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Pulmonary arterial occlusion pressure is not thought to reflect left atrial pressure (Pla) when alveolar pressure (PA) exceeds pulmonary venous pressure because alveolar capillaries collapse and the required continuous fluid column between the pulmonary artery and left atrium is interrupted. However, arterial-to-venous flow can occur when PA exceeds both the pulmonary arterial pressure (Ppa) and pulmonary venous pressure (i.e., in Zone 1 conditions), indicating the existence of a continuous patent vascular channel. Accordingly, Ppa should reflect Pla under these conditions. To investigate this connection cannulas were placed in the pulmonary arteries and left atria of eight excised rabbit lungs. Ppa and Pla were set 5 cm H2O above PA, which ranged from 0 to 25 cm H2O. Pla was then reduced in 2 to 4 cm H2O decrements while recording Ppa when arterial-to-venous flow ceased. At all PAs greater than 0 cm H2O, Pla was accurately reflected by the Ppa when both were exceeded by PA. The greater the PA, the lower the Ppa could track Pla below PA. Pla can be accurately measured by a pulmonary arterial catheter under Zone 1 conditions.

When using Boyle's Law for thoracic gas volume (Vtg) measurement, it is generally assumed that the alveolar pressure (Palv) does not differ from barometric pressure (Pbar) at the start of rarefaction and compression and that the product of the change in volume and pressure (delta P x delta V) is negligibly small. In a gentle panting maneuver in which the difference between Palv and Pbar is small, errors introduced by these assumptions are likely to be small; however, this is not the case when Vtg is measured using a single vigorous inspiratory effort. Discrepancies in the Vtg between the "complex" version of Boyle's Law, which does not ignore delta P x delta V and accounts for large swings in Palv, and the "simplified" version, during both a panting maneuver and a single inspiratory effort were calculated for normal control subjects and patients with cystic fibrosis or asthma. Defining the Vtg from the complete version as "correct," the errors introduced by the simplified version ranged from -3 to +3% for the panting maneuver whereas they ranged from 2 to 9% for the inspiratory maneuver. Using the simplified equation, the Vtg for the inspiratory maneuver was 0.135 +/- 0.237 L greater (p < 0.02) than for the panting maneuver. This discrepancy disappeared when the complete equation was used. While the errors introduced by the use of the simplified version of Boyle's Law are small, they are systematic and unnecessary.

Intrinsic positive end-expiratory pressure (PEEPi) has usually been interpreted as suggesting dynamic hyperinflation, but expiratory muscle activity may also increase end-expiratory alveolar pressure without any additional increase in end-expiratory lung volume. The aim of this study was to assess the influence of expiratory muscle activity, which increases abdominal pressure during expiration and is followed by a sudden drop at end-expiration, on PEEPi measurement in mechanically ventilated patients. We studied eight tracheally intubated patients breathing in an assisted mode in whom expiratory muscle activity was present. PEEPi was measured from the fluctuations of esophageal pressure (Pes) while continuous recording of gastric pressure (Pga) and of changes in abdominal cross-sectional area assessed expiratory muscle activity. PEEPi was also measured by the airway occlusion method in one patient, and diaphragmatic electromyographic activity was recorded to determine the timing of inspiratory muscle activity in two patients. Varying the level of ventilatory support (pressure support level, peak flow rate, or PEEP level) induced increases in measured PEEPi from 6.7 +/- 3.4 to 13.2 +/- 5.9 cm H2O. Concomitantly, the expiratory rise in Pga increased from 3.1 +/- 2.7 to 8.6 +/- 5.0 cm H2O, and the abrupt decay in Pga observed at the end of expiration increased from 4.2 +/- 3.7 to 10.6 +/- 6.1 cm H2O. The drop in Pga and the drop in Pes at end-expiration were synchronous, and these changes, together with electromyographic measurements, were consistent with a concomitant relaxation of the expiratory muscles and activation of the inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

It has recently been shown in several species that lung tissue resistance increases after administration of exogenous bronchoconstrictors. This finding suggests the possibility that lung parenchymal tissues could be involved in the pathophysiology of pulmonary allergic responses. To test this hypothesis, we sensitized Brown Norway rats with ovalbumin (OA) and performed experiments in anesthetized, open-chested, mechanically ventilated (respiratory frequency [f] = 1 Hz, tidal volume [VT] = 9 ml/kg, positive end-expiratory pressure [PEEP] = 3 cm H2O) animals. We affixed alveolar capsules to the lungs to measure alveolar pressure and calculated the resistance of lung (RL), tissue (Rti), and airway (Raw) under control conditions and after aerosol administration of saline (S) (n = 10) or OA (n = 14). To assess lung morphometry during the late response, the lungs of six S and six OA animals were frozen with liquid nitrogen (PEEP = 3 cm H2O) and processed via freeze substitution. Airway constriction was assessed by measuring the ratio of the airway lumen (A) to the ideally relaxed airway (Ar). Tissue distortion was assessed by measuring the mean linear intercept between alveolar walls (Lm), an atelectasis index (ATI) derived by calculating the ratio of tissue/airspace, and the standard deviation (SD) of Lm and ATI. In the OA group, all animals demonstrated an early response (ER; RL, Rti, Raw = 183.5 +/- 7.7, 159.7 +/- 9.9, 232.5 +/- 17.2% baseline, respectively) and 11 animals showed a late response (LR; RL, Rti, Raw = 178.9 +/- 5.1, 191.3 +/- 11.5, 176.6 +/- 17.3% baseline, respectively). Neither ER nor LR were observed in the saline group.(ABSTRACT TRUNCATED AT 250 WORDS)

reasonable to conclude that if PSR inhibition occurred at a higher PaCO2 during PLV than GV then pulmonary stretch must have been higher during PLV than GV. That is, PSR activity was inhibited during PLV at a higher pressure than during GV since PaCO2 was high during PLV. In addition, since the model studied by Sindelar and coworkers was a small lung lavage–injured cat (2.3 1.0 kg), it is unlikely that the impact of perfluorocarbons on dependent lung would be the same as in an adult human. The difference in the height of the lungs (about 3 to 4 cm vs. 15 to 20 cm) would result in marked differences in the effect of the perfluorocarbon on dependent alveoli. Considering the quantity of perfluorocarbon instilled in adult patients (30 ml/kg or about 2,250 ml, 75 kg adult) versus the studied cats (30 ml/kg or about 69 ml, 2.3 kg) and a perfluorocarbon density of 1.9, it is difficult to conceive that the most gravity-dependent alveolar pressure during both inspiration and expiration would be similar during GV and PLV at the same airway gas pressure. It is important to remember that, during PLV, gas ventilation is provided on top of the perfluorocarbon-filled lungs. It is true that with gas ventilation the perfluorocarbon spreads over a larger lung area. However, there is still a column of fluid on top of dependent alveoli that is pressurized by the gas ventilation. Overall, what is clearly needed is additional research into the use of perfluorocarbon-assisted ventilation and the mechanisms associated with both its beneficial and detrimental effects.

Pressure support ventilation (PSV) is almost universally employed in the management of actively breathing ventilated patients with acute respiratory failure. In this partial support mode of ventilation, a fixed pressure is applied to the airway opening, and flow delivery is monitored by the ventilator. Inspiration is terminated when measured inspiratory flow falls below a set fraction of the peak flow rate (flow cutoff); the ventilator then cycles to a lower pressure and expiration commences. We used linear and nonlinear mathematical models to investigate the dynamic behavior of pressure support ventilation and confirmed the predicted behavior using a test lung. Our mathematical and laboratory analyses indicate that pressure support ventilation in the setting of airflow obstruction can be accompanied by marked variations in tidal volume and end-expiratory alveolar pressure, even when subject effort is unvarying. Unstable behavior was observed in the simplest plausible linear mathematical model and is an inherent consequence of the underlying dynamics of this mode of ventilation. The mechanism underlying the observed instability is "feed forward" behavior mediated by oscillatory elevation in end-expiratory pressure. In both mathematical and mechanical models, unstable behavior occurred at impedance values and ventilator settings that are clinically realistic.

The influence of pulmonary vascular congestion on the response of the airways and lung tissue to low doses of inhaled methacholine (MCh) was studied by inflating a balloon catheter in the left atrium of the heart in six piglets, with an additional five piglets serving as control animals. Congestion alone resulted in small increased in baseline airway (Raw) (14.6 +/- 3.7%) and tissue (Rti) resistance (8. 1 +/- 6.5%). Low-dose inhaled MCh (0.3 mg/ml) increased Raw and Rti in the control group by 10.8 +/- 10.3% and 42.2 +/- 29.5%, respectively. The increase in Raw with MCh in the presence of vascular engorgement was significantly greater (67.8 +/- 18.9%) but the increase in Rti (38.1 +/- 13.2%) was similar to that seen in the control group. Morphometric measurements were performed on transverse sections of large and small airways from nine additional piglets (three congested only, three MCh only, and three congestion plus MCh). The thickness of the inner airway wall was similar in all groups. Compared with MCh only piglets, the thickness of the outer airway wall (between the outer border of the smooth muscle and the surrounding lung parenchyma) was increased (p0.05) in engorged only and engorged plus MCh piglets. Compared with MCh only and engorgement only, the amount of airway smooth muscle shortening was greater (p0.05) in all airway size groups in piglets that underwent engorgement plus MCh challenge. The results of this study demonstrate that pulmonary vascular engorgement, induced by increased left atrial pressure, selectively enhances the airway, but not the parenchymal, response to inhaled MCh. These changes are associated with increased thickness of the outer airway wall in response to vascular congestion, suggesting that uncoupling of the mechanical interdependence between the airway smooth muscle and the lung parenchyma may have occurred. Mechanical uncoupling may reduce the load opposing smooth muscle shortening resulting in increased airway narrowing in response to low doses of inhaled methacholine.

With great interest we read the recent article by Kacmarek and colleagues (1). In the trial reported therein, the authors conclude that partial liquid ventilation (PLV) results in a greater number of serious adverse effects and does not improve outcome compared with conventional ventilation in patients with severe ARDS. As one of the reasons for a higher complication rate, the authors suggest the high peak alveolar pressure due to the additional hydrostatic pressure exerted by the perfluorocarbon (PFC), which has to be added to the measured airway pressure. It is obvious that a measurement of the hydrostatic pressure is associated with technical difficulties, though it is possible to estimate it. In this study the PFC was instilled to the carina in the supine position. Therefore, the maximal hydrostatic pressure (cm H2O) can be calculated by multiplying the distance between the liquid surface and the deepest point in the thorax, the dorsovisceral pleura (in cm), and the specific density of the PFC, which is 1.92. To evaluate the effective additional hydrostatic pressure, we measured 40 patients, ages between 18 and 60 yr, median 44.6 12.8 yr, 60% male sex, who had a thoracic CT in the supine position. On the Diagnostic Workstation (Diagnostic DICOM 3.0 Workstation; Agfa-Gevaert Group, Morstel, Belgium), the distance between the level of the carina and the lowest point of the dorsovisceral pleura was measured with the on-screen tool. The median distance retrieved was 7.5 cm 1.2 cm. Using these findings for estimating the actual resulting airway pressure, the distance was multiplied by 1.92. Therefore in the “low-dose” group, the hydrostatic pressure of 14.4 2.36 cm H2O has to be added to the measured plateau pressure as well as to the measured PEEP. Following this estimation, the median plateau pressure would be as high as 45.8 cm H2O with a PEEP of 28.7 cm H2O. These excessively high pressures could explain the higher rate of adverse effects in the “low-dose” group. For the “high-dose” group the resulting pressure would even exceed these findings. As is known from the literature (2), increased airway pressures lead to a worse outcome. Therefore, to avoid barotrauma to the lung during PLV, which probably contributes to a worse outcome, the measured pressure levels during PLV should have been significantly reduced. Therefore, the conclusion based on the findings of this study should be reconsidered.

Mean airway pressure (Pao) has been advocated as a useful index for monitoring hemodynamic performance and risk for barotrauma during mechanical ventilation. This is based on the assumption that Pao closely reflects mean alveolar pressure (Palv). In the present study we have compared Pao with Palv in 12 sedated, paralyzed, mechanically ventilated patients. External PEEP ranged from 0.3 to 8.9 cm H2O. Palv was estimated by measuring Pao after rapid flow interruptions made at different points in time of the breathing cycle, using a modification of the method of Fuhrman and coworkers (4). All subjects exhibited intrinsic PEEP (PEEPi), which ranged from 0.5 to 9.4 cm H2O. A significant negative correlation (p < 0.001) was found between Pao/Palv and PEEPi. On average, at PEEPi of 10 cm H2O, Pao underestimated Palv by about 50%. We conclude that Pao cannot be taken as an index of Palv in patients who exhibit dynamic hyperinflation and PEEPi caused by expiratory flow limitation.

It has been reported that hyperpnea-induced bronchoconstriction in guinea pigs is a potential model for exercise-induced asthma in humans. On the basis of recent studies that show increases in tissue resistance after allergen exposure in sensitized rats, we hypothesized that lung tissues might also be involved in the pathophysiology in this asthma model. We measured tracheal pressure (Ptr) and alveolar pressure (PA) using alveolar capsules in open-chested, mechanically ventilated (respiratory frequency [f] = 1 Hz, tidal volume [VT] = 9 ml/kg, positive end-expiratory pressure [PEEP] = 4 cm H2O) guinea pigs under control conditions (regular breathing of warm, humidified air) and after dry gas hyperpnea challenge (HC, mixture of 95% O2 and 5% CO2, 150 breaths/min, 7 min). We calculated lung elastance (EL) and resistance of lung (RL), tissue (Rti), and airway (Raw) by fitting the equation of motion to changes in Ptr and PA. To assess the effects of volume history, we applied a single deep inflation (three times VT) in five HC animals. We performed morphometric analysis in five control and five HC animals, freezing the lungs with liquid nitrogen and processing the tissues via freeze substitution. HC significantly increased RL, Rti, Raw, and EL (424 +/- 62, 771 +/- 230, 287 +/- 33, 259 +/- 31% baseline, respectively). A deep inflation reduced RL, Rti, Raw, and EL by 30 +/- 4, 31 +/- 4, 29 +/- 6, 23 +/- 5%, respectively. In HC animals, the degree of airway constriction was most prominent in the larger airways; extensive tissue distortion was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)