Effects of expiratory resistive load on respiratory motor output in conscious humans

1987 ◽  
Vol 63 (5) ◽  
pp. 1837-1845 ◽  
Author(s):  
C. S. Poon ◽  
M. Younes ◽  
C. G. Gallagher

We examined, in five conscious human subjects, the steady-state effects of expiratory resistive loading (ERL; R = 8 cmH2O.l–1.s) on the time course of inspiratory and postinspiratory muscle activities (IA and PIA, respectively) and ventilatory pattern during quiet breathing. Driving pressure (DP) was calculated by means of a respiratory neuromechanical model (J. Appl. Physiol. 51: 963–989, 1981) that permitted the derivation, from tidal volume and flow, of the occlusion pressure equivalent (at functional residual capacity) of respiratory neural output throughout the breath. ERL caused a prolongation of both neural inspiratory duration (12.2 +/- 6.9% SD) and expiratory duration (25.0 +/- 10.1%) and an increase in the amplitude of DP (16.5 +/- 10.2%) without any changes in the waveshape of IA and in end-expiratory level. The relative time course of PIA was not altered by ERL. Minute ventilation was depressed (-6.75 +/- 2.88%) during ERL with little change in alveolar PCO2. The results indicate that pulmonary gas exchange may be improved during ERL through increased tidal volume as well as delayed expiratory lung emptying secondary to sustained PIA.

1995 ◽  
Vol 78 (2) ◽  
pp. 555-561 ◽  
Author(s):  
D. A. Sidney ◽  
C. S. Poon

To investigate how breathing is controlled during CO2 stimulation, steady-state ventilatory responses to rebreathing through a tube (DS) and inspiring a fixed PCO2 (INH) were compared in healthy human subjects. Tests were performed in hyperoxia with (IRL) and without (NL) an inspiratory resistive load (15 cmH2O.l–1.s at 1 l/s). The mean slope of the minute ventilation (VE)-end-tidal PCO2 relationship was significantly higher in DS-IRL than in INH-IRL [1.86 +/- 0.67 (SD) vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.01], and it was significantly different between INH-NL and INH-IRL (1.64 +/- 0.41 vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.05) but not between DS-NL and DS-IRL (1.85 +/- 0.72 vs. 1.86 +/- 0.67 l.min-1.Torr-1). The slope of the VE-tidal volume relationship was significantly lower in DS-NL than in INH-NL (19.6 +/- 3.8 vs. 21.2 +/- 5.1 min-1, P < 0.05), but other comparisons in breathing pattern between NL and IRL and between DS and INH failed to reach significance. We concluded that 1) alterations in alveolar PCO2 temporal profile by DS could induce changes in VE-end-tidal PCO2 sensitivity and ventilatory pattern, 2) these changes may be modified by increased mechanical impairment resulting from IRL, and 3) carotid chemoreceptor mediation is not necessary for the observed effects of DS.


1981 ◽  
Vol 51 (5) ◽  
pp. 1162-1168 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora ◽  
J. H. Gaudy

In nine cats and nine human subjects anesthetized with alfaxalone, respiratory activity and tracheal pressure were recorded prior to and during occlusion of the airway at end inspiration or end expiration. Lung inflations at the end of expiration were also performed. In addition, the ventilatory pattern was analyzed during hypercapnia. The results show that occlusions at the end of inspiration or inflations provoked an apnea in both cats and humans. However, concomitant with increases in tidal volume during hypercapnia, inspiratory duration decreased in cats and did not change in human subjects. These results indicate that the Breuer-Hering reflex, which delays the onset of inspiration during inflation was equally operative in cats and humans. In contrast, the “Breuer-Hering threshold curve,” which accounts for the off-switch“ of inspiration was different in cats and humans. Thus, in summary, the Breuer-Hering inflation reflex is operative in human subjects, but it does not seem to be involved in the control of the inspiratory off-switch mechanism during increases respiratory activity resulting from hypercapnia.


2007 ◽  
Vol 102 (2) ◽  
pp. 688-697 ◽  
Author(s):  
Edward S. Schelegle ◽  
William F. Walby ◽  
William C. Adams

We examined the time course of O3-induced changes in breathing pattern in 97 healthy human subjects (70 men and 27 women). One- to five-minute averages of breathing frequency (fB) and minute ventilation (V̇e) were used to generate plots of cumulative breaths and cumulative exposure volume vs. time and cumulative exposure volume vs. cumulative breaths. Analysis revealed a three-phase response; delay, no response detected; onset, fB began to increase; response, fB stabilized. Regression analysis was used to identify four parameters: time to onset, number of breaths at onset, cumulative inhaled dose of ozone at onset of O3-induced tachypnea, and the percent change in fB. The effect of altering O3 concentration, V̇e, atropine treatment, and indomethacin treatment were examined. We found that the lower the O3 concentration, the greater the number of breaths at onset of tachypnea at a fixed ventilation, whereas number of breaths at onset of tachypnea remains unchanged when V̇e is altered and O3 concentration is fixed. The cumulative inhaled dose of O3 at onset of tachypnea remained constant and showed no relationship with the magnitude of percent change in fB. Atropine did not affect any of the derived parameters, whereas indomethacin did not affect time to onset, number of breaths at onset, or cumulative inhaled dose of O3 at onset of tachypnea but did attenuate percent change in fB. The results are discussed in the context of dose response and intrinsic mechanisms of action.


1961 ◽  
Vol 16 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Francisco Moreno ◽  
Harold A. Lyons

The changes produced by body posture on total lung capacity and its subdivisions have been reported for all positions except the prone position. Twenty normal subjects, twelve males and eight females, had determinations of total lung capacity in the three body positions, sitting, supine and prone. Tidal volume, minute ventilation and O2 consumption were also measured. The changes found on assumption of the supine position from the sitting position were similar to those previously reported. For the prone position, a smaller inspiratory capacity and a larger expiratory reserve volume were found. The mean values were changed, respectively, –8% and +37%. Associated with these changes was a significant increase of the functional residual capacity by 636 ml. Ventilation did not change significantly from that found during sitting, unlike the findings associated with the supine position, in which position the tidal volume was decreased. Respiratory frequency remained the same for all positions. Submitted on April 5, 1960


2002 ◽  
Vol 93 (4) ◽  
pp. 1515-1526 ◽  
Author(s):  
Cheng-Li Que ◽  
Christof Kolmaga ◽  
Louis-Gilles Durand ◽  
Suzanne M. Kelly ◽  
Peter T. Macklem

We measured tracheal flow from tracheal sounds to estimate tidal volume, minute ventilation (V˙i), respiratory frequency, mean inspiratory flow (Vt/Ti), and duty cycle (Ti/Ttot). In 11 normal subjects, 3 patients with unstable airway obstruction, and 3 stable asthmatic patients, we measured tracheal sounds and flow twice: first to derive flow-sound relationships and second to obtain flow-volume relationships from the sound signal. The flow-volume relationship was compared with pneumotach-derived volume. When subjects were seated, facing forward and with neck rotation, flexion, and standing, flow-volume relationship was within 15% of pneumotach-derived volume. Error increased with neck extension and while supine. We then measured ventilation without mouthpiece or nose clip from tracheal sounds during quiet breathing for up to 30 min. Normal results ± SD revealed tidal volume = 0.37 ± 0.065 liter, respiratory frequency = 19.3 ± 3.5 breaths/min, V˙i = 6.9 ± 1.2 l/min, Vt/Ti = 0.31 ± 0.06 l/s, and Ti/Ttot = 0.37 ± 0.04. Unstable airway obstruction had large V˙i due to increased Vt/Ti. With the exception of Ti/Ttot, variations in ventilatory parameters were closer to log normal than normal distributions and tended to be greater in patients. We conclude that phonospirometry measures ventilation reasonably accurately without mouthpiece, nose clip, or rigid postural constraints.


1989 ◽  
Vol 67 (6) ◽  
pp. 2357-2368 ◽  
Author(s):  
A. Torres ◽  
W. R. Kimball ◽  
J. Qvist ◽  
K. Stanek ◽  
R. M. Kacmarek ◽  
...  

Through a right thoracotomy in seven sheep we chronically implanted sonomicrometry crystals and electromyographic electrodes in the costal and crural diaphragmatic regions. Awake sheep were studied during recovery for 4-6 wk, both during quiet breathing (QB) and during CO2 rebreathing. Tidal volume, respiratory frequency, and esophageal and gastric pressures were studied before and after surgery. Normalized resting length (LFRC) was significantly decreased for the costal segment on postoperative day 1 compared with postoperative day 28. Fractional costal shortening both during QB and at 10% end-tidal CO2 (ETCO2) increased significantly from postoperative days 1 to 28, whereas crural shortening did not change during QB but progressively increased at 10% ETCO2. Maximal costal shortening during electrophrenic stimulation was constant at 40% LFRC during recovery, although maximal crural shortening increased from 23 to 32% LFRC. Minute ventilation, tidal volume, and transdiaphragmatic pressure at 10% ETCO2 increased progressively after thoracotomy until postoperative day 28. Our results suggest there is profound diaphragmatic inhibition after thoracotomy and crystal implantation in sheep that requires at least 3-4 wk for stable recovery.


1960 ◽  
Vol 15 (5) ◽  
pp. 801-806 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Jerry McDonald ◽  
Frank P. Piccinni

The functional residual capacity (FRC) of paralyzed pump-ventilated dogs was measured by open-circuit helium dilution at various rates and volumes of ventilation and the FRC's of spontaneously ventilated dogs were compared after changes in body position. When tidal volume was constant, increases in rate and minute volume increased FRC. The FRC tended to increase with larger tidal volumes when minute ventilation was constant. An inclination of 30 degrees increased FRC 23.8% (mean for 41 dogs) above the FRC measured in the horizontal position, whereas a declination of 30 degrees decreased FRC by 65.8% (mean for 8 dogs). It is suggested that larger tidal or minute volumes open pulmonary units which are closed by surface tension forces when the volume or duration of inflation is less. Tilting head-up or head-down changes the position of the diaphragm and the abdominal contents in the thoracic ‘cylinder’ to accommodate more or less gas volume in the thorax. Submitted on February 29, 1960


1987 ◽  
Vol 62 (3) ◽  
pp. 1299-1306 ◽  
Author(s):  
R. L. Begle ◽  
J. B. Skatrud ◽  
J. A. Dempsey

The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2–3 min at a constant level (range of increase 160–1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35–50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.


1988 ◽  
Vol 65 (2) ◽  
pp. 934-939 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
N. Munoz ◽  
A. R. Leff ◽  
J. Solway

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.


1996 ◽  
Vol 80 (5) ◽  
pp. 1772-1784 ◽  
Author(s):  
J. A. Spahija ◽  
A. Grassino

To examine the effect of pursed-lips breathing (PLB) on breathing pattern and respiratory mechanics, we studied 11 healthy subjects breathing with and without PLB at rest and during steady-state bicycle exercise. Six of these subjects took part in a second study, which compared the effects of PLB to expiratory resistive loading (ERL). PLB was found to prolong expiratory and total breath durations and to promote a slower and deeper breathing pattern. During exercise, the compensatory increase that occurred in tidal volume was not sufficient to counter the reduction in breathing frequency, causing minute ventilation to be reduced. Although ERL similarly caused minute ventilation and breathing frequency to be decreased, unlike PLB, it produced no change in tidal volume and prolonged expiratory and total breath durations to a lesser extent. PLB and ERL increased the expiratory resistance to a comparable degree, also increasing the expiratory resistive work of breathing and promoting greater expiratory rib cage and abdominal muscle recruitment in response to the expiratory loads. End-expiratory lung volume, which was determined from inspiratory capacity maneuvers, was not altered by PLB; however, with ERL it was increased by 0.20 and 0.24 liter during rest and exercise, respectively. Inspiratory muscle recruitment patterns were not altered by PLB at rest, although small increases in the relative contribution of the rib cage/accessory muscles in conjunction with abdominal muscle relaxation occurred during exercise. Similar trends were observed with ERL. We conclude that, although ERL and PLB induce comparable respiratory muscle recruitment responses, they are not equivalent with respect to breathing pattern changes and effect on end-expiratory lung volume.


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