Fall In Pleural Pressure Research Articles

Fluid responsiveness in critically ill patients.

Fluid responsiveness in critically ill patients.

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.

Respiratory effect of the lower rib displacement produced by the diaphragm

The diaphragm acting alone causes a cranial displacement of the lower ribs and a caudal displacement of the upper ribs. The respiratory effect of the lower rib displacement, however, is uncertain. In the present study, two sets of experiments were performed in dogs to assess this effect. In the first, all the inspiratory intercostal muscles were severed, so that the diaphragm was the only muscle active during inspiration, and the normal inspiratory cranial displacement of the lower ribs was suppressed at regular intervals. In the second experiment, the animals were given a muscle relaxant to abolish respiratory muscle activity, and external, cranially oriented forces were applied to the lower rib pairs to simulate the action of the diaphragm on these ribs. The data showed that 1) holding the lower ribs stationary during spontaneous, isolated diaphragm contraction had no effect on the change in lung volume during unimpeded inspiration and no effect on the fall in pleural pressure (Ppl) during occluded breaths; 2) the procedure, however, caused an increase in the caudal displacement of the upper ribs; and 3) pulling the lower rib pairs cranially induced a cranial displacement of the upper ribs and a small fall in Ppl. These observations indicate that the force applied on the lower ribs by the diaphragm during spontaneous contraction, acting through the interdependence of the ribs, is transmitted to the upper ribs and has an inspiratory effect on the lung. However, this effect is very small compared to that of the descent of the dome.

Mechanisms of the inspiratory action of the diaphragm during isolated contraction

The lung-expanding action of the diaphragm is primarily related to the descent of the dome produced by the shortening of the muscle fibers. However, when the phrenic nerves in dogs are selectively stimulated at functional residual capacity, the muscle insertions into the lower ribs also move caudally. This rib motion should enhance the descent of the dome and increase the fall in pleural pressure (DeltaPpl). To quantify the role of this mechanism in determining DeltaPpl during isolated diaphragm contraction and to evaluate the volume dependence of this role, radiopaque markers were attached to muscle bundles in the midcostal region of the muscle in six animals, and the three-dimensional location of the markers during relaxation at different lung volumes and during phrenic nerve stimulation at the same lung volumes was measured using computed tomography. From these data, accurate measurements of muscle length, dome displacement, and lower rib displacement were obtained. The values of dome displacement were then corrected for lower rib displacement, and the values of DeltaPpl corresponding to the corrected dome displacements were obtained using the measured relationship between DeltaPpl and dome displacement. The measurements showed that phrenic stimulation at all lung volumes causes a caudal displacement of the lower ribs and that this displacement, taken alone, contributes approximately 25% of the DeltaPpl produced by the diaphragm. To the extent that this lower rib displacement is itself caused by DeltaPpl, the lung-expanding action of the diaphragm during isolated contraction may therefore be viewed as a self-facilitating phenomenon.

Role of pleural pressure in the coupling between the intercostal muscles and the ribs

The inspiratory intercostal muscles elevate the ribs and thereby elicit a fall in pleural pressure (DeltaPpl) when they contract. In the present study, we initially tested the hypothesis that this DeltaPpl does, in turn, oppose the rib elevation. The cranial rib displacement (Xr) produced by selective activation of the parasternal intercostal muscle in the fourth interspace was measured in dogs, first with the rib cage intact and then after DeltaPpl was eliminated by bilateral pneumothorax. For a given parasternal contraction, Xr was greater after pneumothorax; the increase in Xr per unit decrease in DeltaPpl was 0.98+/-0.11 mm/cmH2O. Because this relation was similar to that obtained during isolated diaphragmatic contraction, we subsequently tested the hypothesis that the increase in Xr observed during breathing after diaphragmatic paralysis was, in part, the result of the decrease in DeltaPpl, and the contribution of the difference in DeltaPpl to the difference in Xr was determined by using the relation between Xr and DeltaPpl during passive inflation. With diaphragmatic paralysis, Xr during inspiration increased approximately threefold, and 47+/-8% of this increase was accounted for by the decrease in DeltaPpl. These observations indicate that 1) DeltaPpl is a primary determinant of rib motion during intercostal muscle contraction and 2) the decrease in DeltaPpl and the increase in intercostal muscle activity contribute equally to the increase in inspiratory cranial displacement of the ribs after diaphragm paralysis.

Determinants of rib motion in flail chest.

We have previously developed a canine model of isolated flail chest to assess the effects of this condition on the mechanics of breathing, and these studies have led to the conclusion that the respiratory displacement of the fractured ribs is primarily determined by the fall in pleural pressure (Delta Ppl) and the action of the parasternal intercostal muscles. The present studies were designed to test the validity of this conclusion. A flail was induced in six supine anesthetized animals by fracturing both dorsally and ventrally the second to fifth ribs on the right side of the chest, after which the phrenic nerve roots were bilaterally sectioned in the neck. Sectioning the phrenic nerves caused a 34% decrease in Delta Ppl, associated with a 39% increase in parasternal intercostal inspiratory EMG activity (p < 0.05), and resulted in a marked reduction in the inspiratory inward displacement of the ribs. In three animals, the inward rib displacement was even reversed into a small outward displacement. When the airway was then occluded at end-expiration to increase Delta Ppl during the subsequent inspiration, all animals again showed a clear-cut inward rib displacement. These observations therefore confirm that in dogs with flail chest, the inspiratory displacement of the fractured ribs is set by the balance between the force related to pleural pressure and that generated by the parasternal intercostals. These observations also point to the critical importance of the pattern of inspiratory muscle activation in determining the magnitude of rib cage paradox in such patients.

Respiratory Ultrasonography of Human Parasternal Intercostal Muscle In Vivo

The parasternal intercostal muscle (PS) is phasically active during inspiration, but its mechanical function in humans is poorly understood. The aim of this study was to describe PS motion ultrasonographically during respiration. We used a 7.5-MHz curvilinear phased array transducer to obtain ultrasonograms of the second right and left interspace in the sagittal plane, 2–3 cm lateral to the sternum, in 4 seated subjects (3M, 1F), during tidal breathing and at residual volume (RV), functional residual capacity (FRC) and total lung capacity (TLC). Images were recorded on videotape and off-line, digitized, transferred to a workstation, and traced manually to outline the external and pleural borders of the PS muscle in relation to a rectangle bounded by the second and third ribs. To assess PS shape and motion, we measured inter-rib distance (Lics), PS thickness (Tps), and motion of the midpoint of the muscle relative to the midpoint of the reference rectangle (Mps). We also calculated the average radius of curvature of the external and pleural PS borders (Re, Rp) over the mid 50% of Lics, and 1/Re and 1/Rp. During tidal breathing, Mps moved ventrally by 0.42 ± 0.06 mm ( p = 0.001) against the pleural pressure gradient, and 1/Re and 1/Rp decreased by 1.1 × 10 −2 ± 1.6 × 10 −3 mm −1 and 8.4 × 10 −3 ± 1.4 × 10 −3 mm −1, respectively ( p < 0.001). Lics and Tps did not change ( p > 0.19). We conclude that, during inspiration, the PS moves ventrally and straightens, and lung volume, neural activation and pleural pressure influence PS shape and motion. The findings support an intercostal stabilizing function of the PS and suggest a novel mechanism by which the PS may contribute to the inspiratory fall in pleural pressure.

Pathophysiological response of bovine diaphragm function to gastric distension.

Because of the anatomic association of an exceptionally bulky stomach with a striking compartmentation of the chest wall, leading to the most cranial insertion of the diaphragm among mammals, gastric overdistension in the bovine species offers a unique pathophysiological condition for the diaphragm. The purpose of the present study was to determine whether increased intragastric pressure (Pga) (1, 2, 3, 4, and 5 kPa) leads to perturbations of respiratory and diaphragm function in calves. Changes in diaphragmatic strength and inspiratory action followed a biphasic pattern: 1) transdiaphragmatic pressure (Pdi) in response to constant bilateral maximal phrenic nerve stimulation at 30 Hz increased with moderate gastric distension and then fell abruptly as Pga continued to rise and 2) the magnitude of the ratio of the fall in pleural pressure to total Pdi was maintained up to a Pga amounting to 2 kPa but declined at higher pressures. We conclude that gastric distension in the bovine species provokes physiologically significant alterations of the diaphragm excitation-to-pressure generation coupling as well as of its capacity to convert Pdi into useful inspiratory pleural pressure. We suggest that these perturbations resulted from the combination of 1) altered tension-generating capacity due to compromised perfusion, 2) altered diaphragm geometry capable of altering tension-to-pressure generation coupling, and 3) modified coupling of the diaphragm with the chest wall that reduced its ability to drive inspiration.

Breathing muscle activity during expiration in patients with chronic airflow obstruction

During quiet ventilation in 10 patients with severe chronic airflow obstruction (AFO) there were large tidal swings of pleural pressure, 15.8 +/- 5.1 cmH2O, with high negative pressures achieved, 15.2 +/- 5.2 cmH2O. The pattern of pleural pressure mirrored that of tidal expiratory flow with a rapid rise to maximum of pleural pressure and flow at the beginning of expiration, a slow decline of both throughout most of expiration, and just before the onset of inspiration at flow reversal, a sharp fall in pleural pressure and expiratory flow. The shape of expiratory flow and pleural pressure tracings and the pattern of EMG recordings are compatible with loss of post-inspiratory muscle braking of flow. The generally negative pleural pressure and the EMG silence during expiration indicated relaxation of expiratory muscles throughout expiration. Extrapolation of the tidal expiratory flow curve to zero, and calculation of the area under the extrapolated curve showed the volume of dynamic hyperinflation to be a small proportion of the total increase in functional residual capacity above the predicted value in these patients.

Respiratory changes in parasternal intercostal intramuscular pressure

In an attempt to obtain insight in the forces developed by the parasternal intercostal muscles during breathing, changes in parasternal intramuscular pressure (PIP) were measured in 14 supine anesthetized dogs using a microtransducer method. In six animals, during bilateral parasternal stimulation a linear relationship between contractile force exerted on the rib and PIP was demonstrated (r greater than 0.95). In eight animals, during quiet active inspiration, substantial (55 +/- 11.5 cmH2O) PIP was developed. During inspiratory resistive loading and airway occlusion the inspiratory rise in PIP increased in proportion to the inspiratory fall in pleural pressure (r = 0.82). Phrenicotomy and vagotomy resulted in an increase in the inspiratory rise in PIP of 21% and 99%, respectively. During passive deflation, when the parasternal intercostals were passively lengthened, large rises (320 +/- 221 cmH2O) in intramuscular pressure were observed. During passive inflation intramuscular pressure remained constant or even decreased slightly (-8 +/- 25 cmH2O) as expected on the basis of the passive shortening of the muscles. PIP thus invariably increased when tension increased either actively or passively. From PIP it is clear that the parasternals exert significant forces on the ribs during respiratory maneuvers.

Effects of changes in left ventricular loading and pleural pressure on mitral flow.

The cause of the fall in left ventricular (LV) stroke volume (SV) during a fall in pleural pressure (Pp1) has been in dispute for over a century. We have defined the changes in the temporal relationship between LV inflow (Qm) and outflow (Qa) in a canine preparation to test the mutually exclusive hypotheses that the fall in LVSV is caused only by changes during diastole (e.g., ventricular interdependence) or only by changes during systole (e.g., afterload). The ability of the experimental preparation to measure the results of acute changes in right heart volume or output and acute changes in LV afterload was validated in open-chest studies with and without pericardial constraint. In closed-chest studies, with a fall in Pp1 during a Mueller maneuver Qm reached both its inspiratory minimum and expiratory maximum before Qa in 80% of the Mueller maneuvers, invalidating both hypotheses, which each required that one flow lead the other in 100% of the Mueller maneuvers. Review of individual records suggested that if the rapid changes in Pp1 occurred during systole, Qa could vary in a manner independent of the preceding Qm. These studies suggest that both diastolic and systolic events may contribute to the fall in SV, while causing opposite changes in LV volumes.

Mechanics of the parasternal intercostals during occluded breaths in dogs.

The electrical activity and the respiratory changes in length of the third parasternal intercostal muscle were measured during single-breath airway occlusion in 12 anesthetized, spontaneously breathing dogs in the supine posture. During occluded breaths in the intact animal, the parasternal intercostal was electrically active and shortened while pleural pressure fell. In contrast, after section of the third intercostal nerve at the chondrocostal junction and abolition of parasternal electrical activity, the muscle always lengthened. This inspiratory muscle lengthening must be related to the fall in pleural pressure; it was, however, approximately 50% less than the amount of muscle lengthening produced, for the same fall in pleural pressure, by isolated stimulation of the phrenic nerves. These results indicate that 1) the parasternal inspiratory shortening that occurs during occluded breaths in the dog results primarily from the muscle inspiratory contraction per se, and 2) other muscles of the rib cage, however, contribute to this parasternal shortening by acting on the ribs or the sternum. The present studies also demonstrate the important fact that the parasternal inspiratory contraction in the dog is really agonistic in nature.

Effect of lung volume on in vivo contraction characteristics of human diaphragm.

We performed transcutaneous bilateral phrenic nerve stimulation at varying lung volumes between residual volume (RV) and total lung capacity (TLC) in six normal male volunteers. Peak twitch transdiaphragmatic pressure declined from 49.1 +/- 9.1 (SD) cmH2O at RV to 19.6 +/- 5.97 (SD) cmH2O at TLC. Twitch contraction time fell from 91.8 +/- 11.3 (SD) ms at RV to 57.7 +/- 7.4 (SD) ms at TLC. There was a good correlation between changes in contraction time and transdiaphragmatic pressure (r = 0.7). The fall in transdiaphragmatic pressure was almost all due to a fall in pleural pressure, with little change in gastric pressure between RV and TLC. At TLC the pleural pressure in response to phrenic nerve stimulation was -0.58 cmH2O. We conclude that, as lung volume increases and the diaphragm shortens, it becomes less effective as a pressure generator and that pressure it generates is less well converted into useful inspiratory pressure. At a lung volume close to TLC, the diaphragm ceases to act as an inspiratory muscle.

Effect of alterations of pleural pressure on cardiac output.

Cardiac output is determined by the interaction of cardiac pump function and the mechanical properties of the peripheral circulation that govern venous return. Increasing pleural pressure impedes peripheral venous return but aids cardiac ejection; on the other hand, decreasing pleural pressure can augment venous return but impedes the emptying of the left ventricle, creating an increase in aortic pressure. Whether a fall in pleural pressure leads to an increase or decrease in cardiac output depends upon the functional state of the heart and its sensitivity to changes in afterload. Understanding the effect of pleural pressure on cardiac output may lead to the development of therapeutic or diagnostic techniques using altered pleural pressure.

Action of costal and crural parts of the diaphragm on the rib cage in dog.

We studied the action of the costal and crural (vertebral) parts of the diaphragm on the lower rib cage in normal supine dogs. The two parts of the diaphragm were separately stimulated by electrodes directly implanted in the muscle or via the different phrenic nerve roots in the neck. The results of the experiments indicate the following. 1) The costal and crural parts of the diaphragm have a different segmental innervation and a different mechanical action on the rib cage. 2) The costal diaphragm expands the lower rib cage when it contracts. This rib-cage expansion is due mostly to the fulcrum of the abdominal contents and partly to the rise in abdominal pressure that takes place during diaphragmatic contraction. The pericardial attachments play no role in this action of the diaphragm. 3) The action of the crural diaphragm on the lower rib cage depends only on the balance between the inspiratory force exerted by the rise in abdominal pressure and the expiratory force exerted by the fall in pleural pressure. In the intact animal at functional residual capacity, these two opposite effects cancel each other. 4) The inflationary action of both parts on the rib cage decreases progressively as lung volume increases. The findings also suggest that the rise in abdominal pressure which occurs when the diaphragm contracts expands the lower rib cage by acting through the area of apposition of the diaphragm to the rib cage. These findings also strengthen the idea that the diaphragm actually consists of two muscles.

Effects of spontaneous respiration on canine left ventricular function.

The purpose of this study was to determine the mechanism of the decrease in left ventricular stroke volume during spontaneous inspiration. We determined the transmural pressures of the left heart by measuring left atrial and diastolic left ventricular pressures relative to esophageal pressure. We estimated the directional changes in end-systolic and end-diastolic volumes of the left ventricle by determining the transit time of sound transmission between two ultrasonic crystals facing each other across the minor axis of the left ventricle. Left ventricular stroke volume decreased with spontaneous inspiratory effort as pleural pressure fell, regardless of whether lung volume increased or remained constant. The stroke volume was decreased during the fall in pleural pressure because of an increase in end-systolic volume with an essentially unchanged diastolic volume. Thus, the decrease in stroke volume was due to a decrease in ejection, rather than a decrease in filling of the left ventricle. We believe that left ventricular ejection was impeded by the fall in pressure around the heart relative to the pressure in the aorta. In spite of the essentially constant diastolic volume, diastolic left ventricular transmural pressure rose, suggesting that spontaneous inspiration decreases the diastolic compliance of the left ventricle. The change in diastolic compliance contributed to the decrease in stroke volume but was not the primary cause.

Effects of respiration on cardiac performance.

The conventional explanation for the fall in left ventricular stroke volume (LVSV) with inspiration is that blood pools in the lungs, thereby decreasing pulmonary venous return. In anesthetized dogs, we have found an increase in left ventricular filling pressure (LVFP) with both constant and increasing lung volume during an inspiratory effort. Transmural aortic diastolic pressure rises as LVSV falls and LVFP rises consistent with the hypothesis that a fall in pleural pressure afterloads the left ventricle. Additionally the increase found in right ventricular filling pressure with inspiration may adversely affect LV performance by decreasing LV compliance and/or contractility. Our findings are incompatible with pooling of blood in the lungs being the primary determinant of the fall in LVSV with inspiration.