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Peripheral Inert‐Gas Exchange

Peter D. Wagner

10.1002/cphy.cp030414

Source: Supplement 13: Handbook of Physiology, The Respiratory System, Gas Exchange

Originally published: 1987

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Basic Principles of Peripheral Tissue Exchange
1.1 Inclusion of Pulmonary Gas Exchange in Tissue Inert‐Gas Uptake and Elimination
1.2 Comparison of Multicompartment Models With Actual Data
2 Consideration of Tissue‐Blood Diffusion of Inert Gases
2.1 Diffusional Shunts
2.2 Intertissue Diffusion
2.3 Evaluation of Assumptions
3 Application of Inert Gases to Measurement of Organ Perfusion
3.1 Technique 1: Average Organ Blood Flow by Measurement of Prolonged Inert‐Gas Uptake
3.2 Technique 2: Blood Flow by Arterial Bolus Injection and Subsequent Tissue Washout Analysis
3.3 Technique 3: Blood Flow by Arterial Bolus Injection and Measurement of Height‐Area Ratio of Concentration‐Time Curve
3.4 Technique 4: Local Injection of Tracer and Measurement of Blood Flow by Monitoring Subsequent Removal
3.5 Evaluation of Methods for Measuring Tissue Perfusion With Inert Gases
4 Summary
Figure 1. Figure 1.

Important variables in peripheral tissue gas exchange. In this simplest model, tissue tension (Pti) of a gas is uniform both in radial and in axial directions at any point in time. Tissue is characterized by its volume (Vti), blood flow (Q), and solubility (α) for the gas. For blood solubility β, ability of blood to transport gas is βQ. Storage capability of tissue for gas is αVti. Washin or washout of gas in such tissue is exponential, and exponent is Q/(λtiVti), where λti is ratio of α to β and is known as tissue‐blood partition coefficient of gas. Pa, inflowing arterial tension of gas; Pv, outflowing venous tension of gas.
Figure 2. Figure 2.

Calculated concentration‐time profiles for uptake (left graph) and elimination (right graph) of 7 gases in mixed venous blood. During 60 min of uptake, arterial concentration is constant and mixed venous values are given as percentage of that level. Gases are 1) N2, 2) N2O, 3) cyclopropane, 4) fluroxene, 5) enflurane, 6) halothane, and 7) diethyl ether. Note how similar both uptake and elimination curves are for all gases, despite differences in their partition coefficients (Table 2) when arterial levels are held constant.
Figure 3. Figure 3.

Gas tension‐time profiles for uptake (left graphs) and elimination (right graphs) of N2 (A) and N2O (B) in mixed venous blood under conditions identical to those of Fig. 2 (solid lines). Dotted lines for each gas indicate gas tensions in each of 4 standard tissues as labeled. Vessel‐rich tissues equilibrate with inflowing arterial blood in ∼10 min (N2), whereas muscle, vessel‐poor, and fat tissues fail to reach arterial levels within 1 h of uptake (or elimination). Rate of equilibration is determined by conductance‐capacitance ratio of gas in each tissue.
Figure 4. Figure 4.

Organizational arrangement of lungs, circulation, and several tissues, demonstrating their interdependence. For determining gas tensions in lungs, blood, and tissues, 1) the key pulmonary variables are inspired gas tension, alveolar gas tension and volume, pulmonary tissue volume, alveolar ventilation, cardiac output, and blood‐gas partition coefficient and 2) the key tissue variables are tissue gas tension, tissue volume and blood flow, and tissue‐blood partition coefficient.
Figure 5. Figure 5.

Gas tension‐time profiles for uptake (left graphs) and elimination (right graphs) of 7 gases of Fig. 2 computed during 60 min of uptake at constant inspired tension and during 60 min of elimination (0 inspired tension). Tissue variables are as in Fig. 2; however, this figure allows for pulmonary gas exchange and recirculation from tissues to lungs according to model of Fig. 4. Time‐course calculations are shown for both arterial (A) and mixed venous (B) gas tensions. Rate of equilibration is inversely related to blood‐gas partition coefficient, with large differences among gases. In all cases, true equilibrium would be reached when tensions were 100% (uptake) or 0% (elimination) of inspired.
Figure 6. Figure 6.

Comparison of measured and predicted end‐tidal N2O concentrations during uptake (left) and elimination (right). Predictions come from model of Fig. 4 and Eqs. 30–35 in text. Excellent agreement is noted during both phases, indicating that 4 basic tissue compartments and simple convective mass‐balance principles are sufficient to explain actual data.

Measured data from Rackow et al. 70 and Salanitre et al. 72
Figure 7. Figure 7.

Comparison of real arterial and mixed venous cyclopropane concentrations with those predicted from numerical analysis described in text (prediction based on considering 4 tissue compartments and homogeneous lung). From 2 studies 70,75, it is evident that arterial data (•, ○) are quite well followed by simple model. However, there is unexplained difference between actual and predicted mixed venous levels (▪). Tables 3 and 4 give additional comparisons with better agreement between measured and predicted mixed venous levels.
Figure 8. Figure 8.

Comparison of measured and predicted arterial halothane concentrations during uptake. Again, Eqs. 30–35 were used for predictions. Figure emphasizes that standard variable values from Table 2 and 4‐compartment model satisfactorily account for observed arterial values.

Data from Sechzer et al. 77
Figure 9. Figure 9.

Two possible models to explain “diffusional shunts” in tissue. A: there is direct diffusion between inflowing arteriole and outflowing venule. B: arterioles and venules within tissue may be arranged spatially so that they are conducive to significant diffusion between arterioles and venules.

From Roth and Feigl 71
Figure 10. Figure 10.

Nitrous oxide uptake method of Kety and Schmidt 42 applied to kidneys for measuring organ blood flow. The N2O levels are recorded over several minutes in both arterial and venous blood of organ until they are equal. Blood flow per unit tissue volume is then given by product of tissue‐blood partition coefficient and equilibrium concentration of N2O divided by area between arterial and venous curves. A: normal renal flow, 290 ml.100 g−1.min−1. B: slow renal flow, 122 ml.100 g−1.min−1.

From Conn et al. 15
Figure 11. Figure 11.

The 133Xe washout technique for measuring calf muscle blood flow. Small volume (0.1 ml) of 133Xe dissolved in saline is injected directly into muscle, and its subsequent washout is monitored externally by scintillation detector after 2‐min period of ischemic exercise. In normal case washout is rapid, and difference between normal curve and data from patient with occlusive arterial disease is striking. The 133Xe counts on ordinate are on log scale, and blood flow is calculated from log slope of washout curve.

From Lassen and Larsen 51
Figure 12. Figure 12.

Comparison of muscle blood flow (q) measured by 133Xe washout (see Fig. 11) and that measured by radioactive microspheres injected into muscle's arterial supply. Latter measurements correlate well with direct volumetric measurements of venous outflow. Figure shows 1) correlation between 2 methods; 2) much scatter, indicating that individual measurements may be considerably in error; and 3) underestimation of blood flow by about a factor of 2 when 133Xe method is used. Open symbols, muscle stimulated; closed symbols, muscle resting; circles, gastrocnemius; squares, vastus lateralis; triangles, triceps.

From Cerretelli et al. 10


Figure 1.

Important variables in peripheral tissue gas exchange. In this simplest model, tissue tension (Pti) of a gas is uniform both in radial and in axial directions at any point in time. Tissue is characterized by its volume (Vti), blood flow (Q), and solubility (α) for the gas. For blood solubility β, ability of blood to transport gas is βQ. Storage capability of tissue for gas is αVti. Washin or washout of gas in such tissue is exponential, and exponent is Q/(λtiVti), where λti is ratio of α to β and is known as tissue‐blood partition coefficient of gas. Pa, inflowing arterial tension of gas; Pv, outflowing venous tension of gas.



Figure 2.

Calculated concentration‐time profiles for uptake (left graph) and elimination (right graph) of 7 gases in mixed venous blood. During 60 min of uptake, arterial concentration is constant and mixed venous values are given as percentage of that level. Gases are 1) N2, 2) N2O, 3) cyclopropane, 4) fluroxene, 5) enflurane, 6) halothane, and 7) diethyl ether. Note how similar both uptake and elimination curves are for all gases, despite differences in their partition coefficients (Table 2) when arterial levels are held constant.



Figure 3.

Gas tension‐time profiles for uptake (left graphs) and elimination (right graphs) of N2 (A) and N2O (B) in mixed venous blood under conditions identical to those of Fig. 2 (solid lines). Dotted lines for each gas indicate gas tensions in each of 4 standard tissues as labeled. Vessel‐rich tissues equilibrate with inflowing arterial blood in ∼10 min (N2), whereas muscle, vessel‐poor, and fat tissues fail to reach arterial levels within 1 h of uptake (or elimination). Rate of equilibration is determined by conductance‐capacitance ratio of gas in each tissue.



Figure 4.

Organizational arrangement of lungs, circulation, and several tissues, demonstrating their interdependence. For determining gas tensions in lungs, blood, and tissues, 1) the key pulmonary variables are inspired gas tension, alveolar gas tension and volume, pulmonary tissue volume, alveolar ventilation, cardiac output, and blood‐gas partition coefficient and 2) the key tissue variables are tissue gas tension, tissue volume and blood flow, and tissue‐blood partition coefficient.



Figure 5.

Gas tension‐time profiles for uptake (left graphs) and elimination (right graphs) of 7 gases of Fig. 2 computed during 60 min of uptake at constant inspired tension and during 60 min of elimination (0 inspired tension). Tissue variables are as in Fig. 2; however, this figure allows for pulmonary gas exchange and recirculation from tissues to lungs according to model of Fig. 4. Time‐course calculations are shown for both arterial (A) and mixed venous (B) gas tensions. Rate of equilibration is inversely related to blood‐gas partition coefficient, with large differences among gases. In all cases, true equilibrium would be reached when tensions were 100% (uptake) or 0% (elimination) of inspired.



Figure 6.

Comparison of measured and predicted end‐tidal N2O concentrations during uptake (left) and elimination (right). Predictions come from model of Fig. 4 and Eqs. 30–35 in text. Excellent agreement is noted during both phases, indicating that 4 basic tissue compartments and simple convective mass‐balance principles are sufficient to explain actual data.

Measured data from Rackow et al. 70 and Salanitre et al. 72


Figure 7.

Comparison of real arterial and mixed venous cyclopropane concentrations with those predicted from numerical analysis described in text (prediction based on considering 4 tissue compartments and homogeneous lung). From 2 studies 70,75, it is evident that arterial data (•, ○) are quite well followed by simple model. However, there is unexplained difference between actual and predicted mixed venous levels (▪). Tables 3 and 4 give additional comparisons with better agreement between measured and predicted mixed venous levels.



Figure 8.

Comparison of measured and predicted arterial halothane concentrations during uptake. Again, Eqs. 30–35 were used for predictions. Figure emphasizes that standard variable values from Table 2 and 4‐compartment model satisfactorily account for observed arterial values.

Data from Sechzer et al. 77


Figure 9.

Two possible models to explain “diffusional shunts” in tissue. A: there is direct diffusion between inflowing arteriole and outflowing venule. B: arterioles and venules within tissue may be arranged spatially so that they are conducive to significant diffusion between arterioles and venules.

From Roth and Feigl 71


Figure 10.

Nitrous oxide uptake method of Kety and Schmidt 42 applied to kidneys for measuring organ blood flow. The N2O levels are recorded over several minutes in both arterial and venous blood of organ until they are equal. Blood flow per unit tissue volume is then given by product of tissue‐blood partition coefficient and equilibrium concentration of N2O divided by area between arterial and venous curves. A: normal renal flow, 290 ml.100 g−1.min−1. B: slow renal flow, 122 ml.100 g−1.min−1.

From Conn et al. 15


Figure 11.

The 133Xe washout technique for measuring calf muscle blood flow. Small volume (0.1 ml) of 133Xe dissolved in saline is injected directly into muscle, and its subsequent washout is monitored externally by scintillation detector after 2‐min period of ischemic exercise. In normal case washout is rapid, and difference between normal curve and data from patient with occlusive arterial disease is striking. The 133Xe counts on ordinate are on log scale, and blood flow is calculated from log slope of washout curve.

From Lassen and Larsen 51


Figure 12.

Comparison of muscle blood flow (q) measured by 133Xe washout (see Fig. 11) and that measured by radioactive microspheres injected into muscle's arterial supply. Latter measurements correlate well with direct volumetric measurements of venous outflow. Figure shows 1) correlation between 2 methods; 2) much scatter, indicating that individual measurements may be considerably in error; and 3) underestimation of blood flow by about a factor of 2 when 133Xe method is used. Open symbols, muscle stimulated; closed symbols, muscle resting; circles, gastrocnemius; squares, vastus lateralis; triangles, triceps.

From Cerretelli et al. 10
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Article Title: Peripheral Inert‐Gas Exchange
 

How to Cite

Peter D. Wagner. Peripheral Inert‐Gas Exchange. Compr Physiol 2011, Supplement 13: Handbook of Physiology, The Respiratory System, Gas Exchange: 257-281. First published in print 1987. doi: 10.1002/cphy.cp030414