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.

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.

Hemodynamic effects of resistive breathing

1986 ◽  
Vol 60 (3) ◽  
pp. 846-853 ◽  
Author(s):  
R. Olgiati ◽  
G. Atchou ◽  
P. Cerretelli
Keyword(s):  
Minute Ventilation ◽  
Intrathoracic Pressure ◽  
Normal Subjects ◽  
Systemic Arterial Pressure ◽  
O2 Consumption ◽  
Hemodynamic Effects ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Myocardial O2 Consumption ◽  
End Tidal

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.

Effect of expiratory loading on glottic dimensions in humans

1985 ◽  
Vol 58 (2) ◽  
pp. 605-611 ◽  
Author(s):  
T. P. Brancatisano ◽  
D. S. Dodd ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Inverse Relationship ◽  
Time Course ◽  
Normal Subjects ◽  
Positive End Expiratory Pressure ◽  
Expiratory Resistance ◽  
Mouth Pressure ◽  
Internal Impedance ◽  
Resistive Loads ◽  
Increased Activity ◽  
Medullary Neurons

We examined the effects of external mechanical loading on glottic dimensions in 13 normal subjects. When flow-resistive loads of 7, 27, and 48 cmH2O X l-1 X s, measured at 0.2 l/s, were applied during expiration, glottic width at the mid-tidal volume point in expiration (dge) was 2.3 +/- 12, 37.9 +/- 7.5, and 38.3 +/- 8.9% (means +/- SE) less than the control dge, respectively. Simultaneously, mouth pressure (Pm) increased by 2.5 +/- 4, 3.0 +/- 0.4, and 4.6 +/- 0.6 cmH2O, respectively. When subjects were switched from a resistance to a positive end-expiratory pressure at comparable values of Pm, both dge and expiratory flow returned to control values, whereas the level of hyperinflation remained constant. Glottic width during inspiration (unloaded) did not change on any of the resistive loads. There was a slight inverse relationship between the ratio of expiratory to inspiratory glottic width and the ratio of expiratory to inspiratory duration. Our results show noncompensatory glottic narrowing when subjects breathe against an expiratory resistance and suggest that the glottic dimensions are influenced by the time course of lung emptying during expiration. We speculate that the glottic constriction is related to the increased activity of expiratory medullary neurons during loaded expiration and, by increasing the internal impedance of the respiratory system, may have a stabilizing function.

Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults

1993 ◽  
Vol 74 (2) ◽  
pp. 590-595 ◽  
Author(s):  
Y. Akiyama ◽  
M. Nishimura ◽  
S. Kobayashi ◽  
A. Yoshioka ◽  
M. Yamamoto ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Specific Effects ◽  
Mouth Pressure ◽  
End Tidal ◽  
Visual Analogue Scaling ◽  
The Brain ◽  
Normal Adults

To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19–27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.

scholarly journals Control of breathing during sleep assessed by proportional assist ventilation

1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Control Of Breathing ◽  
Respiratory Drive ◽  
Proportional Assist Ventilation ◽  
End Tidal

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men

1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Response Dynamics ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Nonsteady State ◽  
End Tidal

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion

1977 ◽  
Vol 43 (6) ◽  
pp. 971-976 ◽  
Author(s):  
D. J. Riley ◽  
B. A. Legawiec ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Carbon Dioxide Tension ◽  
Base Line ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
Hypercapnic Ventilatory Response ◽  
The Central Nervous System ◽  
End Tidal

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (VE), end-tidal carbon dioxide tension (PETCO2), venous bicarbonate concentration [HCO3-], oxygen consumption (VO2), hypercapnic ventilatory response (deltaVE/deltaPCO2), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 +/- 2.0 mg/dl. VE increased (P less than 0.05, PETCO2 decreased (P less than 0.05), and [HCO3-] did not change significantly during drug ingestion. deltaVE/deltaPCO2 increased gradually to a value 37% greater than control by day 3 and remained constant (P less 0.01). A increased by 251% and VO2 by 18% within 2 h and remained constant for the remainder of the ASA period (P less than 0.01). All values returned to base line within 24 h following cessation of ASA. We conclude that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanically linked to changes in metabolic rate.

Validation of esophageal balloon technique at different lung volumes and postures

1987 ◽  
Vol 62 (1) ◽  
pp. 315-321 ◽  
Author(s):  
A. Baydur ◽  
E. J. Cha ◽  
C. S. Sassoon
Keyword(s):  
Lung Volume ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Lung Volumes ◽  
Pleural Surface ◽  
Mouth Pressure ◽  
Esophageal Balloon ◽  
Balloon Technique ◽  
Pressure Changes

The esophageal balloon technique for measuring pleural surface pressure (Ppl) has recently been shown to be valid in recumbent positions. Questions remain regarding its validity at lung volumes higher and lower than normally observed in upright and horizontal postures, respectively. We therefore evaluated it further in 10 normal subjects, seated and supine, by measuring the ratio of esophageal to mouth pressure changes (delta Pes/delta Pm) during Mueller, Valsalva, and occlusion test maneuvers at FRC, 20, 40, 60, and 80% VC with the balloon placed 5, 10, and 15 cm above the cardia. In general, delta Pes/delta Pm was highest at the 5-cm level, during Mueller maneuvers and occlusion tests, regardless of posture or lung volume (mean range 1.00–1.08). At 10 and 15 cm, there was a progressive increase in delta Pes/delta Pm with volume (from 0.85 to 1.14). During Valsalva maneuvers, delta Pes/delta Pm also tended to increase with volume while supine (range 0.91–1.04), but was not volume-dependent while seated. Qualitatively, observed delta Pes/delta Pm fit predicted corresponding values (based on lung and upper airway compliances). Quantitatively there were discrepancies probably due to lack of measurement of esophageal elastance and to inhomogeneities in delta Ppl. At every lung volume in both postures, there was at least one esophageal site where delta Pes/delta Pm was within 10% of unity.

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.

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