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We present a review and a theoretical analysis of factors determining airway deadspace (VDaw) and alveolar deadspace (VDalv), the two constituents of physiological deadspace (VDphys). VDaw if the volume of gas between the lips and the alveolar/fresh gas interface, the location of which is determined by inspiratory flow pattern and airway geometry. VDalv can be caused by incomplete alveolar gas mixing and associated V/Q mismatching within the terminal respiratory units, temporal V/Q mismatching within units, spatial V/Q mismatching between units, and venous admixture. Most causes of VDphys are influenced by inspiratory flow pattern and the time available for gas diffusion and distribution. Analysis can be made from the single breath test for carbon dioxide (SBT--CO2) which is the plot of fraction of carbon dioxide in expired gas against expired volume. The common causes of VDalv are associated with a sloping SBT-CO2 phase III. Combination of SBT-CO2 with PaCO2 yields VDphys and VDalv. A sloping phase III with a negative arterial-end-tidal PCO2 gradient implies compensation by perfusion for early emptying, overventilated alveoli.

From a cast of a human pulmonary arterial tree, the diameter, length, order, and end branches of all intact branches down to those 0.8 mm in diameter were measured and corrections for broken branches were made. A sample of structures smaller than these (0.8-0.1 mm) was similarly measured. The values for branches less than 0.1 mm in diameter were found by extrapolation and comparison with known data for the precapillary vessels. Therefore, data or estimates for each order of branching in the pulmonary tree were obtained and calculations of cross-sectional area, volume, and flow were made.

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