Measurement of respiratory parameters by using inspired oxygen sinusoidal forcing signals

1996 ◽  
Vol 81 (2) ◽  
pp. 998-1006 ◽  
Author(s):  
E. M. Williams ◽  
R. Hamilton ◽  
L. Sutton ◽  
C. E. Hahn

A companion paper (C. E. W. Hahn. J. Appl. Physiol 81: 985–997, 1996) described a continuous-flow gas-exchange mathematical model, which predicted that forced inspired oxygen sinusoids could be used to measure respiratory parameters rapidly, in place of the inert gas argon. We therefore made simultaneous measurements of dead space volume (VD) and alveolar volume (VA) in an animal model, using argon and oxygen inspired gas concentration sinusoid forcing signals, and then compared the results. Our data confirmed the model prediction that the attenuations of the oxygen and argon sinusoid perturbations are identical in the alveolar gas space, even though there is a net uptake of oxygen by the body. Our results show that the calculated values of VD and VA, obtained by using inspired oxygen forcing signals, were independent of both the mean fractional inspired oxygen concentration (FIO2; range 0.18–0.80% vol/vol) and the oxygen forcing signal amplitude (range +/- 2–6% vol/vol). In these studies, oxygen forcing signals, with forcing periods between 1 and 2 min, were able to measure controlled changes in instrument dead space to within 16 ml and also measure positive end-expiratory pressure-induced changes in VA. Under hyperoxic conditions, intravascular oxygen sensors confirmed that the sinusoidal PO2 signal passed into the arterial blood but not into the mixed-venous blood. However, the sinusoid perturbation PO2 signal did pass into the mixed-venous blood when the mean FIO2 was mildly hypoxic (FIO2 = 0.18% vol/vol). These data show that oxygen can be used instead of argon to measure airways dead space and VA.

1996 ◽  
Vol 81 (2) ◽  
pp. 985-997 ◽  
Author(s):  
C. E. Hahn

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.


2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo

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.


1977 ◽  
Vol 42 (1) ◽  
pp. 39-43 ◽  
Author(s):  
S. M. Cain

O2 stores are kept more intact in apnea than in N2 breathing which removes O2stores from the body. If lactate moves readily into the circulation, arterial lactate should rise sooner with N2 breathing than with apnea because tissue O2 is lowered faster. This was tested in 10 anesthetized, paralyzed dogs made hypoxic both ways. Arterial and mixed venous blood were sampledevery minute until circulation began to fail. Calculated changes in O2 stores would have supported control V O2 for 1.3 min with N2 and 2.7 min with apnea. The PVO2 at those times were 23.1 and 20.1 Torr. Although arterial lactate rose sooner with N2 than with apnea, the mean values for lactate increase for both N2 and apnea were fitted by a single curvilinear relation with PVO2. The PVO2 at which lactate first rosores were depleted. Latent period for lactate rise, therefore, was nearly the same as that for development of tissue hypoxia.


1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  

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


1963 ◽  
Vol 18 (2) ◽  
pp. 345-348 ◽  
Author(s):  
Winnifred F. Storey ◽  
John Butler

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


1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie

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


2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan

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.


1984 ◽  
Vol 56 (2) ◽  
pp. 370-374 ◽  
Author(s):  
B. P. Teisseire ◽  
C. D. Soulard

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.


Perfusion ◽  
2019 ◽  
Vol 34 (5) ◽  
pp. 392-398 ◽  
Author(s):  
R Peter Alston ◽  
Michael Connelly ◽  
Christopher MacKenzie ◽  
George Just ◽  
Natalie Homer

Background:Administering isoflurane 2.5% into the oxygenator during cardiopulmonary bypass results in no patient movement. However, doing so may result in an excessive depth of anaesthesia particularly, when hypothermia is induced. Bispectral index and arterial blood and oxygenator exhaust concentrations of volatile anaesthetics should be related to depth of anaesthesia. The primary aim of this study was to measure the depth of anaesthesia using bispectral index, resulting from administering isoflurane 2.5% into the oxygenator during cardiopulmonary bypass, and secondary aims were to examine the relationships between blood and oxygenator exhaust isoflurane concentrations and bispectral index.Methods:Arterial and mixed-venous blood samples were aspirated at three time points during cardiopulmonary bypass and measured for isoflurane concentration using mass spectrometry. Simultaneously, oxygenator exhaust isoflurane concentration, nasopharyngeal temperature and bispectral index were recorded.Results:When averaged across the three time points, all patients had a bispectral index score below 40 (binomial test, p < 0.001). There were no significant correlations between bispectral index score and arterial or mixed-venous blood isoflurane concentrations (r = –0.082, p = 0.715; r = –0.036, p = 0.874) and oxygenator exhaust gas concentration of isoflurane (r = –0.369, p = 0.091).Conclusion:When 2.5% isoflurane was administered into the sweep gas supply to the oxygenator during cardiopulmonary bypass, all patients experienced a bispectral index score less than 40 and no significant relationship was found between either arterial or mixed-venous blood or oxygenator exhaust concentrations of isoflurane and bispectral index.


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