Inferences about Respiratory Muscle Use after Cardiac Surgery from Compartmental Volume and Pressure Measurements

1995 ◽  
Vol 82 (6) ◽  
pp. 1318-1327. ◽  
Author(s):  
F. Clergue ◽  
W. A. Whitelaw ◽  
J. C. Charles ◽  
I. Gandjbakhch ◽  
J. L. Pansard ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Abdominal Surgery ◽  
Tidal Volume ◽  
Respiratory Muscle ◽  
Muscle Length ◽  
Abdominal Pressure ◽  
Abdominal Muscles ◽  
Muscle Action ◽  
Rib Cage ◽  
Inspiratory Muscles

Background After upper abdominal surgery, patients have been observed to have alterations in respiratory movements of the rib cage and abdomen and respiratory shifts in pleural and abdominal pressure that suggest dysfunction of the diaphragm. The validity of making such deductions about diaphragm function from these observations is open to discussion. Methods In eight adult patients, American Society of Anesthesiologists physical status 2, scheduled for elective cardiac surgery, we measured respiratory rate, tidal volume, rib cage and abdominal cross-section changes, and esophageal (Pes) and gastric (Pga) pressures preoperatively, 1 day postoperatively, and 5 days postoperatively. These data were analyzed in detail by following the variables through each respiratory cycle. Results Mean delta Pga/delta Pes decreased from 0.73 preoperatively to -0.56 1 day postoperatively and recovered to 0.47 5 days postoperatively. Plots of Pes against Pga and rib cage against abdominal expansion (Konno-Mead diagrams) were constructed. Six patients showed a postoperative pattern of breathing similar to that seen in patients who have undergone abdominal surgery: a decrease in the ratio of delta Pga/delta Pes and a shift toward rib cage expansion, with an increase in breathing rate and a decrease in tidal volume. This change was accomplished in most cases by the use of abdominal muscles in expiration with an increase in inspiratory intercostal muscle action without an increase in diaphragm activation, that is, a shift in the normal balance of respiratory muscle use in favor of muscles other than the diaphragm. A different ventilatory pattern was observed in the other two patients, consisting of minimal rib cage excursion and a large abdominal excursion. In these cases tidal volume was generated largely by contraction and relaxation of abdominal muscles with probable reduction in diaphragm activity. In addition, five patients exhibited positive changes in Pes at the end of inspiration that corresponded to closure of the upper airway, relaxation of inspiratory muscles, and subsequent opening of the airway with sudden exhalation, producing a grunt. Conclusions Indirect measurements of respiratory muscle action based on pressure and chest wall motion are easier than are assessments based on implanted electromyogram electrodes and sonomicrometers that measure electric activity and muscle length, respectively, directly. Interpretation requires numerous assumptions and detailed analysis of phase relations among the variables. In patients after thoracic surgery, however, these measurements strongly point to a shift in the distribution of motor output toward muscles other than the diaphragm.

Airway resistance and respiratory muscle function in snorers during NREM sleep

1985 ◽  
Vol 59 (2) ◽  
pp. 328-335 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Muscle Function ◽  
Respiratory Muscle ◽  
Dynamic Compression ◽  
Nrem Sleep ◽  
Abdominal Muscles ◽  
Resistive Load ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Respiratory Muscle Function

The effect of non-rapid-eye-movement (NREM) sleep on total pulmonary resistance (RL) and respiratory muscle function was determined in four snorers and four nonsnorers. RL at peak flow increased progressively from wakefulness through the stages of NREM sleep in all snorers (3.7 +/- 0.4 vs. 13.0 +/- 4.0 cmH2O X 0.1(-1) X s) and nonsnorers (4.8 +/- 0.4 vs. 7.5 +/- 1.1 cmH2O X 1(-1) X s). Snorers developed inspiratory flow limitation and progressive increase in RL within a breath. The increased RL placed an increased resistive load on the inspiratory muscles, increasing the pressure-time product for the diaphragm between wakefulness and NREM sleep. Tidal volume and minute ventilation decreased in all subjects. The three snorers who showed the greatest increase in within-breath RL demonstrated an increase in the contribution of the lateral rib cage to tidal volume, a contraction of the abdominal muscles during a substantial part of expiration, and an abrupt relaxation of abdominal muscles at the onset of inspiration. We concluded that the magnitude of increase in RL leads to dynamic compression of the upper airway during inspiration, marked distortion of the rib cage, recruitment of the intercostal muscles, and an increased contribution of expiratory muscles to inspiration. This increased RL acts as an internal resistive load that probably contributes to hypoventilation and CO2 retention in NREM sleep.

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 .

Partitioning of inspiratory pressure swings between diaphragm and intercostal/accessory muscles

1978 ◽  
Vol 44 (2) ◽  
pp. 200-208 ◽  
Author(s):  
P. T. Macklem ◽  
D. Gross ◽  
G. A. Grassino ◽  
C. Roussos
Keyword(s):  
Total Pressure ◽  
Pleural Pressure ◽  
Inspiratory Pressure ◽  
Abdominal Pressure ◽  
Abdominal Muscles ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Accessory Muscle ◽  
Inspiratory Muscles ◽  
Accessory Muscles

We tested the hypothesis that the inspiratory pressure swings across the rib-cage pathway are the sum of transdiaphragmatic pressure (Pdi) and the pressures developed by the intercostal/accessory muscles (Pic). If correct, Pic can only contribute to lowering pleural pressure (Ppl), to the extent that it lowers abdominal pressure (Pab). To test this we measured Pab and Ppl during during Mueller maneuvers in which deltaPab = 0. Because there was no outward displacement of the rib cage, Pic must have contributed to deltaPpl, as did Pdi. Under these conditions the total pressure developed by the inspiratory muscles across the rib-cage pathway was less than Pdi + Pic. Therefore, we rejected the hypothesis. A plot of Pab vs. Ppl during relaxation allows partitioning of the diaphragmatic and intercostal/accessory muscle contributions to inspiratory pressure swings. The analysis indicates that the diaphragm can act both as a fixator, preventing transmission of Ppl to the abdomen and as an agonist. When abdominal muscles remain relaxed it only assumes the latter role to the extent that Pab increases.

Influence of global inspiratory muscle fatigue on breathing during exercise

1996 ◽  
Vol 80 (4) ◽  
pp. 1270-1278 ◽  
Author(s):  
P. Sliwinski ◽  
S. Yan ◽  
A. P. Gauthier ◽  
P. T. Macklem
Keyword(s):  
Tidal Volume ◽  
Muscle Fatigue ◽  
Minute Ventilation ◽  
Inspiratory Muscle ◽  
Abdominal Muscles ◽  
Maximal Power Output ◽  
Lung Inflation ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Inspiratory Muscle Fatigue

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.

Respiratory response to abdominal and rib cage muscle paralysis in dogs

1993 ◽  
Vol 74 (5) ◽  
pp. 2309-2317 ◽  
Author(s):  
J. F. Brichant ◽  
M. Gorini ◽  
A. De Troyer
Keyword(s):  
Tidal Volume ◽  
Abdominal Cavity ◽  
Emg Activity ◽  
Abdominal Muscles ◽  
Respiratory Response ◽  
Muscle Paralysis ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Arterial Blood

To assess the respiratory response to abdominal and rib cage muscle paralysis, we measured tidal volume, esophageal and gastric pressures, arterial blood gases, and the electromyogram (EMG) of the diaphragm during progressive epidural anesthesia (lidocaine 2%) in 35 supine anesthetized dogs. The EMG activity of the diaphragm was measured with fine-wire electrodes; the abdominal cavity was thus left intact. Paralysis of the abdominal muscles alone did not produce any alterations. In contrast, when all rib cage muscles were also paralyzed, there were substantial increases in the peak height and the rate of rise of diaphragmatic EMG activity that were associated with a decrease in tidal volume and an increase in arterial PCO2 (PaCO2); swings in transdiaphragmatic pressure, however, were unchanged. The increased diaphragmatic activation due to rib cage muscle paralysis persisted after bilateral cervical vagotomy and was well explained by the increased PaCO2. These observations indicate that in the dog 1) the rib cage muscles contribute significantly to tidal volume, and their paralysis causes, through the increased hypercapnic drive, a compensatory increase in diaphragmatic activation; and 2) the rib cage inspiratory muscles enhance the diaphragm's ability to generate pressure during breathing.

Effect of phrenic afferent stimulation on pattern of respiratory muscle activation

1992 ◽  
Vol 73 (2) ◽  
pp. 563-570 ◽  
Author(s):  
M. E. Ward ◽  
A. Deschamps ◽  
C. Roussos ◽  
S. N. Hussain
Keyword(s):  
Tidal Volume ◽  
Phrenic Nerve ◽  
Respiratory Muscle ◽  
Muscle Activation ◽  
Afferent Fiber ◽  
Transversus Abdominis ◽  
Emg Activity ◽  
Abdominal Muscles ◽  
Breathing Frequency ◽  
Inspiratory Muscles

Ventilation and electromyogram (EMG) activities of the right hemidiaphragm, parasternal intercostal, triangularis sterni, transversus abdominis, genioglossus, and alae nasi muscles were measured before and during central stimulation of the left thoracic phrenic nerve in 10 alpha-chloralose anesthetized vagotomized dogs. Pressure in the carotid sinuses was fixed to maintain baroreflex activity constant. The nerve was stimulated for 1 min with a frequency of 40 Hz and stimulus duration of 1 ms at voltages of 5, 10, 20, and 30 times twitch threshold (TT). At five times TT, no change in ventilation or EMG activity occurred. At 10 times TT, neither tidal volume nor breathing frequency increased sufficiently to reach statistical significance, although the change in their product (minute ventilation) was significant (P less than 0.05). At 20 and 30 times TT, increases in both breathing frequency and tidal volume were significant. At these stimulus intensities, the increases in ventilation were accompanied by approximately equal increases in the activity of the diaphragm, parasternal, and alae nasi muscles. The increase in genioglossus activity was much greater than that of the other inspiratory muscles. Phrenic nerve stimulation also elicited inhomogeneous activation of the expiratory muscles. The transversus abdominis activity increased significantly at intensities from 10 to 30 times TT, whereas the activity of the triangularis sterni remained unchanged. The high stimulation intensities required suggest that the activation of afferent fiber groups III and IV is involved in the response. We conclude that thin-fiber phrenic afferent activation exerts a nonuniform effect on the upper airway, rib cage, and abdominal muscles and may play a role in the control of respiratory muscle recruitment.

Effect of intestinal afferent stimulation on pattern of respiratory muscle activation

1989 ◽  
Vol 66 (3) ◽  
pp. 1455-1461 ◽  
Author(s):  
S. B. Gottfried ◽  
A. F. DiMarco
Keyword(s):  
Tidal Volume ◽  
Mechanical Stimulation ◽  
Respiratory Muscle ◽  
Muscle Activation ◽  
Upper Airway ◽  
Visceral Afferents ◽  
Electromyographic Activity ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Stimulation Of

The purpose of the present study was to examine the reflex effects of mechanical stimulation of intestinal visceral afferents on the pattern of respiratory muscle activation. In 14 dogs anesthetized with pentobarbital sodium, electromyographic activity of the costal and crural diaphragm, parasternal intercostal, and upper airway respiratory muscles was measured during distension of the small intestine. Rib cage and abdominal motion and tidal volume were also recorded. Distension produced an immediate apnea (11.16 +/- 0.80 s). During the first postapneic breath, costal (43 +/- 7% control) and crural (64 +/- 6% control) activity were reduced (P less than 0.001). In contrast, intercostal (137 +/- 11%) and upper airway muscle activity, including alae nasi (157 +/- 16%), genioglossus (170 +/- 15%), and posterior cricoarytenoid muscles (142 +/- 7%) all increased (P less than 0.005). There was greater outward rib cage motion although the abdomen moved paradoxically inward during inspiration, resulting in a reduction in tidal volume (82 +/- 6% control) (P less than 0.005). Postvagotomy distension produced a similar apnea and subsequent reduction in costal and crural activity. However, enhancement of intercostal and upper airway muscle activation was abolished and there was a greater fall in tidal volume (65 +/- 14%). In conclusion, mechanical stimulation of intestinal afferents affects the various inspiratory muscles differently; nonvagal afferents produce an initial apnea and subsequent depression of diaphragm activity whereas vagal pathways mediate selective enhancement of intercostal and upper airway muscle activation.

Respiratory muscle coordination and diaphragm length during expiratory threshold loading

1991 ◽  
Vol 70 (4) ◽  
pp. 1554-1562 ◽  
Author(s):  
J. D. Road ◽  
A. M. Leevers ◽  
E. Goldman ◽  
A. Grassino
Keyword(s):  
Lung Volume ◽  
Respiratory Muscle ◽  
Abdominal Muscles ◽  
Muscle Coordination ◽  
Rib Cage ◽  
Relative Contribution ◽  
Volume Functional ◽  
Residual Capacity ◽  
Anesthetized Dogs ◽  
Expiratory Muscles

Active expiration is produced by the abdominal muscles and the rib cage expiratory muscles. We hypothesized that the relative contribution of these two groups to expiration would affect diaphragmatic length and, hence, influence the subsequent inspiration. To address this question we measured the respiratory muscle response to expiratory threshold loading in spontaneously breathing anesthetized dogs. Prevagotomy, the increase in lung volume (functional residual capacity) and decrease in initial resting length of the diaphragm were attenuated by greater than 50% of values predicted by the passive relationships. Diaphragmatic activation (electromyogram) increased and tidal volume (VT) was preserved. Postvagotomy, effective expiratory muscle recruitment was abolished. The triangularis sterni muscle remained active, and the increase in lung volume was attenuated by less than 15% of that predicted by the passive relationship. Diaphragmatic length was shorter than predicted. VT was not restored, even though costal diaphragmatic and parasternal intercostal electromyogram increased. During expiratory threshold loading with abdominal muscles resected and vagus intact, recruitment of the rib cage expiratory muscles produced a reduction in lung volume comparable with prevagotomy; however, diaphragmatic length decreased markedly. Both the rib cage and abdominal expiratory muscles may defend lung volume; however, their combined action is important to restore diaphragmatic initial length and, accordingly, to preserve VT.

scholarly journals Rib Cage Deformities Alter Respiratory Muscle Action and Chest Wall Function in Patients with Severe Osteogenesis Imperfecta

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e35965 ◽  
Author(s):  
Antonella LoMauro ◽  
Simona Pochintesta ◽  
Marianna Romei ◽  
Maria Grazia D'Angelo ◽  
Antonio Pedotti ◽  
...  
Keyword(s):  
Osteogenesis Imperfecta ◽  
Chest Wall ◽  
Respiratory Muscle ◽  
Muscle Action ◽  
Wall Function ◽  
Rib Cage

Respiratory muscle function in the critically ill

2016 ◽  
Author(s):  
Theodoros Vassilakopoulos ◽  
Charis Roussos
Keyword(s):  
Muscle Function ◽  
Respiratory Muscle ◽  
Magnetic Stimulation ◽  
Abdominal Muscles ◽  
Energy Demands ◽  
Inspiratory Muscles ◽  
Respiratory Muscle Function ◽  
Generating Capacity ◽  
Over Time ◽  
Stimulation Of

The inspiratory muscles are the diaphragm, external intercostals and parasternal internal intercostal muscles. The internal intercostals and abdominal muscles are expiratory. The ability of a subject to take one breath depends on the balance between the load faced by the inspiratory muscles and their neuromuscular competence. The ability of a subject to sustain the respiratory load over time (endurance) depends on the balance between energy supplied to the inspiratory muscles and their energy demands. Hyperinflation puts the diaphragm at a great mechanical disadvantage, decreasing its force-generating capacity. In response to acute increases in load the inspiratory muscles become fatigued and inflammed. In response to reduction in load by the use of mechanical ventilation they develop atrophy and dysfunction. Global respiratory muscle function can be tested using maximum static inspiratory and expiratory mouth pressures, and sniff pressure. Diaphragm function can be tested by measuring the transdiaphragmatic and twitch pressures developed upon electrical or magnetic stimulation of the phrenic nerve.

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