A pharmacodynamic model of tidal volume and inspiratory sevoflurane concentration in children during spontaneous breathing

2021 ◽  
Author(s):  
Pyoyoon Kang ◽  
Ji-Hyun Lee ◽  
Young-Eun Jang ◽  
Eun-Hee Kim ◽  
Jin-Tae Kim ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Spontaneous Breathing ◽  
Pharmacodynamic Model ◽  
Sevoflurane Concentration

Augmentation of phrenic neural activity by increased rates of lung inflation

1981 ◽  
Vol 50 (1) ◽  
pp. 149-161 ◽  
Author(s):  
A. I. Pack ◽  
R. G. DeLaney ◽  
A. P. Fishman
Keyword(s):  
Tidal Volume ◽  
Volume Change ◽  
Neural Activity ◽  
Negative Pressure ◽  
Spontaneous Breathing ◽  
Moving Average ◽  
Constant Flow ◽  
Lung Inflation ◽  
Negative Pressure Ventilation ◽  
Single Breath

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.

scholarly journals Strain dependence of the airway response to dry-gas hyperpnea challenge in the rat

1999 ◽  
Vol 86 (1) ◽  
pp. 152-158 ◽  
Author(s):  
X. X. Yang ◽  
W. S. Powell ◽  
L. J. Xu ◽  
J. G. Martin
Keyword(s):  
Tidal Volume ◽  
Receptor Antagonist ◽  
Spontaneous Breathing ◽  
Brown Norway ◽  
Pulmonary Resistance ◽  
Strain Dependence ◽  
Fischer 344 ◽  
Airway Response ◽  
Airway Responses ◽  
Strain Dependent

The aim of the study was to investigate strain dependence and mechanisms of airway responses to dry-gas hyperpnea challenge in the rat. We studied responses in a strain that is hyperresponsive to methacholine, Fischer 344 (F-344); in two normoresponsive strains, Lewis and ACI; and in an atopic but normoresponsive strain, Brown Norway (BN). We examined the effects of a neurokinin (NK) 1-receptor (CP-99994), an NK2-receptor (SR-48968), and a leukotriene D4(LTD4)-receptor antagonist (pranlukast) on responses to hyperpnea challenge in BN rats. The animals were ventilated with a tidal volume of 8 ml/kg and a frequency of 150 breaths/min with either a dry or humidified mixture of 5% CO2-95% O2 for 5 min for hyperpnea challenge, whereas responses to challenge were measured during spontaneous breathing. Pulmonary resistance increased after dry-gas challenge in BN and ACI but not in F-344 and Lewis rats. CP-99994, SR-48968, and pranlukast significantly attenuated the increase in pulmonary resistance after dry-gas challenge. There were no significant differences in responsiveness to airway challenge with LTD4 among the BN, F-344 and ACI rats. We conclude that responses to dry-gas hyperpnea challenge are strain dependent in rats and are mediated by NKs and LTD4.

scholarly journals Hypoxia-induced vagal withdrawal is independent of the hypoxic ventilatory response in men

2019 ◽  
Vol 126 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Christoph Siebenmann ◽  
Camilla K. Ryrsø ◽  
Laura Oberholzer ◽  
James P. Fisher ◽  
Linda M. Hilsted ◽  
...  
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Animal Studies ◽  
Pulmonary Ventilation ◽  
Vagal Activity ◽  
Adrenergic Blockade ◽  
Controlled Breathing ◽  
Vagal Withdrawal

Hypoxia increases heart rate (HR) in humans by sympathetic activation and vagal withdrawal. However, in anaesthetized dogs hypoxia increases vagal activity and reduces HR if pulmonary ventilation does not increase and we evaluated whether that observation applies to awake humans. Ten healthy males were exposed to 15 min of normoxia and hypoxia (10.5% O2), while respiratory rate and tidal volume were volitionally controlled at values identified during spontaneous breathing in hypoxia. End-tidal CO2 tension was clamped at 40 mmHg by CO2 supplementation. β-Adrenergic blockade by intravenous propranolol isolated vagal regulation of HR. During spontaneous breathing, hypoxia increased ventilation by 3.2 ± 2.1 l/min ( P = 0.0033) and HR by 8.9 ± 5.5 beats/min ( P < 0.001). During controlled breathing, respiratory rate (16.3 ± 3.2 vs. 16.4 ± 3.3 breaths/min) and tidal volume (1.05 ± 0.27 vs. 1.06 ± 0.24 l) were similar for normoxia and hypoxia, whereas the HR increase in hypoxia persisted without (8.6 ± 10.2 beats/min) and with (6.6 ± 5.6 beats/min) propranolol. Neither controlled breathing ( P = 0.80), propranolol ( P = 0.64), nor their combination ( P = 0.89) affected the HR increase in hypoxia. Arterial pressure was unaffected ( P = 0.48) by hypoxia across conditions. The hypoxia-induced increase in HR during controlled breathing and β-adrenergic blockade indicates that hypoxia reduces vagal activity in humans even when ventilation does not increase. Vagal withdrawal in hypoxia seems to be governed by the arterial chemoreflex rather than a pulmonary inflation reflex in humans. NEW & NOTEWORTHY Hypoxia accelerates the heart rate of humans by increasing sympathetic activity and reducing vagal activity. Animal studies have indicated that hypoxia-induced vagal withdrawal is governed by a pulmonary inflation reflex that is activated by the increased pulmonary ventilation in hypoxia. The present findings, however, indicate that humans experience vagal withdrawal in hypoxia even if ventilation does not increase, indicating that vagal withdrawal is governed by the arterial chemoreflex rather than a pulmonary inflation reflex.

Sternum dependence of rib displacement during breathing

1993 ◽  
Vol 75 (1) ◽  
pp. 334-340 ◽  
Author(s):  
A. De Troyer ◽  
T. A. Wilson
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Spontaneous Breathing ◽  
Elastic Coupling ◽  
Lateral Expansion ◽  
Rib Cage ◽  
Primary Determinant ◽  
External Forces ◽  
Force Displacement

The parasternal intercostals are the primary determinant of the inspiratory cranial displacement of the ribs in the dog. When they contract, however, these muscles also cause a caudal displacement of the sternum, presumably an expiratory motion. The present studies were designed to assess the effects of this sternal displacement on the cranial displacement of the ribs and on lung volume. Twelve supine anesthetized animals were studied. We first measured, in four paralyzed animals, the displacement of the ribs and sternum produced by known external forces applied to the ribs, the sternum, or both simultaneously. From these measurements, the elastic coupling between the ribs and sternum was determined. We then studied, in eight animals, the effect of sternal motion on rib motion and tidal volume during spontaneous breathing. Rib and sternal displacements and tidal volume were measured first with the sternum free to move caudally during inspiration and then with the sternum constrained to prevent caudal motion. Preventing the sternum from moving caudally caused a 24% increase in the inspiratory cranial displacement of the ribs; this increased displacement of the ribs agreed well with the elastic coupling between the sternum and the ribs as determined from the force-displacement observations. Tidal volume, however, remained unchanged. These observations indicate that the caudal displacement of the sternum produced by the parasternal intercostals reduces the cranial displacement of the ribs but probably increases the lateral expansion of the rib cage.

Mechanical aspects of chest wall distortion

1985 ◽  
Vol 59 (2) ◽  
pp. 295-304 ◽  
Author(s):  
J. P. Mortola ◽  
M. Saetta ◽  
G. Fox ◽  
B. Smith ◽  
S. Weeks
Keyword(s):  
Tidal Volume ◽  
Respiratory System ◽  
Volume Change ◽  
Spontaneous Breathing ◽  
Relaxation Curve ◽  
Abdominal Pressure ◽  
Human Infants ◽  
Adult Rats ◽  
Inspiratory Muscles ◽  
Phrenic Stimulation

During passive inflation of the respiratory system, the rib cage (RC) expands because the pressure applied to it [approximately equal to abdominal pressure (Pab)] increases. Similar Pab-tidal volume (VT) relationships between passive and spontaneous inspirations would occur only if 1) Pab acts on RC equally in the two situations (no distortion) or 2) the extradiaphragmatic inspiratory muscles expand RC, compensating for distortion. In anesthetized adult rats and in sleeping human infants the passive relationships between VT and Pab or abdomen motion (AB) were constructed by occluding the airways during expiration. For a given Pab (or AB) in active breathing VT averaged 55% (rats) and 49% (infants) of the passive volume change. With phrenic stimulation in rats VT was only slightly less than during spontaneous breathing, indicating that, in the latter case, the respiratory system was essentially driven only by the diaphragm. In both species occasional breaths with large RC expansion occurred, and VT was then equal to or larger than the passive volume at iso-Pab. We conclude that 1) RC distortion decreases VT to approximately half of the passive value and 2) being on the relaxation curve reflects “compensated” distortion and not absence of it.

Effect of paced breathing on ventilatory and cardiovascular variability parameters during short-term investigations of autonomic function

2006 ◽  
Vol 290 (1) ◽  
pp. H424-H433 ◽  
Author(s):  
G. D. Pinna ◽  
R. Maestri ◽  
M. T. La Rovere ◽  
E. Gobbi ◽  
F. Fanfulla
Keyword(s):  
Tidal Volume ◽  
Spontaneous Breathing ◽  
Diastolic Pressure ◽  
Minute Ventilation ◽  
Autonomic Control ◽  
Short Term ◽  
Cardiovascular Variability ◽  
Paced Breathing ◽  
Group 2 ◽  
Group 1

Paced breathing (PB) around 0.25 Hz has been advocated as a means to avoid confounding and to standardize measurements in short-term investigations of autonomic cardiovascular regulation. Controversy remains, however, as to whether it causes any alteration in autonomic control. We addressed this issue in 40 supine, middle-aged, healthy volunteers by assessing the changes induced by PB (0.25 Hz for 8 min) on 1) ventilatory parameters, 2) the indexes of autonomic control of cardiovascular function, and 3) the spectral indexes of cardiovascular variability. Subjects were grouped into group 1 ( n = 31), if spontaneous breathing was regular and within the high-frequency (HF) band (0.15–0.45 Hz), or group 2 ( n = 9), if it was irregular or slow (<0.15 Hz). In both groups, PB was accompanied by an increase in minute ventilation (both groups, P < 0.01), whereas tidal volume increased only in group 1 ( P = 0.0003). End-tidal CO2 decreased by [median (lower quartile, upper quartile)] −0.2 (−0.5, −0.1)% ( group 1, P < 0.0001) and −0.6 (−0.8, −0.5)% ( group 2, P = 0.008). Mean R-R interval and systolic and diastolic pressure remained remarkably stable (all P ≥ 0.13, both groups). No significant changes were observed in spectral indexes of R-R and pressure variability (all P ≥ 0.12, measured only in group 1 to avoid confounding), except in the HF power of pressure signals, which significantly increased (all P < 0.05) in association with increased tidal volume. In conclusion, PB at 0.25 Hz causes a slight hyperventilation and does not affect traditional indexes of autonomic control or, in subjects with spontaneous breathing in the HF band, most relevant spectral indexes of cardiovascular variability. These findings support the notion that PB does not alter cardiovascular autonomic regulation compared with spontaneous breathing.

Respiratory sinus arrhythmia in humans: how breathing pattern modulates heart rate

1981 ◽  
Vol 241 (4) ◽  
pp. H620-H629 ◽  
Author(s):  
J. A. Hirsch ◽  
B. Bishop
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Respiratory Sinus Arrhythmia ◽  
Spontaneous Breathing ◽  
Low Frequency ◽  
Corner Frequency ◽  
Breath Hold ◽  
Breathing Frequency ◽  
Quiet Breathing ◽  
Sinus Arrhythmia

The relationship of respiratory sinus arrhythmia amplitude (RSA) to tidal volume and breathing frequency was quantified during voluntarily controlled tidal volume and breathing frequency and spontaneous quiet breathing. Seventeen seated subjects breathed via mouthpiece and nose-clip, maintaining constant tidal volumes at each of several breathing frequencies. Inspiratory breath hold was zero frequency. Log RSA was plotted vs. log frequency for each tidal volume. The large stable RSA for frequencies less than 6 cycles/min was called low-frequency intercept (LFI, 20 +/- 5 beats/min). Low-frequency intercept was inversely proportional to a subject's age only to 35 yr. At higher breathing frequencies above a characteristic corner frequency (fC, 7.2 +/- 1.5 cycles/min) RSA decreased with constant slope (roll-off; 21 +/- 3.4 dB/decade). The RSA-volume relationship was linear permitting normalization of RSA-frequency curves for tidal volume to yield one curve. Spontaneous breathing data points fell on this curve. Voluntarily coupling of heart rate to breathing frequency in integer ratios reduced breath-by-breath variability of RSA without changing mean RSA. In conclusion, low-frequency intercept, corner frequency, and roll-off characterize an individual's RSA-frequency relationship during both voluntarily controlled and spontaneous breathing.

scholarly journals The Interrelationship Between Pulmonary Mechanics and the Spontaneous Breathing Pattern in the Tokay Lizard, Gekko Gecko

1984 ◽  
Vol 113 (1) ◽  
pp. 203-214 ◽  
Author(s):  
WILLIAM K. MILSOM
Keyword(s):  
Tidal Volume ◽  
Spontaneous Breathing ◽  
Breathing Pattern ◽  
Pulmonary Ventilation ◽  
Periodic Breathing ◽  
Breath Holding ◽  
Pulmonary Mechanics ◽  
Respiratory Drive ◽  
Breathing Patterns ◽  
Gekko Gecko

The normal breathing pattern of the Tokay gecko (Gekko gecko) consists of single breaths or bursts of a few breaths separated by periods of breath holding. Increases in pulmonary ventilation that accompany rises in body temperature are caused by increases in respiratory frequency due to shortening of the periods of breath holding. Tidal volume and breath duration remain relatively constant. Measurements of the mechanical work associated with spontaneous breathing yielded values that were similar to those calculated for breaths of the same size and duration based on work curves generated during pump ventilation of anaesthetized animals. In this species, the pattern of periodic breathing and the ventilatory responses to changes in respiratory drive correspond with predictions of optimal breathing patterns based on calculations of the mechanical cost of ventilation. Bilateral vagotomy drastically alters the breathing pattern producing an elevation in tidal volume, a slowing of breathing frequency, and a prolongation of the breath duration. These alterations greatly increase the mechanical cost of ventilation. These data suggest that periodic breathing in this species may represent an adaptive strategy which is under vagal afferent control and which serves to minimize the cost of breathing.

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