Alveolar dead space is believed to be an index of the uniformity of blood flow distribution to the lung. Roughly, the fraction of alveoli without blood flow equals the fraction: alveolar dead space/alveolar tidal volume. Uneven distribution of pulmonary blood flow results not only in the presence of alveolar dead space but is also associated with a difference in Pco2 between end-expired gas and arterial blood. This A-a CO2 difference in the normal dog averaged 3 mm Hg with a range of from 0 to 12 mm Hg. In the absence of uneven ventilation, the A-a CO2 difference and the alveolar dead space are directly related. Pulmonary emboli with 15 ml of air intravenously resulted in an A-a CO2 difference of 30 mm Hg or more. Measurement of both alveolar dead space and A-a CO2 difference suggests that blood flow was interrupted to about of the ventilated alveoli. The A-a oxygen difference was also found to increase at low lung volumes, and decrease at high lung volumes, with tidal volume and rate constant. This is believed to be due primarily to changes in the distribution of alveolar ventilation. The influence of several factors on anatomic dead space is reported. Epinephrine enlarges it about 50%, the effect lasting only 5–10 minutes. Hypoxia (7–10%) constricts the bronchi and reduces the anatomic dead space. Oxygen may result in small and transient increases in anatomic dead space. Increasing respiratory rate also enlarges it, perhaps by increasing oxygen tension. Submitted on January 17, 1956