Pulmonary obstructive diseases are characterized by the narrowing or obstruction of the airways. It is caused by secretions, inflammation of the airways, bronchospasm of smooth muscle or destruction of lung tissue
People with COPD display characteristics of both chronic bronchitis and emphysema
Emphysema: destruction of alveoli
Chronic bronchitis: chronic productive cough for 3 months in 2 successive years
Causes of COPD are cigarette smoking, occupational chemical and dusts, heredity, frequent childhood lung infections
Statistics of COPD:
cigarette smoking is responsible for 80-90% of COPD pts
10% of canadians over 35 have COPD
20% of smokers develop COPD
Tobacco smoke contains over 4000 chemicals, 60 of them are known causes of cancer
Effects of cigarette smoking:
increase of goblet cells = increase mucus production
injures smaller airways
damage ciliary activity (push up the mucus)
damage of alveolar walls
carbon monoxide binds to hemoglobin which decreases its capacity to carry oxygen
Lung changes in COPD
bronchioles lose shape and are clogged with mucus
walls of alveoli are destroyed so there are fewer larger alveoli meaning less possible gas exchange
Noxious particles lead to inflammation of the airways, remodeling of the patient‘s lung and parenchymal (tissue destruction) which then leads to COPD
Important COPD pathophysiologies:
hyperinflation of lungs (barrel chest)
loss of elastic recoil
gas exchange abnormalities
cilia dysfunction
Chronic bronchitis affects the bronchioles (inflammation and excess mucus) VS emphysema affects the alveoli (alveolar membranes break down)
COPD is a ventilation and diffusion problem
Clinical manifestations of COPD are coughing, sputum production and dyspnea. Dyspnea happens with exertion at first, then at rest and then starts interfering with daily activities
Dyspnea scale has 5 grades
Grade 1: after strenuous exercice
Grade 2: when hurrying on the level or walking up a hill
Grade 3: walks slower than people and stops for breaths when walking at a normal pace
Grade 4: stops to breathe after walking 100 yards
Grade 5: too breathless to leave the house
Stages of COPD are mild (grade 2), moderate (grade 3-4), severe (grade 5) and very severe
Diagnostic study for COPD is FEV1, the forced expiratory volume in 1 second (amount of air exhaled). Above 80% is normal
Progression of manifestations include the use of accessory and intercostal muscle, cachexia (severely underweight), anorexia (loss of appetite) and chronic fatigue
Possible physical examination findings for COPD are prolonger expiratory phase, wheezes, decreased breath sounds, anterior and posterior diameter, cyanosis
As COPD progresses, abnormal gas exchange occurs. This results in hypoxemia (decreased oxygen in blood) and hypercapnia (increased CO2 in blood).
The respiratory center in the brain controls our drive to breathe with the accumulation of CO2. As COPD progresses, the respiratory center loses its sensitivity to elevated CO2 levels and our drive to breathe comes from hypoxemia
If we administer too much oxygen to patients with advanced COPD, we suppress their drive to breathe (which is normally hypoxemia). This may result in hypercapnia (too much CO2 in blood)
Complications of COPD include acute exacerbation of COPD, pneumonia, depression and anixety
Acute exacerbation of COPD is a sustained worsening of COPD symptoms with changes in usual dyspnea, cough and sputum. It is often caused by infections (URTI), air pollution, allergens, irritants or cold air.
COPD management includes pulmonary rehabilitation programs (exercice program and breathing exercises), long term oxygen therapy at home and drug therapy
Pursed lip breathing is effective for COPD patients as it imposes a slight obstruction to expiration air flow at the mouth. It helps prop open the airways and assists lung emptying which helps with dyspnea and prevents alveoli collapse
Nursing management for COPD include exercice, nutrition (high calorie and protein diet), energy conserving strategies, sexual activity and end of life issues