Effect of the rebreathing pattern on pulmonary tissue volume and capillary blood flow.

Abstract

Noninvasive rebreathing measurements of pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) theoretically and experimentally vary with the rebreathing maneuver. To determine the cause of these variations and identify ways to minimize them, we examined the consequences of varying the volume inspired (VI), rebreathing rate (f), volume rebreathed (Vreb), and alveolar volume (VA) on the observed Vt and Qc in six normal sitting subjects. When VA was increased by progressively larger VI and Vreb, Vt increased 50 ml/l of VA. Increasing VA while keeping VI and Vreb constant did not significantly alter Vt. Diminishing Vreb while VA and VI constant caused Vt to fall 108 ml/l decrease in Vreb. Therefore the observed Vt is not simply a function of VA but increased with greater penetration of the inspired gas into the lungs. Diminishing f from 40 to 12 breaths/min caused the observed Vt to rise 27%, indicating time allowed for alveolar mixing is an important determinant of Vt. The observed Qc, in contrast, was essentially independent of the same variations in rebreathing. The above findings were similar regardless of solubility of the tracer gas (dimethyl ether instead of acetylene) or changing to the supine position. A two-compartment series lung model derived from the anatomy and rates of gas mixing in normal human pulmonary lobules produced similar changes in Vt. Thus the degree of uneven distribution between ventilation, VA, Vt, and Qc within the normal lung lobule can account for variations in the observed Vt with different ventilatory maneuvers. Slow deep breathing maneuvers tended to reduce variations in Vt. Unlike Qc, the observed value of Vt can be expected to vary substantially with pathological processes that alter pulmonary gas distribution.