Aerosol anesthesia increases hypercapnic ventilation and breathlessness in laryngectomized humans

1987 ◽  
Vol 63 (6) ◽  
pp. 2286-2292 ◽  
Author(s):  
R. D. Hamilton ◽  
A. J. Winning ◽  
A. Perry ◽  
A. Guz
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lower Airway ◽  
Saline Control ◽  
Healthy Male ◽  
Analog Scale ◽  
Cough Reflex ◽  
Vas Scores ◽  
Male Subjects ◽  
Ventilatory Response To Co2

The effect of local anesthetic aerosol inhalation on the ventilatory response and the sensation of breathlessness to CO2 rebreathing was studied in seven healthy male subjects with permanent tracheal stomas after laryngectomy for carcinoma. Inhalation of bupivacaine aerosol sufficient to abolish the cough reflex to mechanical probing below the carina increased the ventilatory response to CO2 in six of seven subjects compared with saline control. This was achieved by an increase in both respiratory frequency (f) and tidal volume (VT) in four subjects, f in one subject, and VT in one subject. All subjects reported that they were more breathless on rebreathing after bupivacaine aerosol. The six subjects who recorded breathlessness with a visual analog scale (VAS) indicated its onset at a lower minute ventilation (VE) and gave higher VAS scores for equivalent levels of VE after threshold. We conclude that the enhanced CO2 sensitivity and breathlessness on rebreathing after airway anesthesia results from altered lower airway receptor discharge.

Effects of upper or lower airway anesthesia on hypercapnic ventilation in humans

1985 ◽  
Vol 59 (4) ◽  
pp. 1090-1097 ◽  
Author(s):  
P. A. Easton ◽  
C. Jadue ◽  
M. E. Arnup ◽  
R. C. Meatherall ◽  
N. R. Anthonisen
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Lower Airway ◽  
Saline Control ◽  
Inspiratory Time ◽  
Lidocaine Solution ◽  
Normal Humans ◽  
Receptor Block ◽  
Ventilatory Response To Co2

To evaluate the contribution of vagal airway receptors to ventilatory control during hypercapnia, we studied 11 normal humans. Airway receptor block was induced by inhaling an aerosol of lidocaine; a preferential upper oropharyngeal block was also induced in a subgroup by gargling a solution of the anesthetic. Inhalation of lidocaine aerosol adequate to increase cough threshold, as measured by citric acid, did not change the ventilatory response to CO2, ratio of the change in minute ventilation to change in alveolar PCO2 (delta VI/delta PACO2), compared with saline control. Breathing pattern at mean CO2-stimulated ventilation of 25 l/min showed significantly decreased respiratory frequency, increased tidal volume, and prolonged inspiratory time compared with saline. Resting breathing pattern also showed significantly increased tidal volume and inspiratory time. In nine of the same subjects gargling a lidocaine solution adequate to extinguish gag response without altering cough threshold did not change delta VI/delta PACO2 or ventilatory pattern during CO2-stimulated or resting ventilation compared with saline. These results suggest that lower but not upper oropharyngeal vagal airway receptors modulate breathing pattern during hypercapnic as well as resting ventilation but do not affect delta VI/delta PACO2.

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

Effects of oxygen inhalation on responses to cold exposure

1961 ◽  
Vol 16 (4) ◽  
pp. 627-632 ◽  
Author(s):  
D. M. Maccanon ◽  
D. D. Eitzman
Keyword(s):  
Cold Exposure ◽  
Ventilatory Response ◽  
Carbon Dioxide Production ◽  
Metabolic Responses ◽  
Body Temperatures ◽  
Healthy Male ◽  
Metabolic Heat ◽  
Oxygen Breathing ◽  
Oxygen Inhalation ◽  
Male Subjects

The effects of oxygen inhalation on shivering and thermal and metabolic responses to exposure to cold (10 C) were determined in ten healthy male subjects. The results showed that oxygen breathing reduced shivering and promoted a feeling of greater comfort. The ventilatory response to cold was diminished, and oxygen consumption was significantly lower during the later periods of the cold exposure. Carbon dioxide production was reduced and the mobilization of nitrogen during the initial periods of cold exposure was also noted. Since body temperatures and their rates of fall were not significantly altered by oxygen inhalation, a shift to more efficient metabolic heat production seems indicated. Submitted on February 6, 1961

Effect of Continuous Positive Airway Pressure on the Ventilatory Response to CO2 in Preterm Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ventilatory Response To Co2

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P < .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P > .1), but the intercept was shifted to the right (P < .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P < .05). In addition, transcutaneous Po2 increased during administration of CPAP (P < .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.

Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise

2008 ◽  
Vol 104 (4) ◽  
pp. 998-1005 ◽  
Author(s):  
Naoto Fujii ◽  
Yasushi Honda ◽  
Keiji Hayashi ◽  
Hideaki Soya ◽  
Narihiko Kondo ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Regression Line ◽  
Hot Water ◽  
Moderate Intensity ◽  
Initial Increase ◽  
Esophageal Temperature ◽  
Healthy Male ◽  
Moderate Intensity Exercise ◽  
Ventilatory Equivalent ◽  
Male Subjects

We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a water-perfused suit were used to increase esophageal temperature (Tes) in 19 healthy male subjects; in the exercise trial, Tes was increased by prolonged submaximal cycling [50% peak O2 uptake (V̇o2)] in the heat (35°C). Minute ventilation (V̇e), ventilatory equivalent for V̇o2 (V̇e/V̇o2) and CO2 output (V̇e/V̇co2), tidal volume (Vt), and respiratory frequency (f) were plotted as functions of Tes. In the exercise trial, V̇e increased linearly with increases (from 37.0 to 38.7°C) in Tes in all subjects; in the rest trial, 14 of the 19 subjects showed a Tes threshold for hyperpnea (37.8 ± 0.5°C). Above the threshold for hyperpnea, the slope of the regression line relating V̇e and Tes was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating V̇e/V̇o2, V̇e/V̇co2, and Tes were significantly greater for the rest than the exercise trial. The increase in V̇e reflected increases in Vt and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to Vt. Finally, the slope of the regression line relating Tes and Vt or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity.

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.

Effects of chest wall vibration on breathlessness during hypercapnic ventilatory response

1998 ◽  
Vol 84 (5) ◽  
pp. 1487-1491 ◽  
Author(s):  
Hidenori Edo ◽  
Hiroshi Kimura ◽  
Mafumi Niijima ◽  
Hideo Sakabe ◽  
Masato Shibuya ◽  
...  
Keyword(s):  
Chest Wall ◽  
Visual Analog Scale ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Vibratory Stimulation ◽  
Analog Scale ◽  
Hypercapnic Ventilatory Response ◽  
Mouth Occlusion Pressure ◽  
Inspiratory Load

Vibratory stimulation applied to the chest wall during inspiration reduces the intensity of breathlessness, whereas the same stimulation during expiration has no effect or may increase breathlessness. The purpose of the present study was to determine whether vibration reduced the intensity of breathlessness during progressive hypercapnia with and without the addition of an external resistive load. A second objective was to see whether the mouth occlusion pressure at 0.2 s (P0.2) was reduced by the vibratory stimulation. Hypercapnic ventilatory response was conducted in 10 healthy male volunteers with simultaneous measurement of visual analog scale, P0.2, and minute ventilation. Hypercapnic ventilatory response was performed and randomly combined with or without vibratory stimulation (100 Hz) as well as with or without inspiratory load. With inspiratory load, in-phase vibration did not cause any significant changes in the slopes of P0.2 and minute ventilation to CO2, whereas the slope of visual analog scale to CO2 significantly decreased from 0.47 ± 0.15 to 0.34 ± 0.11 (SE) cm/Torr ( P < 0.05). We conclude that in-phase vibration could decrease the slope of breathlessness elicited by inspiratory load combined with hypercapnia without changing motor output.

Chronic fluoxetine microdialysis into the medullary raphe nuclei of the rat, but not systemic administration, increases the ventilatory response to CO2

2004 ◽  
Vol 97 (5) ◽  
pp. 1763-1773 ◽  
Author(s):  
Natalie C. Taylor ◽  
Aihua Li ◽  
Adam Green ◽  
Hannah C. Kinney ◽  
Eugene E. Nattie
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Repeated Administration ◽  
Fluoxetine Treatment ◽  
Artificial Cerebrospinal Fluid ◽  
Medullary Raphe ◽  
Chronic Fluoxetine ◽  
Serotonergic Function ◽  
Ventilatory Response To Co2

In conscious rats, focal CO2 stimulation of the medullary raphe increases ventilation, whereas interference with serotonergic function here decreases the ventilatory response to systemic hypercapnia. We sought to determine whether repeated administration of a selective serotonin reuptake inhibitor in this region would increase the ventilatory response to hypercapnia in unanesthetized rats. In rats instrumented with electroencephalogram-electromyogram electrodes, 250 or 500 μM fluoxetine or artificial cerebrospinal fluid (aCSF) was microdialyzed into the medullary raphe for 30 min daily over 15 days. To compare focal and systemic treatment, two additional groups of rats received 10 mg·kg−1·day−1 fluoxetine or vehicle systemically. Ventilation was measured in normocapnia and in 7% CO2 before treatment ( day 0), acutely ( days 1 or 3), on day 7, and on day 15. There was no change in normocapnic ventilation in any treatment group. Rats that received 250 μM fluoxetine microdialysis showed a significant 13% increase in ventilation in wakefulness during hypercapnia on day 7, due to an increase in tidal volume. In rats microdialyzed with 500 μM fluoxetine, there were 16 and 32% increases in minute ventilation during hypercapnia in wakefulness and sleep on day 7, and 20 and 28% increases on day 15, respectively, again due to increased tidal volume. There was no change in the ventilatory response to CO2 in rats microdialyzed with aCSF or in systemically treated rats. Chronic fluoxetine treatment in the medullary raphe increases the ventilatory response to hypercapnia in an unanesthetized rat model, an effect that may be due to facilitation of chemosensitive serotonergic neurons.

DIDS decreases CSF HCO3- and increases breathing in response to CO2 in awake rabbits

1988 ◽  
Vol 64 (1) ◽  
pp. 397-403 ◽  
Author(s):  
E. E. Nattie ◽  
J. M. Adams
Keyword(s):  
Ventilatory Response ◽  
Ph Regulation ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Disulfonic Acid ◽  
Carrier Protein ◽  
Related Effect ◽  
Arterial Pco2 ◽  
Ionic Mechanisms ◽  
Ventilatory Response To Co2

An inhibitor of the HCO3-/Cl- exchange carrier protein, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) or vehicle was infused in mock cerebrospinal fluid (CSF) via the cisterna magna in conscious rabbits at 10 mumol/l for 40 min at 10 microliter/min. Neither treatment had any effect over 2-5 h on the non-CO2-stimulated CSF ion values or blood gases. With CO2 stimulation such that arterial PCO2 (PaCO2) was increased 25 Torr over 3 h, DIDS treatment significantly decreased the stoichiometrically opposite changes in CSF [HCO3-] and [Cl-] that normally accompany hypercapnia and reflect ionic mechanisms of CSF pH regulation. Expressed as delta CSF [HCO3-]/delta PaCO2, DIDS treatment decreased the CSF ionic response by 35%. In a separate paired study design DIDS administration via the same protocol had no effect on resting ventilation but significantly increased the ventilation and tidal volume responses to a 28-Torr increase in PaCO2. Expressed as change in minute ventilation divided by delta PaCO2, DIDS treatment produced a 39.6% increase. The results support the concept of a DIDS-inhibitable anion exchange carrier being involved in CSF pH regulation in hypercapnia and suggest a DIDS-related effect on the ventilatory response to CO2.

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.

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