Thus, the development of pulmonary hypertension at rest represents a major degree of abnormality, associated with the loss of more than 50 percent of the pulmonary vascular bed. The situation is analogous to a waterfall, in which the downstream pressure is no longer a determinant of the flow rate. The value for the pulmonary vascular resistance also varies with the flow rate because portions of the pulmonary vasculature that are normally collapsed become full under conditions of increased flow. The first category is characterized by the loss of portions of the pulmonary vascular bed with normal function in the remaining segments. Such losses might be the result of extensive surgical resection of pulmonary tissue, pulmonary emphysema with loss of many of the alveolar walls, chest wall deformity that reduces the volume of the lungs, or one of many pulmonary parenchymal diseases that replace normal lung tissue with various forms of scar tissue, infiltrates, or inflammatory tissue.
Pulmonary vasoconstriction is mediated by several different mechanisms.
The most potent physiologic stimulus is alveolar hypoxia. The resulting vasoconstriction appears to be a self-regulating response designed to divert blood flow away from hypoxic regions toward better ventilated regions. However, generalized alveolar hypoxia can lead to pulmonary hypertension. Pulmonary hypertension that is chronic and associated with structural changes in the pulmonary vessels leads to a decline in this mediator. The pulmonary vasoconstrictor response to hypoxia is exaggerated in these circumstances.