scholarly journals Deep-breath frequency in bronchoconstricted monkeys (Macaca fascicularis)

2006 ◽  
Vol 100 (3) ◽  
pp. 786-791 ◽  
Author(s):  
Joseph M. Dybas ◽  
Catharine J. Andresen ◽  
Edward S. Schelegle ◽  
Ryan W. McCue ◽  
Natasha N. Callender ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Macaca Fascicularis ◽  
Minute Ventilation ◽  
Mechanical Resistance ◽  
External Resistance ◽  
Deep Breath ◽  
Ventilatory Parameters ◽  
Tissue Compliance ◽  
Airway Opening

Deep-breath frequency has been shown to increase in spontaneously obstructed asthmatic subjects. Furthermore, deep breaths are known to be regulated by lung rapidly adapting receptors, yet the mechanism by which these receptors are stimulated is unclear. This study tested the hypothesis that deep-breath frequency increases during experimentally induced bronchoconstriction, and the magnitude of the increased deep-breath frequency is dependent on the method by which bronchoconstriction is induced. Nine cynomolgus monkeys ( Macaca fascicularis) were challenged with methacholine (MCh), Ascaris suum (AS), histamine, or an external mechanical resistance. Baseline (BL) and challenge deep-breath frequency were calculated from the number of deep breaths per trial period. Airway resistance (Raw) and tissue compliance (Cti), as well as tidal volume, respiratory rate, and minute ventilation, were analyzed for BL and challenged conditions. Transfer impedance measurements were fit with the DuBois model to determine the respiratory parameters (Raw and Cti). The flow at the airway opening was measured and analyzed on a breath-by-breath basis to obtain the ventilatory parameters (tidal volume, respiratory rate, and minute ventilation). Deep-breath frequency resulting from AS and histamine challenges [0.370 (SD 0.186) and 0.467 breaths/min (SD 0.216), respectively] was significantly increased compared with BL, MCh, or external resistance challenges [0.61 (SD 0.046), 0.156 (SD 0.173), and 0.117 breaths/min (SD 0.082), respectively]. MCh and external resistance challenges resulted in insignificant changes in deep-breath frequency compared with BL. All four modalities produced similar levels of bronchoconstriction, as assessed through changes in Raw and Cti, and had similar effects on the ventilatory parameters except that non-deep-breath tidal volume was decreased in AS and histamine. We propose that increased deep-breath frequency during AS and histamine challenge is the result of increased vascular permeability, which acts to increase rapidly adapting receptor activity.

scholarly journals Nasal high flow reduces minute ventilation during sleep through a decrease of carbon dioxide rebreathing

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Ventilation ◽  
Control Ventilation ◽  
High Flow ◽  
Carbon Dioxide Rebreathing ◽  
Anatomical Dead Space

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.

Mechanical Ventilation: Basic Modes

2019 ◽  
pp. 10-16
Author(s):  
Amelia A. Lowell
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Airway Pressure ◽  
Minute Ventilation ◽  
Respiratory Muscles ◽  
Supplemental Oxygen ◽  
Alveolar Ventilation ◽  
Arterial Oxygenation ◽  
Mean Airway Pressure

The main goal of mechanical ventilation is to unload the respiratory muscles to facilitate oxygenation and ventilation. This is accomplished by providing a minute ventilation (VE) (respiratory rate × tidal volume [VT]) that will result in adequate alveolar ventilation coupled with supplemental oxygen and a mean airway pressure that will result in adequate arterial oxygenation.

Ventilatory responses to repeated short hypercapnic challenges

1995 ◽  
Vol 78 (4) ◽  
pp. 1374-1381 ◽  
Author(s):  
D. Gozal ◽  
J. H. Ben-Ari ◽  
R. M. Harper ◽  
T. G. Keens
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Minute Ventilation ◽  
Breathing Patterns ◽  
Ventilatory Strategy ◽  
Continuous Increase ◽  
Ventilatory Responses ◽  
Central Controller ◽  
Controller Gain

In early phases of respiratory disease, patients are more likely to experience intermittent hypercapnia than a continuous increase in PCO2. The effect of intermittent arterial PCO2 elevation on subsequent breathing patterns is unclear. To examine this issue, a series of six ventilatory challenges (CH1-CH6), consisting of 2 min of breathing 5% CO2 in O2, followed by 5 min in room air (RA) were performed in 10 naive healthy subjects (age 12–39 yr). Minute ventilation (VE) increased from 11.9 +/- 1.0 (SE) l/min in RA to 27.6 +/- 3.0 l/min in 5% CO2 (P < 0.0005) in each of the six hypercapnic challenges. Respiratory rate increased from 21.3 +/- 2.6 breaths/min on RA to 29.6 +/- 3.9 breaths/min during CH1 (P < 0.05). However, respiratory rate consistently decreased with successive CO2 challenges (CH6: 21.5 +/- 2.6 breaths/min; P < 0.02). Thus, maintenance of VE was achieved by gradual increases in tidal volume with each of the first four consecutive CO2 challenges (CH1: 1.05 +/- 0.09 liters; CH4: 1.44 +/- 0.13 liters; P < 0.002). Similarly, the ratio of tidal volume to inspiratory time increased from CH1 (1.16 +/- 0.16 l/s) to CH6 (1.57 +/- 0.21 l/s; P < 0.001). These changes in ventilatory strategy were not observed when RA recovery periods were extended to 15 min in five subjects. We conclude that during repeated short hypercapnic challenges similar levels of VE are achieved. However, increased mean inspiratory flows are generated to maintain VE. We speculate that intermittent hypercapnia either modifies central controller gain or induces a long-term modulatory effect to account for the progressive changes in ventilatory components.

Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs

1985 ◽  
Vol 59 (3) ◽  
pp. 869-874 ◽  
Author(s):  
M. A. Bureau ◽  
J. Lamarche ◽  
P. Foulon ◽  
D. Dalle
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Occlusion Pressure ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Postnatal Maturation ◽  
Arterial Po2

The contribution of the carotid body chemoreceptor to postnatal maturation of breathing was evaluated in lambs from 7 to 70 days of age. The study was conducted by comparing the eupneic ventilation and resting pneumograms in intact conscious lambs with those of lambs that were carotid body chemodenervated (CBD) at birth. In comparison to the 1-wk-old intact lambs, the CBD lambs had significant decreases in minute ventilation (VE, 313 vs. 517 ml/kg), tidal volume (VT, 7.2 vs. 10.5 ml/kg), respiratory rate (f, 44 vs. 51 breaths/min), and occlusion pressure (P0.1, 2.8 vs. 7.2 cmH2O). Arterial PO2's were 59 vs. 75 Torr (P less than 0.05) and arterial PCO2's 47 vs. 36 Torr (P less than 0.05), respectively, in CBD and intact lambs. In intact lambs from 7 to 70 days, resting VE decreased progressively from 517 to 274 ml/kg (P less than 0.01) due to a fall in VT, mean inspiratory flow (VT/TI), and f, whereas the ratio of inspiratory time to total breath duration remained constant. P0.1 decreased from 7.2 to 3.9 cmH2O from 7 to 42 days. In contrast the CBD lambs experienced only minimal changes in VE, VT, VT/TI, and f during the same period. VE only decreased from 313 to 218 and P0.1 from 2.8 to 2.4 cmH2O. In contrast to that of intact lambs the resting pneumogram of CBD lambs remained relatively fixed from 7 to 70 days. Three CBD lambs died unexpectedly, without apparent cause, in the 4th and 5th wk of life.

Hyperoxic exposure affects the ventilatory response to hypoxia in awake rats

1988 ◽  
Vol 64 (1) ◽  
pp. 181-186 ◽  
Author(s):  
R. Arieli ◽  
D. Kerem ◽  
Y. Melamed
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hyperoxic Exposure ◽  
Ventilatory Parameters ◽  
Ventilatory Drive ◽  
Co2 Balance ◽  
Hyperbaric O2 ◽  
Hyperbaric Exposure ◽  
Ventilatory Response To Hypoxia

We tested whether hyperbaric O2 (HBO) has an adverse effect on the hypoxic ventilatory drive. Four groups of rats were exposed for 550 min to O2 at 1.67, 1.90, and 2.15 ATA and to air at 1.90 ATA, respectively. Ventilatory parameters (frequency, tidal volume, and minute ventilation) were measured using whole-body plethysmography, before the hyperbaric exposure, immediately after the exposure, and up to 20 days after the exposure. Resting ventilation was not affected after exposure at 1.90 ATA to air or at 1.67 ATA to O2. HBO at 1.90 and 2.15 ATA caused a reduction of frequency and an elevation of tidal volume at different inspired gases: air, 5% CO2 balance O2, 80% O2, and 4.5% O2. However, minute ventilation on the day after the hyperoxic exposure was not different from the control at either air, 5% CO2, or 80% O2 but was markedly attenuated on the first three breaths at 4.5% O2. The hypoxic ventilation decreased to 48 +/- 13 (SD) and 32 + 11% after 1.90 and 2.15 ATA, respectively. The ventilatory parameters recovered in the days after HBO. We conclude that HBO reversibly depresses the hypoxic ventilatory drive, most probably by a direct effect on the carotid O2 chemoreceptors.

Obesity, tidal volume, and pulmonary deposition of fine particulate matter in children with asthma

2021 ◽  
pp. 2100209
Author(s):  
Nima Afshar-Mohajer ◽  
Tianshi David Wu ◽  
Rebecca Shade ◽  
Emily Brigham ◽  
Han Woo ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Minute Ventilation ◽  
Fine Particulate Matter ◽  
Breathing Patterns ◽  
Obese Children ◽  
Fine Particulate ◽  
Children With Asthma

BackgroundObese children with asthma are more vulnerable to air pollution, especially fine particulate matter (PM2.5), but reasons are poorly understood. We hypothesised that differences in breathing patterns (tidal volume, respiratory rate, and minute ventilation) due to elevated body mass index (BMI) may contribute to this finding.ObjectiveTo investigate the association of BMI with breathing patterns and deposition of inhaled PM2.5.MethodsBaseline data from a prospective study of children with asthma was analysed (n=174). Tidal breathing was measured by a pitot-tube flowmeter, from which tidal volume, respiratory rate, and minute ventilation were obtained. The association of BMI z-score with breathing patterns was estimated in a multivariable model adjusted for age, height, race, sex, and asthma severity. A particle dosimetry model simulated PM2.5 lung deposition based on BMI-associated changes in breathing patterns.ResultsHigher BMI was associated with higher tidal volume (adjusted mean difference [aMD] between obese and normal-range BMI of 25 mL, 95% confidence interval [CI] 5–45 mL) and minute ventilation (aMD 453 mL·min−1, 95%CI 123–784 mL·min−1). Higher tidal volumes caused higher fractional deposition of PM2.5 in the lung, driven by greater alveolar deposition. This translated into obese participants having greater per-breath retention of inhaled PM2.5 (aMD in alveolar deposition fraction of 3.4%; 95% CI 1.3–5.5%), leading to worse PM2.5 deposition rates.ConclusionsObese children with asthma breathe at higher tidal volumes that may increase the efficiency of PM2.5 deposition in the lung. This finding may partially explain why obese children with asthma exhibit greater sensitivity to air pollution.

scholarly journals Mechanisms of nasal high flow on ventilation during wakefulness and sleep

2013 ◽  
Vol 114 (8) ◽  
pp. 1058-1065 ◽  
Author(s):  
Toby Mündel ◽  
Sheng Feng ◽  
Stanislav Tatkov ◽  
Hartmut Schneider
Keyword(s):  
Nasal Cavity ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Minute Ventilation ◽  
High Flow ◽  
Cavity Model ◽  
Ventilatory Responses ◽  
State Dependent ◽  
Inspiratory Resistance ◽  
Wake State

Nasal high flow (NHF) has been shown to increase expiratory pressure and reduce respiratory rate but the mechanisms involved remain unclear. Ten healthy participants [age, 22 ± 2 yr; body mass index (BMI), 24 ± 2 kg/m2] were recruited to determine ventilatory responses to NHF of air at 37°C and fully saturated with water. We conducted a randomized, controlled, cross-over study consisting of four separate ∼60-min visits, each 1 wk apart, to determine the effect of NHF on ventilation during wakefulness (NHF at 0, 15, 30, and 45 liters/min) and sleep (NHF at 0, 15, and 30 liters/min). In addition, a nasal cavity model was used to compare pressure/air-flow relationships of NHF and continuous positive airway pressure (CPAP) throughout simulated breathing. During wakefulness, NHF led to an increase in tidal volume from 0.7 ± 0.1 liter to 0.8 ± 0.2, 1.0 ± 0.2, and 1.3 ± 0.2 liters, and a reduction in respiratory rate ( fR) from 16 ± 2 to 13 ± 3, 10 ± 3, and 8 ± 3 breaths/min (baseline to 15, 30, and 45 liters/min NHF, respectively; P < 0.01). In contrast, during sleep, NHF led to a ∼20% fall in minute ventilation due to a decrease in tidal volume and no change in fR. In the nasal cavity model, NHF increased expiratory but decreased inspiratory resistance depending on both the cannula size and the expiratory flow rate. The mechanisms of action for NHF differ from those of CPAP and are sleep/wake-state dependent. NHF may be utilized to increase tidal breathing during wakefulness and to relieve respiratory loads during sleep.

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