Tracheal gas exchange: perfusion-related differences in inert gas elimination

1995 ◽  
Vol 79 (3) ◽  
pp. 918-928 ◽  
Author(s):  
J. E. Souders ◽  
S. C. George ◽  
N. L. Polissar ◽  
E. R. Swenson ◽  
M. P. Hlastala

Exchange of inert gases across the conducting airways has been demonstrated by using an isolated dog tracheal preparation and has been characterized by using a mathematical model (E. R. Swenson, H. T. Robertson, N. L. Polissar, M. E. Middaugh, and M. P. Hlastala, J. Appl. Physiol. 72: 1581–1588, 1992). Theory predicts that gas exchange is both diffusion and perfusion dependent, with gases with a higher blood-gas partition coefficient exchanging more efficiently. The present study evaluated the perfusion dependence of airway gas exchange in an in situ canine tracheal preparation. Eight dogs were studied under general anesthesia with the same isolated tracheal preparation. Tracheal perfusion (Q) was altered from control blood flow (Qo) by epinephrine or papaverine instilled into the trachea and was measured with fluorescent microspheres. Six inert gases of differing blood-gas partition coefficients were used to measure inert gas elimination. Gas exchange was quantified as excretion (E), equal to exhaled partial pressure divided by arterial partial pressure. Data were plotted as ln [E/(l-E)] vs. In (Q/Qo), and the slopes were determined by least squares. Excretion was a positive function of Q, and the magnitude of the response of each gas to changes in Q was similar and highly significant (P < or = 0.0002). These results confirm a substantial perfusion dependence of airway gas exchange.

2004 ◽  
Vol 97 (5) ◽  
pp. 1702-1708 ◽  
Author(s):  
Carmel Schimmel ◽  
Susan L. Bernard ◽  
Joseph C. Anderson ◽  
Nayak L. Polissar ◽  
S. Lakshminarayan ◽  
...  

We studied the airway gas exchange properties of five inert gases with different blood solubilities in the lungs of anesthetized sheep. Animals were ventilated through a bifurcated endobronchial tube to allow independent ventilation and collection of exhaled gases from each lung. An aortic pouch at the origin of the bronchial artery was created to control perfusion and enable infusion of a solution of inert gases into the bronchial circulation. Occlusion of the left pulmonary artery prevented pulmonary perfusion of that lung so that gas exchange occurred predominantly via the bronchial circulation. Excretion from the bronchial circulation (defined as the partial pressure of gas in exhaled gas divided by the partial pressure of gas in bronchial arterial blood) increased with increasing gas solubility (ranging from a mean of 4.2 × 10−5 for SF6 to 4.8 × 10−2 for ether) and increasing bronchial blood flow. Excretion was inversely affected by molecular weight (MW), demonstrating a dependence on diffusion. Excretions of the higher MW gases, halothane (MW = 194) and SF6 (MW = 146), were depressed relative to excretion of the lower MW gases ethane, cyclopropane, and ether (MW = 30, 42, 74, respectively). All results were consistent with previous studies of gas exchange in the isolated in situ trachea.


1992 ◽  
Vol 72 (4) ◽  
pp. 1581-1588 ◽  
Author(s):  
E. R. Swenson ◽  
H. T. Robertson ◽  
N. L. Polissar ◽  
M. E. Middaugh ◽  
M. P. Hlastala

We studied CO2 and inert gas elimination in the isolated in situ trachea as a model of conducting airway gas exchange. Six inert gases with various solubilities and molecular weights (MW) were infused into the left atria of six pentobarbital-anesthetized dogs (group 1). The unidirectionally ventilated trachea behaved as a high ventilation-perfusion unit (ratio = 60) with no appreciable dead space. Excretion of higher-MW gases appeared to be depressed, suggesting a MW dependence to inert gas exchange. This was further explored in another six dogs (group 2) with three gases of nearly equal solubility but widely divergent MWs (acetylene, 26; Freon-22, 86.5; isoflurane, 184.5). Isoflurane and Freon-22 excretions were depressed 47 and 30%, respectively, relative to acetylene. In a theoretical model of airway gas exchange, neither a tissue nor a gas phase diffusion resistance predicted our results better than the standard equation for steady-state alveolar inert gas elimination. However, addition of a simple ln (MW) term reduced the remaining residual sum of squares by 40% in group 1 and by 83% in group 2. Despite this significant MW influence on tracheal gas exchange, we calculate that the quantitative gas exchange capacity of the conducting airways in total can account for less than or equal to 16% of any MW-dependent differences observed in pulmonary inert gas elimination.


1982 ◽  
Vol 52 (3) ◽  
pp. 683-689 ◽  
Author(s):  
H. T. Robertson ◽  
R. L. Coffey ◽  
T. A. Standaert ◽  
W. E. Truog

Pulmonary gas exchange during high-frequency low-tidal volume ventilation (HFV) (10 Hz, 4.8 ml/kg) was compared with conventional ventilation (CV) and an identical inspired fresh gas flow in pentobarbital-anesthetized dogs. Comparing respiratory and infused inert gas exchange (Wagner et al., J. Appl. Physiol. 36: 585--599, 1974) during HFV and CV, the efficiency of oxygenation was not different, but the Bohr physiological dead space ratio was greater on HFV (61.5 +/- 2.2% vs. 50.6 +/- 1.4%). However, the elimination of the most soluble inert gas (acetone) was markedly enhanced by HFV. The increased elimination of the soluble infused inert gases during HFV compared with CV may be related to the extensive intraregional gas mixing that allows the conducting airways to serve as a capacitance for the soluble inert gases. Comparing as exchange during HFV with three different density carrier gases (He, N2, and Ar), the efficiency of elimination of Co2 or the intravenously infused inert gases was greatest with He-O2. However, the alveolar-arterial partial pressure difference for O2 on He-O2 exceeded that on N2-O2 by 5.4 Torr during HFV. The finding agrees with similar observations during CV, suggesting that this aspect of gas exchange is not substantially altered by HFV.


1975 ◽  
Vol 38 (6) ◽  
pp. 1099-1109 ◽  
Author(s):  
P. D. Wagner ◽  
R. B. Laravuso ◽  
E. Goldzimmer ◽  
P. F. Naumann ◽  
J. B. West

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.


2004 ◽  
Vol 96 (5) ◽  
pp. 1894-1898 ◽  
Author(s):  
Thomas V. Brogan ◽  
H. Thomas Robertson ◽  
Wayne J. E. Lamm ◽  
Jennifer E. Souders ◽  
Erik R. Swenson

We have shown previously that inspired CO2 (3-5%) improves ventilation-perfusion (V̇a/Q̇) matching but with the consequence of mild arterial hypercapnia and respiratory acidosis. We hypothesized that adding CO2 only late in inspiration to limit its effects to the conducting airways would enhance V̇a/Q̇ matching and improve oxygenation without arterial hypercapnia. CO2 was added in the latter half of inspiration in a volume aimed to reach a concentration of 5% in the conducting airways throughout the respiratory cycle. Ten mixed-breed dogs were anesthetized and, in a randomized order, ventilated with room air, 5% CO2 throughout inspiration, and CO2 added only to the latter half of inspiration. The multiple inert-gas elimination technique was used to assess V̇a/Q̇ heterogeneity. Late-inspired CO2 produced only very small changes in arterial pH (7.38 vs. 7.40) and arterial CO2 (40.6 vs. 39.4 Torr). Compared with baseline, late-inspired CO2 significantly improved arterial oxygenation (97.5 vs. 94.2 Torr), decreased the alveolar-arterial Po2 difference (10.4 vs. 15.7 Torr) and decreased the multiple inert-gas elimination technique-derived arterial-alveolar inert gas area difference, a global measurement of V̇a/Q̇ heterogeneity (0.36 vs. 0.22). These changes were equal to those with 5% CO2 throughout inspiration (arterial Po2, 102.5 Torr; alveolar-arterial Po2 difference, 10.1 Torr; and arterial-alveolar inert gas area difference, 0.21). In conclusion, we have established that the majority of the improvement in gas exchange efficiency with inspired CO2 can be achieved by limiting its application to the conducting airways and does not require systemic acidosis.


1994 ◽  
Vol 77 (2) ◽  
pp. 912-917 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie ◽  
R. B. Schoene ◽  
R. W. Glenny ◽  
H. T. Robertson

To investigate pulmonary gas exchange during exercise in athletes, 10 high aerobic capacity athletes (maximal aerobic capacity = 5.15 +/- 0.52 l/min) underwent testing on a cycle ergometer at rest, 150 W, 300 W, and maximal exercise (372 +/- 22 W) while trace amounts of six inert gases were infused intravenously. Arterial blood samples, mixed expired gas samples, and metabolic data were obtained. Indexes of ventilation-perfusion (VA/Q) mismatch were calculated by the multiple inert gas elimination technique. The alveolar-arterial difference for O2 (AaDO2) was predicted from the inert gas model on the basis of the calculated VA/Q mismatch. VA/Q heterogeneity increased significantly with exercise and was predicted to increase the AaDO2 by > 17 Torr during heavy and maximal exercise. The observed AaDO2 increased significantly more than that predicted by the inert gas technique during maximal exercise (10 +/- 10 Torr). These data suggest that this population develops diffusion limitation during maximal exercise, but VA/Q mismatch is the most important contributor (> 60%) to the wide AaDO2 observed.


1977 ◽  
Vol 43 (2) ◽  
pp. 357-364 ◽  
Author(s):  
H. T. Robertson ◽  
M. P. Hlastala

A negative aADCO2 has been demonstrated during ventilation with hypercarbic gas mixtures and during rebreathing, but has never been demonstrated during normal gas exchange. This anomalous behavior of CO2 was studied by comparing it to the behavior of five infused inert gases during normal gas exchange in 10 anesthetized mongrel dogs. The distribution of VA/Q heterogeneity and the respiratory dead space in the animals was quantitated using excretion-solubility data from the five infused inert gases. The predicted excretion fraction (PACO2/PVCO2) for CO2 was obtained from the inert gas excretion-solubility curve, using a measured solubility for CO2. The measured excretion fraction for CO2 (PACO2/PVCO2), even after correction for Haldane effect, was significantly greater than the predicted fraction (P less than 0.001). This corresponded to an alveolar PCO2 that exceeded the predicted value by a mean of 5.0 Torr.


1983 ◽  
Vol 55 (1) ◽  
pp. 32-36 ◽  
Author(s):  
W. E. Stewart ◽  
S. M. Mastenbrook

A plot of measured retention-excretion ratios [(Ri/Ei)obs] vs. reciprocal solubility (1/lambda i) for selected inert gases allows quick detection of shunt and ventilation-perfusion (V/Q) inhomogeneity in the lung. We derive simple rules for constructing a smooth R/E function from the data, using a multicompartmental model of the lung. If mixed venous inert gas measurements are available, the values [lambda i(1-Ri)/Ei]obs for the infused gases can be used to estimate the overall VT/QT ratio and provide an additional test of the consistency of the data. For any set of equilibrium compartments ventilated and perfused in parallel, we show that d(R/E)/d(1/lambda) cannot be negative, nor can d2(R/E)/d(1/lambda)2 be greater than zero. A rectilinear R/E function implies a narrow distribution of V/Q among the gas exchange compartments, whereas a downward-concave curve implies a broader distribution. The shunt perfusion and dead-space ventilation can be estimated from the asymptotes of the R/E function. The range of V/Q for the gas exchange compartments can also be bracketed if a well-defined region of curvature is present in the graph. Finally, from the R/E vs. 1/lambda graph and (if mixed venous data are available) from the lambda(1-R)/E values, we can determine quickly whether the data deserve the detailed numerical analysis outlined in our companion paper.


1999 ◽  
Vol 86 (1) ◽  
pp. 93-100 ◽  
Author(s):  
S. R. Hopkins ◽  
C. M. Stary ◽  
E. Falor ◽  
H. Wagner ◽  
P. D. Wagner ◽  
...  

Increased ventilation-perfusion (V˙a/Q˙) inequality is observed in ∼50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O2 difference (A-[Formula: see text]). Despite extensive investigation, the cause remains unknown. As a first step to more direct examination of this problem, we developed an animal model. Eight Yucatan miniswine were studied at rest and during treadmill exercise at ∼30, 50, and 85% of maximal O2 consumption (V˙o 2 max). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-[Formula: see text]increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr during the heaviest exercise level, but arterial[Formula: see text]([Formula: see text]) remained at resting levels during exercise. There was normalV˙a/Q˙inequality [log SD of the perfusion distribution (log[Formula: see text]) = 0.42 ± 0.04] at rest, and moderate increases (log[Formula: see text] = 0.68 ± 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. TheV˙a/Q˙inequality changes are similar to those reported in highly trained humans. However, in swine, unlike in humans, there was no inert gas evidence for pulmonary end-capillary diffusion limitation during heavy exercise; there was no systematic difference in the measured[Formula: see text] and the[Formula: see text] as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise-inducedV˙a/Q˙inequality.


1978 ◽  
Vol 44 (1) ◽  
pp. 124-128 ◽  
Author(s):  
J. S. Lundsgaard ◽  
J. Groenlund ◽  
N. Einer-Jensen

In vivo calibration of blood gas catheters is complicated by the fact that their signals are flow dependent. A calibration method is described here, which permits continuous in vivo calibration. The principle is to compensate for flow dependence through simultaneous measurement on an inspired, inert reference gas of known partial pressure. The method is demonstrated by experiments on three anesthetized dogs, in which the arterial oxygen partial pressure was measured in situ with a flow-dependent blood gas catheter. The compensated signal was in good agreement with the partial pressure of oxygen measured with conventional techniques.


Sign in / Sign up

Export Citation Format

Share Document