Respiratory effect of the lower rib displacement produced by the diaphragm

2012 ◽  
Vol 112 (4) ◽  
pp. 529-534 ◽  
Author(s):  
André De Troyer

The diaphragm acting alone causes a cranial displacement of the lower ribs and a caudal displacement of the upper ribs. The respiratory effect of the lower rib displacement, however, is uncertain. In the present study, two sets of experiments were performed in dogs to assess this effect. In the first, all the inspiratory intercostal muscles were severed, so that the diaphragm was the only muscle active during inspiration, and the normal inspiratory cranial displacement of the lower ribs was suppressed at regular intervals. In the second experiment, the animals were given a muscle relaxant to abolish respiratory muscle activity, and external, cranially oriented forces were applied to the lower rib pairs to simulate the action of the diaphragm on these ribs. The data showed that 1) holding the lower ribs stationary during spontaneous, isolated diaphragm contraction had no effect on the change in lung volume during unimpeded inspiration and no effect on the fall in pleural pressure (Ppl) during occluded breaths; 2) the procedure, however, caused an increase in the caudal displacement of the upper ribs; and 3) pulling the lower rib pairs cranially induced a cranial displacement of the upper ribs and a small fall in Ppl. These observations indicate that the force applied on the lower ribs by the diaphragm during spontaneous contraction, acting through the interdependence of the ribs, is transmitted to the upper ribs and has an inspiratory effect on the lung. However, this effect is very small compared to that of the descent of the dome.

1994 ◽  
Vol 76 (5) ◽  
pp. 2015-2025 ◽  
Author(s):  
B. K. Erickson ◽  
H. V. Forster ◽  
T. F. Lowry ◽  
L. G. Pan ◽  
M. J. Korducki ◽  
...  

The objective of the present study was to determine whether lung and diaphragm afferents contribute to the changes in respiratory muscle activity when end-expiratory lung volume (EELV) is changed in ponies. We studied the responses of the diaphragm and the transversus abdominis (TA) muscles to passive increases in EELV in awake intact (I), diaphragm-deafferented (DD), pulmonary vagal- (hilar nerve) denervated (HND), and DD + HND ponies. Negative pressure of -10 or -20 cmH2O applied around the ponies′ torsos [positive transrespiratory (TR) pressure] increased (P < 0.05) EELV in all ponies; the increases were more (P < 0.05) in HND and less (P < 0.05) in DD than in I ponies. In I ponies, positive TR pressure increased (P < 0.05) the rate of rise of the integrated diaphragmatic electromyogram (EMG), reflecting increased drive to the muscle. This increase was less (P < 0.05) in DD and HND than in I ponies. In DD + HND ponies, there was no significant (P > 0.10) change in drive to the diaphragm during positive TR pressure. In I ponies, positive TR pressure increased (P < 0.05) the duration and mean activity of the TA EMG. In HND and DD + HND ponies, the TA EMG was not altered by positive TR pressure. I and DD ponies decreased (P < 0.05) breathing frequency but maintained tidal volume (VT) during positive TR pressure. HND and DD+HND ponies increased breathing frequency (P < 0.05) and decreased (P < 0.05) VT during positive TR pressure. We conclude that, during positive TR pressure when the diaphragm is presumably at a mechanical disadvantage, diaphragm and vagal afferents mediate increased drive to the diaphragm to prevent VT from decreasing. In addition, during positive TR pressure, vagal afferents mediate an increase in duration of TA activity, which minimizes the increase in EELV.


1992 ◽  
Vol 72 (4) ◽  
pp. 1362-1367 ◽  
Author(s):  
D. M. Ainsworth ◽  
C. A. Smith ◽  
B. D. Johnson ◽  
S. W. Eicker ◽  
K. S. Henderson ◽  
...  

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.


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 &lt; 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.


2010 ◽  
Vol 68 (4) ◽  
pp. 339-343 ◽  
Author(s):  
Gerard J Hutten ◽  
Leo A van Eykern ◽  
Philipp Latzin ◽  
Cindy Thamrin ◽  
Wim M van Aalderen ◽  
...  

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

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Victoria N. Jensen ◽  
Azl Saeed ◽  
Kari A. Seedle ◽  
Sarah Marie Turner ◽  
Steven A. Crone

PEDIATRICS ◽  
1988 ◽  
Vol 81 (3) ◽  
pp. 399-403
Author(s):  
Jeffrey Perlman ◽  
Bradley Thach

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 &lt; .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.


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 ◽  
...  

1988 ◽  
Vol 64 (6) ◽  
pp. 2314-2317 ◽  
Author(s):  
J. Mead ◽  
M. B. Reid

We observed striking differences in respiratory muscle electromyogram activity when active expirations were interrupted in rapid succession, depending on the mode of interruption. When the interruptions were produced at the level of the glottis (utterances, uh-uh-uh-uh, at 5–8 Hz) there were synchronous bursts of activity from expiratory muscles in all three subjects during the periods of no flow and rapid bursts of diaphragmatic activity during the flow phases in one subject. In contrast, when similarly rapid interruptions of active expirations were produced with the tongue on a mouthpiece (utterance, te-te-te-te) or with an external valve, no synchronous bursts were observed. Since all interruptions would have been mechanically similar at expiratory muscular and pulmonary levels, we reasoned that the bursts with glottic interruptions were either programmed centrally or driven reflexly at the laryngeal level.


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