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

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.

1991 ◽  
Vol 70 (2) ◽  
pp. 539-547 ◽  
Author(s):  
D. O. Warner ◽  
J. F. Brichant ◽  
E. L. Ritman ◽  
K. Rehder

To determine the relative contribution of rib cage and abdominal muscles to expiratory muscle activity during quiet breathing, we used lumbar epidural anesthesia in six pentobarbital sodium-anesthetized dogs lying supine to paralyze the abdominal muscles while leaving rib cage muscle motor function substantially intact. A high-speed X-ray scanner (Dynamic Spatial Reconstructor) provided three-dimensional images of the thorax. The contribution of expiratory muscle activity to tidal breathing was assessed by a comparison of chest wall configuration during relaxed apnea with that at end expiration. We found that expiratory muscle activity was responsible for approximately half of the changes in thoracic volume during inspiration. Paralysis of the abdominal muscles had little effect on the pattern of breathing, including the contribution of expiratory muscle activity to tidal breathing, in most dogs. We conclude that, although there is consistent phasic expiratory electrical activity in both the rib cage and the abdominal muscles of pentobarbital-anesthetized dogs lying supine, the muscles of the rib cage are mechanically the most important expiratory muscles during quiet breathing.


1996 ◽  
Vol 84 (2) ◽  
pp. 309-321. ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Prior human studies have shown that halothane attenuates activity in the parasternal intercostal muscle and enhances phasic activity in respiratory muscles with expiratory actions. This expiratory muscle activity could contribute to reductions in the functional residual capacity produced by anesthesia. Termination of this activity could contribute to the maintenance of inspiratory rib cage expansion. The purpose of this study was to estimate in humans the mechanical significance of expiratory muscle activity during halothane anesthesia and to search for the presence of scalene muscle activity during halothane anesthesia that might contribute to inspiratory rib cage expansion. Methods Six subjects (3 males, 3 females) were studied while awake and during 1.2 MAC halothane anesthesia, both during quiet breathing and during carbon dioxide rebreathing. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration was determined using images of the thorax obtained by three-dimensional, fast computed tomography and respiratory impedance plethysmography. Functional residual capacity was measured by a nitrogen dilution technique. Measurements were obtained after paralysis with 0.1 mg/kg vecuronium and mechanical ventilation. Results Phasic inspiratory activity was present in the scalene muscle of four anesthetized subjects during quiet breathing and all anesthetized subjects during rebreathing. Phasic inspiratory activity was present in the parasternal intercostal muscle during halothane anesthesia in only the three female subjects and was enhanced by rebreathing; parasternal intercostal muscle activity was never present in anesthetized males. During anesthesia with quiet breathing, phasic expiratory activity was observed in the transversus abdominis muscles of only the three male subjects. Despite these differences in the pattern of respiratory muscle use, the pattern of chest wall responses to rebreathing was similar between males and females. When expiratory muscle activity was present, paralysis increased the end-expiratory thoracic volume by expanding the rib cage, demonstrating that this activity reduced thoracic volume in these subjects. Changes in thoracic blood volume were significant determinants of the change in functional residual capacity produced by paralysis. Conclusions In humans anesthetized with 1.2 MAC end-tidal halothane, there are marked interindividual differences in respiratory muscle use during quiet breathing that may be related to sex; phasic inspiratory scalene muscle and parasternal intercostal muscle activity may contribute to inspiratory rib cage expansion in some subjects; and when present, expiratory muscle activity significantly constricts the rib cage and contributes to reductions in functional residual capacity caused by halothane anesthesia.


1992 ◽  
Vol 72 (4) ◽  
pp. 1362-1367 ◽  
Author(s):  
D. M. Ainsworth ◽  
C. A. Smith ◽  
B. D. Johnson ◽  
S. W. Eicker ◽  
K. S. Henderson ◽  
...  

Using chronically instrumented awake tracheotomized dogs, we examined the contributions of vagal feedback to respiratory muscle activities, both electrical and mechanical, during normoxic hypercapnia (inspired CO2 fraction = 0.03, 0.04, 0.05, and 0.06) and during mild treadmill exercise (3, 4.3, and 6.4 km/h). Cooling exteriorized vagal loops eliminated both phasic and tonic mechanoreceptor input during either of these hyperpneas. At a given chemical or locomotor stimulus, vagal cooling caused a further increase in costal, crural, parasternal, and rib cage expiratory (triangularis sterni) muscles. No further change in abdominal expiratory muscle activity occurred secondary to vagal cooling during these hyperpneas. However, removal of mechanoreceptor input during hypercapnia was not associated with consistent changes in end-expiratory lung volume, as measured by the He-N2 rebreathe technique. We conclude that during these hyperpneas 1) vagal input is not essential for augmentation of expiratory muscle activity and 2) decrements in abdominal expiratory muscle activity may be offset by increments in rib cage expiratory muscle activity and contribute to the regulation of end-expiratory lung volume.


1990 ◽  
Vol 68 (5) ◽  
pp. 2087-2091 ◽  
Author(s):  
R. C. Pascucci ◽  
M. B. Hershenson ◽  
N. F. Sethna ◽  
S. H. Loring ◽  
A. R. Stark

To test the extent to which diaphragmatic contraction moves the rib cage in awake supine infants during quiet breathing, we studied chest wall motion in seven prematurely born infants before and during spinal anesthesia for inguinal hernia repair. Infants were studied at or around term (postconceptional age 43 +/- 8 wk). Spinal anesthesia produced a sensory block at the T2-T4 level, with concomitant motor block at a slightly lower level. This resulted in the loss of most intercostal muscle activity, whereas diaphragmatic function was preserved. Rib cage and abdominal displacements were measured with respiratory inductance plethysmography before and during spinal anesthesia. During the anesthetic, outward inspiratory rib cage motion decreased in six infants (P less than 0.02, paired t test); four of these developed paradoxical inward movement of the rib cage during inspiration. One infant, the most immature in the group, had inward movement of the rib cage both before and during the anesthetic. Abdominal displacements increased during spinal anesthesia in six of seven infants (P less than 0.05), suggesting an increase in diaphragmatic motion. We conclude that, in the group of infants studied, outward rib cage movement during awake tidal breathing requires active, coordinated intercostal muscle activity that is suppressed by spinal anesthesia.


1989 ◽  
Vol 66 (1) ◽  
pp. 360-369 ◽  
Author(s):  
G. M. Barnas ◽  
N. C. Heglund ◽  
D. Yager ◽  
K. Yoshino ◽  
S. H. Loring ◽  
...  

We measured total chest wall impedance (Zw), "pathway impedances" of the rib cage (Zrcpath), and diaphragm-abdomen (Zd-apath), and impedance of the belly wall including abdominal contents (Zbw+) in five subjects during sustained expiratory (change in average pleural pressure [Ppl] from relaxation = 10 and 20 cmH2O) and inspiratory (change in Ppl = -10 and -20 cmH2O) muscle contraction, using forced oscillatory techniques (0.5–4 Hz) we have previously reported for relaxation (J. Appl. Physiol. 66: 350–359, 1989). Chest wall configuration and mean lung volume were kept constant. Zw, Zrcpath, Zd-apath, and Zbw+ all increased greatly at each frequency during expiratory muscle contraction; increases were proportional to effort. Zw, Zrcpath, and Zd-apath increased greatly during inspiratory muscle contraction, but Zbw+ did not. Resistances and elastances calculated from each of the impedances showed the same changes during muscle contraction as the corresponding impedances. Each of the resistances decreased as frequency increased, independent of effort; elastances generally increased with frequency. These frequency dependencies were similar to those measured in relaxed or tetanized isolated muscle during sinusoidal stretching (P.M. Rack, J. Physiol. Lond. 183: 1-14, 1966). We conclude that during respiratory muscle contraction 1) chest wall impedance increases, 2) changes in regional chest wall impedances can be somewhat independent, depending on which muscles contract, and 3) increases in chest wall impedance are due, at least in part, to changes in the passive properties of the muscles themselves.


1996 ◽  
Vol 85 (4) ◽  
pp. 761-773 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Although epidural anesthesia (EA) can significantly disrupt the function of the respiratory system, data concerning its effects on respiratory muscle activity and the resulting motion of the chest wall are scarce. This study aimed to determine the effects of lumbar EA on human chest wall function during quiet breathing. Methods Six persons were studied while awake and during mid-thoracic (approximately a T6 sensory level) and high (approximately a T1 sensory level) lumbar EA produced by either 2% lidocaine (two persons) or 1.5% etidocaine (four persons) with 1:200,000 epinephrine. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration during high EA was determined using images of the thorax obtained by three-dimensional, fast computed tomography. The functional residual capacity was measured using a nitrogen dilution technique. Results High EA abolished activity in the parasternal intercostal muscles of every participant but one, whereas the mean phasic activity of the scalene muscles was unchanged. High EA significantly decreased the inspiratory volume displacement of the rib cage compared with intact breathing but did not have a significant effect on diaphragm displacement. Therefore, high EA decreased the percentage contribution of rib cage expansion to inspiratory increases in thoracic volume (delta Vth) (from 27 +/- 2 [MSE] to 10 +/- 11% of delta Vth). Paradoxic rib cage motion during inspiration (i.e., a net inward motion during inspiration) developed in only one participant. High EA substantially increased the functional residual capacity (by 295 +/- 89 ml), with a significant net caudad motion of the end expiratory position of the diaphragm. In addition, high EA significantly decreased the volume of liquid in the thorax at end expiration in five of the six participants, a factor that also contributed to the increase in functional residual capacity in these persons. Conclusions Rib cage expansion continues to contribute to tidal volume during high EA in most subjects, even when most of the muscles of the rib cage are paralyzed; the mean phasic electrical activity of unblocked respiratory muscles such as scalenes does not increase in response to rib cage muscle paralysis produced by EA; and high EA increases the functional residual capacity, an increase produced in most participants by a caudad motion of the diaphragm and a decrease in intrathoracic blood volume.


1991 ◽  
Vol 70 (4) ◽  
pp. 1554-1562 ◽  
Author(s):  
J. D. Road ◽  
A. M. Leevers ◽  
E. Goldman ◽  
A. Grassino

Active expiration is produced by the abdominal muscles and the rib cage expiratory muscles. We hypothesized that the relative contribution of these two groups to expiration would affect diaphragmatic length and, hence, influence the subsequent inspiration. To address this question we measured the respiratory muscle response to expiratory threshold loading in spontaneously breathing anesthetized dogs. Prevagotomy, the increase in lung volume (functional residual capacity) and decrease in initial resting length of the diaphragm were attenuated by greater than 50% of values predicted by the passive relationships. Diaphragmatic activation (electromyogram) increased and tidal volume (VT) was preserved. Postvagotomy, effective expiratory muscle recruitment was abolished. The triangularis sterni muscle remained active, and the increase in lung volume was attenuated by less than 15% of that predicted by the passive relationship. Diaphragmatic length was shorter than predicted. VT was not restored, even though costal diaphragmatic and parasternal intercostal electromyogram increased. During expiratory threshold loading with abdominal muscles resected and vagus intact, recruitment of the rib cage expiratory muscles produced a reduction in lung volume comparable with prevagotomy; however, diaphragmatic length decreased markedly. Both the rib cage and abdominal expiratory muscles may defend lung volume; however, their combined action is important to restore diaphragmatic initial length and, accordingly, to preserve VT.


1989 ◽  
Vol 67 (4) ◽  
pp. 1438-1442 ◽  
Author(s):  
G. A. Farkas ◽  
M. Estenne ◽  
A. De Troyer

A change from the supine to the head-up posture in anesthetized dogs elicits increased phasic expiratory activation of the rib cage and abdominal expiratory muscles. However, when this postural change is produced over a 4- to 5-s period, there is an initial apnea during which all the muscles are silent. In the present studies, we have taken advantage of this initial silence to determine functional residual capacity (FRC) and measure the subsequent change in end-expiratory lung volume. Eight animals were studied, and in all of them end-expiratory lung volume in the head-up posture decreased relative to FRC [329 +/- 70 (SE) ml]. Because this decrease also represents the increase in lung volume as a result of expiratory muscle relaxation at the end of the expiratory pause, it can be used to determine the expiratory muscle contribution to tidal volume (VT). The average contribution was 62 +/- 6% VT. After denervation of the rib cage expiratory muscles, the reduction in end-expiratory lung volume still amounted to 273 +/- 84 ml (49 +/- 10% VT). Thus, in head-up dogs, about two-thirds of VT result from the action of the expiratory muscles, and most of it (83%) is due to the action of the abdominal rather than the rib cage expiratory muscles.


1997 ◽  
Vol 83 (4) ◽  
pp. 1256-1269 ◽  
Author(s):  
A. Aliverti ◽  
S. J. Cala ◽  
R. Duranti ◽  
G. Ferrigno ◽  
C. M. Kenyon ◽  
...  

Aliverti, A., S. J. Cala, R. Duranti, G. Ferrigno, C. M. Kenyon, A. Pedotti, G. Scano, P. Sliwinski, Peter T. Macklem, and S. Yan. Human respiratory muscle actions and control during exercise. J. Appl. Physiol. 83(4): 1256–1269, 1997.—We measured pressures and power of diaphragm, rib cage, and abdominal muscles during quiet breathing (QB) and exercise at 0, 30, 50, and 70% maximum workload (W˙max) in five men. By three-dimensional tracking of 86 chest wall markers, we calculated the volumes of lung- and diaphragm-apposed rib cage compartments (Vrc,p and Vrc,a, respectively) and the abdomen (Vab). End-inspiratory lung volume increased with percentage of W˙max as a result of an increase in Vrc,p and Vrc,a. End-expiratory lung volume decreased as a result of a decrease in Vab. ΔVrc,a/ΔVab was constant and independent ofW˙max. Thus we used ΔVab/time as an index of diaphragm velocity of shortening. From QB to 70%W˙max, diaphragmatic pressure (Pdi) increased ∼2-fold, diaphragm velocity of shortening 6.5-fold, and diaphragm workload 13-fold. Abdominal muscle pressure was ∼0 during QB but was equal to and 180° out of phase with rib cage muscle pressure at all percent W˙max. Rib cage muscle pressure and abdominal muscle pressure were greater than Pdi, but the ratios of these pressures were constant. There was a gradual inspiratory relaxation of abdominal muscles, causing abdominal pressure to fall, which minimized Pdi and decreased the expiratory action of the abdominal muscles on Vrc,a gradually, minimizing rib cage distortions. We conclude that from QB to 0% W˙max there is a switch in respiratory muscle control, with immediate recruitment of rib cage and abdominal muscles. Thereafter, a simple mechanism that increases drive equally to all three muscle groups, with drive to abdominal and rib cage muscles 180° out of phase, allows the diaphragm to contract quasi-isotonically and act as a flow generator, while rib cage and abdominal muscles develop the pressures to displace the rib cage and abdomen, respectively. This acts to equalize the pressures acting on both rib cage compartments, minimizing rib cage distortion .


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 ◽  
...  

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.


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