Effects of lung volume on lung and chest wall mechanics in rats

To investigate the effect of lung volume onchest wall and lung mechanics in the rats, we measured theimpedance (Z) under closed- and open-chest conditions at variouspositive end-expiratory pressures (0-0.9 kPa) by using acomputer-controlled small-animal ventilator (T. F. Schuessler andJ. H. T. Bates. IEEE Trans. Biomed. Eng. 42: 860-866, 1995) that we have developed fordetermining accurately the respiratory Z in small animals. The Z oftotal respiratory system and lungs was measured with small-volumeoscillations between 0.25 and 9.125 Hz. The measured Z was fitted to amodel that featured a constant-phase tissue compartment (withdissipation and elastance characterized by constantsG andH, respectively) and a constant airwayresistance (Z. Hantos, B. Daroczy, B. Suki, S. Nagy, and J. J. Fredberg. J. Appl.Physiol. 72: 168-178, 1992). We matched the lungvolume between the closed- and open-chest conditions by using thequasi-static pressure-volume relationship of the lungs to calculate Zas a function of lung volume. Resistance decreased with lung volume andwas not significantly different between total respiratory system andlungs. However, G andH of the respiratory system weresignificantly higher than those of the lungs. We conclude that chestwall in rats has a significant influence on tissue mechanics of thetotal respiratory system.

     

Effect of gravity on chest wall mechanics.

Chest wall mechanics was studied in four subjects on changing gravity in the craniocaudal direction (G(z)) during parabolic flights. The thorax appears very compliant at 0 G(z): its recoil changes only from -2 to 2 cmH(2)O in the volume range of 30-70% vital capacity (VC). Increasing G(z) from 0 to 1 and 1.8 G(z) progressively shifted the volume-pressure curve of the chest wall to the left and also caused a fivefold exponential decrease in compliance. For lung volume <30% VC, gravity has an inspiratory effect, but this effect is much larger going from 0 to 1 G(z) than from 1 to 1.8 G(z). For a volume from 30 to 70% VC, the effect is inspiratory going from 0 to 1 G(z) but expiratory from 1 to 1.8 G(z). For a volume greater than approximately 70% VC, gravity always has an expiratory effect. The data suggest that the chest wall does not behave as a linear system when exposed to changing gravity, as the effect depends on both chest wall volume and magnitude of G(z).     

Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans

Beaumont, Maurice, Damien Lejeune, Henri Marotte, AlainHarf, and Frédéric Lofaso. Effects of chest wallcounterpressures on lung mechanics under high levels of CPAP in humans.J. Appl. Physiol. 83(2): 591-598, 1997.We assessed the respective effects of thoracic (TCP) andabdominal/lower limb (ACP) counterpressures on end-expiratory volume(EEV) and respiratory muscle activity in humans breathing at 40 cmH₂O of continuous positiveairway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (Pga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on thebasis of the transdiaphragmatic pressure-time product (PTPdi). CPAPinduced hyperventilation (+320%) and only a 28% increase in EEVbecause of a high level of expiratory activity (Pga = 24 ± 5 cmH₂O), contrasting with areduction in PTPdi from 17 ± 2 to 9 ± 7 cmH₂O · s¹ · cycle¹during 0 and 40 cmH₂O of CPAP,respectively. When ACP, TCP, or both were added, hyperventilationdecreased and PTPdi increased (19 ± 5, 21 ± 5, and 35 ± 7 cmH₂O · s¹ · cycle¹,respectively), whereas Pga decreased (19 ± 6, 9 ± 4, and 2 ± 2 cmH₂O, respectively). Weconcluded that during high-level CPAP, TCP and ACP limit lunghyperinflation and expiratory muscle activity and restore diaphragmaticactivity.

     

Effects of undernutrition on respiratory mechanics and lung parenchyma remodeling.

Undernutrition thwarts lung structure and function, but there are disagreements about the behavior of lung mechanics in malnourished animals. To clarify this issue, lung and chest wall mechanical properties were subdivided into their resistive, elastic, and viscoelastic properties in nutritionally deprived (ND) rats and correlated with the data gathered from histology (light and electron microscopy and elastic fiber content), and bronchoalveolar lavage fluid analysis (lipid and protein content). Twenty-four Wistar rats were assigned into two groups. In the control (Ctrl) group the animals received food ad libitum. In the ND group, rats received one-third of their usual daily food consumption until they lost 40% of their initial body weight. Lung static elastance, viscoelastic and resistive pressures (normalized by functional residual capacity), and chest wall pressures were higher in the ND group than in the Ctrl group. The ND group exhibited patchy atelectasis, areas of emphysema, interstitial edema, and reduced elastic fiber content. The amount of lipid and protein in bronchoalveolar lavage fluid was significantly reduced in the ND group. Electron microscopy showed 1) type II pneumocytes with a reduction in lamellar body content, multilamellated structures, membrane vesicles, granular debris, and structurally aberrant mitochondria; and 2) diaphragm and intercostals with atrophy, disarrangement of the myofibrils, and deposition of collagen type I fibers. In conclusion, undernutrition led to lung and chest wall mechanical changes that were the result from a balance among the following modifications: 1) distorted structure of diaphragm and intercostals, 2) surfactant content reduction, and 3) decrease in elastic fiber content.     

Effects of acute hyperinflation on chest wall mechanics in dogs

We studied chest wall mechanics at functional residual capacity (FRC) and near total lung capacity (TLC) in 14 supine anesthetized and vagotomized dogs. During breathing near TLC compared with FRC, tidal volume decreased (674 +/- 542 vs. 68 +/- 83 ml; P less than 0.025). Both inspiratory changes in gastric pressure (4.5 +/- 2.5 vs. -0.2 +/- 2.0 cmH2O; P less than 0.005) and changes in abdominal cross-sectional area (25 +/- 17 vs. -1.0 +/- 4.2%; P less than 0.001) markedly decreased; they were both often negative during inspiration near TLC. Parasternal intercostal shortening decreased (-3.0 +/- 3.7 vs. -2.0 +/- 2.7%), whereas diaphragmatic shortening decreased slightly more in both costal and crural parts (costal -8.4 +/- 2.9 vs. -4.3 +/- 4.1%, crural -22.8 +/- 13.2 vs. -10.0 +/- 7.5%; P less than 0.05). As a result, the ratio of parasternal to diaphragm shortening increased near TLC (0.176 +/- 0.135 vs. 0.396 +/- 0.340; P less than 0.05). Electromyographic (EMG) activity in the parasternals slightly decreased near TLC, whereas the EMG activity in the costal and crural parts of the diaphragm slightly increased. We conclude that 1) the mechanical outcome of diaphragmatic contraction near TLC is markedly reduced, and 2) the mechanical outcome of parasternal intercostal contraction near TLC is clearly less affected.     

Lung and chest wall mechanics in microgravity.

We studied the effect of 15-20 s of weightlessness on lung, chest wall, and abdominal mechanics in five normal subjects inside an aircraft flying repeated parabolic trajectories. We measured flow at the mouth, thoracoabdominal and compartmental volume changes, and gastric pressure (Pga). In two subjects, esophageal pressures were measured as well, allowing for estimates of transdiaphragmatic pressure (Pdi). In all subjects functional residual capacity at 0 Gz decreased by 244 +/- 31 ml as a result of the inward displacement of the abdomen. End-expiratory Pga decreased from 6.8 +/- 0.8 cmH2O at 1 Gz to 2.5 +/- 0.3 cmH2O at Gz (P less than 0.005). Abdominal contribution to tidal volume increased from 0.33 +/- 0.05 to 0.51 +/- 0.04 at 0 Gz (P less than 0.001) but delta Pga showed no consistent change. Hence abdominal compliance increased from 43 +/- 9 to 70 +/- 10 ml/cmH2O (P less than 0.05). There was no consistent effect of Gz on tidal swings of Pdi, on pulmonary resistance and dynamic compliance, or on any of the timing parameters determining the temporal pattern of breathing. The results indicate that at 0 G respiratory mechanics are intermediate between those in the upright and supine postures at 1 G. In addition, analysis of end-expiratory pressures suggests that during weightlessness intra-abdominal pressure is zero, the diaphragm is passively tensed, and a residual small pleural pressure gradient may be present.     

Effects of pulse lung inflation on chest wall expiratory motor activity.

The effects of pulse lung inflation (LI) on expiratory muscle activity and phase duration (Te) were determined in anesthetized, spontaneously breathing dogs (n = 20). A volume syringe was used to inflate the lungs at various times during the expiratory phase. The magnitude of lung volume was assessed by the corresponding change in airway pressure (Paw; range 2-20 cmH(2)O). Electromyographic (EMG) activities were recorded from both thoracic and abdominal muscles. Parasternal muscle EMG was used to record inspiratory activity. Expiratory activity was assessed from the triangularis sterni (TS), internal intercostal (IIC), and transversus abdominis (TA) muscles. Lung inflations <7 cmH(2)O consistently inhibited TS activity but had variable effects on TA and IIC activity and expiratory duration. Lung inflations resulting in Paw values >7 cmH(2)O, however, inhibited expiratory EMG activity of each of the expiratory muscles and lengthened Te in all animals. The responses of expiratory EMG and Te were directly related to the magnitude of the lung inflation. The inhibition of expiratory motor activity was independent of the timing of pulse lung inflation during the expiratory phase. The inhibitory effects of lung inflation were eliminated by bilateral vagotomy and could be reproduced by electrical stimulation of the vagus nerve. We conclude that pulse lung inflation resulting in Paw between 7 and 20 cmH(2)O produces a vagally mediated inhibition of expiratory muscle activity that is directly related to the magnitude of the inflation. Lower inflation pressures produce variable effects that are muscle specific.     

Theoretical analysis of chest wall mechanics

A mathematical model of the chest wall partitioned into rib cage, diaphragmatic and abdominal components is developed consistent with published experimental observations. The model describes not only the orthodox chest wall movements (rib cage and abdomen expand together during inspiration) of the quietly breathing standing adult, but also Mueller maneuvers (inspiration against an occluded airway opening) and the paradoxical breathing patterns (rib cage contracts while abdomen expands during inspiration) observed in quadriplegia and in the newborn. The abdomen is inferred to act as a cylinder reinforced by the abdominal muscles functioning similarly to bands around a barrel. The rib cage and abdominal wall are inferred to act not as though they were directly attached to one another, but as though they were being pressed together by the skeleton. Furthermore, transabdominal pressure is visualized as acting, not across the rib cage isolated from the diaphragm, as has been suggested previously, but instead, across the combined rib cage and diaphragm acting as a deformable unit containing the lungs.     

Sigmoidal equation for lung and chest wall volume-pressure curves in acute respiratory failure.

To assess incidence and magnitude of the "lower inflection point" of the chest wall, the sigmoidal equation was used in 36 consecutive patients intubated and mechanically ventilated with acute lung injury (ALI). They were 21 primary and 5 secondary ALI, 6 unilateral pneumonia, and 4 cardiogenic pulmonary edema. The lower inflection point was estimated as the point of maximal compliance increase. The low constant flow inflation method and esophageal pressure were used to partition the volume-pressure curves into their chest wall and lung components on zero end-expiratory pressure. The sigmoidal equation had an excellent fit with coefficients of determination >0.90 in all instances. The point of maximal compliance increase of the chest wall ranged from 0 to 8.3 cmH2O (median 1 cmH2O) with no difference between ALI groups. The chest wall significantly contributed to the lower inflection point of the respiratory system in eight patients only. The occurrence of a significant contribution of the chest wall to the lower inflection point of the respiratory system is lower than anticipated. The sigmoidal equation is able to determine precisely the point of the maximal compliance increase of lung and chest wall.     

Role of the diaphragm in chest wall mechanics.

We analyzed three different assumptions about diaphragm function that determine the thoracoabdominal interaction. In the simplest case, the diaphragm is assumed to be a completely flaccid membrane serving only to partition the thorax and the abdominal cavity. In the second case, it is assumed to have a finite tension but to maintain a relatively flat surface at the base of the rib cage (i.e., a negligible zone of apposition). In the general case, it is assumed that the diaphragm has finite tension and its position may vary (i.e., permitting a zone of apposition). These possible modes of behavior are incorporated into a mathematical model of ventilatory system mechanics that distinguishes the diaphragm, lung, abdomen, and rib cage. The significance of these modes is examined with respect to data from human experiments in which gas or liquid is introduced into the pleural or abdominal spaces, causing a volume change (Vep). We show that the Vep effect on the thoracic and abdominal volumes is sensitive to diaphragm mechanics and depends on the nature of the Vep: gastric distension (with water or air) or pneumothorax. Only the behavior of the general model is consistent with physiological observations, especially the distribution of Vep. Our general mathematical model can quantitatively predict this behavior.     

Effects of volume history and vagotomy on pulmonary and chest wall mechanics in cats

Using the technique of rapid airway occlusion during constant-flow inflation, we studied the effects of inflation volume, different baseline tidal volumes (10, 20, and 30 ml/kg), and vagotomy on the resistive and elastic properties of the lungs and chest wall in six anesthetized tracheotomized paralyzed mechanically ventilated cats. Before vagotomy, airway resistance decreased significantly with increasing inflation volume at all baseline tidal volumes. At any given inflation volume, airway resistance decreased with increasing baseline tidal volume. After vagotomy, airway resistance decreased markedly and was no longer affected by baseline tidal volume. Prevagotomy, pulmonary tissue resistance increased progressively with increasing lung volume and was not affected by baseline tidal volume. Pulmonary tissue resistance decreased postvagotomy. Chest wall tissue resistance increased during lung inflation but was not affected by either baseline tidal volume or vagotomy. The static volume-pressure relationships of the lungs and chest wall were not affected by either baseline tidal volume or vagotomy. The data were interpreted in terms of a linear viscoelastic model of the respiratory system (J. Appl. Physiol. 67: 2276-2285, 1989).     

Pulmonary and chest wall mechanics in anesthetized paralyzed humans

Pulmonary and chest wall mechanics were studied in 18 anesthetized paralyzed supine humans by use of the technique of rapid airway occlusion during constant-flow inflation. Analysis of the changes in transpulmonary pressure after flow interruption allowed partitioning of the overall resistance of the lung (RL) into two compartments, one (Rint,L) reflecting airway resistance and the other (delta RL) representing the viscoelastic properties of the pulmonary tissues. Similar analysis of the changes in esophageal pressure indicates that chest wall resistance (RW) was due entirely to the viscoelastic properties of the chest wall tissues (delta RW = RW). In line with previous measurements of airway resistance, Rint,L increased with increasing flow and decreased with increasing volume. The opposite was true for both delta RL and delta RW. This behavior was interpreted in terms of a viscoelastic model that allowed computation of the viscoelastic constants of the lung and chest wall. This model also accounts for frequency, volume, and flow dependence of elastance of the lung and chest wall. Static and dynamic elastances, as well as delta R, were higher for the lung than for the chest wall.     

Effect of shape and size of lung and chest wall on stresses in the lung.

Conflicting results have been reported on the changes in the distribution of pleural pressures caused by alterations of chest shape. To understand better the effect of shape and size of lung and chest wall on the distribution of stresses, strains, and surface pressures, we analyzed a theoretical model using the technique of finite elements. The study was in two parts. First we investigated the effects of changing the chest wall shape during expansion, and second we studied lungs of a variety of inherent shapes and sizes. We found that, in general, the distributions of alveolar size, mechanical stresses, and surface pressures in the lungs were dominated by the weight of the lung and that changing the shape of the lung or chest wall had relatively little effect. Only at high states of expansion where the lung was very stiff did changing the shape of the chest wall cause substantial changes. Altering the inherent shape of the lung generally had little effect but the topographical differences in stresses and surface pressures were approximately proportional to lung height. The results are generally consistent with those found in dog by Hoppin et al. (J. Appl. Physiol. 27: 863-873, 1969).     

Effects of acute pleural effusion on respiratory system mechanics in dogs

We determined regional (Vr) and overall lung volumes in six head-up anesthetized dogs before and after the stepwise introduction of saline into the right pleural space. Functional residual capacity (FRC), as determined by He dilution, and total lung capacity (TLC) decreased by one-third and chest wall volume increased by two-thirds the saline volume added. Pressure-volume curves showed an apparent increase in lung elastic recoil and a decrease in chest wall elastic recoil with added saline, but the validity of esophageal pressure measurements in these head-up dogs is questionable. Vr was determined from the positions of intraparenchymal markers. Lower lobe TLC and FRC decreased with added saline. The decrease in upper lobe volume was less than that of lower lobe volume at FRC and was minimal at TLC. Saline increased the normal Vr gradient at FRC and created a gradient at TLC. During deflation from TLC to FRC before saline was added, the decrease in lung volume was accompanied by a shape change of the lung, with greatest distortion in the transverse (ribs to mediastinum) direction. After saline additions, deflation was associated with deformation of the lung in the cephalocaudal and transverse directions. The deformation with saline may be a result of upward displacement of the lungs into a smaller cross-sectional area of the thoracic cavity.     

Chest wall and respiratory system mechanics in cats: effects of flow and volume

The effects of inspiratory flow rate and inflation volume on the resistive properties of the chest wall were investigated in six anesthetized paralyzed cats by use of the technique of rapid airway occlusion during constant flow inflation. This allowed measurement of the intrinsic resistance (Rw,min) and overall dynamic inspiratory impedance (Rw,max), which includes the additional pressure losses due to time constant inequalities within the chest wall tissues and/or stress adaptation. These results, together with our previous data pertaining to the lung (Kochi et al., J. Appl. Physiol. 64: 441-450, 1988), allowed us to determine Rmin and Rmax of the total respiratory system (rs). We observed that 1) Rw,max and Rrs,max exhibited marked frequency dependence; 2) Rw,min was independent of flow (V) and inspired volume (delta V), whereas Rrs,min increased linearly with V and decreased with increasing delta V; 3) Rw,max decreased with increasing V, whereas Rrs,max exhibited a minimum value at a flow rate substantially higher than the resting range of V; 4) both Rw,max and Rrs,max increased with increasing delta V. We conclude that during resting breathing, flow resistance of the chest wall and total respiratory system, as conventionally measured, includes a significant component reflecting time constant inequalities and/or stress adaptation phenomena.     

Comparative respiratory system mechanics in rodents.

Because of the wide utilization of rodents as animal models in respiratory research and the limited data on measurements of respiratory input impedance (Zrs) in small animals, we measured Zrs between 0.25 and 9.125 Hz at different levels (0-7 hPa) of positive end-expiratory pressure (PEEP) in mice, rats, guinea pigs, and rabbits using a computer-controlled small-animal ventilator (Schuessler TF and Bates JHT, IEEE Trans Biomed Eng 42: 860-866, 1995). Zrs was fitted with a model, including a Newtonian resistance (R) and inertance in series with a constant-phase tissue compartment characterized by tissue damping (Gti) and elastance (Hti) parameters. Inertance was negligible in all cases. R, Gti, and Hti were normalized to body weight, yielding normalized R, Gti, and Hti (NHti), respectively. Normalized R tended to decrease slightly with PEEP and increased with animal size. Normalized Gti had a minimal dependence on PEEP. NHti decreased with increasing PEEP, reaching a minimum at approximately 5 hPa in all species except mice. NHti was also higher in mice and rabbits compared with guinea pigs and rats at low PEEPs, which we conclude is probably due to a relatively smaller air space volume in mice and rabbits. Our data also suggest that smaller rodents have proportionately wider airways than do larger animals. We conclude that a detailed, comparative study of respiratory system mechanics shows some evidence of structural differences among the lungs of various species but that, in general, rodent lungs obey scaling laws similar to those described in other species.