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.     

Dependence of diaphragmatic length on lung volume and thoracoabdominal configuration

Changes in lung volume can be partitioned into volume displacements of the rib cage and abdomen. Abdominal displacements are often used as estimates of diaphragmatic displacements and changes in lengthening of diaphragmatic muscle. We used X-rays, ultrasound, and linear measurements of thoracic and abdominal diameters to estimate relationships among lung volume, thoracoabdominal configuration and diaphragmatic length, and we found that diaphragmatic length was strongly dependent on rib cage as well as abdominal displacement. In three subjects, the diaphragm shortened 57-85% as much during a breath made without abdominal displacement as during a normal breath in which the abdominal wall moved outward with the rib cage. We conclude that changes in diaphragmatic length can be estimated from surface measurements without radiation and that the length of the diaphragm cannot be estimated from displacements of the abdominal wall alone.     

Mechanical coupling of the rib cage, abdomen, and diaphragm through their area of apposition

Although volumetric displacements of the chest wall are often analyzed in terms of two independent parallel pathways (rib cage and abdomen), Loring and Mead have argued that these pathways are not mechanically independent (J. Appl. Physiol. 53: 756-760, 1982). Because of its apposition with the diaphragm, the rib cage is exposed to two distinct pressure differences, one of which depends on abdominal pressure. Using the analysis of Loring and Mead as a point of departure, we developed a complementary analysis in which mechanical coupling of the rib cage, abdomen, and diaphragm is modeled by a linear translational transformer. This model has the advantage that it possesses a precise electrical analogue. Pressure differences and compartmental displacements are related by the transformation ratio (n), which is the mechanical advantage of abdominal over pleural pressure changes in displacing the rib cage. In the limiting case of very high lung volume, n----0 and the pathways uncouple. In the limit of very small lung volume, n----infinity and the pathways remain coupled; both rib cage and abdomen are driven by abdominal pressure alone, in accord with the Goldman-Mead hypothesis. A good fit was obtained between the model and the previously reported data for the human chest wall from 0.5 to 4 Hz (J. Appl. Physiol. 66:350-359, 1989). The model was then used to estimate rib cage, diaphragm, and abdominal elastance, resistance, and inertance. The abdomen was a high-elastance high-inertance highly damped compartment, and the rib cage a low-elastance low-inertance more lightly damped compartment. Our estimate that n = 1.9 is consistent with the findings of Loring and Mead and suggests substantial pathway coupling.     

Transdiaphragmatic pressure and rib motion in area of apposition during paralysis

Changes in pleural surface pressure in area of apposition of diaphragm to rib cage (delta Ppl,ap), changes in abdominal pressure (delta Pab), and redial displacement of the 11th rib have been recorded in anesthetized, paralyzed dogs during lung inflation or deflation. Above functional residual capacity (FRC) changes in transdiaphragmatic pressure in area of apposition (delta Pdi,ap) were essentially nil in intact (INT) dogs either in lateral or supine posture, and in partially eviscerated (EVS) dogs in lateral posture, either in the 10th or 11th intercostal space. Below FRC delta Pdi,ap could be positive (INT lateral and EVS), nil (EVS), or negative (INT supine and EVS); it could be different in the 10th and 11th intercostal spaces. Hence, with stretched (like with contracted) diaphragm, delta Ppl,ap measured at one site often differs from delta Pab and is not representative of average pressure acting on area of apposition. With volume increase above FRC, the 11th rib moved slightly in and then out in EVS and linearly out in INT. With volume decrease below FRC it moved out progressively in EVS, and it moved in and eventually reversed in INT. In paralyzed dogs in lateral posture the factor having the greatest influence on displacement of the abdominal rib cage is Pab. Mechanical linkage with pulmonary rib cage becomes relevant at large volume, whereas insertional traction of diaphragm becomes relevant at low volume.     

Action of neck accessory muscles on rib cage in dogs

To investigate the action of the neck accessory muscles on the rib cage, we stimulated the sternocleidomastoid and the scalenus muscles separately in supine anesthetized dogs. Hooks screwed into the sternum and ribs were used to measure their axial displacements and the changes in anteroposterior (AP) and transverse (T) diameters of the rib cage. We found that the sternocleidomastoid and scalenus muscles, when they contract alone, cause a large axial displacement of the sternum and the ribs in a cephalad direction and expand the rib cage along both its AP and T diameters. Opening the abdomen increased the cephalad displacement of the ribs and the expansion of the lower rib cage, particularly along its T diameter, but reduced the increase in lung volume. These experiments indicate 1) that the action of the sternocleidomastoid and scalenus muscles on the rib cage is essentially the consequence of a rotation of the ribs' neck axes, resulting from the cephalad displacement of the ribs, and 2) that the fall in abdominal pressure, almost certainly by acting through the zone of apposition of the diaphragm to the rib cage, has a deflationary action on the lower rib cage, more markedly so on its lateral than its anterior wall. The experiments also suggest that the fall in abdominal pressure prevents the diaphragm from moving cephalad and aids the neck accessory muscles in inflating the lungs.     

Mechanics of compartmental models of the chest wall

Standard methods for describing the mechanical properties of a linear elastic system are applied to the two- and three-compartment models of the chest wall. The compliance matrix and the experiments required to determine the entries in this matrix and thereby to describe the mechanical properties of the relaxed chest wall are described. The effective forces exerted by external loads and muscle tension are defined. The formal theory is used to identify relations among variables. From the definition of effective force, it follows that the ratio of the forces exerted by the diaphragm on the rib cage and abdomen is the same as the ratio of the dependence of diaphragm length on rib cage and abdominal volumes. As an example of relations among variables that follow from the symmetry of the compliance matrix, it is shown that the change of gastric pressure caused by raising pleural pressure is related to the change in lung volume caused by changing stomach volume.     

Mechanics of the canine diaphragm in pleural effusion

Pleural effusion is a complicating feature of many diseases of the lung and pleura, but its effects on the mechanics of the diaphragm have not been assessed. In the present study, radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in anesthetized dogs, and the three-dimensional location of the markers during relaxation before and after the stepwise introduction of liquid into the left or right pleural space and during phrenic nerve stimulation in the same conditions was determined using computed tomography. From these data, accurate measurements of diaphragm muscle length and displacement were obtained, and the changes in pleural and abdominal pressure were analyzed as functions of these parameters. The effect of liquid instillation on the axial position of rib 5 was also measured. The data showed that 1) liquid leaked through the dorsal mediastinal sheet behind the pericardium so that effusion was bilateral; 2) effusion caused a caudal displacement of the relaxed diaphragm; 3) this displacement was, compared with passive lung inflation, much larger than the cranial displacement of the ribs; and 4) the capacity of the diaphragm to generate pressure, in particular pleural pressure, decreased markedly as effusion increased, and this decrease was well explained by the decrease in active muscle length. It is concluded that pleural effusion has a major adverse effect on the pressure-generating capacity of the diaphragm and that this is the result of the action of hydrostatic forces on the muscle.     

Relative strengths of the chest wall muscles

We hypothesized that during maximal respiratory efforts involving the simultaneous activation of two or more chest wall muscles (or muscle groups), differences in muscle strength require that the activity of the stronger muscle be submaximal to prevent changes in thoracoabdominal configuration. Furthermore we predicted that maximal respiratory pressures are limited by the strength of the weaker muscle involved. To test these hypotheses, we measured the pleural pressure, abdominal pressure (Pab), and transdiaphragmatic pressure (Pdi) generated during maximal inspiratory, open-glottis and closed-glottis expulsive, and combined inspiratory and expulsive maneuvers in four adults. We then determined the activation of the diaphragm and abdominal muscles during selected maximal respiratory maneuvers, using electromyography and phrenic nerve stimulation. In all subjects, the Pdi generated during maximal inspiratory efforts was significantly lower than the Pdi generated during open-glottis expulsive or combined efforts, suggesting that rib cage, not diaphragm, strength limits maximal inspiratory pressure. Similarly, at high lung volumes, the Pab generated during closed-glottis expulsive efforts was significantly greater than that generated during open-glottis efforts, suggesting that the latter pressure is limited by diaphragm, not abdominal muscle, strength. As predicted, diaphragm activation was submaximal during maximal inspiratory efforts, and abdominal muscle activation was submaximal during open-glottis expulsive efforts at midlung volume. Additionally, assisting the inspiratory muscles of the rib cage with negative body-surface pressure significantly increased maximal inspiratory pressure, whereas loading the rib cage muscles with rib cage compression decreased maximal inspiratory pressure. We conclude that activation of the chest wall muscles during static respiratory efforts is determined by the relative strengths and mechanical advantage of the muscles involved.     

Action of the diaphragm on the rib cage inferred from a force-balance analysis

Displacements of the rib cage are determined by the intrinsic passive properties of the rib cage, rib cage musculature, pleural and abdominal pressures, and the diaphragm. The diaphragm's mechanical actions on the rib cage are inferred from a force-balance analysis in which the diaphragm is seen to cause expansion of the rib cage by pulling cephalad at its insertions on the lower ribs (insertional component) and by raising intra-abdominal pressure, which pushes outward on the diaphragm's zone of apposition to the rib cage (appositional component). Goldman and Mead suggested that the diaphragm, acting alone, could drive both the rib cage and abdomen on their passive characteristics. The force-balance analysis shows that the diaphragm's inspiratory action on the rib cage is less than predicted by Goldman and Mead, but that in the special circumstances of their experiment (low lung volumes), the appositional component is large and the rib cage can be driven close to its passive characteristics. The force-balance analysis is consistent with recent observations by other investigations and is incompatible with the model proposed by Macklem and colleagues and with the Goldman-Mead hypothesis. Experiments on three subjects produced data consistent with the force-balance analysis, showing that the inspiratory action of the diaphragm on the rib cage is greatest at low lung volumes.     

Coupling between rib cage and abdominal compartments of the relaxed chest wall

The volume displacements of the rib cage and abdomen of relaxed seated subjects were measured as functions of pleural pressure with the chest wall expanded by airway pressure and with the chest wall distorted by an external force applied to the rib cage. From the measured displacements for the two independent loads, the three compliances that describe the mechanical properties of the relaxed chest wall modeled as a linear elastic system with two degrees of freedom were obtained. The cross compliance that describes the coupling between the rib cage and abdomen was found to be small and positive, 0.01-0.02 1/cmH2O. The displacement of the rib cage by the external force was consistent with the displacement predicted by use of standard methods for calculating the mechanical advantage of the force.     

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.     

Mechanism of the lung-deflating action of the canine diaphragm at extreme lung inflation

When lung volume in animals is passively increased beyond total lung capacity (TLC; transrespiratory pressure = +30 cmH(2)O), stimulation of the phrenic nerves causes a rise, rather than a fall, in pleural pressure. It has been suggested that this was the result of inward displacement of the lower ribs, but the mechanism is uncertain. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm and to the tenth rib pair in five dogs, and computed tomography was used to measure the displacement, length, and configuration of the muscle and the displacement of the lower ribs during relaxation at seven different lung volumes up to +60 cmH(2)O transrespiratory pressure and during phrenic nerve stimulation at the same lung volumes. The data showed that 1) during phrenic nerve stimulation at 60 cmH(2)O, airway opening pressure increased by 1.5 ± 0.7 cmH(2)O; 2) the dome of the diaphragm and the lower ribs were essentially stationary during such stimulation, but the muscle fibers still shortened significantly; 3) with passive inflation beyond TLC, an area with a cranial concavity appeared at the periphery of the costal portion of the diaphragm, forming a groove along the ventral third of the rib cage; and 4) this area decreased markedly in size or disappeared during phrenic stimulation. It is concluded that the lung-deflating action of the isolated diaphragm beyond TLC is primarily related to the invaginations in the muscle caused by the acute margins of the lower lung lobes. These findings also suggest that the inspiratory inward displacement of the lower ribs commonly observed in patients with emphysema (Hoover's sign) requires not only a marked hyperinflation but also a large fall in pleural pressure.     

Shape of the chest wall in the prone and supine anesthetized dog

The shape of the passive chest wall of six anesthetized dogs was determined at total lung capacity (TLC) and functional residual capacity (FRC) in the prone and supine body positions by use of volumetric-computed tomographic images. The transverse cross-sectional areas of the rib cage, mediastinum, and diaphragm were calculated every 1.6 mm along the length of the thorax. The changes in the volume and the axial distribution of transverse area of the three chest wall components with lung volume and body position were evaluated. The decrease of the transverse area within the rib cage between TLC and FRC, as a fraction of the area at TLC, was uniform from the apex of the thorax to the base. The volume of the mediastinum increased slightly between TLC and FRC (14% of its TLC volume supine and 20% prone), squeezing the lung between it and the rib cage. In the transverse plane, the heart was positioned in the midthorax and moved little between TLC and FRC. The shape, position, and displacement of the diaphragm were described by contour plots. In both postures, the diaphragm was flatter at FRC than at TLC, because of larger displacements in the dorsal than in the ventral region of the diaphragm. Rotation from the prone to supine body position produced a lever motion of the diaphragm, displacing the dorsal portion of the diaphragm cephalad and the ventral portion caudad. In five of the six dogs, bilateral isovolume pneumothorax was induced in the supine body position while intrathoracic gas volume was held constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationships between abdominal and diaphragmatic volume displacements

We investigated the relationship between the volumes displaced by the diaphragm and the abdominal wall during spontaneous breathing in supine anesthetized dogs. Diaphragmatic volume displacement (Vdi) was calculated from measurements taken from anteroposterior fluoroscopic images employing a previously described geometric model. The volume displacement of the abdominal wall (Vabd) was measured with a calibrated Respitrace. Shortening of single diaphragm muscle bundles in costal and crural regions was measured as the distance between radiopaque beads sutured to the peritoneal surface of the muscle. We found that Vdi always exceeded Vabd, but Vabd/Vdi was larger in animals in which the abdominal wall was more compliant. In this preparation, Vdi is better correlated with costal than with crural shortening. Vabd did not correlate with either costal or crural shortening. We infer that the difference between Vdi and Vabd reflects the volume displacement of the lower rib cage caused by diaphragm contraction. This volume difference was tightly correlated with costal shortening. We conclude from these data that coupling between Vdi and Vabd is influenced by the relative compliances of the chest wall and abdomen. Shortening of regions of the diaphragm may have variable relationships to the measured volume displacement, but costal shortening is intimately related to expansion of the lower rib cage.     

Analysis of human chest wall motion using a two-compartment rib cage model.

We present a model of chest wall mechanics that extends the model described previously by Macklem et al. (J. Appl. Physiol. 55: 547-557, 1983) and incorporates a two-compartment rib cage. We divide the rib cage into that apposed to the lung (RCpul) and that apposed to the diaphragm (RCab). We apply this model to determine rib cage distortability, the mechanical coupling between RCpul and RCab, the contribution of the rib cage muscles to the pressure change during spontaneous inspiration (Prcm), and the insertional component of transdiaphragmatic pressure in humans. We define distortability as the relationship between distortion and transdiaphragmatic pressure (Pdi) and mechanical coupling as the relationship between rib cage distortion and the pressure acting to restore the rib cage to its relaxed configuration (Plink), as assessed during bilateral transcutaneous phrenic nerve stimulation. Prcm was calculated at end inspiration as the component of the pressure displacing RCpul not accounted for by Plink or pleural pressure. Prcm and Plink were approximately equal during quiet breathing, contributing 3.7 and 3.3 cmH2O on average during breaths associated with a change in Pdi of 3.9 cmH2O. The insertional component of Pdi was measured as the pressure acting on RCab not accounted for by the change in abdominal pressure during an inspiration without rib cage distortion and was 40 +/- 12% (SD) of total Pdi. We conclude that there is substantial resistance of the human rib cage to distortion, that, along with rib cage muscles, contributes importantly to the fall in pleural pressure over the costal surface of the lung.     

Diaphragmatic work of breathing in premature human infants

Present methods of assessing the work of breathing in human infants do not account for the added load when intercostal muscle activity is lost and rib cage distortion occurs. We have developed a technique for assessing diaphragmatic work in this circumstance utilizing measurements of transdiaphragmatic pressure and abdominal volume displacement. Eleven preterm infants without evidence of lung disease were studied. During periods of minimal rib cage distortion, inspiratory diaphragmatic work averaged 5.9 g X cm X ml-1, increasing to an average of 12.4 g X cm X ml-1 with periods of paradoxical rib cage motion (P less than 0.01). Inspiratory work was strongly correlated with the electrical activity of the diaphragm as measured from its moving time average (P less than 0.05). Assuming a mechanical efficiency of 4% in these infants, the caloric cost of diaphragmatic work may reach 10% of their basal metabolic rate in periods with rib cage distortion. When lung disease is superimposed, the increased metabolic demands of the diaphragm may predispose preterm infants to fatigue and may contribute to a failure to grow.     

Voluntary changes of thoracoabdominal shape and regional lung volumes in humans.

We measured regional lung volumes from apex to base in humans during changes in thoracoabdominal shape which we monitored with magnetometers. In erect subjects, voluntary changes of shape at FRC did not change regional volume distribution. In supine subjects, the effect of negative pressure applied to the abdomen and a similar thoracoabdominal configuration achieved by voluntary means were studied. The distribution of regional volumes in both situations was the same as that measured during relaxation at the same overall lung volumes. We concluded that neither voluntary changes in shape nor negative abdominal pressure influenced the human pleural pressure gradient. This result, which differed from findings in animals, was probably because the human chest was relatively stiff and behaved with one degree of freedom; all parts of the human rib cage changed dimensions proportionally while negative abdominal pressure distorted the rib cage of animals.     

Chest wall distortion and regional lung volume distribution in erect humans.

Using 133Xe measured the regional distribution of FRC and of boluses administered at FRC in seated subjects during relaxation, lateral compression of the lower rib cage, and contraction of the inspiratory muscles so that mouth pressure was 50 cmH2O subatmospheric. Lateral compression increased apex-to-base differences of volume and bolus distribution, suggesting an increase of the apex-to-base gradient of pleural surface pressure. Changes in rib cage shape were measured with magnetometers and were qualitatively similar to those associated with increases in apex-to-base difference of pleural surface pressure in animals. Inspiratory effort decreased apex-to-base difference in volume and induced a similar trend in bolus distribution. Though changes in the rib cage shape were directionally similar, they were much smaller than those associated with decreased pleural surface pressure gradients in animals, and the changes in regional volume we observed were more likely due to forces generated by diaphragmatic contraction. These results were compatible with the apex-to-base gradient of pleural pressure being strongly influenced by shape adaptation between lung and chest wall.     

Dysfunction of the canine respiratory muscle pump in ascites.

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial PCO2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.