Lower pulmonary diffusing capacity in the prone vs. supine posture

We evaluated the effect of prone positioning on gas-transfer characteristics in normal human subjects. Single-breath (SB) and rebreathing (RB) maneuvers were employed to assess carbon monoxide diffusing capacity (DlCO), its components related to capillary blood volume (Vc) and membrane diffusing capacity (Dm), pulmonary tissue volume (Vti), and cardiac output (Q̇c). Alveolar volume (Va) was significantly greater prone than supine, irrespective of the test maneuver used. Nevertheless, DlCO was consistently lower prone than supine, a difference that was enhanced when appropriately corrected for the higher Va prone. When adequately corrected for Va, diffusing capacity significantly decreased by 8% from supine to prone [SB: DlCO,corr supine vs. prone: 32.6 ± 2.3 (SE) vs. 30.0 ± 2 ml·min-1·mmHg-1 stpd; RB: DlCO,corr supine vs. prone: 30.2 ± 2.2 (SE) vs. 27.8 ± 2.0 ml·min-1·mmHg-1 stpd]. Both Vc and Dm showed a tendency to decrease from supine to prone, but neither reached significance. Finally, there were no significant differences in Vti or Q̇c between supine and prone. We interpret the lower diffusing capacity of the healthy lung in the prone posture based on the relatively larger space occupied by the heart in the dependent lung zones, leaving less space for zone 3 capillaries, and on the relatively lower position of the heart, leaving the zone 3 capillaries less engorged.

Pulmonary tissue volume, cardiac output, and diffusing capacity in sustained microgravity

Verbanck, Sylvia, Hans Larsson, Dag Linnarsson, G. Kim Prisk, John B. West, and Manuel Paiva. Pulmonary tissue volume, cardiac output and diffusing capacity in sustained microgravity. J. Appl. Physiol. 83(3): 810–816, 1997.—In microgravity (μG) humans have marked changes in body fluids, with a combination of an overall fluid loss and a redistribution of fluids in the cranial direction. We investigated whether interstitial pulmonary edema develops as a result of a headward fluid shift or whether pulmonary tissue fluid volume is reduced as a result of the overall loss of body fluid. We measured pulmonary tissue volume (Vti), capillary blood flow, and diffusing capacity in four subjects before, during, and after 10 days of exposure to μG during spaceflight. Measurements were made by rebreathing a gas mixture containing small amounts of acetylene, carbon monoxide, and argon. Measurements made early in flight in two subjects showed no change in Vti despite large increases in stroke volume (40%) and diffusing capacity (13%) consistent with increased pulmonary capillary blood volume. Late in-flight measurements in four subjects showed a 25% reduction in Vti compared with preflight controls ( P < 0.001). There was a concomittant reduction in stroke volume, to the extent that it was no longer significantly different from preflight control. Diffusing capacity remained elevated (11%; P< 0.05) late in flight. These findings suggest that, despite increased pulmonary perfusion and pulmonary capillary blood volume, interstitial pulmonary edema does not result from exposure to μG.

Solubility of Freon 22 in human blood and lung tissue

The solubility of Freon 22 in human blood and lung tissue was determined using the chromatographic method of Wagner et al. (J. Appl. Physiol. 36: 600–605, 1974). In normal human blood, the mean Bunsen coefficient of solubility (alpha B) was 0.804 cm3 STPD.cm-3.ATA-1 at 37 degrees C. It increased with hematocrit (Hct) according to the equation alpha B = 0.274 Hct + 0.691. Tissue homogenates were prepared from macroscopically normal lung pieces obtained at thoracotomy from eight patients undergoing resection for lung carcinoma. The Bunsen solubility coefficients were 0.537 +/- 0.068 and 0.635 +/- 0.091 in washed and unwashed lung, respectively. These values can be used in the determination of both cardiac output and pulmonary tissue volume in humans by use of the rebreathing technique.

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

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.

A computerized timing algorithm for determination of pulmonary tissue volume

We developed a computerized method to measure pulmonary tissue volume (Vt) and capillary blood flow (Qc) that requires only a single interface for measurement of a soluble and an insoluble gas. The method uses a timing algorithm that replaces either a marker gas (C18O) or a volume signal. Gas concentrations are stored in digitized form. The data analysis consists of three parts: 1) initial and end-tidal samples found by using minima and maxima; 2) a timing algorithm derived from the end-tidal dead space method (ETDS, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 782-795, 1978); and 3) calculations of Vt and Qc, also by the ETDS method. Both the timing and Vt and Qc agree well with the hand-calculated values, but the coefficient of variation of Vt is slightly improved (6 vs. 7% manually). We conclude that our computerized method is equivalent to the manual ETDS method, but it is faster and more accurate; in addition, it has the advantage of requiring only one interface without the use of expensive gases.

Measurement of pulmonary tissue volume and blood flow in persons with normal and edematous lungs

We measured pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) by a rebreathing method using two soluble gases, acetylene (C2H2) and dimethyl ether (DME), in 32 normal subjects and 14 patients who had had pulmonary edema. In 18 of the normal subjects, studies were performed at three or more different rebreathing volumes (VA). To normalize for differences in body size, results were expressed as the ratio of Vt or VA to predicted total lung capacity (TLC). We found that 1) changes in VA/TLC had a significant effect on Vt/TLC and Qc measured with both gases, 2) the range of normal values for Vt was best defined by expressing the relationship between Vt/TLC and VA/TLC, 3) using this approach, many patients with clinically mild or inapparent pulmonary edema had abnormal values of Vt, and 4) when comparing mean values of C2H2 and DME in 82 simultaneous measurements at constant VA/TLC, Vt was significantly higher in 87% (71/82) and Qc in 63% (52/82) of the paired tests.

Determination of Pulmonary Tissue volume, Pulmonary Capillary Blood Flow and Diffusing Capacity of the Lung before and after Hemodialysis

In order to better understand changes in lung function before and after dialysis, we studied eight patients with end-stage renal disease undergoing chronic hemodialysis. Pulmonary tissue volume (Vt), pulmonary capillary blood flow (Q̇c), the diffusing capacity for carbon monoxide (DLCO), arterial blood gases and body weight were measured before and after dialysis. A single breath, constant expiratory flow technique for determination of DLCO, Q̇c and Vt was used. DLCO, Q̇c, arterial carbon dioxide, and body weight were reduced post dialysis (P ≤ .01) while Vt failed to change. The alveolar-arterial oxygen difference rose 12 mmHg (P = .01). These results are consistent with pulmonary microembolization during dialysis with deterioration of gas exchange and Q̇c. These changes appear to occur independent of significant changes in Vt. Possible physiologic mechanisms are discussed.