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.

Vagal contributions to respiratory muscle activity during eupnea in the awake dog

1992 ◽  
Vol 72 (4) ◽  
pp. 1355-1361 ◽  
Author(s):  
D. M. Ainsworth ◽  
C. A. Smith ◽  
B. D. Johnson ◽  
S. W. Eicker ◽  
K. S. Henderson ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Transversus Abdominis ◽  
Emg Activity ◽  
Expiratory Muscle ◽  
Vagal Blockade ◽  
Inspiratory Activity ◽  
Vagal Cooling ◽  
Respiratory Muscle Activity

We examined the effects of reversible vagal cooling on respiratory muscle activities in awake chronically instrumented tracheotomized dogs. We specifically analyzed electromyographic (EMG) activity and its ventilatory correlates, end-expiratory lung volume (EELV) and diaphragmatic resting length via sonomicrometry. Elimination of phasic and tonic mechanoreceptor activity by vagal cooling doubled the EMG activity of the costal, crural, and parasternal muscles, with activation occurring sooner relative to the onset of inspiratory flow. Diaphragmatic postinspiration inspiratory activity in the intact dog coincided with a brief mechanical shortening of the diaphragm during early expiration; vagal blockade removed both the electrical activity and the mechanical shortening. Vagal blockade also doubled the EMG activity of a rib cage expiratory muscle, the triangularis sterni, but reduced that of an abdominal expiratory muscle, the transversus abdominis. Within-breath electrical activity of both muscles occurred sooner relative to the onset of expiratory flow during vagal blockade. Vagal cooling was also associated with a 12% increase in EELV and a 5% decrease in end-expiratory resting length of the diaphragm. We conclude that vagal input significantly modulates inspiratory and expiratory muscle activities, which help regulate EELV efficiently and optimize diaphragmatic length during eupneic breathing in the awake dog.

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.

Respiratory Origin of Fluctuations in Arterial Blood Pressure in Premature Infants With Respiratory Distress Syndrome

PEDIATRICS ◽  
1988 ◽  
Vol 81 (3) ◽  
pp. 399-403
Author(s):  
Jeffrey Perlman ◽  
Bradley Thach
Keyword(s):  
Premature Infants ◽  
Muscle Activity ◽  
Intraventricular Hemorrhage ◽  
Respiratory Muscle ◽  
Pressure Fluctuations ◽  
Esophageal Pressure ◽  
Arterial Blood ◽  
Gastric Pressure ◽  
Pressure Changes ◽  
Respiratory Muscle Activity

A variable fluctuating pattern of arterial BP often precedes intraventricular hemorrhage in mechanically ventilated preterm infants. To learn more about the origin of this pattern, arterial BP and respiratory muscle activity were studied in five intubated premature infants who were at high risk for intraventricular hemorrhage. We monitored esophageal pressure, gastric pressure, and arterial BP. Consistent findings were: (1) arterial BP fluctuations have the same frequency and direction of change as esophageal and gastric pressure changes associated with spontaneous breathing (R ranged from .93 to .98, P < .001); (2) spontaneous apneic pauses were accompanied by sudden and complete cessation of arterial BP fluctuations; (3) large "cough-like" fluctuations in esophageal and gastric pressures, seen in all infants, were associated with the largest fluctuations in arterial BP; (4) cutaneous stimulation had negligible effect on fluctuation in arterial BP provided no change in esophageal and gastric pressures occurred; (5) the effects of change in esophageal and gastric pressures on arterial BP were nearly simultaneous (0.05 to 0.25 second latency); (6) respirator pressure fluctuations had negligible effects on the fluctuations in arterial BP. These data suggest that the fluctuations in arterial BP are directly related to respiratory muscle activity and are most consistent with the familiar pulsus paradoxus that occurs in various other cardiorespiratory diseases.

Effects of Inspiratory Load on Chest Wall Kinematics, Breathing Pattern, and Respiratory Muscle Activity of Mouth-Breathing Children

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 ◽  
...  
Keyword(s):  
Chest Wall ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Breathing Pattern ◽  
Mouth Breathing ◽  
Chest Wall Kinematics ◽  
Respiratory Muscle Activity ◽  
Inspiratory Load

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.

Effect of chest wall distortion on occlusion pressure and the preterm diaphragm

1983 ◽  
Vol 55 (2) ◽  
pp. 359-364 ◽  
Author(s):  
P. N. LeSouef ◽  
J. M. Lopes ◽  
S. J. England ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Chest Wall ◽  
Preterm Infants ◽  
Face Mask ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Transdiaphragmatic Pressure ◽  
Airway Occlusion ◽  
Mouth Pressure ◽  
Gastric Pressure ◽  
Mouth Occlusion Pressure

We studied the effect of chest wall distortion (CWD) on transdiaphragmatic pressure (Pdi) and/or mouth pressure during end-expiratory airway occlusions in seven preterm infants. We measured mouth occlusion pressure (Pmo) with a face mask and pressure transducer, gastric pressure (Pga) with a fluid-filled catheter, diaphragmatic electromyogram (Edi) using surface electrodes, and rib cage and abdominal motion using magnetometers. We reasoned that Pdi = Pmo - Pga on airway occlusion. Periods with maximal and periods with minimal CWD were compared. We found that 1) when CWD was minimal, an increase in Edi produced an increase in Pmo and Pdi in all infants; when CWD was greatest, large increases in Edi produced no increase in Pmo or Pdi in four infants; 2) when breaths with the same Pmo or Pdi from each period in each infant were compared, those from the period with greatest CWD had an increased Edi (mean increase 76%, P less than 0.005, and 144%, P less than 0.01, for Pmo and Pdi, respectively). We conclude that in preterm infants, Pmo can be a poor indicator of respiratory drive, and CWD markedly limits the effectiveness of the diaphragm as a force generator.

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 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.

Passive mechanics of upright human chest wall during immersion from hips to neck

1986 ◽  
Vol 60 (5) ◽  
pp. 1561-1570 ◽  
Author(s):  
M. B. Reid ◽  
S. H. Loring ◽  
R. B. Banzett ◽  
J. Mead
Keyword(s):  
Chest Wall ◽  
Esophageal Pressure ◽  
Vertical Surface ◽  
Repeated Measurements ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Gastric Pressure ◽  
Length Changes ◽  
Accessory Muscles

We have determined the mechanical effects of immersion to the neck on the passive chest wall of seated upright humans. Repeated measurements were made at relaxed end expiration on four subjects. Changes in relaxed chest wall configuration were measured using magnetometers. Gastric and esophageal pressures were measured with balloon-tipped catheters in three subjects; from these, transdiaphragmatic pressure was calculated. Transabdominal pressure was estimated using a fluid-filled, open-tipped catheter referenced to the abdomen's exterior vertical surface. We found that immersion progressively reduced mean transabdominal pressure to near zero and that the relaxed abdominal wall was moved inward 3–4 cm. The viscera were displaced upward into the thorax, gastric pressure increased by 20 cmH2O, and transdiaphragmatic pressure decreased by 10–15 cmH2O. This lengthened the diaphragm, elevating the diaphragmatic dome 3–4 cm. Esophageal pressure became progressively more positive throughout immersion, increasing by 8 cmH2O. The relaxed rib cage was elevated and expanded by raising water from hips to lower sternum; this passively shortened the inspiratory intercostals and the accessory muscles of inspiration. Deeper immersion distorted the thorax markedly: the upper rib cage was forced inward while lower rib cage shape was not systematically altered and the rib cage remained elevated. Such distortion may have passively lengthened or shortened the inspiratory muscles of the rib cage, depending on their location. We conclude that the nonuniform forcing produced by immersion provides unique insights into the mechanical characteristics of the abdomen and rib cage, that immersion-induced length changes differ among the inspiratory muscles according to their locations and the depth of immersion, and that such length changes may have implications for patients with inspiratory muscle deficits.

Vagal modulation of respiratory muscle activity in awake dogs during exercise and hypercapnia

1992 ◽  
Vol 72 (4) ◽  
pp. 1362-1367 ◽  
Author(s):  
D. M. Ainsworth ◽  
C. A. Smith ◽  
B. D. Johnson ◽  
S. W. Eicker ◽  
K. S. Henderson ◽  
...  
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Respiratory Muscle ◽  
Treadmill Exercise ◽  
Rib Cage ◽  
Expiratory Muscle ◽  
Vagal Modulation ◽  
Vagal Cooling ◽  
Respiratory Muscle Activity

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.

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