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.

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.

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.

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.

PULMONARY FUNCTION IN THE NEWBORN INFANT

PEDIATRICS ◽  
1962 ◽  
Vol 30 (6) ◽  
pp. 963-974
Author(s):  
N. M. Nelson ◽  
L. S. Prod'hom ◽  
R. B. Cherry ◽  
P. J. Lipsitz ◽  
C. A. Smith
Keyword(s):  
Pulmonary Function ◽  
Newborn Infant ◽  
Breathing Circuit ◽  
Co2 Production ◽  
Pulmonary Functions ◽  
Neonatal Physiology ◽  
End Tidal

An open breathing circuit is described that is suitable for the newborn infant. The addition of an end-tidal sampler allows accurate study of many pulmonary functions. Data obtained with this equipment are quite comparable to those obtained with more classic methods in neonatal physiology. The low alveolar CO2 tension commonly observed in the first days of life may result from decreased CO2 production by the fasting newborn infant. [See Fig 7 in Source Pdf]

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

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

scholarly journals Bedside estimates of dead space using end-tidal CO2 are independently associated with mortality in ARDS

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Paola Lecompte-Osorio ◽  
Steven D. Pearson ◽  
Cole H. Pieroni ◽  
Matthew R. Stutz ◽  
Anne S. Pohlman ◽  
...  
Keyword(s):  
Dead Space ◽  
Validation Cohort ◽  
Univariate Analysis ◽  
Multivariable Analysis ◽  
Separate Analysis ◽  
University Of Chicago ◽  
Derivation Cohort ◽  
Ventilator Mode ◽  
The Difference ◽  
End Tidal

Abstract Purpose In acute respiratory distress syndrome (ARDS), dead space fraction has been independently associated with mortality. We hypothesized that early measurement of the difference between arterial and end-tidal CO2 (arterial-ET difference), a surrogate for dead space fraction, would predict mortality in mechanically ventilated patients with ARDS. Methods We performed two separate exploratory analyses. We first used publicly available databases from the ALTA, EDEN, and OMEGA ARDS Network trials (N = 124) as a derivation cohort to test our hypothesis. We then performed a separate retrospective analysis of patients with ARDS using University of Chicago patients (N = 302) as a validation cohort. Results The ARDS Network derivation cohort demonstrated arterial-ET difference, vasopressor requirement, age, and APACHE III to be associated with mortality by univariable analysis. By multivariable analysis, only the arterial-ET difference remained significant (P = 0.047). In a separate analysis, the modified Enghoff equation ((PaCO2–PETCO2)/PaCO2) was used in place of the arterial-ET difference and did not alter the results. The University of Chicago cohort found arterial-ET difference, age, ventilator mode, vasopressor requirement, and APACHE II to be associated with mortality in a univariate analysis. By multivariable analysis, the arterial-ET difference continued to be predictive of mortality (P = 0.031). In the validation cohort, substitution of the arterial-ET difference for the modified Enghoff equation showed similar results. Conclusion Arterial to end-tidal CO2 (ETCO2) difference is an independent predictor of mortality in patients with ARDS.

Expiratory and arterial partial pressure relations under different ventilation-perfusion conditions

1983 ◽  
Vol 54 (6) ◽  
pp. 1745-1753 ◽  
Author(s):  
A. Zwart ◽  
S. C. Luijendijk ◽  
W. R. de Vries
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Gas Analysis ◽  
Lung Model ◽  
Breathing Patterns ◽  
Tracer Gas ◽  
Physiological Dead Space ◽  
Arterial Partial Pressure ◽  
The Difference ◽  
End Tidal

Inert tracer gas exchange across the human respiratory system is simulated in an asymmetric lung model for different oscillatory breathing patterns. The momentary volume-averaged alveolar partial pressure (PA), the expiratory partial pressure (PE), the mixed expiratory partial pressure (PE), the end-tidal partial pressure (PET), and the mean arterial partial pressure (Pa), are calculated as functions of the blood-gas partition coefficient (lambda) and the diffusion coefficient (D) of the tracer gas. The lambda values vary from 0.01 to 330.0 inclusive, and four values of D are used (0.5, 0.22, 0.1, and 0.01). Three ventilation-perfusion conditions corresponding to rest and mild and moderate exercise are simulated. Under simulated exercise conditions, we compute a reversed difference between PET and Pa compared with the rest condition. This reversal is directly reflected in the relation between the physiological dead space fraction (1--PE/Pa) and the Bohr dead space fraction (1--PE/PET). It is argued that the difference (PET--Pa) depends on the lambda of the tracer gas, the buffering capacity of lung tissue, and the stratification caused by diffusion-limited gas transport in the gas phase. Finally some determinants for the reversed difference (PET--Pa) and the significance for conventional gas analysis are discussed.

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document