COPD: Chronic Obstructive Pulmonary Disease
“Chronic or recurrent reduction in expiratory airflow within the lungs”. Lung disease.
A medical “catch phase” of diagnoses for lung disease characterized by increased airway
resistance, specifically prolonged forced exhalation. COPD usually manifests as a combination
of chronic bronchitis, emphysema, asthma and bronchiectasis.
Patients with COPD usually present with wheezing, hyperinflated lungs and a flat diaphragm 
“Barrel chest”
Something is restricting them from getting air out of their lungs.
 Asthma
 Emphysema
 Bronchitis
 bronchiectasis
ASTHMA
Characterized by increased responsiveness of the trachea and bronchi to stimuli. Patients present
with narrowing of bronchial airways [bronchospasm/bronchoconstriction]. A stimulus or
“trigger” causes smooth muscle spasm, inflammation of mucosa and an increased production of
mucus.
Symptoms: “Wheezing, dyspnea, cough, and sputum”
Patients present with an increased respiratory rate, accessory muscle use (to compensate),
prolonged exhalation phase, wheeze and a productive or non-productive cough (there will be lots
of mucus, may or may not come out, airways might be too narrow for it to come out). They tend
to “trap air”.
The Global Initiative for Asthma [1995] defines Asthma as:
1. Asthma – whatever the severity – is a chronic inflammatory disorder of the airway.
2. Airway inflammation is associated with airway hyper-responsiveness, airflow limitation,
and respiratory symptoms.
3. Airway inflammation produces four forms of airflow limitation: acute
bronchoconstriction (acute spasm of smooth muscle), swelling (edema) of the airway
wall, chronic mucus plug formation, and airway wall remodeling (wall will try to thicken
to protect itself).
4. Atopy, the predisposition for developing an IgE-mediated response (overactive
histamines making the person oversensitive) to common environmental allergens, is the
strongest identifiable predisposing factor for developing asthma. OR: People with
allergies are more predisposed to asthma.
5. Considering Asthma an inflammatory disorder has implications for the diagnosis,
prevention, and management of the disorder.
Allergic/ Extrinsic Asthma: diagnosed under 35 y.o., exercise induced asthma, cold air etc, a
know triggers to precipitate the attack (pollen, dust).
Non Allergic / Intrinsic: over age 35. may be related to stress or occupational hazards (inhaled
pollutants/chemicals).
Pathophysiology:
Hyperinflated lungs (air trapping in the lungs during exhalation)
Edematous, inflamed lung mucosa (inner lining gets thicker w/tissue and fluid)
Thickened basement membrane (bigger secretion producing cells/goblet)
Enlarged mucus glands
Increased number of goblet cells
Hypertrophied and thickened bronchial smooth muscle (gets thicker and stronger, closes
airways)
Medical management:
Medical management includes use of inhaled medications (“puffers” such as Ventolin and
Atrovent), supplemental oxygen and education around identification of and avoidance of
triggers, breathing and relaxation techniques etc.
Inhaled medications can include bronchodilators (opens the airways), steroids (corticosteroids –
to control inflammation), adrenalin, muscle relaxants, antihistamines and/or anti-inflammatories.
Reducing triggers in the home is a start.
Find out exactly what type of medications they use and what it is doing for them. This will tell
you the severity of their asthma. Take for health history.
If they have an attack during a MxTx, give them their puffer, talk about continuing or not.
Depends on the client.
The length / severity of an “attack” is always unpredictable (30 seconds to hours).
An attack lasting several hours that is unresponsive to medical treatment is known as
Status Asthmaticus
= MEDICAL EMERGENCY.
The sufferer will become fatigued and lethargic as their respiratory muscles tire,
they will become cyanotic (trapped gases are absorbed, “new” airflow is
obstructed), and may die.
Long term effects of disease process:
May not be able to do sports, go to smoky bars, hang out with family who wears lots of perfume,
cant go to the park because of ragweed season. Social impact.
Cardiovascular health will be poor. High blood pressure – heart has to work harder to pump
blood for gas exchange. Enlarged lungs will compress on the heart and vessels.
Physical / mechanical changes in costovertebral/intercostal, diaphragm muscles and thoracic
cage.

Musculoskeletal:
o Increased use of accessory muscles of inspiration leading to shortening, overuse
syndromes (TOS, forward head posture, TrP’s etc) and weakened cough.
o Barrel chest, increased thoracic kyphosis, lumbar and cervical lordosis – global
decrease in thoracic mobility. (increased risk of arthritis)
 Cardio-Vascular:
o Increased risk of hypertension and heart failure due to increased resistance in
lungs and pulmonary vessels.
o Heart rate increases during “attacks” in attempt to maintain perfusion and oxygen
delivery to tissues.
o Medication may add stress to heart (adrenalin)
 Respiratory:
o Lungs lose elasticity which can cause damage to alveoli (increased tension)
o Net result is an increase in work of breathing and further dyspnea
o Changes to lung parenchyma increase a clients susceptibility to congestion and
infection.
 Emotional impact:
o Dyspnea is frightening! Clients may associate deep breathing with an asthma
attack – will then avoid deep breathing, revert to apical patterns. Clients will
avoid activities and environments they feel may trigger an attack, limiting
opportunity to participate in exercise and leisure activities (avoid outdoors due to
allergies, humidity etc). Exercise itself may be a trigger as respiratory system is
challenged. Disease process may lead to social isolation.
Challenges with clients who have asthma:
o Overuse / chronic strain of respiratory muscles
o Postural dysfunction – kyphosis, lordosis in c-spine, forward head position, barrel chest,
TOS (thoracic outlet syndrome)
o Decreased mechanics of breathing – tight diaphragm, weak resp. muscles, postural
dysfunction
o Increased mucus production – chronic cough, mucous plugging
o Increased SNS activation – working a TrP may be a trigger
o Emotional stress
o Use of face cradle may be claustrophobic and lead to respiratory distress
o Pillowing and/or prone positioning may inhibit diaphragm function.
o Allergens, sensitivities (essential oils, detergents, disinfectants)
o Hypertension CHF/HTN
o Constipation
Things to think about: CI’s, medications
Positioning: how do they sleep, it will be harder for them to breathe in prone it puts strain on
the diaphragm. Seated/semifowlers may be better.
Goals:
o Decrease M tension / strain – normalize length and tone of affected MM.
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Normalize posture
Improve mechanics of breathing
Decrease SNS firing / general relaxation
Facilitate secretion clearance (mucus)
Treatment plan:
o Diaphragmatic and pursed lip breathing exercises. Special breathing: pursed lip breathing
– inhale normally, exhale with lips close together like a whistle. Keeps the lungs open,
ribs open longer, because the mouth is smaller, less air can go out, the exhale is longer. It
increases back pressure in airways to help prevent airway collapse and prolongs
exhalation phase which facilitates gas release.
o Hydro: facial steam (loosen mucus) depends on severity, humid air is difficult to breathe
o Fascial work to decrease restrictions – posture, msk tension
o Address tone/length/strength of resp and postural M. – swedish mx, indirect TrP, general
relaxation work.
o Maintain Thoracic mobilization – ROM, mobility and jt health – jt play, stretching, m
length/tone. rhythmic mobs, rib mobilization
o Tapotement – can loosen mucus, might also be a trigger
o Address compensations, attempt to normalize respiratory function
o Education – avoidance of triggers (allergens, heat, humidity etc)
 Changes to environment (air filters, hypoallergenic products etc)
 Adaptations to exercise programs
EMPHYSEMA
A chronic degenerative lung condition characterized by:
o Abnormal enlargement of air spaces distal to the terminal bronchioles
o Destruction of alveolar walls and capillary beds
This leads to:
o Dev. Of “bullae” = large “pockets” in lung tissue. Must be > 1cm. In diameter to be defined
as Bullae. They cause an increase in overall lung volume., will compress adjacent “healthy”
lung tissue, impairing ventilation and perfusion. They may be surgically removed both to
reduce compression and to avoid “bursting” of bullae which may lead to a pneumothorax.
Loss of lung elasticity.
Causes:
o Majority of cases are related to smoking (both primary and second-hand smoke)!
o A sm. Percentage of cases are related to a genetic defect in the structure of the respiratory
unit.
o Pollution
o Repeated respiratory infections (esp chronic bronchitis)
Types:
Centrilobar: destruction of respiratory bronchiole w/edema, inflammation and thickening of the
bronchiolar wall. Most common in upper half of lungs. Effects men > women. Is rare in nonsmokers – is almost exclusively a disease of smokers.
Panlobar: destructive enlargement of alveoli distal to the terminal bronchiole. Alveoli then
become more prone to collapse during exhalation. Can be found throughout the entire lung. Most
commonly due to smoking but is seen in groups w/genetic defect.
Signs and Symptoms:
o Slow insidious onset of dyspnea
o Tachpynea – rapid, shallow respiration
o Labored inspiration, forced exhalation
This leads to overall poor gas exchange. Client will make attempts to over ventilate to
compensate. Clients often require supplemental home oxygen as the disease process progresses.
Clinical Presentation:
Musculoskeletal:
- Increased use of accessory muscles of inspiration leading to shortening and overuse
syndromes (TOS, forward head posture, TrP’s etc)
- Barrel chest, increased thoracic kyphosis, lumbar and cervical lordosis – global decrease
in thoracic mobility. (increased risk of arthritis)
- Diaphragm flattens (as lungs hyperinflate) – limits respiratory effort, compresses
abdominal contents.
Cardiovascular:
- Increased risk of heart failure and hypertension due to increased resistance in lungs and
pulmonary vessels
Emotional Impact:
- Fear of dyspnea
- Fatigue, chronic hypoxia limits ADL’s
- Leads to frustration, anger, low self esteem
Clinical Considerations:
o Address respiratory muscles for tone, length and strength
o Maintain thoracic rom, mobility and joint health – jt play, stretching, muscle
length/tone, rib mobs (compression not rib springing)
o Address compensations, attempt to normalize respiratory function
o Diaphragmatic and pursed lip breathing exercises
o Promote general relaxation
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Education: - smoking cessation!!
Awareness of individual modifications:
CHF/HTN
Pillowing and or prone positioning may inhibit diaphragm function.