Chronic Obstructive Pulmonary

Disease (COPD)

Dr Kabir O. Abdullahi
PhD, MPH, BNSc
LSN, UOL

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 Objectives:
 At the end of the unit, students will be able to:
 Utilize Functional health pattern to identify
patients problems related to respiratory
disorders including:
 Chronic obstructive pulmonary disorder
(COPD)
 Integrate pathophysiology and pharmacology
concepts of respiratory disease

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 COPD

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COPD
 Any respiratory disease that persistently obstructs
bronchial airflow fall under the broad classification of
COPD, also known as chronic airflow limitations
(CAL). Chronic Obstructive Pulmonary Disease
 (COPD) is a condition of chronic dyspnea with
expiratory airflow limitation that does not
significantly fluctuate. Within that broad category, the
primary cause of the obstruction may vary; examples
include airway inflammation, mucous plugging,
narrowed airway lumina, or airway destruction.

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Cont…
 The term COPD mainly involves two related diseases
— chronic bronchitis and emphysema. Although 
asthma also involves airway inflammation and
periodic narrowing of the airway lumina
(hyperreactivity), the condition is the result of
individual response to a wide variety of
stimuli/triggers and is therefore episodic in nature with
fluctuations/exacerbations of symptoms.
COPD is also called chronic obstructive lung
disease (COLD).

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 Emphysema
 Abnormal permanent enlargement of the air
space distal to the terminal bronchioles

 Accompanied by destruction of bronchioles.

Brunner and Suddarth’s (2010).

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 Chronic Bronchitis
 Presence of chronic productive cough for
 3 or more months in each of 2
successive years in a patient whom other
causes of chronic cough have been excluded.

Brunner and Suddarth’s (2010).

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 COPD
Causes
 Cigarette smoking
 Primary cause of COPD***
 Clinically significant airway obstruction
develops in 15% of smokers
 80% to 90% of COPD deaths are related to
tobacco smoking
 > 1 in 5 deaths is result of cigarette smoking

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 COPD
Causes
 Cigarette smoking
 Nicotine stimulates sympathetic nervous system
resulting in:
  HR

 Peripheral vasoconstriction

  BP and cardiac workload

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 COPD
Causes
 Cigarette smoking
 Compounds problems in a person with CAD
  Ciliary activity
 Possible loss of ciliated cells
 Abnormal dilation of the distal air space
 Alveolar wall destruction
 Carbon monoxide
  O carrying capacity
2
 Impairs psychomotor performance and judgment
 Cellular hyperplasia
 Production of mucus
 Reduction in airway diameter
 Increased difficulty in clearing secretions

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 COPD
Causes
 Secondhand smoke exposure associated with:
  Pulmonary function
  Risk of lung cancer
  Mortality rates from ischemic heart disease

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 COPD
Causes
 Infection
 Major contributing factor to the aggravation and
progression of COPD
 Heredity
 -Antitrypsin (AAT) deficiency (produced by
liver and found in lungs); accounts for < 1% of
COPD cases
 Emphysema results from lysis of lung tissues by proteolytic
enzymes from neutrophils and macrophages

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Pathophysiology of Chronic Bronchitis
and Emphysema

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Fig. 28-7
Emphysema
Pathophysiology
 Hyperinflation of alveoli
 Destruction of alveolar walls
 Destruction of alveolar capillary walls
 Narrowed airways
 Loss of lung elasticity

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Emphysema
Pathophysiology
 Two types:
 Centrilobular (Central part of lobule)

 Most common

 Panlobular (Destruction of whole lobule)

 Usually associated with AAT deficiency

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 Emphysema
Pathophysiology
 Structural changes are:
 Hyperinflation of alveoli
 Destruction of alveolar capillary walls
 Narrowed, tortuous small airways
 Loss of lung elasticity.

Brunner and Suddarth’s (2010).

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Emphysema
Pathophysiology
 Small bronchioles become obstructed as a result
of
 Mucus
 Smooth muscle spasm
 Inflammatory process
 Collapse of bronchiolar walls
 Recurrent infections production/stimulation
of neutrophils and macrophages release
proteolytic enzymes alveolar destruction
inflammation, exudate, and edema

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Emphysema
Pathophysiology
 Elastin and collagen are destroyed
 Air goes into the lungs but is unable to come out
on its own and remains in the lung
 Causes bronchioles to collapse

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Emphysema
Pathophysiology
 Trapped air  hyperinflation and overdistention
 As more alveoli coalesce, blebs and bullae may
develop
 Destruction of alveolar walls and capillaries 
reduced surface area for O2 diffusion
 Compensation is done by increasing respiratory
rate to increase alveolar ventilation
 Hypoxemia usually develops late in disease

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 Emphysema
Clinical Manifestations
 Dyspnea
 Progresses in severity

 Patient will first complain of dyspnea on exertion and

progress to interfering with ADLs and rest.
 Minimal coughing with no to small amounts of sputum
 Overdistention of alveoli causes diaphragm to flatten and
AP diameter to increase.

Brunner and Suddarth’s (2010).

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Emphysema
Clinical Manifestations
 Patient becomes chest breather, relying on
accessory muscles
 Ribs become fixed in inspiratory
position.
 Patient is underweight (despite adequate
calorie intake).

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Chronic Bronchitis
Pathophysiology
Pathologic lung changes are:
 Hyperplasia of mucus-secreting glands
in trachea and bronchi
 Increase in goblet cells
 Disappearance of cilia
 Chronic inflammatory changes and narrrowing
of small airways
 Altered fxn of alveolar macrophages
infections

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Chronic Bronchitis
Pathophysiology
Chronic inflammation
 Primary pathologic mechanism
causing changes
 Narrow airway lumen and reduced
airflow d/t
 hyperplasia of mucus glands
 Inflammatory swelling
 Excess, thick mucus

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 Chronic Bronchitis
Pathophysiology
 Greater resistance to airflow increases work of breathing
 Hypoxemia and hypercapnia develop more frequently in
chronic bronchitis than emphysema.
 Bronchioles are clogged with mucus and pose a physical
barrier to ventilation
 Hypoxemia and hypercapnia d/t lack of ventilation and O 2
diffusion
 Tendency to hypoventilate and retain CO2
 Frequently patients require O2 both at rest and during exercise

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Chronic Bronchitis Pathophysiology

 Cough is often ineffective to remove secretions

because the person cannot breathe deeply
enough to cause air flow distal to the secretions
 Bronchospasm frequently develops
 More common with history of smoking or
asthma

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Chronic Bronchitis
Clinical Manifestations
 Earliest symptoms:
 Frequent, productive cough during winter

 Frequent respiratory infections.

 Bronchospasm at end of paroxysms of coughing

 Cough
 Dyspnea on exertion
 History of smoking
 Normal weight or heavyset

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Chronic Bronchitis
Clinical Manifestations
 Ruddy (bluish-red) appearance d/t
 Polycythemia (increased Hgb d/t chronic
hypoxemia))
 cyanosis

 Hypoxemia and hypercapnia

 Results from hypoventilation and  airway
resistance + problems with alveolar gas
exchange

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Reference:
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