Elevated alveolar PCO2 relative to predicted values during normal gas exchange

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.

1984 ◽  
Vol 56 (1) ◽  
pp. 1-7 ◽  
Author(s):  
M. P. Hlastala

The understanding of pulmonary gas exchange has undergone several major advances since the early 1900‣s. One of the most significant was the development of the multiple inert gas elimination technique for assessing the ventilation-perfusion (VA/Q) distribution in the lung. By measuring the mixed venous, arterial, and mixed expired concentrations of six infused inert gases, it is possible to distinguish shunt, dead space, and the general pattern of VA/Q distribution. As with all mathematical models of complex biological phenomena, there are limitations that can result in errors of interpretation if the technique is applied uncritically. In addition, methodological limitations also can lead to both experimental error and errors of interpretation. Despite these limitations, the multiple inert gas elimination technique remains the most powerful tool developed to date to analyze pulmonary gas exchange.


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.


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.


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.


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.


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.


1996 ◽  
Vol 81 (2) ◽  
pp. 985-997 ◽  
Author(s):  
C. E. Hahn

A sinusoidal forcing function inert-gas-exchange model (C. E. W. Hahn, A. M. S. Black, S. A. Barton, and I. Scott. J. Appl. Physiol. 75: 1863–1876, 1993) is modified by replacing the inspired inert gas with oxygen, which then behaves mathematically in the gas phase as if it were an inert gas. A simple perturbation theory is developed that relates the ratios of the amplitudes of the inspired, end-expired, and mixed-expired oxygen sine-wave oscillations to the airways' dead space volume and lung alveolar volume. These relationships are independent of oxygen consumption, the gas-exchange ratio, and the mean fractional inspired (FIO2) and expired oxygen partial pressures. The model also predicts that blood flow shunt fraction (Qs/QT) is directly related to the oxygen sine-wave amplitude perturbations transmitted to end-expired air and arterial and mixed-venous blood through two simple equations. When the mean FIO2 is sufficiently high for arterial hemoglobin to be fully saturated, oxygen behaves mathematically in the blood like a low-solubility inert gas, and the amplitudes of the arterial and end-expired sine-wave perturbations are directly related to Qs/QT. This relationship is independent of the mean arterial and mixed-venous oxygen partial pressures and is also free from mixed-venous perturbation effects at high forcing frequencies. When arterial blood is not fully saturated, the theory predicts that QS/QT is directly related to the ratio of the amplitudes of the induced-saturation sinusoids in arterial and mixed-venous blood. The model therefore predicts that 1) on-line calculation of airway dead space and end-expired lung volume can be made by the addition of an oxygen sine-wave perturbation component to the mean FIO2; and (2) QS/QT can be measured from the resultant oxygen perturbation sine-wave amplitudes in the expired gas and in arterial and mixed-venous blood and is independent of the mean blood oxygen partial pressure and oxyhemoglobin saturation values. These calculations can be updated at the sine-wave forcing period, typically 2–4 min.


1988 ◽  
Vol 65 (3) ◽  
pp. 1055-1061 ◽  
Author(s):  
P. J. Escourrou ◽  
B. P. Teisseire ◽  
R. A. Herigault ◽  
M. O. Vallez ◽  
A. J. Dupeyrat ◽  
...  

Previous studies have shown a lower arterial PO2 (PaO2) in infants and young animals than in adults. To investigate the mechanism of this impairment of gas exchange we studied 13 piglets from 12 to 65 days of age. Two days after instrumentation we measured the distribution of ventilation-perfusion ratios (VA/Q) by use of the multiple inert gas technique on awake animals. We showed that PaO2 is lower in young animals, increasing from 72 +/- 11.5 Torr before 2 wk to 102 Torr at 2 mo. This hypoxemia is due to an enlarged alveolar-arterial O2 pressure difference that significantly decreases with age. This impairment in gas exchange is not due to shunting (0.6 +/- 1.3%). Mean dead space (36 +/- 11%) was not related to age. Mean modes of perfusion and ventilation did not differ significantly between age groups. However, the dispersion of perfusion as expressed by its logSD decreased significantly with age, whereas dispersion of ventilation remained constant. Furthermore, in the young animals only, a significant difference was evidenced between measured alveolar-arterial PO2 gradient and the value predicted by the inert gas model. We therefore conclude that the impairment of gas exchange in piglets is due to two mechanisms: VA/Q mismatch and diffusion limitation for O2.


1979 ◽  
Vol 47 (4) ◽  
pp. 896-906 ◽  
Author(s):  
J. B. Fortune ◽  
P. D. Wagner

Theoretical gas exchange is compared in lung models having two different types of dead space. In one, the dead space of a lung unit is “personal” and contains gas equivalent in composition to its own alveolar gas; in the other, the dead space is “common” and contains mixed gas from all gas-exchanging units. Formal algebraic analysis of tracer inert gas exchange in two-compartment models shows that values of compartmental ventilation and perfusion can be found that establish one and only one personal dead-space model equivalent for every common dead-space model. When the total dead space and distribution of blood flow and ventilation in the two models are the same, common dead space will always result in improved inert gas elimination. Under these conditions, the amount of improvement is usually greatest when the partition coefficient of the inert gas is between 0.1 and 1.0 and when there is greatest disparity in the ventilation-perfusion ratios (VA/Q). In the inert gas elimination technique that analyzes all dead space as personal, the presence of common dead space consistently causes the recovered VA/Q distributions to be narrower than the actual distributions, but the resultant error is small.


1983 ◽  
Vol 55 (5) ◽  
pp. 1550-1557 ◽  
Author(s):  
R. L. Coffey ◽  
R. K. Albert ◽  
H. T. Robertson

In acute increased-permeability edema, the Bohr physiological dead space (VD/VTCO2) can be influenced by changes in anatomic dead space, ventilation-perfusion (VA/Q) heterogeneity, shunt, and the Haldane effect. We used the multiple inert gas elimination technique to assess the effect of positive end-expiratory pressure (PEEP) on each of these components of VD/VTCO2 in 14 pentobarbital-anesthetized dogs with increased permeability edema induced by infused oleic acid. PEEP of 5, 10, 15, and 20 cmH2O was applied in random sequence. Following injury VD/VTCO2 increased. It decreased with 5 or 10 cmH2O PEEP but increased progressively at higher PEEP levels. The decrease in VD/VTCO2 at 5 or 10 cmH2O PEEP was due to reductions in shunt and midrange VA/Q heterogeneity. The increase in VD/VTCO2 that occurred with higher PEEP levels was due to increased ventilation to high VA/Q regions and a larger anatomic dead space. Haldane effect magnified the shunt component of VD/VTCO2 but reduced the influence of midrange VA/Q heterogeneity.


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