COPD Flashcards
COPD
chronic obstructive pulmonary disease >limitation of airflow through lungs *preventable and treatable *not fully reversible >progressive >pulmonary inflammatory response to noxious particles or gases >eventually systemic symptoms develop
COPD II
chronic bronchitis *upper airway problem emphysema *lower alveolar destruction These conditions co-exist *goal: maintain oxygenation and tissue perfusion
Incidence and prevalence of COPD:
> 12.1 million americans have COPD >18ys old
4th leading cause mortality in U.S. more common in men
women with COPD on rise
highest incidence in white amercians
more than 50% die within 10 years of diagnosis
predicted to become 3rd leading cause of death worldwide by 2020
primary cause-cigarette smoking
Pathophysiology of COPD:
> primary disease process is chronic inflammation
*airways, pulmonary blood vessels, lung parenchyma
inhalation of noxious particles (how disease starts): releases inflammatory cells, increased mucus production, damage and repeated healing, and remodeling and fibrosis
Most common characteristics of COPD:
inability to expire air (hyper airflow of the lungs), airway obstruction leads to progressive air trapping, and residual air+loss of elastic recoil = hyperinflation (barrel chest)*
other common characteristics of COPD:
> gas exchange abnormalities
*alveolar destruction (blebs and bullae), hypoxemia, hypercapnia
mucus hypersecretion and cilia dysfunction
loss of elastic recoil
pulmonary vascular changes
*pulmonary hypertension
*cor pulmonale
Cor pulmonale:
enlargement of the right side of the heart
Pathophysiology: Vascular changes
> pulmonary vascular changes
*blood vessels thicken
*surface area for diffusion of O2 decreases
*hypoxemia at rest=late stage
*may need supplemental O2 earlier with exercise
Cor pulmonale - right sided hypertrophy of pulmonary artery>leads to right sided heart failure
COPD: Chronic bronchitis
> presence of chronic productive cough for 3 or more months in each of 2 successive years when other causes of chronic cough are excluded
bronchi and bronchioles affected
irritants cause:
*inflammation, congestion, bronchospasm, mucosal edema
smaller airways affected first
Chronic bronchitis: Pathophysiology
> inflammation and scarring of bronchiole lining
*decreased airflow, excessive mucous accumulation, cough develops, and ciliary function decreases
bacteria multiply causing infection
COPD: Emphysema
> abnormal permanent enlargement of the air space distal to the terminal bronchioles (alveoli)
10 % of pts with COPD have pure emphysema
*most have mix of chromic bronchitis and emphysema
COPD vs Asthma
High level of proteases
alveoli destroyed: bullae formed
*loss of elastic recoil
*alveoli overstretching
*bronchioles collapse
loss of lung elasticity with lung hyperinflation
results: increased work of breathing, decreased area for gas exchange, air trapping in lungs
Risk factors: COPD
cigarette smoking, occupational risks, air pollution, infection, genetics, and aging
Cigarette smoking:
>smoking causes destruction of alveolar walls *smoke causes hyperplasia of cells *increased mucus production *reduces airway diameter >smoke reduces ciliary action >smoke releases proteases in lungs: *breaks down elastin in found in alveoli
COPD: Cigarette smoking
> clinically significant airway obstruction develops in about 15% of smokers
passive smoking also contributes to respiratory problems (SHS)
COPD: occupation and environment:
> COPD can develop with intense or prolonged exposure to:
- environmental tobacco smoke
- occupational dusts, vapors, irritants, or fumes
- high levels of air pollution
- fumes from indoor heating or cooking with fossil fuel
COPD: infection
> risk factor for and symptom of COPD
recurring infections impair normal defense mechanisms
cycle of chronic inflammation
repeated infections worsen pathologic destruction of lung tissue
haemophilus influenza, streptococcus pneumonia**
Genetic risk:
> alpha 1 antitrypsin deficiency (AAT)
*genetic factor identified for COPD
*serum protein produced by liver
AAT protects lungs from inhaled organisms/pollutants
*inhibits lysis of lung tissue by proteolytic enzymes (proteases)
smoking worsens disease process
symptoms by age 40, minimal tobacco use, family hx
treatment is AAT adm IV
Aging lung changes:
>aging changes similar to emphysema >gradual loss of elastic recoil >lungs become rounded and smaller >loss of alveolar supporting structures >decreased number of functional alveoli >thoracic cage changes from osteoporosis and calcification of costal cartilage >decreased chest compliance and elastic recoil increases work of breathing >decreased ability to clear secretions
Clinical manifestations of COPD:
> symptoms develop slowly
20 pack year smoking history
diagnosis is considered with:
cough, sputum production, dyspnea, and exposure to risk factors
chronic intermittent cough is earliest symptom
progressive dyspnea usually prompts medical attention
*occurs with exertion in early stages and present at rest with advanced disease
Late stage clinical manifestations of COPD:
> Alveoli over distended
* increasing amounts of air trapped
flattened diaphragm
abdominal breathing no longer effective
breathes with intercostal and accessory muscles
not efficient breathing
PE: wheezing, chest tightness, prolonged expiratory phase, decreased breath sounds, accessory muscles, pursed lip breathing, tri-pod position, hypoxemia, hypercapnia, cyanosis, and polycythemia
Weight and muscle mass:
> chronic fatigue
anorexia and weight loss in advanced COPD
underweight with adequate caloric intake
takes all their energy to BREATHE
Chronic bronchitis “blue bloater”:
>right heart failure > obese* >cough with sputum > accessory muscle use > coarse rhonchi/wheezing*
Emphysema “pink puffer”:
> thin, barrel chest* > little or no cough or sputum > pursed lip breathing > accessory muscle use > tripod position > decreased lung sounds or wheezing*
Complications of COPD:
> Cor pulmonale
exacerbations of COPD
acute respiratory failure
depression/anxiety
COPD exacerbations:
> exacerbations are natural coarse of disease
characterized by change in patients baseline: dyspnea, cough, and sputum
acute onset
increased frequency
associated with poorer outcomes
primary cause: bacterial or vial infections, air pollution
careful assessment
changes in plan of care
teaching
Acute respiratory failure:
Caused by:
> exacerbations if COPD
> Cor Pulmonale
> discontinuing bronchodilator or corticosteroid medications
> overuse of sedatives, benzodiazepines, and opioids
> surgery/pain of chest/abdomen
Depression/anxiety:
> depression > anxiety complications > teach about disease > provide emotional support > anti-depressant/ anti anxiolytics > mental health consult
Diagnostic studies:
> pulmonary function test > CXR > ABGS/sputum/CBC/AAT/genealogy > EKG/ echo > SPO2
Pulmonary function testing:
> lung volume test:
* residual volume (air in lung after expiration)
* functional residual capacity ( increased amount of air left after expiration)
flow volume tests:
* FVC ( forced volume capacity)
* FEV1: (forced expired volume in the first second of expiration)**how to rank severity of disease
* FEV1:FVC- ratio
diffusion tests
ABGs:
> low PaO2 > ^ PaCO2 > low pH > ^ bicarbonate level * typical findings in late stages of COPD
Collaborative care:
Primary goal of care: > prevent progression > relieve symptoms > prevent/treat complications > prevent/treat exacerbations > promote patient participation > improve quality of life > decrease mortality risk > evaluate exposure to irritants (control or avoid) > flu/pneumo vx > treat ASAP > smoking cessation (most effective intervention)*
Stages of COPD:
> stage I: mild
stage II: moderate
stage III: severe
stage IV: very severe
