Interaction of lung volume and chemical drive on respiratory muscle EMG and respiratory timing

1977 ◽  
Vol 42 (2) ◽  
pp. 287-295 ◽  
Author(s):  
S. G. Kelsen ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Electrical Activity ◽  
Lung Volume ◽  
Respiratory Muscle ◽  
Vagal Stimulation ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Airway Occlusion ◽  
Continuous Positive Pressure ◽  
Spontaneously Breathing

The effect of increased FRC on the change in respiratory muscle electrical activity (EMG) and the duration of inspiration (Ti) and expiration (Te) produced by increases in chemical drive (i.e., progressive hypercapnia and isocapnic hypoxia) was assessed in 15 anesthetized, spontaneously breathing dogs. FRC was raised by applying continuous positive pressure (4 and 8 cmH2O) to the airway. Progressive hypercapnia and hypoxia were produced by rebreathing techniques. At any PCO2 or PO2, increases in FRC decreased diaphragm EMG (D); increased abdominal muscle EMG (AB); and prolonged Te without affecting Ti. The effect of increased FRC on D, AB, and Te diminished as PCO2 increased or PO2 decreased. The effect of sustained increases in lung volume in the absence of phasic changes was assessed by performing airway occlusion for a single inspiration during rebreathing at both control and increased FRC. The effects of increases in FRC were present during airway occlusion but were eliminated by vagotomy. We conclude, therefore, that tonic vagal stimulation produced by increases in FRC modified the change in respiratory muscle electrical activity and timing produced by increasing chemical drive.

Human respiratory muscle actions and control during exercise

1997 ◽  
Vol 83 (4) ◽  
pp. 1256-1269 ◽  
Author(s):  
A. Aliverti ◽  
S. J. Cala ◽  
R. Duranti ◽  
G. Ferrigno ◽  
C. M. Kenyon ◽  
...  
Keyword(s):  
Lung Volume ◽  
Respiratory Muscle ◽  
Abdominal Muscle ◽  
Abdominal Pressure ◽  
Abdominal Muscles ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Velocity Of Shortening ◽  
And Control ◽  
Muscle Actions

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 .

Physiology of positive-pressure ventilation

2016 ◽  
Author(s):  
Göran Hedenstierna ◽  
Hans Ulrich Rothen
Keyword(s):  
Blood Flow ◽  
Lung Volume ◽  
Respiratory Muscle ◽  
Positive Pressure Ventilation ◽  
Venous Pressure ◽  
Gas Absorption ◽  
Positive Pressure ◽  
Airway Closure ◽  
Dependent Lung ◽  
Oedema Formation

During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).

scholarly journals Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow

2001 ◽  
Vol 91 (2) ◽  
pp. 897-904 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Upper Airway ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Emg Activity ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing ◽  
Respiratory Muscle Activity ◽  
Stimulation Of

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10–15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.

Reflex control of abdominal muscles during positive-pressure breathing

1964 ◽  
Vol 19 (2) ◽  
pp. 224-232 ◽  
Author(s):  
Beverly Bishop
Keyword(s):  
Abdominal Muscle ◽  
Spinal Reflexes ◽  
The Other ◽  
Positive Pressure ◽  
Abdominal Muscles ◽  
Afferent Pathways ◽  
Muscle Response ◽  
Thoracic Spinal ◽  
Vagal Afferent ◽  
Continuous Positive Pressure

Continuous positive-pressure breathing initiates expiratory activity in the abdominal muscle and inhibits the diaphragm in anesthetized cats. This investigation defines neural mechanisms involved in this abdominal muscle response (AMR) to positive-pressure breathing. The AMR is not a segmental reflex since it is abolished by thoracic spinal transection. Bilateral rhizotomy (T8-L3) also eliminates AMR, but laparotomy and abdominal evisceration do not, suggesting that some neural inflow other than from abdominal muscle or viscera is necessary but insufficient for maintaining AMR. Abdominal vagotomy failed to interrupt AMR which was abolished by bilateral cervical vagotomy, indicating that the necessary receptors lie in the thorax. Compression or local anesthesia of the cervical vagi provided the experimental means for abolishing either the inhibition of the diaphragm or the AMR without necessarily interrupting the other. That one response may persist in the absence of the other indicates that vagal afferent pathways subserving AMR are distinct from those mediating diaphragm inhibition. Hence the active expiration of pressure breathing is not a simple corollary of the Hering-Breuer inflation reflex but is a separate reflex served by its own vagal pathway. abdominal muscle response; vagus control of active expiration; abdominal muscle motoneuron pool; vagal afferent pathway in pressure-breathing reflex; thoracic receptors; diaphragm response to pressure breathing; diaphragm; inspiration; expiratory reflexes; inspiratory reflexes; respiratory reflexes; segmental reflexes; spinal reflexes Submitted on February 21, 1963

scholarly journals Nebulization of Poractant alfa via a vibrating membrane nebulizer in spontaneously breathing preterm lambs with binasal continuous positive pressure ventilation

2015 ◽  
Vol 78 (6) ◽  
pp. 664-669 ◽  
Author(s):  
Matthias C. Hütten ◽  
Elke Kuypers ◽  
Daan R. Ophelders ◽  
Maria Nikiforou ◽  
Reint K. Jellema ◽  
...  
Keyword(s):  
Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Vibrating Membrane ◽  
Continuous Positive Pressure ◽  
Spontaneously Breathing

Mechanics of the parasternal intercostals during occluded breaths in dogs

1988 ◽  
Vol 64 (4) ◽  
pp. 1546-1553 ◽  
Author(s):  
A. De Troyer ◽  
G. A. Farkas ◽  
V. Ninane
Keyword(s):  
Electrical Activity ◽  
Intact Animal ◽  
Intercostal Nerve ◽  
Pleural Pressure ◽  
Airway Occlusion ◽  
The Third ◽  
Single Breath ◽  
Supine Posture ◽  
Phrenic Nerves ◽  
Spontaneously Breathing

The electrical activity and the respiratory changes in length of the third parasternal intercostal muscle were measured during single-breath airway occlusion in 12 anesthetized, spontaneously breathing dogs in the supine posture. During occluded breaths in the intact animal, the parasternal intercostal was electrically active and shortened while pleural pressure fell. In contrast, after section of the third intercostal nerve at the chondrocostal junction and abolition of parasternal electrical activity, the muscle always lengthened. This inspiratory muscle lengthening must be related to the fall in pleural pressure; it was, however, approximately 50% less than the amount of muscle lengthening produced, for the same fall in pleural pressure, by isolated stimulation of the phrenic nerves. These results indicate that 1) the parasternal inspiratory shortening that occurs during occluded breaths in the dog results primarily from the muscle inspiratory contraction per se, and 2) other muscles of the rib cage, however, contribute to this parasternal shortening by acting on the ribs or the sternum. The present studies also demonstrate the important fact that the parasternal inspiratory contraction in the dog is really agonistic in nature.

Lung volume and pleural pressure effects on ventricular function

1981 ◽  
Vol 50 (3) ◽  
pp. 630-635 ◽  
Author(s):  
B. H. Culver ◽  
J. J. Marini ◽  
J. Butler
Keyword(s):  
Right Ventricular ◽  
Ventricular Function ◽  
Lung Volume ◽  
Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Pleural Pressure ◽  
Positive Pressure ◽  
Right Ventricular Afterload ◽  
Ventricular Afterload ◽  
Continuous Positive Pressure

To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.

Reflex control of diaphragm activation by thoracic afferents

1993 ◽  
Vol 75 (1) ◽  
pp. 63-69 ◽  
Author(s):  
J. R. Romaniuk ◽  
G. S. Supinski ◽  
A. F. DiMarco
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Respiratory Muscle ◽  
Motor Response ◽  
Airway Occlusion ◽  
Thoracic Level ◽  
Complete Section ◽  
Residual Capacity ◽  
Reflex Control ◽  
The Relationship

Recent studies suggest that chest wall reflexes may have a role in modulating diaphragm activation. The purpose of this study was to more closely examine this issue by assessing the diaphragmatic motor response to airway occlusion. Studies were performed in vagotomized mongrel dogs anesthetized with pentobarbital sodium. Diaphragmatic electromyogram (EMG) and phrenic neurogram (ENG) responses to airway occlusion were evaluated at different precontractile respiratory muscle lengths, achieved by passive inflation and deflation with a volume syringe during the preceding expiration. Lung volume was expressed as the corresponding change in airway pressure. At functional residual capacity, deflation (-5 cmH2O), and large inflation (+25 cmH2O), phrenic ENG during occlusion was 90 +/- 2 (SE), 84 +/- 5, and 86 +/- 3% of the preceding control breaths, respectively (n = 9). Qualitatively similar, but somewhat more pronounced, responses were observed on diaphragmatic EMG. With small lung inflations, the degree of reduction of phrenic ENG with airway occlusion was less. Consequently, the relationship between airway pressure and degree of inhibition was best described as a reverse parabola with the maximum at approximately +10–15 cmH2O. Responses were not significantly affected by bilateral cervical phrenicotomy. Complete section of the spinal cord at the high thoracic level (T1-T2) abolished the observed reduction in phrenic ENG in response to airway occlusion. Our results demonstrate 1) the existence of nonvagal nonphrenic reflex control of diaphragm activation most likely secondary to activation of intercostal afferents and 2) that the magnitude of this reflex is highly dependent on factors related to lung volume.

Effect of transrespiratory pressure on PETCO2-PaCO2 and ventilatory reflexes in humans

1981 ◽  
Vol 51 (3) ◽  
pp. 660-664 ◽  
Author(s):  
R. Banzett ◽  
K. Strohl ◽  
B. Geffroy ◽  
J. Mead
Keyword(s):  
Lung Volume ◽  
Positive Airway Pressure ◽  
Human Subjects ◽  
Positive Pressure ◽  
Healthy Human ◽  
Wide Variability ◽  
The Difference ◽  
End Tidal ◽  
Continuous Positive Pressure ◽  
End Tidal Co2

Inspiratory muscle activity increases when lung volume is increased by continuous positive-pressure breathing in conscious human subjects (Green et al., Respir. Physiol. 35: 283–300, 1978). Because end-tidal CO2 pressure (PETCO2) does not change, these increases have not been attributed to chemoreflexes. However, continuous positive-pressure breathing at 20 cmH2O influences the end-tidal to arterial CO2 pressure differences (Folkow and Pappenheimer, J. Appl. Physiol. 8: 102–110, 1955). We have compared PETCO2 with arterial CO2 pressure (PaCO2). We have compared PETCO2 with arterial CO2 pressure (PaCO2) in healthy human subjects exposed to continuous positive airway pressure (10 cmH2O) or continuous negative pressure around the torso (-15 cmH2O) sufficient to increase mean lung volume by about 650 ml. The difference between PETCO2 and PaCO2 was not decreased, and we conclude that PETCO2 is a valid measure of chemical drive to ventilation in such circumstances. We observed substantial increases in respiratory muscle electromyograms during pressure breathing as seen previously and conclude this response must originate by proprioception. On average, the compensation of tidal volume thus afforded was complete, but the wide variability of individual responses suggests that there was a large cerebral cortical component in the responses seen here.

Effect of hypercapnia and PEEP on expiratory muscle EMG and shortening

1989 ◽  
Vol 66 (3) ◽  
pp. 1408-1413 ◽  
Author(s):  
A. Oliven ◽  
S. G. Kelsen
Keyword(s):  
Electrical Activity ◽  
Abdominal Muscle ◽  
Rectus Abdominis ◽  
Emg Activity ◽  
Expiratory Muscle ◽  
Integrated Emg ◽  
Length Changes ◽  
Expiratory Muscles ◽  
External Oblique ◽  
Spontaneously Breathing

The present study examined the effects of hypercapnia and positive end-expiratory pressure (PEEP) on the electromyographic (EMG) activity and tidal length changes of the expiratory muscles in 12 anesthetized, spontaneously breathing dogs. The integrated EMG activity of both abdominal (external oblique, internal oblique, rectus abdominis, and transverse abdominis) and thoracic (triangularis sterni, internal intercostal) expiratory muscles increased linearly with increasing PCO2 and PEEP. However, with both hypercapnia and PEEP, the percent increase in abdominal muscle electrical activity exceeded that of thoracic expiratory muscle activity. Both hypercapnia and PEEP increased the tidal shortening of the external oblique and rectus abdominis muscles. Changes in tidal length correlated closely with simultaneous increases in muscle electrical activity. However, during both hypercapnia and PEEP, length changes of the external oblique were significantly greater than those of the rectus abdominis. We conclude that both progressive hypercapnia and PEEP increase the electrical activity of all expiratory muscles and augment their tidal shortening but produce quantitatively different responses in the several expiratory muscles.

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