scholarly journals Mixed venous blood gases are superior to arterial blood gases in assessing acid-base status and oxygenation during acute cardiac tamponade in dogs.

1988 ◽  
Vol 82 (3) ◽  
pp. 833-838 ◽  
Author(s):  
D W Mathias ◽  
P S Clifford ◽  
H S Klopfenstein
1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra

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


1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.


1986 ◽  
Vol 61 (5) ◽  
pp. 1914-1919 ◽  
Author(s):  
T. I. Musch ◽  
D. B. Friedman ◽  
G. C. Haidet ◽  
J. Stray-Gundersen ◽  
T. G. Waldrop ◽  
...  

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 64 (5) ◽  
pp. 1947-1952 ◽  
Author(s):  
G. O. Matheson ◽  
D. C. McKenzie

Seven healthy endurance-trained [maximal O2 uptake (VO2max) = 57.1 +/- 4.1 ml.kg-1.min-1)] female volunteers (mean age 24.4 +/- 3.6 yr) served as subjects in an experiment measuring arterial blood gases, acid-base status, and lactate changes while breath holding (BH) during intense intermittent exercise. By the use of a counterbalance design, each subject repeated five intervals of a 15-s on:30-s off treadmill run at 125% VO2max while BH and while breathing freely (NBH). Arterial blood for pH, PO2, PCO2, O2 saturation (SO2) HCO3, and lactate was sampled from a radial arterial catheter at the end of each work and rest interval and throughout recovery, and the results were analyzed using repeated-measures analysis of variance. Significant reductions in pHa (delta mean = 0.07, P less than 0.01), arterial PO2 (delta mean = 24.2 Torr, P less than 0.01), and O2 saturation (delta mean = 4.6%, P less than 0.01) and elevations in arterial PCO2 (delta mean = 8.2 Torr, P less than 0.01) and arterial HCO3 (delta mean = 1.3 meq/l, P = 0.05) were found at the end of each exercise interval in the BH condition. All of the observed changes in arterial blood gases and acid-base status induced by BH were reversed during the rest intervals. During recovery, significantly (P less than 0.025) greater levels of arterial lactate were found in the BH condition.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 13 (11) ◽  
pp. 884-885 ◽  
Author(s):  
MAX HARRY WEIL ◽  
WILLIAM GRUNDLER ◽  
MASANOBU YAMAGUCHI ◽  
SYBIL MICHAELS ◽  
ERIC C. RACKOW

1982 ◽  
Vol 48 (1) ◽  
pp. 45-57 ◽  
Author(s):  
M. Brun-Pascaud ◽  
C. Gaudebout ◽  
M.C. Blayo ◽  
J.J. Pocidalo

1986 ◽  
Vol 30 (5) ◽  
pp. 298
Author(s):  
M. H. WEIL ◽  
W. GRUNDLER ◽  
M. YAMAGUCHI ◽  
S. MICHAELS ◽  
E. C. RACKOW

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.


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