A more general view
Some principles outlined above apply more generally to in vivo systems of tubes which vary their diameter in response to chronic and acute stimuli, such as pulmonary hypertension. Consider the patient with hypoxemia and hypercapnia. This induces pulmonary arteriolar vasoconstriction (von Euler-Liljestrand reflex), which gives rise to an increase in pulmonary artery pressure. This implies an increased afterload to the right ventricle, which may ultimately give rise to cor pulmonale. Sustained pulmonary hypertension gives rise to hypertrophy of the media within the wall of the pulmonary artery, particularly in the smallest pulmonary arteries and the arterioles. This increased wall thickness can result in a fixed component of increased vascular resistance. The smaller the initial diameter of small lung vessels, the greater the increase in vascular resistance and pulmonary artery pressure, for the same drop in oxygen or rise in CO2 pressure. In the presence of medial thickening, improvements in alveolar ventilation will have a greater effect on pulmonary artery pressure than when the vessel waal is normal. Thus there are analogies in the pathophysiological mechanisms underlying the measured constrictor or dilator response ("responsiveness") in pulmonary blood vessels and airways.