Ventilation-perfusion lines and gas exchange in liquid breathing: theory

1980 ◽  
Vol 49 (2) ◽  
pp. 262-269 ◽  
Author(s):  
S. V. Matalon ◽  
L. E. Farhi
Keyword(s):  
Gas Exchange ◽  
Partition Coefficient ◽  
Dissociation Curve ◽  
Co2 Solubility ◽  
Solubility Coefficients ◽  
Ventilation Perfusion Ratio ◽  
Ostwald Coefficients ◽  
Mixed Venous ◽  
Q Values ◽  
Co2 Elimination

Alveolar exchange of a gas is governed by the ventilation-perfusion ratio (VA/Q) and the Ostwald partition coefficient for that species. We altered the Ostwald coefficients for O2 and CO2 by considering an animal breathing water or a fluorocarbon (FC-80) and studied the effects on gas exchange. Among our conclusions are the following. 1) When the ratio of the CO2 to O2 solubility in the inspirate exceeds the ratio of the O2 to the CO2 slope of the blood dissociation curve, as in water breathing, the VA/Q line becomes concave upward, and elements having a low VA/Q differ from each other more in terms of CO2 than of O2. 2) As the ratio of the CO2 to O2 solubility in the inspired medium increases, CO2 elimination becomes more dependent on perfusion. 3) At times, the same R will prevail in areas having different VA/Q values. 4) The alveolar-to-arterial O2 and CO2 differences resulting from a given VA/Q distribution do not depend on the O2 and CO2 solubility coefficients of the inspired medium, but on the inspired and mixed venous concentrations necessary to maintain adequate arterial gas levels in the presence of different inspired media.

Analysis of PCO2 differences during rebreathing due to slow pH equilibration in blood

1978 ◽  
Vol 45 (5) ◽  
pp. 666-673 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Quantitative Analysis ◽  
Gas Exchange ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Transport Processes ◽  
O2 Uptake ◽  
Lung Capillaries ◽  
Mixed Venous ◽  
Co2 Elimination

A quantitative analysis of the reaction and transport processes that occur in blood during and after gas exchange has been used to investigate mechanisms that might account for positive alveolar-mixed venous (A-V) and alveolar-arterial (Aa) PCO2 differences during rebreathing. The analysis was used to determine PCO2 changes that take place in blood as it travels from veins to arteries under conditions in which no CO2 is exchanged in the lung. The predicted A-V and Aa PCO2 differences are all positive and lie within the range of reported measured values. The differences are due to disequilibrium of [H+] between plasma and red blood cells, and to disequilibrium of the reactions CO2 in equilibrium HCO3- + H+ in plasma, as blood leaves the tissue and/or lung capillaries. The differences are increased with exercise and with continued O2 uptake in the lung, the latter due to the Haldane shift. We conclude that the two disequilibria and the Haldane shift contribute to the reported PCO2 differences in rebreathing animals but may not fully account for them. These mechanisms cannot explain any PCO2 differences that might exist during net CO2 elimination from blood in the lung.

Effects of acetone in heparin on the multiple inert gas elimination technique

1985 ◽  
Vol 58 (4) ◽  
pp. 1143-1147 ◽  
Author(s):  
F. L. Powell ◽  
F. A. Lopez ◽  
P. D. Wagner
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Room Temperature ◽  
Inert Gas ◽  
Published Data ◽  
Physiological Mechanisms ◽  
Heparinized Saline ◽  
Partial Pressures ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

We have detected acetone in several brands of heparin. If uncorrected, this leads to errors in measuring acetone in blood collected in heparinized syringes, as in the multiple inert gas elimination technique for measuring ventilation-perfusion ratio (VA/Q) distributions. Error for acetone retention [R = arterial partial pressure-to-mixed venous partial pressure (P-V) ratio] is usually small, because R is normally near 1.0, and the error is similar in arterial and mixed venous samples. However, acetone excretion [E = mixed expired partial pressure (P-E)-to-P-V ratio] will appear erroneously low, because P-E is accurately measured in dry syringes, but P-V is overestimated. A physical model of a homogeneous alveolar lung at room temperature and without dead space shows: the magnitude of acetone E error depends upon the ratio of blood sample to heparinized saline volumes and acetone partial pressures, without correction, acetone E can be less than that of less soluble gases like ether, a situation incompatible with conventional gas exchange theory, and acetone R and E can be correctly calculated using the principle of mass balance if the acetone partial pressure in heparinized saline is known. Published data from multiple inert gas elimination experiments with acetone-free heparin, in our labs and others, are within the limits of experimental error. Thus the hypothesis that acetone E is anomalously low because of physiological mechanisms involving dead space tissue capacitance for acetone remains to be tested.

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.

CO2 elimination as a function of frequency and tidal volume in rabbits during HFO

1984 ◽  
Vol 57 (2) ◽  
pp. 354-359 ◽  
Author(s):  
J. W. Watson ◽  
A. C. Jackson
Keyword(s):  
Gas Exchange ◽  
Tidal Volume ◽  
Co2 Production ◽  
High Frequency Oscillation ◽  
Curvilinear Relationship ◽  
Rabbit Lung ◽  
Frequency Dependent ◽  
Dead Space Volume ◽  
Steady State Levels ◽  
Co2 Elimination

CO2 elimination (VCO2) was monitored during high-frequency oscillation (HFO) over a frequency (f) range of 2–30 Hz in anesthetized and paralyzed rabbits to determine whether effective gas exchange could be achieved in this species, to determine the f and tidal volume (VT) dependence of gas exchange in this species, and to compare these results with those from dog and human studies. We were able to produce VCO2 levels during HFO that exceeded normal steady-state levels of CO2 production with VT's less than the total dead space volume. VCO2 was related to f in a curvilinear fashion, whereas in some rabbits VCO2 became independent of f at higher frequencies. This curvilinear relationship between f and VCO2 is similar to data from humans but contrasts with the linear relationship found in dogs. Evidence is presented indicating frequency-dependent behavior of gas exchange is correlated with a frequency-dependent decrease in respiratory system resistance. We propose that the frequency-dependent mechanical properties of the rabbit lung may also account for the species differences in HFO gas exchange.

Gas-blood PCO2 gradients during avian gas exchange

1975 ◽  
Vol 39 (3) ◽  
pp. 405-410 ◽  
Author(s):  
D. G. Davies ◽  
R. E. Dutton
Keyword(s):  
Gas Exchange ◽  
Exchange System ◽  
Arterial Pco2 ◽  
Charged Membrane ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Gas Exchange System ◽  
Spontaneously Breathing ◽  
Membrane Mechanism ◽  
Mixed Venous

The avian respiratory system is a crosscurrent gas exchange system. One of the aspects of this type of gas exchange system is that end-expired PCO2 is greater than arterial PCO2, the highest possible value being equal to mixed venous PCO2. We made steady-state measurements of arterial, mixed venous, and end-expired PCO2 in anesthetized, spontaneously breathing chickens during inhalation of room air or 4–8% CO2. We found end-expired PCO2 to be higher than both arterial and mixed venous PCO2, the sign of the differences being such as to oppose passive diffusion. The observation that end-expired PCO2 was higher than arterial PCO2 can be explained on the basis of crosscurrent gas exchange. However, the observation that end-expired PCO2 exceeded mixed venous PCO2 must be accounted for by some other mechanism. The positive end-expired to mixed venous PCO2 gradients can be explained if it is postulated that the charged membrane mechanism suggested by Gurtner et al. (Respiration Physiol. 7: 173–187, 1969) is present in the avian lung.

Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange

1996 ◽  
Vol 81 (4) ◽  
pp. 1535-1543 ◽  
Author(s):  
Serge Brimioulle ◽  
Philippe Lejeune ◽  
Robert Naeije
Keyword(s):  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Gas Exchange ◽  
Lung Model ◽  
Arterial Oxygenation ◽  
Blood Gas ◽  
Stimulus Response ◽  
Pulmonary Vasoconstriction ◽  
Lung Compartment ◽  
Mixed Venous

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije.Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange. J. Appl. Physiol. 81(4): 1535–1543, 1996.—Several reports have suggested that hypoxic pulmonary vasoconstriction (HPV) might result in deterioration of pulmonary gas exchange in severe hypoxia. We therefore investigated the effects of HPV on gas exchange in normal and diseased lungs. We incorporated a biphasic HPV stimulus-response curve observed in intact dogs (S. Brimioulle, P. Lejeune, J. L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl. Physiol. 77: 476–480, 1994) into a 50-compartment lung model (J. B. West, Respir. Physiol. 7: 88–110, 1969) to control the amount of blood flow directed to each lung compartment according to the local hypoxic stimulus. The resulting model accurately reproduced the blood gas modifications caused by HPV changes in dogs with acute lung injury. In single lung units, HPV had a moderate protective effect on alveolar oxygenation, which was maximal at near-normal alveolar[Formula: see text] (75–80 Torr), mixed venous[Formula: see text] (35 Torr), and[Formula: see text] at which hemoglobin is 50% saturated (24 Torr). In simulated diseased lungs associated with 40–60 Torr arterial [Formula: see text], however, HPV increased arterial [Formula: see text]by 15–20 Torr. We conclude that HPV can improve arterial oxygenation substantially in respiratory failure.

Effects of Pulmonary Blood Flow and Mixed Venous O2 Tension on Gas Exchange in Dogs

1983 ◽  
Vol 58 (2) ◽  
pp. 130-135 ◽  
Author(s):  
Michael J. Bishop ◽  
Frederick W. Cheney
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Blood Flow ◽  
Mixed Venous

scholarly journals Ventilation‐perfusion ratio: A Mathematical Approach for Gas Exchange in the Lungs

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Alejandro Pizano ◽  
Paola Calvacci ◽  
Felipe Giron ◽  
Juan Cordovez
Keyword(s):  
Gas Exchange ◽  
Mathematical Approach ◽  
Ventilation Perfusion Ratio

Contribution of continuing gas exchange to phase III exhaled PCO2 and PO2 profiles

1987 ◽  
Vol 62 (6) ◽  
pp. 2467-2476 ◽  
Author(s):  
J. Gronlund ◽  
E. R. Swenson ◽  
J. Ohlsson ◽  
M. P. Hlastala
Keyword(s):  
Gas Exchange ◽  
Lung Model ◽  
Phase Iii ◽  
Right Atrial ◽  
Interindividual Variations ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Co2 Flow ◽  
The Relationship ◽  
Mixed Venous

Changes in PCO2 and PO2 during expiration have been ascribed to simultaneous gas exchange, but other factors such as ventilation-perfusion inhomogeneity in combination with sequential emptying may also contribute. An experimental and model approach was used to study the relationship between gas exchange and changes in expired PCO2 and PO2 in anesthetized dogs during prolonged high tidal volume expirations. Changes in PCO2 and PO2 were quantified by taking the area bounded by the sloping exhalation curve and a line drawn horizontally from a point where the Fowler dead space plus 250 ml had been expired. This procedure is similar to using the slope of the exhalation curve but it circumvents problems caused by nonlinearity of the PCO2 and PO2 curves. The gas exchange components of the CO2 and O2 areas were calculated using a single-alveolus lung model whose input parameters were measured in connection with each prolonged expiration. The relationship between changes in experimental CO2 areas caused by sudden reductions in mixed venous PCO2 (produced by right atrial infusions of NaOH) and those calculated by the model was also studied. In seven dogs, calculated CO2 and O2 areas were 13% higher and 25% lower than the respective experimental areas, but interindividual variations were large. Changes in experimental CO2 areas caused by step changes in mixed venous PCO2 were almost identical to changes in the calculated areas. We conclude that the changes in PCO2 and PO2 during expiration cannot be explained solely by gas exchange. However, the single-alveolus lung model accurately predicts changes in the CO2 exhalation curve caused by alterations in the alveolar CO2 flow.

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