Effect of Opposite Changes in Cardiac Output and Arterial PO2on the Relationship between Mixed Venous PO2and Oxygen Transport

1989 ◽  
Vol 140 (4) ◽  
pp. 891-898 ◽  
Author(s):  
Paul V. Carlile ◽  
Barry A. Gray
Keyword(s):  
Cardiac Output ◽  
Oxygen Transport ◽  
The Relationship ◽  
Mixed Venous

Appearance of excess lactate in anesthetized dogs during anemic and hypoxic hypoxia

1965 ◽  
Vol 209 (3) ◽  
pp. 604-610 ◽  
Author(s):  
Stephen M. Cain
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Liver Dysfunction ◽  
Hypoxic Hypoxia ◽  
Blood Gas ◽  
Total Oxygen ◽  
Anesthetized Dogs ◽  
Lactate And Pyruvate ◽  
Mixed Venous

Ten anesthetized, splenectomized dogs were made progressively anemic by replacement of blood with warmed dextran to approximate hematocrits of 30, 20, 15, and 10%. A second group of 10 dogs was made progressively hypoxic by having them inspire 11.4, 9.5, 8.0, and 5.9% O2 in N2. Blood gas contents, pH, and gas tensions were measured in arterial and mixed venous bloods. Cardiac output was calculated from the arteriovenous O2 difference and the O2 uptake. Excess lactate was calculated from measured levels of lactate and pyruvate in blood water. Excess lactate appeared at higher mixed venous Po2 in anemic animals than in hypoxic, 40 mm Hg versus 20 mm Hg. When related to total oxygen transport, however, excess lactate appeared at about the same point (12 ml/kg per min) in both groups. Because liver has been shown to reduce its oxygen uptake with any lowering of perfusate oxygen content, it was suggested that the excess lactate measured during both anemic and hypoxic hypoxia in anesthetized dogs is largely the result of liver dysfunction with respect to lactate.

Cardiodynamic variables and ventilation during treadmill exercise in ponies

1984 ◽  
Vol 57 (3) ◽  
pp. 753-759 ◽  
Author(s):  
L. G. Pan ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
S. M. Dorsey ◽  
M. A. Busch
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Basic Assumption ◽  
Treadmill Exercise ◽  
Biphasic Response ◽  
Exercise Onset ◽  
Relationship Of ◽  
The Relationship ◽  
Cardiovascular Variables ◽  
Mixed Venous

We assessed the relationship of ventilation (VE) to cardiodynamic variables and CO2 transport in seven normal ponies during treadmill exercise. At 1.8, 3, and 6 mph, respectively, VE increased from 15 l/min at rest to 43, 51, and 86 l/min by 1 min and 48, 68, and 125 l/min by 8 min. In three ponies at the same work loads, cardiac output (Qc) increased from approximately 12 l/min at rest to 19.7, 28.1, and 40.3 l/min between 30–60 s (P less than 0.05) and then decreased by about 20% to a steady state by 3–4 min. Heart rate (HR) shows a similar biphasic response during exercise. Mean right ventricular pressure (MRVBP) increased from 9.9 to 15.9 Torr at 1.8 mph, 15.2 Torr at 3 mph, and 23.5 Torr at 6 mph by 1 min (P less than 0.05) and then decreased to 11.8, 12.2, and 15.8 Torr by 8 min of the three respective work intensities. At all work loads, VE increased proportionately faster than these cardiovascular variables in the 1st min. For example, at 6 mph VE increased 470%, whereas Qc and HR increased only 230%. Thereafter, VE generally continued to increase at 3 and 6 mph, whereas MRVBP, Qc, and HR decreased. Therefore, the basic assumption of a cardiodynamic hyperpnea that VE and Qc are equivalently coupled at the exercise onset is rejected for this species. Mixed venous CO2 content (C-vCO2) at 3 and 6 mph, respectively, decreased slightly from 61.6 and 62.3 vol% at rest to 59.6 and 61.9 vol% by 45 s and then increased to 63.3 and 63.5 vol% by 7 min.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

2007 ◽  
Vol 102 (1) ◽  
pp. 331-339 ◽  
Author(s):  
Rebecca S. Syring ◽  
Cynthia M. Otto ◽  
Rebecca E. Spivack ◽  
Klaus Markstaller ◽  
James E. Baumgardner
Keyword(s):  
Cardiac Output ◽  
Lung Injury ◽  
Respiratory Rate ◽  
Pressure Control ◽  
Plateau Pressure ◽  
Control Mode ◽  
Intrinsic Peep ◽  
Mixed Venous Saturation ◽  
Mixed Venous ◽  
Saline Lavage

Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared with PEEPe. In seven New Zealand White rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with a fraction of inspired O2 (FiO2) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH2O, and either 1) high RR ( 24 ) and low PEEPe (3.5) or 2) low RR ( 7 ) and high PEEPe ( 14 ). We assessed cyclical lung recruitment with a fast arterial Po2 probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared with the high PEEPe group ( P < 0.001), and mixed venous saturation was consistently greater in the high RR group ( P < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.

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.

Estimation of ventilation-perfusion inequality by inert gas elimination without arterial sampling

1985 ◽  
Vol 59 (2) ◽  
pp. 376-383 ◽  
Author(s):  
P. D. Wagner ◽  
C. M. Smith ◽  
N. J. Davies ◽  
R. D. McEvoy ◽  
G. E. Gale
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Inert Gas ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Access ◽  
Arterial Blood ◽  
Potential Applications ◽  
Clinical Interest ◽  
Mixed Venous

Estimation of ventilation-perfusion (VA/Q) inequality by the multiple inert gas elimination technique requires knowledge of arterial, mixed venous, and mixed expired concentrations of six gases. Until now, arterial concentrations have been directly measured and mixed venous levels either measured or calculated by mass balance if cardiac output was known. Because potential applications of the method involve measurements over several days, we wished to determine whether inert gas levels in peripheral venous blood ever reached those in arterial blood, thus providing an essentially noninvasive approach to measuring VA/Q mismatch that could be frequently repeated. In 10 outpatients with chronic obstructive pulmonary disease, we compared radial artery (Pa) and peripheral vein (Pven) levels of the six gases over a 90-min period of infusion of the gases into a contralateral forearm vein. We found Pven reached 90% of Pa by approximately 50 min and 95% of Pa by 90 min. More importantly, the coefficient of variation at 50 min was approximately 10% and at 90 min 5%, demonstrating acceptable intersubject agreement by 90 min. Since cardiac output is not available without arterial access, we also examined the consequences of assuming values for this variable in calculating mixed venous levels. We conclude that VA/Q features of considerable clinical interest can be reliably identified by this essentially noninvasive approach under resting conditions stable over a period of 1.5 h.

Hemodynamic Determinants of Coronary Flow: Effect of Changes in Aortic Pressure and Cardiac Output on the Relationship Between Myocardial Oxygen Consumption and Coronary Flow

1957 ◽  
Vol 192 (1) ◽  
pp. 157-163 ◽  
Author(s):  
E. Braunwald ◽  
S. J. Sarnoff ◽  
R. B. Case ◽  
W. N. Stainsby ◽  
G. H. Welch
Keyword(s):  
Cardiac Output ◽  
Coronary Flow ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Filling Pressure ◽  
Heart Preparation ◽  
Ventricular Filling ◽  
The Relationship ◽  
Hemodynamic Determinants

Although the general dependence of coronary flow on myocardial qo2 was confirmed in an in situ heart preparation, changes in aortic pressure and cardiac output were observed to be capable of influencing this relationship. Neither myocardial qo2 nor coronary flow were found to be dependent on left ventricular filling pressure.

Sign in / Sign up

Export Citation Format

Share Document