Transmission of pressure across the chest wall during the rapid thoracic compression technique in infants

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.

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.


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.


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 ◽  
...  

1987 ◽  
Vol 62 (5) ◽  
pp. 2026-2030 ◽  
Author(s):  
C. G. Alex ◽  
R. M. Aronson ◽  
E. Onal ◽  
M. Lopata

To study the effects of continuous positive airway pressure (CPAP) on lung volume, and upper airway and respiratory muscle activity, we quantitated the CPAP-induced changes in diaphragmatic and genioglossal electromyograms, esophageal and transdiaphragmatic pressures (Pes and Pdi), and functional residual capacity (FRC) in six normal awake subjects in the supine position. CPAP resulted in increased FRC, increased peak and rate of rise of diaphragmatic activity (EMGdi and EMGdi/TI), decreased peak genioglossal activity (EMGge), decreased inspiratory time and inspiratory duty cycle (P less than 0.001 for all comparisons). Inspiratory changes in Pes and Pdi, as well as Pes/EMGdi and Pdi/EMGdi also decreased (P less than 0.001 for all comparisons), but mean inspiratory airflow for a given Pes increased (P less than 0.001) on CPAP. The increase in mean inspiratory airflow for a given Pes despite the decrease in upper airway muscle activity suggests that CPAP mechanically splints the upper airway. The changes in EMGge and EMGdi after CPAP application most likely reflect the effects of CPAP and the associated changes in respiratory system mechanics on the afferent input from receptors distributed throughout the intact respiratory system.


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.


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.


1980 ◽  
Vol 49 (4) ◽  
pp. 601-608 ◽  
Author(s):  
B. Gothe ◽  
N. S. Cherniack

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.


1965 ◽  
Vol 32 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Michael S. Hoshiko ◽  
Kenneth W. Berger

1991 ◽  
Vol 70 (6) ◽  
pp. 2611-2618 ◽  
Author(s):  
T. Mutoh ◽  
W. J. Lamm ◽  
L. J. Embree ◽  
J. Hildebrandt ◽  
R. K. Albert

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.


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