Abdominal distension alters regional pleural pressures and chest wall mechanics in pigs in vivo

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.     

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.     

Transmission of airway pressure to pleural space during lung edema and chest wall restriction

To investigate the influence of positive end-expiratory pressure (PEEP) on hemodynamic measurements we examined the transmission of airway pressure to the pleural space during varying conditions of lung and chest wall compliance. Eight ventilated anesthetized dogs were studied in the supine position with the chest closed. Increases in pleural pressure were similar for both small and large PEEP increments (5-20 cmH2O), whether measured in the esophagus (Pes) or in the juxtacardiac space by a wafer sensor (Pj). Increments in Pj exceeded the increments in Pes at all levels of PEEP and under each condition of altered lung and chest wall compliance. When chest wall compliance was reduced by thoracic and abdominal binding, the fraction of PEEP sensed in the pleural space increased as theoretically predicted. Acute edematous lung injury produced by oleic acid (OA) did not alter the deflation limb pressure-volume characteristics of the lung, provided that end-inspiratory volume was adequate. With the chest and abdomen restricted OA was associated with less than normal transmission of airway pressure to the pleural space, most likely because the end-inspiratory volume required to restore normal deflation characteristics was not attained. Together these results indicate that the influence of acute edematous lung injury on the transmission of airway pressure to the pleural space depends importantly on the peak volume achieved during inspiration.     

Respiratory dynamics during laughter.

Lung and chest wall mechanics were studied during fits of laughter in 11 normal subjects. Laughing was naturally induced by showing clips of the funniest scenes from a movie by Roberto Benigni. Chest wall volume was measured by using a three-dimensional optoelectronic plethysmography and was partitioned into upper thorax, lower thorax, and abdominal compartments. Esophageal (Pes) and gastric (Pga) pressures were measured in seven subjects. All fits of laughter were characterized by a sudden occurrence of repetitive expiratory efforts at an average frequency of 4.6 +/- 1.1 Hz, which led to a final drop in functional residual capacity (FRC) by 1.55 +/- 0.40 liter (P < 0.001). All compartments similarly contributed to the decrease of lung volumes. The average duration of the fits of laughter was 3.7 +/- 2.2 s. Most of the events were associated with sudden increase in Pes well beyond the critical pressure necessary to generate maximum expiratory flow at a given lung volume. Pga increased more than Pes at the end of the expiratory efforts by an average of 27 +/- 7 cmH2O. Transdiaphragmatic pressure (Pdi) at FRC and at 10% and 20% control forced vital capacity below FRC was significantly higher than Pdi at the same absolute lung volumes during a relaxed maneuver at rest (P < 0.001). We conclude that fits of laughter consistently lead to sudden and substantial decrease in lung volume in all respiratory compartments and remarkable dynamic compression of the airways. Further mechanical stress would have applied to all the organs located in the thoracic cavity if the diaphragm had not actively prevented part of the increase in abdominal pressure from being transmitted to the chest wall cavity.     

Interrupter technique for measurement of respiratory mechanics in anesthetized cats

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg ip), airflow, changes in lung volume, and tracheal and esophageal pressures were measured. Airflow was interrupted by brief airway occlusions during relaxed expirations (elicited via the Breuer-Hering inflation reflex) and throughout spontaneous breaths. A plateau in tracheal pressure occurred throughout relaxed expirations and the latter part of spontaneous expirations indicating respiratory muscle relaxation. Measurement of tracheal pressure, immediately preceding airflow, and corresponding volume enabled determination of respiratory system elastance and flow resistance. These were partitioned into lung and chest wall components using esophageal pressure. Respiratory system elastance was constant over the tidal volume range, divided approximately equally between the lung and chest wall. While the passive pressure-flow relationship for the respiratory system was linear, those for the lung and chest wall were curvilinear. Volume dependence of chest wall flow resistance was demonstrated. During inspiratory interruptions, tracheal pressure increased progressively; initial tracheal pressure was estimated by backward extrapolation. Inspiratory flow resistance of the lung and total respiratory system were constant. Force-velocity properties of the contracting inspiratory muscles contributed little to overall active resistance.     

Effect of rib cage and abdominal restriction on total respiratory resistance and reactance

In 14 healthy male subjects we studied the effects of rib cage and abdominal strapping on lung volumes, airway resistance (Raw), and total respiratory resistance (Rrs) and reactance (Xrs). Rib cage, as well as abdominal, strapping caused a significant decrease in vital capacity (respectively, -36 and -34%), total lung capacity (TLC) (-31 and -27%), functional residual capacity (FRC) (-28 and -28%), and expiratory reserve volume (-40 and -48%) and an increase in specific airway conductance (+24 and +30%) and in maximal expiratory flow at 50% of control TLC (+47 and +42%). The decrease of residual volume (RV) was significant (-12%) with rib cage strapping only. Abdominal strapping resulted in a minor overall increase in Rrs, whereas rib cage strapping produced a more marked increase at low frequencies; thus a frequency dependence of Rrs was induced. A similar pattern, but with lower absolute values, of Rrs was obtained by thoracic strapping when the subject was breathing at control FRC. Xrs was decreased, especially at low frequencies, with abdominal strapping and even more with thoracic strapping; thus the resonant frequency of the respiratory system was shifted toward higher frequencies. Partitioning Rrs and Xrs into resistance and reactance of lungs and chest wall demonstrated that the different effects of chest wall and abdominal strapping on Rrs and Xrs reflect changes mainly of chest wall mechanics.     

Partitioning of respiratory mechanics in mechanically ventilated patients.

In ten mechanically ventilated patients, six with chronic obstructive pulmonary disease (COPD) and four with pulmonary edema, we have partitioned the total respiratory system mechanics into the lung (l) and chest wall (w) mechanics using the esophageal balloon technique together with the airway occlusion technique during constant-flow inflation (J. Appl. Physiol. 58: 1840-1848, 1985). Intrinsic positive end-expiratory pressure (PEEPi) was present in eight patients (range 1.1-9.8 cmH2O) and was due mainly to PEEPi,L (80%), with a minor contribution from PEEPi,w (20%), on the average. The increase in respiratory elastance and resistance was determined mainly by abnormalities in lung elastance and resistance. Chest wall elastance was slightly abnormal (7.3 +/- 2.2 cmH2O/l), and chest wall resistance contributed only 10%, on the average, to the total. The work performed by the ventilator to inflate the lung (WL) averaged 2.04 +/- 0.59 and 1.25 +/- 0.21 J/l in COPD and pulmonary edema patients, respectively, whereas Ww was approximately 0.4 J/l in both groups, i.e., close to normal values. We conclude that, in mechanically ventilated patients, abnormalities in total respiratory system mechanics essentially reflect alterations in lung mechanics. However, abnormalities in chest wall mechanics can be relevant in some COPD patients with a high degree of pulmonary hyperinflation.     

Respiratory changes in diaphragmatic intramuscular pressure

We attempted to measure diaphragmatic tension by measuring changes in diaphragmatic intramuscular pressure (Pim) in the costal and crural parts of the diaphragm in 10 supine anesthetized dogs with Gaeltec 12 CT minitransducers. During phrenic nerve stimulation or direct stimulation of the costal and crural parts of the diaphragm in an animal with the chest and abdomen open, Pim invariably increased and a linear relationship between Pim and the force exerted on the central tendon was found (r greater than or equal to 0.93). During quiet inspiration Pim in general decreased in the costal part (-3.9 +/- 3.3 cmH2O), whereas it either increased or slightly decreased in the crural part (+3.3 +/- 9.4 cmH2O, P less than 0.05). Similar differences were obtained during loaded and occluded inspiration. After bilateral phrenicotomy Pim invariably decreased during inspiration in both parts (costal -4.3 +/- 6.4 cmH2O, crural -3.1 +/- 0.6 cmH2O). Contrary to the expected changes in tension in the muscle, but in conformity with the pressure applied to the muscle, Pim invariably increased during passive inflation from functional residual capacity to total lung capacity (costal +30 +/- 23 cmH2O, crural +18 +/- 18 cmH2O). Similarly, during passive deflation from functional residual capacity to residual volume, Pim invariably decreased (costal -12 +/- 19 cmH2O, crural -12 +/- 14 cmH2O). In two experiments similar observations were made with saline-filled catheters. We conclude that although Pim increases during contraction as in other muscles, Pim during respiratory maneuvers is primarily determined by the pleural and abdominal pressures applied to the muscle rather than by the tension developed by it.     

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.     

Determinants of transdiaphragmatic pressure in dogs

We measured the transdiaphragmatic pressure (Pdi) during bilateral phrenic nerve stimulation and evaluated the determinants of its change with lung volume, chest wall geometry, and respiratory system impedance in supine dogs. Four rows of radiopaque markers were sewn onto muscle bundles of the costal and crural diaphragm between their origin on the central tendon and their insertion on the rib cage and spine. The length of the diaphragm (L) was determined from the projection images of marker rows using biplane fluoroscopy. Measurements were made at lung volumes between total lung capacity and functional residual capacity before and after the infusion of Ringer lactate solution into the abdominal cavity. In contrast to relaxation, during tetanic stimulation the active lengths of the muscle bundles were similar at all volumes, but the diaphragm assumed different shapes. Although the small differences in active muscle length with volume and liquid loads are consistent with only small changes in muscle force output, Pdi varied by a factor of greater than or equal to 5. There was no single L/Pdi curve that fitted all data during 50-Hz stimulations. We conclude that under these experimental conditions Pdi is not a unique measure of the force produced by the diaphragm and that lung volume, chest wall geometry, and respiratory system impedance are important determinants of the mechanical efficiency of the diaphragm as a pressure generator.     

A two-component simulation model to teach respiratory mechanics

Interactive learning has been proven instrumental for the understanding of complex systems where the interaction of interdependent components is hard to envision. Due to the mechanical properties and mutual coupling of the lung and thorax, respiratory mechanics represent such a complex system, yet their understanding is essential for the diagnosis, prognosis, and treatment of various respiratory disorders. Here, we present a new mechanical model that allows for the simulation of respiratory pressure and volume changes in different ventilation modes. A bellow reflecting the "lung" is positioned within the inverted glass cylinder of a bell spirometer, which is sealed by a water lock and reflects the "thorax." A counterweight attached to springs representing the elastic properties of the chest wall lifts the glass cylinder, thus creating negative "pleural" pressure inside the cylinder and inflating the bellow. Lung volume changes as well as pleural and intrapulmonary pressures are monitored during simulations of spontaneous ventilation, forced expiration, and mechanical ventilation, allowing for construction of respiratory pressure-volume curves. The mechanical model allows for simulation of respiratory pressure changes during different ventilation modes. Individual relaxation curves constructed for the lung and thorax reflect the basic physiological characteristics of the respiratory system. In self-assessment, 232 medical students passing the physiology laboratory course rated that interactive teaching at the simulation model increased their understanding of respiratory mechanics by 70% despite extensive prior didactic teaching. Hence, the newly developed simulation model fosters students' comprehension of complex mechanical interactions and may advance the understanding of respiratory physiology.     

Pleural pressure distribution and its relationship to lung volume and interstitial pressure

The mechanics of the pleural space has long been controversial. We summarize recent research pertaining to pleural mechanics within the following conceptual framework, which is still not universally accepted. Pleural pressure, the force acting to inflate the lung within the thorax, is generated by the opposing elastic recoils of the lung and chest wall and the forces generated by respiratory muscles. The spatial variation of pleural pressure is a result of complex force interactions among the lung and other structures that make up the thorax. Gravity contributes one of the forces that act on these structures, and regional lung expansion and pleural pressure distribution change with changes in body orientation. Forces are transmitted directly between the chest wall and the lung through a very thin but continuous pleural liquid space. The pressure in pleural liquid equals the pressure acting to expand the lung. Pleural liquid is not in hydrostatic equilibrium, and viscous flow of pleural liquid is driven by the combined effect of the gravitational force acting on the liquid and the pressure distribution imposed by the surrounding structures. The dynamics of pleural liquid are considered an integral part of a continual microvascular filtration into the pleural space. Similar concepts apply to the pulmonary interstitium. Regional differences in lung volume expansion also result in regional differences in interstitial pressure within the lung parenchyma and thus affect regional lung fluid filtration.     

Lung volumes after an increase in lung distension in pneumonectomized ferrets

To investigate the role of lung distension in compensatory lung growth, the right lung of each of 21 adult male ferrets was replaced with a silicone rubber balloon filled with mineral oil. Three to thirteen weeks after surgery, the oil was removed through a subcutaneous port. Lung volumes were measured serially until 3-6 wk after balloon deflation. With pneumonectomy the total lung capacity (TLC) decreased to less than 50% of the preoperative value and remained essentially unchanged while the balloon was inflated. At balloon deflation, TLC and vital capacity did not change immediately, whereas functional residual capacity increased by 44%, indicating a change of 2-3 cmH2O in end-expiratory transpulmonary pressure. TLC increased by 10% within 3 days and continued to increase over the subsequent 3-5 wk by a total of 25% over TLC at balloon deflation. There was little difference in this response between animals whose balloons were deflated 3 wk after surgery and those in which deflation was delayed up to 13 wk. After pneumonectomy in the adult ferret, the remaining lung increases in volume in response to an increase in lung distension even weeks or months after surgery. The extent to which this volume increase involves lung tissue growth or depends on previous lung resection is at present unknown. This model may be useful for studies of the mechanisms by which lung distension influences lung volume and compensatory lung growth.     

Breathing strategy of the adult horse (Equus caballus) at rest

To investigate the mechanism underlying the polyphasic airflow pattern of the equine species, we recorded airflow, tidal volum, rib cage and abdominal motion, and the sequence of activation of the diaphragm, intercostal, and abdominal muscles during quiet breathing in nine adult horses standing at rest. In addition, esophageal, abdominal, and transdiaphragmatic pressures were simultaneously recorded using balloon-tipped catheters. Analysis of tidal flow-volume loops showed that, unlike humans, the horse at rest breathes around, rather than from, the relaxed volume of the respiratory system (Vrx). Analysis of the pattern of electromyographic activities and changes in generated pressures during the breathing cycle indicate that the first part of expiration is passive, as in humans, with deflation toward Vrx, but subsequent abdominal activity is responsible for a second phase of expiration: active deflation to below Vrx. From this end-expiratory volume, passive inflation occurs toward Vrx, followed by a second phase of inspiration: active inflation to above Vrx, brought about by inspiratory muscle contraction. Under these conditions the abdominal muscles appear to share the principal pumping duties with the diaphragm. Adoption of this breathing strategy by the horse may relate to its peculiar thoracoabdominal anatomic arrangement and to its very low passive chest wall compliance. We conclude that there is a passive and active phase to both inspiration and expiration due to the coordinated action of the respiratory pump muscles responsible for the resting adult horse's biphasic inspiratory and expiratory airflow pattern. This unique breathing pattern perhaps represents a strategy of minimizing the high elastic work of breathing in this species, at least at resting breathing frequencies.     

On defining total lung capacity in the mouse.

Maximal lung volume or total lung capacity in experimental animals is dependent on the pressure to which the lungs are inflated. Although 25-30 cm H2O are nominally used for such inflations, mouse pressure-volume (P-V) curves show little flattening on inflation to those pressures. In the present study, we examined P-V relations and mean alveolar chord length in three strains (C3H/HeJ, A/J, and C57BL/6J) at multiple inflation pressures. Mice were anesthetized, and their lungs were degassed in vivo by absorption of 100% O2. P-V curves were then recorded in situ with increasing peak inflation pressure in 10-cm H2O increments up to 90 cm H2O. Lungs were quickly frozen at specific pressures for morphometric analysis. The inflation limbs never showed the appearance of a plateau, with lung volume increasing 40-60% as inflation pressure was increased from 30 to 60 cm H2O. In contrast, parallel flat deflation limbs were always observed, regardless of the inflation pressure, indicating that the presence of a flat deflation curve cannot be used to justify measurement of total lung capacity in mice. Alveolar size increased monotonically with increasing pressure in all strains, and there was no evidence of irreversible lung damage from these inflations to high pressures. These results suggest that the mouse lung never reaches a maximal volume, even up to nonphysiological pressures >80 cm H2O.     

Respiratory mechanical effects of abdominal distension

We develop a theory to predict the partitioning of a change in volume of the abdominal contents into the end-expiratory volume changes of the lung, rib cage, and anterior abdominal wall. First, we calculate the distribution of such a volume change using the relative compliances of the three compartments. We then consider the inspiratory influence of abdominal pressure on the rib cage and its effect on the distribution of this volume. We test our theory by inducing gastric distension in three experienced laboratory personnel. We instilled and subsequently withdrew 1 liter of water from a gastric balloon and examined the effects of this change in gastric volume on the relaxation characteristics of the respiratory system. The distribution of the volume change that would be expected from the observed relative compliances of the three compartments would be approximately 66% into change in lung volume, 25% into change in rib cage volume, and 9% into change in abdominal volume. Instead, in line with our predictions for acute gastric distension, approximately 33% went into decrease in lung volume, 40% into increase in rib cage volume, and 26% into increase in abdominal volume. These results suggest that the interactions among the rib cage, abdomen, and diaphragm are such as to defend against large changes in end-expiratory lung volume in the face of abdominal distension.     

Frequency-dependent effects of hypercapnia on respiratory mechanics of cats

The effect of increasing arterial partial pressure of CO2 (PaCO2) on respiratory mechanics was investigated in six anesthetized, paralyzed cats ventilated by constant-flow inflation. Respiratory mechanics were studied after end-inspiratory occlusions. Zero frequency resistance (Rmax), infinite frequency resistance (Rmin), and static elastance (Est) were calculated for the respiratory system, lung, and chest wall. Alveolar ventilation was manipulated by the addition of dead space to achieve a range of PaCO2 values of 29.3-87.3 mmHg. Cats did not become hypoxic during the experiment. Under control conditions marked frequency dependence in Rmax, Rmin, and Est of the respiratory system, lungs, and chest wall was demonstrated. The chest wall contributed 50% of the total resistance of the respiratory system. With increasing PaCO2 the only resistance observed to increase was Rmax of the lung (P less than 0.01). There were also no changes in the static elastic properties of either the lungs or the chest wall. These results suggest that hypercapnia increases resistance by changes in the lung periphery and not in the conducting airways.     

Respiratory abdominal muscle recruitment and chest wall motion in myotonic muscular dystrophy.

Abdominal muscles are selectively active in normal subjects during stress and may increase the potential energy for inspiration by reducing the end-expiratory lung volume (EELV). We hypothesized that a similar process would occur in subjects with myotonic muscular dystrophy (MMD), but would be less effective, because of to their weakness and altered chest wall mechanics. Fine-wire electromyography (EMG) of the transversus abdominis (TA), internal oblique (IO), external oblique, and rectus abdominis was recorded in 10 MMD and 10 control subjects. EMG activity, respiratory inductive plethysmography, and gastric pressure were recorded during static pressure measurement and at increasing levels of inspiratory resistance breathing. EELV was reduced and chest wall motion was synchronous only in controls. Although the TA and IO were selectively recruited in both groups, EMG activity of the MMD group was twice that of controls at the same inspiratory pressure. In MMD subjects with mildly reduced forced vital capacity, significant differences can be seen in abdominal muscle recruitment, wall motion, work of breathing, and ventilatory parameters.     

Sustained inflation during HFOV improves pulmonary mechanics and oxygenation

Effective use of high-frequency oscillatory ventilation (HFOV) may require maintenance of adequate lung volume to optimize gas exchange. To determine the impact of inflation during HFOV, sustained inflation was applied at pressures of 5, 10, and 15 cmH2O above mean airway pressure for 3, 10, and 30 s to 15 intubated, paralyzed, anesthetized rabbits after saline lavage to induce surfactant deficiency. Arterial blood gases were recorded in all rabbits while static compliance, resistance, time constant, and changes in functional residual capacity were recorded using the interrupter technique and plethysmograph in seven rabbits. Parameters were recorded before and 2 min after sustained inflation. Arterial PO2, compliance of the respiratory system, and functional residual capacity increased after sustained inflation at pressure levels of at least 10 cmH2O and 10-s duration. As the presence or duration of a sustained inflation was increased, oxygenation improved (P less than or equal to 0.01), but arterial PCO2 increased as longer sustained inflations were used (P less than or equal to 0.005). Sustained inflations of 5 cmH2O above mean airway pressure or of 3-s duration were ineffective. We conclude that either a critical pressure or duration of sustained inflation is needed to improve oxygenation and pulmonary mechanics during HFOV.     

Static lung-lung interactions in unilateral emphysema.

Motivated by the introduction of single-lung transplantation into clinical practice, we compared the static mechanical properties of the respiratory system in six supine dogs before (at baseline) with those after the induction of unilateral emphysema. Relaxation volume (Vrel), total lung capacity (TLC), and static compliance of the emphysematous lung increased to 214 +/- 68, 186 +/- 39, and 253 +/- 95% (SD) of baseline, respectively. Vrel of the nonemphysematous lung fell to 81 +/- 28% of baseline, with no significant change in TLC of the nonemphysematous lung or its pressure-volume relationship, indicating that unilateral hyperinflation does not cause dropout of contralateral lung units. After unilateral emphysema, the chest wall shifted to a higher unstressed or neutral volume (when pleural pressure equals atmospheric pressure) in three of six animals, minimizing the anticipated decrease in lung recoil pressure at the higher respiratory system Vrel. The pattern of relative lung emptying in the intact dog and in the excised lungs was similar during stepwise deflations from TLC, suggesting that mean pleural pressure of the hemithoraces is equal. We conclude that in the dog the static volume distribution between emphysematous and nonemphysematous lungs is determined only by differences in lung recoil and compliance.