Using conventional concepts, it is possible that a single pathologic entity, pulmonary telangiectases, can produce hypoxia by 3 physiologic mechanisms; shunt, diffusion defect, and ventilation-perfusion abnormalities. The estimation of shunt or shunt-like effect is traditionally calculated by measuring the Po2 of arterial blood during the breathing of 100 per cent 02. This method, however, did not determine blood flow through large alveolar vessels in a patient with familial hemorrhagic telangiectasis who was severely hypoxemic while breathing air. This case served to test the concept that blood flowing through large vessels in the airspaces may be hypoxemic when the patient breathes air, but not 02. Blood flow through these vessles can be estimated by use of radionuclide lung perfusion techniques and estimation of the quantity of radioactive particles that pass through an abnormal pulmonary vascular bed and lodge in kidney and brain. Conventional approaches to estimating blood flow through these fistulas underestimated their effect.

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