Arterial lactate responses in dogs made apneic or breathing nitrogen

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.

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.


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.


Perfusion ◽  
1998 ◽  
Vol 13 (1) ◽  
pp. 45-51 ◽  
Author(s):  
F Cavaliere

A nomogram providing the arterial mixed venous haemoglobin saturation difference (Sa-vO2) corresponding to normal oxygen consumption (VO2) during cardiopulmonary bypass (CPB) was produced. Normal VO2 during CPB (95.8 ± 20.1 ml/min/m2 at 37°C) was obtained from the literature. The nomogram computes the Sa-vO2 from the body surface, pump flow, blood haemoglobin and patient temperature; a table is also presented which supplies the Sa-vO2 ranges corresponding to VO2 mean ±1 and ±2SD. The nomogram was tested on 10 subjects undergoing CPB for myocardial revascularization. Sa-vO2 was determined by arterial and mixed venous blood oximetry 5, 20, and 35 min after the start of CPB. The measured Sa-vO2 was 27.1 ± 7.2% while Sa-vO2 obtained from the nomogram was 24.9 ± 4.0%, the difference was not statistically significant. Eighteen values (60%) were within the range corresponding to VO2 mean ±1SD. One value was lower than the Sa-vO2 value corresponding to VO2 mean - 2SD and was associated with the lowest value of blood haemoglobin. Two values were higher than the Sa-vO2 value corresponding to VO2 mean + 2SD and were associated with inadequate muscle relaxation. By comparing measured Sa-vO2 values with those obtained by the nomogram and the table, anaesthesiologists and perfusionists can easily detect patients presenting abnormally low or high VO2 values.


1961 ◽  
Vol 16 (3) ◽  
pp. 507-510 ◽  
Author(s):  
Johannes Piiper

The factors determining the alveolar-arterial O2 pressure difference, AaD, have been theoretically reinvestigated, taking into account the effect of unequal distribution of pulmonary diffusing capacity, D, to pulmonary perfusion, Q. It is shown that, for a given inspired gas and a given mixed venous blood, the AaD is determined by two parameters, the ratios diffusing capacity :perfusion, D/Q, and alveolar ventilation :perfusion, Va/Q. Two characteristics of both of these ratios, the mean value and the variation, affect the AaD. Submitted on May 23, 1960


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.


1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams

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)


1962 ◽  
Vol 17 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Albert H. Niden ◽  
Charles Mittman ◽  
Benjamin Burrows

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


1962 ◽  
Vol 17 (1) ◽  
pp. 126-130
Author(s):  
Leon Bernstein ◽  
Chiyoshi Yoshimoto

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


1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra

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