Pulmonary receptor discharge and expiratory muscle activity

1982 ◽  
Vol 47 (2) ◽  
pp. 219-229 ◽  
Author(s):  
J.P. Farber
Keyword(s):  
Muscle Activity ◽  
Expiratory Muscle ◽  
Pulmonary Receptor

Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia

1992 ◽  
Vol 72 (3) ◽  
pp. 881-887 ◽  
Author(s):  
Y. Wakai ◽  
M. M. Welsh ◽  
A. M. Leevers ◽  
J. D. Road
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Ventilatory Threshold ◽  
Minute Ventilation ◽  
Abdominal Muscle ◽  
Transversus Abdominis ◽  
Abdominal Muscles ◽  
Lung Inflation ◽  
Expiratory Muscle ◽  
Intramuscular Electrodes

Expiratory muscle activity has been shown to occur in awake humans during lung inflation; however, whether this activity is dependent on consciousness is unclear. Therefore we measured abdominal muscle electromyograms (intramuscular electrodes) in 13 subjects studied in the supine position during wakefulness and non-rapid-eye-movement sleep. Lung inflation was produced by nasal continuous positive airway pressure (CPAP). CPAP at 10–15 cmH2O produced phasic expiratory activity in two subjects during wakefulness but produced no activity in any subject during sleep. During sleep, CPAP to 15 cmH2O increased lung volume by 1,260 +/- 215 (SE) ml, but there was no change in minute ventilation. The ventilatory threshold at which phasic abdominal muscle activity was first recorded during hypercapnia was 10.3 +/- 1.1 l/min while awake and 13.8 +/- 1 l/min while asleep (P less than 0.05). Higher lung volumes reduced the threshold for abdominal muscle recruitment during hypercapnia. We conclude that lung inflation alone over the range that we studied does not alter ventilation or produce recruitment of the abdominal muscles in sleeping humans. The internal oblique and transversus abdominis are activated at a lower ventilatory threshold during hypercapnia, and this activation is influenced by state and lung volume.

scholarly journals Expiratory muscle activity in preterm babies.

1987 ◽  
Vol 62 (8) ◽  
pp. 825-829 ◽  
Author(s):  
M South ◽  
C J Morley ◽  
G Hughes
Keyword(s):  
Muscle Activity ◽  
Expiratory Muscle ◽  
Preterm Babies

scholarly journals Respiratory Muscle Effort during Expiration in Successful and Failed Weaning from Mechanical Ventilation

2018 ◽  
Vol 129 (3) ◽  
pp. 490-501 ◽  
Author(s):  
Jonne Doorduin ◽  
Lisanne H. Roesthuis ◽  
Diana Jansen ◽  
Johannes G. van der Hoeven ◽  
Hieronymus W. H. van Hees ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Electrical Activity ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Weaning From Mechanical Ventilation ◽  
Expiratory Muscle ◽  
Diaphragm Electrical Activity ◽  
Gastric Pressure ◽  
Weaning Failure ◽  
Expiratory Muscles

Abstract What We Already Know about This Topic What This Article Tells Us That Is New Background Respiratory muscle weakness in critically ill patients is associated with difficulty in weaning from mechanical ventilation. Previous studies have mainly focused on inspiratory muscle activity during weaning; expiratory muscle activity is less well understood. The current study describes expiratory muscle activity during weaning, including tonic diaphragm activity. The authors hypothesized that expiratory muscle effort is greater in patients who fail to wean compared to those who wean successfully. Methods Twenty adult patients receiving mechanical ventilation (more than 72 h) performed a spontaneous breathing trial. Tidal volume, transdiaphragmatic pressure, diaphragm electrical activity, and diaphragm neuromechanical efficiency were calculated on a breath-by-breath basis. Inspiratory (and expiratory) muscle efforts were calculated as the inspiratory esophageal (and expiratory gastric) pressure–time products, respectively. Results Nine patients failed weaning. The contribution of the expiratory muscles to total respiratory muscle effort increased in the “failure” group from 13 ± 9% at onset to 24 ± 10% at the end of the breathing trial (P = 0.047); there was no increase in the “success” group. Diaphragm electrical activity (expressed as the percentage of inspiratory peak) was low at end expiration (failure, 3 ± 2%; success, 4 ± 6%) and equal between groups during the entire expiratory phase (P = 0.407). Diaphragm neuromechanical efficiency was lower in the failure versus success groups (0.38 ± 0.16 vs. 0.71 ± 0.36 cm H2O/μV; P = 0.054). Conclusions Weaning failure (vs. success) is associated with increased effort of the expiratory muscles and impaired neuromechanical efficiency of the diaphragm but no difference in tonic activity of the diaphragm.

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

1991 ◽  
Vol 71 (5) ◽  
pp. 1795-1800 ◽  
Author(s):  
S. B. Hollstien ◽  
M. L. Carl ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Muscle Activity ◽  
Vagal Afferents ◽  
Oblique Muscle ◽  
Vagus Nerves ◽  
Expiratory Muscle ◽  
C Fibers ◽  
C Fiber ◽  
Before And After ◽  
Afferent Vagal ◽  
Alpha Chloralose

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Excitatory lung reflex may stress inspiratory muscle by suppressing expiratory muscle activity

2001 ◽  
Vol 90 (3) ◽  
pp. 857-864 ◽  
Author(s):  
J. Yu ◽  
Y. Wang ◽  
G. Soukhova ◽  
L. C. Collins ◽  
J. C. Falcone
Keyword(s):  
Duty Cycle ◽  
Muscle Activity ◽  
Breathing Pattern ◽  
Lung Parenchyma ◽  
Abdominal Muscle ◽  
Inspiratory Muscle ◽  
Nerve Activity ◽  
Expiratory Muscle ◽  
Inspiratory Activity ◽  
Inspiratory Muscle Fatigue

Recently, a vagally mediated excitatory lung reflex (ELR) causing neural hyperpnea and tachypnea was identified. Because ventilation is regulated through both inspiratory and expiratory processes, we investigated the effects of the ELR on these two processes simultaneously. In anesthetized, open-chest, and artificially ventilated rabbits, we recorded phrenic nerve activity and abdominal muscle activity to assess the breathing pattern when the ELR was evoked by directly injecting hypertonic saline (8.1%, 0.1 ml) into lung parenchyma. Activation of the ELR stimulated inspiratory activity, which was exhibited by increasing amplitude, burst rate, and duty cycle of the phrenic activity (by 22 ± 4, 33 ± 9, and 57 ± 11%, respectively; n = 13; P < 0.001), but suppressed expiratory muscle activity. The expiratory muscle became silent in most cases. On average, the amplitude of expiratory muscle activity decreased by 88 ± 5% ( P < 0.002). The suppression reached the peak at 6.9 ± 1 s and lasted for 200 s (median). Injection of H2O2 into the lung parenchyma produced similar responses. By suppressing expiration, the ELR produces a shift in the workload from expiratory muscle to inspiratory muscle. Therefore, we conclude that the ELR may contribute to inspiratory muscle fatigue, not only by directly increasing the inspiratory activity but also by suppressing expiratory activity.

Anesthesia and chest wall function in dogs

1994 ◽  
Vol 76 (6) ◽  
pp. 2802-2813 ◽  
Author(s):  
D. O. Warner ◽  
M. J. Joyner ◽  
E. L. Ritman
Keyword(s):  
Chest Wall ◽  
Muscle Activity ◽  
High Speed ◽  
Respiratory Muscles ◽  
Suitable Model ◽  
Wall Function ◽  
Pentobarbital Anesthesia ◽  
Expiratory Muscle ◽  
Anesthetic Drugs ◽  
Computed Tomography Scanning

Three anesthetics (pentobarbital, halothane, and isoflurane) were studied in six mongrel dogs to systematically compare their effects on chest wall function during spontaneous breathing. Each dog received each anesthetic on separate occasions. Electrical activities of several respiratory muscles were measured with chronically implanted electrodes, and chest wall motion was assessed by high-speed three-dimensional computed tomography scanning. Phasic expiratory muscle activity was markedly depressed by volatile anesthetics halothane and isoflurane compared with pentobarbital. In contrast, inspiratory activity in parasternal intercostal muscles was relatively well preserved during anesthesia with these volatile agents. The contribution of expiratory muscles to tidal volume was diminished during halothane and isoflurane compared with pentobarbital anesthesia. As anesthesia was deepened, expiratory muscle activity was unchanged during pentobarbital anesthesia, enhanced in some dogs during isoflurane anesthesia, and remained absent during halothane anesthesia. Activity in parasternal intercostal muscle was depressed as inspired concentration of halothane or isoflurane was increased, whereas diaphragmatic activity was unchanged. Depression of expiratory muscle activity by halothane persisted when breathing was stimulated by positive end-expiratory pressure, with significant mechanical consequences for chest wall configuration. Many of these findings are in contrast with previous observations in humans and suggest that the dog is not a suitable model for the study of the effects of anesthetic drugs on the pattern of human respiratory muscle activity.

Release of expiratory muscle activity by graded focal cold block in the medulla

1985 ◽  
Vol 124 (3) ◽  
pp. 341-351 ◽  
Author(s):  
KRYSTYNA BUDZIŃSKA ◽  
CURT EULER ◽  
FREDERICK F. KAO ◽  
TITO PANTALEO ◽  
YUJI YAMAMOTO
Keyword(s):  
Muscle Activity ◽  
Expiratory Muscle

Chest Wall Responses to Rebreathing in Halothane-anesthetized Dogs

1995 ◽  
Vol 83 (4) ◽  
pp. 835-843. ◽  
Author(s):  
David O. Warner ◽  
Michael J. Joyner ◽  
Erik L. Ritman
Keyword(s):  
Chest Wall ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Species Differences ◽  
Minimum Alveolar Concentration ◽  
Electromyographic Activity ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Expiratory Muscle ◽  
Anesthetized Dogs

Background The pattern of respiratory muscle use during halothane-induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (VE) and PCO2 (0.34 +/- 0.04 [M +/- SE] and 0.28 +/- 0.05 l.min-1.mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated VE at a PCO2 of 60 mmHg (from 7.4 +/- 1.2 to 4.0 +/- 0.6 l.min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (delta Vth), with percentage of delta Vth attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 +/- 6% to 48 +/- 2% of delta Vth). Conclusions Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.

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