Download COPD

Obstructive and Inflammatory
Lung Disease
DR. ISAZAEHFAR
Obstructive and Inflammatory
Lung Disease
Emphysema
 Chronic Bronchitis
 Asthma

Chronic Obstructive
Pulmonary Disease: COPD
Disease of airflow obstruction
that is not totally reversible
Chronic
Bronchitis
Emphysema
New Definition



Chronic obstructive pulmonary disease (COPD) is a
preventable and treatable disease state
characterized by airflow limitation that is not fully
reversible.
The airflow limitation is usually progressive and is
associated with an abnormal inflammatory
response of the lungs to noxious particles or gases,
primarily caused by cigarette smoking.
Although COPD affects the lungs, it also produces
significant systemic consequences.
COPD
COPD

In COPD, less air flows in and out of the airways
because of one or more of the following:

The airways and air sacs lose their elastic
quality.
The walls between many of the air sacs are
destroyed.
The walls of the airways become thick and
inflamed.
The airways make more mucus than usual,
which tends to clog them.



COPD: Etiology
Cigarette smoking
 Recurrent respiratory infection
 Alpha 1-antitrypsin deficiency
 Aging

Chronic Bronchitis
Recurrent or chronic productive cough for
a minimum of 3 months for 2 consecutive
years.
 Risk factors

Cigarette smoke
 Air pollution

Chronic Bronchitis
Pathophysiology




Chronic inflammation
Hypertrophy &
hyperplasia of
bronchial glands that
secrete mucus
Increase number of
goblet cells
Cilia are destroyed
Chronic Bronchitis
Pathophysiology

Narrowing of airway
Starting w/ bronchi 
smaller airways
airflow resistance
work of breathing
Hypoventilation & CO2
retention  hypoxemia &
hypercapnea




Chronic Bronchitis
Pathophysiology
Bronchospasm often occurs
 End result

Hypoxemia
 Hypercapnea
 Polycythemia (increase RBCs)
 Cyanosis
 Cor pulmonale (enlargement of right side of heart)

Chronic Bronchitis:
Clinical Manifestations

In early stages




Clients may not recognize early symptoms
Symptoms progress slowly
May not be diagnosed until severe episode with a
cold or flu
Productive cough
• Especially in the morning
• Typically referred to as “cigarette cough”


Bronchospasm
Frequent respiratory infections
Chronic Bronchitis:
Clinical Manifestations

Advanced stages
Dyspnea on exertion Dyspnea at rest
 Hypoxemia & hypercapnea
 Polycythemia
 Cyanosis
 Bluish-red skin color
 Pulmonary hypertension Cor pulmonale

Chronic Bronchitis:
Diagnostic Tests

PFTs




ABGs



FVC:  Forced vital capacity
FEV1:  Forcible exhale in 1 second
FEV1/FVC = <70%
 PaCO2
 PaO2
CBC

 Hct
Emphysema



Abnormal distension of
air spaces
Actual cause is unknown
Abnormal permanent
enlargement of the
airspaces distal to the
terminal bronchioles
accompanying
destruction of the
airspaces walls
Emphysema: Pathophysiology

Structural changes




Hyperinflation of alveoli
Destruction of alveolar &
alveolar-capillary walls
Small airways narrow
Lung elasticity decreases
Emphysema: Pathophysiology

Mechanisms of
structural change

Obstruction of small
bronchioles
Proteolytic enzymes destroy
alveolar tissue
Elastin & collagen are
destroyed




Support structure is destroyed
“paper bag” lungs
Emphysema: Pathophysiology






The end result:
Alveoli lose elastic recoil, then distend, &
eventually blow out.
Small airways collapse or narrow
Air trapping
Hyperinflation
Decreased surface area for ventilation
Emphysema:
Clinical Manifestations

Early stages




Dyspnea
Non productive cough
Diaphragm flattens
A-P diameter increases
• “Barrel chest”

Hypoxemia may occur
• Increased respiratory rate
• Respiratory alkalosis

Prolonged expiratory phase
Emphysema:
Clinical Manifestations

Later stages
Hypercapnea
 Purse-lip breathing
 Use of accessory muscles to breathe
 Underweight

• No appetite & increase breathing workload

Lung sounds diminished
Emphysema: Clinical
Manifestations
COPD
Symptoms
 Productive
cough
 Breathlessness
 Chest infection
 Other symptoms of COPD can
be more vague, weight loss,
tiredness and ankle swelling.
Emphysema: Clinical
Manifestations

Pulmonary function
•  residual volume,  lung capacity, DECREASED FEV1,
vital capacity maybe normal

Arterial blood gases




Normal in moderate disease
May develop respiratory alkalosis
Later: hypercapnia and respiratory acidosis
Chest x-ray


Flattened diaphragm
hyperinflation
COPD
Diagnostic tests
Symptoms
 Physical examination
 Sample of sputum
 Chest x-ray
 High-resolution CT (HRCT scan)
 Pulmonary function test (spirometery)
 Arterial blood gases test
 Pulse oximeter

Goals of Treatment: Emphysema
& Chronic Bronchitis
Improved ventilation
 Remove secretions
 Prevent complications
 Slow progression of signs & symptoms
 Promote patient comfort and participation
in treatment

Collaborative Care: Emphysema &
Chronic Bronchitis
Treat respiratory infection
 Monitor spirometry and PEFR
 Nutritional support
 Fluid intake 3 lit/day
 O2 as indicated

Collaborative Care: Medications

Anti-inflammatory


Bronchodilators






Corticosteroids
Beta-adrenergic agonist: Proventil
Methylxanthines: Theophylline
Anticholinergics: Atrovent
Mucolytics: Mucomyst
Expectorants: Guaifenisin
Antihistamines: non-drying
Collaborative Care: Emphysema &
Chronic Bronchitis

Client teaching



Support to stop smoking
Conservation of energy
Breathing exercises
• Pursed lip breathing
• Diaphragm breathing

Chest physiotherapy
• Percussion, vibration
• Postural drainage

Self-manage medications
• Inhaler & oxygen equipment
COPD
Medical management





Give antibiotics to treat infection
Give bronchodilators to relieve bronchospasm,
reduce airway obstruction, mucosal edema and
liquefy secretions.
Chest physiotherapy and postural drainage to
improve pulmonary ventilation.
Proper hydration helps to cough up secretions or
tracheal suctioning when the patient is unable to
cough.
Steroid therapy if the patient fails to respond to
more conservative treatment.
COPD classification based on spirometry
Severity
Postbronchodilator
FEV1/FVC
Postbronchodilator
FEV1% predicted
At risk
>0.7
>80
Mild COPD
<0.7
>80
Moderate
COPD
<0.7
50-80
Severe COPD
<0.7
30-50
Very severe
COPD
<0.7
<30
SPIROMETRY is not to substitute for clinical judgment in the
evaluation of the severity of disease in individual patients.
Management based on GOLD
Postbronchodilator
FEV1
(% predicted)
COPD
Preventive measures

To prevent irritation and infection of the
airways, instruct the patient to:

Avoid exposure to cigarette, pipe, and cigar
smoke as well as to dusts and powders.

Avoid use of aerosol sprays.

Stay indoors when the pollen count is high.

Stay indoors when temperature and humidity
are both high
COPD
Preventive measures (cont…)

Use air conditioning to help decrease pollutants
and control temperature

Avoid exposure to persons known to have colds
or other respiratory tract infection

Avoid enclosed, crowded areas during cold and
flu season.

Obtain
immunization
against
influenza
and
COPD
Preventive measures (cont…)

To ensure prompt, effective treatment of
a developing respiratory infection,
instruct the patient to do the following:-

Report any change in sputum color
character, increased tightness of the
chest, increased dyspnea, or fatigue.

Call the physician if ordered antibiotics
do not relieve symptoms within 24 hours.
Asthma
Reversible inflammation & obstruction
 Intermittent attacks
 Sudden onset
 Varies from person to person
 Severity can vary from shortness of
breath to death

Difference between COPD and Asthma

In COPD there is permanent damage to the airways.
The narrowed airways are fixed, and so symptoms are
chronic (persistent). Treatment to open up the airways,
is therefore limited.

In asthma there is inflammation in the airways which
makes the muscles in the airways constrict. This
causes the airways to narrow. The symptoms tend to
come and go, and vary in severity from time to time.
Treatment to reduce inflammation and to open up the
airways usually works well.

COPD is more likely than asthma to cause a chronic
(ongoing) cough with sputum.
Difference between COPD and asthma (cont…)

Night time waking with breathlessness or
wheeze is common in asthma and
uncommon in COPD.

COPD is rare before the age of 35 whilst
asthma is common in under-35.
Asthma

Triggers
Allergens
 Exercise
 Respiratory infections
 Drugs and food additives
 Nose and sinus problems
 GERD
 Emotional stress

Asthma: Pathophysiology


Swelling of mucus
membranes (edema)
Spasm of smooth
muscle in bronchioles


Increased airway
resistance
Increased mucus
gland secretion
Asthma: Pathophysiology

Early phase response: 30 – 60 minutes

Allergen or irritant activates mast cells

Inflammatory mediators are released
• histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines

Intense inflammation occurs
• Bronchial smooth muscle constricts
• Increased vasodilation and permeability
• Epithelial damage

Bronchospasm
• Increased mucus secretion
• Edema
Asthma: Pathophysiology

Late phase response: 5 – 6 hours

Characterized by inflammation

Eosinophils and neutrophils infiltrate
Mediators are released
mast cells release
histamine and additional mediators
Self-perpetuating cycle
Lymphocytes and monocytes invade as well
Future attacks may be worse because of increased
airway reactivity that results from late phase
response




• Individual becomes hyperresponsive to specific allergens
and non-specific irritants such as cold air and dust
• Specific triggers can be difficult to identify and less
stimulation is required to produce a reaction
Asthma: Early Clinical
Manifestations








Expiratory & inspiratory wheezing
Dry or moist non-productive cough
Chest tightness
Dyspnea
Anxious &Agitated
Prolonged expiratory phase
Increased respiratory & heart rate
Decreased PEFR
Asthma: Early Clinical
Manifestations

Wheezing

Chest tightness
Dyspnea
 Cough
 Prolonged expiratory phase [1:3 or 1:4]

Asthma: Severe Clinical
Manifestations








Hypoxia
Confusion
Increased heart rate & blood pressure
Respiratory rate up to 40/minute & pursed lip
breathing
Use of accessory muscles
Diaphoresis & pallor
Cyanotic nail beds
Flaring nostrils
Endotracheal Intubation
Classifications of Asthma

Mild intermittent
Mild persistent
 Moderate persistent
 Severe persistent

Asthma: Diagnostic Tests

Pulmonary Function Tests

FEV1 decreased
• Increase of 12% - 15% after bronchodilator indicative of asthma



PEFR decreased
Symptomatic patient

eosinophils > 5% of total WBC

Increased serum IgE

Chest x-ray shows hyperinflation
ABGs

Early: respiratory alkalosis, PaO2 normal or near-normal

severe: respiratory acidosis, increased PaCO2,
Asthma: Collaborative Care

Mild intermittent

Avoid triggers
Premedicate before exercising
 May not need daily medication


Mild persistent asthma

Avoid triggers
Premedicate before exercising
 Low-dose inhaled corticosteroids

Asthma: Collaborative Care

Moderate persistent asthma

Low-medium dose inhaled corticosteroids

Long-acting beta2-agonists
Can increase doses or use theophylline or
leukotriene-modifier [singulair, accolate, zyflo]


Severe persistent asthma

High-dose inhaled corticosteroids

Long-acting inhaled beta2-agonists
Corticosteroids if needed

Asthma: Collaborative Care

Acute episode

FEV1, PEFR, pulse oximetry compared to baseline

O2 therapy
Beta2-adrenergic agonist

• via MDI w/spacer or nebulizer
• Q20 minutes – 4 hours prn

Corticosteroids if initial response insufficient
• Severity of attack determines po or IV
• If poor response, consider IV aminophylline
Asthma Medications: Antiinflammatory

Corticosteroids



Not useful for acute attack
Beclomethasone: vanceril,
beclovent, qvar

Leukotriene modifiers

Interfere with synthesis or
block action of leukotrienes

Have both bronchodilation
and anti-inflammatory
properties
Not recommended for acute
asthma attacks
Should not be used as only
therapy for persistent
asthma
Accolate, Singulair, Zyflo
Cromolyn & nedocromil

Inhibits immediate response
from exercise and allergens

Prevents late-phase response
Useful for premedication for
exercise, seasonal asthma
Intal, Tilade





Asthma Medications:
Bronchodilators

2-adrenergic agonists

Rapid onset: quick relief of bronchoconstriction

Treatment of choice for acute attacks
If used too much causes tremors, anxiety, tachycardia, palpitations,
nausea
Too-frequent use indicates poor control of asthma
Short-acting



• Albuterol[proventil]; metaproterenol [alupent]; bitolterol [tornalate];
pirbuterol [maxair]

Long-acting
• Useful for nocturnal asthma
• Not useful for quick relief during an acute attack
• Salmeterol [serevent]
Asthma Medications:
Bronchodilators con’t

Methylxanthines

Anticholinergics

Less effective than betaadrenergics

Inhibit parasympathetic
effects on respiratory system

Useful to alleviate
bronchoconstriction of early
and late phase, nocturnal
asthma
Does not relieve
hyperresponsiveness
Side effects: nausea,
headache, insomnia,
tachycardia, arrhythmias,
seizures
Theophylline, aminophylline

Increased mucus

Smooth muscle contraction
Useful for pts w/adverse
reactions to beta-adrenergics
or in combination w/betaadrenergics





Ipratropium [atrovent]

Ipratropium + albuterol
[Combivent]
Asthma: Client Teaching


Correct use of medications
Signs & symptoms of an attack





Dyspnea, anxiety, tight chest, wheezing, cough
Relaxation techniques
When to call for help, seek treatment
Environmental control
Cough & postural drainage techniques