Relationship between cardiac output and mixed venous-arterial Pco2 gradient in sodium bicarbonate-treated dogs

Resuscitation ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 266
Author(s):  
K Okamoto ◽  
H Kishi ◽  
H Choi ◽  
M Kurose ◽  
T Sato ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Bicarbonate ◽  
Arterial Pco2 ◽  
Mixed Venous

Effect of analyzer on determination of mixed venous PCO2 and cardiac output during exercise

1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands
Keyword(s):  
Cardiac Output ◽  
Gas Mixture ◽  
Arterial Pco2 ◽  
Venous Pco2 ◽  
The Face ◽  
High O2 ◽  
Collision Broadening ◽  
Rebreathing Methods ◽  
Mixed Venous

Cardiac output (CO) during exercise can be determined noninvasively by using the indirect Fick CO2-rebreathing technique. CO2 measurements for this technique are usually performed with an infrared analyzer (IA) or mass spectrometer (MS). However, IA CO2 measurements are susceptible to underreading in the face of high O2 concentrations because of collision broadening. We compared an IA (Ametek model CD-3A) with a MS (Marquette model MGA-1100) to see the effect this would have on mixed venous PCO2 (PVCO2) and CO measurements. After calibration with room air and a gas mixture of 5% CO2–12% O2–83% N2, both devices were tested with three different gas mixtures of CO2 in O2. For each gas mixture, IA gave lower CO2 values than did the MS (4.1% CO2: IA, 3.85 +/- 0.01% and MS, 4.13 +/- 0.01%; 9.2% CO2: IA, 8.44 +/- 0.07% and MS, 9.19 +/- 0.01%; 13.8% CO2: IA, 12.57 +/- 0.15% and MS, 13.82 +/- 0.01%). Warming and humidifying the gases did not alter the results. The IA gave lower values than did the MS for eight other medical gases in lower concentrations of O2 (40–50%). Equilibrium and exponential rebreathing procedures were performed. Values determined by the IA were > 10% higher than those determined by the MS for both rebreathing methods. We conclude that all IAs must be checked for collision broadening if they are to be used in environments where the concentration of O2 is > 21%. If collision broadening is present, then either a special high O2-CO2 calibration curve must be constructed, or the IA should not be used for both arterial PCO2 and PVCO2 estimates because it may produce erroneously low PVCO2 values, with resultant overestimation of CO.

Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema

1985 ◽  
Vol 59 (6) ◽  
pp. 1698-1703 ◽  
Author(s):  
J. R. Catterall ◽  
P. M. Calverley ◽  
W. MacNee ◽  
P. M. Warren ◽  
C. M. Shapiro ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Chronic Bronchitis ◽  
Rem Sleep ◽  
Normal Subjects ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Nocturnal Hypoxemia ◽  
Voluntary Hypoventilation ◽  
Arterial Po2 ◽  
Mixed Venous

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

Relationship between cardiac output and mixed venous-arterial PCO 2 gradient in sodium bicarbonate-treated dogs

1994 ◽  
Vol 8 (2) ◽  
Author(s):  
Kazufumi Okamoto ◽  
Hiroshi Kishi ◽  
Hyun Choi ◽  
Mitsuro Kurose ◽  
Toshihide Sato ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Bicarbonate ◽  
Mixed Venous

Effect of water immersion on cardiopulmonary physiology at high gravity (+Gz)

1986 ◽  
Vol 61 (5) ◽  
pp. 1686-1692 ◽  
Author(s):  
R. Arieli ◽  
U. Boutellier ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Functional Residual Capacity ◽  
Water Immersion ◽  
Systemic Circulation ◽  
Co2 Production ◽  
Arterial Pco2 ◽  
Residual Capacity ◽  
Gravitational Influence ◽  
End Tidal ◽  
Mixed Venous

We compared the cardiopulmonary physiology of eight subjects exposed to 1, 2, and 3 Gz during immersion (35 degrees C) to the heart level with control dry rides. Immersion should almost cancel the effects of gravity on systemic circulation and should leave the lung alone to gravitational influence. During steady-state breathing we measured ventilation, O2 consumption (VO2), CO2 production, end-tidal PCO2 (PACO2), and heart frequency (fH). Using CO2 rebreathing techniques, we measured cardiac output, functional residual capacity, equivalent lung tissue volume, and mixed venous O2 content, and we calculated arterial PCO2 (PaCO2). As Gz increased, ventilation, fH, and VO2 rose markedly, and PACO2 and PaCO2 decreased greatly in dry ride, but during immersion these variables changed very little in the same direction. Functional residual capacity was lower during immersion and decreased in both the dry and immersed states as Gz increased, probably reflecting closure effects. Cardiac output decreased as Gz increased in dry rides and was elevated and unaffected by Gz during immersion. We conclude that most of the changes we observed during acceleration are due to the effect on the systemic circulation, rather than to the effect on the lung itself.

Relationship between cardiac output and mixed venous-arterialPco 2 gradient in sodium bicarbonate-treated dogs

1994 ◽  
Vol 8 (2) ◽  
pp. 204-207 ◽  
Author(s):  
Kazufumi Okamoto ◽  
Hiroshi Kishi ◽  
Hyun Choi ◽  
Mitsuro Kurose ◽  
Toshihide Sato ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Bicarbonate ◽  
Mixed Venous

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.

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

1989 ◽  
Vol 256 (5) ◽  
pp. H1316-H1321 ◽  
Author(s):  
J. I. Shapiro ◽  
M. Whalen ◽  
R. Kucera ◽  
N. Kindig ◽  
G. Filley ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Ammonium Chloride ◽  
Respiratory Acidosis ◽  
Arterial Pco2 ◽  
Bicarbonate Therapy ◽  
Brain Ph ◽  
Dose Dependent ◽  
Intracellular Alkalinization

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

Increases in coronary vein CO2 during cardiac resuscitation

1990 ◽  
Vol 68 (4) ◽  
pp. 1405-1408 ◽  
Author(s):  
C. V. Gudipati ◽  
M. H. Weil ◽  
R. J. Gazmuri ◽  
H. G. Deshmukh ◽  
J. Bisera ◽  
...  
Keyword(s):  
Spontaneous Circulation ◽  
Co2 Production ◽  
Acid Base ◽  
Coronary Vein ◽  
Arterial Pco2 ◽  
Control Value ◽  
Great Cardiac Vein ◽  
Aortic Blood ◽  
Highly Correlated ◽  
Mixed Venous

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

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.

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