inhaled beta-2 agonist
 Beclomethasone, oral inhalation 200μg, BID.
 Decrease the dose to 100μg, BID if symptoms are controlled
after three months.
OR (Preferred if symptoms are more severe or if response is not
optimal to Beclomethasone)
 Fluticasone/Salmeterol, 250/50μg oral inhalation, BID
 Dosage forms: 250/50μg per dose, 500/50μg per dose

Cont.….
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PLUS
 Theophedrine (Ephedrine +Theophylline), P.O., 131mg 12
hourly.
 Doasage forms:Tablet, 11mg + 120mg
PLUS
 Long term home O 2 (>15 hrs per day) For patients with
resting hypoxemia with signs of
 pulmonary hypertension or right Heart Failure , the use of
O2 has been demonstrated to have a significant impact on
mortality rate.

Cont.….
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 Management of Acute exacerbation
1. Oxygen via nasal cannula or facemask for hypoxic patients to
keep O2 saturation above 90%
PLUS
Short-acting beta2 agonists
Salbutamol, MDI, 200 mcg 6 hourly as needed using a spacer
PLUS
3. Corticosteroids
Prednisolone, 30- 40mg/day or its equivalent for 7-14
PLUS
4. Antibiotic therapy in patients with a moderate to severe
COPD exacerbation (increased dyspnea, increased sputum
volume, or increased sputum purulence or requiring
hospitalization)

Cont.….
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 First line for moderate exacerbation managed as
out patient
Doxycycline, 100mg, P.O., BID for 7 days
OR
Azithromycin, 500mg, P.O., daily for 3days
OR
Clarithromycin, 500mg, P.O., BID for 7 days
If there is high risk for Pseudomonas (frequent use of
antibiotics, recent admission and frequent use of
antibiotics)
PLUS
Ciprofloxacin, 500mg, P.O., BID for 7 days

Cont.….
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 Alternative
Cefuroxime, 500mg, P.O., BID for 7 days
OR
Amoxicillin /Clavulanate, 500/165mg, P.O.,TID for 7 days
For severe exacerbations requiring hospitalization
Ceftriaxone, 1gm, IV, BID for 7-10 days or until discharge
whichever is shorter.
 On discharge change to oral antibiotic mentioned above.
PLUS
Doxycycline, 100mg, oral, BID
OR
Clarithromycin, 500mg, oral, BID

Nursing management
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Nursing diagnosis
 Impaired gas exchange
 Ineffective airway clearance
 Ineffective breathing pattern
 Self-care deficits
 Activity intolerance
 Ineffective coping
 Deficient knowledge

Nursing interventions
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 Achieving Airway Clearance
 administering of corticosteroids and bronchodilators
 Clear the airway
 Chest physiotherapy and directed or controlled coughing
 Elimination lung irritants (cessation of smoking)
 Improving Activity Tolerance
 Rehabilitative therapies to promote independence in
executing AODL

Nursing interventions …
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 Improving Breathing Patterns
 Inspiratory muscle training and breathing retraining
 Training in diaphragmatic breathing
 Pursed-lip breathing
 Monitoring and Managing for potential complications such as
pulmonary hypertension and pneumothorax.
 Monitors pulse oximetry - O2 therapy is variable in COPD
patients; its aim in COPD is to achieve an acceptable oxygen
level without a fall in the pH

Nursing interventions …
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 Vaccinations against influenza and S. pneumoniae,
 Promoting Home and Community-Based Care
 Teaching Patients Self-Care
 Emphasize primary prevention to occupational exposures.
 Evaluate current exposures to risk factors occupational
toxins, indoor and outdoor air pollution (e.g. smoking,
pollution, toxic fumes, and chemicals).
 Educate regarding types of indoor and outdoor air
pollution
 Evaluate current smoking status, educate regarding
smoking cessation

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ASTHMA

Objectives
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At the end of the session the students will able to:
 Describe Asthma
 Describe patho-physiology of chronic bronchitis and
emphysema asthma
 List clinical features of asthma
 Identify managements of asthma
 Develop nursing process for the patients with bronchial
asthma

Asthma
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 Is a chronic inflammatory disease of the airways that
causes:-
 Airway hyperresponsiveness
 Mucosal edema
 Mucus production.

Asthma
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ETIOLOGY
Allergy is the strongest predisposing factor for asthma.
Common allergens can be
 Seasonal (grass, tree, and weed pollens) or
 Perennial (eg, mold, dust, roaches, animal dander).
Common triggers for asthma symptoms and exacerbations
 Airway irritants (eg, air pollutants, cold, heat, weather changes,
strong odors or perfumes, smoke)
 Exercise, stress or emotional upset
 Rhinosinusitis with postnasal drip
 Medications
 Viral respiratory tract infections
 Gastroesophageal reflux.

Asthma….
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Epidemiology & WHO response
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 Asthma affected an estimated 262 million people in 2019 and
caused 455 000 deaths globally.
 Asthma is included in the WHO Global Action Plan for the
Prevention and Control of NCDs and the United Nations 2030
Agenda for Sustainable Development.
 WHO is taking action to extend diagnosis of and treatment for
asthma in a number of ways.
 The WHO Package of Essential Non-communicable Disease
Interventions (PEN) was developed to help improve NCD
management in primary health care in low-resource settings.
 PEN includes protocols for the assessment, diagnosis and
management of chronic respiratory diseases (asthma and chronic
obstructive pulmonary disease), and modules on healthy lifestyle
counseling, including tobacco cessation and self-care.

……
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 Reducing tobacco smoke exposure is important for both
primary prevention of asthma and disease management. The
Framework Convention on Tobacco Control is enabling
progress in this area as are WHO initiatives such as
MPOWER and mTobacco Cessation.
 The Global Alliance against Chronic Respiratory Diseases
(GARD) contributes to WHO’s work to prevent and
control chronic respiratory diseases.
 GARD is a voluntary alliance of national and international
organizations and agencies from many countries committed
to the vision of a world where all people breathe freely.

Asthma….
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Clinical Manifestations
The three most common symptoms of asthma are
 Cough
 Dyspnea
 Wheezing
As the exacerbation progresses
 Diaphoresis
 Tachycardia
 Hypoxemia and central cyanosis (a late sign of poor
oxygenation)

Cont…..
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Asthma…..
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Asthma….
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Assessment and Diagnostic Findings
Hx
Physical examination
Chest X-ray
Sputum increase viscosity
CBC- eosinophills
Lung Function Tests
Arterial blood gas analysis and pulse oximetry

Investigations
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- Spirometry or Peak expiratory flow meter-to confirm the
diagnosis and assess severity.
- Chest X-ray-is not routinely needed. It is indicated when
superimposed pneumonia is strongly suspected or when
there is evidence of complications (Pneumothorax)
- The diagnosis of bronchial asthma is mainly clinical.
- Confirmation of diagnosis is done by demonstrating airflow
obstruction and its reversibility with bronchodilators with
spirometer or peak expiratory flow meter.

Treatment of acute asthma attack
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Objectives
- Prevent respiratory failure
- Relieve symptoms promptly
- Shorten hospital stay

A. Non-pharmacologic
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Hospital admission-Admit patients with any feature of a severe
attack persisting after initial treatment in the emergency room to
wards.
Admit patients with life threatening attacks directly to ICU.
2. Oxygen-give supplementary oxygen via face mask or nasal
cannula to all hypoxic patients with acute asthma to maintain a SpO2
level of >90%.
Lack of pulse oximetry should not prevent the use of oxygen.
3. Positioning-sitting upright and/or leaning.
4. Hydration-most patients need IV hydration

B. Pharmacologic
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First-line
Salbutamol, 4 to 6 puffs every 20 minutes in the first 1-4
hours.
Then the same dose every 1- 4 hours depending on the
patient need.
OR
Salbutamol, 2 –5mg every 20 minutes for 3 doses, then
2.5–10mg every 1–4 hours as needed, or 10–15mg/hour
continuously
PLUS
Ipratropium bromide, 4–8 puffs every 20 minutes as
needed up to 3 hours, 0.25–0.5mg every 20 minutes for 3
doses, then as needed. OR
Aminophylline, IV 250mg IV bolus slowly over 20 minutes

Cont.….
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 When there are no other options:
Adrenaline, 1:1000, 0.5ml sc. Repeat after 1/2 if patient
doesn’t respond.
PLUS
Systemic steroids
 Hydrocortisone, 200mg IV as a single dose.
 Further IV doses are needed only if oral dosing is not
possible (100mg, IV, 3-4 X per day).
 Followed by
Prednisolone, 40-60mg P.O., should be started immediately,
for 5-7 days.
 Discontinuation does not need tapering

Maintenance therapy for chronic asthma
in adults
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Objectives
 Prevent chronic and troublesome symptoms
 Minimize use of inhaled SABA for quick relief of symptoms
 Maintain (near) normal pulmonary function
 Maintain normal activity levels.
 Prevent recurrent exacerbations
 Minimize adverse effects of therapy

Cont.….
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 Non pharmacologic
- Avoid identified allergens and smoking
 Pharmacologic
- Depends on the severity of asthma
- Assess the severity of asthma and scale up or down
treatment based on the severity.

Cont.….
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 Intermittent asthma
First line
Salbutamol, inhaler 200microgram/puff, 2 puffs to be
taken as needed but not more than 3-4 times a day, or
tablet, 2-4mg 3-4 times a day
Alternative
Ephedrine +Theophylline, 11mg + 120mg P.O., BID
OR TID

Cont.…….
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Persistent mild asthma
 Salbutamol, inhaler, 200micro gram/puff 1-2 puffs to be
taken, as needed but not more than 3-4 times/day, or
tablet, 2-4mg 3-4 times a day
PLUS (Inhaled corticosteroid)
Beclomethasone, oral inhalation 200μg, BID.
 Decrease the dose to 100μg, BID if symptoms are
controlled after three months.

Cont.….
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Persistent moderate asthma
 Salbutamol, inhalation 200/puff 1-2pμg/puffs as needed PRN not
more than 3-4 times a day. PLUS (Inhaled corticosteroid)
 Beclomethasone, oral inhalation 200μg, BID.
 Decrease the dose to 100μg, BID if symptoms are controlled
after three months. OR (Preferred if symptoms are more severe
or if response is not optimal to Beclomethasone )
Fluticasone/Salmeterol, 250/50μg oral inahalation, BID
PLUS (if required): Ephedrine + Theophylline, 11mg + 120mg P.O.,
BID ORTID

Cont.…..
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Severe persistent asthma
 Salbutamol, inhalation 200/puff 1-2pμg/puffs as needed PRN
not more than 3-4 times a day.
PLUS (Inhaled corticosteroid)
 Beclomethasone, oral inhalation 200μg, BID.
Decrease the dose to 100μg, BID if symptoms are controlled
after three months. OR (Preferred if symptoms are more severe
or if response is not optimal to Beclomethasone)
 Fluticasone/Salmeterol, 250/50μg oral inahalation, BID

Cont.…..
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PLUS
 Ephedrine +Theophylline, 11mg + 120mg P.O., BID
OR TID
PLUS (if required)
 Prednisolone, 5-10mg P.O., QOD. Doses of 20-40mg
daily for seven days may be needed forshort-term
exacerbations in patients not responding to the above
treatment.

Asthma….
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Nursing management
 Assessing patients respiratory status
 The purpose and action of each medication Triggers to
avoid, and how to do so
 Proper inhalation technique

Asthma….
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Complications
Status asthmaticus
Respiratory failure
Pneumonia
Atelectasis

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