Effect of chest wall vibration on breathlessness in normal subjects

1991 ◽  
Vol 71 (1) ◽  
pp. 175-181 ◽  
Author(s):  
H. L. Manning ◽  
R. Basner ◽  
J. Ringler ◽  
C. Rand ◽  
V. Fencl ◽  
...  
Keyword(s):  
Steady State ◽  
Chest Wall ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Potential Contribution ◽  
Resistive Load ◽  
Residual Capacity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Hypercapnic Response

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.

Response of normal subjects to inspiratory resistive unloading

1989 ◽  
Vol 66 (3) ◽  
pp. 1113-1119 ◽  
Author(s):  
C. G. Gallagher ◽  
R. Sanii ◽  
M. Younes
Keyword(s):  
Average Rate ◽  
Minute Ventilation ◽  
Co2 Concentration ◽  
Normal Subjects ◽  
Resistive Load ◽  
Mouth Pressure ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Resistive Loads ◽  
End Tidal

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.

Steady-state response of quadriplegic subjects to inspiratory resistive load

1986 ◽  
Vol 60 (5) ◽  
pp. 1482-1492 ◽  
Author(s):  
V. Im Hof ◽  
H. Dubo ◽  
V. Daniels ◽  
M. Younes
Keyword(s):  
Steady State ◽  
Chest Wall ◽  
Muscle Spindles ◽  
Normal Subjects ◽  
Afferent Feedback ◽  
Resistive Load ◽  
State Response ◽  
The Face ◽  
Inspiratory Resistance

Normal subjects preserve tidal volume (VT) in the face of added inspiratory resistance by increasing maximal amplitude and duration of the rising phase of respiratory driving pressure (DP) and by changing the shape of this phase to one that is more concave to the time axis. To explore the possible role of chest wall afferents in mediating these responses, we determined averaged DP in eight quadriplegic subjects during steady-state unloaded breathing and while breathing through an inspiratory resistance (8.5 cmH2O X 1(-1) X s). As with normal subjects, quadriplegics preserved VT (loaded VT = 106% control) by utilizing all three mechanisms. However, prolongation of the inspiratory duration derived from the DP waveform (+22% vs. +42%) and shape response were significantly less in the quadriplegic subjects. Shape response was completely absent in subjects with C4 lesions. The results provide strong evidence that respiratory muscle spindles are responsible for shape response and that changes in afferent feedback from the chest wall play an important role in mediating inspiratory prolongation.

External thoracic restriction, respiratory sensation, and ventilation during exercise in men

1999 ◽  
Vol 86 (4) ◽  
pp. 1142-1150 ◽  
Author(s):  
Helen R. Harty ◽  
Douglas R. Corfield ◽  
Richard M. Schwartzstein ◽  
Lewis Adams
Keyword(s):  
Chest Wall ◽  
Minute Ventilation ◽  
Residual Volume ◽  
Exercise Tests ◽  
Arterial Blood ◽  
Residual Capacity ◽  
Respiratory Discomfort ◽  
End Tidal ◽  
The Impact ◽  
Insight Into

Multiple factors may contribute to the dyspnea associated with restrictive ventilatory disease (RVD). Simple models that examine specific features of this problem are likely to provide insight into the mechanisms. Previous models of RVD utilizing elastic loads may not represent completely the impact on pulmonary and chest wall receptors derived from breathing at low thoracic volumes. The purpose of this study was to investigate the sensory consequences of breathing at low lung volumes induced by external thoracic restriction in an attempt to further elucidate the etiology of dyspnea in this setting. Ten men were studied, with and without an inelastic corset applied at residual volume (restriction resulted in mean reductions in vital capacity, functional residual capacity, residual volume, and forced expired volume in 1 s of 44, 31, 12.5, and 42%, respectively). During 10-min steady-state exercise tests (at a workload set to achieve ∼65% maximum heart rate), restriction resulted in significant increases, compared with control, in minute ventilation (61 vs. 49 l/min), respiratory frequency (43 vs. 23 breaths/min), and visual analog scale measurements of respiratory discomfort (65 vs. 20 mm). Alveolar hyperventilation (end-tidal [Formula: see text] = 39 vs. 44 Torr for control) and mild O2 desaturation (arterial blood O2 saturation = 93 vs. 95% for control) occurred. Hypoxemia, atelectasis, increased work and effort of breathing, or a decrease in the volume-related feedback from chest wall and/or lungs could be responsible for the increased dyspnea reported. External thoracic restriction provides a useful model to study mechanisms of dyspnea in RVD.

Steady-state response of normal subjects to inspiratory resistive load

1986 ◽  
Vol 60 (5) ◽  
pp. 1471-1481 ◽  
Author(s):  
V. Im Hof ◽  
P. West ◽  
M. Younes
Keyword(s):  
Steady State ◽  
Normal Subjects ◽  
Driving Pressure ◽  
Resistive Load ◽  
Steady State Response ◽  
Occlusion Pressure ◽  
State Response ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Loaded Breathing

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.

Response to hypercapnia and exercise hyperpnea in graded anesthesia

1984 ◽  
Vol 57 (6) ◽  
pp. 1796-1802 ◽  
Author(s):  
T. Chonan ◽  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Exercise Hyperpnea ◽  
Sciatic Nerves ◽  
End Tidal ◽  
Response To Exercise ◽  
The Relationship ◽  
End Tidal Co2 ◽  
Rebreathing Method

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of mechanical loading on expiratory and inspiratory muscle activity during NREM sleep

1990 ◽  
Vol 68 (3) ◽  
pp. 1195-1202 ◽  
Author(s):  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey ◽  
R. L. Begle
Keyword(s):  
Steady State ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Abdominal Muscles ◽  
Compensatory Response ◽  
Load Compensation ◽  
Resistive Loading ◽  
Chemical Stimuli ◽  
End Tidal ◽  
End Tidal Co2

We investigated the effect of acute and sustained inspiratory resistive loading (IRL) on the activity of expiratory abdominal muscles (EMGab) and the diaphragm (EMGdi) and on ventilation during wakefulness and non-rapid-eye-movement (NREM) sleep in healthy subjects. EMGdi and EMGab were measured with esophageal and transcutaneous electrodes, respectively. During wakefulness, EMGdi increased in response to acute loading (18 cmH2O.l-1.s) (+23%); this was accompanied by preservation of tidal volume (VT) and minute ventilation (VE). During NREM sleep, no augmentation was noted in EMGdi or EMGab. Inspiratory time (TI) was prolonged (+5%), but this was not sufficient to prevent a decrease in both VT and VE (-21 and -20%, respectively). During sustained loading (12 cmH2O.l-1 s) in NREM sleep, control breaths (C) were compared with the steady-state loaded breaths (SS) defined by breaths 41-50. Steady-state IRL was associated with augmentation of EMGdi (12%) and EMGab (50%). VT returned to control levels, expiratory time shortened, and breathing frequency increased. The net result was the increase in VE above control levels (+5%, P less than 0.01). No change was noted in end-tidal CO2 or O2. We concluded that 1) wakefulness is a prerequisite for immediate load compensation (in its absence, TI prolongation is the only compensatory response) and 2) during sustained IRL, the augmentation of EMGdi and EMGab can lead to complete ventilatory recovery without measurable changes in chemical stimuli.

Influence of prior ventilatory experience on the estimation of breathlessness during exercise

1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones
Keyword(s):  
Exercise Test ◽  
Prior Experience ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Borg Scale ◽  
Exercise Tests ◽  
Loaded Breathing ◽  
Inspiratory Load

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.

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

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.

Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation

1983 ◽  
Vol 55 (3) ◽  
pp. 813-822 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Positive Pressure ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Apnea Duration ◽  
O2 Concentration ◽  
End Tidal ◽  
End Tidal Co2

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].

Effect of body posture on lung volumes

1961 ◽  
Vol 16 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Francisco Moreno ◽  
Harold A. Lyons
Keyword(s):  
Tidal Volume ◽  
Prone Position ◽  
Supine Position ◽  
Total Lung Capacity ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Body Posture ◽  
Mean Values ◽  
Lung Capacity ◽  
Residual Capacity

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

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