COPD Flashcards
List the major COPD states and why they fit under this category
- emphysema (destruction and enlargement of lung alveoli)
- chronic bronchitis (chronic cough and phelgm)
* note: without chronic airflow obstruction, chronic bronchitis is not included within COPD)* - small airway disease (small bronchioles are narrowed)
**all conditions cause obstruction to getting air out of lung **
explain the airway hyperresponsiveness and COPD
-increased bronchoconstriction in response to exogenous stimuli (like metacholine and histamine)
metacholine acts in parasympathetic nervous system, so would constrict the bronchioles
-Dutch hypothesis says both asthma AND COPD share this feature
explain the following changes you expect to see in COPD of the following:
- Forced expiratory flow rates:
- Residual volume:
- residual volume/total lung capacity ratio:
- ventilation distribution:
- V/Q:
- FEV1/FVC
- Forced expiratory flow rates: decreased
- Residual volume: increased
- residual volume/total lung capacity ratio: increased
- ventilation distribution: nonuniform
- V/Q: mismatch
- FEV1/FVC: decreases
airflow during forced exhalation is the result of the balance between these two factors:
- elastic recoil = promotes flow
- resistance of airways = limits flow
Why does maximal expiratory flow diminish as the lungs empty? Does this happen in normal and/or COPD pts?
-lung parenchyma provides progressively less elastic recoil and cross sectional area of airway falls, raising the resistance to airflow
occurs in lungs affected by COPD and normal lungs
What happens to lung volumes in COPD? How does this affect maximum expiratory airflow?
“air trapping”
increased RV and RV/TLC
progressive hyperinflation (increased TLC)
-hyperinflation of the thorax during tidal breathing actually helps to preserve max exp airflow: as lung volume increases, elastic pressure increases, and airways enlarge so that airway resistance decreases
While hyperinflamation is a way to help expiration, how does it effect inspiration?
Overall,compromises inspiration in 3 ways:
less effective positive abdominal pressure –> hinders rib cage movement –> impaired inspiration
bigger lung volume flattens diaphgram –> shorter muscle fibers –> **less capable of generating inspiratory pressures **
diaphagram must generate greater tension to develop the transpulmonary pressure needed to produce tidal breathing, also inspiratory muscles must do more work to overcome the resistance of the thoracic cage (since chest wall isnt helping with its natural recoil outward towards resting volume)
cigarette smoke causes different responses whether there are changes in large airways or small airways and alveoli. Explain
large airways: cause cough and sputum <– mucous gland enlargement and goble cell hyperplasia
these define chronic bronchitis, but not related to airflow limitation
small airways and alveoli: physiologic alterations <–luminal narrowing by fibrosis, excess mucus, edema, and cellular infiltration, mucus secreting cells replace surfactant secreting, which may increase surface tension, increased airway narrowing or collapse
What characterizes emphysema
destruction of gas-exchanging air spaces (respiratory bronchioles, alveolar ducts, and alveoli)
small distinct airspaces –> abnormal large ones
macrophages are >95% of total cell count
Centriacinar vs. panacinar emphysema
centriacinar = associated w cigarette smoke = bigger air spaces foudn intiially in association with respiratory bronchioles, usually in upper lobes
panacinar = a1AT deficiency = large air spaces evenly distrbuted across acinar units, usually lower lobes
what causes the cell death in emphysema?
increased oxidant stress both directly from cigarette smoke and from inflammation
3 most common symptoms in COPD
cough, sputum, exertional dyspnea
physical findings of COPD
barrel chest, expiratory wheezing, prolonged expiratory phase, cyanosis may develop\
“pink puffers” (stay pink, pursed lips and prolonged expiration to overcome obstruction
blue bloaters are associateed with chronic bronchitis, but really you see elements of both in each type of patient
change in pH with PCO2 for acute and chronic state
PCO2 level for classification of ventilatory failure
0.08 units/10 mmHg acutely and 0.03 units/10 mmHg in the chronic state
pCO2>45 mmHg