Transpulmonary pressures and lung mechanics with glossopharyngeal insufflation and exsufflation beyond normal lung volumes in competitive breath-hold divers.

Throughout life, most mammals breathe between maximal and minimal lung volumes determined by respiratory mechanics and muscle strength. In contrast, competitive breath-hold divers exceed these limits when they employ glossopharyngeal insufflation (GI) before a dive to increase lung gas volume (providing additional oxygen and intrapulmonary gas to prevent dangerous chest compression at depths recently greater than 100 m) and glossopharyngeal exsufflation (GE) during descent to draw air from compressed lungs into the pharynx for middle ear pressure equalization. To explore the mechanical effects of these maneuvers on the respiratory system, we measured lung volumes by helium dilution with spirometry and computed tomography and estimated transpulmonary pressures using an esophageal balloon after GI and GE in four competitive breath-hold divers. Maximal lung volume was increased after GI by 0.13-2.84 liters, resulting in volumes 1.5-7.9 SD above predicted values. The amount of gas in the lungs after GI increased by 0.59-4.16 liters, largely due to elevated intrapulmonary pressures of 52-109 cmH(2)O. The transpulmonary pressures increased after GI to values ranging from 43 to 80 cmH(2)O, 1.6-2.9 times the expected values at total lung capacity. After GE, lung volumes were reduced by 0.09-0.44 liters, and the corresponding transpulmonary pressures decreased to -15 to -31 cmH(2)O, suggesting closure of intrapulmonary airways. We conclude that the lungs of some healthy individuals are able to withstand repeated inflation to transpulmonary pressures far greater than those to which they would normally be exposed.     

Surrounding structures affect pressure-diameter behavior of excised dog bronchi

The effects of adjacent large blood vessels, fibroelastic membrane, and parenchyma on pressure-diameter (P-D) behavior of intrapulmonary bronchi were studied in five dog lung lobes. Central lobar airways were inflated separately by blocking all branches with beads and inflating the distal lobar air spaces via pleural capsules. After bronchial P-D curves were obtained at fixed pleural pressures (Ppl) of -30, -10, and -5 cmH2O, the P-D properties of the isolated bronchi were measured in each of four stages of dissection: 1) lobar artery and vein were left attached to the bronchus, but parenchyma was removed to within 1-2 mm of the limiting membranes; 2) all remaining parenchyma was carefully removed; 3) the large vessels were removed, leaving the bronchial fibroelastic membrane intact; and 4) the fibroelastic membrane was peeled from the bronchus. From stage 1 it was deduced that in the intact lobes, peak peribronchial parenchymal stress (Px) averaged -29.2 cmH2O at Ppl = -30 cmH2O). In stage 2 bronchial recoil was reduced only approximately 5%. The major decrease (approximately 35%) occurred in stage 3, indicating that interaction between vessels and bronchi contributed significantly to bronchial stiffness. A final decrease of approximately 10% was seen in stage 4. We conclude that Px in the intact state is similar to Ppl at a transpulmonary pressure of 30 cmH2O and that stages 1 or 2 may provide a better basis for estimating Px than the commonly employed bronchus free of vessels and tissue.     

Elastic properties of the bronchial mucosa: epithelial unfolding and stretch in response to airway inflation.

The bronchial mucosa contributes to elastic properties of the airway wall and may influence the degree of airway expansion during lung inflation. In the deflated lung, folds in the epithelium and associated basement membrane progressively unfold on inflation. Whether the epithelium and basement membrane also distend on lung inflation at physiological pressures is uncertain. We assessed mucosal distensibility from strain-stress curves in mucosal strips and related this to epithelial length and folding. Mucosal strips were prepared from pig bronchi and cycled stepwise from a strain of 0 (their in situ length at 0 transmural pressure) to a strain of 0.5 (50% increase in length). Mucosal stress and epithelial length in situ were calculated from morphometric data in bronchial segments fixed at 5 and 25 cmH(2)O luminal pressure. Mucosal strips showed nonlinear strain-stress properties, but regions at high and low stress were close to linear. Stresses calculated in bronchial segments at 5 and 25 cmH(2)O fell in the low-stress region of the strain-stress curve. The epithelium of mucosal strips was deeply folded at low strains (0-0.15), which in bronchial segments equated to < or =10 cmH(2)O transmural pressure. Morphometric measurements in mucosal strips at greater strains (0.3-0.4) indicated that epithelial length increased by approximately 10%. Measurements in bronchial segments indicated that epithelial length increased approximately 25% between 5 and 25 cmH(2)O. Our findings suggest that, at airway pressures <10 cmH(2)O, airway expansion is due primarily to epithelial unfolding but at higher pressures the epithelium also distends.     

Mechanical modulation of pressure-volume characteristics of contracted canine airways in vitro

In normal humans and dogs, the airways do not constrict to closure even when maximally stimulated. However, airway closure can be produced in isolated canine lobes and bronchial segments that are stimulated with maximal concentrations of bronchoconstrictors. These observations suggest that under normal conditions, physiological mechanisms to limit bronchoconstriction exist in vivo. In this investigation, we evaluated how mechanical factors that influence airway smooth muscle contractility contribute to the modulation of the pressure-volume characteristics of contracted canine intraparenchymal airways in vitro. Our results demonstrated that maximal and even submaximal contractile stimuli can produce airway closure in bronchi that are allowed to contract under isobaric conditions. However, the effectiveness of bronchoconstrictors is significantly reduced when the airways are subjected to tidal volume oscillations during contraction. In addition, airways contracted isovolumetrically at low volumes exhibit a markedly reduced sensitivity to submaximal concentrations of acetylcholine. This may limit bronchoconstriction at low lung volumes and transpulmonary pressures where the effectiveness of parenchymal stress in keeping the airways open is reduced. Together these factors could provide a mechanism by which bronchoconstriction is limited to low levels of airway resistance under normal conditions in vivo.     

Mechanical properties of porcine intralobar pulmonary arteries

The isobaric and isovolumetric properties of intrapulmonary arteries were evaluated by placing a highly compliant balloon inside arterial segments. The passive pressure-volume (P-V) curve was obtained by changing volume (0.004 ml/s) and measuring pressure. The isobaric active volume change (delta V) or isovolumetric active pressure change (delta P) generated by submaximal histamine was measured at four different transmural pressures (Ptm's) reached by balloon inflation. The maximal delta P = 11.2 +/- 0.6 cmH2O (mean +/- SE) was achieved at 30.8 +/- 1.2 cmH2O Ptm and maximal delta V = 0.20 +/- 0.02 ml at 16.7 +/- 1.7 cmH2O Ptm. The P-V relationships were similar when volume was increased after either isobaric or isovolumetric contraction. The calculated length-tension (L-T) relationship showed that the active tension curve was relatively flat and that the passive tension at the optimal length was 149 +/- 11% of maximal active tension. These data show that 1) a large elastic component operates in parallel with the smooth muscle in intralobar pulmonary arteries, and 2) the change in resistance associated with vascular expansion of the proximal arteries is independent of the type of contraction that occurs in the more distal arterial segments.     

High lung volume increases stress failure in pulmonary capillaries.

We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.     

Influence of lung volume on pulmonary microvascular pressure-volume characteristics.

The pressure-volume (P-V) characteristics of the lung microcirculation are important determinants of the pattern of pulmonary perfusion and of red and white cell transit times. Using diffuse light scattering, we measured capillary P-V loops in seven excised perfused dog lobes at four lung volumes, from functional residual capacity (FRC) to total lung capacity (TLC), over a wide range of vascular transmural pressures (Ptm). At Ptm 5 cmH(2)O, specific compliance of the microvasculature was 8.6%/cmH(2)O near FRC, decreasing to 2.7%/cmH(2)O as lung volume increased to TLC. At low lung volumes, the vasculature showed signs of strain stiffening (specific compliance fell as Ptm rose), but stiffening decreased as lung volume increased and was essentially absent at TLC. The P-V loops were smooth without sharp transitions, consistent with vascular distension as the primary mode of changes in vascular volume with changes in Ptm. Hysteresis was small (0.013) at all lung volumes, suggesting that, although surface tension may set basal capillary shape, it does not strongly affect capillary compliance.     

Chronic strain alters the passive and contractile properties of rabbit airways.

Pathophysiological conditions of the lung may shift the balance of forces so as to chronically alter the amount of strain imposed on the airways. This chronic strain could result in changes in the structure and/or function of the airways that affect its physiological properties. We evaluated the effects of imposing physiological levels of chronic mechanical strain on the passive and active physiological properties of intraparenchymal rabbit airways. Isolated bronchial segments were cultured for 48 h at transmural pressures of 0 cmH(2)O (No Strain) or 7 cmH(2)O (Strain). Effects of strain on small parenchymal airways were evaluated in lung tissue slices cultured under conditions of No Strain or approximately 50% increased in diameter (Strain). Chronic strain resulted in a higher passive compliance of the bronchial segments and larger airway lumen size. In addition, bronchi not subjected to chronic Strain were more responsive to ACh than bronchi subjected to chronic Strain, and airways in lung slices subjected to No Strain narrowed more in response to ACh than airways in lung slices subjected to Strain. The greatest effects of chronic strain occurred in the smallest sized airways. Our results suggest that chronic distension of the airways has physiologically important effects on their passive and active properties, which are most prominent in the smaller, more peripheral airways.     

Effect of intravenous papain on tracheal pressure-volume curves in rabbits

To investigate the effects of airway cartilage softening on tracheal mechanics, pressure-volume (PV) curves of excised tracheas were studied in 12 rabbits treated with 100 mg/kg iv papain, whereas 14 control animals received no pretreatment. The animals were killed 24 h after the injection and the excised specimens studied 24 h later. Treated tracheas exhibited decreased ability to withstand negative transmural pressures, reflected in increased collapse compliance: 6.2 +/- 2.1 vs. 2.0 +/- 0.5% peak volume (Vmax)/cmH2O means +/- SD, P less than 0.001, (Vmax = extrapolated maximal tracheal volume), increased kc (exponential constant that reflects the shape of collapse limb of the PV curve): 0.244 +/- 0.077 vs. 0.065 +/- 0.015 (P less than 0.001). The distension limb of the PV curve greater than 2.5 cmH2O transmural pressure (Ptm) was no different. Compliance between 0 and 2.5 cmH2O Ptm was increased in papain-treated rabbits: 4.97 +/- 1.73 vs. 2.30 +/- 0.31% Vmax/cmH2O (P less than 0.001). Tracheal volume, and therefore mean diameter, was decreased at 0 Ptm: 2.7 +/- 0.26 vs. 3.2 +/- 0.27 mm (P less than 0.001). We conclude that airway cartilage softening increases the compliance of the trachea at pressures less than 2.5 cmH2O Ptm.     

Alveolar pressure inhomogeneity during low-frequency oscillation of excised canine lobes

To quantify the inhomogeneity of alveolar pressures (PA) during cyclic changes in lung volume similar to those present during spontaneous breathing, inhomogeneity of PA was measured with an alveolar capsule technique in six excised canine lungs. The lungs were ventilated by a quasi-sinusoidal pump with a constant end-expiratory lung volume and tidal volumes of 10, 20, and 40% of vital capacity at breathing frequencies ranging from 5 to 45 breaths/min. Inhomogeneity of PA was quantified as the sample standard deviation of pressures measured in three capsules. A component of inhomogeneity in phase with flow and a smaller component out of phase with flow were present. The in-phase component increased approximately linearly with flow. The ratio of inhomogeneity to flow was smaller at large tidal volumes and, at the two higher tidal volumes studied, the ratio was greater during inspiration than during expiration. If these data are interpreted in terms of a simple circuit model, this degree of inhomogeneity implies an approximately twofold variation in regional time constants. Despite these considerable differences in time constants, the absolute amount of inhomogeneity as defined by the sample standard deviation of the three PA's was small (maximum 0.57 +/- 0.32 cmH2O at the highest breathing frequency and tidal volume) because airway resistance in the canine lung was small.     

Cigarette smoke acutely increases collateral resistance in excised dog lobes

The acute effects of cigarette smoke or drug inhalation on collateral conductance (Gcoll) were studied in freshly excised dog lobes held at fixed volumes. A double-lumen catheter was wedged into a segmental bronchus, and air, smoke, or aerosol flowed into the blocked segment at a constant pressure of 2 cmH2O. A capsule glued over a small area of perforated pleura of the segment was used to measure alveolar pressure; the capsule could also be used to measure small airway flow (Vcap) through the segment. Gcoll was almost linearly dependent on lung volume, rising about fivefold between 20 and 100% inflation (30 cmH2O). During smoke inhalation Gcoll began decreasing almost immediately, roughly halving with the first cigarette and falling to about 20% after two cigarettes. Similar proportions were obtained at other lung volumes. Pulmonary conductance (oscillator) in the remainder of the lobe decreased only modestly to 78% of control after two cigarettes. In lobes exposed to 4.5% CO2 after air Gcoll rose 25-50%, but Vcap increased only 5-10%. However, acetylcholine chloride aerosol reduced both flows by similar ratios. Isoproterenol did not prevent or reverse smoke-induced collateral constriction but did reverse the effects of acetylcholine on both pathways. These results suggest that in excised lungs aerosols acted on larger segmental airways in series with collateral channels and with peripheral airways, whereas CO2 and particularly cigarette smoke provoked more marked effects on the most distal smooth muscle.     

Different ventilation strategies alter surfactant responses in preterm rabbits.

The effect of ventilation strategy on in vivo function of different surfactants was evaluated in preterm rabbits delivered at 27 days gestational age and ventilated with either 0 cmH2O positive end-expiratory pressure (PEEP) at tidal volumes of 10-11 ml/kg or 3 cmH2O PEEP at tidal volumes of 7-8 ml/kg after treatment with one of four different surfactants: sheep surfactant, the lipids of sheep surfactant stripped of protein (LH-20 lipid), Exosurf, and Survanta. The use of 3 cmH2O PEEP decreased pneumothoraces in all groups except for the sheep surfactant group where pneumothoraces increased (P < 0.01). Ventilatory pressures (peak pressures - PEEP) decreased more with the 3 cmH2O PEEP, low-tidal-volume ventilation strategy for Exosurf-, Survanta-, and sheep surfactant-treated rabbits (P < 0.05), whereas ventilation efficiency indexes (VEI) improved only for Survanta- and sheep surfactant-treated rabbits with 3 cmH2O PEEP (P < 0.01). Pressure-volume curves for sheep surfactant-treated rabbits were better than for all other treated groups (P < 0.01), although Exosurf and Survanta increased lung volumes above those in control rabbits (P < 0.05). The recovery of intravascular radiolabeled albumin in the lungs and alveolar washes was used as an indicator of pulmonary edema. Only Survanta and sheep surfactant decreased protein leaks in the absence of PEEP, whereas all treatments decreased labeled albumin recoveries when 3 cmH2O PEEP was used (P < 0.05). These experiments demonstrate that ventilation style will alter a number of measurements of surfactant function, and the effects differ for different surfactants.     

Effect of resting smooth muscle length on contractile response in resistance airways

We studied the effect of resting smooth muscle length on the contractile response of the major resistance airways (generations 0-5) in 18 mongrel dogs in vivo using tantalum bronchography. Dose-response curves to 10(-10) to 10(-7) mol/kg methacholine (MCh) were generated [at functional residual capacity (FRC)] by repeated intravenous bolus administration using tantalum bronchography after each dose. Airway constriction varied substantially with dose-equivalent stimulation and varied sequentially from trachea (8.8 +/- 2.2% change in airway diam) to fifth-generation bronchus (49.8 +/- 3.0%; P less than 0.001). Length-tension curves were generated for each airway to determine the airway diameter (i.e., resting in situ smooth muscle length) at which maximal constriction was elicited using bolus intravenous injection of 10(-8) mol/kg MCh. A Frank-Starling relationship was obtained for each airway; the transpulmonary pressure at which maximal constriction was elicited increased progressively from 2.50 +/- 1.12 cmH2O for trachea (approximately FRC) to 18.3 +/- 1.05 cmH2O for fifth-generation airways (approximately 50% TLC) (P less than 0.001). A similar relationship was obtained when change in airway diameter was plotted as a function of airway radius. We demonstrate substantial heterogeneity in the lung volumes at which maximal constriction is elicited and in distribution of parasympathomimetic constriction within the first few generations of resistance bronchi. Our data also suggest that lung hyperinflation may lead to augmented airway contractile responses by shifting resting smooth muscle length toward optimum resting smooth muscle length.     

Mechanical properties of small airways in excised pony lungs.

We evaluated the pressure-flow relationships in collaterally ventilating segments of excised pony lungs by infusing N2, He, Ne, or SF6 at known flows (V) through a catheter wedged in a peripheral airway. Measurements were made at segment- (Ps) to-airway opening (Pao) pressure differentials of 3-15 cmH2O when the lungs were held at transpulmonary pressures of 5, 10, and 15 cmH2O. The data were analyzed both by calculating collateral resistance (Ps-Pao/V) and by constructing Moody-type plots of normalized pressure drop [(Ps-Pao)/(1/2 rho U2, where rho is density and U is velocity)] against Reynolds number to assess the pattern of flow through the segment and the change in dimension of the flow channels as Ps and Pao were changed. The interpretations from these analyses were compared with radiographic measurements of the diameters of small airways within the collaterally ventilating lung segment at similar pressures. Collateral resistance increased as Ps-Pao increased at high Reynolds numbers, i.e., high flows or dense gas (SF6). Analysis of the Moody-type plots revealed that flow was density dependent at Reynolds number greater than 100, which frequently occurred when N2 was the inflow gas. The radiographic data revealed that small airway diameter increased as Ps-Pao increased at all lung volumes. In addition, at 5 cmH2O Pao, small-airway diameter was smaller for a given Ps in the nonhomogeneous case (Ps greater than Pao) than small-airway diameter for the same Ps in the homogeneous case (Ps = Pao). We interpret these data to suggest that the surrounding lung prevented the segment from expanding in the nonhomogeneous case.(ABSTRACT TRUNCATED AT 250 WORDS)     

Active and passive respiratory mechanics in anesthetized dogs

In six spontaneously breathing anesthetized dogs (pentobarbital sodium, 30 mg/kg) airflow, volume, and tracheal and esophageal pressures were measured. The active and passive mechanical properties of the total respiratory system, lung, and chest wall were calculated. The average passive values of respiratory system, lung, and chest wall elastances amounted to, respectively, 50.1, 32.3, and 17.7 cmH2O X l-1. Resistive pressure-vs.-flow relationships for the relaxed respiratory system, lung, and chest wall were also determined; a linear relationship was found for the former (the total passive intrinsic resistance averaged 4.1 cmH2O X l-1 X s), whereas power functions best described the others: the pulmonary pressure-flow relationship exhibited an upward concavity, which for the chest wall presented an upward convexity. The average active elastance and resistance of the respiratory system were, respectively, 64.0 cmH2O X l-1 and 5.4 cmH2O X l-1 X s. The greater active impedance reflects pressure losses due to force-length and force-velocity properties of the inspiratory muscles and those due to distortion of the respiratory system from its relaxed configuration.     

Intravenous papain-induced cartilage softening decreases preload of tracheal smooth muscle

To study the interaction between tracheal cartilage and the trachealis muscle we measured trachealis muscle contraction in response to electrical field stimulation and methacholine in excised tracheal segments from control and papain-treated rabbits. Papain treatment softened the tracheal cartilage and altered the passive pressure volume curve of the tracheal segments at transmural pressures below 5 cmH2O. The transmural pressure required for maximal active changes in volume (isobaric contraction) with electrical field stimulation was increased in papain-treated animals. We conclude that tracheal cartilage provides a preload which stretches the trachealis muscle toward optimal length and that papain, by altering the elastic mechanical properties of cartilage, decreases this preload.     

Effect of inflation on trachealis muscle tone in canine tracheal segments in vitro

Isolated tracheal segments were studied in vitro to determine how inflation affects the length and tension of the contracted and relaxed trachealis muscle. Circumferential trachealis muscle lengths were measured from cross-sectional radiographs taken during stepwise inflation of intact 20-cm-long tracheal segments to an inflation pressure of 25 cmH2O. A tracheal length spanning two cartilage rings was then cut out and mounted in a tissue bath using clips attached at the points of muscle insertion into the cartilage. The ring was stretched open along the axis of the muscle, and the resulting forces of the relaxed and contracted muscle and the cartilage were measured. Muscle lengths and tensions during inflation of the trachea were determined by comparing pressure vs. length and force vs. length measurements. During inflation from 0 to 25 cmH2O, the circumferential length of the trachealis muscle contracted with 10(-5) M acetylcholine increased from 48 to 70% of its length of maximal active tension (Lmax), while the relaxed muscle increased from 80 to 93% Lmax. The length of the contracted muscle was maintained at a nearly constant proportion of its relaxed length at each pressure.     

Effect of flow direction on collateral ventilation in excised dog lung lobes

We determined the effect of flow direction on the relationship between driving pressure and gas flow through a collaterally ventilating lung segment in excised cranial and caudal dog lung lobes. He, N2, and SF6 were passed through the lung segment distal to a catheter wedged in a peripheral airway. Gases were pushed through the segment by raising segment pressure (Ps) relative to airway opening pressure (Pao) and pulled from the segment by ventilating the lobe with the test gas, then lowering Ps relative to Pao. Driving pressures (Ps - Pao) between 0.25 and 2 cmH2O were evaluated at Pao values of 5, 10, and 15 cmH2O. Results were similar in cranial and caudal lobes. Flow increased as Ps - Pao increased and was greatest at Pao = 15 cmH2O for the least-dense gas (He). Although flow direction was not a significant first-order effect, there was significant interaction between volume, driving pressure, and flow direction. Dimensional analysis suggested that, although flow direction had no effect at Pao = 10 and 15 cmH2O, at Pao = 5 cmH2O, raising Ps relative to Pao increased the characteristic dimension of the flow pathways, and reducing Ps relative to Pao reduced the dimension. These data suggest that at large lobe volumes, airways (including collateral pathways) within the segment are maximally dilated and the stiffness of the parenchyma prevents any significant distortion when Ps is altered. At low lobe volumes, these pathways are affected by changes in transmural pressure due to the increased airway and parenchymal compliance.     

Volume-related and volume-independent effects of posture on esophageal and transpulmonary pressures in healthy subjects.

Ventilator management decisions in acute lung injury could be better informed with knowledge of the patient's transpulmonary pressure, which can be estimated using measurements of esophageal pressure. Esophageal manometry is seldom used for this, however, in part because of a presumed postural artifact in the supine position. Here, we characterize the magnitude and variability of postural effects on esophageal pressure in healthy subjects to better assess its significance in patients with acute lung injury. We measured the posture-related changes in relaxation volume and total lung capacity in 10 healthy subjects in four postures: upright, supine, prone, and left lateral decubitus. Then, in the same subjects, we measured static pressure-volume characteristics of the lung over a wide range of lung volumes in each posture by using an esophageal balloon catheter. Transpulmonary pressure during relaxation (PLrel) averaged 3.7 (SD 2.0) cmH2O upright and -3.3 (SD 3.2) cmH2O supine. Approximately 58% of the decrease in PLrel between the upright and supine postures was due to a corresponding decrease in relaxation volume. The remaining 2.9-cmH2O difference is consistent with reported values of a presumed postural artifact. Relaxation volumes and pressures in prone and lateral postures were intermediate. To correct estimated transpulmonary pressure for the effect of lying supine, we suggest adding 3 cmH2O (95% confidence interval: -1 to +7 cmH2O). We conclude that postural differences in estimated transpulmonary pressure at a given lung volume are small compared with the substantial range of PLrel in patients with acute lung injury.     

Influence of passive changes of lung volume on upper airways

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.