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

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.

Influence of Bohr-Haldane effect on steady-state gas exchange

1982 ◽  
Vol 52 (5) ◽  
pp. 1330-1337 ◽  
Author(s):  
B. J. Grant
Keyword(s):  
Steady State ◽  
Gas Exchange ◽  
Venous Blood ◽  
Gas Composition ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Venous Blood Gas ◽  
Mixed Venous ◽  
Haldane Effect

The influence of the Bohr-Haldane effect (BH) on steady-state gas exchange has previously been described by its effect of gas transfer from the blood when arterial and venous blood gas tensions were held constant. This report quantifies by computer analysis the effects of BH when either or both arterial and venous blood gas tensions are subject to change. When mixed venous blood gas composition is held constant, elimination of BH from a single lung unit typically reduces CO2 output by 6.5% and O2 uptake by 0.5%. Similar effects occur in a two-compartment lung model whether alveolar ventilation-perfusion (VA/Q) mismatch occurs in a parallel or series ventilatory arrangement. When arterial blood gas composition is held constant, elimination of BH increases systemic venous CO2 partial pressure, but O2 partial pressure is hardly affected in the absence of metabolic acidosis. When both mixed venous and arterial blood gas tensions vary and gas exchange is stressed by VA/Q inequality, altitude, anemia, or exercise, elimination of BH predominantly affects mixed venous rather than arterial blood gas tensions. it is concluded that BH may act primarily to reduce tissue acidosis.

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

Lactate, pyruvate, glucose, and free fatty acid in mixed venous and arterial blood

1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cardiac Output ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Venous Blood ◽  
Average Concentration ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Acquired Heart Disease ◽  
Mixed Venous

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963

Gas-blood CO2 equilibration in parabronchial lungs of birds

1976 ◽  
Vol 41 (3) ◽  
pp. 302-309 ◽  
Author(s):  
M. Meyer ◽  
H. Worth ◽  
P. Scheid
Keyword(s):  
Steady State ◽  
Venous Blood ◽  
Blood Perfusion ◽  
Co2 Exchange ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Mixed Venous ◽  
Haldane Effect

We have conducted two experimental series in the chicken in order to study CO2 exchange in the parabronchial lungs of birds.In the first series, the animals were artifically ventilated and end-expired PCO2, PE'CO2,was measured and compared with mixed venous PCO2, PVCO2. On the average, PECO2 exceeded PVCO2 by 2.8 Torr. In the second series, rebreathing was used to investigate the mechanism of this positive (PE'-PV)CO2 difference.Lung gas PCO2 was found to equilibrate with PVCO2 if both CO2 and O2 exchange in the lung was abolished during rebreathing. Only if O2 uptake continued, we observed a positive gas-to-mixed venous blood PCO2 difference. The results suggest that positive gas-blood PCO2 differences both during rebreathing and steady-state ventilation are brought about by the Haldane effect.Model calculations show that in the homogeneous avian lung, unlike in the alveolar lung, the Haldane effect can produce positive (PE'-PV)CO2 differences during steady-state breathing due to the peculiarities of the crosscurrent arrangement and parabronchial ventilation and blood perfusion.

Evidence that the Pco2 of mixed venous blood is not a regulator of ventilation during exercise

1963 ◽  
Vol 18 (2) ◽  
pp. 345-348 ◽  
Author(s):  
Winnifred F. Storey ◽  
John Butler
Keyword(s):  
Venous Blood ◽  
Muscular Exercise ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Cardiac Lesions ◽  
Pulmonary Arterial ◽  
Mixed Venous

We studied 10 patients with intracardiac left-to-right shunt and 13 patients with other cardiac lesions during exercise. The hyperpnea of muscular exercise was independent of the mixed venous Pco2. In the 13 patients without shunt both the pulmonary arterial Pco2 and the ventilation increased during exercise. In the 10 patients who had shunts ventilation increased during exercise even when the Pco2 in the pulmonary arterial blood did not rise. Submitted on July 5, 1962

Changes in blood gases and acid-base balance in the exercising dog

1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Respiratory Alkalosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Mixed Venous Blood ◽  
Acid Base Balance ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood ◽  
Mixed Venous

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962

NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds

2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Physiological Saline ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Exercise Induced ◽  
Mixed Venous

The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.

Pulmonary vasoconstrictor response to acute decrease in blood P50

1984 ◽  
Vol 56 (2) ◽  
pp. 370-374 ◽  
Author(s):  
B. P. Teisseire ◽  
C. D. Soulard
Keyword(s):  
Right Ventricular ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Venous Blood ◽  
Systolic Pressure ◽  
Mixed Venous Blood ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Alveolar Hypoxia ◽  
Mixed Venous

The O2 sensor that triggers hypoxic pulmonary vasoconstriction may be sensitive not only to alveolar hypoxia but also to hypoxia in mixed venous blood. A specific test of the blood contribution would be to lower mixed venous PO2 (PvO2), which can be accomplished by increasing hemoglobin-O2 affinity. When we exchanged transfused rats with cyanate-treated erythrocytes [PO2 at 50% hemoglobin saturation (P50) = 21 Torr] or with Creteil erythrocytes (P50 = 13.1 Torr), we lowered PvO2 from 39 +/- 5 to 25 +/- 4 and to 14 +/- 4 Torr, respectively, without altering arterial blood gases or hemoglobin concentration. Right ventricular systolic pressure increased from 32 +/- 2 to 36 +/- 3 Torr with cyanate erythrocytes and to 44 +/- 5 Torr with Creteil erythrocytes. Cardiac output was unchanged. Control exchange transfusions with normal rat or 2,3-diphosphoglycerate-enriched human erythrocytes had no effect on PvO2 or right ventricular pressure. Alveolar hypoxia plus high O2 affinity blood caused a greater increase in right ventricular systolic pressure than either stimulus alone. We concluded that PvO2 is an important determinant of pulmonary vascular tone in the rat.

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