Effects of neuromuscular blockade on respiratory mechanics in conscious man

1979 ◽  
Vol 47 (6) ◽  
pp. 1162-1168 ◽  
Author(s):  
A. De Troyer ◽  
J. Bastenier-Geens

The effect of submaximal neuromuscular blockade (SMNB) on lung and chest wall mechanics was studied in six normal, awake subjects infused with pancuronium. Measurements of static lung volumes, specific airway conductance (sGaw), maximum expiratory and inspiratory flow-volume (MEFV, MIFV) curves, and static pressure-volume (PV) curves of the lung and of the relaxed chest wall were obtained after lung recoil pressure (Pst(L)) at full inflation had been reduced to 60 +/- 10% of control. Inspiratory capacity was decreased, but residual volume was not increased. Inspiratory PV curve of the lung was not modified, and the observed decrease in expiratory compliance and the slight increase in Pst(L) during deflation were compatible with the altered lung volume history. SMNB did not modify sGaw nor the relationship between Pst(L) and MEF; by contrast it markedly reduced MIF rates. Finally, SMNB transposed the chest wall PV curve to higher levels on the pressure axis (it decreased the outward pull of the chest wall) without greatly affecting its slope, and thereby it reduced the resting level of the respiratory system. We conclude that 1) muscle weakness per se does not affect the eleastic properties of the lungs and airways, and 2) involuntary respiratory muscle activity influences the elastic recoil of the chest wall. We believe this muscle activity originates from muscle spindles, and lies essentially in the inspiratory portion of the intercostal musculature.

1985 ◽  
Vol 58 (2) ◽  
pp. 339-345 ◽  
Author(s):  
K. Harada ◽  
T. Mutsuda ◽  
N. Saoyama ◽  
N. Hamaguchi ◽  
Y. Shimada

Total gas pressure in the pleural space is more subatmospheric than that in the alveolar cavity. This pressure difference minus elastic recoil pressure of the lung was termed stress pressure. We investigated the relationship between stress pressure and a force that would hold the lung against the chest wall to prevent accumulation of liquid. The condition was a pleural space with an enlarged pleural surface pressure. Dogs anesthetized with pentobarbital sodium were placed in a box maintained subatmospherically at approximately -30 cmH2O and breathed atmospheric air for 4 h. Liquid volume in the pleural space of the dogs was measured under conditions of thoracotomy. In the normal group, the volume of the pleural liquid was within the normal range of approximately 2.0 ml and the visceral and the parietal pleura made contact. In the pneumothorax group, established by injecting 50 ml of air into the pleural space, the liquid increased significantly in all cases by a mean value of approximately 12 ml. Thus pleural stress pressure seems to be an important force holding the lung against the chest wall and aiding in the control of accumulation of liquid in a more subatmospheric pleural space.


2020 ◽  
Vol 65 (9) ◽  
pp. 1285-1294
Author(s):  
Jéssica Danielle Medeiros da Fonsêca ◽  
Vanessa Regiane Resqueti ◽  
Kadja Benício ◽  
Valéria Soraya de Farias Sales ◽  
Luciana Fontes Silva da Cunha Lima ◽  
...  

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Tom Schepens ◽  
Koen Janssens ◽  
Sabine Maes ◽  
Davina Wildemeersch ◽  
Jurryt Vellinga ◽  
...  

Abstract Background The use of neostigmine after neuromuscular blockade (NMB) has been associated with postoperative respiratory complications. In previous studies, we found lower diaphragmatic activity after neostigmine reversal of NMB, compared to sugammadex. It is still unclear whether the adequate use of neostigmine guarantees normal respiratory muscle function after NMB. In this study, we wanted to assess the effect of commonly used degrees of NMB and their possible reversal strategies on respiratory muscle activity after the return of normal neuromuscular transmission. Methods This is a randomized, controlled, parallel-group, single-centre, double-blind study in patients scheduled for intracranial surgery at a tertiary academic hospital in Belgium. All participants received target controlled propofol/remifentanil anesthesia and were randomized into one of five groups, receiving either a shallow NMB with no reversal (shallow/saline), a shallow NMB with sugammadex reversal (shallow/sugammadex), a moderate NMB with neostigmine reversal (moderate/neostigmine), a moderate NMB with sugammadex reversal (moderate/sugammadex), or a deep NMB with sugammadex reversal (deep/sugammadex). Primary and secondary outcome parameters were diaphragm and intercostal electromyographic (EMG) activity at the moment of resumed spontaneous breathing activity, defined as a maximal interval of 10 min after the first spontaneous breath. Results For the five groups, a total of 55 patients could be included in the final analysis. Median time of spontaneous breathing analyzed was 5 min (IQR 3–9.5 min). Both the moderate/sugammadex and the moderate/neostigmine groups had lower levels of diaphragm EMG compared to the shallow/sugammadex group. The moderate/neostigmine group had lower levels of intercostal EMG activity compared to the shallow/saline group. Conclusions In this study, the depth of neuromuscular blockade and type of reversal strategy impacts respiratory muscle activity at the moment of resumed spontaneous breathing and recovery of neuromuscular blockade. Both groups that received moderate NMB had lower levels of diaphragm EMG, compared to the shallow NMB group with sugammadex reversal. Compared to the shallow NMB group with no reversal, the moderate NMB with neostigmine reversal group had lower intercostal EMG activity. Trial registration Clinicaltrials.gov NCT01962298 on October 9, 2013 and EudraCT 2013–001926-25 on October 10, 2013.


2010 ◽  
Vol 5 ◽  
Author(s):  
Giorgio Scano

Our understanding of the nature and mechanisms of dyspnea has greatly evolved over the last two centuries. Although the relationship was never form- ally specified, discomfort was always assumed to accompany respiratory muscle activity. Hypotheses and theories of dyspnea thus became synonymous with the factors controlling the extremes of respira- tory muscle activity, with expiratory muscle activity and discomfort now being known to be controlled by the same factors.


1989 ◽  
Vol 32 (3) ◽  
pp. 657-667 ◽  
Author(s):  
David H. McFarland ◽  
Anne Smith

Bipolar electromyographic (EMG) recordings were made from six chest wall and nasal sites with disk electrodes attached to the skin. Electrode locations were based on previous studies of nonspeech breathing and were designed to sample the activity of both primary and accessory respiratory muscles. EMG activity was sampled while subjects performed a series of speech and nonspeeeh tasks. The results revealed that surface electrodes could sample the activity of respiratory muscles during speech and other ventilatory tasks, particularly during the expiratory phases of the breathing cycle.


1995 ◽  
Vol 82 (1) ◽  
pp. 6-19 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Data concerning chest wall configuration and the activities of the major respiratory muscles that determine this configuration during anesthesia in humans are limited. The aim of this study was to determine the effects of halothane anesthesia on respiratory muscle activity and chest wall shape and motion during spontaneous breathing. Methods Six human subjects were studied while awake and during 1 MAC halothane anesthesia. 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. Tidal changes in gas volume were measured by integrating respiratory gas flow, and the functional residual capacity was measured by a nitrogen dilution technique. Results While awake, ribcage expansion was responsible for 25 +/- 4% (mean +/- SE) of the total change in thoracic volume (delta Vth) during inspiration. Phasic inspiratory activity was regularly present in the diaphragm and parasternal intercostal muscles. Halothane anesthesia (1 MAC) abolished activity in the parasternal intercostal muscles and increased phasic expiratory activity in the abdominal muscles and lateral ribcage muscles. However, halothane did not significantly change the ribcage contribution to delta Vth (18 +/- 4%). Intrathoracic blood volume, measured by comparing changes in total thoracic volume and gas volume, increased significantly during inspiration both while awake and while anesthetized (by approximately 20% of delta Vth, P < 0.05). Halothane anesthesia significantly reduced the functional residual capacity (by 258 +/- 78 ml), primarily via an inward motion of the end-expiratory position of the ribcage. Although the diaphragm consistently changed shape, with a cephalad displacement of posterior regions and a caudad displacement of anterior regions, the diaphragm did not consistently contribute to the reduction in the functional residual capacity. Halothane anesthesia consistently increased the curvature of the thoracic spine measured in the saggital plane. Conclusions The authors conclude that (1) ribcage expansion is relatively well preserved during halothane anesthesia despite the loss of parasternal intercostal muscle activity; (2) an inward displacement of the ribcage accounts for most of the decrease in functional residual capacity caused by halothane anesthesia, accompanied by changes in diaphragm shape that may be related to motion of its insertions on the thoracoabdominal wall; and (3) changes in intrathoracic blood volume constitute a significant fraction of delta Vth during tidal breathing.


1994 ◽  
Vol 76 (4) ◽  
pp. 1411-1416 ◽  
Author(s):  
S. Stick ◽  
D. Turner ◽  
P. LeSouef

During the rapid thoracic compression maneuver in infants, the transmission of pressure from compression jacket to pleural space and airway is less at functional residual capacity than at end inspiration. To examine whether reduced pressure transmission at functional residual capacity vs. higher lung volumes is explained by passive characteristics of the chest wall rather than by respiratory muscle activity, we assessed the pressure transmitted across the chest wall in nine anesthetized infants and young children after muscle relaxation. We measured esophageal and airway occlusion pressure during chest compressions at different lung volumes determined by varying distending pressure. In six subjects studied under static conditions, there was an approximately linear relationship between distending pressure and the proportion of pressure transmitted to the airway and esophagus from the compression jacket. The mean r2 value (95% confidence interval) was 0.80 (0.09) for pressure transmission to the airway and 0.85 (0.04) for pressure transmission to the esophagus. This relationship between lung volume and pressure transmission observed under static conditions was also demonstrated dynamically. Thus the reduced transmission of pressure from compression jacket to airway and pleural space at low lung volumes occurs independently of respiratory muscle activity.


1997 ◽  
Vol 83 (2) ◽  
pp. 591-598 ◽  
Author(s):  
Maurice Beaumont ◽  
Damien Lejeune ◽  
Henri Marotte ◽  
Alain Harf ◽  
Frédéric Lofaso

Beaumont, Maurice, Damien Lejeune, Henri Marotte, Alain Harf, and Frédéric Lofaso. Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans. J. Appl. Physiol. 83(2): 591–598, 1997.—We assessed the respective effects of thoracic (TCP) and abdominal/lower limb (ACP) counterpressures on end-expiratory volume (EEV) and respiratory muscle activity in humans breathing at 40 cmH2O of continuous positive airway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (ΔPga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on the basis of the transdiaphragmatic pressure-time product (PTPdi). CPAP induced hyperventilation (+320%) and only a 28% increase in EEV because of a high level of expiratory activity (ΔPga = 24 ± 5 cmH2O), contrasting with a reduction in PTPdi from 17 ± 2 to 9 ± 7 cmH2O ⋅ s−1 ⋅ cycle−1during 0 and 40 cmH2O of CPAP, respectively. When ACP, TCP, or both were added, hyperventilation decreased and PTPdi increased (19 ± 5, 21 ± 5, and 35 ± 7 cmH2O ⋅ s−1 ⋅ cycle−1, respectively), whereas ΔPga decreased (19 ± 6, 9 ± 4, and 2 ± 2 cmH2O, respectively). We concluded that during high-level CPAP, TCP and ACP limit lung hyperinflation and expiratory muscle activity and restore diaphragmatic activity.


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