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The aim of this study is to assess how analysis of the spectral characteristics of lung sounds can help in detecting lung injury and subsequent recruitment as verified by computed tomography (CT).Lung sounds were recorded at four locations (ventral and dorsal on right and left side) in six ventilated pigs before and after unilateral oleic acid-induced lung injury during sequential increase of positive end-expiratory pressure (PEEP) from 0 to 20 cmH(2)O. CT scans of the chest were used for comparison with lung aeration. Sound characteristics were compared by computer-aided analysis in the time and frequency domain as well as by clinicians.The presence of lung injury and its location were detected by substantial acoustic spectral components above 500 Hz (frequency) and -70 dB (amplitude). Application of increasing PEEP gradually reduced the pathological components as CT analysis verified recruitment. At 20 cmH(2)O PEEP there was no further tidal recruitment of injured lung and the pathological sounds had disappeared, rendering the lung sounds of the injured lung similar to those of the control lung. This was mirrored by the clinicians' characterization of the sounds.Computer-aided analysis of lung sounds is suitable for detection of pathological lung sounds and may guide in detection and recruitment of poorly/nonaerated lung.

Following a previous analysis that was performed on lung sounds of right and left apexes [Chaos, Solitons & Fractals 2004;21:869–77], in the present paper we studied tracheal sounds by recurrence quantification analysis, adding chaos analysis as estimation of correlation dimension and Lyapunov spectrum. The results confirm the presence of singularities indicating that respiratory dynamics is controlled by a discrete non-deterministic dynamics based on violation of Lipschitz conditions. On the basis of the results, it is also evidenced the possibility to introduce new indexes having interest in respiratory diagnostic routine.

Using Recurrence Quantification Analysis it was possible to detect singularities in non-stationary lung sounds recorded on both right and left apexes. This result indicates that respiratory dynamics is controlled by a discrete non-deterministic dynamics based on violation of Lipschitz conditions.

In this study we evaluated whether a technology based on artificial neural networks (ANN) could estimate the static compliance (C(RS)) of the respiratory system, even in the absence of an end-inspiratory pause, during continuous mechanical ventilation. A porcine model of acute lung injury was used to provide recordings of different respiratory mechanics conditions. Each recording consisted of 10 or more consecutive breaths in volume-controlled mechanical ventilation, followed by a breath having an end-inspiratory pause used to calculate C(RS) according to the interrupter technique (IT). The volume-pressure loop of the breath immediately preceding the one with pause was given to the ANN for the training, together with the C(RS) separately calculated by the IT. The prospective phase consisted of giving only the loops to the trained ANN and comparing the results yielded by it to the compliance separately calculated by the investigators. Determination of measurement agreement between ANN and IT methods showed an error of -0.67 +/- 1.52 mL/cm H(2)O (bias +/- SD). We could conclude that ANN, during volume-controlled mechanical ventilation, can extract C(RS) without needing to stop inspiratory flow.We studied the application of artificial neural networks (ANN) to the estimation of respiratory compliance during mechanical ventilation. The study was performed on an animal model of acute lung injury, testing the performance of ANN in both healthy and diseased conditions of the lung.

During positive-pressure ventilation parenchymal deformation can be assessed as strain (volume increase above functional residual capacity) in response to stress (transpulmonary pressure). The aim of this study was to explore the relationship between stress and strain on the regional level using computed tomography in anesthetized healthy pigs in two postures and two patterns of breathing. Airway opening and esophageal pressures were used to calculate stress; change of gas content as assessed from computed tomography was used to calculate strain. Static stress-strain curves and dynamic strain-time curves were constructed, the latter during the inspiratory phase of volume and pressure-controlled ventilation, both in supine and prone position. The lung was divided into nondependent, intermediate, dependent, and central regions: their curves were modeled by exponential regression and examined for statistically significant differences. In all the examined regions, there were strong but different exponential relations between stress and strain. During mechanical ventilation, the end-inspiratory strain was higher in the dependent than in the nondependent regions. No differences between volume- and pressure-controlled ventilation were found. However, during volume control ventilation, prone positioning decreased the end-inspiratory strain of dependent regions and increased it in nondependent regions, resulting in reduced strain gradient. Strain is inhomogeneously distributed within the healthy lung. Prone positioning attenuates differences between dependent and nondependent regions. The regional effects of ventilatory mode and body positioning should be further explored in patients with acute lung injury.

To compare the efficacy of 0.75% levobupivacaine with that of 3% mepivacaine for pain control after surgical removal of impacted mandibular third molars.Forty-two subjects (23 females and 19 males, mean age 23.5 +/- 4) underwent surgical removal of third molars in two separate sessions. Within each patient, levobupivacaine was used to anesthetize one extraction side and for the other side, mepivacaine. Onset of anesthesia, duration of surgery, lip numbness, timing of pain appearance and analgesic consumption were evaluated.There were no significant differences in onset of anesthesia, duration of surgical procedure, and lower lip numbness between the two groups (P.05). Timing of pain appearance and of first drug consumption was significantly lower in the mepivacaine group (P.05). Patients with levobupivacaine anesthesia had significantly lower visual analog (VAS) pain scores at 1 and 2 hours postoperatively than those with mepivacaine anesthesia.Levobupivacaine is a valid alternative to traditional local anesthetics for surgical removal of lower third molars. It presents better pain relief when compared to mepivacaine in the immediate postoperative period as evidenced by lower VAS scores.

Computerized lung sounds analysis offers a new technique to monitor regional ventilation during spontaneous breathing. The purpose of the present study was to assess the acoustic behaviour of the respiratory system in healthy pigs during mechanical ventilation when a positive end-expiratory pressure (PEEP) is applied. Lung sounds were recorded during mechanical ventilation and different PEEP levels of 0, 5, 10, 15 and 20 cm H(2)O were applied. The increase in end-expiratory lung volume (EELV) related to the PEEP application was also measured and the correlation between changes in EELV (DeltaEELV) and sound amplitude (DeltaA) was examined. The amplitude of normal lung sounds was reduced by application of PEEPor=10 cm H(2)O (P0.05). The increase in PEEP from 0 to 20 cm H(2)O reduced the acoustic energy of lung sounds recorded at ZEEP by 0.3 dB (PEEP 5), 2 dB (PEEP 10), 5 dB (PEEP 15) and 7 dB (PEEP 20), which corresponds to 1%, 6%, 14% and 21% in acoustic attenuation, respectively. The variations in DeltaA correlated with changes in lung volume (P0.05) and with changes in compliance of the respiratory system (P0.05), but were not correlated with changes of the resistance of respiratory system. The frequency analysis showed a downward shifting of the spectra at frequencies between 150 and 600 Hz for PEEP levelsor=10 cm H(2)O and frequencies between 75 and 600 Hz for PEEP levelsor=15 cm H(2)O. The application of increasing levels of PEEP reduced the amplitude and changed the spectral characteristics of normal lung sounds.

We evaluated 1) the performance of an artificial neural network (ANN)-based technology in assessing the respiratory system resistance (Rrs) and compliance (Crs) in a porcine model of acute lung injury and 2) the possibility of using, for ANN training, signals coming from an electrical analog (EA) of the lung. Two differently experienced ANNs were compared. One ANN (ANNBIO) was trained on tracings recorded at different time points after the administration of oleic acid in 10 anesthetized and paralyzed pigs during constant-flow mechanical ventilation. A second ANN (ANNMOD) was trained on EA simulations. Both ANNs were evaluated prospectively on data coming from four different pigs. Linear regression between ANN output and manually computed mechanics showed a regression coefficient ( R) of 0.98 for both ANNs in assessing Crs. On Rrs, ANNBIO showed a performance expressed by R= 0.40 and ANNMOD by R = 0.61. These results suggest that ANNs can learn to assess the respiratory system mechanics during mechanical ventilation but that the assessment of resistance and compliance by ANNs may require different approaches.

Objective: Cardiopulmonary bypass (CPB) is associated with abnormalities of lung function characterized by an increase in static elastance of the respiratory system. We examined the following: a) the effects of CPB on the total inspiratory volume-pressure (V-P) relationship of the respiratory system; b) the relative contribution of the chest wall and lung to the impairment of respiratory system mechanics; and c) the time-course of such impairment. Design: Prospective, interventional study. Setting: Surgical and medical intensive care units in a teaching hospital. Patients: Eight adult patients scheduled for elective open heart surgery to correct valvular dysfunction. Interventations: V-P curves (interrupter technique) of the respiratory system were partitioned between the chest wall and lung by measurements of esophageal pressure. Measurements were obtained before stemotomy (control), immediately after, 4 hrs after, and 7 hrs after separation from CPB. Measurements and Main Results : Control V-P relationships of the respiratory system and lung showed lower inflection points (P flex ) at pressure values of 5.9 ± 2.3 and 4.3 ± 2.5 cm H 2 O, respectively. Immediately after and 4 hrs after separation from CPB, both curves had sigmoid shapes because of lower P flex and formation of upper inflection (UIP) points. The pressures corresponding to the P flex increased significantly (p

The incorporation of microprocessors into the design of ventilators has produced a confounding array of products, each with its own peculiar features and modes of operation. This confusion has been compounded in the medical literature with unproved statements favouring one new device or mode of ventilation over another. We believe that physicians concerned with the ventilatory management of patients with respiratory failure must base their approach on physiologic principles and an understanding of patient-ventilator interactions [1].

Proportional assist ventilation (PAV) [1–3] is an innovative ventilatory assistance technique devised by Dr. Magdy Younes of Manitoba University and intended for clinical use in patients who, though having an adequate respiratory “drive”, are not capable of “sustaining” the respiratory work completely.

Background Acute respiratory failure may develop in patients with chronic obstructive pulmonary disease because of intrinsic positive end-expiratory pressure (PEEPi) and increased resistive and elastic loads. Proportional assist ventilation is an experimental mode of partial ventilatory support in which the ventilator generates flow to unload the resistive burden (flow assistance: FA) and volume to unload the elastic burden (volume assistance: VA) proportionally to inspiratory muscle effort, and PEEPi can be counterbalanced by application of external PEEP. The authors assessed effects of proportional assist ventilation and optimal ventilatory settings in patients with chronic obstructive pulmonary disease and acute respiratory failure. Methods Inspiratory muscles and diaphragmatic efforts were evaluated by measurements of esophageal, gastric, and transdiaphragmatic pressures. Minute ventilation and breathing patterns were evaluated by measuring airway pressure and flow. Measurements were performed during spontaneous breathing, continuous positive airway pressure, FA, FA+PEEP, VA, VA+PEEP, FA+VA, and FA+VA+PEEP. Results FA+PEEP provided the greatest improvement in minute ventilation (89 +/- 3%) and dyspnea (62 +/- 2%). The largest reduction in pressure time product per breath of the respiratory muscles and diaphragm (44 +/- 3% and 33 +/- 2%, respectively) also was observed during FA+PEEP condition. When VA was added to this setting, a reduction in respiratory rate (50 +/- 3%), an increase in inspiratory time (102 +/- 6%), and a further reduction in pressure time product per minute (65 +/- 2% and 64% for the respiratory muscles and diaphragm, respectively) was observed. However, values of pressure time product per liter of minute ventilation during FA+VA+PEEP did not differ with those observed during FA+PEEP condition. Worsening of patient-ventilator interaction and breathing asynchrony occurred when VA was implemented. Conclusions Application of PEEP to counterbalance PEEPi and FA to unload the resistive burden provided the optimal conditions in such patients. Ventilator over-assistance and patient-ventilator asynchrony was observed when VA was added to this setting. The clinical use of proportional assist ventilation should be based on continuous measurements of respiratory mechanics.

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.

Conflicting data are available on the relative contribution of the chest wall (cw) to the intrinsic positive end-expiratory pressure of the total respiratory system (PEEPi,rs) in patients with chronic obstructive pulmonary disease (COPD). In order to assess the chest wall and lung contribution to the elastic properties of the respiratory system in COPD patients during acute ventilatory failure, using the "interrupter technique", static inflation volume-pressure (V-P) curves of the total respiratory system (rs), lung (L) and cw were obtained in seven mechanically-ventilated COPD patients during application of zero end-expiratory pressure (ZEEP) and different levels (0-15 cmH2O) of PEEP. On ZEEP, PEEPi,rs was present in all patients (range 10.5-13.1 cmH2O), to which PEEPi,cw and PEEPi,L contributed 17 +/- 2 and 83 +/- 1%, respectively. The static V-P curves of the rs, L, and cw on ZEEP were concave toward the horizontal axis, indicating that elastance increased with inflating volume. Application of PEEP did not affect lung and chest wall mechanics until PEEP levels exceeding 90% of PEEPi,cw on ZEEP (critical value of PEEP (Pcrit)). At PEEP levels higher than Pcrit, and relative to the V-P curves on ZEEP, we observed that: 1) the V-P curve of the rs showed an initial shift along the curve on ZEEP followed by a downward displacement with inflating volume; 2) the V-P curve of the L was shifted along the curve on ZEEP throughout inflating volume; and 3) the V-P curve of the cw was initially displaced along the curve on ZEEP, whilst a downward displacement appeared at higher lung volume. In conclusion, our data show that, in chronic obstructive pulmonary disease patients with flow limitation, the increase in pleural pressure does not make a significant contribution to the intrinsic positive end-expiratory pressure of the total respiratory system. However, during tidal ventilation, a substantial increase in elastance of the chest wall is present. The critical values of positive end-expiratory pressure below which there are no changes in chest wall and lung mechanics amount to 90% of the total PEEPi,rs on ZEEP. Positive end-expiratory pressure levels higher than such critical value cause important alterations of the elastic properties of the lung and chest wall.

In patients with acute respiratory distress syndrome (ARDS), a ventilator strategy based on large tidal volumes (VT) and PEEP has been proposed [1–4]. VT of 10–15 mL/kg are used to prevent the micro atelectasis that accompanies shallow breathing, adjusting respiratory rate to normalize pH and/or arterial carbon dioxide tension (PaCO2). Sufficient levels of positive end-expiratory pressure (PEEP) to recruit previously collapsed alveoli and ensure arterial oxygenation at an inspiratory oxygen fraction (FiO2) that does not cause oxygen toxicity, have also been suggested [1–4].

To examine the effects of external positive end-expiratory pressure (PEEP) on right ventricular function in chronic obstructive pulmonary disease (COPD) patients with intrinsic PEEP (PEEPi).Prospective study.General intensive care unit in a university teaching hospital.Seven mechanically ventilated flow-limited COPD patients (PEEPi = 9.7 +/- 1.3 cmH2O, mean +/- SD) with acute respiratory failure.Hemodynamic and respiratory mechanic data were collected at four different levels of PEEP (0-5-10-15 cmH2O).Hemodynamic parameters were obtained by a Swan-Ganz catheter with a fast response thermistor. Cardiac index (CI) and end-expiratory lung volume (EELV) reductions started simultaneously when the applied PEEP was approximately 90% of PEEPi measured on 0 cmH2O (ZEEP). Changes in transmural intrathoracic pressure (PEEPi,cw) started only at a PEEP value much higher (120%) than PEEPi. The reduction in CI was related to a decrease in the right end-diastolic ventricular volume index (RVEDVI) (r = 0.61; p0.001). No correlation between CI and transmural right atrial pressure was observed. The RVEDVI was inversely correlated with PEEP-induced changes in EELV (r = -55; p0.001), but no with PEEPi,cw (r = -0.08; NS). The relationship between RVEDVI and right ventricular stroke work index, considered an index of contractility, was significant in three patients, i.e., PEEP did not change contractility. In the other patients, an increase in contractility seemed to occur.In COPD patients an external PEEP exceeding 90% of PEEPi causes lung hyperinflation and reduces the CI due to a preload effect. The reduction in RVEDVI seems related to changes in EELV, rather than to changes in transmural pressures, suggesting a lung/heart volume interaction in the cardiac fossa. Thus, in COPD patients, application of an external PEEP level lower than PEEPi may affect right ventricular function.

Background In patients with acute respiratory distress syndrome (ARDS), the ventilatory approach is based on tidal volume (VT) of 10-15 ml/kg and positive end-expiratory pressure (PEEP). To avoid further pulmonary injury, decreasing VT and allowing PaCO2 to increase (permissive hypercapnia) has been suggested. Effects of 10 cmH2O of PEEP on respiratory mechanics, hemodynamics, and gas exchange were compared during mechanical ventilation with conventional (10-15 ml/kg) and low (5-8 ml/kg) VT. Methods Nine sedated and paralyzed patients were studied. VT was decreased gradually (50 ml every 20-30 min). Static volume-pressure (V-P) curves, hemodynamics, and gas exchange were measured. Results During mechanical ventilation with conventional VT, V-P curves on PEEP 0 (ZEEP) exhibited an upward convexity in six patients reflecting a progressive reduction in compliance with inflating volume, whereas PEEP resulted in a volume displacement along the flat part of this curve. After VT reduction, V-P curves in the same patients showed an upward concavity, reflecting progressive alveolar recruitment with inflating volume, and application of PEEP resulted in alveolar recruitment. The other three patients showed a V-P curve with an upward concavity; VT reduction increased this concavity, and application of PEEP induced greater alveolar recruitment than during conventional VT. With PEEP, cardiac index decreased by, respectively, 31% during conventional VT and 11% during low VT (P < 0.01); PaO2 increased by 32% and 71% (P < 0.01), respectively, whereas right-to-left venous admixture (Qs/Qt) decreased by 11% and 40%, respectively (P < 0.01). The greatest values of PaO2, static compliance, and oxygen delivery and the lowest values of Qs/Qt (best PEEP) were obtained during application of PEEP with low VT (P < 0.01). Conclusions Although PEEP induced alveolar hyperinflation in most patients during mechanical ventilation with conventional VT, at low VT, there appeared to be a significant alveolar collapse, and PEEP was able to expand these units, improving gas exchange and hemodynamics.

The incorporation of microprocessors into the design of ventilators has produced a confounding array of products, each with its own peculiar features and modes of operation. This confusion has been compounded in the medical literature with unproved statements favoring one new device or mode of ventilation over another. We believe that physicians concerned with the ventilatory management of patients with respiratory failure must base their approach on physiologic principles and an understanding of patient-ventilator interactions [1].

Synchronized intermittent mandatory ventilation (SIMV) intermixes assisted and spontaneous breaths. Its ability as a weaning technique has been questioned on the basis that patients show little adaptation to ventilator assistance. We studied inspiratory effort and patient-ventilator interaction at different levels (SIMV, 100, 50, and 0%) of flow-triggered SIMV versus pressure-triggered SIMV in patients during the weaning period. The two triggering systems were evaluated during constant flow and constant pressure mandatory SIMV breaths. Inspiratory effort was estimated as the esophageal pressure time product (PTP) per breath (PTP/b) and per minute (PTP/min). The PTP/b and PTP/min of both mandatory and spontaneous breaths were significantly lower during flow triggering than during pressure triggering SIMV, irrespective of the ventilatory mode. During pressure-triggered SIMV PTP/b and PTP/min were identical for mandatory and spontaneous breaths, whereas during flow-triggered SIMV PTP/b and PTP/min were significantly lower for mandatory than for spontaneous breaths. This difference was greatest when flow triggering and constant pressure ventilation were associated. These data show that flow triggering reduces inspiratory effort during both mandatory and spontaneous SIMV breaths and obtains a better patient-ventilator interaction.

The effects of positive end-expiratory pressure (PEEP) on static ("rapid airway occlusion" technique) and dynamic ("constant flow" technique) volume-pressure (V-P) curves were studied in 19 patients with adult respiratory distress syndrome (ARDS). To describe the shape of both curves, the nonlinear coefficient of a second-order polynomial equation fitted to the static (static nonlinear coefficient) and dynamic (dynamic nonlinear coefficient) V-P curves on zero end-expiratory pressure (ZEEP) was used. Two distinct patterns were observed: (1) in ten patients, the static and dynamic V-P curves on ZEEP exhibited a convex shape with a progressive decrease in slope with increasing inflation volume (nonlinear coefficients: negative). In these patients PEEP induced a volume displacement along the static and dynamic V-P curves on ZEEP (hyperinflation). (2) In nine patients, the static and dynamic V-P curves on ZEEP showed a concave shape with a progressive increase in slope with increasing volume (nonlinear coefficients: positive) and PEEP shifted both curves upward along the volume axis (alveolar recruitment). A correlation (p < 0.0001) between static and dynamic nonlinear coefficients was found at all levels of PEEP. Both static and dynamic nonlinear coefficients on ZEEP were correlated (p < 0.0001) with the amount of lung volume recruited with PEEP, and the variations of cardiac index (CI), O2 delivery (DO2), right-to-left venous admixture (Qs/Qt), and PaO2 with PEEP. Besides, the effects of PEEP on Cl, DO2, Qs/Qt, and PaO2 were less pronounced (p < 0.001) in patients with convex V-P curves than in patients with concave V-P curves.(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEPi) are observed in patients with chronic obstructive pulmonary disease (COPD) and flow limitation. Several reports suggest that PEEP levels approaching PEEPi reduce inspiratory load due to PEEPi, without further hyperinflation. Hence PEEP should not increase intrathoracic pressure or affect hemodynamics and gas exchange. To verify this hypothesis, the effects of PEEP (0 to 15 cm H2O) on respiratory mechanics, hemodynamics, and gas exchange were studied in nine COPD patients during controlled mechanical ventilation. PEEP levels approaching PEEPi (9.8 +/- 0.5 cm H2O) did not affect the expiratory flow/volume relationship, confirming the presence of flow limitation. PEEP levels of 5 and 10 cm H2O did not change lung volume and PEEPi in the respiratory system (PEEPtot,rs) and chest wall (PEEPtot,cw) or affect hemodynamics and gas exchange. When applied PEEP overcame PEEPi, changes in lung volume and the expiratory flow/volume relationship were observed. PEEPtot,rs and PEEPtot,cw also increased. Under these circumstances, PEEP increased static elastance in both the respiratory system and the chest wall, reducing cardiac index and affecting hemodynamics and gas exchange. Our data show that in mechanically ventilated COPD patients with PEEPi due to flow limitation, PEEP levels exceeding the 85% of PEEPi (Pcrit) caused further hyperinflation and compromised hemodynamics and gas exchange.

Eight patients mechanically ventilated for acute respiratory failure were submitted to increasing levels of PEEP, from 0 to 15 cm H2O. Right ventricular ejection fraction (RVEF) and end-diastolic volume index (RVEDVI) were measured using the fast response thermistor Swan-Ganz catheter. PEEP induced a linear decrease of cardiac index, while the pulmonary artery pressure increased. In three patients (group A) with a RVEDVI larger than 120 ml at ZEEP, RVEF decreased and RVEDVI increased with PEEP. In the other five patients (RVEDVI less than 120 ml, group B), RVEF was unchanged and RVEDVI decreased at PEEP 15 cm H2O. This study suggest that RV changes induced by PEEP are probably a function of the initial RVEF and RVEDVI.

PEEP is indicated in patients with COPD only to unload the respiratory muscles from the auto-PEEP resulting from expiratory flow limitation. If auto-PEEP is not caused by flow limitation, application of PEEP will cause further hyperinflation, worsening respiratory mechanics, muscle activity, and hemodynamics. To assess the presence of expiratory flow limitation correctly, to measure auto-PEEP correctly, and to identify the maximal PEEP level to be used, measurements of flow and opening pressure must be obtained during a brief period of suspended respiratory muscle activity (obtained by sedation) with the patient's own breathing pattern reproduced accurately.