Derivation of CO2 output from oscillations in arterial pH

1987 ◽  
Vol 62 (3) ◽  
pp. 880-891 ◽  
Author(s):  
B. A. Cross ◽  
R. P. Stidwill ◽  
K. D. Leaver ◽  
S. J. Semple

Theory predicts that the rate of rise of the oscillation in arterial CO2 partial pressure (PaCO2) is linearly dependent on CO2 flux from venous blood to alveolar gas. We have measured, in the anesthetized cat, CO2 output (VCO2) and oscillations in arterial pH. The pH signal was differentiated to give the maximum rate of fall of pH on the downstroke of the oscillation (dpH/dt decreases max). Since oscillations in pH are due to oscillations in arterial PCO2, dpH/dt decreases max was considered to be equivalent to the maximum rate of rise of the PCO2 oscillation. VCO2 was increased by ventilating the intestines with CO2 and by the intra-arterial infusion of 2,4-dinitrophenol. VCO2 was decreased by filling the intestines with isotonic tris(hydroxymethyl)methylamine buffer. The maximum range of VCO2 covered was 7.8–51 ml/min, and the mean range was from 13.6 +/- 1.3 to 29.7 +/- 1.6 (SE) ml/min. Although CO2 loading produced a small rise and CO2 unloading a small fall in mean PaCO2, the changes were not statistically significant, so that overall the response was close to isocapnia. Over the limited range of VCO2 studied there was a highly significant linear association between dpH/dt decreases max and VCO2 which supports the contention that the slope of the upstroke of the PaCO2 oscillation is determined by the CO2 flux from mixed venous blood to alveolar gas. As such this slope is a potential chemical signal linking ventilation to CO2 production.

1965 ◽  
Vol 20 (4) ◽  
pp. 763-766 ◽  
Author(s):  
K. Klausen

The cardiac output during rest and work was determined by a CO2 rebreathing method as suggested by Defares. The partial pressure of CO2 in the mixed venous blood (PvCOCO2) was calculated from the rise of the CO2 percent in a Grollman bag during rebreathing. In the rest experiments the partial pressure of CO2 in arterial blood (PaCOCO2) was obtained from analysis of alveolar samples taken by the Haldane-Priestley direct sampling method. In the work experiments the PaCOCO2 was calculated using the Bohr formula and a dead space estimated from Asmussen and Nielsen's data. The metabolic rate including both O2 uptake and CO2 output was determined by the Douglas bag method. In each experiment the acetylene method as described by Christensen was applied after the CO2 rebreathing method. The values obtained by the two methods were almost identical, the standard deviation for all experiments being ±7.3%, and were of the same magnitude as those obtained by others with the dye-dilution or direct Fick method both during rest and work. cardiac output at rest and work; arterial Pco2 and venous Pco2 at rest and work; stroke volume at rest and work Submitted on November 25, 1964


1995 ◽  
Vol 78 (2) ◽  
pp. 654-662 ◽  
Author(s):  
N. Pelletier ◽  
D. E. Leith

Thoroughbred horses (TB) have no ventilatory response to added CO2 during near-maximal exercise. To see whether that reflects mechanical limits to ventilation or the control of breathing, we examined the effects of varying inspired O2 fraction (0.16, 0.21, or 0.30) in five normal TB standing quietly and galloping at 10 and 14 m/s on a level treadmill. We measured gas exchange (O2 consumption and CO2 production) and ventilation with a flow-through mask system. We also measured PO2, PCO2, and O2 contents in arterial and mixed venous blood and calculated cardiac output by using the Fick equation. Low inspired O2 fraction (0.16 vs. 0.21) had significant effects in TB galloping at 14 m/s. Arterial PO2 then was 38 Torr compared with 56 Torr for horses on air. Tidal volume and minute ventilation were 20% greater than their corresponding values on air, which were 12 liters and 1,475 l/min, respectively, whereas respiratory frequency did not change. O2 consumption and CO2 production were unchanged, but alveolar ventilation was 6% greater, despite increased alveolar and physiological dead spaces, so arterial PCO2 was lower (45 vs. 50 Torr on air). Thus, hypoxia was an effective stimulus to breathing, and minute ventilation was not mechanically limited in TB breathing air at the speeds studied.


1982 ◽  
Vol 52 (5) ◽  
pp. 1272-1277 ◽  
Author(s):  
R. D. Tallman ◽  
F. S. Grodins

The possible role of intrapulmonary CO2 receptors (IPC) in arterial CO2 partial pressure (PaCO2) homeostasis was investigated by comparing the arterial blood gas and ventilatory responses to CO2 loading via the inspired gas and via the venous blood. Adult male Pekin ducks were decerebrated 1 wk prior to an experiment. Venous CO2 loading was accomplished with a venovenous extracorporeal blood circuit that included a silicone-membrane blood oxygenator. The protocol randomized four states: control (no loading), venous CO2 loading, inspired CO2 loading, and venous CO2 unloading. Intravenous and inspired loading both resulted in hypercapnic hyperpnea. Comparison of the ventilatory sensitivity (delta VE/delta PaCO2) showed no significant difference between the two loading regimes. Likewise, venous CO2 unloading led to a significant hypocapnic hypopnea. Sensitivity to changes in PaCO2 could explain the response of ventilation under these conditions. The ventilatory pattern, however, was differentially sensitive to the route of CO2 loading; inspired CO2 resulted in slower deeper breathing than venous loading. It is concluded that IPC play a minor role in adjusting ventilation to match changes in pulmonary CO2 flux but rather are involved in pattern determination.


2021 ◽  
Vol 11 (3) ◽  
pp. 164
Author(s):  
Mahmoud Al-Obeidallah ◽  
Dagmar Jarkovská ◽  
Lenka Valešová ◽  
Jan Horák ◽  
Jan Jedlička ◽  
...  

Porcine model of peritonitis-induced sepsis is a well-established clinically relevant model of human disease. Interindividual variability of the response often complicates the interpretation of findings. To better understand the biological basis of the disease variability, the progression of the disease was compared between animals with sepsis and septic shock. Peritonitis was induced by inoculation of autologous feces in fifteen anesthetized, mechanically ventilated and surgically instrumented pigs and continued for 24 h. Cardiovascular and biochemical parameters were collected at baseline (just before peritonitis induction), 12 h, 18 h and 24 h (end of the experiment) after induction of peritonitis. Analysis of multiple parameters revealed the earliest significant differences between sepsis and septic shock groups in the sequential organ failure assessment (SOFA) score, systemic vascular resistance, partial pressure of oxygen in mixed venous blood and body temperature. Other significant functional differences developed later in the course of the disease. The data indicate that SOFA score, hemodynamical parameters and body temperature discriminate early between sepsis and septic shock in a clinically relevant porcine model. Early pronounced alterations of these parameters may herald a progression of the disease toward irreversible septic shock.


1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.


1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)


1962 ◽  
Vol 17 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Albert H. Niden ◽  
Charles Mittman ◽  
Benjamin Burrows

Methods have been presented for assessing pulmonary diffusion by the “equilibration technique” in the experimental intact dog and perfused lung while controlling ventilation with a whole body respirator. No significant change in diffusion of carbon monoxide was noted between open and closed chest anesthetized animals, with duration of anesthesia in the intact dog, or with duration of perfusion of the isolated dog's lung. There was no demonstrable difference in diffusion when arterialized blood was used as the perfusate in place of mixed venous blood in the lung perfusions suggesting that within the range studied the Po2, Pco2, and pH of pulmonary artery blood does not directly affect the diffusion of carbon monoxide. Retrograde perfusions of dogs' lungs did not significantly alter diffusion, suggesting that pulmonary venous resistance was not significantly lower than pulmonary arterial resistance in the perfused dog lung at the flows and pressures studied. The equilibration technique for measuring pulmonary diffusion and assessing the uniformity of diffusion was well suited to the study of pulmonary diffusing characteristics in the experimental animal. Submitted on January 8, 1962


1962 ◽  
Vol 17 (1) ◽  
pp. 126-130
Author(s):  
Leon Bernstein ◽  
Chiyoshi Yoshimoto

The analyzer described was de signed for measuring the concentration of carbon dioxide in the bag of gas from which the subject rebreathes in the “rebreathing method” for estimating the tension of carbon dioxide in mixed venous blood. Its merits are that it is cheap, robust, simple to construct and to service, easy to operate, and accurate when used by untrained operators. (Medical students, unacquainted with the instrument, and working with written instructions only, obtained at their first attempt results accurate to within ±0.36% [sd] of carbon dioxide.) The instrument is suitable for use by nurse or physician at the bedside, and also for classes in experimental physiology. Some discussion is presented of the theoretical principles underlying the design of analyzers employing thermal conductivity cells. Submitted on July 13, 1961


1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.


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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