Cardiac output, arterial and mixed-venous O2 saturation, and blood O2 dissociation curve in growing rats adapted to a simulated altitude of 3500 m

1972 ◽  
Vol 335 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Z. Turek ◽  
B. E. M. Ringnalda ◽  
L. J. C. Hoofd ◽  
A. Frans ◽  
F. Kreuzer
Keyword(s):  
Cardiac Output ◽  
Dissociation Curve ◽  
Simulated Altitude ◽  
Growing Rats ◽  
O2 Dissociation Curve ◽  
Venous O2 Saturation ◽  
Mixed Venous ◽  
O2 Dissociation

Central venous O2 saturation and rate of arterial desaturation during obstructive apnea

1989 ◽  
Vol 66 (3) ◽  
pp. 1477-1485 ◽  
Author(s):  
E. C. Fletcher ◽  
R. Kass ◽  
J. I. Thornby ◽  
J. Rosborough ◽  
T. Miller
Keyword(s):  
Cardiac Output ◽  
Continuous Monitoring ◽  
Base Line ◽  
Central Venous ◽  
Cuffed Endotracheal Tube ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Spontaneously Breathing ◽  
Venous O2 Saturation ◽  
Mixed Venous

We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.

Simple, accurate equations for human blood O2 dissociation computations

1979 ◽  
Vol 46 (3) ◽  
pp. 599-602 ◽  
Author(s):  
J. W. Severinghaus
Keyword(s):  
Temperature Coefficient ◽  
Human Blood ◽  
Single Sample ◽  
Dissociation Curve ◽  
Hill’S Equation ◽  
Hill's Equation ◽  
O2 Dissociation Curve ◽  
O2 Dissociation

Hill's equation can be slightly modified to fit the standard human blood O2 dissociation curve to within plus or minus 0.0055 fractional saturation (S) from O less than S less than 1. Other modifications of Hill's equation may be used to compute Po2 (Torr) from S (Eq. 2), and the temperature coefficient of Po2 (Eq. 3). Variations of the Bohr coefficient with Po2 are given by Eq. 4. S = (((Po2(3) + 150 Po2)(-1) x 23,400) + 1)(-1) (1) In Po2 = 0.385 In (S-1 - 1)(-1) + 3.32 - (72 S)(-1) - 0.17(S6) (2) DELTA In Po2/delta T = 0.058 ((0.243 X Po2/100)(3.88) + 1)(-1) + 0.013 (3) delta In Po2/delta pH = (Po2/26.6)(0.184) - 2.2 (4) Procedures are described to determine Po2 and S of blood iteratively after extraction or addition of a defined amount of O2 and to compute P50 of blood from a single sample after measuring Po2, pH, and S.

Micromethod for dynamic determination of O2 dissociation curves using a PO2 electrode

1984 ◽  
Vol 56 (3) ◽  
pp. 795-797 ◽  
Author(s):  
M. C. Barnhart
Keyword(s):  
Human Blood ◽  
Time Course ◽  
Gas Mixtures ◽  
Dissociation Curve ◽  
Permeable Membrane ◽  
Standard Values ◽  
Dissociation Curves ◽  
O2 Dissociation Curve ◽  
O2 Dissociation

A nonspectrophotometric method is described for measurement of the O2 dissociation curve and O2 capacity of a 50-microliter sample of fluid. PO2 is recorded by a microprocessor as the sample is oxygenated and then deoxygenated by exposure to isocapnic gas mixtures across a gas-permeable membrane. The time course of deoxygenation and the O2 conductance of the membrane are used in calculating the O2 capacity of the sample and the dissociation curve. The method is sensitive and is best suited to samples of low O2 capacity and affinity. Measurements on buffer-diluted human blood agree with standard values.

Effect of simulated altitude erythrocythemia in women on hemoglobin flow rate during exercise

1988 ◽  
Vol 64 (4) ◽  
pp. 1644-1649 ◽  
Author(s):  
R. J. Robertson ◽  
R. Gilcher ◽  
K. F. Metz ◽  
C. J. Caspersen ◽  
T. G. Allison ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Flow Rate ◽  
Maximal Exercise ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Peak Exercise ◽  
Simulated Altitude ◽  
Test Conditions ◽  
Placebo Infusion ◽  
Mixed Venous

The effect of simulated altitude erythrocythemia on hemoglobin flow rate and maximal O2 uptake (VO2max) was determined for nine women sea-level residents. Test conditions included normoxia and normobaric hypoxia (16% O2-84% N2). Cycle tests were performed under normoxia (T1-N) and hypoxia (T1-H) at prereinfusion control and under hypoxia 48 h after a placebo infusion (T2-H) and 48 h after autologous infusion of 334 ml of erythrocytes (T3-H). Hematocrit (38.1-44.9%) and hemoglobin concentration (12.7-14.7 g.dl-1) increased from control to postreinfusion. At peak exercise, VO2max decreased from T1-N (2.40 l.min-1) to T1-H (2.15 l.min-1) then increased at T3-H (2.37 l.min-1). Maximal arterial-mixed venous O2 difference decreased from T1-N to T1-H and increased at T3-H. Cardiac output (Q), stroke volume, heart rate, and total peripheral resistance during maximal exercise were unchanged from T1-N through T3-H. Hemoglobin flow rate (Hb flow) at maximum did not change from T1-N to T1-H but increased at T3-H. When compared with submaximal values for T1-N, VO2 was unchanged at T1-H and T3-H; Q increased at T1-H and decreased at T3-H; arterial-mixed venous O2 difference decreased at T1-H and increased at T3-H; Hb flow did not change at T1-N but increased at T3-H. For young women, simulated altitude erythrocythemia increased peak Hb flow and decreased physiological altitude (227.8 m) but did not affect maximum cardiac output (Qmax).

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