Effects of voluntary constraining of thoracic displacement during hypercapnia

1987 ◽  
Vol 63 (5) ◽  
pp. 1822-1828 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
N. S. Cherniack ◽  
M. D. Altose

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.

1992 ◽  
Vol 72 (3) ◽  
pp. 842-850 ◽  
Author(s):  
F. Cerny ◽  
L. Armitage ◽  
J. A. Hirsch ◽  
B. Bishop

We hypothesized that the hyperinflation and pulmonary dysfunction of cystic fibrosis (CF) would distort feedback and therefore alter the abdominal muscle response to graded expiratory threshold loads (ETLs). We compared the respiratory and abdominal muscle responses with graded ETLs of seven CF patients with severe lung dysfunction with those of matched healthy control subjects in the supine and 60 degrees head-up positions. Breathing frequency, tidal volume, and ventilatory timing were determined from inspiratory flow recordings. Abdominal electromyograms (EMGs) were detected with surface electrodes placed unilaterally over the external and internal oblique and the rectus abdominis muscles. Thresholds, times of onset, and durations of phasic abdominal activity were determined from raw EMGs; peak amplitudes were determined from integrated EMGs. Graded ETLs were imposed by submerging a tube from the expiratory port of the breathing valve into a column of water at depths of 0–25 cmH2O. We found that breathing frequency, tidal volume, and expired minute ventilation were higher in CF patients than in control subjects during low ETLs; a change in body position did not alter these ventilatory responses in the CF patients but did in the control subjects. All CF patients, but none of the control subjects, had tonic abdominal activity while supine. CF patients recruited abdominal muscles at lower loads, earlier in the respiratory cycle, and to a higher recruitment level in both positions than the control subjects, but burst duration of phasic activity was not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 73 (2) ◽  
pp. 440-445 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. Calverley

Although inspiratory resistive loading (IRL) reduces the ventilatory response to CO2 (VE/PCO2) and increases the sensation of inspiratory effort (IES), there are few data about the converse situation: whether CO2 responsiveness influences sustained load compensation and whether awareness of respiratory effort modifies this behavior. We studied 12 normal men during CO2 rebreathing while free breathing and with a 10-cmH2O.l-1.s IRL and compared these data with 5 min of resting breathing with and without the IRL. Breathing pattern, end-tidal PCO2, IES, and mouth occlusion pressure (P0.1) were recorded. Free-breathing VE/PCO2 was inversely related to an index of effort perception (IES/VE; r = -0.63, P less than 0.05), and the reduction in VE/PCO2 produced by IRL was related to the initial free-breathing VE/PCO2 (r = 0.87, P less than 0.01). IRL produced variable increases in inspiratory duration (TI), IES, and P0.1 at rest, and the change in tidal volume correlated with both VE/PCO2 (r = 0.63, P less than 0.05) and IES/VE (r = -0.69, P less than 0.05), this latter index also predicting the changes in TI with loading (r = -0.83, P less than 0.01). These data suggest that in normal subjects perception of inspiratory effort can modify free-breathing CO2 responsiveness and is as important as CO2 sensitivity in determining the response to short-term resistive loading. Individuals with good perception choose a small-tidal volume and short-TI breathing pattern during loading, possibly to minimize the discomfort of breathing.


1976 ◽  
Vol 41 (3) ◽  
pp. 341-347 ◽  
Author(s):  
L. J. Bynum ◽  
J. E. Wilson ◽  
A. K. Pierce

Distribution of ventilation (V) and perfusion (Q) was studied with 133Xe in eight supine, normal subjects comparing spontaneous breathing (SB) and intermittent positive-pressure breathing (IPPB). Tidal volume, inspiratory flow, and breathing frequency measured during SB were closely matched during automatically triggered IPPB. V and Q in the lung bases (adjacent to the diaphragm) were decreased relative to other regions during SB and further diminished by IPPB at similar volumes. During IPPB, basilar V and Q improvedwhen tidal volume was increased; however; spontaneous hyperinflation resulted in significantly higher basilar V and Q than large tidal volumes delivered by IPPB. Thus, changes in lung volumes and gas exchange in the supine posture are attributable to impaired V and Q in the bases but not in dependent (posterior) regions. IPPB further reduces basilar V and Q, possibly due to loss of interdependence resulting from diminished respiratory muscle contraction. These findings may explain atelectasis during prolonged IPPB in supine patients. Although large tidal volumes improve basilar V during IPPB, spontaneous deep breaths are more effective and may prevent atelectasis better than IPPB at similar tidal volumes.


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


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.


Author(s):  
William J.M. Kinnear ◽  
James H. Hull

This chapter describes how the amount of air going in and out of the lungs increases on exercise. The predicted value for minute ventilation (VE) is calculated for each subject from their own forced expiratory volume in one second (FEV1), rather than taken from published tables. Normally, ventilation does not limit exercise and VE does not reach 80% of the predicted value. If VE at peak exercise is more than 80% of predicted, it is likely there is something wrong with the lungs. VE increases by a combination of a larger tidal volume and an increase in breathing frequency. The pattern of increase is normally gradual. An erratic pattern suggests dysfunctional breathing.


1993 ◽  
Vol 84 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Rachel C. Wilson ◽  
W. L. G. Oldfield ◽  
P. W. Jones

1. The effect of residence at altitude on the perception of breathlessness after return to sea level was examined in normal subjects. Breathlessness (Borg scale), minute ventilation, respiratory frequency, tidal volume, ‘oxygen pulse’ (oxygen consumption/heart rate) and the ventilatory equivalent for oxygen (minute ventilation/oxygen consumption) were measured at exercise (cycle-ergometer) during 5 months of training before 4 weeks at 4000 m and during the 6 month period after return to sea level. 2. There was no change in the subjects' pattern of breathing (respiratory frequency and tidal volume) or ‘oxygen pulse’ after the period at altitude (P = 0.0001). The ventilatory equivalent for oxygen was increased at all work rates after the period at altitude (P = 0.02). This ratio was slightly lower after 6 weeks and had returned to normal by 6 months (P = 0.4). 3. During training there was no change in breathlessness score (P = 0.6). On return to sea level, breathlessness score relative to ventilation was reduced (P = 0.0001). This was maintained for at least 6 weeks, but not as long as 6 months. 4. This study has demonstrated that, in normal subjects, the otherwise stable and reproducible relationship between breathlessness and ventilation may be disrupted for several weeks by factors other than lung disease. 5. The mechanism responsible for this is not clear, but the observations are consistent with the hypothesis that prior experience of breathlessness may condition subsequent estimates of breathlessness.


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.


1993 ◽  
Vol 74 (6) ◽  
pp. 2750-2756 ◽  
Author(s):  
W. D. Pitcher ◽  
H. S. Cunningham

Hypercapnia is associated with a shallow breathing pattern in patients with severe chronic obstructive pulmonary disease (COPD). We sought to determine the oxygen cost of increasing tidal volume and to relate this to hypercapnia [arterial PCO2 (PaCO2) > or = 45 Torr] and diaphragm flattening. We studied 3 normal subjects and 12 patients with stable but comparably severe COPD (forced expired volume in 1 s 1.01 +/- 0.09 liters) who had baseline PaCO2 ranging from 36 to 56 Torr. Oxygen consumption was measured during the subject's native breathing pattern and then while tidal volume was increased by 20%; minute ventilation was held constant by proportionately slowing frequency. There was a significant oxygen cost of increasing tidal volume for hypercapnic patients (235 +/- 23 to 260 +/- 25 ml O2/min; P = 0.002); no significant oxygen cost was observed in normal or eucapnic patients. This oxygen cost was positively correlated to baseline PaCO2 (r2 = 0.88, P < 0.001) and degree of diaphragm flattening assessed from chest radiographs (r2 = 0.74, P < 0.05). Although others have shown that force generation is preserved during chronic hyperinflation (G. A. Farkas and C. Roussos. J. Appl. Physiol. 54: 1635–1640, 1983; T. Similowski et al. N. Engl. J. Med. 325: 917–923, 1991), we conclude that diaphragm flattening produces mechanical inefficiency that may contribute to limiting the effective operating range of the respiratory muscles during tidal breathing.


Sign in / Sign up

Export Citation Format

Share Document