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C Physiology of Airflow Obstruction
1. Loss of elastic recoil:
Destruction of lung tissues
leads to more compliant lung. The airways lose the "tethering" effect of the
surrounding lung tissue making them more susceptible to collapse during
exhalation. Moreof the expiratory curve is "flow limited," i.e., more effort by
the patient does not produce greater expiratory flows.
2. Equal pressure point:
Tendency of airways to
collapse as a result of loss of elastic recoil. With positive intrathoracic
pressure during exhalation, the equal pressure point (the point where the
pressure outside the airway and inside the airway are equal) moves toward more
distal (and morecompressible) airways. Greater tendency to airways collapse
which limits airflow regardless of the expiratory "effort." Patients with
emphysema spend much of their expiratory cycle on the "effortindependent"
portion of the expiratory curve.
3. Hyperinflation:
With early collapse of
airways, air is trapped and the patient breathes at higher lung volumes. This
places the respiratory muscles at a relatively inefficient position on their
length-tension curve leading to greater use of accessory muscles and more
difficulty generating negative intrapleural pressures.
4. AutoPEEP:
Given expiratory flow
limitation through much of the expiratory cycle, expiratory time is increased.
Patients may be forced to initiate the next inspiration before function residual
capacity (FRC) is reached. Thus, there is still positive pressure in the airways
at the end of expiration (PEEP). To generate negative pressure for the next
breath, the patient must overcome this PEEP before any inspiratory flow occurs.
This poses what has been termed an inspiratory threshold load" on the system and
increases the work of breathing.
5. Airways reactivity:
1/3 of patients will have
evidence of reversible airways obstruction after a single dose of a
bronchodilator. Up to 2/3 of patients will demonstrate improved lung function
with repeated testing.
6. Natural history:
Under normal conditions, lung
function decreases by approximately 25-30 mL/year. Rate of decline is steeper in
smokers and, with greater number of cigarettes there is a greater rate of
decline. Once an individual stops smoking, however, the rate of decline returns
toward that of a nonsmoker. Patients with chronic bronchitis who stop smoking
may have improvement in cough and sputum as well as oxygenation. After an acute
respiratory infection, there may a decline in lung function and oxygenation,
which does not return back to previous baseline for 30-90 days. Mortality: with
FEV1 < 0.75 L, the mortality rate at one year is 30%, and at ten years is 95%.
However, some patients "beat the odds" for quite a while.
III. Assessment of the Patient
with COPD
A. History:
Smoking history, presence of
acute changes in symptoms suggestive of airways reactivity or myocardial
ischemia, quantification of exercise capability (patients often make subtle
changes in lifestyle to compensate for increasing shortness of breath and tell
you that they don't have much dyspnea), frequency of and precipitating factors
for acute decompensations, evidence of right heart failure, quality of their
shortness of breath. Most patients whose exercise capability is reduced by
emphysema will describe "increased effort and work of breathing" while those who
have bronchospasm may describe a sense of "chest tightness," and those who are
limited by deconditioning will note "huffing and puffing" or "heavy breathing."
B. Physical examination:
1. Assessment of severity of
airways obstruction: use of accessory muscles, supraclavicular and intercostal
retractions, pulsus paradoxus
2. Assessment of
hyperinflation: AP diameter, Hoover's sign (inward motion of lower lateral rib
cage on inflation, which is indicative of a flat diaphragm), hyperresonance on
percussion
3. Assessment of right
ventricular function: right sided S3; elevated jugular venous pressure, enlarged
liver, peripheral edema
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