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

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.

1987 ◽  
Vol 63 (3) ◽  
pp. 951-961 ◽  
Author(s):  
D. R. Hillman ◽  
K. E. Finucane

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.


1985 ◽  
Vol 58 (5) ◽  
pp. 1646-1653 ◽  
Author(s):  
E. R. Ringel ◽  
S. H. Loring ◽  
J. Mead ◽  
R. H. Ingram

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.


1997 ◽  
Vol 83 (5) ◽  
pp. 1531-1537 ◽  
Author(s):  
A. De Groote ◽  
M. Wantier ◽  
G. Cheron ◽  
M. Estenne ◽  
M. Paiva

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.


1996 ◽  
Vol 81 (4) ◽  
pp. 1528-1534 ◽  
Author(s):  
Sheng Yan ◽  
Pawel Sliwinski ◽  
Peter T. Macklem

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.


1990 ◽  
Vol 68 (5) ◽  
pp. 2087-2091 ◽  
Author(s):  
R. C. Pascucci ◽  
M. B. Hershenson ◽  
N. F. Sethna ◽  
S. H. Loring ◽  
A. R. Stark

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.


1993 ◽  
Vol 74 (3) ◽  
pp. 1398-1405 ◽  
Author(s):  
S. J. Cala ◽  
J. Edyvean ◽  
L. A. Engel

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.


Physiology ◽  
1990 ◽  
Vol 5 (6) ◽  
pp. 233-237
Author(s):  
PT Macklem

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.


1993 ◽  
Vol 74 (5) ◽  
pp. 2242-2252 ◽  
Author(s):  
J. G. Venegas ◽  
K. Tsuzaki ◽  
B. J. Fox ◽  
B. A. Simon ◽  
C. A. Hales

Apparently conflicting differences between the regional chest wall motion and gas transport have been observed during high-frequency ventilation (HFV). To elucidate the mechanism responsible for such differences, a positron imaging technique capable of assessing dynamic chest wall volumetric expansion, regional lung volume, and regional gas transport was developed. Anesthetized supine dogs were studied at ventilatory frequencies (f) ranging from 1 to 15 Hz and eucapnic tidal volumes. The regional distribution of mean lung volume was found to be independent of f, but the apex-to-base ratio of regional chest wall expansion favored the lung bases at low f and became more homogeneous at higher f. Regional gas transport per unit of lung volume, assessed from washout maneuvers, was homogeneous at 1 Hz, favored the bases progressively as f increased to 9 Hz, and returned to homogeneity at 15 Hz. Interregional asynchrony (pendelluft) and right-to-left differences were small at this large regional scale. Analysis of the data at a higher spatial resolution showed that the motion of the diaphragm relative to the excursions of the rib cage decreased as f increased. These differences from apex to base in regional chest wall expansion and gas transport were consistent with a simple model including lung, rib cage, and diaphragm regional impedances and a viscous coupling between lungs and chest wall caused by the relative sliding between pleural surfaces. To further test this model, we studied five additional animals under open chest conditions. These studies resulted in a homogeneous and f-independent regional gas transport. We conclude that the apex-to-base distribution of gas transport observed during HFV is not caused by intrinsic lung heterogeneity but rather is a result of chest wall expansion dynamics and its coupling to the lung.


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