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.

Chest wall motion during epidural anesthesia in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 539-547 ◽  
Author(s):  
D. O. Warner ◽  
J. F. Brichant ◽  
E. L. Ritman ◽  
K. Rehder
Keyword(s):  
Chest Wall ◽  
Epidural Anesthesia ◽  
Muscle Activity ◽  
High Speed ◽  
Abdominal Muscles ◽  
Tidal Breathing ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Expiratory Muscle ◽  
Anesthetized Dogs

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.

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.

Surface Recordings of Respiratory Muscle Activity during Speech

1989 ◽  
Vol 32 (3) ◽  
pp. 657-667 ◽  
Author(s):  
David H. McFarland ◽  
Anne Smith
Keyword(s):  
Chest Wall ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Respiratory Muscles ◽  
Emg Activity ◽  
Breathing Cycle ◽  
Surface Electrodes ◽  
Disk Electrodes ◽  
Respiratory Muscle Activity ◽  
Accessory Respiratory Muscles

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.

Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans

1997 ◽  
Vol 83 (2) ◽  
pp. 591-598 ◽  
Author(s):  
Maurice Beaumont ◽  
Damien Lejeune ◽  
Henri Marotte ◽  
Alain Harf ◽  
Frédéric Lofaso
Keyword(s):  
Chest Wall ◽  
Muscle Activity ◽  
Lung Mechanics ◽  
Transdiaphragmatic Pressure ◽  
Expiratory Muscle ◽  
Pressure Time ◽  
Gastric Pressure ◽  
Inspiratory Activity ◽  
High Level ◽  
Respiratory Muscle Activity

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.

Human Chest Wall Function during Epidural Anesthesia

1996 ◽  
Vol 85 (4) ◽  
pp. 761-773 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman
Keyword(s):  
Chest Wall ◽  
Functional Residual Capacity ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Sensory Level ◽  
Wall Function ◽  
Rib Cage ◽  
Residual Capacity ◽  
The Mean ◽  
Respiratory Muscle Activity

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.

Effect of respiratory muscle tension on lung volume

1992 ◽  
Vol 73 (6) ◽  
pp. 2283-2288 ◽  
Author(s):  
T. A. Wilson ◽  
A. De Troyer
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Airway Pressure ◽  
Linear Prediction ◽  
Muscle Tension ◽  
Muscle Length ◽  
Respiratory Muscles ◽  
Active Tension ◽  
Airway Opening ◽  
Measured Change

The chest wall is modeled as a linear system for which the displacements of points on the chest wall are proportional to the forces that act on the chest wall, namely, airway opening pressure and active tension in the respiratory muscles. A standard theorem of mechanics, the Maxwell reciprocity theorem, is invoked to show that the effect of active muscle tension on lung volume, or airway pressure if the airway is closed, is proportional to the change of muscle length in the relaxation maneuver. This relation was tested experimentally. The shortening of the cranial-caudal distance between a rib pair and the sternum was measured during a relaxation maneuver. These data were used to predict the respiratory effect of forces applied to the ribs and sternum. To test this prediction, a cranial force was applied to the rib pair and a caudal force was applied to the sternum, simulating the forces applied by active tension in the parasternal intercostal muscles. The change in airway pressure, with lung volume held constant, was measured. The measured change in airway pressure agreed well with the prediction. In some dogs, nonlinear deviations from the linear prediction occurred at higher loads. The model and the theorem offer the promise that existing data on the configuration of the chest wall during the relaxation maneuver can be used to compute the mechanical advantage of the respiratory muscles.

scholarly journals P1.08-061 Clinical Experience of Rib Resection for Lung Cancer with Chest Wall Invasion Using a Pneumatic High Speed Power Drill System

2017 ◽  
Vol 12 (1) ◽  
pp. S768-S769
Author(s):  
Yuichiro Ueda ◽  
Tatsuo Nakagawa ◽  
Yasuaki Tomioka ◽  
Toshiya Toyazaki ◽  
Masashi Gotoh
Keyword(s):  
Lung Cancer ◽  
Chest Wall ◽  
Clinical Experience ◽  
High Speed ◽  
Chest Wall Invasion ◽  
Rib Resection ◽  
Power Drill ◽  
Wall Invasion ◽  
Drill System

The C-start escape response ofPolypterus senegalus: bilateral muscle activity and variation during stage 1 and 2

2002 ◽  
Vol 205 (17) ◽  
pp. 2591-2603 ◽  
Author(s):  
Eric D. Tytell ◽  
George V. Lauder
Keyword(s):  
Muscle Activity ◽  
Escape Response ◽  
High Speed ◽  
Wave Speed ◽  
Activity Patterns ◽  
Motor Pattern ◽  
The Body ◽  
Wide Range ◽  
Fast Start ◽  
Stage 1

SUMMARYThe fast-start escape response is the primary reflexive escape mechanism in a wide phylogenetic range of fishes. To add detail to previously reported novel muscle activity patterns during the escape response of the bichir, Polypterus, we analyzed escape kinematics and muscle activity patterns in Polypterus senegalus using high-speed video and electromyography (EMG). Five fish were filmed at 250 Hz while synchronously recording white muscle activity at five sites on both sides of the body simultaneously (10 sites in total). Body wave speed and center of mass velocity, acceleration and curvature were calculated from digitized outlines. Six EMG variables per channel were also measured to characterize the motor pattern. P. senegalus shows a wide range of activity patterns, from very strong responses, in which the head often touched the tail, to very weak responses. This variation in strength is significantly correlated with the stimulus and is mechanically driven by changes in stage 1 muscle activity duration. Besides these changes in duration, the stage 1 muscle activity is unusual because it has strong bilateral activity, although the observed contralateral activity is significantly weaker and shorter in duration than ipsilateral activity. Bilateral activity may stiffen the body, but it does so by a constant amount over the variation we observed; therefore, P. senegalus does not modulate fast-start wave speed by changing body stiffness. Escape responses almost always have stage 2 contralateral muscle activity, often only in the anterior third of the body. The magnitude of the stage 2 activity is the primary predictor of final escape velocity.

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.

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