Analysis of the effects of hematocrit on pulmonary CO2 transfer

1982 ◽  
Vol 53 (2) ◽  
pp. 413-418 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Gas Exchange ◽  
Venous Blood ◽  
Total Surface Area ◽  
Pulmonary Vasculature ◽  
Mixed Venous Blood ◽  
Red Cell Membrane ◽  
Dehydration Reactions ◽  
High Buffer Capacity ◽  
Different Levels ◽  
Co2 Excretion

A mathematical model of the chemical and transport events in blood during and after gas exchange has been used to examine the rates of CO2 excretion (Vco2) and O2 uptake (Vo2) in the lung at different levels of hematocrit (Hct), assuming fixed mixed venous blood O2 and CO2 contents and alveolar gases and constant cardiac output. The results show that a reduction in Hct from 45 to 30% leads to approximately 25% reduction in Vco2 compared with approximately 30% reduction in Vo2. Reduction of Hct from 45 to 15% results in approximately 50% reduction in Vco2 and approximately 63% reduction in Vo2. An increase in Hct from 45 to 60% results in approximately 25% increase in Vco2, accompanied by approximately 30% increase in Vo2. These fractional changes in gas exchange are only slightly affected by the extent of catalysis of the plasma CO2-H2CO3 hydration-dehydration reactions in the pulmonary vasculature. The reduction in Vco2 with reductions in Hct are due to 1) decrease in the total quantity of Bohr protons released during diminution of Vo2, 2) decrease in the size of the high buffer capacity intraerythrocytic pool, and 3) decrease in the total surface area available for HCO-3/Cl- exchange across the red cell membrane. We conclude that hitherto unrecognized changes in Vco2 (in addition to the well-known changes in Vo2) may occur as a consequence of alterations in Hct.

Analysis of postcapillary pH changes in blood in vivo after gas exchange

1978 ◽  
Vol 44 (5) ◽  
pp. 770-781 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall ◽  
R. E. Forster
Keyword(s):  
Gas Exchange ◽  
Time Course ◽  
Quantitative Description ◽  
Carbonic Anhydrase Activity ◽  
Transport Processes ◽  
Red Cell Membrane ◽  
Ph Changes ◽  
Pulmonary Capillaries ◽  
Dehydration Reactions

A quantitative description of the reaction and transport processes that take place in blood during and after gas exchange in capillaries is developed and used to interpret recently reported experimental results. Included in the computation are 1) CO2-H2CO3 hydration-dehydration reactions in plasma and erythrocytes, 2) CO2 reactions with hemoglobin, 3) O2 binding to hemoglobin, 4) buffering of H+ intra- and extracellularly, 5) HCO3- Cl- exchange across the red cell membrane, 6) diffusion of gases between alveolar gas and blood, and 7) transcellular movement of water. Ion and water fluxes are described assuming passive diffusion down their electrochemical potential gradients. Recent data on the magnitude of the Bohr and Haldane shifts and on carbamate formation in the presence of 2,3-diphosphoglycerate are used. The analysis is used to examine the direction, magnitude, and time course of plasma pH changes in blood leaving the pulmonary capillaries and is shown to preduct results that agree very closely with recently reported experimental measurements in vivo. The time computed for plasma pH equilibration after gas exchange when carbonic anhydrase activity is absent from plasma is so great that blood may never be in complete electrochemical equilibrium as it travels around the circulation in normal man.

Influence of G-suit abdominal bladder inflation on gas exchange during +GZ stress

1985 ◽  
Vol 58 (2) ◽  
pp. 506-513
Author(s):  
H. I. Modell ◽  
P. Beeman ◽  
J. Mendenhall
Keyword(s):  
Gas Exchange ◽  
Time Course ◽  
Venous Blood ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Mixed Venous Blood ◽  
Blood Gas ◽  
Series Of Experiments ◽  
Spontaneously Breathing ◽  
Arterial Po2

Available data relating duration of +GZ stress to blood gas exchange status is limited. Furthermore, studies focusing on pulmonary gas exchange during +GZ stress when abdominal restriction is imposed have yielded conflicting results. To examine the time course of blood gas changes occurring during exposure to +GZ stress in dogs and the influence of G-suit abdominal bladder inflation on this time course, seven spontaneously breathing pentobarbital-anesthetized adult mongrel dogs were exposed to 60 s of up to +5 GZ stress with and without G-suit abdominal bladder inflation. Arterial and mixed venous blood were sampled for blood gas analysis during the first and last 20 s of the exposure and at 3 min postexposure. Little change in blood gas status was seen at +3 GZ regardless of G-suit status. However, with G-suit inflation, arterial PO2 fell by a mean of 14.7 Torr during the first 20 s at +4 Gz (P less than 0.01, t test) and 20.6 Torr at +5 GZ (P less than 0.01). It continued to fall an additional 10 Torr during the next 40 s at both +4 and +5 GZ. Arterial PO2 was still 5–10 Torr below control values (P less than 0.05) 3 min postexposure. A second series of experiments paralleling the first focused on blood gas status during repeated exposure to acceleration. Blood gas status was assessed in five dogs during the late 20 s of two 60-s exposures separated by 3 min at 0 GZ. No significant differences between the initial and repeated exposures were detected. The data indicate that G-suit abdominal bladder inflation promotes increased venous admixture.

Influence of blood Po2 on the stability of agitated saline contrast

2020 ◽  
Vol 129 (6) ◽  
pp. 1341-1347
Author(s):  
Lindsey M. Boulet ◽  
Tyler D. Vermeulen ◽  
Paul D. Cotton ◽  
Glen E. Foster
Keyword(s):  
Regulatory Mechanism ◽  
Venous Blood ◽  
Pulmonary Vasculature ◽  
Mixed Venous Blood ◽  
Arteriovenous Anastomoses ◽  
Stabilizing Effect ◽  
Flow Through ◽  
Exercise Induced ◽  
The Stability ◽  
Mixed Venous

Hyperoxic blood has a small stabilizing effect on agitated saline contrast compared with mixed venous blood, lending support to studies that show the reversal of exercise-induced blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) with hyperoxia. These data support the possible presence of a local O2-dependent regulatory mechanism within the pulmonary vasculature that may play a role in Q̇IPAVA regulation.

In vivo regulation of plasma [H+] in ponies during acute changes in PCO2

1990 ◽  
Vol 68 (1) ◽  
pp. 316-321 ◽  
Author(s):  
H. V. Forster ◽  
C. L. Murphy ◽  
A. G. Brice ◽  
L. G. Pan ◽  
T. F. Lowry
Keyword(s):  
Venous Blood ◽  
Strong Ion Difference ◽  
Mixed Venous Blood ◽  
Arterial Pco2 ◽  
Acute Changes ◽  
Different Levels ◽  
In Vitro Data ◽  
Mixed Venous

The major objective of this study was to test the hypothesis that in ponies the change in plasma [H+] resulting from a change in PCO2 (delta H+/delta PCO2) is less under acute in vivo conditions than under in vitro conditions. Elevation of inspired CO2 and lowering of inspired O2 (causing hyperventilation) were used to respectively increase and decrease arterial PCO2 (Paco2) by 5-8 Torr from normal. Arterial and mixed venous blood were simultaneously sampled in 12 ponies during eucapnia and 5-60 min after Paco2 had changed. In vitro data were obtained by equilibrating blood in a tonometer at five different levels of PCO2. The in vitro slopes of the H+ vs. PCO2 relationships were 0.73 +/- 0.01 and 0.69 +/- 0.01 neq.1-1.Torr-1 for oxygenated and partially deoxygenated blood, respectively. These slopes were greater (P less than 0.001) than the in vivo H+ vs. PCO2 slopes of 0.61 +/- 0.03 and 0.57 +/- 0.03 for arterial and mixed venous blood, respectively. The delta HCO3-/delta pH (Slykes) was 15.4 +/- 1.1 and 17.0 +/- 1.1 for in vitro oxygenated and partially deoxygenated blood, respectively. These values were lower (P less than 0.001) than the in vivo values of 23.3 +/- 2.7 and 25.2 +/- 4.7 Slykes for arterial and mixed venous blood, respectively. In vitro, plasma strong ion difference (SID) increased 4.5 +/- 0.2 meq/l (P less than 0.001) when Pco2 was increased from 25 to 55 Torr. A 3.5-meq/l decrease in [Cl-] (P less than 0.001) and a 1.3 +/- 0.1 meq/l increase in [Na+] (P less than 0.001) accounted for the SID change.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of abnormalities of capillary CO2 exchange in vivo

1991 ◽  
Vol 70 (4) ◽  
pp. 1686-1699 ◽  
Author(s):  
A. Bidani
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Venous Blood ◽  
Co2 Exchange ◽  
Transport Processes ◽  
Complete Inhibition ◽  
Mixed Venous Blood ◽  
Moderate Exercise ◽  
Significant Chemical

Capillary CO2 exchange in vivo is affected by several interdependent reactions and transport processes. A mathematical model that includes all the significant chemical and transport events that are presumed to occur during capillary gas exchange has been used to investigate the effect of inhibition of 1) erythrocyte HCO(3-)-Cl- exchange, 2) lung carbonic anhydrase (CA) activity with access to plasma, and 3) erythrocyte CA activity on overall pulmonary CO2 excretion (VCO2) during rest and moderate exercise. Any decrement in VCO2 due to inhibition of HCO(3-)-Cl- exchange and/or CA activity, should result in compensatory alterations in cardiac output and/or an increase in the mixed venous blood-to-alveolar PCO2 gradient [(delta PCO2)V-A] to restore steady-state VCO2. Our computations show that complete inhibition of erythrocyte anion exchange would require a compensatory increment in cardiac output of approximately 30-40% or an increase in (delta PCO2)V-A from 6 to 8.3 Torr at rest and from 12 to 15.6 Torr during moderate exercise, if lung CA activity is intact. In the absence of availability of lung CA activity to plasma, the necessary (delta PCO2)V-A is 10.5 Torr at rest and 19.5 Torr during moderate exercise. Complete inhibition of lung and erythrocyte CA activity is predicted to require (delta PCO2)V-A of 39.1 Torr at rest and 74.2 Torr during moderate exercise. These results suggest that HCO(3-)-Cl- exchange might not be vital to maintenance of CO2 transfer and perhaps has a more important role in minimizing the changes in plasma pH associated with microvascular gas exchange in vivo.

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

Effect of local pulmonary blood flow control on gas exchange: theory

1982 ◽  
Vol 53 (5) ◽  
pp. 1100-1109 ◽  
Author(s):  
B. J. Grant
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Flow Control ◽  
Pulmonary Blood Flow ◽  
Venous Blood ◽  
Pulmonary Gas Exchange ◽  
Mixed Venous Blood ◽  
Regulatory Effect ◽  
Local Ventilation ◽  
Blood Flow Control

The effect of local pulmonary blood flow control by local alveolar O2 tension on steady-state pulmonary gas exchange is analyzed with techniques derived from control theory. In a single homogeneous lung unit with normal inspired and mixed venous blood gas composition, the homeostatic effect on local ventilation-perfusion ratios (VA/Q) regulation occurs over a restricted range of VA/Q. The homeostatic effect is maximal at a moderately low VA/Q (about 0.4) due to the slope of the O2 dissociation curve. In a multicompartment lung with a lognormal distribution of VA/Q, regulation of arterial O2 tension varies with the extent of inhomogeneity. At mild degrees of inhomogeneity where local pulmonary blood flow (Q) control acts predominantly on the lower VA/Q of the Q distribution, the regulatory effect is best. At severe degrees of inhomogeneity where local Q control acts mainly on the higher VA/Q of the Q distribution, the regulatory effect is worse, and positive-feedback behavior may occur. Local Q control has the potential of reducing the deleterious effects of lung disease on pulmonary gas exchange particularly when it operates in association with other regulatory mechanisms.

scholarly journals The Role of the Gills and Branchiostegites in Gas Exchange in a Bimodally Breathing Crab, Holthuisana Transversa: Evidence for a Facultative Change in the Distribution of the Respiratory Circulation

1984 ◽  
Vol 111 (1) ◽  
pp. 103-121 ◽  
Author(s):  
H. H. TAYLOR ◽  
PETER GREENAWAY
Keyword(s):  
Gas Exchange ◽  
Venous Return ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Substantial Fraction ◽  
Air Breathing ◽  
Arterial Circulation ◽  
Circulation Patterns ◽  
Gill Lamellae

The respiratory circulation was investigated in air-breathing and waterbreathing Holthuisana transversa von Martens by analysis of the distribution of radioactive microspheres injected into the haemocoel at seven locations. The gills and putative lungs (branchiostegites and membraneous thoracic walls) both trap approximately 90% of the microspheres entrained in their afferent circulations. The main blood supply to the branchiostegites is from the venous sinuses and constitutes a substantial fraction of the total venous return, which is consistent with earlier inferences, based on morphological information, of their possible involvement in gas exchange. In airbreathing crabs, a mechanism exists which directs a greater proportion of the total venous return via the lungs. From the sinus at the base of walking leg 2, the ratio lung: gill flow was estimated as 86.9: 13.1 ± 5.7% in hydrated crabs that had been air-breathing for more than 1 day, and 19.5:80.5 ± 7.12% in water-breathers. A factor in this circulatory switch may be an increase in branchial resistance in air caused by surface tension of water adherent to the gill lamellae. The direct arterial circulation to the gills represents about 3% of cardiac output and is therefore an insignificant component of the total respiratory circulation. Patterns of microsphere distribution among different gills and different regions of the lung provide information on flow patterns within the thoracic sinus. Neither the thoracic sinus as a whole nor the inf rabranchial sinuses can be considered as reservoirs of truly mixed venous blood in H. transversa.

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.

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