Alveolar gas exchange during exercise: a single-breath analysis

1984 ◽  
Vol 57 (6) ◽  
pp. 1704-1709 ◽  
Author(s):  
C. J. Allen ◽  
N. L. Jones ◽  
K. J. Killian
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Heavy Exercise ◽  
Single Breath ◽  
Arterial Blood ◽  
Co2 Output ◽  
Dead Space Volume ◽  
Airway Dead Space ◽  
Male Subjects ◽  
Alveolar Gas Exchange

Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.

Inspiratory airway CO2 loading in the pony

1984 ◽  
Vol 57 (4) ◽  
pp. 1097-1103 ◽  
Author(s):  
H. W. Shirer ◽  
J. A. Orr ◽  
J. L. Loker
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Blood Gases ◽  
Minute Volume ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Airway Dead Space ◽  
Arterial Po2 ◽  
Stimulation Of

To determine if CO2-sensitive airway receptors are important in the control of breathing, CO2 was preferentially loaded into the respiratory airways in conscious ponies. The technique involved adding small amounts of 100% CO2 to either the latter one-third or latter two-thirds of the inspiratory air in an attempt to raise CO2 concentrations in the airway dead space independent of the arterial blood. Arterial blood gas tensions (PCO2 and PO2) and pH, as well as respiratory output (minute volume, tidal volume, and respiratory rate), were measured in a series of 20 experiments on 5 awake ponies. Elevation of airway CO2 to approximately 12% by addition of CO2 to the latter portion of the inspiratory tidal volume did not alter either ventilation or arterial blood gases. When CO2 was added earlier in the inspiratory phase to fill more of the airway dead space, a small but significant increase in minute volume (2.1 l X min-1 X m-2) and tidal volume (0.1 l X m-2) was accompanied by an increase in arterial PCO2, arterial PO2, and a fall in pH (0.96 Torr, 10.5 Torr, 0.007 units, respectively). A second series of 12 experiments on 6 awake ponies using radiolabeled 14CO2 determined that the increases in breathing were minimal when compared with the large increase that occurred when these animals inhaled 6% 14CO2 (12.7 l X min-1 X m-2). Also, stimulation of systemic arterial or central nervous system chemoreceptors cannot be eliminated from the response since significant amounts of 14CO2 were present in the arterial blood when this marker gas was added to the latter two-thirds of the inspiratory tidal volume. The results, therefore, provide no evidence for CO2-sensitive airway receptors that can increase breathing when stimulated during the latter part of the inspiratory cycle.

Time and volume dependence of dead space in healthy and surfactant-depleted rat lungs during spontaneous breathing and mechanical ventilation

2013 ◽  
Vol 115 (9) ◽  
pp. 1268-1274 ◽  
Author(s):  
Constanze Dassow ◽  
David Schwenninger ◽  
Hanna Runck ◽  
Josef Guttmann
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Dead Space ◽  
Spontaneous Breathing ◽  
Small Animals ◽  
Single Breath ◽  
Dead Space Volume ◽  
The Dead ◽  
Gas Volume ◽  
Space Volume

Volumetric capnography is a standard method to determine pulmonary dead space. Hereby, measured carbon dioxide (CO2) in exhaled gas volume is analyzed using the single-breath diagram for CO2. Unfortunately, most existing CO2 sensors do not work with the low tidal volumes found in small animals. Therefore, in this study, we developed a new mainstream capnograph designed for the utilization in small animals like rats. The sensor was used for determination of dead space volume in healthy and surfactant-depleted rats ( n = 62) during spontaneous breathing (SB) and mechanical ventilation (MV) at three different tidal volumes: 5, 8, and 11 ml/kg. Absolute dead space and wasted ventilation (dead space volume in relation to tidal volume) were determined over a period of 1 h. Dead space increase and reversibility of the increase was investigated during MV with different tidal volumes and during SB. During SB, the dead space volume was 0.21 ± 0.14 ml and increased significantly at MV to 0.39 ± 0.03 ml at a tidal volume of 5 ml/kg and to 0.6 ± 0.08 ml at a tidal volume of 8 and 11 ml/kg. Dead space and wasted ventilation during MV increased with tidal volume. This increase was mostly reversible by switching back to SB. Surfactant depletion had no further influence on the dead space increase during MV, but impaired the reversibility of the dead space increase.

Effect of salicylates on ventilatory response to inhaled carbon dioxide in normal subjects

1960 ◽  
Vol 15 (5) ◽  
pp. 826-828 ◽  
Author(s):  
Philip Samet ◽  
Eugene M. Fierer ◽  
William H. Bernstein
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
The Other ◽  
Compressed Air ◽  
Arterial Blood ◽  
Dead Space Volume ◽  
Basic Purpose ◽  
Space Volume

The basic purpose of this investigation was to determine whether salicylates increase the sensitivity of the respiratory center to inhaled CO2. The problem was approached by noting the effect of salicylates upon ventilation and arterial blood Co2 tension and pH during inhalation of compressed air and 3% and 5% Co2 in air. These studies were performed in 30 subjects, 15 of whom ingested 2.1 gm salicylate; the other 15 ingested 3.6 gm. The results demonstrate that the ventilatory response to CO2 was increased only by the larger dose of salicylate. Variations in dead-space volume secondary to increments in tidal volume were observed. Dead-space volume increased in approximately linear fashion with increase in tidal volume. Submitted on October 28, 1959

Assessment of cardiorespiratory function using oscillating inert gas forcing signals

1994 ◽  
Vol 76 (5) ◽  
pp. 2130-2139 ◽  
Author(s):  
E. M. Williams ◽  
J. B. Aspel ◽  
S. M. Burrough ◽  
W. A. Ryder ◽  
M. C. Sainsbury ◽  
...  
Keyword(s):  
Blood Flow ◽  
Nitrous Oxide ◽  
Dead Space ◽  
Confidence Limit ◽  
Pulmonary Blood Flow ◽  
Mean Difference ◽  
Alveolar Volume ◽  
Single Breath ◽  
Cardiorespiratory Function ◽  
Airway Dead Space

A theoretical model (Hahn et al. J. Appl. Physiol. 75: 1863–1876, 1993) predicts that the amplitudes of the argon and nitrous oxide inspired, end-expired, and mixed expired sinusoids at forcing periods in the range of 2–3 min (frequency 0.3–0.5 min-1) can be used directly to measure airway dead space, lung alveolar volume, and pulmonary blood flow. We tested the ability of this procedure to measure these parameters continuously by feeding monosinusoidal argon and nitrous oxide forcing signals (6 +/- 4% vol/vol) into the inspired airstream of nine anesthetized ventilated dogs. Close agreement was found between single-breath and sinusoid airway dead space measurements (mean difference 15 +/- 6%, 95% confidence limit), N2 washout and sinusoid alveolar volume (mean difference 4 +/- 6%, 95% confidence limit), and thermal dilution and sinusoid pulmonary blood flow (mean difference 12 +/- 11%, 95% confidence limit). The application of 1 kPa positive end-expiratory pressure increased airway dead space by 12% and alveolar volume from 0.8 to 1.1 liters but did not alter pulmonary blood flow, as measured by both the sinusoid and comparator techniques. Our findings show that the noninvasive sinusoid technique can be used to measure cardiorespiratory lung function and allows changes in function to be resolved in 2 min.

Labeled carbon dioxide (C18O2): an indicator gas for phase II in expirograms

2004 ◽  
Vol 97 (5) ◽  
pp. 1755-1762 ◽  
Author(s):  
Holger Schulz ◽  
Anne Schulz ◽  
Gunter Eder ◽  
Joachim Heyder
Keyword(s):  
Carbon Dioxide ◽  
Phase Ii ◽  
Dead Space ◽  
Moment Analysis ◽  
Cumulative Distribution ◽  
Breath Holding ◽  
Power Moment ◽  
Single Breath ◽  
Dead Space Volume ◽  
Space Volume

Carbon dioxide labeled with 18O (C18O2) was used as a tracer gas for single-breath measurements in six anesthetized, mechanically ventilated beagle dogs. C18O2 is taken up quasi-instantaneously in the gas-exchanging region of the lungs but much less so in the conducting airways. Its use allows a clear separation of phase II in an expirogram even from diseased individuals and excludes the influence of alveolar concentration differences. Phase II of a C18O2 expirogram mathematically corresponds to the cumulative distribution of bronchial pathways to be traversed completely in the course of exhalation. The derivative of this cumulative distribution with respect to respired volume was submitted to a power moment analysis to characterize volumetric mean (position), standard deviation (broadness), and skewness (asymmetry) of phase II. Position is an estimate of dead space volume, whereas broadness and skewness are measures of the range and asymmetry of functional airway pathway lengths. The effects of changing ventilatory patterns and of changes in airway size (via carbachol-induced bronchoconstriction) were studied. Increasing inspiratory or expiratory flow rates or tidal volume had only minor influence on position and shape of phase II. With the introduction of a postinspiratory breath hold, phase II was continually shifted toward the airway opening (maximum 45% at 16 s) and became steeper by up to 16%, whereas skewness showed a biphasic response with a moderate decrease at short breath holding and a significant increase at longer breath holds. Stepwise bronchoconstriction decreased position up to 45 ± 2% and broadness of phase II up to 43 ± 4%, whereas skewness was increased up to twofold at high-carbachol concentrations. Under all circumstances, position of phase II by power moment analysis and dead space volume by the Fowler technique agreed closely in our healthy dogs. Overall, power moment analysis provides a more comprehensive view on phase II of single-breath expirograms than conventional dead space volume determinations and may be useful for respiratory physiology studies as well as for the study of diseased lungs.

CO2 and acid-base transients after hyperventilation

1962 ◽  
Vol 17 (5) ◽  
pp. 805-811 ◽  
Author(s):  
Joseph A. Lipsky ◽  
Joseph F. Tomashefski ◽  
Earl T. Carter
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Recovery Period ◽  
The Body ◽  
Positive Pressure ◽  
Acid Base ◽  
Alveolar Air ◽  
Arterial Blood ◽  
Intermittent Positive Pressure Breathing ◽  
Male Subjects

Fourteen male subjects were mechanically hyperventilated by intermittent positive pressure breathing. Tidal volume and respiratory frequency were increased approximately three times and one and one-half times control, respectively. Breath-by-breath analyses of CO2 output indicate a loss of approximately 2.5 liters of CO2 from the body stores in 12 min. Only one-third of that volume was restored during the ensuing 12-min recovery period, mostly as a result of hypoventilation rather than apnea. Over the entire recovery period, the volume of CO2 regained by the blood store approximated 75% of the CO2 content lost during hyperventilation. Under the conditions of these experiments, tissues regained less than 20% of the depleted CO2 store. CO2 retention patterns may be more effective than arterial blood or alveolar air analyses in determining a return to a steady state when tissue stores have been considerably reduced. Submitted on August 24, 1961

scholarly journals Effects of inspiratory pause on CO2 elimination and arterial Pco2 in acute lung injury

2008 ◽  
Vol 105 (6) ◽  
pp. 1944-1949 ◽  
Author(s):  
Jérôme Devaquet ◽  
Björn Jonson ◽  
Lisbet Niklason ◽  
Anne-Gaëlle Si Larbi ◽  
Leif Uttman ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Gas Diffusion ◽  
Arterial Pco2 ◽  
Mechanically Ventilated ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Single Breath Test ◽  
Airway Dead Space

A high respiratory rate associated with the use of small tidal volumes, recommended for acute lung injury (ALI), shortens time for gas diffusion in the alveoli. This may decrease CO2 elimination. We hypothesized that a postinspiratory pause could enhance CO2 elimination and reduce PaCO2 by reducing dead space in ALI. In 15 mechanically ventilated patients with ALI and hypercapnia, a 20% postinspiratory pause (Tp20) was applied during a period of 30 min between two ventilation periods without postinspiratory pause (Tp0). Other parameters were kept unchanged. The single breath test for CO2 was recorded every 5 min to measure tidal CO2 elimination (VtCO2), airway dead space (VDaw), and slope of the alveolar plateau. PaO2, PaCO2, and physiological and alveolar dead space (VDphys, VDalv) were determined at the end of each 30-min period. The postinspiratory pause, 0.7 ± 0.2 s, induced on average <0.5 cmH2O of intrinsic positive end-expiratory pressure (PEEP). During Tp20, VtCO2 increased immediately by 28 ± 10% (14 ± 5 ml per breath compared with 11 ± 4 for Tp0) and then decreased without reaching the initial value within 30 min. The addition of a postinspiratory pause significantly decreased VDaw by 14% and VDphys by 11% with no change in VDalv. During Tp20, the slope of the alveolar plateau initially fell to 65 ± 10% of baseline value and continued to decrease. Tp20 induced a 10 ± 3% decrease in PaCO2 at 30 min (from 55 ± 10 to 49 ± 9 mmHg, P < 0.001) with no significant variation in PaO2. Postinspiratory pause has a significant influence on CO2 elimination when small tidal volumes are used during mechanical ventilation for ALI.

Effect of common dead space on VA/Q distribution in the dog

1990 ◽  
Vol 68 (6) ◽  
pp. 2488-2493 ◽  
Author(s):  
K. Tsukimoto ◽  
J. P. Arcos ◽  
W. Schaffartzik ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Blood Flow ◽  
Tidal Volume ◽  
Dead Space ◽  
Volume Ratio ◽  
Inert Gas ◽  
Base Line ◽  
Heavy Exercise ◽  
The Common ◽  
Technique Comparison ◽  
Condition B

Several previous studies have shown worsening ventilation-perfusion (VA/Q) relationships in humans during heavy exercise at sea level. However, the mechanism of this deterioration remains unclear because of the correlation with ventilatory and circulatory variables. Our hypothesis was that the decrease in the series dead space-to-tidal volume ratio during exercise might be partly responsible because mixing in the common dead space can reduce apparent inequality. We tested this notion in 10 resting anesthetized normocapnic dogs passively hyperventilated by increase tidal volume and a) inspired CO2 or b) external dead space. We predicted less apparent VA/Q inequality in condition b because of mixing in the added dead space. After base-line measurements, conditions a and b were randomly assigned, and after a second set of base-line measurements they were repeated in the reverse order in each dog. VA/Q inequality was measured by the multiple inert gas elimination technique. Comparison of conditions a and b demonstrated that additional external dead space improved (P less than 0.001) the blood flow distributions as hypothesized [log standard deviation of perfusion = 0.49 +/- 0.02 (SE) in condition b and 0.61 +/- 0.03 in condition a with respect to 0.52 +/- 0.03 at base line]. This study suggests that the increased tidal volume during exercise could uncover VA/Q inequality not evident at rest because of the higher ratio of common dead space to tidal volume at rest.

scholarly journals Combining Dynamic Hyperinflation with Dead Space Volume during Maximal Exercise in Patients with Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 9 (4) ◽  
pp. 1127 ◽  
Author(s):  
Ming-Lung Chuang
Keyword(s):  
Dead Space ◽  
Maximal Exercise ◽  
Control Group ◽  
Chronic Obstructive ◽  
Study Group ◽  
Dynamic Hyperinflation ◽  
Obstructive Pulmonary Disease ◽  
Dead Space Volume ◽  
Male Subjects ◽  
Space Volume

Physiological dead space volume (VD) and dynamic hyperinflation (DH) are two different types of abnormal pulmonary physiology. Although they both involve lung volume, their combination has never been advocated, and thus their effect and implication are unclear. This study aimed (1) to combine VD and DH, and (2) investigate their relationship and clinical significance during exercise, as well as (3) identify a noninvasive variable to represent the VD fraction of tidal volume (VD/VT). Forty-six male subjects with chronic obstructive pulmonary disease (COPD) and 34 healthy male subjects matched for age and height were enrolled. Demographic data, lung function, and maximal exercise were investigated. End-expiratory lung volume (EELV) was measured for the control group and estimated for the study group using the formulae reported in our previous study. The VD/VT ratio was measured for the study group, and reference values of VD/VT were used for the control group. In the COPD group, the DHpeak/total lung capacity (TLC, DHpeak%) was 7% and the EELVpeak% was 70%. After adding the VDpeak% (8%), the VDDHpeak% was 15% and the VDEELVpeak% was 78%. Both were higher than those of the healthy controls. In the COPD group, the VDDHpeak% and VDEELVpeak% were more correlated with dyspnea score and exercise capacity than that of the DHpeak% and EELV%, and had a similar strength of correlation with minute ventilation. The VTpeak/TLC (VTpeak%), an inverse marker of DH, was inversely correlated with VD/VT (R2 ≈ 0.50). Therefore, we recommend that VD should be added to DH and EELV, as they are physiologically meaningful and VTpeak% represents not only DH but also dead space ventilation. To obtain VD, the VD/VT must be measured. Because obtaining VD/VT requires invasive arterial blood gases, further studies on noninvasive predicting VD/VT is warranted.

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