Pulmonary resistance in cardiovascular context.
Comparison of the human cardiovascular system with arrangements of circulatory systems found in lower vertebrates and invertebrates allows appreciation of the functional elegance of our double circulation with systemic and pulmonary vascular trees served by a single looped and septated heart. In the pulmonary part of the circulation, consideration of the nature of alveolar microvessels in relation to the system as a whole may throw light on the pathophysiology of pulmonary regurgitation and pulmonary hypertension. Pulmonary microvessels impose remarkably little resistance to flow compared with the systemic. This may be attributed to their delicate, compliant structure, with tissue support on one side only, their respiratory walls remaining relatively free to expand in alveolar air. Low resistance may also depend on the branch pattern of alveolar capillaries, with almost immediate proximity between bifurcations and confluences in a uniquely dense, interconnected network. In the presence of free pulmonary regurgitation, pulmonary microvessels probably play a valve-like role, representing a low-resistance boundary or watershed between pulmonary arteries and veins. This microvascular watershed imposes little resistance to systolic forward flow, but in diastole, with venous pressures being kept low by function of the left heart, there is presumably little or no reversal of gradient to move blood back through the capillaries. The delicacy and potential vulnerability of alveolar capillaries to elevation of flow and pressure is likely, however, to go with a protective feedback circuit which, in abnormal circumstances, could contribute to development of arteriolar medial hypertrophy and pulmonary arterial hypertension.