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.

Effects of inspiratory elastic load on respiratory control in hypercapnia and exercise

1989 ◽  
Vol 66 (5) ◽  
pp. 2400-2406 ◽  
Author(s):  
C. S. Poon
Keyword(s):  
Steady State ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Occlusion Pressure ◽  
Stimulus Input ◽  
Elastic Load ◽  
Co2 Output ◽  
End Tidal ◽  
Inspiratory Load

Five healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with a discontinuous inspiratory elastic load (IEL) of approximately 10 cmH2O/l. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0–5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE-VCO2) relationship in NL and IEL. Compared with NL, the VE-VCO2 slope was depressed by IEL, more so in hypercapnic [-28.7 +/- 7.2 (SE) %] than in eucapnic exercise (-16.0 +/- 2.8%). The steady-state hypercapnic ventilatory response at rest was also markedly depressed (-32.1 +/- 11.2%). Occlusion pressure response was augmented in response to IEL during eucapnic exercise (88.7 +/- 13.3%) but not during CO2 inhalation at rest or during exercise. Breathing pattern characteristics were similar regardless of the type of stimulus input and the level of inspiratory load. Results are consistent with the notion that the control of VE and breathing pattern may both be influenced by a balance between the prevailing chemical drive and a propensity of the controller to reduce respiratory effort.

Effects of inspiratory resistive load on respiratory control in hypercapnia and exercise

1989 ◽  
Vol 66 (5) ◽  
pp. 2391-2399 ◽  
Author(s):  
C. S. Poon
Keyword(s):  
Steady State ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Resistive Load ◽  
Occlusion Pressure ◽  
Inspiratory Time ◽  
Co2 Output ◽  
End Tidal ◽  
Inspiratory Load

Eight healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with an inspiratory resistive load (IRL) of approximately 12 cmH2O.1–1.s. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0–5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE - VCO2) relationship in NL and IRL. Compared with NL, the VE - VCO2 slope was depressed by IRL, more so in hypercapnic [-19.0 +/- 3.4 (SE) %] than in eucapnic exercise (-6.0 +/- 2.0%), despite a similar increase in the slope of the occlusion pressure at 100 ms - VCO2 (P100 - VCO2) relationship under both conditions. The steady-state hypercapnic ventilatory response at rest was markedly depressed by IRL (-22.6 +/- 7.5%), with little increase in P100 response. For a given inspiratory load, breathing pattern responses to separate or combined hypercapnia and exercise were similar. During IRL, VE was achieved by a greater tidal volume (VT) and inspiratory duty cycle (TI/TT) along with a lower mean inspiratory flow (VT/TI). The increase in TI/TT was solely because of a prolongation of inspiratory time (TI) with little change in expiratory duration for any given VT. The ventilatory and breathing pattern responses to IRL during CO2 inhalation and exercise are in favor of conservation of respiratory work.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

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.

Effect of sleep and sleep deprivation on ventilatory response to bronchoconstriction

1990 ◽  
Vol 69 (2) ◽  
pp. 490-497 ◽  
Author(s):  
R. D. Ballard ◽  
W. C. Tan ◽  
P. L. Kelly ◽  
J. Pak ◽  
R. Pandey ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Airway Resistance ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lower Airway ◽  
Occlusion Pressure ◽  
Arousal Threshold ◽  
Asthmatic Patients ◽  
Ventilatory Responses ◽  
Normal Sleep

To characterize ventilatory responses to bronchoconstriction during sleep and to assess the effect of prior sleep deprivation on ventilatory and arousal responses to bronchoconstriction, bronchoconstriction was induced in eight asthmatic subjects while they were awake, during normal sleep, and during sleep after a 36-h period of sleep deprivation. Each subject was bronchoconstricted with increasing concentrations of aerosolized methacholine while ventilatory patterns and lower airway resistance (Rla) were continually monitored. The asthmatic patients maintained their minute ventilation as Rla increased under all conditions, demonstrating a stable tidal volume with a mild increase in respiratory frequency. Inspiratory drive, as measured by occlusion pressure (P0.1), increased progressively and significantly as Rla increased under all conditions (slopes of P0.1 vs. Rla = 0.249, 0.112, and 0.154 for awake, normal sleep, and sleep after sleep deprivation, respectively, P less than 0.0006). Chemostimuli did not appear to contribute significantly to the observed increases in P0.1. Prior sleep deprivation had no effect on ventilatory and P0.1 responses to bronchoconstriction but did significantly raise the arousal threshold to induced bronchoconstriction. We conclude that ventilatory responses to bronchoconstriction, unlike extrinsic loading, are not imparied by the presence of sleep, nor are they chemically mediated. However, prior sleep deprivation does increase the subsequent arousal threshold.

Awake baboon's ventilatory response to venous and inhaled CO2 loading

1975 ◽  
Vol 39 (3) ◽  
pp. 417-422 ◽  
Author(s):  
S. M. Lewis
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Venous Blood ◽  
Minute Volume ◽  
Arteriovenous Shunt ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Change In Mean

Steady-state ventilatory responses to CO2 in trained awake baboons were studied to determine the response to a venous CO2 load. CO2 was loaded either directly into the venous blood through an arteriovenous shunt or by addition to the inhaled air. The two modes of loading were adjusted to produce the same increase in minute volume. Minute volume, tidal volume respiratory frequency, end-tidal PCO2, PaCO2, and pHa were measured. PaCO2 and PETCO2 increased the same amount during the two modes of CO2 loading; thus, the response to changes in arterial PCO2, deltaVE/deltaPaCO2, was the same. I conclude that the ventilatory response to venous CO2 loading occurs only through the change in mean arterial PCO2 and thus it is unlikely that there are any important venous CO2 receptors.

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

Effect of ketamine on control of breathing in cats

1983 ◽  
Vol 55 (3) ◽  
pp. 851-859 ◽  
Author(s):  
N. Jaspar ◽  
M. Mazzarelli ◽  
C. Tessier ◽  
J. Milic-Emili
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Time Profile ◽  
Occlusion Pressure ◽  
Tracheal Occlusion ◽  
Co2 Partial Pressure ◽  
Convex Upward ◽  
End Tidal ◽  
Ventilatory Response To Co2

We studied minute ventilation, breathing pattern, end-tidal CO2 partial pressure (PACO2), and tracheal occlusion pressure in cats anesthetized with ketamine (40 and 80 mg/kg) before and after CO2 inhalation. Before CO2 administration ventilation was reduced and PACO2 increased relative to unanesthetized cats at both ketamine doses. Breathing pattern was of the “apneustic” type, being characterized by 1) prolonged inspiratory duration and relatively short expiratory time and 2) markedly curvilinear (convex upward) inspiratory volume-time profile. The latter reflected a similar curvilinearity in the tracheal occlusion pressure waveform. During CO2 inhalation, the ventilatory response to CO2 was similar to that in unanesthetized cats in spite of a depressed tracheal occlusion pressure response. This discrepancy was due to the fact that in the presence of a convex upward inspiratory volume-time profile, the shortening of inspiratory duration with increasing CO2 results in a marked increase of mean inspiratory flow, and hence the ventilatory response to CO2 remains high.

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.

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