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.

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.

scholarly journals A Pilot Study on the Association of Mitochondrial Oxygen Metabolism and Gas Exchange During Cardiopulmonary Exercise Testing: Is There a Mitochondrial Threshold?

2020 ◽  
Vol 7 ◽  
Author(s):  
Philipp Baumbach ◽  
Christiane Schmidt-Winter ◽  
Jan Hoefer ◽  
Steffen Derlien ◽  
Norman Best ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Partial Pressure ◽  
Cardiopulmonary Exercise Testing ◽  
Oxygen Metabolism ◽  
Capillary Blood ◽  
Blood Gas ◽  
Cardiopulmonary Exercise ◽  
Blood Gas Analyses ◽  
End Tidal

Background: Mitochondria are the key players in aerobic energy generation via oxidative phosphorylation. Consequently, mitochondrial function has implications on physical performance in health and disease ranging from high performance sports to critical illness. The protoporphyrin IX-triplet state lifetime technique (PpIX-TSLT) allows in vivo measurements of mitochondrial oxygen tension (mitoPO2). Hitherto, few data exist on the relation of mitochondrial oxygen metabolism and ergospirometry-derived variables during physical performance. This study investigates the association of mitochondrial oxygen metabolism with gas exchange and blood gas analysis variables assessed during cardiopulmonary exercise testing (CPET) in aerobic and anaerobic metabolic phases.Methods: Seventeen volunteers underwent an exhaustive CPET (graded multistage protocol, 50 W/5 min increase), of which 14 were included in the analysis. At baseline and for every load level PpIX-TSLT-derived mitoPO2 measurements were performed every 10 s with 1 intermediate dynamic measurement to obtain mitochondrial oxygen consumption and delivery (mitoV.O2, mitoD.O2). In addition, variables of gas exchange and capillary blood gas analyses were obtained to determine ventilatory and lactate thresholds (VT, LT). Metabolic phases were defined in relation to VT1 and VT2 (aerobic: <VT1, aerobic-anaerobic transition: ≥VT1 and <VT2 and anaerobic: ≥VT2). We used linear mixed models to compare variables of PpIX-TSLT between metabolic phases and to analyze their associations with variables of gas exchange and capillary blood gas analyses.Results: MitoPO2 increased from the aerobic to the aerobic-anaerobic phase followed by a subsequent decline. A mitoPO2 peak, termed mitochondrial threshold (MT), was observed in most subjects close to LT2. MitoD.O2 increased during CPET, while no changes in mitoV.O2 were observed. MitoPO2 was negatively associated with partial pressure of end-tidal oxygen and capillary partial pressure of oxygen and positively associated with partial pressure of end-tidal carbon dioxide and capillary partial pressure of carbon dioxide. MitoD.O2 was associated with cardiovascular variables. We found no consistent association for mitoV.O2.Conclusion: Our results indicate an association between pulmonary respiration and cutaneous mitoPO2 during physical exercise. The observed mitochondrial threshold, coinciding with the metabolic transition from an aerobic to an anaerobic state, might be of importance in critical care as well as in sports medicine.

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.

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)

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

1996 ◽  
Vol 81 (5) ◽  
pp. 1978-1986 ◽  
Author(s):  
C. Tantucci ◽  
P. Bottini ◽  
M. L. Dottorini ◽  
E. Puxeddu ◽  
G. Casucci ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Autonomic Neuropathy ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Subjects ◽  
Inhibitory Modulation ◽  
End Tidal ◽  
And Control ◽  
Response To Exercise ◽  
Maximal Voluntary Ventilation

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response to exercise in diabetic subjects with autonomic neuropathy. J. Appl. Physiol. 81(5): 1978–1986, 1996.—We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan+) and 10 without (Dan−) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan− subjects achieved lower O2 consumption and CO2 production (V˙co 2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (V˙e) or adjusted ventilation (V˙e/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan+ than in Dan− and control subjects ( P < 0.05). The slope of the linearV˙e/V˙co 2relationship was 0.032 ± 0.002, 0.027 ± 0.001 ( P < 0.05), and 0.025 ± 0.001 ( P < 0.001) ml/min in Dan+, Dan−, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasingV˙co 2 were progressively higher in Dan+ than in Dan− and control subjects. At peak of exercise, end-tidal [Formula: see text] was much lower in Dan+ (35.9 ± 1.6 Torr) than in Dan− (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.

Is hypercapnia necessary for the ventilatory response to exercise in man?

1987 ◽  
Vol 73 (6) ◽  
pp. 617-625 ◽  
Author(s):  
K. Murphy ◽  
R. P. Stidwill ◽  
Brenda A. Cross ◽  
Kathryn D. Leaver ◽  
E. Anastassiades ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Co2 Production ◽  
Moderate Exercise ◽  
Arterial Ph ◽  
Arteriovenous Shunts ◽  
Exercise Period ◽  
Leg Exercise ◽  
End Tidal ◽  
Response To Exercise ◽  
End Tidal Co2

1. Continuous recordings of arterial pH, ventilation, airway CO2 and heart rate were made during rest and during 3–4 min periods of rhythmic leg exercise in four renal patients with arteriovenous shunts. 2. The patients were anaemic (haemoglobin 6.5–9.0 g/dl) but had a normal ventilatory response to exercise as judged by the ratio of the change in ventilation to the change in CO2 production. 3. Breath-by-breath oscillations in arterial pH disappeared for the majority of the exercise period in each patient. 4. Changes in mean arterial pH and end-tidal CO2 tension with exercise were inconsistent between subjects but consistent within a given subject. On average, mean arterial pH rose by 0.011 pH unit. Changes in end-tidal CO2 tension reflected changes in mean pHa by falling on average by 1 mmHg (0.13 kPa). 5. Hypercapnia and acidaemia were not found to be necessary for the ventilatory response to moderate exercise.

The Ventilatory Response to Hypoxia Below the Carbon Dioxide Threshold

1997 ◽  
Vol 22 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Theodore Rapanos ◽  
James Duffin
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Ventilatory Response ◽  
Pressure Threshold ◽  
Partial Pressures ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia ◽  
Lower Carbon

The ventilatory response to acute progressive hypoxia below the carbon dioxide threshold using rebreathing was investigated. Nine subjects rebreathed after 5 min of hyperventilation to lower carbon dioxide stores. The rebreathing bag initially contained enough carbon dioxide to equilibrate alveolar and arterial partial pressures of carbon dioxide to the lowered mixed venous partial pressure (≈ 30 mmHg), and enough oxygen to establish a chosen end-tidal partial pressure (50-70 mmHg), within one circulation time. During rebreathing, end-tidal partial pressure of carbon dioxide increased while end-tidal partial pressure of oxygen fell. Ventilation increased linearly with end-tidal carbon dioxide above a mean end-tidal partial pressure threshold of 39 ± 2.7 mmHg. Below this peripheral-chemoreflex threshold, ventilation did not increase, despite a progressive fall in end-tidal oxygen partial pressure to a mean of 37 ± 4.1 mmHg. In Conclusion, hypoxia does not stimulate ventilation when carbon dioxide is below its peripheral-chemoreflex threshold. Key words: peripheral chemoreflex, rebreathing technique, hyperventilation

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.

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