Response of normal subjects to inspiratory resistive unloading

1989 ◽  
Vol 66 (3) ◽  
pp. 1113-1119 ◽  
Author(s):  
C. G. Gallagher ◽  
R. Sanii ◽  
M. Younes

The purpose of this study was to examine the role of the normal inspiratory resistive load in the regulation of respiratory motor output in resting conscious humans. We used a recently described device (J. Appl. Physiol. 62: 2491–2499, 1987) to make mouth pressure during inspiration positive and proportional to inspiratory flow, thus causing inspiratory resistive unloading (IRUL); the magnitude of IRUL (delta R = -3.0 cmH2O.1(-1).s) was set so as to unload most (approximately 86% of the normal inspiratory resistance. Six conscious normal humans were studied. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963–1001, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. IRUL resulted in small but significant changes in minute ventilation (0.6 1/min) and in end-tidal CO2 concentration (-0.11%) with no significant change in tidal volume or respiratory frequency. There was a significant shortening of the duration (neural inspiratory time) of the rising phase of the DP waveform and the shape of the rising phase became more convex to the time axis. There was no change in the average rate of rise of DP or in the duration or shape of the declining phase. We conclude that 1) the normal inspiratory resistance is an important determinant of the duration and shape of the rising phase of DP and 2) the neural responses elicited by the normal inspiratory resistance are similar to those observed with added inspiratory resistive loads.

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.


1991 ◽  
Vol 71 (1) ◽  
pp. 175-181 ◽  
Author(s):  
H. L. Manning ◽  
R. Basner ◽  
J. Ringler ◽  
C. Rand ◽  
V. Fencl ◽  
...  

This study evaluated the effect of chest wall vibration (115 Hz) on breathlessness. Breathlessness was induced in normal subjects by a combination of hypercapnia and an inspiratory resistive load; both minute ventilation and end-tidal CO2 were kept constant. Cross-modality matching was used to rate breathlessness. Ratings during intercostal vibration were expressed as a percentage of ratings during the control condition (either deltoid vibration or no vibration). To evaluate their potential contribution to any changes in breathlessness, we assessed several aspects of ventilation, including chest wall configuration, functional residual capacity (FRC), and the ventilatory response to steady-state hypercapnia. Intercostal vibration reduced breathlessness ratings by 6.5 +/- 5.7% compared with deltoid vibration (P less than 0.05) and by 7.0 +/- 8.3% compared with no vibration (P less than 0.05). The reduction in breathlessness was accompanied by either no change or negligible change in minute ventilation, tidal volume, frequency, duty cycle, compartmental ventilation, FRC, and the steady-state hypercapnic response. We conclude that chest wall vibration reduces breathlessness and speculate that it may do so through stimulation of receptors in the chest wall.


1986 ◽  
Vol 60 (5) ◽  
pp. 1471-1481 ◽  
Author(s):  
V. Im Hof ◽  
P. West ◽  
M. Younes

Tidal volume (VT) is usually preserved when conscious humans are made to breathe against an inspiratory resistance. To identify the neural changes responsible for VT compensation we calculated the respiratory driving pressure waveform during steady-state unloaded and loaded breathing (delta R = 8.5 cmH2O X 1(-1) X s) in eight conscious normal subjects. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963–989, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. VT during resistance breathing was 108% of unloaded VT, as opposed to a predicted value of 82% of control in the absence of neural compensation. Compensation was accomplished through three changes in the DP waveform: 1) peak amplitude increased (+/- 23%), 2) the duration of the rising phase increased (+42%); and 3) the rising phase became more concave to the time axis. There were no changes in the relative decay rate of inspiratory pressure during expiration, in the shape of the declining phase of DP, or in end-expiratory lung volume.


1977 ◽  
Vol 53 (2) ◽  
pp. 117-123 ◽  
Author(s):  
N. K. Burki ◽  
L. K. Mitchell ◽  
B. A. Chaudhary ◽  
F. W. Zechman

1. Simultaneous measurements of mouth pressure at the end of the first 0·1 s of inspiratory occlusion (P0·1) at functional residual capacity and the maximum rate of rise of this pressure (dP/dt max.) were made repeatedly in five normal subjects during resting respiration; the coefficient of variation of dP/dt max. was 36·2%, compared with 50·6% for P0·1. 2. During both isocapnic hypoxia and hyperoxic hypercapnia in five normal subjects there was a close correlation between ventilation (V̇E) and both P0·1 and dP/dt max., and between end-tidal Pco2 or Po2 and P0·1 and dP/dt max.; during both procedures there was a close correlation between P0·1 and dP/dt max. 3. The time at which dP/dt max. occurred (Tmax.) was not correlated with changes of dP/dt max. in either procedure. Tmax. was greater than 0·12 s in most studies. 4. The regression coefficients of P0·1 and dP/dt max. on V̇E were significantly different in hypoxia as compared with hypercapnia in four out of the five subjects; on repeated hypercapnic stimulation in two out of three subjects these regression coefficients again varied significantly. Changes in lung volume or inspiratory volume-timing relationship were not responsible for these differences. These results suggest that mouth occlusion pressure, as reflected by P0·1 or dP/dt max., is a complex variable, reflecting the motor output of the respiratory centre, but also affected by random variations in the measurements and probably by changes in lung volume.


1979 ◽  
Vol 46 (5) ◽  
pp. 897-904 ◽  
Author(s):  
C. Roussos ◽  
M. Fixley ◽  
D. Gross ◽  
P. T. Macklem

The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.


1986 ◽  
Vol 60 (3) ◽  
pp. 846-853 ◽  
Author(s):  
R. Olgiati ◽  
G. Atchou ◽  
P. Cerretelli

To examine the acute hemodynamic effects induced by large swings in intrathoracic pressure such as may be generated by obstructive lung disease, airway obstruction was simulated by means of two different fixed external alinear resistances and the results were compared with those for unobstructed breathing (C). Eight normal subjects breathed through external resistances during inspiration (I), expiration (E), or both (IE) at rest (Re) and exercise (Ex). The resistances were chosen to induce similar mouth pressure (Pm) swings at Re and Ex. Pleural pressures (Ppl) were found to correlate closely with Pm. During IE resistive breathing mean swings in Pm were -31 and +19 cmH2O at Re and -38 and +22 cmH2O at Ex, with a corresponding decrease in minute ventilation (-30 and -18%) and an increase in end-tidal PCO2 (+5.6 and +4.2 Torr); these were associated with an increase in heart rate (delta HR = 4 and 6 beats/min) and systolic systemic arterial pressure (delta Psas = 10 and 14 Torr at Re and Ex, respectively). O2 consumption and cardiac output did not change. The myocardial O2 consumption, estimated from the product HR X (Psas--Ppl), increased by 17 and 20% at Re and Ex, respectively. Changes in mechanics, gas exchange, and hemodynamics were less pronounced during I or E resistive loading. It is concluded that breathing through a tight external resistance during IE at Re and Ex increases the metabolic load on the myocardium.


1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.


1980 ◽  
Vol 49 (4) ◽  
pp. 601-608 ◽  
Author(s):  
B. Gothe ◽  
N. S. Cherniack

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.


1981 ◽  
Vol 51 (5) ◽  
pp. 1261-1267 ◽  
Author(s):  
J. W. Shepard ◽  
V. D. Minh ◽  
G. F. Dolan

Gas exchange was studied under conditions of zero perfusion both in situ and in vitro. Six dogs, anesthetized with pentobarbital sodium, underwent surgical interruption of both pulmonary and bronchial circulations to the left lung. Despite the absence of perfusion, O2 uptake for the left lung ranged from 0.76 to 0.98 ml/min, whereas CO2 elimination greatly exceeded O2 uptake ranging from 1.68 to 4.34 ml/min. In addition, CO2 output was observed to vary directly with the level of minute ventilation (VE) and inversely with end-tidal CO2 concentration. To investigate the mechanisms responsible for these findings we studied 20 excised, ventilated, but nonperfused dog lungs to evaluate the relative roles of tissue metabolism and transpleural diffusion to gas exchange. The results obtained with these excised lungs under conditions of varying VE and extrapleural gas concentrations indicate that the high respiratory exchange ratios observed in situ can be explained by the greater rate with which CO2 diffuses through the pleura, and that reduced ventilation decreases total gas transfer by decreasing the transpleural partial pressure driving gradient. Our data further document that the concentration of CO2 in alveolar gas may differ significantly from that present in inspired gas under conditions of ventilation-perfusion ratio equal to infinity, and that tissue metabolism as well as transpleural diffusion contribute to gas exchange in nonperfused lung.


1988 ◽  
Vol 65 (2) ◽  
pp. 760-766 ◽  
Author(s):  
D. S. Dodd ◽  
P. W. Collett ◽  
L. A. Engel

We examined the combined effect of an increase in inspiratory flow rate and frequency on the O2 cost of inspiratory resistive breathing (VO2 resp). In each of three to six pairs of runs we measured VO2 resp in six normal subjects breathing through an inspiratory resistance with a constant tidal volume (VT). One of each pair of runs was performed at an inspiratory muscle contraction frequency of approximately 10/min and the other at approximately 30/min. Inspiratory mouth pressure was 45 +/- 2% (SE) of maximum at the lower contraction frequency and 43 +/- 2% at the higher frequency. Duty cycle (the ratio of contraction time to total cycle time) was constant at 0.51 +/- 0.01. However, during the higher frequency runs, two of every three contractions were against an occluded airway. Because VT and duty cycle were kept constant, mean inspiratory flow rate increased with frequency. Careful selection of appropriate parameters allowed the pairs of runs to be matched both for work rate and pressure-time product. The VO2 resp did not increase, despite approximately threefold increases in both inspiratory flow rate and contraction frequency. On the contrary, there was a trend toward lower values for VO2 resp during the higher frequency runs. Because these were performed at a slightly lower mean lung volume, a second study was designed to measure the VO2 resp of generating the same inspiratory pressure (45% maximum static inspiratory mouth pressure at functional residual capacity) at the same frequency but at two different lung volumes. This was achieved with a negligibly small work rate.(ABSTRACT TRUNCATED AT 250 WORDS)


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