Haemodynamic and Metabolic Evaluations by Rebreathing Methods

Author(s):  
M. Girardis ◽  
C. Lombardini ◽  
A. Pasetto
Keyword(s):  
1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands

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.


1983 ◽  
Vol 55 (1) ◽  
pp. 205-211 ◽  
Author(s):  
G. M. Burma ◽  
G. M. Saidel

As the basis for comparing rebreathing methods of estimating pulmonary blood flow (Q) and tissue-capillary volume (Vtc), we use a dynamic mass-balance model for gas species having different physicochemical properties (e.g., He, CO, C2H2). The model accounts for the effects of ventilation and perfusion inhomogeneities, breathing pattern variation, lung and rebreathing-bag volumes, and recirculation. Also, we examine the variability of the estimates caused by random error. In addition to analyzing two well-known methods, we show how an appropriate synthesis of these methods can lead to improved estimates.


2007 ◽  
Vol 159 (1) ◽  
pp. 34-44 ◽  
Author(s):  
Jaideep J. Pandit ◽  
Ravi M. Mohan ◽  
Nicole D. Paterson ◽  
Marc J. Poulin

2017 ◽  
Vol 38 (3) ◽  
pp. 483-490 ◽  
Author(s):  
Nduka C. Okwose ◽  
Shakir Chowdhury ◽  
David Houghton ◽  
Michael I. Trenell ◽  
Christopher Eggett ◽  
...  

2007 ◽  
Vol 102 (5) ◽  
pp. 593-599 ◽  
Author(s):  
Djordje G. Jakovljevic ◽  
David Nunan ◽  
Gay Donovan ◽  
Lynette D. Hodges ◽  
Gavin R. H. Sandercock ◽  
...  

2003 ◽  
Vol 137 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Jaideep J Pandit ◽  
Ravi M Mohan ◽  
Nicole D Paterson ◽  
Marc J Poulin

1985 ◽  
Vol 63 (3) ◽  
pp. 188-192 ◽  
Author(s):  
K. R. Chapman ◽  
A. Perl ◽  
N. Zamel ◽  
A. S. Rebuck

We measured, in 11 healthy volunteers, the contributions of rib cage and abdomen–diaphragm compartments to increased ventilation caused by hypercapnia, hypoxia, and exercise to determine whether different stimuli produce similar or different patterns of ventilation with respect to the motion of rib cage and abdominal compartments. Progressive hypcroxic hypercapnia and progressive isocapnic hypoxia were induced by rebreathing methods and graded exercise performed on a treadmill, and compartmental tidal volume (VT) was measured by respiratory inductive plethysmography. For each stimulus, the wide range of VT responses among individuals was determined primarily by the range of rib cage contributions to VT, the abdominal compartment VT response slopes accounting for less of this range. There were no significant differences between hypercapnia and hypoxia in either rib cage or abdominal contributions to ventilation (for both, p < 0.3). However, exercise rib cage and abdominal contributions to ventilation were significantly different from those during chemically driven breathing: for the rib cage compartment, p < 0.0001 and for the abdominal compartment, p < 0.05. Whereas, in 8 of 10 subjects the rib cage contribution to VT during exercise was similar to or exceeded that during rebreathing, in 7 of 10 subjects the abdomen–diaphragm contribution fell below that measured during both hypercapnia and hypoxia. There was a significant correlation between hypercapnia and hypoxia in the VT contribution of each compartment at equivalent levels of ventilation (rib cage, p < 0.0001; abdomen, p < 0.0005), but there was no significant correlation in the VT contribution of either compartment between exercise and hypercapnia or exercise and hypoxia. The pattern of compartmental contributions to ventilation during treadmill exercise differs significantly from that observed during chemically driven breathing.


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