Different Syndromes? |
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
ABSTRACT |
|---|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
To assess the possible differences in respiratory mechanics between the acute respiratory distress
syndrome (ARDS) originating from pulmonary disease (ARDSp) and that originating from extrapulmonary disease (ARDSexp) we measured the total respiratory system (Est,rs), chest wall (Est,w) and
lung (Est,L) elastance, the intra-abdominal pressure (IAP), and the end-expiratory lung volume
(EELV) at 0, 5, 10, and 15 cm H2O positive end-expiratory pressure (PEEP) in 12 patients with ARDSp
and nine with ARDSexp. At zero end-expiratory pressure (ZEEP), Est,rs and EELV were similar in both
groups of patients. The Est,L, however, was markedly higher in the ARDSp group than in the ARDSexp
group (20.2 ± 5.4 versus 13.8 ± 5.0 cm H2O/L, p < 0.05), whereas Est,w was abnormally increased in the ARDSexp group (12.1 ± 3.8 versus 5.2 ± 1.9 cm H2O/L, p < 0.05). The IAP was higher in ARDSexp
than in ARDSp (22.2 ± 6.0 versus 8.5 ± 2.9 cm H2O, p < 0.01), and it significantly correlated with Est,w (p < 0.01). Increasing PEEP to 15 cm H2O caused an increase of Est,rs in ARDSp (from 25.4 ± 6.2 to 31.2 ± 11.3 cm H2O/L, p < 0.01) and a decrease in ARDSexp (from 25.9 ± 5.4 to 21.4 ± 55.5 cm
H2O/L, p < 0.01). The estimated recruitment at 15 cm H2O PEEP was 
0.031 ± 0.092 versus 0.293 ± 0.241 L in ARDSp and ARDSexp, respectively (p < 0.01). The different respiratory mechanics and response to PEEP observed are consistent with a prevalence of consolidation in ARDSp as opposed to
prevalent edema and alveolar collapse in ARDSexp.
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The acute respiratory distress syndrome (ARDS) is thought to be a uniform expression of a diffuse and overwhelming inflammatory reaction of the pulmonary parenchyma to a variety of serious underlying diseases. The most frequent causes include sepsis, severe pneumonia, peritonitis, and multiple trauma (1, 2).
However, the possible differences in lung dysfunction between ARDS resulting from pulmonary disease and that resulting from extrapulmonary disease have not been examined systematically. Mechanical properties of the respiratory system may be related to underlying pathology, at least in the early phases of ARDS (3). For instance, when the prevalent pathology is lung tissue consolidation such as in pneumonia, application of positive end-expiratory pressure (PEEP) should induce only a moderate lung recruitment, increased elastance of the respiratory system (i.e., reduction of respiratory compliance), and possible alveolar overdistension. On the other hand, when the prevalent pathology is interstitial edema and alveolar collapse, PEEP should induce remarkable lung recruitment, with a decrease of the elastance of the respiratory system (i.e., increase in respiratory compliance).
We hypothesized that ARDS caused by pulmonary disease is associated with predominant consolidation, whereas ARDS caused by extrapulmonary disease is associated with prevalent interstitial edema and alveolar collapse. To test this hypothesis, we studied patients with ARDS of different origins and divided them into two groups. The first group included patients with ARDS caused by a "direct" insult to the lung, i.e., pulmonary ARDS (ARDSp), and the second group included patients with ARDS developing after an "indirect" insult, i.e., extrapulmonary ARDS (ARDSexp). We report here the respiratory mechanics observed in the two types of the syndrome and discuss possible physiopathologic and clinical implications.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Study Population and Classification of Patients
Approval for this investigation was granted by the Ethical Committee of our Institution, and informed consent was obtained from the next of kin of the patients before inclusion in the study. Between December 1994 and June 1996, 21 unselected consecutive mechanically ventilated patients with ARDS were examined. Nineteen of them were in-hospital patients and two were patients transferred from other hospitals. ARDS was defined according to the criteria established by the American-European Consensus Conference on ARDS (4), i.e., acute onset, PaO2/FIO2 < 200 mm Hg (regardless of PEEP level), bilateral infiltrates seen on frontal chest radiograph, and pulmonary artery occlusion pressure below 18 mm Hg. We excluded patients in whom air leaks prevented a correct measurement of respiratory mechanics.
These 21 patients made up the total population and their data were compared for similarities to and differences from previous studies on ARDS. Twelve patients were assigned to the ARDSp group, and nine were assigned to the ARDSexp group by three independent physicians, blinded as to the results of the measurements, and the clinical course. Assignment was based on history, clinical presentation, and microbiological results (Table 1). As shown in the table all of the patients were studied during the early phase of ARDS. Eleven of the 12 patients with ARDSp had diffuse pneumonia with positive airway cultures, and none had positive blood cultures. In the nine patients with ARDSexp airway cultures were positive in three; these three also had positive blood cultures. Of the nine patients with ARDSexp, seven had undergone surgery 10 ± 7 d before the study.
|
Every patient had an arterial cannula, a Swan-Ganz pulmonary- artery catheter and a urinary catheter inserted for clinical monitoring. The Simplified Acute Physiology Score (SAPS) (5) and the number of organ dysfunctions (6) were recorded on the day of the study. The characteristics of the patients population are summarized in Table 2.
|
Procedure
In all patients while in the supine position, we measured the elastic properties of the lung and chest wall (in triplicate), the end-expiratory lung volume (EELV), and the intra-abdominal pressure at four different PEEP levels (0, 5, 10, and 15 cm H2O) applied in random order. The other ventilator settings were kept constant throughout the entire protocol, which lasted between 25 and 30 min.
All the patients were ventilated with a Siemens Servo 900 C ventilator in the volume control mode with constant inspiratory flow (Table 3). The patients of both groups were ventilated following the guidelines recommended by the American College of Chest Physicians (7). Before the investigation, the patients were sedated with fentanyl (2 to 3 µg/kg) and diazepam (0.1 to 0.2 mg/kg), and paralyzed with pancuronium bromide (0.1 to 0.2 mg/kg).
|
Respiratory Mechanics
Respiratory mechanics were assessed as previously reported (8). Airway pressure (Pao) and gas flow were measured and recorded by a computerized system (CP-100 Pulmonary Monitor; Bicore Monitoring System, Irvine, CA) at the endotracheal tube opening. Esophageal pressure (Pes) was determined from an esophageal balloon inflated with 0.5-1 ml of air, positioned at the lower third of the esophagus, as confirmed by the chest roentgenograph. The validity of Pes was verified by the "occlusion test" according to the principle of Baydur and colleagues (9). Volume was obtained by digital integration of the flow signal.
Static Elastance of Total Respiratory System, Lung, and Chest Wall
We recorded Pao and Pes during a 3 to 4 s airway occlusion at end-
expiration and at end-inspiration. Static elastance of the total respiratory system (Est,rs) was computed as Est,rs = DPao/VT, where DPao
is the difference between end-inspiratory and end-expiratory airway
pressure and VT is the tidal volume. Static elastance of the chest wall
(Est,w) was computed as DPes/VT, where DPes is the difference between end-inspiratory and end-expiratory esophageal pressure. Static
lung elastance (Est,L) was calculated as (Est,L = Est,rs Est,w).
End-expiratory volume corresponded to the elastic equilibrium volume in each patient, as evidenced by zero flow during an expiratory
pause and absence of changes in Pao after airway occlusion.
Resistance of the Total Respiratory System, Lung, and Chest Wall
Maximal (Rmax,rs) and minimal (Rmin,rs) resistances of the respiratory system were computed from Pao as (Pmax' P2)/
and (Pmax'
P1)/, where Pmax' is the maximal pressure value after occlusion corrected for the tube resistance, P1 is the pressure recorded after the immediate drop from Pmax, P2 is the plateau pressure and is the flow
immediately preceding the occlusion. Rmin,rs represents the "ohmic"
resistive component of the respiratory system, and Rmax,rs includes
Rmin,rs plus the "additional" respiratory resistance (DR,rs) caused
by stress relaxation and/or time-constant inequalities within the respiratory system tissues. Because there was no appreciable drop in Pes
immediately after the occlusion (i.e., P1 in the esophageal tracings was
not identifiable), Rmin,rs reflects essentially airway resistance
(Rmin,L), and minimal chest wall resistance (Rmin,w) can be considered negligible. As a consequence, maximal chest wall resistance
(Rmax,w) is entirely due to the viscoelastic properties of the chest
wall tissues (i.e., Rmax,w = DR,w). "Additional" resistance of the
lung (DR,L) was obtained as DR,rs-DR,w whereas the sum of
Rmin,L + DR,L gives the maximal lung resistance (Rmax,L).
End-expiratory Lung Volume (EELV)
EELV was measured at zero end-expiratory pressure (ZEEP) using a
closed-circuit helium dilution method (10). To compute EELV at
each level of PEEP, we measured the total exhaled volume after
PEEP removal during an expiratory period long enough to reach zero
flow. This total exhaled volume represented the volume of the lung
above the EELV at ZEEP, at the end of tidal inspiration. Therefore,
EELV was computed as: EELV at ZEEP + (total exhaled volume tidal volume).
Estimated Lung Recruitment
To estimate the lung recruitment by PEEP, we had to differentiate, in
the measured lung volume, the component caused by the inflation of
pulmonary units already open and the component caused by the recruitment of previously collapsed pulmonary units. To do so we assumed that pulmonary units open at ZEEP inflate with tidal volume
or PEEP according to the elastance present at ZEEP (predicted volume). This was calculated by adding to EELV the amount expected to
be gained with PEEP according to the elastance (DPao/VT) determined at ZEEP. Lung volume recruitment was then computed as
measured minus predicted volume, i.e., EELV at PEEP (EELV at
ZEEP + PEEP/Est,rs at ZEEP).
The basic assumption for this estimate of alveolar recruitment relies on the finding that specific elastance of pulmonary units in ARDS is near to normal (3, 11), indicating that the elastance decrease with PEEP is likely due to the recruitment of the new pulmonary units. This assumption has been adopted by other investigators also (12).
Intra-abdominal Pressure
Intra-abdominal pressure was measured using a transurethral bladder catheter (13). One hundred milliliters of normal saline were infused through the urinary catheter into the bladder. The catheter was then clamped and the intra-abdominal pressure was recorded by a pressure transducer as mean pressure at end-expiration. Zero was set at the level of the pubis.
Statistical Methods
Data are expressed as mean ± standard deviation (SD), unless otherwise specified. In each group, statistical comparisons between PEEP levels were done using analysis of variance (ANOVA). Individual comparisons (ZEEP versus PEEP) were obtained using Student's paired t test. Individual comparisons between the two groups, at each level of PEEP, were performed using Student's unpaired t test. Bonferroni's correction for multiple comparisons was applied.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The anthropometric characteristics, number of organ dysfunctions, acute physiology score, and outcome for all patients are summarized in Table 2. We found no differences in any variable between the ARDSp or ARDSexp groups, except for age, which was significantly lower in the patients with ARDSp. Similarly, as shown in Table 3, no differences were noted for the ventilatory setting, gas exchange, and hemodynamic variables measured before the PEEP trial. The average daily water balance from the onset of ARDS to the day of the study was also similar between the ARDSp and the ARDSexp groups.
Elastance of the Total Respiratory System, Lung, and Chest Wall
The total population. The high values of Est,rs and Est,L, the moderate increase in Est,w, and low EELV are typical of ARDS (Table 4). When PEEP was increased from 0 to 15 cm H2O, Est,rs and Est,L did not change significantly, Est,w decreased slightly, and intra-abdominal pressure increased by an average of 1.8 ± 1.7 cm H2O. As expected, EELV increased significantly with PEEP.
|
ARDS of pulmonary versus extrapulmonary origin at ZEEP. As shown in Figure 1, Est,rs was similar for both types of ARDS at ZEEP (25.4 ± 6.2 versus 26 ± 5.4 cm H2O/L, p = NS), but Est,L was higher in ARDSp (20.2 ± 5.4 versus 13.8 ± 5.0 cm H2O/L in ARDSexp, p < 0.01) indicating a stiffer lung. Est,w was more than twofold higher in ARDSexp than in ARDSp (12.1 ± 3.8 versus 5.2 ± 1.9 cm H2O/L, p < 0.01), indicating a stiffer chest wall. This latter finding was possibly due to higher intra-abdominal pressure, which amounted to 22.2 ± 6.0 and 8.5 ± 2.9 cm H2O in ARDSexp and ARDSp, respectively (p < 0.01). The close correctional between Est,w and intra-abdominal pressure is shown in Figure 2.
|
p < 0.05 versus Group 1;
|
Because the fluid management in the individual patients might account for the differences we found in respiratory system mechanics, we looked for a possible relationship between mechanics of the total respiratory system, lung, and chest wall and IAP versus the daily fluid balance of the day of the study, the cumulative fluid balance of the 48 h before the study, and the cumulative fluid balance from the day of intubation and the day of ARDS onset to the day of the study. None of these relationships reached statistical significance.
PEEP response in ARDS of pulmonary or extrapulmonary origin. Increasing PEEP from 0 to 15 cm H2O led to opposite effects on elastance in the two types of ARDS, as shown in Figure 1. In ARDSp (upper panel), increasing PEEP caused an increase of Est,rs mainly caused by an increase in Est,L whereas in ARDSexp (lower panel) PEEP resulted in a significant decrease in Est,rs caused by the reduction in both Est,L and Est,w. Increasing PEEP from 0 to 15 cm H2O led to a slight increase in intra-abdominal pressure (p < 0.01) in both groups and amounted, at 15 cm H2O PEEP, to 10.0 ± 3.4 and 24.3 ± 6.1 cm H2O in ARDSp and ARDSexp, respectively. These results indicate a stiffer lung in ARDSp, which does not improve with PEEP, while in ARDSexp there is a stiffer thoracoabdominal cage and a more compliant lung, which both improve with increasing PEEP. As shown in Figure 3 (left panel), the pressure-volume relationship of the total respiratory system of patients with ARDSp was essentially the same at each PEEP level. This suggests that, at end-expiration, PEEP keeps already open pulmonary units more inflated, but no recruitment occurs. This pattern is substantially different in ARDSexp (right panel) where an upwards shift of the pressure-volume curve of the total respiratory system was observed, indicating significant recruitment of pulmonary units by PEEP. The difference in response between ARDSp and ARDSexp with regard to end-expiratory lung volume and recruitment is shown in Table 5.
|
|
Resistance of the total respiratory system, lung, and chest wall. In Table 6 are summarized, for the whole population, the resistances ("ohmic" and additional) of the total respiratory system, lung, and chest wall as a function of PEEP. As shown, we observed a significant decrease with PEEP of the "ohmic" resistance, whereas DR,rs significantly increased mainly because of the lung component.
|
This pattern was somewhat different in ARDSp versus ARDSexp. As shown in Figure 4, with PEEP, Rmax,rs increased significantly in ARDSp, but it remained constant in ARDSexp. As in both groups the "ohmic" resistances decreased significantly, the major difference between the two types of ARDS was a clear increase in DR,L with PEEP in the former, whereas in the latter DR,L remained immodified. The DR,w was higher in ARDSexp and correlated with the IAP (r = 0.66, p < 0.01).
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The main finding of the present study is a different response of respiratory mechanics in ARDS of pulmonary versus extrapulmonary origin. This may correspond to different underlying pathology resulting from two different pathogenetic pathways (4): a "direct" insult to the lung parenchyma in ARDS caused by pulmonary disease such as diffuse pneumonia versus an "indirect" insult to the lung parenchyma in ARDS caused by extrapulmonary disease such as abdominal sepsis or pancreatitis. The prevalent pathogenetic pathway has never been considered in clinical studies on ARDS; patients with both types of ARDS are usually grouped together. Our findings suggest that this differentiation may be important.
The distinction between pulmonary and extrapulmonary origins of ARDS seems not to be controversial nor difficult, since the three physicians who independently classified our study population agreed in all cases but one, an allergic-hemorrhagic alveolitis, finally classified as pulmonary ARDS. The distinction may be more difficult if there is an overlap of the two mechanisms, as in ARDS from peritoneal sepsis with later pulmonary superinfection. As this difficulty can increase with time, we limited our study to the early phases of ARDS. Our two groups included primarily diffuse pneumonia as pulmonary ARDS and abdominal sepsis as extrapulmonary ARDS, as we did not observe in this study population other etiologies that might possibly lead to "direct" or "indirect" lung injury such as near drowning, aspiration, meningitis, etc. The etiologies we observed in our patients, however, cover the majority of ARDS cases commonly presenting in intensive care units (1, 2).
Respiratory, Lung, and Chest Wall Mechanics at ZEEP
In the total population, at ZEEP, the low end-expiratory lung volume (0.576 ± 0.264 L) and the high Est,rs (25.7 ± 5.7 cm H2O/L) were typical of ARDS.
It is traditionally thought that in ARDS the high Est,rs is mainly due to the lung component, with the assumption that Est,w is normal. This assumption, however, is not correct, since the few studies that have specifically addressed this question found a consistent increase in Est,w, ranging from 7.2 to 15 cm H2O/L (normal values, 3.0 to 5.0 cm H2O/L) (10, 14- 17). In the total population our Est,w values (8.2 ± 4.5 cm H2O/L) are in the range of those reported previously. However, in ARDS caused by pulmonary disease Est,w was normal (5.2 ± 1.9 cm H2O/L), whereas in ARDS secondary to an extrapulmonary cause Est,w was markedly elevated (12.1 ± 3.8 cm H2O/L).
We cannot rule out, however, a possible role of age to explain the differences in lung and chest wall elastance we observed between the two groups. The ARDSexp patients, in fact, were 17.3 yr older than the ARDSp patients. In normal subjects the elastance of the respiratory system increases with age, and this increase results from a decreased Est,L (0.1 to 0.2 cm H2O/yr loss of recoil at total lung capacity), which is offset by the increase of Est,w (18). However, in our study population we did not find any relationship between age and Est,rs (r = 0.11). Moreover, the differences in Est, L and Est,w we found between the two groups, largely exceed the possible age-related differences (19). (In 38 normal preoperative anesthetized-paralyzed supine patients 13 to 94 yr of age, we found a significant increase of Est,w with age according to the following equation [unpublished data]: Est,w [cm H2O/L] = 3.65 + 0.04 × age [yr], r = 0.57; p < 0.01. This accounts for a "physiologic" increase of Est,w of only 0.69 cm H2O/L over 17.3 yr of age difference.)
Our findings suggest that in ARDS the increased Est,rs is produced by two different mechanisms: in ARDS caused by a direct pulmonary insult, a high Est,L is the major component (ratio Est,L/Est,rs = 0.79 ± 0.07), whereas in ARDS caused by extrapulmonary disease, increased Est,L and Est,w equally contribute to the high Est,rs (ratio Est,L/Est,rs = 0.53 ± 0.15).
The mean IAP was threefold greater in ARDS of extrapulmonary than of pulmonary origin, and it appears closely related to Est,w (Figure 2). A similar correlation has been observed both in animal models (20) and in normal subjects when IAP was altered artificially (21). In critically ill patients, data on IAP are surprisingly rare. In our patients, the elevated values can be explained, in most patients, by primary abdominal disease or edema of the gastrointestinal tract after shock or trauma.
The resistance of the chest wall was also elevated in ARDS because of extrapulmonary causes and significantly related to IAP, suggesting that IAP affects the viscoelastic properties of the thoracoabdominal region.
In summary, although at ZEEP ARDS of both origins have an equal increase of Est,rs, in ARDS caused by pulmonary disease this is primarily due to an altered Est,L, whereas in ARDS caused by extrapulmonary disease, Est,L is less affected, and Est,w and IAP are markedly increased.
Respiratory, Lung, and Chest Wall Mechanics at Different PEEP Levels
For the total patient population, no significant changes in Est,rs with PEEP were seen. Other groups have reported an increase (14, 16), decrease (15, 22), or no change (10, 23) in Est,rs with PEEP. These apparently contradictory findings may be due to different proportions in each study of patients with ARDS caused by pulmonary or extrapulmonary diseases. The two types of ARDS, in fact, show opposite responses to PEEP; patients with direct lung injury significantly increase Est,rs, mainly the Est,L component, whereas in secondary lung injury PEEP decreases Est,rs and both of its components, Est,L and Est,w.
It is known that in the early phases of ARDS, PEEP regionally stretches the pulmonary units that are already open, i.e., increases elastance. PEEP simultaneously maintains open, at end-expiration, the pulmonary units, which collapse at lower pressure, i.e., increases the number of open units, thereby decreasing Est,rs (24). The global variations of Est,rs depend on the prevalence in a given lung of each of these two mechanisms. The global variations of Est,rs with PEEP, found in ARDS caused by pulmonary disease, suggest the prevalence of stretching phenomena, whereas the decrease of Est,rs in ARDS from extrapulmonary disease indicates a prevalence of recruitment of previously closed alveolar spaces.
The decrease of Est,w with PEEP in extrapulmonary ARDS may be due to a greater increase in lung volume, which may place the thoracic cage in a more favorable part of its pressure-volume curve.
Airway resistance decreased in both groups, as expected, probably because of the increase in lung volume induced by PEEP (10). However, the DR,L markedly increased with PEEP in ARDS caused by pulmonary disease, where stretching phenomena seem prevalent. Although the physiologic meaning of DR,L is still unclear, these data suggest that stretching may affect the viscoelastic resistance of the lung tissue.
In this study, we explored the PEEP level up to 15 cm H2O. We cannot exclude that higher levels of PEEP and inspiratory plateau pressure could result in recruitment in pulmonary ARDS and in further recruitment in extrapulmonary ARDS. However, while this possibility is likely in extrapulmonary ARDS, it seems unlikely in pulmonary ARDS, where stretching phenomena (i.e., an increase in Est,rs and Est,L) are evident already at 15 cm H2O PEEP (see Figure 3).
Pathologic Changes in ARDS Caused by Pulmonary and Extrapulmonary Disease
There is a general belief that ARDS is the extreme form of a spectrum of lung injury caused by a uniform inflammatory mechanism that is independent of the precipitating disease. This assumption mainly originates from pathology studies, which have consistently indicated that the lung response to injury is stereotyped, with transition from acute alveolar capillary damage to a late proliferative phase, quite independently of the initial cause (25). Unfortunately, most of the studies report late or terminal events, and pathologic features of early phases of ARDS such as interstitial edema and alveolar collapse are not easily recognized unless special techniques are used for obtaining lung specimens and processing the tissue.
In experimental ARDS, different lung responses have been reported when the injury is applied directly to the alveoli, as with intratracheal instillation of endotoxin (26, 27), complement (28), tumor necrosis factor (29), or bacteria (30), or when the lung is injured indirectly by a toxic substance injected intravenously (31) or intraperitoneally (32). After a "direct" insult the alveolar damage includes edema, fibrin, collagen, neutrophil aggregates, and red cells seen in the alveoli, whereas the "indirect" insult results in a prevalent microvascular congestion, interstitial edema and less severe alveolar damage such as typically seen after intravenously administered Escherichia coli endotoxin (33). The pathologic differences between "direct" and "indirect" insult are well illustrated in models where the two types of insult can be observed (34, 35). "Direct" injury by live bacteria causes intra-alveolar damage with loss of compartmentalization (29) in the instilled regions, whereas in lung areas not directly instilled, vascular congestion and interstitial edema are noted. If pulmonary lesions in human ARDS are similar to those observed in animal models, prevalent consolidation is expected in "direct" injury type ARDS, and prevalent interstitial edema and alveolar collapse in "indirect" injury type ARDS. These pathologic mechanisms may explain our data: lung volume recruitment is marginal when the underlying pathology is prevalent consolidation, whereas in ARDS caused by extrapulmonary diseases, recruitment by PEEP is remarkable, possibly because of prevalent interstitial edema and alveolar collapse. The morphologic data reported by Lamy and colleagues (36) are in line with our interpretation. In patients in whom gas exchange did not improve with PEEP in early ARDS, severe lung tissue damage was seen, with alteration of alveolar spaces by hemorrhage and purulent exudate, whereas the responders to PEEP had less severe lung damage but diffuse congestion, microatelectasis, and some alveolar damage.
It is possible that these different responses to PEEP disappear in late ARDS where the lung structure undergoes important changes such as remodeling the fibrosis (37, 38).
Possible Clinical Consequences
We believe that the recognition of the two forms of ARDS, pulmonary and extrapulmonary, may lead to an improved clinical management.
Two major complications of positive pressure ventilation in patients with ARDS are barotrauma and hemodynamic impairment, both related to the elevated Est,rs. We can speculate that for a similar Est,rs, the differences between Est,L and Est,w between pulmonary and extrapulmonary ARDS identify the former at a greater risk of barotrauma and the latter at a greater risk of hemodynamic impairment. High Est,L and low Est,w in pulmonary ARDS, in fact, result in elevated transmural pressure, a risk factor for barotrauma, and low pleural pressure, whereas lower Est,L and Higher Est,w in extrapulmonary ARDS result in elevated pleural pressure, with consecutive possible impairment of venous return, cardiac filling, and cardiac output. The lack of recruitment with PEEP we observed in ARDS from pulmonary disease does not necessarily imply that PEEP is unuseful in this type of ARDS. PEEP may, in fact, improve gas exchange through mechanisms other than recruitment as regional diversion of ventilation or perfusion (39).
Finally, our data suggest, in agreement with recent work (40, 41), the importance of respiratory mechanics partitioning for a better characterization of ARDS underlying pathology and for a possible improvement in the clinical management.
| |
Footnotes |
|---|
Correspondence and requests for reprints should be addressed to Prof. Luciano Gattinoni, Istituto di Anestesia e Rianimazione, Universita' de Milano, Ospedale Maggiore via F.Sforza 35, I-20122, Milano, Italy.
(Received in original form August 7, 1997 and in revised form November 12, 1997).
Acknowledgments: Supported in part by Grant No. 32.043637.95 from the Swiss National Research Foundation to P. M. Suter.
| |
References |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1. Sloane, P. J., M. H. Gee, and J. E. Gotlieb. 1992. A multicenter registry of patients with acute respiratory distress syndrome. Am. Rev. Respir. Dis 146: 419-426 [Medline].
2. Knaus, W. A., X. Sun, R. B. Hakim, and D. P. Wagner. 1994. Evaluation of definitions for adult respiratory distress syndrome. Am. J. Respir. Crit. Care Med 150: 311-317 [Abstract].
3. Gattinoni, L., A. Pesenti, L. Avalli, F. Rossi, and M. Bombino. 1987. Pressure-volume curve of total respiratory system in acute respiratory failure. Am. Rev. Respir. Dis 136: 730-736 [Medline].
4. Bernard, G. R., A. Artigas, K. L. Brigham, J. Carlet, K. Falke, L. Hudson, M. Lamy, J. R. Le Gall, A. Morris, R. Spragg, and the Consensus Committee. 1994. The American-European consensus conference on ARDS. Definition, mechanisms, relevant outcomes, and clinical trial coordination. Am. J. Respir. Crit. Care Med 149: 818-824 [Abstract].
5. Le Gall, J. R., P. Loirat, and A. Alperovitch. 1984. A simplified acute physiology score for ICU patients. Crit. Care Med 12: 975-977 [Medline].
6.
Gattinoni, L.,
L. Brazzi,
P. Pelosi,
R. Latini,
G. Tognoni,
A. Pesenti, and
R. Fumagalli.
1995.
A trail of goal-oriented hemodynamic therapy in
critically ill patients.
N. Engl. J. Med
333:
1025-1032
7. Slutsky, A. S. 1993. ACCP Consensus Conference: mechanical ventilation. Chest 104:1833-1859. (Also in Intensive Care Med. 1994:20:64- 79.)
8.
D'Angelo, E.,
F. M. Robatto,
E. Calderini,
M. Tavola,
D. Bono,
G. Torri, and
J. Milic-Emili.
1991.
Pulmonary and chest wall mechanics in
anesthetized paralyzed humans.
J. Appl. Physiol
70:
2602-2610
9. Baydur, A., P. K. Behrakis, W. A. Zin, M. Jaeger, and J. Milic-Emili. 1992. A simple method for assessing the validity of the esophageal balloon technique. Am. Rev. Respir. Dis 126: 788-791 .
10. Pelosi, P., M. Cereda, G. Foti, M. Giacomini, and A. Pesenti. 1995. Alterations of lung and chest wall mechanics in patients with acute lung injury: effects of positive end-expiratory pressure. Am. J. Respir. Crit. Care Med 152: 531-537 [Abstract].
11.
Gattinoni, L.,
L. D'Andrea,
P. Pelosi,
A. Pesenti, and
R. Fumagalli.
1993.
Regional effects and mechanism of positive end-expiratory pressure in early adult respiratory distress syndrome.
J.A.M.A.
269:
2122-2127
12. Ranieri, V. M., N. T. Eissa, C. Corbeil, M. Chassé, J. Braidy, N. Matar, and J. Milic-Emili. 1991. Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in patients with the adult respiratory distress syndrome. Am. Rev. Respir. Dis 144: 544-551 [Medline].
13. Iberti, T. J., C. E. Lieber, and E. Benjamin. 1989. Determination of intra-abdominal pressure using a transurethral bladder catheter: clinical validation of the technique. Anesthesiology 70: 47-50 [Medline].
14.
Suter, P. M.,
H. B. Fairley, and
M. D. Isenberg.
1978.
Effect of tidal volume and positive end-expiratory pressure on compliance during mechanical ventilation.
Chest
73:
158-162
15.
Katz, J. A.,
S. E. Zinn,
G. M. Ozanne, and
H. B. Fairley.
1981.
Pulmonary, chest wall and lung-thorax elastances in acute respiratory failure.
Chest
80:
304-311
16.
Jardin, F.,
B. Genevray,
D. Brun-Ney, and
J. P. Bourdarias.
1985.
Influence of lung and chest wall compliances on transmission of airway
pressure to the pleural space in critically ill patients.
Chest
88:
653-658
17.
Polese, G.,
A. Rossi,
L. Appendini,
G. Brandi,
J. H. T. Bates, and
R. Brandolese.
1996.
Partitioning of respiratory mechanics in mechanically ventilated patients.
J. Appl. Physiol
71:
2425-2433
18. Anthonisen, N. R. 1986. Tests of mechanical function. In P. T. Macklem and J. Mead, editors. Handbook of Physiology, American Physiological Society, Bethesda, Maryland. 753-784.
19. Frank, N. R., J. Mead, and B. G. Ferris. 1957. The mechanical behavior of the lungs in healthy elderly persons. J. Clin. Invest 36: 1680-1687 .
20.
Mutoh, T.,
J. Wayne,
W. J. E. Lamm,
J. Embree,
J. Hildebrandt, and
R. K. Albert.
1992.
Volume infusion produces abdominal distension,
lung compression, and chest wall stiffening in pigs.
J. Appl. Physiol
72:
575-582
21. Pelosi, P., G. Foti, M. Cereda, P. Vicardi, and L. Gattinoni. 1996. Effects of carbon dioxide insufflation for laparoscopic cholecystectomy on the respiratory system. Anaesthesia 51: 744-749 [Medline].
22.
Eissa, N. T.,
V. M. Ranieri,
C. Corbeil,
M. Chassé,
J. Braidy, and
J. Milic-Emili.
1992.
Effect of PEEP on the mechanics of the respiratory
system in ARDS patients.
J. Appl. Physiol
73:
1728-1735
23. Pesenti, A., P. Pelosi, N. Rossi, A. Virtuani, L. Brazzi, and A. Rossi. 1991. The effects of positive end-expiratory pressure on respiratory resistance in patients with the adult respiratory distress syndrome and in normal anesthetized subjects. Am. Rev. Respir. Dis 144: 101-107 [Medline].
24. Gattinoni, L., P. Pelosi, S. Crotti, and F. Valenza. 1995. Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am. J. Respir. Crit. Care Med 151: 1807-1814 [Abstract].
25. Tomashefski, J. F.. 1990. Pulmonary pathology of the adult respiratory distress syndrome. Clin. Chest Med 11: 593-619 [Medline].
26. Tasaka, S., A. Ishizaka, and K. Sayama. 1996. Heat-killed Corynebacterium parvum enhances endotoxin lung injury with increased TNF production in guinea pigs. Am. J. Respir. Crit. Care Med 153: 1047-1055 [Abstract].
27. Terashima, T., M. Kanazawa, and K. Sayama. 1994. Granulocyte colony-stimulating factor exacerbates acute lung injury induced by intratracheal endotoxin in guinea pigs. Am. J. Respir. Crit. Care Med 149: 1295-1303 [Abstract].
28. Shaw, J. O., P. M. Henson, J. Henson, and R. O. Webster. 1980. Lung inflammation induced by complement-derived chemotatic fragments in the alveolus. Lab. Invest 42: 547-558 [Medline].
29. Tutor, J. D., C. M. Mason, E. Dobard, C. Beckerman, W. R. Summer, and S. Nelson. 1994. Loss of compartimentalization of alveolar tumor necrosis factor after lung injury. Am. J. Respir. Crit. Care Med 149: 1107-1111 [Abstract].
30. Johanson, W. G., J. H. Higuchi, D. E. Woods, P. Gomez, and J. J. Coalson. 1985. Dissemination of Pseudomonas aeruginosa during lung infection in hamsters. Am. Rev. Respir. Dis 132: 358-361 [Medline].
31. Muller-Leisse, C., B. Klosterhalfen, and S. Hauptmann. 1993. Computed tomography and histologic results in the early stages of endotoxin- injury lungs as a model for adult respiratory distress syndrome. Invest. Radio 28: 39-45 .
32. Seidenfeld, J. J., R. Curtix, Mullins, S. R. Fowler, and W. G. Johanson. 1986. Bacterial infection and acute lung injury in hamsters. Am. Rev. Respir. Dis 134: 22-26 [Medline].
33. Brigham, K. L., and B. Meyrick. 1986. Endotoxin and lung injury. Am. Rev. Respir. Dis 133: 913-927 [Medline].
34. Wiener-Kronish, J. P., K. H. Albertine, M. A. Matthay, and with the technical assistance of O. Osorio and M. Neuberger. 1991. Differential responses of the endothelial and epithelial barriers of the lung in sheep to Escherichia coli endotoxin. J. Clin. Invest 88: 864-875 .
35. Terashima, T., H. Matsubara, and M. Nakamura. 1996. Local pseudomonas instillation induces contralateral injury and plasma cytokines. Am. J. Respir. Crit. Care Med 153: 1600-1605 [Abstract].
36. Lamy, M., R. J. Fallat, and E. Koeniger. 1976. Pathologic features and mechanisms of hypoxemia in adult respiratory distress syndrome. Am. Rev. Respir. Dis 114: 267-284 [Medline].
37. Bitterman, P. B. 1992. Pathogenesis of fibrosis in acute lung injury. Am. J. Med. 92:6-39S-43S.
38.
Gattinoni, L.,
M. Bombino,
P. Pelosi,
A. Lissoni,
A. Pesenti,
R. Fumagalli, and
M. Tagliabue.
1994.
Lung structure and function in different
stages of severe adult respiratory distress syndrome.
J.A.M.A.
271:
1772-1779
39. Rossi, A., and V. M. Ranieri. 1994. Positive end-expiratory pressure. In M. J. Tobin, editor. Principles and Practice of Mechanical Ventilation, 1st ed. McGraw-Hill, New York, NY. 259-303.
40.
Mergoni, M.,
A. Martelli,
A. Volpi,
S. Primavera,
P. Zuccoli, and
A. Rossi.
1977.
Impact of positive end-expiratory pressure on chest wall
and lung pressure-volume curve in acute respiratory failure.
Am. J. Respir. Crit. Care Med.
156:
846-854
41.
Ranieri, V. M.,
N. Brienza,
S. Santostasi,
F. Puntillo,
L. Mascia,
N. Vitale,
R. Giuliani,
V. Memeo,
F. Bruno,
T. Fiore,
A. Brienza, and
A. S. Slutsky.
1997.
Impairment of lung and chest wall mechanics in patients
with acute respiratory distress syndrome: role of abdominal distension.
Am. J. Respir. Crit. Care Med
156:
1082-1091
This article has been cited by other articles:
 |
|
 |
|
  E. Borges, M. Pinheiro, A. Eleto-Silva, M. Caliari, and M. Rodrigues-Machado Glycogen content is affected differently in acute pulmonary and extra-pulmonary lung injury Human and Experimental Toxicology, September 1, 2009; 28(9): 583 - 590. [Abstract] [PDF]
|
|
|
|
 |
|
 S. Grasso, T. Stripoli, M. Sacchi, P. Trerotoli, F. Staffieri, D. Franchini, V. De Monte, V. Valentini, P. Pugliese, A. Crovace, et al. Inhomogeneity of Lung Parenchyma during the Open Lung Strategy: A Computed Tomography Scan Study Am. J. Respir. Crit. Care Med., September 1, 2009; 180(5): 415 - 423. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Gusmao, A. C. Tanner, J. M. Teles, R. Valentini, P. Rodriguez, I. Bonelli, A. J. Walkey, A. Vieillard-Baron, F. Jardin, D. Talmor, et al. Esophageal Pressure in Acute Lung Injury N. Engl. J. Med., February 19, 2009; 360(8): 831 - 833. [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Kress Acute Respiratory Distress Syndrome ACCP Crit Care Med Brd Rev, January 1, 2009; 20(0): 279 - 288. [Full Text] [PDF]
|
|
|
|
 |
|
 J L Davis, A Morris, R H Kallet, K Powell, A S Chi, M Bensley, J M Luce, and L Huang Low tidal volume ventilation is associated with reduced mortality in HIV-infected patients with acute lung injury Thorax, November 1, 2008; 63(11): 988 - 993. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. J. H. Taut, G. Rippin, P. Schenk, G. Findlay, W. Wurst, D. Hafner, J. F. Lewis, W. Seeger, A. Gunther, and R. G. Spragg A Search for Subgroups of Patients With ARDS Who May Benefit From Surfactant Replacement Therapy: A Pooled Analysis of Five Studies With Recombinant Surfactant Protein-C Surfactant (Venticute) Chest, October 1, 2008; 134(4): 724 - 732. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Sevransky, G. S. Martin, P. Mendez-Tellez, C. Shanholtz, R. Brower, P. J. Pronovost, and D. M. Needham Pulmonary vs Nonpulmonary Sepsis and Mortality in Acute Lung Injury Chest, September 1, 2008; 134(3): 534 - 538. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Chiumello, E. Carlesso, P. Cadringher, P. Caironi, F. Valenza, F. Polli, F. Tallarini, P. Cozzi, M. Cressoni, A. Colombo, et al. Lung Stress and Strain during Mechanical Ventilation for Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., August 15, 2008; 178(4): 346 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Gattinoni and P. Caironi Ventilation Strategies for Acute Lung Injury and Acute Respiratory Distress Syndrome--Reply JAMA, July 2, 2008; 300(1): 42 - 43. [Full Text] [PDF]
|
|
|
|
|
|
A. L. Lagan, G. J. Quinlan, S. Mumby, D. D. Melley, P. Goldstraw, G. J. Bellingan, M. R. Hill, D. Briggs, P. Pantelidis, R. M. du Bois, et al. Variation in Iron Homeostasis Genes Between Patients With ARDS and Healthy Control Subjects Chest, June 1, 2008; 133(6): 1302 - 1311. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Agarwal, R. Srinivas, A. Nath, and S. K. Jindal Is the Mortality Higher in the Pulmonary vs the Extrapulmonary ARDS?: A Metaanalysis Chest, June 1, 2008; 133(6): 1463 - 1473. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. O. Meade, D. J. Cook, G. H. Guyatt, A. S. Slutsky, Y. M. Arabi, D. J. Cooper, A. R. Davies, L. E. Hand, Q. Zhou, L. Thabane, et al. Ventilation Strategy Using Low Tidal Volumes, Recruitment Maneuvers, and High Positive End-Expiratory Pressure for Acute Lung Injury and Acute Respiratory Distress Syndrome: A Randomized Controlled Trial JAMA, February 13, 2008; 299(6): 637 - 645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Grasso, T. Stripoli, M. De Michele, F. Bruno, M. Moschetta, G. Angelelli, I. Munno, V. Ruggiero, R. Anaclerio, A. Cafarelli, et al. ARDSnet Ventilatory Protocol and Alveolar Hyperinflation: Role of Positive End-Expiratory Pressure Am. J. Respir. Crit. Care Med., October 15, 2007; 176(8): 761 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Perl, C.-S. Chung, U. Perl, J. Lomas-Neira, M. de Paepe, W. G. Cioffi, and A. Ayala Fas-induced Pulmonary Apoptosis and Inflammation during Indirect Acute Lung Injury Am. J. Respir. Crit. Care Med., September 15, 2007; 176(6): 591 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. B. Santos, L. K. S. Nagato, N. M. Boechem, E. M. Negri, A. Guimaraes, V. L. Capelozzi, D. S. Faffe, W. A. Zin, and P. R. M. Rocco Time course of lung parenchyma remodeling in pulmonary and extrapulmonary acute lung injury J Appl Physiol, January 1, 2006; 100(1): 98 - 106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Fan, D. M. Needham, and T. E. Stewart Ventilatory Management of Acute Lung Injury and Acute Respiratory Distress Syndrome JAMA, December 14, 2005; 294(22): 2889 - 2896. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Q. Curley, P. L. Hibberd, L. D. Fineman, D. Wypij, M.-C. Shih, J. E. Thompson, M. J. C. Grant, F. E. Barr, N. Z. Cvijanovich, L. Sorce, et al. Effect of Prone Positioning on Clinical Outcomes in Children With Acute Lung Injury: A Randomized Controlled Trial JAMA, July 13, 2005; 294(2): 229 - 237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. L. S. Menezes, P. T. Bozza, H. C. C. Faria Neto, A. P. Laranjeira, E. M. Negri, V. L. Capelozzi, W. A. Zin, and P. R. M. Rocco Pulmonary and extrapulmonary acute lung injury: inflammatory and ultrastructural analyses J Appl Physiol, May 1, 2005; 98(5): 1777 - 1783. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. L. Farias, D. S. Faffe, D. G. Xisto, M. C. E. Santana, R. Lassance, L. F. M. Prota, M. B. Amato, M. M. Morales, W. A. Zin, and P. R. M. Rocco Positive end-expiratory pressure prevents lung mechanical stress caused by recruitment/derecruitment J Appl Physiol, January 1, 2005; 98(1): 53 - 61. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Esteban, P. Fernandez-Segoviano, F. Frutos-Vivar, J. A. Aramburu, L. Najera, N. D. Ferguson, I. Alia, F. Gordo, and F. Rios Comparison of Clinical Criteria for the Acute Respiratory Distress Syndrome with Autopsy Findings Ann Intern Med, September 21, 2004; 141(6): 440 - 445. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Allen and J. H. T. Bates Dynamic mechanical consequences of deep inflation in mice depend on type and degree of lung injury J Appl Physiol, January 1, 2004; 96(1): 293 - 300. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Gattinoni, E. Carlesso, P. Cadringher, F. Valenza, F. Vagginelli, and D. Chiumello Physical and biological triggers of ventilator-induced lung injury and its prevention Eur. Respir. J., November 16, 2003; 22(47_suppl): 15s - 25s. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Pereira, J. Bohe, S. Rosselli, E. Combourieu, C. Pommier, J.-P. Perdrix, J.-C. Richard, M. Badet, S. Gaillard, F. Philit, et al. Sigmoidal equation for lung and chest wall volume-pressure curves in acute respiratory failure J Appl Physiol, November 1, 2003; 95(5): 2064 - 2071. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. L. Jackson Jr. Management of Acute Renal Failure Ann Intern Med, September 16, 2003; 139(6): 529 - 530. [Full Text] [PDF]
|
|
|
|
|
|
S.M. Maggiore, J-C. Richard, and L. Brochard What has been learnt from P/V curves in patients with acute lung injury/acute respiratory distress syndrome Eur. Respir. J., August 1, 2003; 22(42_suppl): 22s - 26s. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J-J. Rouby, Q. Lu, and S. Vieira Pressure/volume curves and lung computed tomography in acute respiratory distress syndrome Eur. Respir. J., August 1, 2003; 22(42_suppl): 27s - 36s. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Pelosi, N. Bottino, D. Chiumello, P. Caironi, M. Panigada, C. Gamberoni, G. Colombo, L. M. Bigatello, and L. Gattinoni Sigh in Supine and Prone Position during Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., February 15, 2003; 167(4): 521 - 527. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Gama de Abreu, M. Heintz, A. Heller, R. Szechenyi, D. M. Albrecht, and T. Koch One-Lung Ventilation with High Tidal Volumes and Zero Positive End-Expiratory Pressure Is Injurious in the Isolated Rabbit Lung Model Anesth. Analg., January 1, 2003; 96(1): 220 - 228. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Allen, L. K. A. Lundblad, P. Parsons, and J. H. T. Bates Transient mechanical benefits of a deep inflation in the injured mouse lung J Appl Physiol, November 1, 2002; 93(5): 1709 - 1715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Messerole, P. Peine, S. Wittkopp, J. J. Marini, and R. K. Albert The Pragmatics of Prone Positioning Am. J. Respir. Crit. Care Med., May 15, 2002; 165(10): 1359 - 1363. [Full Text] [PDF]
|
|
|
|
|
|
J. J. ROUBY, Q. LU, and I. GOLDSTEIN Selecting the Right Level of Positive End-Expiratory Pressure in Patients with Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., April 15, 2002; 165(8): 1182 - 1186. [Full Text] [PDF]
|
|
|
|
|
|
M. D. Eisner, B. T. Thompson, D. Schoenfeld, A. Anzueto, M. A. Matthay, and the Acute Respiratory Distress Syndrome Network Airway Pressures and Early Barotrauma in Patients with Acute Lung Injury and Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., April 1, 2002; 165(7): 978 - 982. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Zijlstra, J. J.M. Ligtenberg, T. S. van der Werf, K. Thorburn, S. J. Kerr, P. B. Baines, A. Malhotra, N. Ayas, R. Kacmarek, L. Gattinoni, et al. Prone Positioning of Patients with Acute Respiratory Failure N. Engl. J. Med., January 24, 2002; 346(4): 295 - 297. [Full Text] [PDF]
|
|
|
|
|
|
A. VILLAGRA, A. OCHAGAVIA, S. VATUA, G. MURIAS, M. DEL MAR FERNANDEZ, J. L. AGUILAR, R. FERNANDEZ, and L. BLANCH Recruitment Maneuvers during Lung Protective Ventilation in Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., January 15, 2002; 165(2): 165 - 170. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. GATTINONI, P. CAIRONI, P. PELOSI, and L. R. GOODMAN What Has Computed Tomography Taught Us about the Acute Respiratory Distress Syndrome? Am. J. Respir. Crit. Care Med., November 1, 2001; 164(9): 1701 - 1711. [Full Text] [PDF]
|
|
|
|
|
|
R. G. Brower, L. B. Ware, Y. Berthiaume, and M. A. Matthay Treatment of ARDS Chest, October 1, 2001; 120(4): 1347 - 1367. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. D. BERSTEN, T. HUNT, T. E. NICHOLAS, and I. R. DOYLE Elevated Plasma Surfactant Protein-B Predicts Development of Acute Respiratory Distress Syndrome in Patients with Acute Respiratory Failure Am. J. Respir. Crit. Care Med., August 15, 2001; 164(4): 648 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. D. EISNER, T. THOMPSON, L. D. HUDSON, J. M. LUCE, D. HAYDEN, D. SCHOENFELD, M. A. MATTHAY, and the Acute Respiratory Distress Syndrome Network Efficacy of Low Tidal Volume Ventilation in Patients with Different Clinical Risk Factors for Acute Lung Injury and the Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., July 15, 2001; 164(2): 231 - 236. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. RIALP, A. J. BETBESE, M. PEREZ-MARQUEZ, and J. MANCEBO Short-term Effects of Inhaled Nitric Oxide and Prone Position in Pulmonary and Extrapulmonary Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., July 15, 2001; 164(2): 243 - 249. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Mergoni, A. Volpi, C. Bricchi, and A. Rossi Lower inflection point and recruitment with PEEP in ventilated patients with acute respiratory failure J Appl Physiol, July 1, 2001; 91(1): 441 - 450. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. CROTTI, D. MASCHERONI, P. CAIRONI, P. PELOSI, G. RONZONI, M. MONDINO, J. J. MARINI, and L. GATTINONI Recruitment and Derecruitment during Acute Respiratory Failure . A Clinical Study Am. J. Respir. Crit. Care Med., July 1, 2001; 164(1): 131 - 140. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Tobin Advances in Mechanical Ventilation N. Engl. J. Med., June 28, 2001; 344(26): 1986 - 1996. [Full Text] [PDF]
|
|
|
|
|
|
M. A. Martynowicz, B. J. Walters, and R. D. Hubmayr Mechanisms of recruitment in oleic acid-injured lungs J Appl Physiol, May 1, 2001; 90(5): 1744 - 1753. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Hering, H. Wrigge, R. Vorwerk, K. A. Brensing, S. Schroder, J. Zinserling, A. Hoeft, T. V. Spiegel, and C. Putensen The Effects of Prone Positioning on Intraabdominal Pressure and Cardiovascular and Renal Function in Patients with Acute Lung Injury Anesth. Analg., May 1, 2001; 92(5): 1226 - 1231. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. A. Raimondi, A. C. Raimondi, R. Rodriquez-Roisin, C. Santos, M. Ferrer, J. Roca, A. Torres, and C. Hernandez RESPONSE TO OXYGEN BREATHING IN ALI/ARDS PATIENTS Am. J. Respir. Crit. Care Med., March 1, 2001; 163(3): 793 - 794. [Full Text] [PDF]
|
|
|
|
 |
|
 S. R. Desai, A. U. Wells, G. Suntharalingam, M. B. Rubens, T. W. Evans, and D. M. Hansell Acute Respiratory Distress Syndrome Caused by Pulmonary and Extrapulmonary Injury: A Comparative CT Study Radiology, March 1, 2001; 218(3): 689 - 693. [Abstract] [Full Text]
|
|
|
|
|
|
A. Kornecki, H. Frndova, A. L. Coates, and S. D. Shemie 4A Randomized Trial of Prolonged Prone Positioning in Children With Acute Respiratory Failure Chest, January 1, 2001; 119(1): 211 - 218. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J DAKIN and T W EVANS Progress in ARDS research: a protection racket? Thorax, January 1, 2001; 56(1): 2 - 3. [Full Text]
|
|
|
|
 |
|
 M. Lichtwarck-Aschoff, V. Kessler, U. H. Sjostrand, A. Hedlund, G. Mols, S. Rubertsson, A. M. Markstrom, and J. Guttmann Static versus dynamic respiratory mechanics for setting the ventilator Br. J. Anaesth., October 1, 2000; 85(4): 577 - 586. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A.Q. Curley, J. E. Thompson, and J. H. Arnold The Effects of Early and Repeated Prone Positioning in Pediatric Patients With Acute Lung Injury Chest, July 1, 2000; 118(1): 156 - 163. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. E.V. d. KLOOT, L. BLANCH, A. MELYNNE YOUNGBLOOD, C. WEINERT, A. B. ADAMS, J. J. MARINI, R. S. SHAPIRO, and A. NAHUM Recruitment Maneuvers in Three Experimental Models of Acute Lung Injury . Effect on Lung Volume and Gas Exchange Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1485 - 1494. [Abstract] [Full Text]
|
|
|
|
|
|
A. ALIVERTI, R. DELLACÁ, P. PELOSI, D. CHIUMELLO, A. PEDOTTI, and L. GATTINONI Optoelectronic Plethysmography in Intensive Care Patients Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1546 - 1552. [Abstract] [Full Text]
|
|
|
|
|
|
A. VIEILLARD-BARON, E. GIROU, E. VALENTE, C. BRUN-BUISSON, F. JARDIN, F. LEMAIRE, and L. BROCHARD Predictors of Mortality in Acute Respiratory Distress Syndrome . Focus on the Role of Right Heart Catheterization Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1597 - 1601. [Abstract] [Full Text]
|
|
|
|
|
|
C. SANTOS, M. FERRER, J. ROCA, A. TORRES, C. HERNÁNDEZ, and R. RODRIGUEZ-ROISIN Pulmonary Gas Exchange Response to Oxygen Breathing in Acute Lung Injury Am. J. Respir. Crit. Care Med., January 1, 2000; 161(1): 26 - 31. [Abstract] [Full Text]
|
|
|
|
|
|
T. T Bauer, C. Montón, A. Torres, H. Cabello, X. Fillela, A. Maldonado, J.-M. Nicolás, and E. Zavala Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome, severe pneumonia, and controls Thorax, January 1, 2000; 55(1): 46 - 52. [Abstract] [Full Text]
|
|
|
|
|
|
International Consensus Conferences in Intensive Care Medicine: Ventilator-associated Lung Injury in ARDS . THIS OFFICIAL CONFERENCE REPORT WAS COSPONSORED BY THE AMERICAN THORACIC SOCIETY, THE EUROPEAN SOCIETY OF INTENSIVE CARE MEDICINE, AND THE SOCIETE DE REANIMATION DE LANGUE FRANCAISE, AND WAS APPROVED BY THE ATS BOARD OF DIRECTORS, JULY 1999 Am. J. Respir. Crit. Care Med., December 1, 1999; 160(6): 2118 - 2124. [Full Text]
|
|
|
|
|
|
L. R. Goodman, R. Fumagalli, P. Tagliabue, M. Tagliabue, M. Ferrario, L. Gattinoni, and A. Pesenti Adult Respiratory Distress Syndrome Due to Pulmonary and Extrapulmonary Causes: CT, Clinical, and Functional Correlations Radiology, November 1, 1999; 213(2): 545 - 552. [Abstract] [Full Text]
|
|
|
|
 |
|
 T. Gluecker, P. Capasso, P. Schnyder, F. Gudinchet, M.-D. Schaller, J.-P. Revelly, R. Chiolero, P. Vock, and S. Wicky Clinical and Radiologic Features of Pulmonary Edema RadioGraphics, November 1, 1999; 19(6): 1507 - 1531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. H. Ketai Invited Commentary RadioGraphics, November 1, 1999; 19(6): 1532 - 1533. [Full Text] [PDF]
|
|
|
|
|
|
B. JONSON, J.-C. RICHARD, C. STRAUS, J. MANCEBO, F. LEMAIRE, and L. BROCHARD Pressure-Volume Curves and Compliance in Acute Lung Injury . Evidence of Recruitment Above the Lower Inflection Point Am. J. Respir. Crit. Care Med., April 1, 1999; 159(4): 1172 - 1178. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. PELOSI, P. CADRINGHER, N. BOTTINO, M. PANIGADA, F. CARRIERI, E. RIVA, A. LISSONI, and L. GATTINONI Sigh in Acute Respiratory Distress Syndrome Am. J. Respir. Crit. Care Med., March 1, 1999; 159(3): 872 - 880. [Abstract] [Full Text]
|
|
|
|
|
|
J. B. Hall Respiratory System Mechanics in Adult Respiratory Distress Syndrome . Stretching Our Understanding Am. J. Respir. Crit. Care Med., July 1, 1998; 158(1): 1 - 2. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Proc. Am. Thorac. Soc. | Am. J. Respir. Cell Mol. Biol. |