Role of Impaired Inspiratory Muscle Function in Limiting the Ventilatory Response to Carbon Dioxide in Chronic Airflow Obstruction

1983 ◽  
Vol 64 (5) ◽  
pp. 487-495 ◽  
Author(s):  
H. R. Gribbin ◽  
I. T. Gardiner ◽  
G. J. Heinz ◽  
G. J. Gibson ◽  
N. B. Pride
Keyword(s):  
Muscle Activation ◽  
Ventilatory Response ◽  
Work Of Breathing ◽  
Airflow Obstruction ◽  
Normal Subjects ◽  
Inspiratory Muscle ◽  
Pleural Pressure ◽  
Pulmonary Mechanics ◽  
Respiratory Drive ◽  
Inspiratory Muscles

1. Twenty patients with severe chronic airflow obstruction (CAFO), four of whom were hypercapnic, had greatly reduced ventilatory responses to rebreathing CO2 under hyperoxic conditions, compared with the responses in normal subjects. 2. Mouth occlusion pressure (P0.1) responses to CO2 were also reduced in the patients compared with those of normal subjects but the reduction was less severe than in the ventilatory response. 3. in ten patients with CAFO minimum pleural pressure during tidal breathing [Ppl min. (dynamic)] at a Pco2 of 8.0 kPa was only slightly less negative than in the normal subjects (−16.2 cm water vs −23.4 cm water). 4. During rebreathing end-expiratory volume (EEV) fell progressively in the normal subjects (mean fall = 800 ml); in the patients there was a progressive rise in EEV (mean rise = 390 ml). 5. When Ppl min. (dynamic) was compared with minimum static pleural pressures at the same lung volume the patients were generating a much higher proportion of their available static pressure (47.0%) than the normal subjects (26.4%) at a Pco2 of 8.0 kPa, suggesting that despite the slightly less negative Ppl min. (dynamic), inspiratory muscle activation was greater in the patients than in normal subjects. Similar conclusions were reached from an analysis of the inspiratory work of breathing. 6. We conclude that hyperinflation, by impairing the capacity of the inspiratory muscles to lower pleural pressure, reduces the ventilatory response to CO2 and adds to the effects of abnormalities in pulmonary mechanics so that measurements of absolute pleural pressure or work of breathing underestimate inspiratory muscle activation in patients with severe CAFO. 7. Hyperinflation and severe airflow obstruction also reduce the change in P0.1 for a given degree of inspiratory muscle activation. 8. Our results suggest that, despite the impaired pressure and ventilatory response to rebreathing CO2 in the patients, their central respiratory drive was greater than that of the normal subjects.

The Rate of Isometric Inspiratory Pressure Development as a Measure of Responsiveness to Carbon Dioxide in Man

1975 ◽  
Vol 49 (1) ◽  
pp. 57-68 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell
Keyword(s):  
Initial Rate ◽  
Ventilatory Response ◽  
Pressure Change ◽  
Normal Subjects ◽  
Inspiratory Pressure ◽  
Pulmonary Mechanics ◽  
Inspiratory Muscles ◽  
Pressure Development ◽  
Respiratory Centre ◽  
Very High

1. A technique has been developed for assessing CO2 responsiveness by measuring the maximum rate of isometric inspiratory pressure change at the mouth [(dP/dt)max.]. 2. By use of a rebreathing technique, the (dP/dt)max. response to CO2 was shown to correlate well with the ventilatory response in thirty-two normal subjects. 3. The addition of an external flow resistance sufficient to reduce the ventilatory response by a mean of 33.4% produced no significant mean change in the (dP/dt)max. response in thirty subjects. 4. In six patients recovering from bronchial asthma, reduction of airways obstruction led to a mean increase in the ventilatory response of 109% without any significant mean change in the (dP/dt)max. response. 5. An increase in lung volume did not reduce the (dP/dt)max. response in five normal subjects. 6. At very high lung volumes, six normal subjects were able to develop a higher (dP/dt)max. during voluntary inspiratory efforts than has been recorded during spontaneous breathing response to CO2. 7. It is believed that (dP/dt)max. represents the initial rate of development of force by the inspiratory muscles before this can be modified by mechanical loading, proprioceptive feedback mechanisms or conscious response and can therefore be used to study changes in the motor output of the respiratory centre in response to ventilatory stimuli independently of pulmonary mechanics.

Influence of lung volume on oxygen cost of resistive breathing

1986 ◽  
Vol 61 (1) ◽  
pp. 16-24 ◽  
Author(s):  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Lung Volume ◽  
Work Of Breathing ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Constant Load ◽  
Inspiratory Muscle ◽  
Mechanical Coupling ◽  
Inspiratory Muscles ◽  
Inspiratory Resistance ◽  
Residual Capacity

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.

Pressure-flow effects on endurance of inspiratory muscles

1986 ◽  
Vol 60 (1) ◽  
pp. 299-303 ◽  
Author(s):  
F. D. McCool ◽  
D. R. McCann ◽  
D. E. Leith ◽  
F. G. Hoppin
Keyword(s):  
Normal Subjects ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Inspiratory Muscle ◽  
Negative Slope ◽  
Muscle Endurance ◽  
Inspiratory Muscles ◽  
Wide Range ◽  
Flow Effects ◽  
Forced Breathing

We examined the effects of varying inspiratory pressures and flows on inspiratory muscle endurance. Four normal subjects performed voluntary forced breathing with various assigned inspiratory tasks. Duty cycle, tidal volume, and mean lung volume were the same in all tasks. Mean esophageal pressure, analogous to a pressure-time integral (PTes), was varied over a wide range. In each task the subject maintained an assigned PTes while breathing on one of a range of inspiratory resistors, and this gave a range of inspiratory flows at any given PTes. Inspiratory muscle endurance for each task was assessed by the length of time the task could be maintained (Tlim). For a given resistor, Tlim increased as PTes decreased. At a given PTes, Tlim increased as the external resistance increased and therefore as mean inspiratory flow rate (VI) decreased. Furthermore, for a given Tlim, PTes and VI were linearly related with a negative slope. We conclude that inspiratory flow, probably because of its relationship to the velocity of muscle shortening, is an independent variable importantly influencing endurance of the inspiratory muscles.

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.

Ventilatory compensation for changes in functional residual capacity during sleep

1987 ◽  
Vol 62 (3) ◽  
pp. 1299-1306 ◽  
Author(s):  
R. L. Begle ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Functional Residual Capacity ◽  
Minute Ventilation ◽  
Muscle Length ◽  
Normal Subjects ◽  
Conscious State ◽  
Inspiratory Muscle ◽  
Compensatory Response ◽  
Inspiratory Muscles ◽  
Residual Capacity

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.

scholarly journals Mechanisms of Orthopnoea in Patients with Advanced COPD

2020 ◽  
pp. 2000754
Author(s):  
Amany F. Elbehairy ◽  
Azmy Faisal ◽  
Hannah McIsaac ◽  
Nicolle J. Domnik ◽  
Kathryn M. Milne ◽  
...  
Keyword(s):  
Supine Position ◽  
Minute Ventilation ◽  
Pulmonary Function Tests ◽  
Work Of Breathing ◽  
Airflow Obstruction ◽  
Lung Compliance ◽  
Chronic Obstructive ◽  
Inspiratory Muscles ◽  
Elastic Loading ◽  
Dynamic Lung Compliance

Many patients with severe chronic obstructive pulmonary disease (COPD) report unpleasant respiratory sensation at rest, further amplified by adoption of supine position (orthopnoea). The mechanisms of this acute symptomatic deterioration are poorly understood.16 patients with advanced COPD and history of orthopnoea and 16 age- and sex-matched healthy controls (CTRL) underwent pulmonary function tests and detailed sensory-mechanical measurements including inspiratory neural drive (IND, diaphragm electromyography), oesophageal and gastric pressures in sitting and supine positions.Patients had severe airflow obstruction (FEV1: 40±18%predicted) and lung hyperinflation. Regardless of the position, patients had lower inspiratory capacity (IC) and higher IND for a given tidal volume (i.e. greater neuromechanical dissociation (NMD)), higher intensity of breathing discomfort, minute ventilation (⩒E) and breathing frequency (Fb) compared with CTRL (all p<0.05). In supine position in CTRL (versus sitting erect): IC increased (by 0.48L) with a small drop in ⩒E mainly due to reduced Fb (all p<0.05). By contrast, patients’ IC remained unaltered, but dynamic lung compliance decreased (p<0.05) in the supine position. Breathing discomfort, inspiratory work of breathing, inspiratory effort, IND, NMD and neuro-ventilatory uncoupling all increased in COPD in the supine position (p<0.05), but not in CTRL. Orthopnoea was associated with acute changes in IND (r=0.65, p=0.01), neuro-ventilatory uncoupling (r=0.76, p=0.001) and NMD (r=0.73, p=0.002).In COPD, onset of orthopnoea coincided with an abrupt increase in elastic loading of the inspiratory muscles in recumbency in association with increased IND and greater neuromechanical dissociation of the respiratory system.

scholarly journals Performance Evaluation of Fixed Sample Entropy in Myographic Signals for Inspiratory Muscle Activity Estimation

Entropy ◽  
2019 ◽  
Vol 21 (2) ◽  
pp. 183 ◽  
Author(s):  
Manuel Lozano-García ◽  
Luis Estrada ◽  
Raimon Jané
Keyword(s):  
Muscle Activity ◽  
Muscle Activation ◽  
Cardiac Activity ◽  
Sample Entropy ◽  
Inspiratory Muscle ◽  
Chronic Obstructive ◽  
Inspiratory Muscles ◽  
Fixed Sample ◽  
Cross Covariance ◽  
Activity Estimation

Fixed sample entropy (fSampEn) has been successfully applied to myographic signals for inspiratory muscle activity estimation, attenuating interference from cardiac activity. However, several values have been suggested for fSampEn parameters depending on the application, and there is no consensus standard for optimum values. This study aimed to perform a thorough evaluation of the performance of the most relevant fSampEn parameters in myographic respiratory signals, and to propose, for the first time, a set of optimal general fSampEn parameters for a proper estimation of inspiratory muscle activity. Different combinations of fSampEn parameters were used to calculate fSampEn in both non-invasive and the gold standard invasive myographic respiratory signals. All signals were recorded in a heterogeneous population of healthy subjects and chronic obstructive pulmonary disease patients during loaded breathing, thus allowing the performance of fSampEn to be evaluated for a variety of inspiratory muscle activation levels. The performance of fSampEn was assessed by means of the cross-covariance of fSampEn time-series and both mouth and transdiaphragmatic pressures generated by inspiratory muscles. A set of optimal general fSampEn parameters was proposed, allowing fSampEn of different subjects to be compared and contributing to improving the assessment of inspiratory muscle activity in health and disease.

Effects of progressive hypoxia on parasternal, costal, and crural diaphragm activation

1989 ◽  
Vol 66 (6) ◽  
pp. 2579-2584 ◽  
Author(s):  
G. B. Darian ◽  
A. F. DiMarco ◽  
S. G. Kelsen ◽  
G. S. Supinski ◽  
S. B. Gottfried
Keyword(s):  
Chest Wall ◽  
Neural Control ◽  
Muscle Activation ◽  
Electromyographic Activity ◽  
Respiratory Drive ◽  
Intercostal Muscle ◽  
Inspiratory Muscles ◽  
Rate Of Increase ◽  
Progressive Hypoxia ◽  
Crural Diaphragm

The distribution of motor drive to the costal and crural diaphragm and parasternal intercostal muscles was evaluated during progressive isocapnic hypoxia in anesthetized dogs. Bipolar stainless steel wire electrodes were placed unilaterally into the costal and crural portions of the diaphragm and into the parasternal intercostal muscle in the second or third intercostal space. Both peak and rate of rise of electromyographic activity of each chest wall muscle increased in curvilinear fashion in response to progressive hypoxia. Both crural and parasternal intercostal responses, however, were greater than those of the costal diaphragm. The onset of crural activation preceded that of the costal portion of the diaphragm and parasternal intercostal muscle activation. Despite differences in the degree of activation among the various chest wall muscles, the rate of increase in activation for any given muscle was linearly related to the rate of increases for the other two. This suggests that respiratory drive during progressive hypoxia increases in fixed proportion to the different chest wall inspiratory muscles. Our findings lend further support to the concept that the costal and crural diaphragm are governed by separate neural control mechanisms and, therefore, may be considered separate muscles.

Pulmonary mechanics during the ventilatory response to hypoxemia in the newborn monkey

1983 ◽  
Vol 55 (3) ◽  
pp. 1008-1014 ◽  
Author(s):  
W. A. LaFramboise ◽  
R. D. Guthrie ◽  
T. A. Standaert ◽  
D. E. Woodrum
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lung Compliance ◽  
Pulmonary Mechanics ◽  
Base Line ◽  
Respiratory Drive ◽  
Pulmonary Resistance ◽  
Residual Capacity ◽  
Dynamic Lung Compliance ◽  
Sustained Increase

Dynamic lung compliance (CL), inspiratory pulmonary resistance (RL), and functional residual capacity (FRC) were measured in 10 unanesthetized 48 h-old newborn monkeys and seven 21-day-old infant monkeys during acute exposures to an equivalent level of hypoxemia. End-expiratory airway occlusions were performed and the pressure developed by 200 ms (P0.2) was utilized as an index of central respiratory drive. P0.2 demonstrated a sustained increase throughout the period of hypoxemia on day 2 despite the fact that minute ventilation (VI) initially increased but then fell back to base-line levels. Dynamic lung compliance fell and FRC increased by 5 min of hypoxemia in the newborns. The 21-day-old monkeys exhibited a sustained increase in both VI and P0.2 throughout the hypoxic period with no change in CL and FRC. RL did not change at either postnatal age during hypoxemia. These data indicate that the neonatal monkey is subject to changes in pulmonary mechanics (decreased CL and increased FRC) during hypoxemia and that these changes are eliminated with maturation.

Inspiratory muscle relaxation rate after voluntary maximal isocapnic ventilation in humans

1991 ◽  
Vol 70 (5) ◽  
pp. 2173-2180 ◽  
Author(s):  
D. A. Mulvey ◽  
N. G. Koulouris ◽  
M. W. Elliott ◽  
C. M. Laroche ◽  
J. Moxham ◽  
...  
Keyword(s):  
Relaxation Rate ◽  
Flow Rate ◽  
Early Onset ◽  
Minute Ventilation ◽  
Muscle Relaxation ◽  
Normal Subjects ◽  
Inspiratory Muscle ◽  
Inspiratory Flow Rate ◽  
Inspiratory Muscles ◽  
Progressive Loss

We have investigated whether the capacity of the inspiratory muscles to generate pressure and flow during a ventilatory load is related to changes in inspiratory muscle relaxation rate. Five highly motivated normal subjects performed voluntary maximal isocapnic ventilation (MIV) for 2 min. Minute ventilation and esophageal, gastric, and transdiaphragmatic pressures were measured breath by breath. We observed that ventilation, peak inspiratory and expiratory pressures, and inspiratory flow rate declined from the start of the run to reach a plateau at 60 s that was sustained for the remainder of the exercise. In a subsequent series of studies, MIV was performed for variable durations between 15 and 120 s. The normalized maximum relaxation rate of unoccluded inspiratory sniffs (sniff MRR, %pressure loss/10 ms) was determined immediately on stopping MIV. Sniff MRR slowed as the duration of MIV increased and paralleled the decline in inspiratory pressure and ventilation observed during the 2-min exercise. No further slowing in MRR occurred when ventilation became sustainable. We conclude that, during MIV, the progressive loss of ventilation and capacity to generate pressure is associated with the early onset and progression of a peripheral fatiguing process within the inspiratory muscles.

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