Atelectasis and Chest Wall Shape during Halothane Anesthesia

1996 ◽  
Vol 85 (1) ◽  
pp. 49-59 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Anesthesia produces atelectasis in the dependent areas of the lungs by mechanisms that remain unknown. It has been proposed that anesthesia produces a cephalad shift in the end-expiratory position of the diaphragm, which compresses the lungs and produces atelectasis. This study tested the hypothesis that the extent of atelectasis is correlated with the cephalad displacement of the dependent portion of the diaphragm produced by halothane anesthesia in healthy young human subjects. Methods Twelve volunteers (mean age 34 yr) were studied while awake and during approximately 1.2 minimum alveolar concentration halothane anesthesia. Chest wall configuration was determined using images of the thorax obtained by three-dimensional fast computed tomography. Functional residual capacity was measured by a nitrogen dilution technique. Measurements were performed during quiet breathing in all subjects and after paralysis with 0.1 mg/kg vecuronium and mechanical ventilation in six subjects. Atelectasis was assumed to be present in regions of the lung that showed radiographic attenuation values similar to solid organs such as the liver. Results Atelectasis in dependent lung regions was not apparent in scans performed while the subjects were awake. Anesthesia with spontaneous breathing increased the volume of atelectasis measured at end-expiration by more than 1 ml in 9 of 12 subjects. For all subjects, the volume of atelectasis was 29 +/- 10 ml (M +/- SE), representing 0.67 +/- 0.23% of the total thoracic volume. The distribution of atelectasis varied along the cephalocaudal axis, with less atelectasis in more cephalad transverse sections. Paralysis and mechanical ventilation significantly decreased the volume of atelectasis present at end-expiration. There was no correlation between the average amount of cephalad displacement of the most dependent region of the diaphragm and the amount of atelectasis, nor was there any correlation between the amount of atelectasis and anesthesia-induced changes in the end-expiratory position of any chest wall structure. Conclusions The dependent lung atelectasis produced by halothane anesthesia does not appear to be related to changes in the position of any single chest wall structure in these healthy young subjects, but rather to an interaction of several factors that remain to be identified.

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 < 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.


1996 ◽  
Vol 84 (2) ◽  
pp. 309-321. ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Prior human studies have shown that halothane attenuates activity in the parasternal intercostal muscle and enhances phasic activity in respiratory muscles with expiratory actions. This expiratory muscle activity could contribute to reductions in the functional residual capacity produced by anesthesia. Termination of this activity could contribute to the maintenance of inspiratory rib cage expansion. The purpose of this study was to estimate in humans the mechanical significance of expiratory muscle activity during halothane anesthesia and to search for the presence of scalene muscle activity during halothane anesthesia that might contribute to inspiratory rib cage expansion. Methods Six subjects (3 males, 3 females) were studied while awake and during 1.2 MAC halothane anesthesia, both during quiet breathing and during carbon dioxide rebreathing. 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 and respiratory impedance plethysmography. Functional residual capacity was measured by a nitrogen dilution technique. Measurements were obtained after paralysis with 0.1 mg/kg vecuronium and mechanical ventilation. Results Phasic inspiratory activity was present in the scalene muscle of four anesthetized subjects during quiet breathing and all anesthetized subjects during rebreathing. Phasic inspiratory activity was present in the parasternal intercostal muscle during halothane anesthesia in only the three female subjects and was enhanced by rebreathing; parasternal intercostal muscle activity was never present in anesthetized males. During anesthesia with quiet breathing, phasic expiratory activity was observed in the transversus abdominis muscles of only the three male subjects. Despite these differences in the pattern of respiratory muscle use, the pattern of chest wall responses to rebreathing was similar between males and females. When expiratory muscle activity was present, paralysis increased the end-expiratory thoracic volume by expanding the rib cage, demonstrating that this activity reduced thoracic volume in these subjects. Changes in thoracic blood volume were significant determinants of the change in functional residual capacity produced by paralysis. Conclusions In humans anesthetized with 1.2 MAC end-tidal halothane, there are marked interindividual differences in respiratory muscle use during quiet breathing that may be related to sex; phasic inspiratory scalene muscle and parasternal intercostal muscle activity may contribute to inspiratory rib cage expansion in some subjects; and when present, expiratory muscle activity significantly constricts the rib cage and contributes to reductions in functional residual capacity caused by halothane anesthesia.


1980 ◽  
Vol 49 (2) ◽  
pp. 300-305 ◽  
Author(s):  
P. Southorn ◽  
K. Rehder ◽  
R. E. Hyatt

Functional residual capacity (FRC) and quasi-static deflation pressure-volume (PV) curves of the total respiratory system, lung, and chest wall were measured in eight trained dogs lying supine, first awake and then anesthetized with halothane. Two of the eight dogs were repetitively examined 10 times during a 15-mo period. FRC decreased with anesthesia in six of the eight dogs and incresed with anesthesia in the remaining two dogs. There was a significant mean anesthesia-induced reduction in FRC of 16.9% (P 〜 0.05). FRC change with anesthesia varied between studies in one of the two dogs repetitively examined. Mean PV curves of the total system, lung, and chest wall of the six dogs whose FRC decreased with anesthesia were shifted to the right by anesthesia. PV curves from the two dogs whose FRC increased with anesthesia were shifted to the left. Anesthesia produced a significant reduction (P 〜 0.05) in mean lung compliance and significant increases (P 〜0.05) in mean chest wall and total system compliances.


1981 ◽  
Vol 50 (1) ◽  
pp. 55-64 ◽  
Author(s):  
G. Hedenstierna ◽  
L. Bindslev ◽  
J. Santesson ◽  
O. P. Norlander

Airway closure and functional residual capacity (FRC) were assessed for each lung separately in the anesthetized subject by means of a double-lumen tracheal catheter. Airway closure was studied by argon-bolus and nitrogen-washout techniques, and FRC was calculated from single-breath nitrogen washout. Recordings were done with subjects in the supine and lateral postures. In the supine position, closing capacity (CC) exceeded FRC in each lung. Airway closure occurred synchronously in the two lungs. Argon CC was 0.05-0.1 liter larger than nitrogen CC of either lung. Minor gas trapping occurred during the vital capacity (VC) maneuver, so that inspired VC exceeded expired VC by 3%. In the left lateral posture, CC remained unaltered in either lung, whereas FRC was markedly increased in the nondependent and reduced in the dependent lung. Airway closure occurred asynchronously in the two lungs, and its distribution was discontinuous between them. Onset of airway closure in the dependent lung caused an early (60% VC) upstroke on the overall tracer gas recording (sampling of mixed expirate at the mouth), whereas onset of airway closure in the nondependent lung caused an additional upstroke at 10% VC. Gas trapping was more marked in the dependent lung than in the supine position, but some gas was released (expired VC greater than inspired VC) n the nondependent lung.


1989 ◽  
Vol 66 (3) ◽  
pp. 1179-1189 ◽  
Author(s):  
D. O. Warner ◽  
S. Krayer ◽  
K. Rehder ◽  
E. L. Ritman

We measured the volume change of the thoracic cavity (delta Vth) and the volumes displaced by the diaphragm (delta Vdi) and rib cage (delta Vrc) in six pentobarbital-anesthetized dogs lying supine. A high-speed X-ray scanner (dynamic spatial reconstructor) provided three-dimensional images of the thorax during spontaneous breathing and during mechanical ventilation with paralysis. Tidal volume (VT) was measured by integrating gas flow. Changes in thoracic liquid volume (delta Vliq, presumably caused by changes in thoracic blood volume) were calculated as delta Vth - VT. Absolute volume displaced by the rib cage was not significantly different during the two modes of ventilation. During spontaneous breathing, thoracic blood volume increased during inspiration; delta Vliq was 12.3 +/- 4.1% of delta Vth. During mechanical ventilation, delta Vliq was nearly zero. Configuration of the relaxed chest wall was similar during muscular relaxation induced by either pharmacological paralysis or hyperventilation. Expiratory muscle activity produced 50 +/- 11% of the delta Vth during spontaneous breathing. We conclude that at constant VT the volume displaced by the rib cage is remarkably similar during the transition from spontaneous breathing to mechanical ventilation, while both diaphragmatic volume displacement and changes in intrathoracic blood volume decrease by a similar amount.


2002 ◽  
Vol 93 (6) ◽  
pp. 2044-2052 ◽  
Author(s):  
D. Bettinelli ◽  
C. Kays ◽  
O. Bailliart ◽  
A. Capderou ◽  
P. Techoueyres ◽  
...  

The volume-pressure relationship of the lung was studied in six subjects on changing the gravity vector during parabolic flights and body posture. Lung recoil pressure decreased by ∼2.7 cmH2O going from 1 to 0 vertical acceleration (Gz), whereas it increased by ∼3.5 cmH2O in 30° tilted head-up and supine postures. No substantial change was found going from 1 to 1.8 Gz. Matching the changes in volume-pressure relationships of the lung and chest wall (previous data), results in a decrease in functional respiratory capacity of ∼580 ml at 0 Gz relative to 1 Gz and of ∼1,200 ml going to supine posture. Microgravity causes a decrease in lung and chest wall recoil pressures as it removes most of the distortion of lung parenchyma and thorax induced by changing gravity field and/or posture. Hypergravity does not greatly affect respiratory mechanics, suggesting that mechanical distortion is close to maximum already at 1 Gz. The end-expiratory volume during quiet breathing corresponds to the mechanical functional residual capacity in each condition.


1987 ◽  
Vol 63 (5) ◽  
pp. 1837-1845 ◽  
Author(s):  
C. S. Poon ◽  
M. Younes ◽  
C. G. Gallagher

We examined, in five conscious human subjects, the steady-state effects of expiratory resistive loading (ERL; R = 8 cmH2O.l–1.s) on the time course of inspiratory and postinspiratory muscle activities (IA and PIA, respectively) and ventilatory pattern during quiet breathing. Driving pressure (DP) was calculated by means of a respiratory neuromechanical model (J. Appl. Physiol. 51: 963–989, 1981) that permitted the derivation, from tidal volume and flow, of the occlusion pressure equivalent (at functional residual capacity) of respiratory neural output throughout the breath. ERL caused a prolongation of both neural inspiratory duration (12.2 +/- 6.9% SD) and expiratory duration (25.0 +/- 10.1%) and an increase in the amplitude of DP (16.5 +/- 10.2%) without any changes in the waveshape of IA and in end-expiratory level. The relative time course of PIA was not altered by ERL. Minute ventilation was depressed (-6.75 +/- 2.88%) during ERL with little change in alveolar PCO2. The results indicate that pulmonary gas exchange may be improved during ERL through increased tidal volume as well as delayed expiratory lung emptying secondary to sustained PIA.


1994 ◽  
Vol 76 (1) ◽  
pp. 223-229 ◽  
Author(s):  
A. M. Boriek ◽  
T. A. Wilson ◽  
J. R. Rodarte

Radiopaque markers were attached at 1- to 2-cm intervals along three nearby muscle bundles to cover rectangular regions of the mid-costal diaphragms of seven dogs. The markers were tracked by biplane video fluoroscopy during spontaneous breathing (SB), mechanical ventilation with the same tidal volume (MV), and at inflation to total lung capacity (TLC) in the prone and supine positions. The three-dimensional positions of the markers at functional residual capacity (FRC), at end inspiration during SB and MV, and at TLC were determined, and the strains in the plane of the diaphragm relative to FRC were calculated. The principal strains were found to lie nearly along the muscle bundle direction and perpendicular to it. The principal strains along the muscle bundles, which describe muscle shortening, were uniform among the three bundles and uniform along the bundle for MV. For SB, in the prone and supine positions, shortening was approximately 30% greater in the middle of the bundle than near the central tendon and chest wall. Although the tidal volumes were the same for SB and MV, the shortening was larger for SB. The strains perpendicular to the bundle direction were not significantly different from zero. It appears that, for the loads that occur during tidal breathing, the diaphragm is inextensible in the direction perpendicular to the muscle direction. There is a very small displacement of the costal diaphragm at its insertion on the chest wall. The displacement at the central tendon is primarily a result of muscle shortening and rotation of the arc of the muscle around its insertion on the chest wall.


1987 ◽  
Vol 63 (6) ◽  
pp. 2467-2475 ◽  
Author(s):  
R. D. Hubmayr ◽  
J. R. Rodarte ◽  
B. J. Walters ◽  
F. M. Tonelli

We evaluated the effects of the different patterns of chest wall deformation that occur with different body positions and modes of breathing on regional lung deformation and ventilation. Using the parenchymal marker technique, we determined regional lung behavior during mechanical ventilation and spontaneous breathing in five anesthetized recumbent dogs. Regional lung behavior was related to the patterns of diaphragm motion estimated from X-ray projection images obtained at functional residual capacity (FRC) and end inspiration. Our results indicate that 1) in the prone and supine positions, FRC was larger during mechanical ventilation than during spontaneous breathing; 2) there were significant differences in the patterns of diaphragm motion and regional ventilation between mechanical ventilation and spontaneous breathing in both body positions; 3) in the supine position only, there was a vertical gradient in lung volume at FRC; 4) in both positions and for both modes of breathing, regional ventilation was nonlinearly related to changes in lobar and overall lung volumes; and 5) different patterns of diaphragm motion caused different sliding motions and differential rotations of upper and lower lobes. Our results are inconsistent with the classic model of regional ventilation, and we conclude that the distribution of ventilation is determined by a complex interaction of lung and chest wall shapes and by the motion of the lobes relative to each other, all of which help to minimize distortion of the lung parenchyma.


Author(s):  
Béatrice Satiat-Jeunemaitre ◽  
Chris Hawes

The comprehension of the molecular architecture of plant cell walls is one of the best examples in cell biology which illustrates how developments in microscopy have extended the frontiers of a topic. Indeed from the first electron microscope observation of cell walls it has become apparent that our understanding of wall structure has advanced hand in hand with improvements in the technology of specimen preparation for electron microscopy. Cell walls are sub-cellular compartments outside the peripheral plasma membrane, the construction of which depends on a complex cellular biosynthetic and secretory activity (1). They are composed of interwoven polymers, synthesised independently, which together perform a number of varied functions. Biochemical studies have provided us with much data on the varied molecular composition of plant cell walls. However, the detailed intermolecular relationships and the three dimensional arrangement of the polymers in situ remains a mystery. The difficulty in establishing a general molecular model for plant cell walls is also complicated by the vast diversity in wall composition among plant species.


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