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.

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.

scholarly journals Impact of cervical spinal cord contusion on the breathing pattern across the sleep-wake cycle in the rat

2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee
Keyword(s):  
Spinal Cord ◽  
Tidal Volume ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Breathing Patterns ◽  
Cord Injury ◽  
Spinal Contusion ◽  
Cervical Spinal Injury

The present study was designed to investigate breathing patterns across the sleep-wake state following a high cervical spinal injury in rats. The breathing patterns (e.g., respiratory frequency, tidal volume, and minute ventilation), neck electromyogram, and electroencephalography of unanesthetized adult male rats were measured at the acute (i.e., 1 day), subchronic (i.e., 2 wk), and/or chronic (i.e., 6 wk) injured stages after unilateral contusion of the second cervical spinal cord. Cervical spinal cord injury caused a long-term reduction in the tidal volume but did not influence the sleep-wake cycle duration. The minute ventilation during sleep was usually lower than that during the wake period in uninjured animals due to a decrease in respiratory frequency. However, this sleep-induced reduction in respiratory frequency was not observed in contused animals at the acute injured stage. By contrast, the tidal volume was significantly lower during sleep in contused animals but not uninjured animals from the acute to the chronic injured stage. Moreover, the frequency of sigh and postsigh apnea was elevated in acutely contused animals. These results indicated that high cervical spinal contusion is associated with exacerbated sleep-induced attenuation of the tidal volume and higher occurrence of sleep apnea, which may be detrimental to respiratory functional recovery after cervical spinal cord injury. NEW & NOTEWORTHY Cervical spinal injury is usually associated with sleep-disordered breathing. The present study investigated breathing patterns across sleep-wake state following cervical spinal injury in the rat. Unilateral cervical spinal contusion significantly impacted sleep-induced alteration of breathing patterns, showing a blunted frequency response and exacerbated attenuated tidal volume and occurrence of sleep apnea. The result enables us to investigate effects of cervical spinal injury on the pathogenesis of sleep-disordered breathing and evaluate potential therapies to improve respiration.

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 Micron-sized intrapulmonary particle deposition in the developing rat lung

2012 ◽  
Vol 112 (5) ◽  
pp. 759-765
Author(s):  
Holger Schulz ◽  
Gunter Eder ◽  
Ines Bolle ◽  
Akira Tsuda ◽  
Stefan Karrasch
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Surface Area ◽  
Lung Development ◽  
Particle Deposition ◽  
Structural Changes ◽  
Breathing Patterns ◽  
Respiratory Parameters ◽  
Wistar Kyoto ◽  
Postnatal Lung Development

Little is known about the effects of postnatal developmental changes in lung architecture and breathing patterns on intrapulmonary particle deposition. We measured deposition in the developing Wistar-Kyoto rat, whose lung development largely parallels that of humans. Deposition of 2-μm sebacate particles was determined in anesthetized, intubated, spontaneously breathing rats on postnatal days (P) 7 to 90 by aerosol photometry (Karrasch S, Eder G, Bolle I, Tsuda A, Schulz H. J Appl Physiol 107: 1293–1299, 2009). Respiratory parameters were determined by body plethysmography. Tidal volume increased substantially from P7 (0.19 ml) to P90 (2.1 ml) while respiratory rate declined from 182 to 107/min. Breath-specific deposition was lowest (9%) at P7 and P90 and markedly higher at P35 (almost 16%). Structural changes of the alveolar region include a ninefold increase in surface area (Bolle I, Eder G, Takenaka S, Ganguly K, Karrasch S, Zeller C, Neuner M, Kreyling WG, Tsuda A, Schulz H. J Appl Physiol 104: 1167–1176, 2008). Particle deposition per unit of time and surface area peaked at P35 and showed a minimum at P90. At an inhaled particle number concentration of 105/cm3, there was an estimated 450, 690, and 330 particles/(min × cm2) at P7, P35, and P90, respectively. Multiple regression models showed that deposition depends on the mean linear intercept as structural component and the breathing parameters, tidal volume, and respiratory rate ( r2 > 0.9). In conclusion, micron-sized particle deposition was dependent on the stage of postnatal lung development. A maximum was observed during late alveolarization (P35), which corresponds to human lungs of about eight years of age. Children at this age may therefore be more susceptible to micron-sized airborne environmental health hazards.

Effect of respiratory apparatus on respiration

1984 ◽  
Vol 57 (2) ◽  
pp. 475-480 ◽  
Author(s):  
C. Weissman ◽  
J. Askanazi ◽  
J. Milic-Emili ◽  
J. M. Kinney
Keyword(s):  
Tidal Volume ◽  
Duty Cycle ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Percentage Increase ◽  
Breathing Patterns ◽  
Normal Volunteers ◽  
Abdominal Operation ◽  
Respiratory Apparatus

A mouthpiece plus noseclip (MP & NC) is frequently used in performing measurements of breathing patterns. Although the effects the apparatus exerts on breathing patterns have been studied, the mechanism of the changes it causes remains unclear. The current study examines the effects on respiratory patterns of a standard (17-mm-diam) MP & NC during room air (RA) breathing and the administration of 2 and 4% CO2 in normal volunteers and in patients 2–4 days after abdominal operation. When compared with values obtained with a noninvasive canopy system, the MP & NC induced increases in minute ventilation (VE), tidal volume (VT), and mean inspiratory flow (VT/TI), but not frequency (f) or inspiratory duty cycle, during both RA and CO2 administration. The percentage increase in VE, VT, and VT/TI caused by the MP & NC decreased as the concentration of CO2 increased. During RA breathing, the application of noseclip alone resulted in a decrease in f and an increase in VT, but VE and VT/TI were unchanged. The changes were attenuated during the administration of 2 and 4% CO2. Reducing the diameter of the mouthpiece to 9 mm abolished the alterations in breathing pattern observed with the larger (17-mm) diameter MP.

scholarly journals Ventilatory responses during and following hypercapnic gas challenge are impaired in male but not female endothelial NOS knock-out mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulina M. Getsy ◽  
Sripriya Sundararajan ◽  
Walter J. May ◽  
Graham C. von Schill ◽  
Dylan K. McLaughlin ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Inspiratory Time ◽  
Male And Female ◽  
Knock Out ◽  
Ventilatory Responses ◽  
Knock Out Mice ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractThe roles of endothelial nitric oxide synthase (eNOS) in the ventilatory responses during and after a hypercapnic gas challenge (HCC, 5% CO2, 21% O2, 74% N2) were assessed in freely-moving female and male wild-type (WT) C57BL6 mice and eNOS knock-out (eNOS-/-) mice of C57BL6 background using whole body plethysmography. HCC elicited an array of ventilatory responses that were similar in male and female WT mice, such as increases in breathing frequency (with falls in inspiratory and expiratory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flows, and inspiratory and expiratory drives. eNOS-/- male mice had smaller increases in minute ventilation, peak inspiratory flow and inspiratory drive, and smaller decreases in inspiratory time than WT males. Ventilatory responses in female eNOS-/- mice were similar to those in female WT mice. The ventilatory excitatory phase upon return to room-air was similar in both male and female WT mice. However, the post-HCC increases in frequency of breathing (with decreases in inspiratory times), and increases in tidal volume, minute ventilation, inspiratory drive (i.e., tidal volume/inspiratory time) and expiratory drive (i.e., tidal volume/expiratory time), and peak inspiratory and expiratory flows in male eNOS-/- mice were smaller than in male WT mice. In contrast, the post-HCC responses in female eNOS-/- mice were equal to those of the female WT mice. These findings provide the first evidence that the loss of eNOS affects the ventilatory responses during and after HCC in male C57BL6 mice, whereas female C57BL6 mice can compensate for the loss of eNOS, at least in respect to triggering ventilatory responses to HCC.

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.

The Effect of Temperature and Hypoxia Hypercapnia on the Respiratory Pattern of the Unrestrained Lizard, Pogona Vitticeps

1995 ◽  
Vol 43 (2) ◽  
pp. 165 ◽  
Author(s):  
S Crafter ◽  
MI Soldini ◽  
CB Daniels ◽  
AW Smits
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Work Of Breathing ◽  
Average Frequency ◽  
Respiratory Pattern ◽  
Effect Of Temperature ◽  
Breath Holding ◽  
Breathing Patterns ◽  
Pogona Vitticeps ◽  
Lower Temperature

The effect of altering body temperature and the oxygen and carbon dioxide composition of inspired air on the respiratory pattern of the unrestrained lizard Pogona vitticeps was determined using pneumotachometry that did not require restraining the animal. P. vitticeps demonstrated a typical reptilian breathing pattern of groups of breaths separated by periods of breath-holding. Respiratory patterns were measured at 18 degrees C and at 37 degrees C. Minute ventilation decreased at the lower temperature as a result of a decrease in average frequency. Tidal volume was temperature independent. The change in average frequency resulted from both a decrease in the instantaneous inspiratory time and an increase in the time spent in a non-ventilatory period. As a result, the work of breathing was less at 18 degrees C than at 37 degrees C. With the exception of tidal volume, breathing patterns were independent of changes to the composition of inspired air. At both 18 degrees C and 37 degrees C, inspiring a 5% CO2/13% O-2/82% N-2 gas mixture increased tidal volume but did not increase minute ventilation.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

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