Assessment of Responsiveness to Carbon Dioxide in Patients with Chronic Airways Obstruction by Rate of Isometric Inspiratory Pressure Development

1976 ◽  
Vol 50 (3) ◽  
pp. 199-205 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Pressure Change ◽  
Significant Negative Correlation ◽  
Inspiratory Pressure ◽  
Normal Range ◽  
Ventilatory Responses ◽  
Airways Obstruction ◽  
Pressure Development ◽  
Mechanical Factors

1. Responsiveness to CO2 was measured in forty patients with chronic airways obstruction in terms of ventilation and rate of isometric inspiratory pressure change [(dP/dt)max.]. 2. The ventilatory response was below the normal range in eighteen out of twenty-two patients with normal arterial CO2 tensions and in all of eighteen patients with CO2 retention. 3. The (dP/dt)max. response was distributed throughout the normal range in all but one of the patients with normal arterial CO2 tension. In all the patients with CO2 retention the (dP/dt)max. response was either at or below the lower limit of the normal range. 4. Although the ventilatory responses correlated significantly with FEV1 there was no such correlation for the (dP/dt)max. responses. 5. The (dP/dt)max. response showed a significant negative correlation with Pa,co2. 6. It is believed that the (dP/dt)max. response to CO2 can be used to assess central CO2 responsiveness in subjects with airways obstruction independently of mechanical factors limiting their ventilation.

The Rate of Isometric Inspiratory Pressure Development as a Measure of Responsiveness to Carbon Dioxide in Man

1975 ◽  
Vol 49 (1) ◽  
pp. 57-68 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell
Keyword(s):  
Initial Rate ◽  
Ventilatory Response ◽  
Pressure Change ◽  
Normal Subjects ◽  
Inspiratory Pressure ◽  
Pulmonary Mechanics ◽  
Inspiratory Muscles ◽  
Pressure Development ◽  
Respiratory Centre ◽  
Very High

1. A technique has been developed for assessing CO2 responsiveness by measuring the maximum rate of isometric inspiratory pressure change at the mouth [(dP/dt)max.]. 2. By use of a rebreathing technique, the (dP/dt)max. response to CO2 was shown to correlate well with the ventilatory response in thirty-two normal subjects. 3. The addition of an external flow resistance sufficient to reduce the ventilatory response by a mean of 33.4% produced no significant mean change in the (dP/dt)max. response in thirty subjects. 4. In six patients recovering from bronchial asthma, reduction of airways obstruction led to a mean increase in the ventilatory response of 109% without any significant mean change in the (dP/dt)max. response. 5. An increase in lung volume did not reduce the (dP/dt)max. response in five normal subjects. 6. At very high lung volumes, six normal subjects were able to develop a higher (dP/dt)max. during voluntary inspiratory efforts than has been recorded during spontaneous breathing response to CO2. 7. It is believed that (dP/dt)max. represents the initial rate of development of force by the inspiratory muscles before this can be modified by mechanical loading, proprioceptive feedback mechanisms or conscious response and can therefore be used to study changes in the motor output of the respiratory centre in response to ventilatory stimuli independently of pulmonary mechanics.

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.

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

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.

Maximal Oxygen Uptake, Lung Volume and Ventilatory Response to Carbon Dioxide and Hypoxia in a Pair of Identical Twin Athletes

1975 ◽  
Vol 48 (3) ◽  
pp. 235-238 ◽  
Author(s):  
A. G. Leitch ◽  
L. Clancy ◽  
D. C. Flenley
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Major Part ◽  
Genetic Factors ◽  
Ventilatory Response ◽  
Identical Twin ◽  
Lung Volumes ◽  
Ventilatory Responses ◽  
High Degree

1. Maximal oxygen uptake (V̇o2 max.), lung volumes, and ventilatory responses to carbon dioxide and hypoxia have been measured in identical twin athletes, who were trained to a similar high degree. 2. The results confirm previous findings for V̇o2 max. and lung volumes in identical twins, and are in keeping with the suggestion that genetic factors play a major part in determining the ventilatory response to carbon dioxide and hypoxia.

Influences of Subanesthetic Isoflurane on Ventilatory Control in Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 478-490. ◽  
Author(s):  
Maarten van den Elsen ◽  
Albert Dahan ◽  
Jacob DeGoede ◽  
Aad Berkenbosch ◽  
Jack van Kleef
Keyword(s):  
Carbon Dioxide ◽  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Carbon Dioxide Tension ◽  
Central Component ◽  
Ventilatory Control ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia

Background The purpose of this study was to quantify in humans the effects of subanesthetic isoflurane on the ventilatory control system, in particular on the peripheral chemoreflex loop. Therefore we studied the dynamic ventilatory response to carbon dioxide, the effect of isoflurane wash-in upon sustained hypoxic steady-state ventilation, and the ventilatory response at the onset of 20 min of isocapnic hypoxia. Methods Study 1: Square-wave changes in end-tidal carbon dioxide tension (7.5-11.5 mmHg) were performed in eight healthy volunteers at 0 and 0.1 minimum alveolar concentration (MAC) isoflurane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set (apneic threshold). Study 2: The ventilatory changes due to the wash-in of 0.1 MAC isoflurane, 15 min after the induction of isocapnic hypoxia, were studied in 11 healthy volunteers. Study 3: The ventilatory responses to a step decrease in end-tidal oxygen (end-tidal oxygen tension from 110 to 44 mmHg within 3-4 breaths; duration of hypoxia 20 min) were assessed in eight healthy volunteers at 0, 0.1, and 0.2 MAC isoflurane. Results Values are reported as means +/- SF. Study 1: The peripheral carbon dioxide sensitivities averaged 0.50 +/- 0.08 (control) and 0.28 +/- 0.05 l.min-1.mmHg-1 (isoflurane; P < 0.01). The central carbon dioxide sensitivities (control 1.20 +/- 0.12 vs. isoflurane 1.04 +/- 0.11 l.min-1.mmHg-1) and off-sets (control 36.0 +/- 0.1 mmHg vs. isoflurane 34.5 +/- 0.2 mmHg) did not differ between treatments. Study 2: Within 30 s of exposure to 0.1 MAC isoflurane, ventilation decreased significantly, from 17.7 +/- 1.6 (hypoxia, awake) to 15.0 +/- 1.5 l.min-1 (hypoxia, isoflurane). Study 3: At the initiation of hypoxia ventilation increased by 7.7 +/- 1.4 (control), 4.1 +/- 0.8 (0.1 MAC; P < 0.05 vs. control), and 2.8 +/- 0.6 (0.2 MAC; P < 0.05 vs. control) l.min-1. The subsequent ventilatory decrease averaged 4.9 +/- 0.8 (control), 3.4 +/- 0.5 (0.1 MAC; difference not statistically significant), and 2.0 +/- 0.4 (0.2 MAC; P < 0.05 vs. control) l.min-1. There was a good correlation between the acute hypoxic response and the hypoxic ventilatory decrease (r = 0.9; P < 0.001). Conclusions The results of all three studies indicate a selective and profound effect of subanesthetic isoflurane on the peripheral chemoreflex loop at the site of the peripheral chemoreceptors. We relate the reduction of the ventilatory decrease of sustained hypoxia to the decrease of the initial ventilatory response to hypoxia.

Fetal chemoreception: a developing story

1996 ◽  
Vol 8 (3) ◽  
pp. 471 ◽  
Author(s):  
DF Teitel
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Current Knowledge ◽  
Chemical Stimulus ◽  
Lung Inflation ◽  
Ventilatory Responses ◽  
Central Inhibition ◽  
Chemical Stimuli ◽  
The Difference ◽  
Efficient Uptake

The central and peripheral chemoreceptors are critical to the efficient uptake and delivery of oxygen and the removal of carbon dioxide after birth. However, the importance and activity of fetal chemoreception has been questioned, since oxygen uptake and carbon dioxide removal are not regulated in the lungs in the fetus. Early studies suggested that chemotransduction-the conversion of a chemical stimulus to cardiovascular and ventilatory responses via the integration of chemoreceptor stimulation, neural afferent activity and neurohormonal effector mechanisms-was immature in its individual components or their interaction. However, it now appears that the chemoreceptor cascade is structurally and functionally intact in the late-term fetus, and responds actively to normal and other chemical stimuli. The differences between fetal and postnatal chemotransduction appear to be primarily dependent on the central inhibition of the ventilatory response, the inhibitory area being localized to the lateral pons. It appears to be mediated in part by a placental factor which is removed at birth, allowing for the expression of the ventilatory response. The suppression of this response is also responsible for the difference in the heart rate response: the postnatal tachycardia is caused by the lung inflation reflex; when abolished, bradycardia is seen, just as in the fetus. Despite the suppression of the ventilatory component of chemoreception, the fetal carotid chemoreceptor is more important than the aortic, even though it has been considered to be more important to ventilatory than to cardiovascular stability. This review discusses current knowledge of the various components of the mature chemoreceptor cascade, and presents the fetal story within that framework.

scholarly journals Ventilatory responses to acute hypoxia and hypercapnia in humans with a patent foramen ovale

2019 ◽  
Vol 126 (3) ◽  
pp. 730-738 ◽  
Author(s):  
James T. Davis ◽  
Lindsey M. Boulet ◽  
Alyssa M. Hardin ◽  
Alex J. Chang ◽  
Andrew T. Lovering ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
High Altitude ◽  
Patent Foramen Ovale ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Acute Exposure ◽  
Foramen Ovale ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
Peripheral Chemoreflex

Subjects with a patent foramen ovale (PFO) have blunted ventilatory acclimatization to high altitude compared with subjects without PFO. The blunted response observed could be because of differences in central and/or peripheral respiratory chemoreflexes. We hypothesized that compared with subjects without a PFO (PFO−), subjects with a PFO (PFO+) would have blunted ventilatory responses to acute hypoxia and hypercapnia. Sixteen PFO+ subjects (9 female) and 15 PFO− subjects (8 female) completed four 20-min trials on the same day: 1) normoxic hypercapnia (NH), 2) hyperoxic hypercapnia (HH), 3) isocapnic hypoxia (IH), and 4) poikilocapnic hypoxia (PH). Hypercapnic trials were completed before the hypoxic trials, the order of the hypercapnic (NH & HH) and hypoxic (IH & PH) trials were randomized, and trials were separated by ≥40 min. During the NH trials but not the HH trials subjects who were PFO+ had a blunted hypercapnic ventilatory response compared with subjects who were PFO− (1.41 ± 0.46 l·min−1·mmHg−1 vs. 1.98 ± 0.71 l·min−1·mmHg−1, P = 0.02). There were no differences between the PFO+ and PFO− subjects with respect to the acute hypoxic ventilatory response during IH and PH trials. Hypoxic ventilatory depression was similar between subjects who were PFO+ and PFO− during IH. These data suggest that compared with subjects who were PFO−, subjects who were PFO+ have normal ventilatory chemosensitivity to acute hypoxia but blunted ventilatory chemosensitivity to carbon dioxide, possibly because of reduced carbon dioxide sensitivity of either the central and/or the peripheral chemoreceptors. NEW & NOTEWORTHY Patent foramen ovale (PFO) is found in ~25%–40% of the population. The presence of a PFO appears to be associated with blunted ventilatory responses during acute exposure to normoxic hypercapnia. The reason for this blunted ventilatory response during acute exposure to normoxic hypercapnia is unknown but may suggest differences in either central and/or peripheral chemoreflex contribution to hypercapnia.

Effect of mechanical factors on respiratory work and ventilatory responses to CO2

1959 ◽  
Vol 14 (5) ◽  
pp. 721-726 ◽  
Author(s):  
Frederic Eldridge ◽  
John M. Davis
Keyword(s):  
Airway Resistance ◽  
Ventilatory Response ◽  
Work Of Breathing ◽  
Normal Subjects ◽  
Limiting Factor ◽  
Ventilatory Responses ◽  
Mechanical Factors ◽  
Respiratory Apparatus ◽  
End Tidal ◽  
Respiratory Stimulation

The end-tidal pCo2, mechanical work of breathing, and ventilation were determined in normal subjects breathing air, 2.2, 4.2 and 5.8 per cent Co2, with no added resistance and with three grades of added airway resistance. With increasing resistance, pCo2 and work rose in parallel whereas ventilation remained constant or even decreased. In the presence of a constant Co2 stimulus, increasing airway resistance caused a progressive decrease in ventilatory response to Co2. The maximum breathing capacity was not in itself the limiting factor in the ventilatory response to Co2. It is concluded that mechanical abnormalities of the respiratory apparatus are an important factor in reducing the ventilatory response to Co2, and that work of breathing is a more satisfactory index of respiratory stimulation than ventilation. Since patients with obstructive emphysema have nonelastic resistance values in the same range as those used in this study, it is concluded that the low ventilatory response to Co2 in these patients can, in large part, be explained by the mechanical abnormalities. Submitted on April 28, 1959

The Ventilatory Response to Carbon Dioxide in Asthmatic Children, Measured by the Mouth-Occlusion Method (PM100)

PEDIATRICS ◽  
1976 ◽  
Vol 57 (6) ◽  
pp. 952-959
Author(s):  
John F. Cosgrove ◽  
Naftoli Neuburger ◽  
Henry Levison
Keyword(s):  
Carbon Dioxide ◽  
Bronchial Asthma ◽  
Ventilatory Response ◽  
Carbon Dioxide Concentration ◽  
Forced Expiratory Volume ◽  
Healthy Children ◽  
Paradoxical Response ◽  
Asthmatic Children ◽  
Ventilatory Responses ◽  
The One

Ventilatory responses to carbon dioxide vary widely in patients with bronchial asthma; some have a high response despite increased airway resistance. This paradoxical response was studied in 31 asthmatic children and 22 age-matched healthy children. Measurement of the ventilatory response to carbon dioxide with a conventional rebreathing method showed wide variation in the patients, paralleling the degree of their airway obstruction as measured by the one-second forced expiratory volume and maximal midexpiratory flow rate, but their mean response was similar to that in the control subjects. The ventilatory response was then determined with a new index (PM100), which rises linearly with increasing carbon dioxide concentration. Despite wide variation in the slope of PM100 in the patients, their mean response significantly exceeded normal, confirming that the neurochemical drive is increased in bronchial asthma.

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