Measurement of Mouth Occlusion Pressure as an Index of Respiratory Centre Output in Man

1977 ◽  
Vol 53 (2) ◽  
pp. 117-123 ◽  
Author(s):  
N. K. Burki ◽  
L. K. Mitchell ◽  
B. A. Chaudhary ◽  
F. W. Zechman
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Close Correlation ◽  
Regression Coefficients ◽  
Occlusion Pressure ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Respiratory Centre ◽  
Mouth Occlusion Pressure ◽  
End Tidal

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.

Lung volume, closing volume, and gas exchange

1982 ◽  
Vol 52 (6) ◽  
pp. 1453-1457 ◽  
Author(s):  
S. C. Morrison ◽  
D. G. Stubbing ◽  
P. V. Zimmerman ◽  
E. J. Campbell
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Normal Subjects ◽  
Close Correlation ◽  
Closing Volume ◽  
Tidal Breathing ◽  
Co2 Partial Pressure ◽  
Residual Capacity ◽  
End Tidal ◽  
Arterial O2 Saturation

The effect of a voluntary reduction in lung volume on arterial O2 saturation (SaO2) was studied in 10 normal subjects aged 19–63 yr. SaO2 was measured by ear oximetry first during tidal breathing at functional residual capacity, and then during tidal breathing at 380 ml above residual volume. Tidal volume and breathing frequency were kept constant, and end-tidal CO2 partial pressure remained stable or fell in 9 out of 10 subjects. When lung volume was reduced, SaO2 fell by a mean of 1.5% (range 0–3%). Closing volume (CV) was measured by the N2-washout method (mean 0.89 liter, range 0.41–1.44). There was a close correlation between CV and the fall in SaO2 (r = 0.867, P = 0.001). Arterial and mixed venous CO2 were measured in one subject; the results indicated some fall in cardiac output following the lung volume change, but this accounted for less than half of the fall in SaO2. The relationship between CV and the lung volume at which tidal breathing occurs is an important determinant of pulmonary gas exchange through its effect on the matching of ventilation to perfusion.

Diaphragmatic EMG and occlusion pressure response to elastic loading during CO2 rebreathing in humans

1980 ◽  
Vol 49 (4) ◽  
pp. 669-675 ◽  
Author(s):  
M. Lopata ◽  
J. L. Pearle
Keyword(s):  
Average Rate ◽  
Normal Subjects ◽  
Occlusion Pressure ◽  
Load Compensation ◽  
Co2 Rebreathing ◽  
Elastic Loading ◽  
Inspiratory Activity ◽  
Mouth Occlusion Pressure ◽  
End Tidal ◽  
Change In Mean

The effects of external elastic loading (EL) (19 cmH2O/l), applied continuously (C) and intermittently (I) during CO2 rebreathing, on diaphragmatic electromyogram (EMGdi), mouth occlusion pressure (P0.15), and ventilation (VI) were studied in normal subjects. EMGdi was analyzed as moving time average and quantitated in terms of peak (mean p) and average rate of rise of inspiratory activity (mean p/TI). CEL resulted in an increased mean p/TI response to CO2 in all subjects with P0.15 increasing in proportion to EMGdi. Tidal volume (VT) during rebreathing was decreased in all cases with VI being preserved in four of six runs due to increased breathing frequency (f). Although mean p was increased for a given end-tidal CO2 (PACO2) level during CEL, for a given rate of rise of inspiratory activity mean p was decreased in three of five subjects, indicating a diminished threshold for inspiratory "off-switch." CEL results in an augmented inspiratory drive that serves to increase muscle output and stabilize VT; the increased drive and decrease inspiratory off-switch threshold shorten TI mediating the compensatory increase in f. The first breath IEL resulted in decreased VT and mean p without change in mean p/TI, and all increased with subsequent loaded breaths independent of changes in PCO2. Load compensation for externally applied EL is mediated by neural mechanisms independent of chemical drive.

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.

Lung mechanics and neuromuscular output during CO2 inhalation after airway anesthesia

1987 ◽  
Vol 63 (6) ◽  
pp. 2542-2548 ◽  
Author(s):  
T. Y. Sullivan ◽  
E. L. DeWeese ◽  
P. L. Yu ◽  
G. R. Aronoff
Keyword(s):  
Mechanical Load ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Pleural Pressure ◽  
Detectable Effect ◽  
Occlusion Pressure ◽  
Air Breathing ◽  
Residual Capacity ◽  
Mouth Occlusion Pressure

Airway anesthesia with aerosolized lidocaine has been associated with an increase in minute ventilation (VE) during CO2 inhalation. The increase in VE may be due to increased neuromuscular output or decreased mechanical load on breathing. To evaluate this we measured VE, breathing pattern, mouth occlusion pressure, and lung mechanics in 20 normal subjects during room-air breathing and then inhalation of 6% CO2–94% O2, before and after airway anesthesia. Measurements of lung mechanics included whole-lung resistance, dynamic and static compliance, and functional residual capacity. Airway anesthesia had no detectable effect on any measurements during room-air breathing. During CO2 inhalation, airway anesthesia produced increases in VE and mean inspiratory flow rate (VT/TI) and more negative inspiratory pleural pressure but had no detectable effect on lung mechanics or mouth occlusion pressure. Pleural pressure was more negative during the latter 25% of inspiration. We concluded that airway receptors accessible to airway anesthesia play a role in determining neuromuscular output during CO2 inhalation.

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.

Inspiratory muscles during exercise: a problem of supply and demand

1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Supply And Demand ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Maximum Exercise ◽  
Lung Capacity ◽  
Inspiratory Muscles ◽  
Residual Capacity

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.

Influence of inspiratory flow rate and frequency on O2 cost of resistive breathing in humans

1988 ◽  
Vol 65 (2) ◽  
pp. 760-766 ◽  
Author(s):  
D. S. Dodd ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Flow Rate ◽  
Duty Cycle ◽  
Normal Subjects ◽  
Work Rate ◽  
Inspiratory Flow ◽  
Inspiratory Flow Rate ◽  
Contraction Frequency ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Residual Capacity

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)

scholarly journals Lung elastic recoil during breathing at increased lung volume

1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  
Keyword(s):  
Stress Relaxation ◽  
Tidal Volume ◽  
Lung Volume ◽  
Normal Subjects ◽  
Dynamic Hyperinflation ◽  
Airway Closure ◽  
Elastic Recoil ◽  
Volume Increase ◽  
Before And After ◽  
Residual Capacity

During dynamic hyperinflation with induced bronchoconstriction, there is a reduction in lung elastic recoil at constant lung volume (R. Pellegrino, O. Wilson, G. Jenouri, and J. R. Rodarte. J. Appl. Physiol. 81: 964–975, 1996). In the present study, lung elastic recoil at control end inspiration was measured in normal subjects in a volume displacement plethysmograph before and after voluntary increases in mean lung volume, which were achieved by one tidal volume increase in functional residual capacity (FRC) with constant tidal volume and by doubling tidal volume with constant FRC. Lung elastic recoil at control end inspiration was significantly decreased by ∼10% within four breaths of increasing FRC. When tidal volume was doubled, the decrease in computed lung recoil at control end inspiration was not significant. Because voluntary increases of lung volume should not produce airway closure, we conclude that stress relaxation was responsible for the decrease in lung recoil.

Gravity effects on upper airway area and lung volumes during parabolic flight

1998 ◽  
Vol 84 (5) ◽  
pp. 1639-1645 ◽  
Author(s):  
Maurice Beaumont ◽  
Redouane Fodil ◽  
Daniel Isabey ◽  
Frédéric Lofaso ◽  
Dominique Touchard ◽  
...  
Keyword(s):  
Lung Volume ◽  
Parabolic Flight ◽  
Upper Airway ◽  
Normal Subjects ◽  
Lung Volumes ◽  
Acoustic Reflection ◽  
Volume Functional ◽  
Airway Caliber ◽  
Gravity Effects ◽  
Residual Capacity

We measured upper airway caliber and lung volumes in six normal subjects in the sitting and supine positions during 20-s periods in normogravity, hypergravity [1.8 + head-to-foot acceleration (Gz)], and microgravity (∼0 Gz) induced by parabolic flights. Airway caliber and lung volumes were inferred by the acoustic reflection method and inductance plethysmography, respectively. In subjects in the sitting position, an increase in gravity from 0 to 1.8 +Gz was associated with increases in the calibers of the retrobasitongue and palatopharyngeal regions (+20 and +30%, respectively) and with a concomitant 0.5-liter increase in end-expiratory lung volume (functional residual capacity, FRC). In subjects in the supine position, no changes in the areas of these regions were observed, despite significant decreases in FRC from microgravity to normogravity (−0.6 liter) and from microgravity to hypergravity (−0.5 liter). Laryngeal narrowing also occurred in both positions (about −15%) when gravity increased from 0 to 1.8 +Gz. We concluded that variation in lung volume is insufficient to explain all upper airway caliber variation but that direct gravity effects on tissues surrounding the upper airway should be taken into account.

Respiratory movements of the vocal cords

1983 ◽  
Vol 54 (5) ◽  
pp. 1269-1276 ◽  
Author(s):  
T. Brancatisano ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Lung Volume ◽  
Respiratory Control ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Tight Coupling ◽  
Tidal Breathing ◽  
Vocal Cords ◽  
Residual Capacity ◽  
The Relationship ◽  
Respiratory Movements

We examined the movements of the vocal cords during tidal breathing, panting, and large changes in lung volume in 12 normal subjects. The glottis was observed with a fiber-optic bronchoscope, and the glottic image was recorded together with flow, volume, and a time marker onto videotape. Phasic respiratory swings in glottic width (dg) and glottic area (Ag) were reproducible in all subjects but differed substantially between subjects. In the group as a whole dg and Ag increased during inspiration to 10.1 +/- 5.6 mm and 126 +/- 8 mm2 (mean +/- SE), respectively, whereas during expiration the lowest values were 5.7 +/- 0.5 mm and 70 +/- 7 mm2, respectively. These extreme dimensions corresponded closely to the midtidal volume points in the respiratory cycle. Glottic width during vital capacity (VC) expirations was nearly 30% greater at a flow of 1.2 l/s than at 0.5 l/s, but the relationship between dg and lung volume differed between subjects. When swings in dg were minimized by panting, there was no difference in dg between functional residual capacity (FRC) and a volume corresponding to midinspiratory capacity. However, tidal breathing at this lung volume was associated with a 20% decrease in dg compared with breathing at FRC. Our observations indicate a tight coupling between the pattern of glottic movement and the respiratory volume cycle. The results suggest that during voluntary respiratory maneuvers both intrinsic laryngeal and respiratory muscles are recruited, participating as effector organs in ventilatory and respiratory control.

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