A model of the respiratory pump

1987 ◽  
Vol 63 (3) ◽  
pp. 951-961 ◽  
Author(s):  
D. R. Hillman ◽  
K. E. Finucane
Keyword(s):  
Chest Wall ◽  
Volume Change ◽  
Active Component ◽  
Wall Motion ◽  
Respiratory Muscles ◽  
Passive Components ◽  
Rib Cage ◽  
Lever System ◽  
Chest Wall Motion ◽  
Applied Forces

The interaction of forces that produce chest wall motion and lung volume change is complex and incompletely understood. To aid understanding we have developed a simple model that allows prediction of the effect on chest wall motion of changes in applied forces. The model is a lever system on which the forces generated actively by the respiratory muscles and passively by impedances of rib cage, lungs, abdomen, and diaphragm act at fixed sites. A change in forces results in translational and/or rotational motion of the lever; motion represents volume change. The distribution and magnitude of passive relative to active forces determine the locus and degree of rotation and therefore the effect of an applied force on motion of the chest wall, allowing the interaction of diaphragm, rib cage, and abdomen to be modeled. Analysis of moments allow equations to be derived that express the effect on chest wall motion of the active component in terms of the passive components. These equations may be used to test the model by comparing predicted with empirical behavior. The model is simple, appears valid for a variety of respiratory maneuvers, is useful in interpreting relative motion of rib cage and abdomen and may be useful in quantifying the effective forces acting on the rib cage.

Chest wall distortion during resistive inspiratory loading

1985 ◽  
Vol 58 (5) ◽  
pp. 1646-1653 ◽  
Author(s):  
E. R. Ringel ◽  
S. H. Loring ◽  
J. Mead ◽  
R. H. Ingram
Keyword(s):  
Chest Wall ◽  
Wall Motion ◽  
Respiratory Muscles ◽  
Underlying Mechanism ◽  
Abdominal Muscles ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Circular Configuration ◽  
Chest Wall Motion ◽  
Resistive Loads

We studied six (1 naive and 5 experienced) subjects breathing with added inspiratory resistive loads while we recorded chest wall motion (anteroposterior rib cage, anteroposterior abdomen, and lateral rib cage) and tidal volumes. In the five experienced subjects, transdiaphragmatic and pleural pressures, and electromyographs of the sternocleidomastoid and abdominal muscles were also measured. Subjects inspired against the resistor spontaneously and then with specific instructions to reach a target pleural or transdiaphragmatic pressure or to maximize selected electromyographic activities. Depending on the instructions, a wide variety of patterns of inspiratory motion resulted. Although the forces leading to a more elliptical or circular configuration of the chest wall can be identified, it is difficult to analyze or predict the configurational results based on insertional and pressure-related contributions of a few individual respiratory muscles. Although overall chest wall respiratory motion cannot be readily inferred from the electromyographic and pressure data we recorded, it is clear that responses to loading can vary substantially within and between individuals. Undoubtedly, the underlying mechanism for the distortional changes with loading are complex and perhaps many are behavioral rather than automatic and/or compensatory.

Chest wall motion and distribution of inspired gas in anesthetized supine dogs

1980 ◽  
Vol 49 (2) ◽  
pp. 279-286 ◽  
Author(s):  
E. R. Schmid ◽  
K. Rehder ◽  
T. J. Knopp ◽  
R. E. Hyatt
Keyword(s):  
Chest Wall ◽  
Wall Motion ◽  
Regional Distribution ◽  
Vertical Gradient ◽  
Spontaneous Respiration ◽  
Regional Ventilation ◽  
Muscle Paralysis ◽  
Rib Cage ◽  
Chest Wall Motion ◽  
Anterior Posterior

Changes in the anterior-posterior (AP) and lateral diameters of the rib cage and abdomen were assessed by magnetometry in seven anesthetized supine dogs during spontaneous respiration (SR) and mechanical ventilation after muscle paralysis (MV). Regional distribution of inspired gas was measured for both modes of ventilation by determining regional 133Xe clearances. Marked differences in chest wall motion were observed between SR and MV: during MV, the changes in lateral rib cage diameter from FRC to end inspiration were larger, and the changes in both abdominal diameters smaller than during SR. AP rib cage diameter changes were similar for both modes of ventilation. Inward motion of the lateral rib cage during initial inspiration was observed in four dogs during SR; it disappeared consistently with MV. Regional 133Xe clearances were not significantly different: there was no cephalocaudal gradient, and the vertical gradient in regional ventilation was similar with MV and SR. We conclude that significant changes in chest wall motion and shape are not necessarily associated with detectable differences in the distribution of regional ventilation.

Chest wall motion during tidal breathing

1997 ◽  
Vol 83 (5) ◽  
pp. 1531-1537 ◽  
Author(s):  
A. De Groote ◽  
M. Wantier ◽  
G. Cheron ◽  
M. Estenne ◽  
M. Paiva
Keyword(s):  
Chest Wall ◽  
Wall Motion ◽  
Costal Cartilage ◽  
Three Dimensional ◽  
Normal Subjects ◽  
Costal Margin ◽  
Tidal Breathing ◽  
Lateral Direction ◽  
Rib Cage ◽  
Chest Wall Motion

De Groote, A., M. Wantier, G. Cheron, M. Estenne, and M. Paiva. Chest wall motion during tidal breathing. J. Appl. Physiol. 83(5): 1531–1537, 1997.—We have used an automatic motion analyzer, the ELITE system, to study changes in chest wall configuration during resting breathing in five normal, seated subjects. Two television cameras were used to record the x-y-z displacements of 36 markers positioned circumferentially at the level of the third (S1) and fifth (S2) costal cartilage, corresponding to the lung-apposed rib cage; midway between the xyphoid process and the costal margin (S3), corresponding to the abdomen-apposed rib cage; and at the level of the umbilicus (S4). Recordings of different subsets of markers were made by submitting the subject to five successive rotations of 45–90°. Each recording lasted 30 s, and three-dimensional displacements of markers were analyzed with the Matlab software. At spontaneous end expiration, sections S1–3 were elliptical but S4 was more circular. Tidal changes in chest wall dimensions were consistent among subjects. For S1–2, changes during inspiration occurred primarily in the cranial and ventral directions and averaged 3–5 mm; displacements in the lateral direction were smaller (1–2 mm). On the other hand, changes at the level of S4 occurred almost exclusively in the ventral direction. In addition, both compartments showed a ventral displacement of their dorsal aspect that was not accounted for by flexion of the spine. We conclude that, in normal subjects breathing at rest in the seated posture, displacements of the rib cage during inspiration are in the cranial, lateral outward, and ventral directions but that expansion of the abdomen is confined to the ventral direction.

Association of chest wall motion and tidal volume responses during CO2 rebreathing

1996 ◽  
Vol 81 (4) ◽  
pp. 1528-1534 ◽  
Author(s):  
Sheng Yan ◽  
Pawel Sliwinski ◽  
Peter T. Macklem
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Wall Motion ◽  
Forced Expiratory Volume ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Chest Wall Motion ◽  
Variable Recruitment ◽  
The Individual ◽  
End Tidal

Yan, Sheng, Pawel Sliwinski, and Peter T. Macklem.Association of chest wall motion and tidal volume responses during CO2 rebreathing. J. Appl. Physiol. 81(4): 1528–1534, 1996.—The purpose of this study is to investigate the effect of chest wall configuration at end expiration on tidal volume (Vt) response during CO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory and end-inspiratory volume of the rib cage (ΔVrc,e and ΔVrc,i, respectively) and abdomen (ΔVab,eand ΔVab,i, respectively) measured by linearized magnetometers were expressed as a function of end-tidal[Formula: see text]([Formula: see text]). The changes in end-expiratory and end-inspiratory volumes of the chest wall (ΔVcw,e and ΔVcw,i, respectively) were calculated as the sum of the respective rib cage and abdominal volumes. The magnetometer coils were placed at the level of the nipples and 1–2 cm above the umbilicus and calibrated during quiet breathing against the Vt measured from a pneumotachograph. The ΔVrc,e/[Formula: see text]slope was quite variable among subjects. It was significantly positive ( P < 0.05) in five subjects, significantly negative in four subjects ( P < 0.05), and not different from zero in the remaining two subjects. The ΔVab,e/[Formula: see text]slope was significantly negative in all subjects ( P < 0.05) with a much smaller intersubject variation, probably suggesting a relatively more uniform recruitment of abdominal expiratory muscles and a variable recruitment of rib cage muscles during CO2rebreathing in different subjects. As a group, the mean ΔVrc,e/[Formula: see text], ΔVab,e/[Formula: see text], and ΔVcw,e/[Formula: see text]slopes were 0.010 ± 0.034, −0.030 ± 0.007, and −0.020 ± 0.032 l / Torr, respectively; only the ΔVab,e/[Formula: see text]slope was significantly different from zero. More interestingly, the individual ΔVt/[Formula: see text]slope was negatively associated with the ΔVrc,e/[Formula: see text]( r = −0.68, P = 0.021) and ΔVcw,e/[Formula: see text]slopes ( r = −0.63, P = 0.037) but was not associated with the ΔVab,e/[Formula: see text]slope ( r = 0.40, P = 0.223). There was no correlation of the ΔVrc,e/[Formula: see text]and ΔVcw,e/[Formula: see text]slopes with age, body size, forced expiratory volume in 1 s, or expiratory time. The group ΔVab,i/[Formula: see text]slope (0.004 ± 0.014 l / Torr) was not significantly different from zero despite the Vt nearly being tripled at the end of CO2 rebreathing. In conclusion, the individual Vtresponse to CO2, although independent of ΔVab,e, is a function of ΔVrc,e to the extent that as the ΔVrc,e/[Formula: see text]slope increases (more positive) among subjects, the Vt response to CO2 decreases. These results may be explained on the basis of the respiratory muscle actions and interactions on the rib cage.

Chest wall motion of infants during spinal anesthesia

1990 ◽  
Vol 68 (5) ◽  
pp. 2087-2091 ◽  
Author(s):  
R. C. Pascucci ◽  
M. B. Hershenson ◽  
N. F. Sethna ◽  
S. H. Loring ◽  
A. R. Stark
Keyword(s):  
Spinal Anesthesia ◽  
Chest Wall ◽  
Muscle Activity ◽  
Wall Motion ◽  
Sensory Block ◽  
Intercostal Muscle ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Diaphragmatic Function ◽  
Chest Wall Motion

To test the extent to which diaphragmatic contraction moves the rib cage in awake supine infants during quiet breathing, we studied chest wall motion in seven prematurely born infants before and during spinal anesthesia for inguinal hernia repair. Infants were studied at or around term (postconceptional age 43 +/- 8 wk). Spinal anesthesia produced a sensory block at the T2-T4 level, with concomitant motor block at a slightly lower level. This resulted in the loss of most intercostal muscle activity, whereas diaphragmatic function was preserved. Rib cage and abdominal displacements were measured with respiratory inductance plethysmography before and during spinal anesthesia. During the anesthetic, outward inspiratory rib cage motion decreased in six infants (P less than 0.02, paired t test); four of these developed paradoxical inward movement of the rib cage during inspiration. One infant, the most immature in the group, had inward movement of the rib cage both before and during the anesthetic. Abdominal displacements increased during spinal anesthesia in six of seven infants (P less than 0.05), suggesting an increase in diaphragmatic motion. We conclude that, in the group of infants studied, outward rib cage movement during awake tidal breathing requires active, coordinated intercostal muscle activity that is suppressed by spinal anesthesia.

Human Chest Wall Function while Awake and during Halothane Anesthesia 

1995 ◽  
Vol 82 (1) ◽  
pp. 20-31 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner
Keyword(s):  
Carbon Dioxide ◽  
Chest Wall ◽  
Respiratory Muscle ◽  
Wall Motion ◽  
Respiratory Muscles ◽  
Respiratory Drive ◽  
Halothane Anesthesia ◽  
Neural Drive ◽  
Carbon Dioxide Rebreathing ◽  
Chest Wall Motion

Background Changes in the distribution of respiratory drive to different respiratory muscles may contribute to respiratory depression produced by halothane. The aim of this study was to examine factors that are responsible for halothane-induced depression of the ventilatory response to carbon dioxide rebreathing. Methods In six human subjects, respiratory muscle activity in the parasternal intercostal, abdominal, and diaphragm muscles was measured using fine-wire electromyography electrodes. Chest wall motion was determined by respiratory impedance plethysmography. Electromyography activities and chest wall motion were measured during hyperpnea produced by carbon dioxide rebreathing while the subjects were awake and during 1 MAC halothane anesthesia. Results Halothane anesthesia significantly reduced the slope of the response of expiratory minute ventilation to carbon dioxide (from 2.88 +/- 0.73 (mean +/- SE) to 2.01 +/- 0.45 l.min-1.mmHg-1). During the rebreathing period, breathing frequency significantly increased while awake (from 10.3 +/- 1.4 to 19.7 +/- 2.6 min-1, P &lt; 0.05) and significantly decreased while anesthetized (from 28.8 +/- 3.9 to 21.7 +/- 1.9 min-1, P &lt; 0.05). Increases in respiratory drive to the phrenic motoneurons produced by rebreathing, as estimated by the diaphragm electromyogram, were enhanced by anesthesia. Anesthesia attenuated the response of parasternal electromyography and accentuated the response of the transversus abdominis electromyography to rebreathing. The compartmental response of the ribcage to rebreathing was significantly decreased by anesthesia (from 1.83 +/- 0.58 to 0.48 +/- 0.13 l.min-1.mmHg-1), and marked phase shifts between ribcage and abdominal motion developed in some subjects. However, at comparable tidal volumes, the ribcage contribution to ventilation was similar while awake and anesthetized in four of the six subjects. Conclusions Halothane anesthesia enhances the rebreathing response of neural drive to the primary respiratory muscle, the diaphragm. These findings provide direct evidence that, at the dose examined in this study, halothane-induced respiratory depression is caused by alterations in the distribution and timing of neural drive to the respiratory muscles, rather than a global depression of respiratory motoneuron drive.

Abdominal compliance, parasternal activation, and chest wall motion

1993 ◽  
Vol 74 (3) ◽  
pp. 1398-1405 ◽  
Author(s):  
S. J. Cala ◽  
J. Edyvean ◽  
L. A. Engel
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Wall Motion ◽  
Normal Subjects ◽  
Rib Cage ◽  
Mechanical Coupling ◽  
Co2 Rebreathing ◽  
Abdominal Compliance ◽  
Chest Wall Motion ◽  
The Difference

We measured abdominal compliance (Cab) and rib cage displacement (delta Vrc) relative to abdominal displacement (delta Vab) during relaxation and tidal breathing in upright (U) and supine (S) postures in five normal subjects. In S, an abdominal binder was used to decrease Cab in two to five increments. We also measured the electrical activity of the parasternal muscle (EMGps) with the use of fine-wire intramuscular electrodes during CO2 rebreathing in U and in supine unbound (SU) and supine bound (SB) postures. During maximum binding (SB2), Cab decreased to 39 +/- 7% of the SU value (P = 0.01), matching Cab in U (P = 0.16). In the SB condition, the ratio of tidal delta Vrc/delta Vab to relaxation delta Vrc/delta Vab increased as Cab decreased, matching the data in U. For the group, this ratio decreased during SU to 47 +/- 10% (P = 0.02) but increased during SB2 to 86 +/- 7% (P = 0.18) of the value in U. During CO2 rebreathing, EMGps increased linearly with tidal volume (r > 0.727, P < 0.01). However, at any given tidal volume, the SU and SB2 EMGps were not significantly different (P = 0.12), and both were less than that in U (P < 0.02). The results suggest that the differences in chest wall motion between U and S may be due to the difference in Cab and not to different patterns of respiratory muscle recruitment. The mechanism may relate to changes in mechanical coupling between the diaphragm and the rib cage.

The Act of Breathing

Physiology ◽  
1990 ◽  
Vol 5 (6) ◽  
pp. 233-237
Author(s):  
PT Macklem
Keyword(s):  
Chest Wall ◽  
Wall Motion ◽  
Compartment System ◽  
Rib Cage ◽  
Chest Wall Motion

During the last 30 years, quantification of chest wall motion, partitioning and analysis of pressures displacing chest wall, recognition that the diaphragm is composed of 2 muscles, and realization that rib cage is a 2-compartment system, each exposed to different pressure, has produced new insights into how mammals breathe.

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