Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

Effort sensation, chemoresponsiveness, and breathing pattern during inspiratory resistive loading

1992 ◽  
Vol 73 (2) ◽  
pp. 440-445 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. Calverley
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Sustained Load ◽  
Resistive Loading ◽  
End Tidal ◽  
Few Data ◽  
Normal Men

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.

scholarly journals Effect of expiratory resistive loading on the noninvasive tension-time index in COPD

2000 ◽  
Vol 89 (5) ◽  
pp. 2007-2014 ◽  
Author(s):  
William H. Thompson ◽  
Paula Carvalho ◽  
James P. Souza ◽  
Nirmal B. Charan
Keyword(s):  
Normal Subjects ◽  
Respiratory Cycle ◽  
Inspiratory Pressure ◽  
Occlusion Pressure ◽  
Time Index ◽  
Inspiratory Muscles ◽  
Copd Patients ◽  
Resistive Loading ◽  
Tension Time ◽  
Mouth Occlusion Pressure

Expiratory resistive loading (ERL) is used by chronic obstructive pulmonary disease (COPD) patients to improve respiratory function. We, therefore, used a noninvasive tension-time index of the inspiratory muscles (TTmus =P̄i/Pi max × Ti/Tt, where P̄i is mean inspiratory pressure estimated from the mouth occlusion pressure, Pi max is maximal inspiratory pressure, Ti is inspiratory time, and Tt is total respiratory cycle time) to better define the effect of ERL on COPD patients. To accomplish this, we measured airway pressures, mouth occlusion pressure, respiratory cycle flow rates, and functional residual capacity (FRC) in 14 COPD patients and 10 normal subjects with and without the application of ERL. TTmus was then calculated and found to drop in both COPD and normal subjects ( P < 0.05). The decline in TTmus in both groups resulted solely from a prolongation of expiratory time with ERL ( P < 0.001 for COPD, P < 0.05 for normal subjects). In contrast to the COPD patients, normal subjects had an elevation in P̄i and FRC, thus minimizing the decline in TTmus. In conclusion, ERL reduces the potential for inspiratory muscle fatigue in COPD by reducing Ti/Tt without affecting FRC andP̄i.

Augmentation of CO2 drives by chlormadinone acetate, a synthetic progesterone

1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Pressure Response ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Physiological Basis ◽  
Load Compensation ◽  
Chlormadinone Acetate ◽  
Arterial Blood ◽  
Resistive Loading

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

Costal and crural diaphragm in early inspiration: free breathing and occlusion

1987 ◽  
Vol 63 (4) ◽  
pp. 1622-1628 ◽  
Author(s):  
P. A. Easton ◽  
J. W. Fitting ◽  
A. E. Grassino
Keyword(s):  
Pressure Measurement ◽  
Neural Control ◽  
Free Breathing ◽  
Inspiratory Effort ◽  
Electromyographic Activity ◽  
Occlusion Pressure ◽  
Airway Occlusion ◽  
Co2 Rebreathing ◽  
Control Patterns ◽  
Crural Diaphragm

Changes in length of costal and crural segments of the canine diaphragm were measured by sonomicrometry within the first 100–300 ms of inspiration during CO2 rebreathing in anesthetized animals. Both segments showed small but significant decreases in end-expiratory length during progressive hypercapnia. Although both costal and crural segments showed electromyographic activity within the first 100 ms of inspiration, in early inspiration crural shortening predominated with minimal costal shortening. Neither segment contracted isometrically early in inspiration in the presence of airway occlusion. The amount of crural shortening during airway occlusion exceeded costal shortening; both segments showed increased shortening with prolonged occlusion and increasing CO2. Costal and crural shortening at 100 ms was not different for unoccluded and occluded states. These observations suggest that neural control patterns evoke discrete and unequal contributions from the diaphragmatic segments at the beginning of an inspiration; the crural segment may be predominately recruited in early inspiration. Despite traditional assumptions about occlusion pressure measurement (P0.1), diaphragm segments do not contract isometrically during early inspiratory effort against an occluded airway.

Effect of chest wall distortion on occlusion pressure and the preterm diaphragm

1983 ◽  
Vol 55 (2) ◽  
pp. 359-364 ◽  
Author(s):  
P. N. LeSouef ◽  
J. M. Lopes ◽  
S. J. England ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Chest Wall ◽  
Preterm Infants ◽  
Face Mask ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Transdiaphragmatic Pressure ◽  
Airway Occlusion ◽  
Mouth Pressure ◽  
Gastric Pressure ◽  
Mouth Occlusion Pressure

We studied the effect of chest wall distortion (CWD) on transdiaphragmatic pressure (Pdi) and/or mouth pressure during end-expiratory airway occlusions in seven preterm infants. We measured mouth occlusion pressure (Pmo) with a face mask and pressure transducer, gastric pressure (Pga) with a fluid-filled catheter, diaphragmatic electromyogram (Edi) using surface electrodes, and rib cage and abdominal motion using magnetometers. We reasoned that Pdi = Pmo - Pga on airway occlusion. Periods with maximal and periods with minimal CWD were compared. We found that 1) when CWD was minimal, an increase in Edi produced an increase in Pmo and Pdi in all infants; when CWD was greatest, large increases in Edi produced no increase in Pmo or Pdi in four infants; 2) when breaths with the same Pmo or Pdi from each period in each infant were compared, those from the period with greatest CWD had an increased Edi (mean increase 76%, P less than 0.005, and 144%, P less than 0.01, for Pmo and Pdi, respectively). We conclude that in preterm infants, Pmo can be a poor indicator of respiratory drive, and CWD markedly limits the effectiveness of the diaphragm as a force generator.

Effect of ethanol and naloxone on control of ventilation and load perception

1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte
Keyword(s):  
Normal Subjects ◽  
Ethanol Ingestion ◽  
Resistive Load ◽  
Load Compensation ◽  
Ventilatory Responses ◽  
Resistive Loading ◽  
Resistive Loads ◽  
Mouth Occlusion Pressure ◽  
Load Perception ◽  
Respiratory Depressant

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.

Effect of resistive loading on ventilatory response to hypoxia

1975 ◽  
Vol 38 (6) ◽  
pp. 965-968 ◽  
Author(s):  
A. S. Rebuck ◽  
E. F. Juniper
Keyword(s):  
Response Curve ◽  
Mechanical Load ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Normal Subjects ◽  
Arterial Oxygen ◽  
Resistive Load ◽  
O2 Concentration ◽  
Resistive Loading ◽  
Ventilatory Response To Hypoxia

Ventilatory responses to hypoxia, with and without an inspiratory resistive load, were measured in eight normal subjects, using a rebreathing technique. During the studies, the end-tidal P-CO2 was kept constant at mixed venous level (Pv-CO2) by drawing expired gas through a variable CO2-absorbing bypass. The initial bag O2 concentration was 24% and rebreathing was continued until the O2 concentration in the bag fell to 6% or the subject's arterial oxygen saturation (Sa-O2), monitored continuously by ear oximetry, fell to 70%. Studies with and without the load were performed in a formally randomized order for each subject. Linear regressions for rise in ventilation against fall in Sa-O2 were calculated. The range of unloaded responses was 0.78–3.59 1/min per 1% fall in Sa-O2 and loaded responses 0.37–1.68 1/min per 1% fall in Sa-O2. In each subject, the slope of the response curve during loading fell by an almost constant fraction of the unloaded response, such that the ratio of loaded to unloaded slope in all subjects ranged from 0.41 to 0.48. However, the extrapolated intercept of the response curve on the Sa-O2 axis did not alter significantly indicating that the P-CO2 did not alter between experiments. These results suggest that the change in ventilatory response to hypoxia during inspiratory resistive loading is related to the mechanical load applied, with the loaded slope being directly proportional to the unloaded one.

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 to external inspiratory resistive loading and bronchospasm in anesthetized dogs

1982 ◽  
Vol 53 (2) ◽  
pp. 355-360 ◽  
Author(s):  
J. Savoy ◽  
M. E. Arnup ◽  
N. R. Anthonisen
Keyword(s):  
Breathing Pattern ◽  
External Loading ◽  
Vagal Activity ◽  
Occlusion Pressure ◽  
Ventilatory Drive ◽  
Resistive Loading ◽  
Lung Resistance ◽  
Anesthetized Dogs ◽  
Mouth Occlusion Pressure ◽  
Pentobarbital Sodium Anesthesia

Mouth occlusion pressure (P0.1) and breathing-pattern responses to external inspiratory resistive loading and methacholine chloride-induced bronchospasm were assessed in six dogs under pentobarbital sodium anesthesia. There was no change in P0.1 with external loading, but, in response to bronchospasm, we observed a P0.1 increase proportional to the change in lung resistance. These results indicate that, unlike external loading, the ventilatory-drive adaptation to bronchospasm does not require consciousness of the animal. The breathing-pattern response to bronchospasm consisted of tachypnea associated with decreased tidal volume (VT), decreased inspiratory duration (TI), and unchanged mean inspiratory flow (VT/TI). In response to resistive loading there was no tachypnea, VT decreased, TI was unchanged, and VT/TI decreased. We suggest that in response to resistive loading there was no modification of vagal activity, whereas in bronchospasm there was an increase of vagal activity, which was responsible for the changes in breathing pattern and, at least in part, for the changes in P0.1.

Respiratory Drive in Nonsmokers and Smokers Assessed by Passive Tilt and Mouth Occlusion Pressure

CHEST Journal ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 6-10 ◽  
Author(s):  
T.S. Chadha ◽  
E. Lang ◽  
S. Birch ◽  
M. A Sackner
Keyword(s):  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Mouth Occlusion Pressure
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