Mechanism of improvement in pulmonary gas exchange during growth in awake piglets

1988 ◽  
Vol 65 (3) ◽  
pp. 1055-1061 ◽  
Author(s):  
P. J. Escourrou ◽  
B. P. Teisseire ◽  
R. A. Herigault ◽  
M. O. Vallez ◽  
A. J. Dupeyrat ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pressure Difference ◽  
Age Groups ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Significant Difference ◽  
Arterial Po2 ◽  
And Diffusion

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.

Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation

1994 ◽  
Vol 77 (2) ◽  
pp. 912-917 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie ◽  
R. B. Schoene ◽  
R. W. Glenny ◽  
H. T. Robertson
Keyword(s):  
Gas Exchange ◽  
Aerobic Capacity ◽  
Maximal Exercise ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Inert Gases ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Maximal Aerobic Capacity ◽  
Arterial Blood

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.

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Slight Improvement ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Po2

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

Multiple inert gas elimination technique

1984 ◽  
Vol 56 (1) ◽  
pp. 1-7 ◽  
Author(s):  
M. P. Hlastala
Keyword(s):  
Gas Exchange ◽  
Mathematical Models ◽  
Dead Space ◽  
Experimental Error ◽  
General Pattern ◽  
Pulmonary Gas Exchange ◽  
Inert Gases ◽  
Inert Gas ◽  
Biological Phenomena ◽  
Mixed Venous

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.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Effect of change in P50 on exercise tolerance at high altitude: a theoretical study

1982 ◽  
Vol 53 (6) ◽  
pp. 1487-1495 ◽  
Author(s):  
H. Z. Bencowitz ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Exercise Tolerance ◽  
Theoretical Study ◽  
Dissociation Curve ◽  
Diffusion Limitation ◽  
Rightward Shift ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Very High ◽  
Alveolar Capillary

Acclimatization to altitude often results in a rightward shift of the O2 dissociation curve (ODC). However, a left-shifted ODC is reported to increase exercise tolerance in humans at medium altitude and increase survival in rats breathing hypoxic gas mixtures. We examined this paradox using a computer model of pulmonary gas exchange. A Bohr integration procedure allowed for alveolar-capillary diffusion. When diffusion equilibration was complete, mixed venous (PVO2) and arterial PO2 fell as O2 consumption (VO2) was increased, but PVO2 approached a plateau. Under these conditions a right-shifted ODC is advantageous (higher PVO2) at all but very high altitudes. However, diffusion limitation of O2 transfer may occur at any altitude if VO2 is increased sufficiently. If this occurs, a left-shifted ODC results in higher calculated VO2max (compared with the standard ODC). Further, diffusion limitation always occurs at a lower VO2 with a right-shifted ODC than with a left-shifted ODC. We conclude that whether a leftward or rightward shift in the ODC is advantageous to gas exchange at altitude depends on the presence or absence of diffusion limitation.

Diffusion limitation in normal humans during exercise at sea level and simulated altitude

1985 ◽  
Vol 58 (3) ◽  
pp. 989-995 ◽  
Author(s):  
J. R. Torre-Bueno ◽  
P. D. Wagner ◽  
H. A. Saltzman ◽  
G. E. Gale ◽  
R. E. Moon
Keyword(s):  
Sea Level ◽  
Minute Ventilation ◽  
Inert Gas ◽  
Diffusion Resistance ◽  
Diffusion Limitation ◽  
O2 Concentration ◽  
Normal Humans ◽  
Respiratory Gases ◽  
Arterial Po2 ◽  
Alveolar Capillary

The relative roles of ventilation-perfusion (VA/Q) inequality, alveolar-capillary diffusion resistance, postpulmonary shunt, and gas phase diffusion limitation in determining arterial PO2 (PaO2) were assessed in nine normal unacclimatized men at rest and during bicycle exercise at sea level and three simulated altitudes (5,000, 10,000, and 15,000 ft; barometric pressures = 632, 523, and 429 Torr). We measured mixed expired and arterial inert and respiratory gases, minute ventilation, and cardiac output. Using the multiple inert gas elimination technique, PaO2 and the arterial O2 concentration expected from VA/Q inequality alone were compared with actual values, lower measured PaO2 indicating alveolar-capillary diffusion disequilibrium for O2. At sea level, alveolar-arterial PO2 differences were approximately 10 Torr at rest, increasing to approximately 20 Torr at a metabolic consumption of O2 (VO2) of 3 l/min. There was no evidence for diffusion disequilibrium, similar results being obtained at 5,000 ft. At 10 and 15,000 ft, resting alveolar-arterial PO2 difference was less than at sea level with no diffusion disequilibrium. During exercise, alveolar-arterial PO2 difference increased considerably more than expected from VA/Q mismatch alone. For example, at VO2 of 2.5 l/min at 10,000 ft, total alveolar-arterial PO2 difference was 30 Torr and that due to VA/Q mismatch alone was 15 Torr. At 15,000 ft and VO2 of 1.5 l/min, these values were 25 and 10 Torr, respectively. Expected and actual PaO2 agreed during 100% O2 breathing at 15,000 ft, excluding postpulmonary shunt as a cause of the larger alveolar-arterial O2 difference than accountable by inert gas exchange.

Effect of inspired CO2 on ventilation and perfusion heterogeneity in hyperventilated dogs

1993 ◽  
Vol 75 (3) ◽  
pp. 1306-1314 ◽  
Author(s):  
K. B. Domino ◽  
E. R. Swenson ◽  
N. L. Polissar ◽  
Y. Lu ◽  
B. L. Eisenstein ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Partial Pressure ◽  
Respiratory Rate ◽  
Dead Space ◽  
Pressure Difference ◽  
Inert Gas ◽  
Ventilation Distribution ◽  
Pentobarbital Sodium ◽  
Ventilation And Perfusion ◽  
Paco2 Level

We studied the effect of inspired CO2 on ventilation-perfusion (VA/Q) heterogeneity in dogs hyperventilated under two different tidal volume (VT) and respiratory rate conditions with the use of the multiple inert gas elimination technique. Dogs anesthetized with pentobarbital sodium were hyperventilated with an inspired fraction of O2 of 0.21 by using an increased VT (VT = 30 ml/kg at 18 breaths/min) or an increased respiratory rate (VT = 18 ml/kg at 35 breaths/min). The arterial CO2 tension (PaCO2) was varied to three levels (20, 35, and 52 Torr) by altering the inspired PCO2. The orders of type of ventilation and PaCO2 level were randomized. Compared with normocapnia, VA/Q heterogeneity was increased during hypocapnia induced by increased respiratory rate ventilation, which was indicated by an increase in dispersion indexes and arterial-alveolar inert gas partial pressure difference areas (P < 0.01). In contrast, VA/Q heterogeneity was not affected by hypocapnia when a large VT ventilation was used. Under the conditions of our study, hypercapnia did not result in statistically significant changes in VA/Q heterogeneity with either type of ventilation. Increased VT ventilation reduced dead space at all PaCO2 levels (P < 0.01) and reduced the log standard deviation of the ventilation distribution during normocapnia (P < 0.05) and hypocapnia (P < 0.01). We conclude that hypocapnia increased VA/Q heterogeneity when hyperventilation was achieved with a rapid respiratory rate. Therefore, a lack of improvement in VA/Q matching with inhaled CO2 may be associated with the use of a large VT. These data suggest that hypocapnic bronchoconstriction may be important in mediating hypocapnia-induced VA/Q inequality in dogs.

Single breath‐hold measurement of pulmonary gas exchange and diffusion in humans with hyperpolarized 129 Xe MR

2019 ◽  
Vol 32 (5) ◽  
pp. e4068 ◽  
Author(s):  
Junshuai Xie ◽  
Haidong Li ◽  
Huiting Zhang ◽  
Xiuchao Zhao ◽  
Lei Shi ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Breath Hold ◽  
Single Breath ◽  
Single Breath Hold ◽  
And Diffusion

Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs

1975 ◽  
Vol 38 (6) ◽  
pp. 1099-1109 ◽  
Author(s):  
P. D. Wagner ◽  
R. B. Laravuso ◽  
E. Goldzimmer ◽  
P. F. Naumann ◽  
J. B. West
Keyword(s):  
Pulmonary Embolism ◽  
Steady State ◽  
Gas Exchange ◽  
Clinical Investigation ◽  
Inert Gas ◽  
Blood Gas ◽  
Gas Barrier ◽  
Initial Application ◽  
Arterial Po2 ◽  
Made In

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.

Oxygen-induced alteration of ventilation-perfusion relationships in rats

1979 ◽  
Vol 47 (5) ◽  
pp. 1112-1117 ◽  
Author(s):  
W. E. Truog ◽  
M. P. Hlastala ◽  
T. A. Standaert ◽  
H. P. McKenna ◽  
W. A. Hodson
Keyword(s):  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Small Animals ◽  
Difference Curve ◽  
Oxygen Breathing ◽  
Anesthetized Rats ◽  
Effect Of Oxygen ◽  
Breathing Room

The effect of oxygen breathing on shunt and ventilation-perfusion ratios (VA/Q) in anesthetized rats was studied using a modification of the multiple inert gas elimination technique. Base-line analyses showed hypoxemia in some animals breathing room air (arterial O2 tensions 48-70 Torr) associated with intrapulmonary shunts ranging from 0 to 22%, and variable low VA/Q lung regions as determined by calculation of the inert gas arterial-alveolar difference curve. Of nine rats that breathed 100% oxygen for 30 min, three showed increases in shunt (0% leads to 19%, 1.5% leads to 16%, 11% leads to 40%). These three animals had larger preexisting low VA/Q regions than the six that developed no shunt (0.48 +/- 0.15 vs. 0.17 +/- 0.03 (mean +/- SD); P less than 0.05). These data are compatible with the theory of absorption atelectasis. This study documents the usefulness of the inert gas elimination technique for studying pulmonary gas exchange problems in small animals.

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