Abstract
The physiologic derangements of patients with chronic obstructive pulmonary disease can be grouped in two categories: those that stem from the anatomic alterations produced by the disease and those that represent adaptations that, if optimally carried out, prolong survival. For instance, increased airway resistance, hyperinflation, ventilation–perfusion inhomogeneity, and hypoxemia can all be considered direct consequences of the anatomic changes in the lung. But polycythemia, increased cardiac output, hypoxic pulmonary vasoconstriction, and chronic shifts in the oxyhemoglobin dissociation curve can more readily be considered in the category of adaptive physiology.Support for such a grouping can be adduced from recent studies . . .