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The acute respiratory distress syndrome (ARDS) is a very serious pathology caused by inflammation of the lung, usually infectious or traumatic. The alveoli are filled with inflammatory fluid, impairing gas exchange. Mechanical ventilation is the inevitable treatment, but it must ensure specific levels of alveolar pressure, tidal volume, and positive end-expiratory pressure (PEEP) not to exacerbate inflammation and ARDS. This is called protective ventilation but it does not always guarantee satisfactory blood gases, only the extra-corporeal membrane oxygenation (ECMO) can provide. Management of ARDS patient under ECMO is complex because it combines the care related to intensive care patient, very restrictive mechanical ventilation and ECMO. Intensive care nurse requires a very good knowledge of lung disease and respiratory assistance constraints, whether ventilatory or extra-corporeal.

Summary Body plethysmography allows to assess functional residual capacity ( FRC pleth ) and specific airway resistance ( sRaw ) as primary measures. In combination with deep expirations and inspirations, total lung capacity (TLC) and residual volume (RV) can be determined. Airway resistance ( Raw ) is calculated as the ratio of sRaw to FRC pleth . Raw is a measure of airway obstruction and indicates the alveolar pressure needed to establish a flow rate of 1 L s −1 . In contrast, sRaw can be interpreted as the work to be performed by volume displacement to establish this flow rate. These measures represent different functional aspects and should both be considered. The measurement relies on the fact that generation of airflow needs generation of pressure. Pressure generation means that a mass of air is compressed or decompressed relative to its equilibrium volume. This difference is called "shift volume". As the body box is sealed and has rigid walls, its free volume experiences the same, mirror image-like shift volume as the lung. This shift volume can be measured via the variation of box pressure. The relationship between shift volume and alveolar pressure is assessed in a shutter maneuver, by identifying mouth and alveolar pressure under zero-flow conditions. These variables are combined to obtain FRC pleth , sRaw and Raw . This presentation aims at providing the reader with a thorough and precise but non-technical understanding of the working principle of body plethysmography. It also aims at showing that this method yields significant additional information compared to spirometry and even bears a potential for further development.

Background and objective: The origin of frequency dependence of respiratory resistance has been explained by ventilation inhomogeneity; however, it is unclear which components in the respiratory system generate the frequency dependence. The author constructed a 4D pulmonary lobule model and analysed relationships between airflow rate, pressure and airway resistance by the use of computational fluid dynamics. Methods: The lobule model contained bifurcated bronchioles with two adjacent acini in which deformable inter-acinar septa and alveolar duct walls were designed. Constrictive conditions of respective bronchioles were designed, too. 4D finite element models for computational fluid dynamics were generated and airflow simulations were performed under moving boundary conditions of the arbitrary Lagrangean-Eulerean method. From the simulation results, airway resistances for various conditions were calculated. Results: Tissue resistance emerged under the condition of different acinar pressures caused by unequal airway resistances. If the inter-acinar septum was shifted so as to cancel the pressure difference, the acinar pressures were equal in spite of unequal airway resistances, and hence, tissue resistances did not emerge. Therefore, the tissue resistance in the former case is thought to be an index of alveolar pressure inequality (which could be cancelled by mechanical interaction of lung parenchyma), rather than a material property of the tissue itself. Conclusions: Inequality of alveolar pressure decreases as the input oscillatory frequency increases. Therefore, frequency dependence of the respiratory resistance should be regarded as a conditional index of the alveolar pressure inequality caused by heterogeneous changes in the intra-pulmonary airway and/or the lung parenchyma.

Introduction: Potentially recruitable lung has been assessed previously in patients with acute lung injury (ALI) by computed tomography. A large variability in lung recruitability was observed between patients. In this study, we assess whether a new non-radiological bedside technique could determine potentially recruitable lung volume (PRLV) in ALI patients. Methods: Sixteen mechanically ventilated patients with early ALI/ARDS were subjected to a recruitment manoeuvre and decremental PEEP titration. Electric impedance tomography, together with measurements of end-expiratory lung volume (EELV) and tracheal pressure, were used to determine PRLV. The method defines fully recruited open lung volume (OLV) as the volume reached at the end of two consecutive vital capacity manoeuvres to 40 cmH2O. It also uses extrapolation of the baseline alveolar pressure/volume curve up to 40 cmH2O, the volume reached being the non-recruited lung volume. The difference between the fully recruited and the non-recruited volume was defined as PRLV. Results: We observed a considerable heterogeneity among the patients in lung recruitability, PRLV range 11–47%. In a post hoc analysis, dividing the patients into two groups, a high and a low PRLV group, we found at baseline before the recruitment manoeuvre that the high PRLV group had lower compliance and a lower fraction of EELV/OLV. Conclusions: Using non-invasive radiation-free bedside methods, it may be possible to measure PRLV in ALI/ARDS patients. It is possible that this technique could be used to determine the need for recruitment manoeuvres and to select PEEP level on the basis of lung recruitability.

Background The mechanical in-exsufflator (MIE) is commonly used to augment cough in patients with neuromuscular disease from infancy to adulthood. Little is known about the alveolar pressures, lung volumes, and expiratory flow rates generated by the MIE when used via tracheostomy tube in infants and children. Methods A high-fidelity mechanical lung model was programmed to simulate infants with tracheostomy tubes. Generated pressures, volumes, and expiratory flows using the MIE device at variable insufflation/exsufflation pressures and times were recorded. The primary measure of interest was maximal expiratory flow (MEF). Results Pressure equilibration across the tracheostomy tube did not occur with insufflation time 70% vital capacity attained at insufflation pressures as low as 20 cmH2O. Though higher insufflation pressures resulted in increased expiratory flow rates, more negative exsufflation pressure had a greater absolute impact on MEF. Conclusions Using the MIE via tracheostomy tube in an infant lung model, we found that an insufflation time of >1 sec is required for equilibration of insufflation pressure and alveolar pressure. Longer exsufflation time does not significantly alter MEF. Higher insufflation and exsufflation pressures both increased MEF, but greater exsufflation pressure had more substantial impact. Pediatr Pulmonol. 2011; 46:211–217. © 2011 Wiley-Liss, Inc.

Background and objective: The interrupter resistance (Rint) can be calculated from various estimates of alveolar pressure based on mouth pressure during occlusion. We compared Rint, as measured by the opening interrupter technique (Rint1), and the linear back-extrapolation method (Rint2), with the ‘gold standard’ airway resistance measured by plethysmography (Raw). Methods: The study included 32 asthmatic children and 11 children with cystic fibrosis, aged 5 to 18 years, who were categorized into non-obstructed (NObs) (n = 27) and obstructed (Obs) (n = 16) groups. Spirometry and the three different resistance measurements were performed on all children. Rint1 and Raw were assessed after a bronchodilator (BD) test in 16 and nine children, respectively, in the Obs group. Results: Raw (0.48 ± 0.20 kPa.s/L) was lower than Rint1 (1.04 ± 0.34 kPa.s/L) and Rint2 (0.63 ± 0.18 kPa.s/L) (P

A complex dynamic model of the closed cardiovascular and respiratory systems including their interaction is considered. It is proposed to substitute a single-component model of the alveolar volume with a multi-component one. A refined structure of the vascular network based on experimental data is suggested. Resonance properties of the alveolar volume components are investigated with the help of the proposed multi-component model. Computational results are presented showing an amplitude-dependent decrease in oxygen concentration in the venous part of the pulmonary circuit when the alveolar volume is subject to periodic disturbances at its eigenfrequencies

Gas exchange is the main function of the lungs. Oxygen and carbon dioxide diffuse along the gradient of their partial pressures across the alveolar capillary membrane. Lungs have a vast area for gas exchange. Alveolar ventilation and pulmonary circulation are closely interlinked to provide efficient gas exchange in the lungs. This means that gas exchange can be impaired after surgery and in various disease states, leading to hypoxia. Hypoxaemia often results from ventilation–perfusion ( V ⋅ / Q ⋅ ) mismatching and an increase in fractional inspired oxygen ( F i o 2 ) does not fully correct it. A reduced transfer factor for carbon monoxide (TLCO) indicates disease of the pulmonary parenchyma or pulmonary circulation. Various tests are available to assess the pulmonary function including gas exchange. These tests can be used for the purposes of diagnosis, follow-up and fitness for undergoing anaesthesia and surgery.

Pulmonary emphysema is usually the result of chronic exposure to cigarette smoke in at risk individuals. To investigate the hypothesis that lung damage in emphysema results from coincident weakening in the structural properties of the tissue and increased mechanical forces--as one explanation of the continued development of pulmonary emphysema after smoking cessation--we developed a three dimensional, geometric dodecahedron-based acinar model. Using the model numerical analysis of the stress distribution in normal conditions could be compared with those resulting in emphysematous conditions. Finite element analysis was used to evaluate the model at a number of lung inflation levels, using quasi-static loading of the alveolar pressure. When internal alveolar pressure was increased along with the adjustment of the material properties to represent a weakening of one wall in the acinus, increased stress resulted at the perimeters of the weakened area. In particular this increased stress was localized at the junction points of the internal alveolar septa. It was also found that under the proposed simulated emphysematous conditions, a significant disruption in the stress distribution within the acinus model occurred at low, rather than high, lung volumes. This is supportive of the physiological observation that destruction of the diseased tissue can occur under less stress than those existing in the normal state.

Mechanical ventilation is used during respiratory failure in many patients. High-frequency oscillatory ventilation is used as a rescue therapy at adult patients. High-frequency ventilation has minimum monitoring and even tidal volume is not routinely measured. Models of the respiratory system can contribute to better understanding about principle of high-frequency oscillatory ventilation. The identification of simple RLC model is described in the study and effect of lung compliance upon tidal volume and alveolar pressure is discussed. It was shown that reduced lung compliance has a minimal effect upon tidal volume whereas it significantly affects an amplitude of alveolar pressure.

Dynamic hyperinflation during high frequency oscillatory ventilation (HFOV) is defined as a situation when the mean alveolar pressure (mPalv) is higher than the mean airway pressure (mPaw). Lower inspiratory to expiratory time ratio (I:E) is recommended to prevent dynamic hyperinflation. Some studies document a possibility of the opposite effect — dynamic hypoinflation (mPalv

A patient-specific non-uniform pressure outlet boundary condition was developed and used in unsteady simulations of cyclic breathing in a large-scale model of the lung airway from the oronasal opening to the terminal bronchioles. The computational domain is a reduced-geometry model, in which some airway branches in each generation were truncated, and only selected paths were retained to the terminal generation. To characterize pressure change through airway tree extending from the truncated outlets to pulmonary zone, virtual airways represented by extended volume mesh zones were constructed in order to apply a zero-dimensional airway resistance model. The airway resistances were prescribed based on a precursor steady simulation under constant ventilation condition. The virtual airways accommodate the use of patient-specific alveolar pressure conditions. Furthermore, the time-dependent alveolar pressure profile was composed with the physiologically accurate pleural pressure predicted by the whole-body simulation software HumMod, and the transpulmonary pressure evaluated based on lung compliance and local air volume change. To investigate airway flow patterns of healthy and diseased lungs, unsteady breathing simulations were conducted with varying lung compliances accounting for healthy lungs, and lungs with emphysema or interstitial fibrosis. Results show that the simulations using this patient-specific pressure boundary condition are capable of reproducing physiologically realistic flow patterns corresponding to abnormal pulmonary compliance in diseased lungs, such as the hyperventilation in lungs with emphysema, and the demand of more mechanic work for breathing in lungs with fibrosis.

We develop a lung ventilation model based on a continuum poroelastic representation of lung parenchyma that is strongly coupled to a pipe network representation of the airway tree. The continuous system of equations is discretized using a low-order stabilised finite element method. The framework is applied to a realistic lung anatomical model derived from computed tomography data and an artificially generated airway tree to model the conducting airway region. Numerical simulations produce physiologically realistic solutions and demonstrate the effect of airway constriction and reduced tissue elasticity on ventilation, tissue stress and alveolar pressure distribution. The key advantage of the model is the ability to provide insight into the mutual dependence between ventilation and deformation. This is essential when studying lung diseases, such as chronic obstructive pulmonary disease and pulmonary fibrosis. Thus the model can be used to form a better understanding of integrated lung mechanics in both the healthy and diseased states. Copyright © 2015 John Wiley and Sons, Ltd.

Motivated by this evidence, we compare the acid-base parameters with a peculiar feature of hemodialysis patients, namely the percentage of interdialytic weight gain (IWG). This parameter is obtained by measuring the patient weight at time of the blood sampling and that at the end of the previous hemodialysis treatment. As already reported in (1), the mean IWG (±SD) is 2.8 % (±1.6). It turns out that a few percent of the analyzed samples exhibits values of IWG known to be associated with adverse outcome: only 11.2 or 4.1 %, depending on the value chosen to identify the adverse outcome [6]. Remarkably, we find a correlation (r = −0.17) between IWG and pCO2 at high level of significance (p = 0.001). More specifically, with reference to Table 1, we see that by increasing the IWG (say, from below 2 to above 4 %), there is a significant decrease of pCO2 (with p value 0.0002), while the same is not true for other blood gas analysis parameters, for which the p value does not allow us to conclude with sufficient reliability that a change occurs. We may conjecture that the decreasing of pCO2 is the early evidence of subclinical, i.e., asymptomatic, pulmonary interstitial edema, which is typically present before the hemodialysis treatment [7, 8]. Indeed, interstitial and peribronchial edema fluid may leak without interfering with respiratory exchange, as it happens in the case of left heart failure [9] and as it would seem to occur in our dataset in which, by increasing the IWG, the value of pO2 is certainly not decreasing. What is relevant here is that such interstitial edema could cause a mild degree of hyperventilation and consequently may lower the value of pCO2 in asymptomatic hemodialysis patients. This also agrees with recent experimental evidence [10]. Our aforementioned conjecture would explain both the occurrence of lower pCO2 in patients with relatively larger IWG and the frequent occurrence of respiratory Editor

The alveolar air equation allows the accurate estimation of the partial pressure of oxygen in the alveoli using straightforward measurements and assumptions. Once so estimated, arterial oxygen partial pressures may then be simply derived. This derived prediction can be compared with actual measured values to assess the state of respiratory health of a patient under virtually any commonly encountered physiological condition. The understanding of the alveolar air equation requires basic knowledge of gas physics, respiratory physiology and metabolism and so is often considered arcane and difficult. However, these concepts are relatively straightforward and even intuitive once the fundamentals are understood. This article reviews the basis of calculating alveolar air composition in a practical manner and describes how it can be used in the clinical setting with minimal mathematics.

Our aim was to assess the influence of oscillatory frequency, inspiratory-to-expiratory (I:E) ratio and airway pressure on gas trapping during high frequency oscillatory ventilation (HFOV). A lung model was used, which had a high compliance (4.0 ml (cmH(2)O)(-1)) and resistance (160 cmH(2)O l(-1) s(-1)) resulting in a long time constant (0.64 s). To assess whether gas trapping occurred, the mean pressure within the lung model (equivalent to alveolar pressure) was compared to the mean airway pressure (MAP) measured at the manifold (manifold MAP) of the two oscillators used, the SLE 5000 (I:E ratio 1:1) and the Sensor Medics 3100A (tested at I:E ratios of 1:2 and 1:1). The effects were assessed of raising the MAP from 15 to 35 cmH(2)O, the oscillatory amplitude from 30 to 70 cmH(2)O and the frequency from 5 to 15 Hz (5 to 20 Hz SLE only). There were no significant trends for differences between the pressure within the lung model and the 'manifold' MAP to increase (i.e. no evidence of gas trapping), as MAP, amplitude or frequency was increased, regardless of which oscillator or I:E ratio was used. Increasing the pressure amplitude led to a progressive fall in the pressure within the lung model when an I:E ratio of 1:2 was used (p < 0.05). Our results suggest that significant gas trapping does not occur during HFOV even if there is high compliance and resistance.

Polymorphonuclear leukocytes (PMN) play an important role in ventilator-induced lung injury (VILI), but the mechanisms of pulmonary PMN recruitment, particularly early intravascular PMN sequestration during VILI, have not been elucidated. We investigated the physiological and molecular mechanisms of pulmonary PMN sequestration in an in vivo mouse model of VILI. Anesthetized C57/BL6 mice were ventilated for 1 h with high tidal volume (injurious ventilation), low tidal volume and high positive end-expiratory pressure (protective ventilation), or normal tidal volume (control ventilation). Pulmonary PMN sequestration analyzed by flow cytometry of lung cell suspensions was substantially enhanced in injurious ventilation compared with protective and control ventilation, preceding development of physiological signs of lung injury. Anesthetized, spontaneously breathing mice with continuous positive airway pressure demonstrated that raised alveolar pressure alone does not induce PMN entrapment. In vitro leukocyte deformability assay indicated stiffening of circulating leukocytes in injurious ventilation compared with control ventilation. PMN sequestration in injurious ventilation was markedly inhibited by administration of anti-L-selectin antibody, but not by anti-CD18 antibody. These results suggest that mechanical ventilatory stress initiates pulmonary PMN sequestration early in the course of VILI, and this phenomenon is associated with stretch-induced inflammatory events leading to PMN stiffening and mediated by L-selectin-dependent but CD18-independent mechanisms.

A strain energy function for the human alveolar wall in vivo is developed based on its length-tension properties. Using large deformation theory, this function is employed to determine the relationship between circumferential stress and stretch ratio as well as between alveolar pressure and stretch ratio. We find that both the circumferential stress and the pressure in the alveolar wall rise very rapidly if the wall is stretched even slightly more than that which occurs at the pressures attained during mechanical in-exsufflation (MI-E). MI-E involves producing a high inspiratory air pressure and then quickly switching to a large negative air pressure in order to remove mucus from the airways.

Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. In patients who have ARDS or ALI, however, VILI cannot be distinguished from exacerbation of the primary condition. Animal and clinical studies that clearly show elevated levels of cytokines when PPV is applied beyond certain limits support the concept that an inflammatory process is activated by PPV. Whether the induction of inflammatory mediators contributes to the mortality or morbidity of the ventilated patient has not been established. A potential role for anti-inflammatory therapeutic agents is promising. Therefore, the following considerations can guide the clinical care of ventilator patients: Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O. Positive end-expiratory pressure should be applied to avoid end-expiratory collapse and reopening. Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation. Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.

A class of one-compartment models for pressure controlled mechanical ventilation is studied. The resistive pressure term in the general model is of the form: R"1Q + R"2Q|Q| where Q denotes the flow in and out of the compartment. This Rohrer-type model (R"1 0 and R2 0) is compared against the special cases: 1.(i) R"1 = R"L and R"2 = 0 (linear model); 2.(ii) R"1 = 0 and R"2 = R"N (nonlinear model). For clinical ranges of resistances (R"2 and R"2), compliance (C), applied pressure (P"s"e"t), frequency (f), and inspiratory time-fraction (D), the Rohrer model is used to compute the key outcome variables: tidal volume, average volume, end-expiratory pressure, and mean alveolar pressure. These values are compared against those obtained using equivalent RL and RN values. It is demonstrated that for clinically relevant ranges of the physiologic and ventilator parameters, little difference is observed between the Rohrer and nonlinear model.

We evaluated an algorithm for continuous on-line monitoring of alveolar pressure over time in a lung model with lower and upper inflection points and variable resistance ratios and in patients with acute lung injury. The algorithm is based on "static" pressure/volume curves obtained from tracheal pressure measurements under dynamic conditions.Experimental and clinical evaluation of algorithm in a university hospital laboratory and intensive care unit.Ten patients undergoing postoperative respiratory therapy (feasibility of tracheal measurement) and ten patients with acute lung injury undergoing ventilator treatment (evaluation of algorithm).Direct tracheal pressure measurements with a catheter inserted through the endotracheal tube. Comparison of measured alveolar and the dynostatic alveolar pressure vs. time in a lung model with changes in five ventilatory parameters. Examples of clinical monitoring are reported. In the model there was excellent agreement between alveolar pressures obtained by the algorithm, the dynostatic alveolar pressure, and measured alveolar pressure at all ventilator settings. For inspiratory/expiratory resistance ratios between 1:2.1-2.1:1, the dynostatic alveolar pressure was within +/-1.5 cm H(2)O of measured alveolar pressure. In patients the technique for direct tracheal pressure measurement using a catheter inserted through the endotracheal tube functioned satisfactorily with intermittent air flushes for cleansing.Using a thin tracheal pressure catheter inserted through the endotracheal tube alveolar pressure allows continuous bedside monitoring with ease and precision using the dynostatic algorithm. The method is unaffected by tube and connector geometry or by secretions.

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.

A nonlinear mathematical model for pressure controlled, variable compliance ventilation is proposed, solved, and analyzed. The effect of the variable compliance on the key outcome variables, tidal volume, average lung volume, total PEEP, and mean alveolar pressure, is presented. Using human data, the variable compliance model is used to investigate effects of recruitment maneuvers on the key outcome variables.

Background High-frequency oscillatory ventilation (HFOV) allows for small tidal volumes at mean airway pressures (mPaw) above that of conventional mechanical ventilation (CMV), but the effect of HFOV on hemodynamics, oxygen metabolism, and tissue perfusion in acute respiratory distress syndrome (ARDS) remains unclear. We investigated the effects of HFOV and CMV in sheep models with ARDS. Methods After inducing ARDS by repeated lavage, twelve adult sheep were randomly divided into a HFOV or CMV group. After stabilization, standard lung recruitments (40 cmH2O × 40 seconds) were performed. The optimal mPaw or positive end-expiratory pressure was obtained by lung recruitment and decremental positive end-expiratory pressure titration. The animals were then ventilated for 4 hours. The hemodynamics, tissue perfusion (superior mesenteric artery blood flow, pHi, and Pg-aCO2), oxygen metabolism and respiratory mechanics were examined at baseline before saline lavage, in the ARDS model, after model stabilization, and during hourly mechanical ventilation for up to 4 hours. A two-way repeated measures analysis of variance was applied to evaluate differences between the groups. Results The titrated mPaw was higher and the tidal volumes lower in the HFOV group than the positive end-expiratory pressure in the CMV group. There was no significant difference in hemodynamic parameters between the HFOV and CMV groups. There was no difference in the mean alveolar pressure between the two groups. After lung recruitment, both groups showed an improvement in the oxygenation, oxygen delivery, and DO2. Lactate levels increased in both groups after inducing the ARDS model. Compared with the CMV group, the superior mesenteric artery blood flow and pHi were significantly higher in the HFOV group, but the Pg-aCO2 decreased in the HFOV group. Conclusion Compared with CMV, HFOV with optimal mPaw has no significant side effect on hemodynamics or oxygen metabolism, and increases gastric tissue blood perfusion.

The compensatory responses of the respiratory system to simulated central hypervolemia (CHV) were investigated in 14 normal subjects. The central hypervolemia was caused by a short-time passive head-down tilt (HDT, −30°, 30 min). The results show that CHV increased the mechanical respiratory load and the airway resistance, slowed the inspiratory flow, increased the duration of the inspiratory phase, reduced the respiratory rate, but not changed the minute ventilation. CHV induced a significant rise in inspiratory swings of alveolar pressure (184 %), based on the inspiratory occlusion pressure measurement. These changes indicate a compensatory increase in the inspiratory muscle contraction force. A stable level of minute ventilation during CHV was an effect of increased EMG activity of parasternal muscles more than twice (P < 0.01). A contribution of the diaphragm and scalene muscles to ventilation during spontaneous breathing in HDT was reduced. An increase of genioglossus contractile activity during HDT contributed to the stabilization of airway patency. These results suggest that a coordinated modulation of inspiratory muscles activity allows preserving a constant level of minute ventilation during a short-time intrathoracic blood volume expansion. The mechanisms of respiratory load compensation seem to be mediated by afferent information from the lung and respiratory muscle receptors and from the segmentary reflexes and intrinsic properties of the muscle fibers.

Background/Purpose: Pulmonary injury from mechanical ventilation has been attributed to application of excess alveolar pressure (barotrauma) or volume (volutrauma). The authors questioned whether partial liquid ventilation (gas ventilation of the perfluorocarbon filled lung, PLV) would reduce ventilator-induced lung injury. Methods: A tracheostomy tube and carotid artery catheter were placed in anesthetized Sprague-Dawley rats (500 ± 50 g). Bovine serum albumin (BSA) labeled with Iodine (I) 125 was administered intraarterially. Ventilation with tidal volume (TV) of 5 mL/kg was initiated. The rats were then selected randomly to a 30-minute experimental period of one of the following ventilation protocols: continued atraumatic gas ventilation (GV, TV, 5 mL/kg; n=10); atraumatic gas ventilation combined with intratracheal administration of 10 mL/kg perfluorocarbon (GV-PLV, TV, 5 mL/kg, n=10); barotrauma (BT, peak inspiratory pressure [PIP], 45 cm H 2 O; n=10); barotrauma with PLV (BT-PLV, PIP, 45 cm H 2 O; n=8); volutrauma (VT, TV, 30 mL/kg; n=8); or volutrauma with PLV (VT-PLV, TV, 30 mL/kg; n=10). Animals were killed and the amount of radiolabeled BSA in both lungs was measured and normalized to the counts in 1 mL of blood from that animal (injury index). Data were analyzed by analysis of variance (ANOVA) with post-hoc t test comparison between groups. Results: There was a significant difference in the 125 I-BSA injury index when all groups were compared ( P P =.024) and VT versus VT-PLV ( P =.014). Conclusion: 125 I-BSA leak produced during high-pressure or high-volume mechanical ventilation is reduced by partial liquid ventilation. J Pediatr Surg 36:1333-1336. Copyright © 2001 by W.B. Saunders Company.

Background: Closed system suctioning, CSS, has been advocated to avoid alveolar collapse. However, ventilator manufacturers indicate that extreme negative pressure levels can be obtained during closed system suctioning, impeding the performance of the ventilator. Methods: Suctioning with a 12 or 14 Fr catheter with a vacuum level of −50 kPa was either performed with an open technology or a CSS, where the catheter is introduced through a tight-fitting connection through the endotracheal tube, ETT. The lung model was ventilated with a Servo 900C or 300 ventilator with an I:E ratio of 1:2, 1:1 and 2:1 and extrinsic positive end-expiratory pressure (PEEP) at 0 or 10 cm H2O. Respiratory volumes and alveolar pressure were measured at the lung model alveolus. Results: The initial suctioning flow was >40 l/min with a 14 Fr catheter. When inserting the catheter through a no. 7 ETT, PEEP rose from 11 to 23 cm H2O during volume control ventilation with an I:E ratio 1:1. During suctioning the alveolar pressure fell to 10 cm H2O below the set PEEP level. CSS during pressure control ventilation had fewer effects. Low tidal volumes, inverse I:E ratio and secretions in the tube resulted in pressures down to −92 cm H2O. Conclusion: CSS should not be used in volume control ventilation due to risk of high intrinsic PEEP levels at insertion of the catheter and extreme negative pressures during suctioning. Pressure control ventilation produces less intrinsic PEEP effect. The continuous positive airway pressure (CPAP) mode offers the least intrinsic PEEP during insertion of the catheter and least sub-atmospheric pressure during suctioning.

Background: All monitoring of respiratory mechanics should depend on tracheal pressures (Trach-P) as endotracheal tube resistance (ETT-Res) will otherwise distort them. The aim of this study was to investigate factors that may vary ETT-Res, causing difficulties in ETT-Res estimation clinically, and to evaluate a method for direct Trach-P measurements to obviate these problems. Methods: In a model we studied: 1) The influence on ETT-Res caused by different connectors and secretions; 2) Direct Trach-P measurements with a catheter (o.d. 2 mm, i.d. 0.9 mm) with either end or side hole, filled with either air or liquid, introduced through the ETT lumen and evaluated regarding response time and position. Results: The pressure drop between trachea and Y-piece increased by 15% when respectively a swivel connector and a humidification device were connected to the ETT. When injecting 1 ml and 2 ml gel into the ETT lumen the inspiratory resistance increased 100% and 600% respectively. The response time of all catheters was ≤12 ms. During constant flow in inspiratory and expiratory directions the pressure difference between an end hole catheter positioned from 2 cm above the ETT tip to 4 cm below and a reference pressure in the artificial trachea was less than 1.5 cmH2O. Conclusions: ETT connections and secretions cause a variance in resistance. Tracheal pressure can be measured with high precision with an air- or liquid-filled catheter. An end hole catheter placed within 2 cm above or below the ETT tip will give sufficiently precise measurements for clinical purposes.

Patients suffering from chronic obstructive pulmonary diseases, frequently exhibit expiratory airflow limitation. We propose a mathematical model describing the mechanical behavior of the ventilated respiratory system. This model has to simulate applied positive end-expiratory pressure (PEEP) effects during expiration, a process used by clinicians to improve airflow. The proposed model consists of a nonlinear two-compartment system. One of the compartments represents the collapsible airways and mimics its dynamic compression, the other represents the lung and chest wall compartment. For all clinical conditions tested (n=16), the mathematical model simulates the removal of expiratory airflow limitation at PEEP lower than 70–80% of intrinsic end-expiratory pressure (PEEPi), i.e. the end-expiratory alveolar pressure (PAet) without PEEP. It also shows the presence of an optimal PEEP. The optimal PEEP contributes to decrease PAet from 7.4 ± 0.9 (SD) to 5.4 ± 0.9 hPa (p < 0.0001; mild flow limitation) and from 11.8 ± 1.1 to 7.8 ± 0.7 hPa (p < 0.0001; severe flow limitation). Resistance of the collapsible compartment is decreased from 53 ± 7 to 8.2 ± 5.9 hPa.L−1.s (p < 0.0001; mild flow limitation) and from 80 ± 11 to 6.9 ± 5.4 hPa.L−1.s (p < 0.0001; severe flow limitation). This simplistic mathematical model gives a plausible explanation of the expiratory airflow limitation removal with PEEP and a rationale to the practice of PEEP application to airflow limited patients.

Objective: When positive end-expiratory pressure (PEEP) is applied, the intracavitary left ventricular end-diastolic pressure (LVEDP) exceeds the LV filling pressure because pericardial pressure exceeds 0 at end-expiration. Under those conditions, the LV filling pressure is itself better reflected by the transmural LVEDP (tLVEDP) (LVEDP minus pericardial pressure). By extension, end-expiratory pulmonary artery occlusion pressure (eePAOP), as an estimate of end-expiratory LVEDP, overestimates LV filling pressure when pericardial pressure is >0, because it occurs when PEEP is present. We hypothesized that LV filling pressure could be measured from eePAOP by also knowing the proportional transmission of alveolar pressure to pulmonary vessels calculated as index of transmission = (end-inspiratory PAOP - eePAOP)/ (plateau pressure - total PEEP). We calculated transmural pulmonary artery occlusion pressure (tPAOP) with this equation: tPAOP = eePAOP - (index of transmission x total PEEP). We compared tPAOP with airway disconnection nadir PAOP measured during rapid airway disconnection in subjects undergoing PEEP with and without evidence of dynamic pulmonary hyperinflation. Design: Prospective study. Setting: Medical intensive care unit of a university hospital. Patients: We studied 107 patients mechanically ventilated with PEEP for acute respiratory failure. Patients without dynamic pulmonary hyperinflation (group A; n = 58) were analyzed separately from patients with dynamic pulmonary hyperinflation (group B; n = 49). Intervention: Transient airway disconnection. Measurements and Main Results: In group A, tPAOP (8.5 ± 6.0 mm Hg) and nadir PAOP (8.6 ± 6.0 mm Hg) did not differ from each other but were lower than eePAOP (12.4 ± 5.6 mm Hg; p < .05). The agreement between tPAOP and nadir PAOP was good (bias, 0.15 mm Hg; limits of agreement, -1.5-1.8 mm Hg). In group B, tPAOP (9.7 ± 5.4 mm Hg) was lower than both nadir PAOP and eePAOP (12.1 ± 5.4 and 13.9 ± 5.2 mm Hg, respectively; p

To estimate regional lung volume during ventilation with liquids (e.g. perfluorochemicals, PFC) we developed a multi-compartment mathematical model of a lung and thorax. The height of the fluid column and the fluid’s density determine alveolar pressure (P a ). The weight of thoracic contents above any given gravitational plane influences pleural pressure (P pl ). Transpulmonary pressure (P tp =P a− P pl ) and compliance of the lung and chest wall permit estimation of volumes. The results indicate the lung inflates almost uniformly during total liquid ventilation despite a substantial vertical P a gradient. Inflation uniformity is due to the offsetting vertical P pl gradient created by the added weight of the PFC and sustained by the relative rigidity of the chest wall. During partial liquid ventilation our model indicates that the combination of uniform P a with a large vertical gradient in P pl leads to a vertical P tp gradient and therefore relative over-inflation of the top of the lung. This effect increases with increasing PFC dose and with lung height.

Insight into the physiology of a forced expiration is the most important prerequisite for understanding and correctly interpreting the most common pulmonary function tests like spirometry and recording of a maximum expiratory flow-volume curve. Along the airway, intraluminal pressure falls progressively from alveolar pressure in the periphery to atmospheric pressure at the airway opening. Downstream of the equal pressure point, where intraluminal equals transthoracic pressure, the airway is dynamically compressed. Once the forced expiration is flow limited, more transthoracic pressure will rather effect more compression than a further increase in flow. It follows that the achieved maximum expiratory flow rates are then exclusively defined by the resistance of the intrathoracic airways and no longer by muscular effort. The end of a forced expiration is determined by the elastic resistance of the thoracic cage and by airway closure.

Mechanical support of the lungs used to preserve life or during any kind of surgery may have an adverse effect on the cardiovascular system. Usually, positive pressure in alveoli diminishes lung perfusion, venous return and cardiac output. Positive pressure during the respiratory cycle is transfered into the thoracic space. The aim of this study was to assess how synchronization of the respirator with spontaneous breathing influences the distribution of pressure and ventilation in nonhomogeneous lungs and how it should influence hemodynamics. For this purpose a multicompartmental model of respiratory system mechanics was used in the electrical analog of a respirator-lung circuit, which enabled us to simultaneously simulate ventilatory support and spontaneous breathing. Mechanical properties of the respiratory system were modeled by lumped parameters: resistances and capacitances of constant values, independent of lung volume or inspiratory flow changes. A multicompartmental model of the respiratory system enabled us to simulate lung pathology characterized by non-homogeneity of the mechanical properties of the different parts of the lungs. The results of simulations presented in the paper enable us to conclude that lung volume increase, independent of the respirator-patient breathing synchronization, may be modeled as the increase in pulmonary vascular resistance and alveolar pressure increase, dependent on respirator-patient breathing synchronization, may be averaged by esophageous balloon measurements which show intrathoracic pressure changes.

The pressure in the alveoli of the lungs, created by the elastic recoil of the lungs and respiratory muscle activity, is referred to as alveolar pressure (P a ). The extent to which tracheal pressure (P t ) approximates P a depends on the resistance to airflow offered by structures above and below the point at which tracheal pressure is measured. An understanding of the relationship among P a , P t , and upper and lower airway resistance, and how these values fluctuate during speech, could aid in interpretation and modeling of speech aerodynamics. The purpose of this study was to (a) obtain values for lower airway resistance (R law ), (b) use these R law values to estimate P a during speech, and (c) quantify the degree to which P t approximates P a during production of voiced and voiceless sounds, in comparison to inhalation. In addition, the results were discussed in terms of the degree to which the respiratory system functions as a pressure source. Tracheal pressure (obtained with tracheal puncture) and airflow were measured during sentence production in 6 subjects. Using a technique introduced in this paper, R law was determined from measures of tracheal pressure and flow obtained during a sudden change in upper airway resistance because of release of a voiceless plosive. Mean R law values ranged from 0.14 to 0.32 kPa/(l/s). Each subject's mean R law was used to derive a time-varying measure of P a during speech from continuous measures of tracheal pressure and airflow. P t was approximately 95% of P a during phonation (i.e., when the vocal folds were adducted), 75% of P a during release of the voiceless stop consonant /p/, and 55% of P a during inhalation (i.e., when the vocal folds were abducted). Therefore, the degree to which the respiratory system functioned as an ideal pressure source varied during speech. The ability to estimate P a provides a measure of the pressure produced by the respiratory system that is not influenced by laryngeal activity.

Thoracic gas volume (TGV) may be measured and total respiratory impedance (Zrs) may be partitioned into its airway and tissue (Zti) components by combining forced oscillations and plethysmographic measurements of alveolar gas compression (Vpl) (Peslin, Duvivier, 1998, J. Appl. Physiol. 84, 553-561 and 862-867). The method requires that the thermal component of Vpl (Vpl,th) be eliminated by conditioning inspired gas to BTPS. We have evaluated a technically simpler method where Vpl,th is corrected using a thermal gain (G) and a thermal time constant (theta). Zrs and the relationship between Vpl and flow (Hpl) were measured in 15 healthy subjects at frequencies from 4 to 29 Hz. G was obtained from the breathing component of Vpl in phase with volume. Zti and TGV (TGVos) were computed from Zrs and from Hpl after the latter was corrected using G and different values of theta. With theta = 27.5 ms both the difference between TGVos and standard plethysmographic TGV, and the difference between Zti spectra obtained with and without gas conditioning were minimal. We conclude that the simpler method is adequate for both purposes.

The alveolar septum consists of a skeleton of fine collagen and elastin fibers, which are interlaced with a capillary network. Its mechanical characteristics play an important role in the overall performance of the lung. An alveolar sac model was developed for numerical analysis of the internal stress distribution and septal displacements within the alveoli of both normal and emphysematic saline-filled lungs. A scanning electron micrograph of the parenchyma was digitized to yield a geometric replica of a typical two-dimensional alveolar sac. The stress-strain relationship of the alveolar tissue was adopted from experimental data. The model was solved by using commercial finite-element software for quasi-static loading of alveolar pressure. Investigation of the state of stresses and displacements in a healthy lung simulation yielded values that compared well with experimentally reported data. Alteration of the mechanical characteristics of the alveolar septa to simulate elastin destruction in the emphysematic model induced significant stress concentrations (e.g., at a lung volume of 60% total capacity, tensions at certain parts in an emphysematic lung were up to 6 times higher than those in a normal lung). The combination of highly elevated stress sites together with the cyclic loading of breathing may explain the observed progressive damage to elastin fibers in emphysematic patients.

圧支持換気(pressure support ventilation, PSV)の設定圧が肺内でどのように伝播するかを調べるため,PSV中の肺胞圧を測定した。雑種成犬6頭をペントバルビタールで麻酔し,フジシステムズ製内径8.5mmのユニベントチューブを気管挿管した。犬を側臥位とし肋間筋を分け,「閉胸式カプセル法」によりカプセルを肺に接着し,その圧を肺胞圧とした。気管内圧はユニベントチューブのオクルージョンカテーテルより導出した。回路内圧,気管内圧および肺胞圧は圧トランスデューサで測定し,同時にポリグラフで記録した。PSVは呼気終末陽圧(PEEP)5cmH2O,立上がり時間0.5secで,設定圧5,10cmH2Oの2通りを検討した。回路内圧波形は設定圧に達するとプラトーとなったが,気管,肺胞圧波形ではプラトー部分はなかった。気管と肺胞の圧差は設定圧によらず極めて小さかった。正常な犬で肺内の気道抵抗は,PSV時の圧の伝播にほとんど影響を及ぼさないと考えられた。

The determinants of the shape of the pulmonary input impedance spectrum were investigated using a mathematical model based on Womersley's equations for pulsatile flow in constrained viscoelastic tubes and structural data (morphometry, elasticity, and rheology) provided for the entire cat lung by Zhuang et al. Mean distending pressures and diameters of vessels were determined from the structural data and four independent variables: cardiac output and left atrial, pleural, and alveolar pressures. Studies were performed in a control model and a model whose structure was designed to imitate that of a subject with pulmonary vascular impairment. Model simplifications were investigated. Increasing left atrial pressure or cardiac output caused passive distention of vessels that increased total blood volume and decreased vascular resistance, creating a slight spectral shift downward and to the right. Increasing pleural pressure decreased total blood volume and increased vascular resistance, creating a spectral shift upward and to the right. Increasing levels of alveolar pressure resulted in increased vascular resistance and pressures and a shift in blood volume from the capillaries to the arteries without significant change in total blood volume, creating a spectral shift that was slightly downward and to the right . Model simplification studies demonstrated that (1) all vessels distal to the tenth generation (arteries with zero distending pressure diameters < 50 μM) can be modelled as a simple resistor or (2) all vessels distal to the fourth generation can be modelled as a modified Windkessel. Results obtained from the passive studies were consistent with those obtained from normal lambs and lambs with chronically elevated pulmonary blood flow. To model a hypertensive state created by injury to the lung microvasculature, the number and size of small vessels and the compliance constants of all arteries were decreased and the viscoelastic constant was increased, which created the requisite shift to the right and upward. To better match the modulus fluctuation and negative phase angles at higher frequencies in the hypertensive animals, the development of a major reflection site between the main and branch arteries was hypothesized.

There is injury caused in numerous animal species when overdistending airway pressure and volume are delivered. The extent of this injury is attenuated by the application of PEEP. Patient case series point to the benefit of LPVS. In randomized controlled trials, the data may appear confusing. However, based on the data from the Amato and colleagues' trial, it seems prudent to employ an LPVS based on the individual patient's lung mechanics. Based on the trials discussed it appears that many have been convinced of the detrimental effects of high peak alveolar pressure. It remains to convince clinicians of the beneficial effects of the use of higher PEEP early in ARDS based on respiratory system mechanics of the individual patient and to use recruitment maneuvers. In conclusion, I concur with Dreyfuss and Saumon and Slutsky and Tremblay that the use of an LPVS may not only attenuate the severity of ARDS by preventing VALI, but may also prevent MODS or attenuate its severity.

Sir: Patient-ventilator non-synchrony is common [1–6] and may increase morbidity [4]. Some possible reasons for its adverse effects include increased need for sedation, sleep disruption, respiratory muscle injury and errors in assessing weanability (see [7] for review). Extension of the ventilator’s inflation phase much beyond the end of inspiratory effort (delayed cycling-off) is a very common form of non-synchrony, particularly with pressure support (PSV) [2, 3, 5, 6; see 8–10 for mechanisms]. With delayed cycling-off, the lungs are being forcibly inflated when the patient wants them to deflate. When this occurs in alert individuals, it results in considerable discomfort. Often, expiratory muscles are activated in an effort to force cycling-off [11–13]. Airway pressure (PAW) frequently overshoots the set PSV level before the ventilator cycles off [13]. Given the reported expiratory muscle activation in association with delayed cycling-off [11, 12], some researchers interpret the PAW overshoot as indicative of expiratory recruitment in response to delayed cycling-off (i.e. patient is fighting the ventilator). Whereas expiratory muscle activation may result in pressure overshoot, an overshoot need not reflect expiratory muscle activation or even excessive delayed cycling-off. This is important to recognize, since concluding that the patient is fighting the ventilator, or that cycling-off delay is excessive when it is not, may lead to unnecessary sedation or to increasing the cycling-off flow threshold when this is not indicated. The latter situation may result in the equally undesirable premature termination of the inflation cycle. To understand the mechanism of PAW overshoot it is necessary to review how the ventilator controls PAW. When gas is flowing into the patient, PAW (i.e. upstream pressure) is higher than downstream pressure (alveolar pressure; PALV) by an amount corresponding to flow rate and respiratory resistance (RRS; Fig. 1): PAW = PALV + Flow× RRS . Eq. (1)

A general mathematical model for the dynamic behaviour of a single-compartment respiratory system in response to an arbitrary applied inspiratory airway pressure and arbitrary respiratory muscle activity is investigated. The model is used to compute explicit expressions for ventilation and pressure variables of clinical interest for clinician-selected and impedance-determined inputs. The outcome variables include tidal volume, end-expiratory pressure, minute ventilation, mean alveolar pressure, average pleural pressure, as well as the work performed by the ventilator and the respiratory muscles. It is also demonstrated that under suitable conditions, there is a flow reversal that can occur during inspiration.

Lung inflation was compared in isolated perfused lungs of control (C) and chronically hypoxic (CH) rats; in the latter, there is muscularization and loss of compliance in the pulmonary arterial system. During ventilation hypoxia, high alveolar pressure (Palv) elevated the pulmonary artery pressure (Ppa) less in C than in CH rats; Ppa fell during sustained inflation, rose on deflation, and after inflation hypoxic vasoconstriction was attenuated. Opposite changes took place in CH rats; Ppa often rose during inflation, fell on deflation, and after inflation hypoxic vasoconstriction was enhanced. Inflation also increased Ppa more in CH than C rats during air ventilation. Ppa/Palv relations measured during incremental inflation revealed normoxic tone in "extra-alveolar" vessels in both rat groups, which usually increased during hypoxia. In CH, but not C rats, there was also evidence for constriction in "alveolar" vessels during hypoxia. The effects of inflation were not changed by NO synthase blockade in either rat group. Pulmonary hypertensive effects of inflation in chronically hypoxic rats can be attributed to vascular remodelling.

The aim of this study was to assess the respective role of a small elevation in pulmonary capillary pressure, airway pressure, or both on alveolar capillary barrier permeability in an isolated perfused rat lung model.Four groups were studied with low or high airway pressure (LA: 10 mL/kg (tidal volume); HA: 20 mL/kg), low or high pulmonary artery pressure (LP: 9 mm Hg; HP: 12 mm Hg): LALP, HALP, LAHP, and HAHP. The lungs were ventilated and perfused ex vivo for 30 minutes. Quantification of fluorescein isothiocyanate-labeled (FITC) dextran in bronchoalveolar lavage (BAL) fluid and radiolabeled tracers assessed alveolar capillary barrier permeability.BALF FITC-dextran was similar in the three groups with either one or two low-pressure parameters (LALP, LAHP, HALP), but high amounts were found in the HAHP group (375.2 x 10(-6) mg/mL v, respectively, 21.4, 26.2, and 30 x 10(-6) mg/mL, P = .0001). These results were consistent with the albumin space and extravascular lung water: higher values only in the HAHP group statistically different from the other groups (P.002). Interalveolar pore examined with scanning electron microscopy showed an increase in diameters between LALP and HAHP (P.0001).We can conclude that elevation of either the pulmonary artery pressure from 8 to 11 mm Hg or the alveolar pressure from 10 to 15 mm Hg alone does not change the permeability of the alveolar capillary membrane; however, there is an additive effect of these pressures.

Lung tissue resistance (Rti) measured in air-filled guinea pig lungs by the alveolar capsule technique was a large part of total lung resistance (Rl), and we wondered whether similar results applied to saline-filled lungs. We used the micropuncture method to measure alveolar pressure (Palv) in saline-filled lungs of 21 guinea pigs. Palv and airway opening pressure (Pao) were measured before and after a sudden interruption of flow during an inflation or deflation maneuver. On stopping flow, there was an immediate large change in Pao followed by a smaller slower change in Pao. Palv was nearly constant immediately after flow interruption but followed the slower change in Pao. The initial change in Pao on flow interruption was interpreted as the resistive pressure loss in the airways. The small change in Pao and Palv was interpreted as the pressure loss caused by tissue stress adaptation. Airway resistance (R(aw)) and Rti were obtained by dividing the pressure losses by the flow before the interruption. Rl was the sum of R(aw) and Rti. The calcium blocker nifedipine reduced both R(aw) and Rti and abolished the difference in Rti between inflation and deflation. Values of Rti were 10-29% of Rl. However, with correction for viscosity, Rti predicted in air-filled lungs would dominate Rl.

Eleven open-chest piglets were studied to examine the effects of vascular engorgement on partitioned airway and lung tissue mechanics, and to investigate the role of vagal denervation on lung function during engorgement. Alveolar pressure was measured using alveolar capsules. Pulmonary elastance (EL) and resistance (RL), airway (Raw), and tissue (Vti) resistance were calculated during mechanical ventilation. Acute fluid administration with polygeline (10 mL/kg boluses up to a total of 30 mL/kg) resulted in an increase of RL with increases in both Raw and Vti. Vti rose 2-3-fold in comparison with Raw. To increase left atrial pressure, a balloon catheter was inserted into the left atrium of the heart and inflated with different volumes. The responses of EL, RL, Raw and Vti were comparable to those with acute fluid load. Alterations in pulmonary mechanics were closely correlated to mean pulmonary artery blood pressure. In another six animals the effect of vagotomy on vascular engorgement was studied. Vagotomy did not alter baseline airway or tissue mechanics. Furthermore, vagotomy did not influence the change of pulmonary mechanics to fluid load or increase of left atrial pressure. Our data indicate that in young piglets vascular engorgement causes alterations in airway and lung tissue mechanics that are not dependent on vagal influences.

Background Sevoflurane is a new volatile anesthetic agent that may be a useful alternative to halothane for anesthesia in children. However, there is insufficient information about its effects on respiratory mechanics, particularly in the presence of constrictor stimuli. Methods Eighteen piglets had anesthesia induced and maintained with either pentobarbital (control: n = 8), 1 minimum alveolar concentration (MAC) sevoflurane (sevo: n = 5), or 1 MAC halothane (halo: n = 5). Pressure, flow, and volume were measured at the airway opening and used to calculate lung compliance (C(L)) and resistance (R(L)). Resistance was partitioned into airway (Raw) and parenchymal (Vti) components using alveolar pressure. Methacholine was infused intravenously in a dose sufficient (15 microg x kg(-1) x h(-1)) to approximately double R(L). Results The increase in R(L) seen in the control group was almost entirely due to an increase in Vti. Sevoflurane and halothane prevented the increase in R(L) and Vti (both P < 0.02) and the decrease in C(L) (both P < 0.02). Conclusions Sevoflurane and halothane can prevent methacholine-induced changes in lung function.

We studied respiratory system resistance by the interrupter technique (Rint) in healthy and asthmatic children, paying special attention to the effect of cheek compliance and the effects of supporting the cheeks, the influence of lung volume at which interruption was performed, the effect of direction of flow before occlusion (inspiration vs. expiration), and short-term reproducibility of this method. One hundred and thirty-two children (36 controls and 96 asthmatics) were included in the study (mean, 9.0 ± SD 3.6 years). Rint was calculated from the ratio of the alveolar pressure (estimated from mouth pressure during occlusion) to the flow prior to interruption. We observed that (1) underestimation of airway resistance due to upper airway compliance can be minimized by supporting the cheeks; Rint was significantly lower when measured without supporting the cheeks than with support of the cheeks in controls (3.9 ± 0.9 vs. 4.7 ± 1.2 cmH2O · L−1 · s, respectively) and asthmatics (5.2 ± 1.6 vs 6.9 7 plusmn; 2.0 cmH2O · L−1 · s); the quantitative differences of Rint with and without cheek support was larger in small children and in the most obstructed children; (2) performing occlusion at mid-tidal volume accurately reflected the respiratory system resistance of the whole respiratory cycle since we observed no difference in Rint when performing occlusion at different volumes during quiet respiration or at the middle of tidal volume; (3) Rint measured during expiration was higher than Rint obtained during inspiration in controls and in asthmatics; moreover, the effect of direction of flow before occlusion was greater in the small children; (4) Rint was closely correlated to height in controls (r = −0.82; P < 0.001); and (5) short-term reproducibility (at 15 min intervals) was satisfactory in controls and asthmatics (coefficients of variation were 9% and 7%, respectively). Pediatr. Pulmonol. 1997;24:78–85. © 1997 Wiley-Liss, Inc.

In 11 anaesthetised pigs the accuracy of the three-element (WK3) and the four-element (WK4) Windkessel models to describe hemodynamic properties of the pulmonary circulation was compared during six different experimental conditions increasing pulmonary arterial pressure: increase in left atrial pressure, increase in alveolar pressure, increase in pulmonary blood flow, endotoxin shock, mechanical obstruction of left pulmonary artery or histamine infusion. Our results showed that WK4 fitted better the data than did WK3 because values of 1-R2 decreased from 6 percent (WK3) to 1.4 percent (WK4) when WK4 was used (P < 0.0005). 1-R2 was an adequate marker of the accuracy of the linear regression used to solve equations of both models. Compliance values estimated by WK4 were decreased by 5% comparatively to WK3 (P = 0.008). However, this difference can be considered as not physiologically relevant. Values of characteristic resistance corresponding to R1 + (L/R2C) in WK4 and to R1 in WK3 were not different (P = 0.22). The relative changes in R1, R2, and C observed due to the different experimental conditions were comparable regardless of the model. In conclusion, the conversion of WK3 in WK4 by adding an inductance, whose physiological meaning is not clear, resulted in an increased statistical accuracy of the model, but did not seem to have relevant influence on parameters or their evolution during experimental conditions.