A model evaluation of estimates of breath-to-breath alveolar gas exchange

1983 ◽  
Vol 55 (6) ◽  
pp. 1936-1941 ◽  
Author(s):  
G. D. Swanson ◽  
D. L. Sherrill
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Indirect Measurement ◽  
Alveolar Volume ◽  
Gas Concentration ◽  
Inherent Error ◽  
Sinusoidal Flow ◽  
End Tidal ◽  
Exercise In Humans ◽  
Alveolar Gas Exchange

A mathematical model has been implemented for evaluation of methods for estimating breath-to-breath alveolar gas exchange during exercise in humans. This model includes a homogeneous alveolar gas exchange compartment, a dead space compartment, and tissue spaces for CO2 (alveolar and dead space). The dead space compartment includes a mixing portion surrounded by tissue and an unmixed (slug flow) portion which is partitioned between anatomical and apparatus contributions. A random sinusoidal flow pattern generates a breath-to-breath variation in pulmonary stores. The Auchincloss algorithm for estimating alveolar gas exchange (Auchincloss et al., J. Appl. Physiol. 21: 810-818, 1966) was applied to the model, and the results were compared with the simulated gas exchange. This comparison indicates that a compensation for changes in pulmonary stores must include factors for alveolar gas concentration change as well as alveolar volume change and thus implies the use of end-tidal measurements. Although this algorithm yields reasonable estimates of breath-to-breath alveolar gas exchange, it does not yield a “true” indirect measurement because of inherent error in the estimation of a homogeneous alveolar gas concentration at the end of expiration.

Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model

1997 ◽  
Vol 82 (6) ◽  
pp. 1963-1971 ◽  
Author(s):  
Thierry Busso ◽  
Peter A. Robbins
Keyword(s):  
Gas Exchange ◽  
Lung Model ◽  
Gas Composition ◽  
Breathing Patterns ◽  
Alveolar Volume ◽  
Gas Concentration ◽  
Pulmonary Capillaries ◽  
Partial Pressures ◽  
End Tidal ◽  
Alveolar Gas Exchange

Busso, Thierry, and Peter A. Robbins. Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model. J. Appl. Physiol. 82(6): 1963–1971, 1997.—The purpose of this study was to evaluate algorithms for estimating O2 and CO2 transfer at the pulmonary capillaries by use of a nine-compartment tidally ventilated lung model that incorporated inhomogeneities in ventilation-to-volume and ventilation-to-perfusion ratios. Breath-to-breath O2 and CO2 exchange at the capillary level and at the mouth were simulated by using realistic cyclical breathing patterns to drive the model, derived from 40-min recordings in six resting subjects. The SD of the breath-by-breath gas exchange at the mouth around the value at the pulmonary capillaries was 59.7 ± 25.5% for O2 and 22.3 ± 10.4% for CO2. Algorithms including corrections for changes in alveolar volume and for changes in alveolar gas composition improved the estimates of pulmonary exchange, reducing the SD to 20.8 ± 10.4% for O2 and 15.2 ± 5.8% for CO2. The remaining imprecision of the estimates arose almost entirely from using end-tidal measurements to estimate the breath-to-breath changes in end-expiratory alveolar gas concentration. The results led us to suggest an alternative method that does not use changes in end-tidal partial pressures as explicit estimates of the changes in alveolar gas concentration. The proposed method yielded significant improvements in estimation for the model data of this study.

Short-term modulation of the exercise ventilatory response in young men

2008 ◽  
Vol 104 (1) ◽  
pp. 244-252 ◽  
Author(s):  
Helen E. Wood ◽  
Gordon S. Mitchell ◽  
Tony G. Babb
Keyword(s):  
Dead Space ◽  
Animal Studies ◽  
Ventilatory Response ◽  
Young Men ◽  
Neural Mechanism ◽  
Short Term ◽  
Response Slope ◽  
Ventilatory Drive ◽  
End Tidal ◽  
Exercise In Humans

Arterial isocapnia is a hallmark of moderate exercise in humans and is maintained even when resting arterial Pco2 (PaCO2) is raised or lowered from its normal level, e.g., with chronic acid-base changes or acute increases in respiratory dead space. When resting ventilation and/or PaCO2 are altered, maintenance of isocapnia requires active adjustments of the exercise ventilatory response [slope of the ventilation (V̇e)-CO2 production (V̇co2) relationship, ΔV̇e/ΔV̇co2]. On the basis of animal studies, it has been proposed that a central neural mechanism links the exercise ventilatory response to the resting ventilatory drive without need for changes in chemoreceptor feedback from rest to exercise, a mechanism referred to as short-term modulation (STM). We tested the hypothesis that STM is elicited by increased resting ventilatory drive associated with added external dead space (DS) in humans. Twelve young men were studied in control conditions and with added DS (200, 400, and 600 ml; randomized) at rest and during mild-to-moderate cycle exercise. ΔV̇e/ΔV̇co2 increased progressively as DS volume increased ( P < 0.0001). While resting end-tidal Pco2 (PetCO2) increased with DS, the change in PetCO2 from rest to exercise was not increased, indicating that increased chemoreceptor feedback from rest to exercise cannot account for the greater exercise ventilatory response. We conclude that STM of the exercise ventilatory response is induced in young men when resting ventilatory drive is increased with external DS, confirming the existence of STM in humans.

Repeated exercise paired with “imperceptible” dead space loading does not alter V˙e of subsequent exercise in humans

2002 ◽  
Vol 92 (3) ◽  
pp. 1159-1168 ◽  
Author(s):  
S. H. Moosavi ◽  
A. Guz ◽  
L. Adams
Keyword(s):  
Associative Learning ◽  
Dead Space ◽  
Breathing Circuit ◽  
Conditioning Session ◽  
Repeated Exercise ◽  
Session Type ◽  
End Tidal ◽  
Response To Exercise ◽  
Exercise In Humans ◽  
Test Control

We employed an associative learning paradigm to test the hypothesis that exercise hyperpnea in humans arises from learned responses forged by prior experience. Twelve subjects undertook a “conditioning” and a “nonconditioning” session on separate days, with order of performance counterbalanced among subjects. In both sessions, subjects performed repeated bouts of 6 min of treadmill exercise, each separated by 5 min of rest. The only difference between sessions was that all the second-to-penultimate runs of the conditioning session were performed with added dead space in the breathing circuit. Cardiorespiratory responses during the first and last runs (the “control” and “test” runs) were compared for each session. Steady-state exercise end-tidal Pco 2 was significantly lower ( P= 0.003) during test than during control runs for both sessions (dropping by 1.8 ± 2 and 1.4 ± 3 Torr during conditioning and nonconditioning sessions, respectively). This and all other test-control run differences tended to be greater during the first session performed regardless of session type. Our data provide no support for the hypothesis implicating associative learning processes in the ventilatory response to exercise in humans.

Pulmonary gas exchange and its determinants during sustained microgravity on Spacelabs SLS-1 and SLS-2

1995 ◽  
Vol 79 (4) ◽  
pp. 1290-1298 ◽  
Author(s):  
G. K. Prisk ◽  
A. R. Elliott ◽  
H. J. Guy ◽  
J. M. Kosonen ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pulmonary Gas Exchange ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

Lung cytokinetics after exposure to hypobaria and/or hypoxia and undernutrition in growing rats

1995 ◽  
Vol 79 (4) ◽  
pp. 1299-1309 ◽  
Author(s):  
H. S. Sekhon ◽  
W. M. Thurlbeck
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Normal Gravity ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

scholarly journals Ventilatory response to exercise in cardiopulmonary disease: the role of chemosensitivity and dead space

2018 ◽  
Vol 51 (2) ◽  
pp. 1700860 ◽  
Author(s):  
Jason Weatherald ◽  
Caroline Sattler ◽  
Gilles Garcia ◽  
Pierantonio Laveneziana
Keyword(s):  
Gas Exchange ◽  
Partial Pressure ◽  
Dead Space ◽  
Ventilatory Response ◽  
Heart Function ◽  
Cardiopulmonary Exercise Testing ◽  
Cardiopulmonary Disease ◽  
The Difference ◽  
End Tidal ◽  
Response To Exercise

The lungs and heart are irrevocably linked in their oxygen (O2) and carbon dioxide (CO2) transport functions. Functional impairment of the lungs often affects heart function andvice versa. The steepness with which ventilation (V′E) rises with respect to CO2production (V′CO2) (i.e.theV′E/V′CO2slope) is a measure of ventilatory efficiency and can be used to identify an abnormal ventilatory response to exercise. TheV′E/V′CO2slope is a prognostic marker in several chronic cardiopulmonary diseases independent of other exercise-related variables such as peak O2uptake (V′O2). TheV′E/V′CO2slope is determined by two factors: 1) the arterial CO2partial pressure (PaCO2) during exercise and 2) the fraction of the tidal volume (VT) that goes to dead space (VD) (i.e.the physiological dead space ratio (VD/VT)). An alteredPaCO2set-point and chemosensitivity are present in many cardiopulmonary diseases, which influenceV′E/V′CO2by affectingPaCO2. Increased ventilation–perfusion heterogeneity, causing inefficient gas exchange, also contributes to the abnormalV′E/V′CO2observed in cardiopulmonary diseases by increasingVD/VT. During cardiopulmonary exercise testing, thePaCO2during exercise is often not measured andVD/VTis only estimated by taking into account the end-tidal CO2partial pressure (PETCO2); however,PaCO2is not accurately estimated fromPETCO2in patients with cardiopulmonary disease. Measuring arterial gases (PaO2andPaCO2) before and during exercise provides information on the real (and not “estimated”)VD/VTcoupled with a true measure of gas exchange efficiency such as the difference between alveolar and arterial O2partial pressure and the difference between arterial and end-tidal CO2partial pressure during exercise.

Breath-by-breath alveolar gas exchange

1983 ◽  
Vol 55 (2) ◽  
pp. 583-590 ◽  
Author(s):  
D. Giezendanner ◽  
P. Cerretelli ◽  
P. E. Di Prampero
Keyword(s):  
Gas Exchange ◽  
Open Circuit ◽  
Single Breath ◽  
Alveolar Level ◽  
Expired Gas ◽  
The Difference ◽  
Computer Monitors ◽  
End Tidal ◽  
Breath Measurement ◽  
Alveolar Gas Exchange

A method is described for breath-by-breath measurement of alveolar gas exchange corrected for changes of lung gas stores. In practice, the subject inspires from a spirometer, and each expired tidal volume is collected into a rubber bag placed inside a rigid box connected to the same spirometer. During the inspiration following any given expiration the bag is emptied by a vacuum pump. A computer monitors inspiratory and expiratory tidal volumes, drives four solenoid valves allowing appropriate operation of the system, and memorizes end-tidal gas fractions as well as mixed expired gas composition analyzed by mass spectrometer. Thus all variables for calculating alveolar gas exchange, based on the theory developed by Auchincloss et al. (J. Appl. Physiol. 21: 810-818, 1966), are obtained on a single-breath basis. Mean resting and steady-state exercise gas exchange data are equal to those obtained by conventional open-circuit measurements. Breathing rates up to 30 X min-1 can be followed. The breath-to-breath variability of O2 uptake at the alveolar level is less (25-35%) than that measured at the mouth as the difference between the inspired and expired volumes, both at rest and during exercise up to 0.7 of maximum O2 consumption.

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.

A Note of Caution About the Continuous Use of Colorimetric End-Tidal CO2 Detectors in Children

PEDIATRICS ◽  
1995 ◽  
Vol 95 (5) ◽  
pp. 800-801
Author(s):  
Mananda S. Bhende ◽  
David LaCovey
Keyword(s):  
Endotracheal Tube ◽  
Dead Space ◽  
Spontaneous Circulation ◽  
End Tidal ◽  
Continuous Use ◽  
End Tidal Co2

Colorimetric end-tidal CO2 (ETCO2) detectors (Easy Cap, Nellcor Inc, Hayward, CA) are extremely useful in determining the position of the endotracheal tube (ETT) in the airway and have been validated in animals, children, and adults.1-6 They have not been labelled for use in children weighing 15 kg because of their large dead space of 38 mL.1-3 We have demonstrated in numerous studies that the ETCO2 detector accurately verifies the ETT position in infants weighing &gt;2 kg with spontaneous circulation.1-3

Sign in / Sign up

Export Citation Format

Share Document