Dynamic End-Tidal Forcing Technique: Modelling the Ventilatory Response to Carbon Dioxide

1989 ◽  
pp. 59-69 ◽  
Author(s):  
Jacob DeGoede ◽  
Adriaan Berkenbosch
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Tidal Forcing ◽  
End Tidal

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

Effect of intravenous dopamine on hypercapnic ventilatory response in humans

1983 ◽  
Vol 55 (5) ◽  
pp. 1418-1425 ◽  
Author(s):  
D. S. Ward ◽  
J. W. Bellville
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Carbon Dioxide Concentration ◽  
Carbon Dioxide Tension ◽  
Model Parameters ◽  
Loop Gain ◽  
Loop Contribution ◽  
Dopamine Infusion ◽  
Hypercapnic Ventilatory Response ◽  
End Tidal

This study assessed the effect of low-dose intravenous dopamine (3 micrograms X kg-1 X min-1) on the hypercapnic ventilatory response in humans. Six normal healthy subjects were studied. By manipulating the inspired carbon dioxide concentration, the end-tidal carbon dioxide tension was raised in a stepwise fashion from 41 to 49 Torr and held at this level for 4 min. The end-tidal CO2 tension was then lowered back to 41 Torr in a stepwise fashion. The end-tidal O2 tension was held constant at 106 Torr throughout the experiment. The ventilatory response to this normoxic hypercapnic stimulus was analyzed by fitting two exponential functions, allowing the response to be separated into slow and fast chemoreflex loops. Each loop is described by a gain, time constant, and time delay. A single eupneic threshold was used for both loops. Nine control experiments and eight experiments performed during dopamine infusion were analyzed. The dopamine infusion caused the fast loop gain to be significantly (P less than 0.05) reduced from 0.64 to 0.19 l X min-1 X Torr-1, while the slow loop gain was unchanged. The fast loop contribution was reduced from 28 to 11% of the total ventilatory response. None of the other model parameters were significantly affected by the dopamine infusion. Exogenously administered dopamine substantially reduces the sensitivity of the fast chemoreflex loop to carbon dioxide.

scholarly journals Dynamic Forcing of End-Tidal Carbon Dioxide and Oxygen Applied to Functional Magnetic Resonance Imaging

2007 ◽  
Vol 27 (8) ◽  
pp. 1521-1532 ◽  
Author(s):  
Richard G Wise ◽  
Kyle TS Pattinson ◽  
Daniel P Bulte ◽  
Peter A Chiarelli ◽  
Stephen D Mayhew ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Oxygenation ◽  
Dynamic Responses ◽  
Bold Signal ◽  
Tidal Forcing ◽  
Partial Pressures ◽  
Oxygenation Level ◽  
Mri Environment ◽  
Dynamic Forcing ◽  
End Tidal

Investigations into the blood oxygenation level-dependent (BOLD) functional MRI signal have used respiratory challenges with the aim of probing cerebrovascular physiology. Such challenges have altered the inspired partial pressures of either carbon dioxide or oxygen, typically to a fixed and constant level (fixed inspired challenge (FIC)). The resulting end-tidal gas partial pressures then depend on the subject's metabolism and ventilatory responses. In contrast, dynamic end-tidal forcing (DEF) rapidly and independently sets end-tidal oxygen and carbon dioxide to desired levels by altering the inspired gas partial pressures on a breath-by-breath basis using computer-controlled feedback. This study implements DEF in the MRI environment to map BOLD signal reactivity to CO2. We performed BOLD (T2*) contrast FMRI in four healthy male volunteers, while using DEF to provide a cyclic normocapnichypercapnic challenge, with each cycle lasting 4 mins (PetCO2 mean±s.d., from 40.9 ± 1.8 to 46.4 ± 1.6 mm Hg). This was compared with a traditional fixed-inspired (FiCO2 = 5%) hypercapnic challenge (PetCO2 mean±s.d., from 38.2 ± 2.1 to 45.6 ± 1.4 mm Hg). Dynamic end-tidal forcing achieved the desired target PetCO2 for each subject while maintaining PetCO2 constant. As a result of CO2-induced increases in ventilation, the FIC showed a greater cyclic fluctuation in PetCO2. These were associated with spatially widespread fluctuations in BOLD signal that were eliminated largely by the control of PetCO2 during DEF. The DEF system can provide flexible, convenient, and physiologically well-controlled respiratory challenges in the MRI environment for mapping dynamic responses of the cerebrovasculature.

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

Dynamics of the Ventilatory Response to Step Changes in End-Tidal PCO2 in Older Humans

1997 ◽  
Vol 22 (4) ◽  
pp. 368-383 ◽  
Author(s):  
Marc J. Poulin ◽  
David A. Cunningham ◽  
Donald H. Paterson
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Older Men ◽  
Young Group ◽  
Control Of Breathing ◽  
Ventilatory Responses ◽  
Key Words Ageing ◽  
Younger Men ◽  
End Tidal ◽  
Mild Hypoxia

The purpose of this study was to examine the ventilatory response to carbon dioxide (CO2) in young and older men. Six square-wave steps of end-tidal CO2 (PETCO2) were administered in euoxia (PETO2 = 100 torr), hyperoxia (PETO2 = 500 torr), and mild hypoxia (PETO2 = 60 torr) The peripheral and central chemoreflex loops were described by three parameters including a gain (gp and gc), time constant of the response(τp, τc), and a time delay (Tp, Tc), respectively. The young and older men showed similar characteristics for Tp and Tc, with Tp, being 3 to 5 s shorter than Tc. In hypoxia, the ventilatory responses of the old group were characterised by a significantly smaller gc and a smaller gp. In hypoxia, τc was significantly shortened from its euoxic value in the young group, but not in the old group. Thus, this study demonstrated that in older men, the ventilatory responses to CO2 in euoxia and hyperoxia are similar to younger men, while in hypoxia the ventilatory responses are characterised by smaller gain terms. Key words: ageing, hypercapnia, hypoxia, hyperoxia, control of breathing

scholarly journals Activation of Opioid μ Receptors in Caudal Medullary Raphe Region Inhibits the Ventilatory Response to Hypercapnia in Anesthetized Rats

2007 ◽  
Vol 107 (2) ◽  
pp. 288-297 ◽  
Author(s):  
Zhenxiong Zhang ◽  
Fadi Xu ◽  
Cancan Zhang ◽  
Xiaomin Liang
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Central Area ◽  
Mu Receptor ◽  
Medullary Raphe ◽  
Mu Receptors ◽  
End Tidal ◽  
Spontaneously Breathing ◽  
Made In

Background : Opioids, extensively used as analgesics, markedly depress ventilation, particularly the ventilatory responsiveness to hypercapnia in humans and animals predominantly via acting on mu receptors. The medullary raphe region (MRR) contains abundant mu receptors responsible for analgesia and is also an important central area involving carbon dioxide chemoreception and contributing to the ventilatory responsiveness to hypercapnia. Therefore, the authors asked whether activation of mu receptors in the caudal, medial, or rostral MRR depressed ventilation and the response to hypercapnia, respectively. Methods : Experiments were conducted in 32 anesthetized and spontaneously breathing rats. Ventilation and it response to progressive hypercapnia were recorded. The slopes obtained from plotting minute ventilation, respiratory frequency, and tidal volume against the corresponding levels of end-tidal pressure of carbon dioxide were used as the indices of the respiratory responsiveness to carbon dioxide. DAMGO ([d-Ala2, N-Me-Phe4, Gly-ol]-enkephalin), a mu-receptor agonist, was systemically administered (100 mug/kg) before and/or after local injection of CTAP (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2) (100 ng/100 nl), a mu-receptor antagonist, into the caudal MRR, or locally administered (35 ng/100 nl) into the MRR subnuclei. Results : The authors found that systemic DAMGO significantly inhibited ventilation and the response to carbon dioxide by 20% and 31%, respectively, and these responses were significantly diminished to 11% and 14% after pretreatment of the caudal MRR with CTAP. Local administration of DAMGO into the caudal MRR also reduced ventilation and the response to carbon dioxide by 22% and 28%, respectively. In sharp contrast, these responses were not observed when the DAMGO microinjection was made in the middle MRR or rostral MRR. Conclusions : These results lead to the conclusion that mu receptors in the caudal MRR rather than the middle MRR or rostral MRR are important but not exclusive for attenuating the hypercapnic ventilatory response.

Factors Determining the Ventilatory Response to Carbon Dioxide in Chronic Obstructive Airways Disease

1970 ◽  
Vol 39 (5) ◽  
pp. 653-662 ◽  
Author(s):  
T. K. C. King ◽  
D. Yu
Keyword(s):  
Carbon Dioxide ◽  
Response Curve ◽  
Ventilatory Response ◽  
Chronic Obstructive ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Obstructive Airways Disease ◽  
End Tidal ◽  
Chronic Obstructive Airways Disease ◽  
Carbon Dioxide Response

1. The ventilatory response to carbon dioxide was measured in a group of patients with chronic obstructive airways disease using a rebreathing method. 2. The slope of the carbon dioxide response curve was obtained by plotting the ventilation at successive half minutes against the corresponding mean end tidal Pco2. 3. The slope of the carbon dioxide response curve was positively correlated with (a) the FEV1 and (b) the reciprocal of the resting arterial Pco2, both these correlations being statistically significant. 4. Reference to FEV1 alone could explain more than 80% of the variation in the slope of the CO2 response curve. This explained variation was not significantly improved by the additional consideration of the resting arterial Pco2. 5. It was suggested that whatever the underlying complex mechanisms that determine the response to CO2, the FEV1 can be used as an empirical factor for the prediction of this response in patients with chronic obstructive airways disease.

Influences of Morphine on the Ventilatory Response to Isocapnic Hypoxia 

1997 ◽  
Vol 86 (6) ◽  
pp. 1342-1349 ◽  
Author(s):  
Aad Berkenbosch ◽  
Luc J. Teppema ◽  
Cees N. Olievier ◽  
Albert Dahan
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Shape Parameter ◽  
Ventilatory Response ◽  
Depressant Effect ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
Ventilatory Response To Hypoxia ◽  
Carbon Dioxide Sensitivity

Background The ventilatory response to hypoxia is composed of the stimulatory activity from peripheral chemoreceptors and a depressant effect from within the central nervous system. Morphine induces respiratory depression by affecting the peripheral and central carbon dioxide chemoreflex loops. There are only few reports on its effect on the hypoxic response. Thus the authors assessed the effect of morphine on the isocapnic ventilatory response to hypoxia in eight cats anesthetized with alpha-chloralose-urethan and on the ventilatory carbon dioxide sensitivities of the central and peripheral chemoreflex loops. Methods The steady-state ventilatory responses to six levels of end-tidal oxygen tension (PO2) ranging from 375 to 45 mmHg were measured at constant end-tidal carbon dioxide tension (P[ET]CO2, 41 mmHg) before and after intravenous administration of morphine hydrochloride (0.15 mg/kg). Each oxygen response was fitted to an exponential function characterized by the hypoxic sensitivity and a shape parameter. The hypercapnic ventilatory responses, determined before and after administration of morphine hydrochloride, were separated into a slow central and a fast peripheral component characterized by a carbon dioxide sensitivity and a single offset B (apneic threshold). Results At constant P(ET)CO2, morphine decreased ventilation during hyperoxia from 1,260 +/- 140 ml/min to 530 +/- 110 ml/ min (P < 0.01). The hypoxic sensitivity and shape parameter did not differ from control. The ventilatory response to carbon dioxide was displaced to higher P(ET)CO2 levels, and the apneic threshold increased by 6 mmHg (P < 0.01). The central and peripheral carbon dioxide sensitivities decreased by about 30% (P < 0.01). Their ratio (peripheral carbon dioxide sensitivity:central carbon dioxide sensitivity) did not differ for the treatments (control = 0.165 +/- 0.105; morphine = 0.161 +/- 0.084). Conclusions Morphine depresses ventilation at hyperoxia but does not depress the steady-state increase in ventilation due to hypoxia. The authors speculate that morphine reduces the central depressant effect of hypoxia and the peripheral carbon dioxide sensitivity at hyperoxia.

scholarly journals Reproducibility of hypercapnic ventilatory response measurements with steady-state and rebreathing methods

2018 ◽  
Vol 4 (1) ◽  
pp. 00141-2017
Author(s):  
Denise C. Mannée ◽  
Timon M. Fabius ◽  
Michiel Wagenaar ◽  
Michiel M.M. Eijsvogel ◽  
Frans H.C. de Jongh
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Rating Scales ◽  
Ventilatory Response ◽  
Intraclass Correlation ◽  
Carbon Dioxide Tension ◽  
Secondary Outcome ◽  
Hypercapnic Ventilatory Response ◽  
Steady State Method ◽  
End Tidal

In this study, the hypercapnic ventilatory response (HCVR) was measured, defined as the ventilation response to carbon dioxide tension (PCO2). We investigated which method, rebreathing or steady-state, is most suitable for measurement of the HCVR in healthy subjects, primarily based on reproducibility. Secondary outcome parameters were subject experience and duration.20 healthy adults performed a rebreathing and steady-state HCVR measurement on two separate days. Subject experience was assessed using numeric rating scales (NRS). The intraclass correlation coefficient (ICCs) of the sensitivity to carbon dioxide above the ventilatory recruitment threshold and the projected apnoea threshold were calculated to determine the reproducibility of both methods.The ICCs of sensitivity were 0.89 (rebreathing) and 0.56 (steady-state). The ICCs of the projected apnoea threshold were 0.84 (rebreathing) and 0.25 (steady-state). The steady-state measurement was preferred by 16 out of 20 subjects; the differences in NRS scores were small.The hypercapnic ventilatory response measured using the rebreathing setup provided reproducible results, while the steady-state method did not. This may be explained by high variability in end-tidal PCO2. Differences in subject experience between the methods are small.

Respiratory Sites of Action of Propofol

2001 ◽  
Vol 95 (4) ◽  
pp. 889-895 ◽  
Author(s):  
Diederik Nieuwenhuijs ◽  
Elise Sarton ◽  
Luc J. Teppema ◽  
Erik Kruyt ◽  
Ida Olievier ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Binary Sequence ◽  
Total Duration ◽  
Carbon Dioxide Concentration ◽  
Central Component ◽  
End Tidal ◽  
Sites Of Action ◽  
Peripheral Chemoreflex ◽  
Carbon Dioxide Sensitivity

Background Propofol has a depressant effect on metabolic ventilatory control, causing depression of the ventilatory response to acute isocapnic hypoxia, a response mediated via the peripheral chemoreflex loop. In this study, the authors examined the effect of sedative concentrations of propofol on the dynamic ventilatory response to carbon dioxide to obtain information about the respiratory sites of action of propofol. Methods In 10 healthy volunteers, the end-tidal carbon dioxide concentration was varied according to a multifrequency binary sequence that involved 13 steps into and 13 steps out of hypercapnia (total duration, 1,408 s). In each subject, two control studies, two studies at a plasma target propofol concentration of 0.75 microg/ml (P(low)), and two studies at a target propofol concentration of 1.5 microg/ml (P(high)) were performed. The ventilatory responses were separated into a fast peripheral component and a slow central component, characterized by a time constant, carbon dioxide sensitivity, and apneic threshold. Values are mean +/- SD. Results Plasma propofol concentrations were approximately 0.5 microg/ml for P(low) and approximately 1.3 mg/ml for P(high), Propofol reduced the central carbon dioxide sensitivity from 1.5 +/- 0.4 to 1.2 +/- 0.3 (P(low); P < 0.01 vs. control) and 0.9 +/- 0.1 l x min(-1) x mmHg(-1) (P(high); P < 0.001 vs. control). The peripheral carbon dioxide sensitivity remained unaffected by propofol (control, 0.5 +/- 0.3; P(low), 0.5 +/- 0.2; P(high), 0.5 +/- 0.2 l x min(-1) x mmHg(-1)). The apneic threshold was reduced from 36.3 +/- 2.7 (control) to 35.0 +/- 2.1 (P(low); P < 0.01 vs. control) and to 34.6 +/- 1.9 mmHg (P(high); P < 0.01 vs. control). Conclusions Sedative concentrations of propofol have an important effect on the control of breathing, showing depression of the ventilatory response to hypercapnia. The depression is attributed to an exclusive effect within the central chemoreflex loop at the central chemoreceptors. In contrast to low-dose inhalational anesthetics, the peripheral chemoreflex loop, when stimulated with carbon dioxide, remains unaffected by propofol.

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