Do canine scalene and sternomastoid muscles play a role in breathing?

1994 ◽  
Vol 76 (1) ◽  
pp. 242-252 ◽  
Author(s):  
A. De Troyer ◽  
M. Cappello ◽  
J. F. Brichant

To assess the respiratory function of the scalene and sternomastoid muscles in the dog, we studied the effect of graded increases in inspiratory airflow resistance and single-breath airway occlusion on the electrical activity of these muscles in 18 supine anesthetized spontaneously breathing animals. The sternomastoids never showed any activity, and the scalenes showed some inspiratory activity during occlusion in only two animals. The adoption of the prone position and bilateral cervical vagotomy did not affect this pattern. Hypercapnia also did not elicit any sternomastoid activity and induced scalene inspiratory activity during occlusion in only four of nine animals. On microscopic examination, however, both muscles were found to contain large numbers of spindles, suggesting that they have the capacity to respond to stretch. In addition, with increases in inspiratory resistance, both the sternum and ribs were displaced in the caudal direction. As a result, the scalenes demonstrated a gradual inspiratory lengthening and the normal inspiratory lengthening of the sternomastoids was accentuated. Additional studies in three unanesthetized animals showed consistent activity in the scalene and sternomastoid muscles during movements of the trunk and neck but no activity during breathing, including occluded breathing. These observations thus indicate that the alpha-motoneurons of the scalene and sternomastoid muscles in the dog have very small central respiratory drive potentials with respect to their critical firing threshold. In this animal, these muscles do not have a significant respiratory function.

1984 ◽  
Vol 56 (4) ◽  
pp. 940-947 ◽  
Author(s):  
T. Trippenbach ◽  
R. Affleck ◽  
G. Kelly

Effects of prolonged airway occlusion were investigated in anesthetized and vagotomized 9-to 15-day-old pups and adult rabbits. The changes and temporal relationships between “integrated” phrenic activity, external intercostal electromyogram (INT), and esophageal pressure (Pes) were examined. Each occlusion resulted in hyperpnea, apnea, and gasping. Blood pressure recorded during the occlusion showed a marked decrease. During hyperpnea, the rate of changes and maximal amplitudes in Pes and INT were similar in both age groups. The increase in integrated phrenic activity (PHR) was significantly greater in young rabbits. In both age groups, changes in INT during gasping followed a similar time course and exceeded those in PHR. Maximal values of the three parameters were concurrent in adults, whereas the increase in INT peaked later than PHR and Pes in rabbit pups. In adult rabbits, PHR, INT, and Pes, during the last gasp, decreased to the values of the first hyperpnea breath. In rabbit pups, Pes of the last gasp decreased significantly below this value while INT was still elevated. This Pes decrease could result from inspiratory muscle dysfunction in the pups. Thus in rabbit pups, 1) greater changes in PHR were necessary to produce a given change in Pes than in adult rabbits; 2) activity of the external intercostal muscles was not efficient in developing pressure under conditions of asphyxia; and 3) the independent activation of diaphragmatic and intercostal motoneurons is not of vagal origin. Additionally, the results led us to conclude that Pes can serve as a close approximation of respiratory drive in adult rabbits. This parameter, however, cannot be used as an index of central inspiratory activity during gasping in rabbit pups.


1988 ◽  
Vol 64 (4) ◽  
pp. 1546-1553 ◽  
Author(s):  
A. De Troyer ◽  
G. A. Farkas ◽  
V. Ninane

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.


1989 ◽  
Vol 66 (3) ◽  
pp. 1414-1420 ◽  
Author(s):  
A. De Troyer ◽  
G. A. Farkas

We have previously demonstrated that the shortening of the canine parasternal intercostals during inspiration results primarily from the muscles' own activation (J. Appl. Physiol. 64: 1546–1553, 1988). In the present studies, we have tested the hypothesis that other inspiratory rib cage muscles may contribute to the parasternal inspiratory shortening. Eight supine, spontaneously breathing dogs were studied. Changes in length of the third or fourth right parasternal intercostal were measured during quiet breathing and during single-breath airway occlusion first with the animal intact, then after selective denervation of the muscle, and finally after bilateral phrenicotomy. Denervating the parasternal virtually eliminated the muscle shortening during quiet inspiration and caused the muscle to lengthen during occluded breaths. After phrenicotomy, however, the parasternal, while being denervated, shortened again a significant amount during both quiet inspiration and occluded breaths. These data thus confirm that a component of the parasternal inspiratory shortening is not active and results from the action of other inspiratory rib cage muscles. Additional studies in four animals demonstrated that the scalene and serratus muscles do not play any role in this phenomenon; it must therefore result from the action of intrinsic rib cage muscles.


1984 ◽  
Vol 57 (1) ◽  
pp. 197-204 ◽  
Author(s):  
W. B. Van de Graaff ◽  
S. B. Gottfried ◽  
J. Mitra ◽  
E. van Lunteren ◽  
N. S. Cherniack ◽  
...  

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xu-Ying Luo ◽  
Xuan He ◽  
Yi-Min Zhou ◽  
Yu-Mei Wang ◽  
Jing-Ran Chen ◽  
...  

Abstract Background Patient–ventilator asynchrony is common in mechanically ventilated patients and may be related to adverse outcomes. Few studies have reported the occurrence of asynchrony in brain-injured patients. We aimed to investigate the prevalence, type and severity of patient–ventilator asynchrony in mechanically ventilated patients with brain injury. Methods This prospective observational study enrolled acute brain-injured patients undergoing mechanical ventilation. Esophageal pressure monitoring was established after enrollment. Flow, airway pressure, and esophageal pressure–time waveforms were recorded for a 15-min interval, four times daily for 3 days, for visually detecting asynchrony by offline analysis. At the end of each dataset recording, the respiratory drive was determined by the airway occlusion maneuver. The asynchrony index was calculated to represent the severity. The relationship between the prevalence and the severity of asynchrony with ventilatory modes and settings, respiratory drive, and analgesia and sedation were determined. Association of severe patient–ventilator asynchrony, which was defined as an asynchrony index  ≥ 10%, with clinical outcomes was analyzed. Results In 100 enrolled patients, a total of 1076 15-min waveform datasets covering 330,292 breaths were collected, in which 70,156 (38%) asynchronous breaths were detected. Asynchrony occurred in 96% of patients with the median (interquartile range) asynchrony index of 12.4% (4.3%–26.4%). The most prevalent type was ineffective triggering. No significant difference was found in either prevalence or asynchrony index among different classifications of brain injury (p > 0.05). The prevalence of asynchrony was significantly lower during pressure control/assist ventilation than during other ventilatory modes (p < 0.05). Compared to the datasets without asynchrony, the airway occlusion pressure was significantly lower in datasets with ineffective triggering (p < 0.001). The asynchrony index was significantly higher during the combined use of opioids and sedatives (p < 0.001). Significantly longer duration of ventilation and hospital length of stay after the inclusion were found in patients with severe ineffective triggering (p < 0.05). Conclusions Patient–ventilator asynchrony is common in brain-injured patients. The most prevalent type is ineffective triggering and its severity is likely related to a long duration of ventilation and hospital stay. Prevalence and severity of asynchrony are associated with ventilatory modes, respiratory drive and analgesia/sedation strategy, suggesting treatment adjustment in this particular population. Trial registration The study has been registered on 4 July 2017 in ClinicalTrials.gov (NCT03212482) (https://clinicaltrials.gov/ct2/show/NCT03212482).


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Shinichiro Ohshimo

AbstractAcute respiratory distress syndrome (ARDS) is a fatal condition with insufficiently clarified etiology. Supportive care for severe hypoxemia remains the mainstay of essential interventions for ARDS. In recent years, adequate ventilation to prevent ventilator-induced lung injury (VILI) and patient self-inflicted lung injury (P-SILI) as well as lung-protective mechanical ventilation has an increasing attention in ARDS.Ventilation-perfusion mismatch may augment severe hypoxemia and inspiratory drive and consequently induce P-SILI. Respiratory drive and effort must also be carefully monitored to prevent P-SILI. Airway occlusion pressure (P0.1) and airway pressure deflection during an end-expiratory airway occlusion (Pocc) could be easy indicators to evaluate the respiratory drive and effort. Patient-ventilator dyssynchrony is a time mismatching between patient’s effort and ventilator drive. Although it is frequently unrecognized, dyssynchrony can be associated with poor clinical outcomes. Dyssynchrony includes trigger asynchrony, cycling asynchrony, and flow delivery mismatch. Ventilator-induced diaphragm dysfunction (VIDD) is a form of iatrogenic injury from inadequate use of mechanical ventilation. Excessive spontaneous breathing can lead to P-SILI, while excessive rest can lead to VIDD. Optimal balance between these two manifestations is probably associated with the etiology and severity of the underlying pulmonary disease.High-flow nasal cannula (HFNC) and non-invasive positive pressure ventilation (NPPV) are non-invasive techniques for supporting hypoxemia. While they are beneficial as respiratory supports in mild ARDS, there can be a risk of delaying needed intubation. Mechanical ventilation and ECMO are applied for more severe ARDS. However, as with HFNC/NPPV, inappropriate assessment of breathing workload potentially has a risk of delaying the timing of shifting from ventilator to ECMO. Various methods of oxygen administration in ARDS are important. However, it is also important to evaluate whether they adequately reduce the breathing workload and help to improve ARDS.


1975 ◽  
Vol 38 (5) ◽  
pp. 768-773 ◽  
Author(s):  
N. N. Stanley ◽  
M. D. Altose ◽  
S. G. Kelsen ◽  
C. F. Ward ◽  
N. S. Cherniack

Experiments were conducted on human subjects to study the effect of lung inflation during breath holding on respiratory drive. Two series of experiments were performed: the first to examine respiratory drive during a single breath hold, the second designed to examine the sustained effect of lung inflation on subsequent breath holds. The experiments involved breath holding begun either at the end of a normal expiration or after a maximum inspiration. When breath holding was repeated at 10-min intervals, the increase in BHT produced by lung inflation was greater in short breath holds (after CO2 rebreathing) than in long breath holds (after hyperventilation). If breath holds were made in rapid succession, the first breath hold was much longer when made at total lung capacity than at functional residual capacity, but this effect of lung inflation diminished in subsequent breath holds. It is concluded that the inhibitory effect of lung inflation decays during breath holding and is regained remarkably slowly during the period of breathing immediately after breath holding.


1981 ◽  
Vol 51 (4) ◽  
pp. 990-1001 ◽  
Author(s):  
M. Younes ◽  
W. Riddle ◽  
J. Polacheck

In the preceding two communications we described a model for the relation between respiratory neural and mechanical outputs. In the present report we test the accuracy of the model in predicting volume and flow from occlusion pressure wave forms, and vice versa. We performed single-breath airway occlusions in 21 unconscious subjects and determined the time course of occlusion pressure. We also measured the passive properties of the respiratory system. The time course of volume and flow was predicted from the occlusion pressure wave forms, and the results were compared with the spontaneous breaths immediately preceding occlusion. Inspiratory duration, shape and amplitude of occlusion-pressure wave forms, and the passive properties of the respiratory system varied widely among subjects. There was good agreement between predicted and observed values in all cases. Except for some prolongation of inspiration (Hering-Breuer reflex), diaphragmatic activity did not change during occlusion. Since occlusion pressure is proportional to inspiratory activity, we conclude that the model described provides a good approximation of the relation between inspiratory activity and spirometric output.


1986 ◽  
Vol 61 (2) ◽  
pp. 719-727 ◽  
Author(s):  
E. van Lunteren ◽  
N. S. Cherniack

In nine anesthetized supine spontaneously breathing dogs, we compared moving average electromyograms (EMGs) of the costal diaphragm and the third parasternal intercostal muscles with their respective respiratory changes in length (measured by sonomicrometry). During resting O2 breathing the pattern of diaphragm and intercostal muscle inspiratory shortening paralleled the gradually incrementing pattern of their moving average EMGs. Progressive hypercapnia caused progressive increases in the amount and velocity of respiratory muscle inspiratory shortening. For both muscles there were linear relationships during the course of CO2 rebreathing between their peak moving average EMGs and total inspiratory shortening and between tidal volume and total inspiratory shortening. During single-breath airway occlusions, the electrical activity of both the diaphragm and intercostal muscles increased, but there were decreases in their tidal shortening. The extent of muscle shortening during occluded breaths was increased by hypercapnia, so that both muscles shortened more during occluded breaths under hypercapnic conditions (PCO2 up to 90 Torr) than during unoccluded breaths under normocapnic conditions. These results suggest that for the costal diaphragm and parasternal intercostal muscles there is a close relationship between their electrical and mechanical behavior during CO2 rebreathing, this relationship is substantially altered by occluding the airway for a single breath, and thoracic respiratory muscles do not contract quasi-isometrically during occluded breaths.


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