Modelling Inert Gas Exchange in Tissue and Mixed–Venous Blood Return to the Lungs

2001 ◽  
Vol 209 (4) ◽  
pp. 431-443 ◽  
Author(s):  
J.P. WHITELEY ◽  
D.J. GAVAGHAN ◽  
C.E.W. HAHN
Keyword(s):  
Gas Exchange ◽  
Venous Blood ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Mixed Venous

Oxygen respiratory gas analysis by sine-wave measurement: a theoretical model

1996 ◽  
Vol 81 (2) ◽  
pp. 985-997 ◽  
Author(s):  
C. E. Hahn
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Venous Blood ◽  
Sine Wave ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Partial Pressures ◽  
The Mean ◽  
Mixed Venous

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.

Mechanism of pulmonary gas exchange and CO2 transport during breath holding

1959 ◽  
Vol 14 (5) ◽  
pp. 706-710 ◽  
Author(s):  
John C. Mithoefer
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Venous Blood ◽  
Volume Shrinkage ◽  
Breath Holding ◽  
Mixed Venous Blood ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Mixed Venous ◽  
Haldane Effect

Experiments describe the changes in PaCOCO2 and lung volume shrinkage during breath holding with O2 in man and the PaCOCO2, pH and CO2 content of arterial and mixed venous blood during breath holding in the dog. An explanation is offered for the aberrations in CO2 transport and exchange which occur during apnea. A self-perpetuating cycle is established during breath holding which is initiated by the arrest of the ventilatory output of Co2. The arterial PaCOCo2 rises rapidly as a result of decreased clearance of Co2 from venous blood, the concentrating effect of lung volume shrinkage and the Haldane effect from oxygenation of hemoglobin. The venous PaCOCO2 rises more slowly because of the uptake of Co2 by the tissues and the Haldane effect from reduction of oxyhemoglobin. By this mechanism the Co2 output into the lungs progressively falls and eventually stops. The cycle then is reversed and Co2 moves from lungs to arterial blood. Submitted on March 2, 1959

Instability of lung units with low Va/Q ratios during O2 breathing

1975 ◽  
Vol 38 (5) ◽  
pp. 886-895 ◽  
Author(s):  
David R. Dantzker ◽  
Peter D. Wagner ◽  
John B. West
Keyword(s):  
Venous Blood ◽  
Capillary Blood ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Gas Uptake ◽  
Oxygen Breathing ◽  
Infusion Method ◽  
Net Flux ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

Using a multiple inert gas infusion method, we have observed the development of shunts during oxygen breathing in lungs which contained areas of low ventilation-perfusion ratios while breathing air. This paper gives a theoretical analysis of the factors involved. When the inspired ventilation-perfusion ratio (VaI/Q) of a lung unit is gradually reduced, a point is reached where the expired ventilation falls to zero. Such a unit will no longer eliminate gas but may continue gas uptake unless it becomes atelectatic. This critical VaI/Q is determined by the net flux of O2, CO2, and N2 from alveolar gas to capillary blood, and its value increases from about 0.001 to 0.1 as the inspired gas is changed from air to 100% O2. The critical VaI/Q at any inspired O2 concentration is raised if the O2 or N2content of mixed venous blood are reduced or if N2 is replaced by a more soluble gas. In distributions of ventilation-perfusion ratios, the amount of shunt which develops during oxygen breathing depends on the degree of dispersion of the VaI ratios. The release of hypoxic vasoconstruction following O2 administration, in general, reduces the amount of shunt.

Central venous bubbles and mixed venous nitrogen in goats following decompression

1981 ◽  
Vol 51 (5) ◽  
pp. 1238-1244 ◽  
Author(s):  
B. G. D'Aoust ◽  
H. T. Swanson ◽  
R. White ◽  
R. Dunford ◽  
J. Mahoney
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Bubble Formation ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Central Venous ◽  
Output Measurement ◽  
General Response ◽  
Nitrogen Elimination ◽  
Mixed Venous

Decompression of awake goats from saturation at 1, 2, and 3 ATA of air has been carried out using ultrasonic Doppler bubble detection, central venous blood inert gas measurement, and cardiac output measurement. The results of these experiments indicate that the decrease in nitrogen elimination rate as an apparent result of decompression cannot be due to excessive cardiac output or mass transport of a large amount of inert gas to the lungs as bubbles. Rather, the rapid drop in mixed venous nitrogen content is consistent with a generalized decrease in tissue-to-blood nitrogen elimination. This in turn appears to be due to a cardiovascular response to the decompression insult as was previously reported for dogs (D'Aoust et al., J. Appl. Physiol. 41: 348--355, 1976) at 1, 2, and 3 ATA; addition of ultrasonic Doppler monitoring and cardiac output in the present studies allowed measurement of the degree of latency in the appearance of bubbles at a central venous location. This time period includes that required for bubble formation, growth, and vascular transport of the bubbles to the Doppler detector. All results of these studies are consistent with the interpretation that due to a decompression insult, which probably includes bubble formation, some degree of hemostasis, and other hematologic sequelae, the transport of tissue inert gas to the capillary venous blood is retarded, thus providing the rapid apparent decrease in mixed venous blood inert gas content. These results demonstrate what is most likely a general response to a severe but not crucial decompression by the cardiovascular system.

Is inert gas washout from the tissues limited by diffusion?

1978 ◽  
Vol 45 (6) ◽  
pp. 903-907 ◽  
Author(s):  
Y. Ohta ◽  
S. H. Song ◽  
A. C. Groom ◽  
L. E. Farhi
Keyword(s):  
Molecular Weight ◽  
Theoretical Analysis ◽  
Time Course ◽  
Gas Transport ◽  
Venous Blood ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Initial Value ◽  
Washout Curves ◽  
Mixed Venous

To determine the extent to which diffusion may limit the exchange of gases stored in the tissues, nine dogs were allowed to breathe an O2-N2-Ar mixture until saturation was achieved; the inspired gas was then changed to one containing neither N2 nor Ar, and the level of these two species in the arterial and in the mixed venous blood was monitored during the washout. A theoretical analysis shows that in a situation where peripheral gas transport is limited entirely by perfusion, the washout curves should be identical, provided concentrations are expressed as a fraction of the initial value. When the process is restricted by diffusion through the tissues, Ar is expected to lag because of its higher molecular weight. In all animals, the rate of elimination of the two tracers was the same, indicating that the time course of storage or release of inert gas from body stores is governed (mainly or entirely) by perfusion.

Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition

1998 ◽  
Vol 84 (2) ◽  
pp. 683-694 ◽  
Author(s):  
Victor Cardenas ◽  
Thomas A. Heming ◽  
Akhil Bidani
Keyword(s):  
Mathematical Model ◽  
Gas Exchange ◽  
Carbonic Anhydrase ◽  
Blood Cells ◽  
Venous Blood ◽  
Hysteresis Loops ◽  
Mixed Venous Blood ◽  
Carbonic Anhydrase Inhibition ◽  
Kinetics Of ◽  
Mixed Venous

Cardenas, Victor, Jr., Thomas A. Heming, and Akhil Bidani.Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition. J. Appl. Physiol. 84(2): 683–694, 1998.—Inhibition of carbonic anhydrase (CA) activity (activity in red blood cells and activity available on capillary endothelium) results in decrements in CO2 excretion (V˙co 2) and plasma-erythrocyte CO2-[Formula: see text]-H+disequilibrium as blood travels around the circulation. To investigate the kinetics of changes in blood [Formula: see text]and pH during progressive CA inhibition, we used our previously detailed mathematical model of capillary gas exchange to analyze experimental data of V˙co 2and blood-gas/pH parameters obtained from anesthetized, paralyzed, and mechanically ventilated dogs after treatment with acetazolamide (Actz, 0–100 mg/kg iv). Arterial and mixed venous blood samples were collected via indwelling femoral and pulmonary arterial catheters, respectively. Cardiac output was measured by thermodilution. End-tidal[Formula: see text], as a measure of alveolar[Formula: see text], was obtained from continuous records of airway [Formula: see text] above the carina. Experimental results were analyzed with the aid of a mathematical model of lung and tissue-gas exchange. Progressive CA inhibition was associated with stepwise increments in the equilibrated mixed venous-alveolar [Formula: see text] gradient (9, 19, and 26 Torr at 5, 20, and 100 mg/kg Actz, respectively). The maximum decrements in V˙co 2were 10, 24, and 26% with 5, 20, and 100 mg/kg Actz, respectively, without full recovery ofV˙co 2 at 1 h postinfusion. Equilibrated arterial [Formula: see text]overestimated alveolar [Formula: see text], and tissue [Formula: see text] was underestimated by the measured equilibrated mixed venous blood[Formula: see text]. Mathematical model computations predicted hysteresis loops of the instantaneous CO2-[Formula: see text]-H+relationship and in vivo blood[Formula: see text]-pH relationship due to the finite reaction times for CO2-[Formula: see text]-H+reactions. The shape of the hysteresis loops was affected by the extent of Actz inhibition of CA in red blood cells and plasma.

Gas uptake from an unventilated area of lung: computer model of absorption atelectasis

1993 ◽  
Vol 74 (3) ◽  
pp. 1107-1116 ◽  
Author(s):  
C. J. Joyce ◽  
A. B. Baker ◽  
R. R. Kennedy
Keyword(s):  
Computer Model ◽  
Venous Blood ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Gas Uptake ◽  
Fractional Concentration ◽  
Mixed Venous

A computer model of gas uptake from an area of nonventilated lung, such as a pulmonary lobe with an occluded bronchus or an alveolus with an occluded airway, is presented. Previous analyses have assumed that when an inert gas is present, equilibration of O2 and CO2 with mixed venous blood is sufficiently rapid to be treated as instantaneous. This is valid for insoluble gases such as N2 or He when the fractional concentration of inspired O2 (FIO2) is < or = 0.6 but is invalid for a relatively soluble gas such as N2O. When a mixture of O2 and an inert gas is breathed, the time for an area of unventilated lung to collapse depends on the solubility of the inert gas and FIO2. When the solubility is low (N2 or He), collapse takes longer than when 100% O2 is breathed, and the lower the FIO2 the longer the time to collapse. When the gas is more soluble (N2O) and FIO2 is > 0.3, collapse is more rapid than when 100% O2 is breathed.

Effects of cocaine on incremental treadmill exercise in horses

1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams
Keyword(s):  
Right Ventricular ◽  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Ventricular Pressure ◽  
Mixed Venous Blood ◽  
Work Intensity ◽  
Venous Blood Lactate ◽  
Mixed Venous

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary diffusion in the dog lung

1962 ◽  
Vol 17 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Albert H. Niden ◽  
Charles Mittman ◽  
Benjamin Burrows
Keyword(s):  
Carbon Monoxide ◽  
Pulmonary Artery ◽  
Experimental Animal ◽  
Venous Blood ◽  
Whole Body ◽  
Mixed Venous Blood ◽  
Pulmonary Diffusion ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
Mixed Venous

Methods have been presented for assessing pulmonary diffusion by the “equilibration technique” in the experimental intact dog and perfused lung while controlling ventilation with a whole body respirator. No significant change in diffusion of carbon monoxide was noted between open and closed chest anesthetized animals, with duration of anesthesia in the intact dog, or with duration of perfusion of the isolated dog's lung. There was no demonstrable difference in diffusion when arterialized blood was used as the perfusate in place of mixed venous blood in the lung perfusions suggesting that within the range studied the Po2, Pco2, and pH of pulmonary artery blood does not directly affect the diffusion of carbon monoxide. Retrograde perfusions of dogs' lungs did not significantly alter diffusion, suggesting that pulmonary venous resistance was not significantly lower than pulmonary arterial resistance in the perfused dog lung at the flows and pressures studied. The equilibration technique for measuring pulmonary diffusion and assessing the uniformity of diffusion was well suited to the study of pulmonary diffusing characteristics in the experimental animal. Submitted on January 8, 1962

An electrical analyzer for carbon dioxide in respiratory gases

1962 ◽  
Vol 17 (1) ◽  
pp. 126-130
Author(s):  
Leon Bernstein ◽  
Chiyoshi Yoshimoto
Keyword(s):  
Carbon Dioxide ◽  
Thermal Conductivity ◽  
Medical Students ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
The Subject ◽  
Respiratory Gases ◽  
Rebreathing Method ◽  
Mixed Venous

The analyzer described was de signed for measuring the concentration of carbon dioxide in the bag of gas from which the subject rebreathes in the “rebreathing method” for estimating the tension of carbon dioxide in mixed venous blood. Its merits are that it is cheap, robust, simple to construct and to service, easy to operate, and accurate when used by untrained operators. (Medical students, unacquainted with the instrument, and working with written instructions only, obtained at their first attempt results accurate to within ±0.36% [sd] of carbon dioxide.) The instrument is suitable for use by nurse or physician at the bedside, and also for classes in experimental physiology. Some discussion is presented of the theoretical principles underlying the design of analyzers employing thermal conductivity cells. Submitted on July 13, 1961

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