三维超声测量胎儿肺体积及其在常见胎儿肺病变随访中的应用

目的利用三维超声技术测量胎儿肺体积,建立肺体积正常值范围,评价胎儿肺发育。方法选择显示满意的300胎18～36周正常胎儿肺三维容积图像,利用VOCAL技术测量其左、右肺体积,并对肺总体积(TLV)与孕周(GA)进行回归分析。随机抽取20胎正常胎儿TLV测值进行可信度分析。对4胎超声诊断为肺囊性腺瘤样畸形或隔离肺胎儿进行随访,测量其TLV,与正常胎儿TLV行散点图比较,观察其变化趋势。结果胎儿肺三维图像满意者占91.74%(300/327)。正常胎儿TLV随GA增加而增大,最适回归方程为:TLV=1.139-1.418GA+0.093GA2(r=0.99,P<0.01)。三维超声测量胎儿TLV的可信度很高(内部一致性系数为0.99,组内相关系数为0.99)。4胎肺病变胎儿TLV均随GA增加而增大,但变化趋势各不相同。结论三维超声能够很好地测量胎儿肺体积,在评价胎儿肺发育中具有重要作用。     

Stimulation of human leukocyte elastase by platelet factor 4. Physiologic, morphologic, and biochemical effects on hamster lungs in vitro.

The purpose of this study was to determine if human platelet factor 4 (PF4) stimulates human leukocyte elastase (HLE) against lung elastin. Lung elastin was purified from hamster lungs and tritiated by reduction with NaB3H4. We found that HLE activity against this substrate is increased by concentrations of PF4 as low as 1.6 microgram/ml, and that this stimulation increased linearly with additional PF4. Lungs removed from hamsters and inflated with solutions containing buffer alone, low dose HLE, HLE plus PF4, or PF4 alone were incubated for 2 h at 37 degrees C. Whereas low-dose HLE failed to lower lung elastin when compared to control animals, HLE stimulated by PF4 lowered lung elastin by 20%. PF4 alone had no effect. Furthermore, low-dose HLE failed to alter the mechanical properties of hamster lungs as measured by pressure-volume curves in saline, although there was a significant loss of lung elasticity in the mid- and high-lung volume ranges in lungs treated with HLE and PF4. Morphologic studies revealed that low dose HLE resulted in a minimal emphysemalike lesion whereas HlE plus PF4 caused a significantly more severe lesion. PF4 is capable of stimulating HLE against lung elastin, and this effect may have a role in the pathogenesis of emphysema.     

Elastic properties of the centrilobular emphysematous space

Bronchograms were performed using finely particulate lead on emphysematous lungs obtained at necropsy. X-ray films were taken of these lungs at distending pressures of 0, 5, 10, and 20 cm H(2)O. The volumes of individual centrilobular emphysematous spaces were calculated at each distending pressure from measurements made on these bronchograms and pressure-volume curves were constructed for each space. The pressure-volume characteristics of seven normal lungs and one lung with centrilobular emphysema was also measured. The normal lungs, the lung with centrilobular emphysema, and the centrilobular emphysematous spaces were compared by expressing the volume of air contained in them at each distending pressure as a per cent of the volume contained at 20 cm H(2)O distending pressure. We conclude that centrilobular emphysematous spaces have a high residual volume, are less compliant than normal lung tissue, and are much less compliant than the emphysematous lungs which contain them. Furthermore, these spaces undergo little volume change in the tidal breathing range and probably add a relatively nondistensible series dead space to the surrounding lung parenchyma.     

Estimation of regional lung volume changes by electrical impedance pressures tomography during a pressure-volume maneuver

OBJECTIVE: To assess the degree of linearity between lung volume and impedance change by electrical impedance tomography (EIT) in pigs with acute lung injury and to investigate regional impedance changes during a pressure-volume maneuver. DESIGN AND SETTING: Experimental animal study in a university research laboratory. PATIENTS AND PARTICIPANTS: Nine pigs with lung injury induced by lung lavage. INTERVENTIONS: The lungs were insufflated to four different lung volumes. Next the lungs were inflated in steps up to 40 cm H(2)O and then in steps deflated. MEASUREMENTS AND RESULTS: EIT measurements were performed. Impedance was highly linear with lung volume ( r(2)=0.97). From the pressure-volume maneuver regional pressure-impedance (P-I) curves were obtained in the upper half (ventral) and lower half (dorsal) of the thoracic cross-section. Excellent fit was found of the regional P-I curves with a predefined sigmoid equation ( r(2)=0.998). The P-I curves after lavage were markedly different than before lavage. The P-I curves recorded after lavage displayed a strong heterogeneity on the inflation limb: Lower corner pressure (traditionally lower inflection point) was significantly higher in the dorsal (28.3+/-4.1 cm H(2)O) than in the ventral region (17.5+/-4.3 cm H(2)O). The deflation limb displayed a more homogeneous pattern. Upper corner pressure and true inflection point, where the curve slope is maximal, in the dorsal region were only slightly higher than in the ventral region (1-2 cm H(2)O). CONCLUSIONS: EIT and automated curve fitting provide information on regional lung inflation and deflation which may be of clinical use for optimizing ventilator settings.     

Bleomycin-Induced Diffuse Interstitial Pulmonary Fibrosis in Baboons

Pulmonary fibrosis was induced in eight baboons with bleomycin; five untreated animals were controls. After 45-65 U/kg of bleomycin, lung volumes and diffusing capacity were reduced, and static lung pressure-volume curves were shifted to the right. Right middle lobes were resected at this time in five bleomycin-treated and two control animals. Compared to controls, right middle lobes from bleomycintreated animals had increased weight and contained increased amounts of total protein, collagen, elastin, and DNA; synthesis of collagen and noncollagen protein were also elevated. Occasional alveolar septae were edematous and infiltrated by mononuclear inflammatory cells; a slight increase in collagen was demonstrable histologically. Four of six treated animals died with extensive diffuse interstitial fibrosis after 95 U/kg of bleomycin. Biochemical analyses revealed significantly elevated lobar contents of dry weight, protein, elastin, and collagen. Two animals survived 95 U/kg of bleomycin and were terminated 6 mo after treatment. In these animals, physiologic studies were indicative of restrictive lung disease, but lung histology was nearly normal. Lung weight, total protein, and DNA had returned to control values, but collagen and elastin were increased in amount and concentration. Bleomycin induces an intense inflammatory response in the lung. During this inflammation, connective tissue proliferation occurs in concert with proliferation of other tissue components. Cessation of bleomycin treatment is followed by resolution of inflammation manifested by decreases in tissue mass, cellular content, and nonconnective tissue protein. Collagen and elastin deposited during inflammation are less successfully removed during resolution, leading to a stage characterized by increased concentrations of these proteins. A similar sequence of tissue alterations may occur in idiopathic diffuse interstitial fibrosis of man in response to various lung injuries.     

Static pressure-volume curves of the respiratory system: were they just a passing fad?

PURPOSE OF REVIEW: The aim of this article is to describe the physiologic utility, correlation with lung morphology, difficulties in interpretation and current clinical applications of static respiratory system pressure-volume curves at the bedside in patients with acute lung injury or acute respiratory distress syndrome. RECENT FINDINGS: Complex interpretation of pressure-volume curves indicates that alveolar reopening continues past the lower inflection point on the linear part of the curve and suggests the presence of homogeneous lung disease in which recruitment is still possible by positive end-expiratory pressure application. Setting positive end-expiratory pressure above the lower inflection point and tidal ventilation (approximately 6 ml/kg) in the linear portion of the respiratory system pressure-volume curve improved mortality and ameliorated lung and plasma inflammatory mediators compared with ventilation with the lowest positive end-expiratory pressure at traditional tidal volumes. Recent studies have found that regular use of pressure-volume curves provides useful physiological data that help to optimize mechanical ventilation at the bedside. SUMMARY: The physiologic data obtained by measuring the static pressure-volume curves have helped clinicians to better understand the behavior of the respiratory system when positive-pressure ventilation is applied. The advanced technology incorporated into modern ventilators allows routine measurement of pressure-volume curves under sedation without paralysis, with acceptable variability and no serious adverse effects.     

单肺通气时降低吸入氧浓度对兔肺损伤的影响

目的观察单肺通气(OLV)时降低吸入氧浓度(FiO2)对兔肺损伤的影响。方法新西兰白兔30只,随机均分为三组:60%FiO2组(L组)、100%FiO2组(H组)和对照组即双肺通气(TLV)组(C组,60%FiO2)。L组和H组TLV30min后行右OLV3h,C组TLV30min后继续TLV3h。三组于TLV30min(T0)和OLV10min(T1)、30min(T2)、60min(T3)、120min(T4)、180min(T5)时抽取动脉血行血气分析并计算氧合指数(OI)。股动脉置管监测血压(ABP)、心率(HR),记录气道峰压(Ppeak)。各组实验结束后处死动物,取双侧肺组织行肺病理组织学损伤评分,并测量双侧肺组织匀浆液中超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果与H组比较,L组动脉氧分压(PaO2)在T4、T5时明显降低,动脉氧饱和度(SaO2)在T5时明显降低,T5时SOD含量明显增高,MDA含量明显降低,肺损伤评分降低(P<0.05);H组镜下肺泡腔内可见大量红细胞渗出,L组镜下可见较少的炎性细胞浸润、肺泡渗出液、肺泡间质破坏。结论OLV时降低FiO2到60%虽然增加低氧血症的发生率,但能显著减轻兔肺损伤,这可能与减轻了肺组织氧化应激水平有关。     

Static and dynamic pressure-volume curves reflect different aspects of respiratory system mechanics in experimental acute respiratory distress syndrome.

INTRODUCTION: A lower inflection point, an upper inflection (or deflection) point, and respiratory system compliance can be estimated from an inspiratory static pressure-volume (SPV) curve of the respiratory system. Such data are often used to guide selection of positive end-expiratory pressure (PEEP)/tidal volume combinations. Dynamic pressure-volume (DPV) curves obtained during tidal ventilation are effortlessly displayed on modern mechanical ventilator monitors and bear a theoretical but unproven relationship to the more labor-intensive SPV curves. OBJECTIVE: Attempting to relate the SPV and DPV curves, we assessed both curves under a range of conditions in a canine oleic acid lung injury model. METHODS: Five mongrel dogs were anesthetized, paralyzed, and monitored to assure a stable preparation. Acute lung injury was induced by infusing oleic acid. SPV curves were constructed by the super-syringe method. DPV curves were constructed for a range of PEEP and inspiratory constant flow settings while ventilating at a frequency of 15 breaths/min and tidal volume of 350 mL. Functional residual capacity at PEEP = 0 cm H2O was measured by helium dilution. The change in lung volume by PEEP at 8, 16, and 24 cm H2O was measured by respiratory inductance plethysmography. RESULTS: The slope of the second portion of the DPV curve did not parallel the corresponding slope of the SPV curve. The mean lower inflection point of the SPV curve was 13.2 cm H2O, whereas the lower inflection point of the DPV curve was related to the prevailing flow and PEEP settings. The absolute lung volume during the DPV recordings exceeded (p < 0.05) that anticipated from the SPV curves by (values are mean +/- SEM) 267 +/- 86 mL, 425 +/- 129 mL, and 494 +/- 129 mL at end expiration for PEEP = 8, 16, and 24 cm H2O, respectively. CONCLUSIONS: The contours of the SPV curve are not reflected by those of the DPV curve in this model of acute lung injury. Therefore, this study indicates that DPV curve should not be used to guide the selection of PEEP/tidal volume combinations. Furthermore, an increase in end-expiratory lung volume occurs during tidal ventilation that is not reflected by the classical SPV curve, suggesting a stable component of lung volume recruitment attributable to tidal ventilation, independent of PEEP.     

Respiratory compliance but not gas exchange correlates with changes in lung aeration after a recruitment maneuver: an experimental study in pigs with saline lavage lung injury

Introduction

Atelectasis is a common finding in acute lung injury, leading to increased shunt and hypoxemia. Current treatment strategies aim to recruit alveoli for gas exchange. Improvement in oxygenation is commonly used to detect recruitment, although the assumption that gas exchange parameters adequately represent the mechanical process of alveolar opening has not been proven so far. The aim of this study was to investigate whether commonly used measures of lung mechanics better detect lung tissue collapse and changes in lung aeration after a recruitment maneuver as compared to measures of gas exchange

Methods

In eight anesthetized and mechanically ventilated pigs, acute lung injury was induced by saline lavage and a recruitment maneuver was performed by inflating the lungs three times with a pressure of 45 cmH₂O for 40 s with a constant positive end-expiratory pressure of 10 cmH₂O. The association of gas exchange and lung mechanics parameters with the amount and the changes in aerated and nonaerated lung volumes induced by this specific recruitment maneuver was investigated by multi slice CT scan analysis of the whole lung.

Results

Nonaerated lung correlated with shunt fraction (r = 0.68) and respiratory system compliance (r = 0.59). The arterial partial oxygen pressure (PaO₂) and the respiratory system compliance correlated with poorly aerated lung volume (r = 0.57 and 0.72, respectively). The recruitment maneuver caused a decrease in nonaerated lung volume, an increase in normally and poorly aerated lung, but no change in the distribution of a tidal breath to differently aerated lung volumes. The fractional changes in PaO₂, arterial partial carbon dioxide pressure (PaCO₂) and venous admixture after the recruitment maneuver did not correlate with the changes in lung volumes. Alveolar recruitment correlated only with changes in the plateau pressure (r = 0.89), respiratory system compliance (r = 0.82) and parameters obtained from the pressure-volume curve.

Conclusion

A recruitment maneuver by repeatedly hyperinflating the lungs led to an increase of poorly aerated and a decrease of nonaerated lung mainly. Changes in aerated and nonaerated lung volumes were adequately represented by respiratory compliance but not by changes in oxygenation or shunt.     

Total respiratory compliance as a function of lung volume in patients with mechanical ventilation

In normal subjects breathing spontaneously, complicance has been shown to be influenced by the lung volume from which deflation started. We wondered whether this would also be true for patients with acute respiratory failure who required mechanical ventilation and we accordingly studied 15 such patients. Chest inflation was performed using a continuous flow device (ATM-PV 102), and total compliance was measured as the slope of the pressure-volume relationship during deflation. As inflated lung volumes were increased by 10 to 15, 20 and 25 ml/kg body weight above FRC, mean compliance increased to 38.2, 45.5, 52.2 and 59.3 ml/cmH₂O respectively. Each of these increases in mean compliance was statistically significant (p<0.001). Increasing the inflated lung volume to 30 ml/kg produced no further significant increase in mean compliance. This study showed that, in patients with acute respiratory failure requiring mechanical ventilation, compliance measured during deflation is a function of the inflated lung volume. We recommed that the compliance should be measured from a constant and high lung volume, equal to 25 ml/kg body weight above FRC.     

Effects of positive end-expiratory pressure on hyaline membrane formation in a rabbit model of the neonatal respiratory distress syndrome

Sixteen rabbits were anaesthetized and subjected to saline lavage of the lungs to produce surfactant deficiency. This resulted in an arterial oxygen tension of less than 12 kPa on 100% inspired oxygen and an inflection point on the pressure-volume curve at a pressure of 8–12 mmHg. After lavage the animals were randomly assigned to receive either conventional mechanical ventilation (CMV) with a positive end-expiratory pressure (PEEP) of 1–2 mmHg (group I —low PEEP) or CMV with PEEP equal to the inflection point pressure (group II — high PEEP). Mean airway pressures were kept at 14–16 mmHg in both groups by increasing the inspiratory: expiratory time ratios in the low PEEP group. The 5-h protocol was completed by 4 animals in group I and 6 animals in group II, early death usually being associated with a metabolic acidosis. On 100% oxygen, the mean PaO₂ at 2-h post-lavage was 15.2±8.3 kPa in group I and 39.6±21.8 kPa in group II. Group I had much lower end-expiratory lung volumes (3.0±1.5 ml above FRC) than group II (34.9±12.2 ml above FRC). Histological examination of the lungs revealed significantly less hyaline membrane formation in group II (p=0.001). Thus, the prevention of alveolar collapse by the use of high PEEP levels appears to reduce lung damage in this preparation.     

Repair of protease-damaged elastin in neonatal rat aortic smooth muscle cell cultures.

The objective of this study was to investigate the elastin repair process in the rat aortic smooth muscle cell culture after proteolytic injury. Although little studied in vivo, elastin repair is thought to occur through a sequential process involving enzymatic removal (debridement) of damaged fibers followed by synthesis of tropoelastin, its subsequent processing, and eventual incorporation into new insoluble elastin. A second repair mechanism of proteolytically damaged elastin in a culture system is reported here. Repair in this system relates directly to restoration of resistance to elastin solubilization by hot alkali. As expected, severe injuries were observed with porcine pancreatic elastase (PPE). Using PPE, only 6% of the elastin, relative to control, was resistant to hot alkali immediately after elastase treatment. 4 wk later, resistance to hot alkali had increased dramatically to a mean of 90%. Repair took longer after injury with 75 micrograms of PPE as compared with 50 micrograms of PPE. The limited elastic fiber proteolysis induced by either human neutrophil elastase or porcine trypsin was repaired in culture within 2 wk. Elastin that had been radiolabeled with [3H]lysine 4-5 wk before injury was converted from a hot NaOH-susceptible to a NaOH-resistant elastin fraction during recovery from PPE injury. At the same time, the frayed elastic fibers that were seen with the electron microscope immediately after PPE treatment were replaced by continuous bands of elastin that resembled those in control cultures. Restoration of NaOH resistance did not require a net increase in total cell layer elastin, suggesting that relatively little new tropoelastin incorporation into the cell layer was required for this type of repair. These results suggested a salvage repair mechanism for proteolytically damaged elastin.     

Prevention of Collagen Deposition Following Pulmonary Oxygen Toxicity in the Rat by Cis-4-Hydroxy-l-Proline

Exposure of rats to high oxygen tensions causes increased collagen content of lungs and alveolar enlargement in 3-6 wk. We tested whether cis-hydroxyproline, a proline analogue that inhibits collagen synthesis, could prevent the collagen accumulation and alveolar enlargement. Rats were exposed to hyperoxia for 60 h and then to room air and hyperoxia for alternate 24-h periods for 11.5 d. Treated oxygen-exposed rats received 200 mg/kg cis-hydroxyproline twice daily over the 14-d exposure period. Control rats breathed room air. Examination of lungs on day 14 showed collagen content of oxygen-exposed lungs to be 48% greater than control (P < 0.05). The collagen content of the treated oxygen-exposed lungs was −12% of control (NS). Total lung volume was 16% greater than control in oxygen-exposed rats (P < 0.05) and 8% greater than control in treated oxygen-exposed rats (NS). Morphometric studies showed alveolar size was greater than control in oxygen-exposed rats (188±11 [SE] vs. 143±6 μμl [P < 0.05]). Oxygen-exposed, treated rats had a mean alveolar volume of 150±7 μμl. Lung pressure-volume curves were significantly shifted to the left of control in the oxygen-exposed rats, whereas the curves of the oxygen-exposed, treated group were identical to control. These data suggest that cis-hydroxyproline prevented the accumulation of collagen in the lungs in pulmonary oxygen toxicity. In addition, there was apparent protection from airspace dilatation and decreased lung elasticity, suggesting that alveolar enlargement after oxygen toxicity is linked to the deposition in lung tissue of new connective tissue fibers.     

Peak volume history and peak pressure-volume curve pressures independently affect the shape of the pressure-volume curve of the respiratory system

OBJECTIVE: To determine the specific effect of peak volume history pressure on the inflation limb of the pressure-volume curve and peak pressure-volume curve pressure on the deflation limb of the pressure-volume curve. DESIGN: Prospective assessment of pressure-volume curves in saline, lung lavage injured sheep. SETTING: Large animal laboratory of a university-affiliated hospital. SUBJECTS: Eight female Dorset sheep. INTERVENTIONS:: The effect of two volume history pressures (40 and 60 cm H2O) and three pressure-volume curve peak pressures (40, 50, and 60 cm H2O) were randomly compared. MEASUREMENTS AND MAIN RESULTS: Peak volume history pressure affected the inflation curve beyond the lower inflection point but did not affect the inflection point (Pflex). Peak pressure-volume curve pressure affected the deflation curve. Increased peak volume history pressure increased inflation compliance (p <.05). Increased peak pressure-volume curve pressure increased the point of maximum compliance change on the deflation limb and deflation compliance and decreased compliance between peak pressure and the point of maximum curvature on the deflation limb (p <.05). CONCLUSION: Peak volume history pressure must be considered when interpreting the inflation limb of the pressure-volume curve of the respiratory system beyond the inflection point. The peak pressure achieved during the pressure-volume curve is important during interpretation of deflation compliance and the point of maximum compliance change on the deflation limb.     

Estimation of left ventricular compliance using on-line echocardiographic automated border detection and pressure data

The end-diastolic pressure-volume relationship can be used to describe left ventricular (LV) compliance. The objective of this study was to utilize measurements of LV cavity area by echocardiographic automated border detection and pressure data to estimate the end-diastolic pressure-volume curve in an isolated heart preparation where true volume could be measured by an intraventricular balloon. Six dog hearts were excised for placement of an intraventricular balloon and a micromanometer catheter and perfused in anex vivo circuit. Mid-ventricular short-axis images were used to measure cross-sectional area by automated border detection while LV volumes were increased from 5 ml to maximal volume (30–40 ml) in each preparation. Simultaneous area and pressure data were recorded on a computer workstation through a customized interface with the ultrasound system. Three runs of varying LV volumes at 1 ml increments were performed on each of 6 hearts for a total of 1,080 simultaneous measurements. Pressure-volume and pressure-area curves were analyzed by linear regression analyses, the slope of which was used to estimate compliance. End-diastolic pressure-area and pressure-volume relationships were significantly correlated with mean r=0.97 ± 0.02 (p<0.001) from individual hearts. The slopes which served to estimate compliance of the individual pressure-area and pressure-volume curves were similar and differed by only 7±4%. A similar correlation was observed by second order regression analyses with r=0.97±0.01 (p<0.001) for pressure-area and r=0.98±0.01 (p<0.001) for pressure-volume relationships. The end-diastolic pressure-area curves may potentially be used to estimate LV compliance, although the clinical application of this method remains to be validated.     

Airway pressure-volume curve estimated by flow interruption during forced expiration

The pressure-volume characteristics of the airway downstream to the choke point was estimated with abrupt interruption of airflow at the mouth during forced expiration. The pressure was measured at the mouth and the volume was given by the maximum flow immediately before interruption multiplied by interruption time. The compliance of the airway downstream to the choke point, i.e., a slope of the pressure-volume curve, was 1.04 ml/cmH2O at 50% FVC, and increased in lower lung volumes, in 7 healthy subjects. Whereas, in a case of tracheo-bronchopathia osteochondroplastica, its value decreased markedly.     

Temporal change,reproducibility, and interobserver variability in pressure-volume curves in adults with acute lung injury and acute respiratory distress syndrome

OBJECTIVES: To assess the reproducibility of the static pressure-volume curve of the respiratory system by using a "mini-syringe" technique; to assess the temporal change in upper (UIP) and lower inflection points (LIP) measured from pressure-volume curves of the respiratory system; to assess the inter- and intraobserver variability in detection of the UIP and LIP in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS); and to compare the syringe and multiple occlusion techniques for determining LIP and UIP. DESIGN: Prospective observational study. SETTING: Academic medical-surgical critical care unit. PATIENTS: Consecutive patients with ALI or ARDS. INTERVENTIONS: Static inspiratory pressure-volume curves of the respiratory system were determined twice on day 1 of diagnosis of ALI/ARDS and then once daily for up to 6 days by using the syringe technique. Pressure-volume curves were determined from zero positive end-expiratory pressure. At each time point, three separate measurements of the pressure-volume curve were made to determine reproducibility. A 100-mL graduated syringe was used to inflate patients' lungs with 50- to 100-mL increments up to an airway pressure of 45 cm H2O or a total volume of 2 L; each volume step was maintained for 2-3 secs until a plateau airway pressure was recorded. On day 1, the static pressure-volume curve also was determined by using the multiple occlusion technique. In a random and blinded sequence, the pressure-volume curves were examined visually by three critical care physicians on three different occasions, to determine the intra- and interobserver variability in visual detection of the LIP and UIP. Observers were given objective instructions to visually identify LIP and UIP. MEASUREMENTS AND MAIN RESULTS: Eleven patients were enrolled, with a total of 134 pressure-volume curves generated. LIP and UIP could be detected in 90-94% and 61-68% of curves, respectively. When the three successive pressure-volume curves were compared, both the LIP and UIP were within 3 cm H2O in >65% of curves. The index of reliability (intraclass correlation coefficient) in LIP and UIP was 0.92 and 0.89 for interobserver variability and 0.90 and 0.88 for intraobserver variability. Daily variability was as high as 7 cm H2O for LIP and 5 cm H2O for UIP. When pressure-volume curves obtained by using the multiple occlusion and syringe techniques were compared, LIP was within 2 cm H2O, and UIP was within 4 cm H2O with the two techniques. CONCLUSIONS: The static pressure-volume curve of the respiratory system is reasonably reproducible, thus avoiding the need for multiple measurements at a single time. We found excellent interobserver and intraobserver correlation in manual identification of the LIP and UIP. Both LIP and UIP show appreciable daily variability in patients with ALI/ARDS. The multiple occlusion and syringe techniques generate similar values for LIP and UIP.     

Pulmonary pressure-volume relationship in acute respiratory distress syndrome in adults: Role of positive end expiratory pressure

During the early phase of the acute respiratory distress syndrome in adults (ARDS), pulmonary pressure-volume (P-V) curves exhibit a peculiar pattern, with increased hysteresis and an inflection in the ascending limb (Matamis et al, Chest 86:58-661984). End-expiratory lung volume is also markedly reduced. We traced P-V curves using a 2-L syringe in six patients with ARDS (group 2) and five patients without ARDS (group 1). End-expiratory lung volume, measured using the closed circuit helium dilution technique, was markedly reduced in both groups (39% ± 7% predicted in group 1, and 27% ± 7% in group 2). In the ARDS group, P-V curve was grossly abnormal, with an inflection at low lung volume and increased hysteresis: lung volume difference during inflation and deflation at a pressure 10 cm H₂O higher than end-expiratory pressure was 803 ± 127 mL in group 2 and was only 450 ± 189 mL in group 1. Compliance measured during deflation was only slightly reduced in group 2. Application of first positive end-expiratory pressure 10, then 20 cm H₂O, restored end-expiratory lung volume in all patients, and, in group 2 (ARDS), suppressed the inflection of the ascending limb, reduced hysteresis, and shifted the P-V trace upward and to the left. We conclude that, in ARDS patients, an abnormal pattern of P-V curve is explained by loss of volume, and by increased surface tension, since lung volume was similarly reduced in both groups. Increasing the level of end-expiratory pressure restores the normal pulmonary P-V relationship by suppressing the airway closure.     

Application of continuous positive airway pressure to trace static pressure-volume curves of the respiratory system

OBJECTIVE: To evaluate a new technique for pressure-volume curve tracing. DESIGN: Prospective experimental study. SETTING: Animal research laboratory. SUBJECTS: Six anesthetized rats. INTERVENTIONS: Two pressure-volume curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H2O in 5 cm H2O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further pressure-volume curves were traced. Pressure-volume pairs were fitted to a mathematical model. MEASUREMENTS AND MAIN RESULTS: Pressure-volume curves were equivalent for each method, with intraclass correlation coefficients being higher than.75 for each pressure level measured. Bias and precision for volume values were 0.46 +/- 0.875 mL in basal measurements and 0.31 +/- 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being.97 (.58,.99),.85 (.55,.95), and.94 (.81,.98) (p <.001 for each one). When inflection points were estimated by observers, the correlation coefficient between methods was.90 (.67,.98) for lower inflection points (p <.001). However, estimations for upper inflection points and maximum curvature point were significantly different. CONCLUSIONS: The CPAP method for tracing pressure-volume curves is equivalent to the super-syringe method. It is easily applicable at the bedside, avoids disconnection from the ventilator, and can be used to obtain both the inspiratory and the deflation limbs of the pressure-volume curve. Use of regression techniques improves determination of inflection points.     

Dynamic versus static respiratory mechanics in acute lung injury and acute respiratory distress syndrome

OBJECTIVES: It is not clear whether the mechanical properties of the respiratory system assessed under the dynamic condition of mechanical ventilation are equivalent to those assessed under static conditions. We hypothesized that the analyses of dynamic and static respiratory mechanics provide different information in acute respiratory failure. DESIGN: Prospective multiple-center study. SETTING: Intensive care units of eight German university hospitals. PATIENTS: A total of 28 patients with acute lung injury and acute respiratory distress syndrome. INTERVENTIONS: None. MEASUREMENTS: Dynamic respiratory mechanics were determined during ongoing mechanical ventilation with an incremental positive end-expiratory pressure (PEEP) protocol with PEEP steps of 2 cm H2O every ten breaths. Static respiratory mechanics were determined using a low-flow inflation. MAIN RESULTS: The dynamic compliance was lower than the static compliance. The difference between dynamic and static compliance was dependent on alveolar pressure. At an alveolar pressure of 25 cm H2O, dynamic compliance was 29.8 (17.1) mL/cm H2O and static compliance was 59.6 (39.8) mL/cm H2O (median [interquartile range], p < .05). End-inspiratory volumes during the incremental PEEP trial coincided with the static pressure-volume curve, whereas end-expiratory volumes significantly exceeded the static pressure-volume curve. The differences could be attributed to PEEP-related recruitment, accounting for 40.8% (10.3%) of the total volume gain of 1964 (1449) mL during the incremental PEEP trial. Recruited volume per PEEP step increased from 6.4 (46) mL at zero end-expiratory pressure to 145 (91) mL at a PEEP of 20 cm H2O (p < .001). Dynamic compliance decreased at low alveolar pressure while recruitment simultaneously increased. Static mechanics did not allow this differentiation. The decrease in static compliance occurred at higher alveolar pressures compared with the dynamic analysis. CONCLUSIONS: Exploiting dynamic respiratory mechanics during incremental PEEP, both compliance and recruitment can be assessed simultaneously. Based on these findings, application of dynamic respiratory mechanics as a diagnostic tool in ventilated patients should be more appropriate than using static pressure-volume curves.