Biomedical Engineering Reference
In-Depth Information
COPD are considered, several indices of bronchiolar inflammation correlate
with the degree of airflow obstruction. Indeed, the most consistent relation-
ship between lung function and airway and pulmonary structure found in
subjects with severe COPD is between severe emphysema and severe airflow
limitation. The most important factor is emphysema and loss of elastic
recoil. Most studies in advanced COPD find that the best reflection of the
severity of airflow limitation is the extent of pulmonary emphysema. Thus,
although both the destruction of alveolar attachments to the outer wall of
the peripheral airways and the loss of lung elastic recoil produced by emphy-
sema have been implicated in the pathogenesis of peripheral airways
obstruction, direct measurements of peripheral airways resistance show that
the structural changes in the airway wall are the most important cause of the
increase in peripheral airways resistance in COPD. Thus, when COPD
becomes moderate or severe, loss of elastic recoil becomes overwhelmingly
important and may mask the effects of bronchiolar disease on chronic
airflow limitation (1).
Advanced COPD is also associated with gas-exchange abnormalities,
i.e. hypoxemia and, later on, hypercapnia. Abnormal gas exchange may
be due to several factors, such as alveolar hypoventilation, altered gas trans-
fer, inequalities in ventilation-perfusion (V
=
Q) ratio, and right-left blood
shunting. Several studies have demonstrated a negative relationship between
single breath or steady-state carbon monoxide transfer factor (TLCO) and
the degree of emphysema (23,24). In COPD, regardless of the stage of dis-
ease and the presence or absence of emphysema, V
=
Q inequality is generally
accepted to be the major mechanism that impairs gas exchange and leads to
arterial hypoxemia. Impaired V
=
Q relationships may be caused by multiple
pathological changes in different lung structures, including the airways, par-
enchyma, and pulmonary vasculature. Bronchiolar lesions are associated
with V
=
Q mismatching, as indicated by a significant correlation between
bronchiolar inflammation and the distribution of ventilation. Low V
=
Q units
in the lungs may represent areas with a partially blocked airway. Destruction
of the lung surface area by emphysema reduces the diffusing capacity and
interferes with gas exchange (23). The severity of pulmonary emphysema
appears to be related to the overall inefficiency of the lung as a gas exchanger.
This is reflected by the good correlation between the diffusing capacity of car-
bon monoxide per liter of alveolar volume (TLCO
=
VA) and the severity of
macroscopic emphysema. Reduced ventilation due to loss of elastic recoil
in emphysematous lung together with loss of the capillary bed and generalized
inhomogeneity of ventilation due to the patchy nature of these changes leads
to areas of V
=
Q mismatching which result in arterial hypoxemia. Of the four
classic mechanisms determining hypoxemia and
=
or hypercapnia—alveolar
hypoventilation, alveolar-end capillary diffusion limitation to oxygen,
increased intrapulmonary shunt, and ventilation-perfusion mismatching—
the last is by far the most common intrapulmonary determinant of hypoxe-
