Biomedical Engineering Reference
In-Depth Information
mia in COPD. The role of shunt is almost negligible, even in the most life-
threatening conditions, and diffusion limitation is conspicuously absent.
Hypercapnia can be induced by ventilation-perfusion imbalance and
=
or
alveolar hypoventilation, the latter being predominant during exacerbations.
Pulmonary hypertension develops late in the natural history of
patients with COPD is usually associated with the development of severe
hypoxemia (PaO
2
<
8KPa or 60mmHg), and often of hypercapnia as well.
It represents the main cardiovascular complication associated with the
development of right ventricular hypertrophy (cor pulmonale). Several fac-
tors are known to contribute to the development of pulmonary hypertension
in patients with COPD, i.e. (a) thickening of pulmonary vessel walls and
reduction of lumen, (b) hypoxia, which causes pulmonary vascular smooth
muscle to contract and further reduces the lumen, (c) impaired endothelium-
dependent vasodilation (reduction of nitric oxide (NO) synthesis or release
in response to hypoxemia), (d) abnormal secretion of vasoconstrictor
peptides such as endothelin-1, (e) destruction of the capillary bed, which
further increases the pressure required to perfuse the pulmonary circulation.
Cor pulmonale is defined as ''hypertrophy of the right ventricle result-
ing from diseases affecting the function and
=
or structure of the lungs, except
when these pulmonary alterations are the result of diseases that primarily
affect the left side of the heart, as in congenital heart disease.'' This is a
pathological definition and the clinical diagnosis and assessment of right
ventricular hypertrophy is difficult in life. The prevalence and natural
history of cor pulmonale in COPD are not yet clear. Pulmonary hyperten-
sion and reduction of the vascular bed due to emphysema can lead to right
ventricular hypertrophy and right heart failure. Right heart failure is asso-
ciated with venous stasis and thrombosis that may result in pulmonary
embolism and further compromise the pulmonary circulation.
B. Asthma
Similar to COPD, also in asthma structural changes occur in both large and
small airways and may lead to the characteristic clinical manifestations and
lung function changes of the disease, i.e. respiratory symptoms (i.e. wheez-
ing, dyspnea, chest tightness), often reversible airflow limitation, and in
some cases, gas-exchange abnormalities (1). At variance with COPD,
asthma is usually not associated with emphysema, i.e. the lung parenchyma
is usually preserved even in most severe asthmatics.
Asthma is a complex inflammatory disease state characterized by a
specific pattern of inflammation involving many inflammatory cells, media-
tors, with multiple inflammatory effects, including bronchoconstriction,
plasma exudation, mucus hypersecretion, and sensory nerve activation.
Genetic factors are involved in the predisposition to atopy, the most
important risk factor for asthma together with allergen exposure. There is
