Respective Role of PEEP and a Recruitment Maneuver | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
ABSTRACT |
|---|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. Fifteen patients with ARDS were successively ventilated using conventional VT (CVT = 10 ± 1 ml/kg) and low VT (LVT = 6 ± 1 ml/ kg); total PEEP (PEEPtot) was individually set at the lower inflection point (Plip) of the pressure-volume curve (PEEPtot = 11 ± 4 cm H2O). Pressure-volume curves were recorded from zero PEEP (ZEEP) and from PEEP, and recruited volume (Vrec) was calculated as the volume difference between the two curves for a given pressure. Despite a similar PEEPtot, Vrec was significantly lower with LVT than with CVT, indicating low VT-induced alveolar derecruitment. Reduction in VT was associated with a reduced SaO2. In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H2O), and after an increase in PEEP (by 4 cm H2O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Plip.
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Injury caused by or associated with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS) has become a subject of great concern (1). Various experimental studies have described the physiologic mechanism by which MV may lead to ventilation-induced lung injury (VILI) (2, 3). The factors that mainly contribute to VILI include high distending transalveolar pressure or overdistension, related to high pressures and volumes that occur at the end of inspiration (4), and transalveolar pressure falling below the critical closing pressure of alveolar units at the end of expiration, inducing repetitive opening-closing phenomenon (3, 5, 6). Although these factors occur either at high lung volume (i.e., overdistension) or at low lung volume (i.e., opening closing), they are often associated throughout the respiratory cycle in the ARDS lung because of the uneven distribution of lung disease.
On the basis of these clinical and experimental factors, it is now recommended that, in order to limit VILI, plateau pressure should be kept below 30 to 35 cm H2O while maintaining the lung open with sufficient positive end-expiratory pressure (PEEP) (7). Reduction of tidal volume (VT) is the cornerstone of this strategy, and PEEP should be set at a sufficient level in order to avoid end-expiratory collapse.
Three recent controlled trials that compared low (6 to 8 ml/kg) versus conventional (10 to 11 ml/kg) VT for a given PEEP level set empirically, failed to demonstrate any benefit of a pressure-limited strategy with regard to morbidity and mortality (8). In contrast, two other studies showed a significant benefit on mortality by reducing VT (11, 12). One of these studies associated the reduction in VT to a high PEEP level, whereas the most recent and largest trial to date has used a high respiratory rate in the low VT group, which could lead to gas trapping and a higher total PEEP. In addition, a recent clinical trial demonstrated that the use of high PEEP and low VT reduced inflammatory cytokines level both at the bronchoalveolar lavage and in the blood (2). As previously suggested, a high PEEP level could be particularly important in this low VT strategy, because hypoventilation may lead to progressive derecruitment. For this reason, it has been proposed to add recruitment maneuvers to the standard approach of reduced VT (12).
The aim of this study was to test the hypothesis that, for a total PEEP kept constant at the lower inflection point (Plip) on the pressure-volume (Pel-V) curve of the respiratory system, a reduction in VT from 10 to 6 ml/kg could be responsible for alveolar derecruitment. The respective efficacy of a recruitment maneuver and an increase in PEEP level above Plip was also assessed by means of the Pel-V curve.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Patients
Patients requiring MV for more than 24 h and fulfilling the criteria for acute lung injury as defined by a PaO2/FIO2 ratio < 300 mm Hg, bilateral opacities on chest radiograph, and no history suggesting elevated left atrial pressure, were candidates for inclusion (13). Patients presenting with a documented history of chronic obstructive pulmonary disease or a contraindication for sedation and paralysis were not included in the study. The protocol was approved by the Henri Mondor Hospital Ethics Committee, and informed consent was obtained from patient's next of kin.
Fifteen consecutive patients were enrolled in the study. All patients were sedated, paralyzed, and ventilated in the volume-controlled mode (Servo Ventilator 900C; Siemens-Elema AB, Solna, Sweden).
Pel-V Curve Recording
The system, including a computer-controlled Servo Ventilator 900C, and the technique for performing Pel-V curves, based on the low-flow insufflation method, have been previously described in detail (14). This allowed Pel-V curves to be obtained either from PEEP or from zero end-expiratory pressure (ZEEP).
Each Pel-V curve was analyzed according to a mathematical model that divided the curve into three segments, separated by a lower and upper inflection point (LIP and UIP, respectively) (15). (See online data supplement.)
Alveolar Recruitment
PEEP Pel-V curve was plotted on the same volume axis as the ZEEP Pel-V curve, using PEEP-related end-expiratory lung-volume variation measured during the passive expiration from PEEP to ZEEP. PEEP-related recruitment was defined, for a given elastic pressure (Pel), by the volume difference between both curves, taking into account intrinsic PEEP (PEEPi) (14). This volume represented the PEEP-related recruitment of previously collapsed lung units, and was identified by the upward shift along the volume axis of the PEEP Pel-V curve, relative to the ZEEP Pel-V curve. Recruitment could be quantified at any elastic pressure studied.
Protocol
The first Pel-V curve was obtained from ZEEP, without modifying
previous ventilator settings, in order to determine pressure at the LIP
(Plip). The total PEEP (PEEPtot) level (taking into account PEEPi)
was set close to Plip and kept constant whatever the VT tested, by
modifying external PEEP level when necessary. The respiratory rate
(from 18 to 22 min
1), the inspiratory/total time ratio (0.33), and the
FIO2 were also kept constant.
First part of the study (15 patients). Patients were successively ventilated with conventional VT (CVT = 10 ml/kg of "dry" body weight) and low VT (LVT = 6 ml/kg) randomly applied. Patients were ventilated 1 h in each mode. After sampling blood for arterial blood gas measurements, the following measurements were made during the last 10 min of each condition (CVT and LVT). (1) The PEEP Pel-V curve was recorded after a prolonged expiration during which PEEP was maintained. (2) The ZEEP Pel-V curve was then recorded after a prolonged expiration during which PEEP was eliminated (i.e., from the elastic equilibrium volume reached at ZEEP).
Second part of the study (10 patients). Similar measurements were made, respectively, with CVT and LVT immediately after two successive recruitment maneuvers consisting of a 45 cm H2O pressure-limited breath applied for 15 s.
Third part of the study (10 patients). The PEEP level was then increased by 4 cm H2O, taking into account PEEPi to keep PEEPtot constant whatever the VT. Pel-V curve recordings and recruitment calculation were repeated after 1 h of CVT and LVT ventilation combined with the high level of PEEP.
Statistics
Values are given as means ± SD. At a given PEEP level, alveolar recruitment (calculated for any given Pel), ventilatory settings, hemodynamic data, and arterial blood gases measured with CVT and LVT, were compared using Wilcoxon's test for paired samples. The effect of a recruitment maneuver and increasing PEEP was compared with those observed before recruitment maneuver or PEEP increase using the same test. Significant differences were considered for p < 0.05.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Arterial blood gases and Pel-V curves recorded from PEEP set at Plip, and from ZEEP, were obtained in 15 patients with CVT and LVT, respectively. The mean LIP was 10 ± 4 cm H2O. Pel-V curves were also recorded after a recruitment maneuver and after an increase in PEEP by 4 cm H2O in 10 patients of the whole population. The characteristics of the patients are presented in Table 1.
|
Influence of VT Keeping PEEP Constant
Both strategies were well tolerated by all patients. Ventilatory settings, plateau pressure (Pplat), setPEEP, and PEEPtot are given in Table 2. PEEPtot observed with CVT did not differ from LVT, and this was achieved by individual adaptation of external PEEP level. As expected, PaCO2 was significantly higher with LVT (Table 3). Hemodynamic parameters were not affected by change in VT (Table 3).
|
|
Over the Pel range from 15 to 30 cm H2O, recruitment was significantly higher with CVT than with LVT, for a similar PEEPtot level. Recruitment calculated for 20, 25, and 30 cm H2O of Pel, is illustrated in Figure 1. Expressed as a percentage of the amount of recruitment observed with CVT, recruitment with LVT was only 69% at 15 cm H2O and 59% at 30 cm H2O. PaO2, as well as PaO2/FIO2, were not significantly altered by reduction of VT. SaO2 was significantly lower with LVT than with CVT (Table 3).
|
Effect of a Recruitment Maneuver on the Derecruitment Induced by Low VT
In the 10 patients in whom a recruitment maneuver was performed, PEEPtot set at LIP and Pplat were: 13 ± 3 versus 13 ± 4 cm H2O, NS, and 36 ± 7 versus 28 ± 7 cm H2O, p < 0.01, for CVT and LVT, respectively. The comparison of recruitment between CVT and LVT before the recruitment maneuver showed the same difference as in the 15 patients.
With LVT, a recruitment maneuver induced a significant increase in recruitment (175 ± 108 ml versus 254 ± 137 ml, expressed at a Pel of 20 cm H2O, p < 0.01). In contrast, the same recruitment maneuver did not significantly affect recruitment with CVT (266 ± 157 ml versus 264 ± 120 ml, NS). As a result, PEEP-induced recruitment became similar for LVT and CVT after the recruitment maneuver (Figure 1).
Effect of Increasing PEEP on the Derecruitment Induced by Low VT
In the same 10 patients, the 4 cm H2O increase in PEEP modified PEEPtot and Pplat to 17 ± 3 versus 16 ± 3 cm H2O, NS, and to 41 ± 9 versus 32 ± 7 cm H2O, p < 0.01 for CVT and LVT, respectively.
The increase in PEEP induced an increase in recruitment for both VT (expressed at 20 cm H2O of Pel: 175 ± 108 versus 332 ± 91 ml with LVT, p < 0.05, and 266 ± 157 versus 464 ± 216 ml with CVT, p < 0.05) (Figure 1). At this high PEEP level, the difference in recruitment between LVT and CVT (Figure 1) did not reach significance.
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The present study has demonstrated that a reduction in VT from 10 to 6 ml/kg, keeping PEEPtot constant at the LIP, was responsible for a significant lung volume loss corresponding to alveolar derecruitment. This effect may have participated, at least in part, to the negative results of three recent clinical trials that failed to demonstrate any benefit of a ventilatory strategy aiming at systematically reducing VT (8). This hypothesis is corroborated by the significant reduction in mortality rate associated with a lung protective strategy recently reported by Amato and colleagues (12). In this study, particular attention was given to the PEEP setting, as well as to repeated sighs, performed to preserve lung recruitment during low VT ventilation. In contrast, the recent NIH Network trial seems to indicate that reduction in VT alone is effective to reduce mortality. However, the possibility of a PEEPi effect in the low VT group, caused by the high respiratory frequencies used, makes the interpretation of these results still open.
The apparent conflicting results of these recent clinical trials could also suggest that, first, reduction in VT from 10 to 6 ml/kg alone fails to improve mortality and, second, that a specific strategy to avoid harmful alveolar derecruitment may be beneficial. In addition, a recent clinical study has indicated that a low PEEP associated with high VT may lead to systemic inflammatory response and possibly promotes lung injury (2).
Alveolar Derecruitment
Several studies based on CT scan, Pel-V curves, or gas exchange have demonstrated that recruitment is a continuous and
progressive phenomenon that not only depends on PEEP but
also on peak inflation volume (14, 16). Considering a given
PEEP level, if tidal inflation induces recruitment, a reduction
in VT could thus be responsible for alveolar derecruitment. It
has been demonstrated that low VT ventilation during anesthesia could be responsible for alveolar collapse in healthy
lungs (19, 20). Several factors, including the use of high FIO2 in
the presence of low 
/
ratio, the use of low VT, sedation, and
paralysis may facilitate atelectasis and promote denitrogenation atelectasis in patients with ARDS (21). Cereda and
colleagues (24) have shown that low VT ventilation could induce a progressive decrease in compliance, indicating a time-dependent derecruitment, which could be prevented by higher PEEP level. The influence of VT on PEEP-related cardiorespiratory effect was also studied by Ranieri and colleagues (25)
in a group of nine patients with ARDS. Recruitment based on
Pel-V curve analysis was measured in each patient during low
and high tidal ventilation for a constant PEEP level. In all
patients, the Pel-V curve from ZEEP during low VT ventilation exhibited a concavity toward the volume axis, which suggested a recruitable lung, whereas the Pel-V curves recorded
with high VT were convex in six patients, indicating a progressive decrease in compliance suggesting overdistension. These
investigators concluded that with high VT, PEEP mainly induced hyperinflation of alveoli already recruited by tidal ventilation, whereas with low VT, PEEP induced alveolar recruitment and counterbalanced low VT-related derecruitment.
Despite some discrepancies with our results, possibly related
to methodologic differences, the results reported by Ranieri
and colleagues showed that low VT ventilation might affect
lung recruitment. A recent study corroborating these findings
suggested that the size of VT might interfere with recruitment
by modifying the behavior of airway resistance and time constant (26). In the present study, the significant alveolar derecruitment associated with VT reduction was recovered by increasing PEEP, which confirmed that the lung was not fully
recruited during low VT ventilation. However, because we kept
VT constant at the two different PEEP levels (either with LVT
or with CVT), the Pplat increased with the higher PEEP level.
Therefore, we cannot determine whether the greater recruitment was a result of the Pplat causing inflation of more lung
units at end-inspiration or higher PEEP preventing more time
dependent end-expiratory collapse or both.
Influence on Oxygenation
It is known that oxygenation depends on recruitment, and therefore a worsening in oxygenation could have been expected with low VT. In the present study, PaO2 did not significantly change with the reduction in VT but arterial oxygen saturation worsened. A right-shift in the oxyhemoglobin dissociation curve caused by acidosis may have participated to this latter finding. However, the influence of VT reduction on gas exchange remains controversial in the studies that have specifically addressed this issue. Several mechanisms, not directly related to recruitment, could be involved in the oxygenation changes occurring after VT reduction. Hypercapnia associated with VT reduction tends to increase cardiac output (27). This effect may improve PaO2 by increasing mixed venous oxygen saturation or decrease PaO2 by increasing shunt. In the study reported by Ranieri and colleagues (26), PaO2 was significantly improved when VT was reduced from 12 to 7 ml/kg. These results greatly differ from those of Blanch and colleagues (30) who reported a better recruitment as well as a PaO2 improvement associated with an increase in VT. In this study, minute ventilation was matched by increasing respiratory rate with low VT in order to limit hypercapnia induced by VT reduction. Kiiski and colleagues (31, 32) studied the influence of VT on gas exchange and oxygen delivery during, respectively, nonmatched and matched minute ventilation. Both studies suggested that changes in gas exchange observed with low VT not only depend on recruitment but also on the hemodynamic effects associated with hypercapnia. Our results concerning oxygenation should be interpreted with caution because of the relatively small number of patients. The absence of invasive hemodynamic monitoring makes it difficult to interpret the effects of both ventilatory strategies on oxygenation.
Recruitment Maneuver
The lung protective approach reported by Amato and colleagues (12) included the application of systematic sighs after tracheal suctioning, with the aim of avoiding harmful alveolar collapse. The rationale for using a recruitment maneuver is to forestall collapsed lung units, which suggests that this technique is effective when the lung has previously been derecruited. Several studies have demonstrated the effect of sighs on atelectasis observed during general anesthesia (19, 20). Pelosi and colleagues (33) investigated the effects of sighs on gas exchange in patients with acute lung injury. These investigators demonstrated that application of sighs during lung protective strategy could improve lung volume and oxygenation. These results indicate that a low VT strategy may not provide full lung recruitment despite the relatively high PEEP level (14 ± 2 cm H2O) applied. A recent study confirmed these findings but also suggested that recruitment maneuvers were less efficient than PEEP increase (34). In our study, the increase in recruitment resulting from the recruitment maneuver was observed only during low VT ventilation. Interestingly, the same maneuver did not lead to any significant beneficial effect during CVT ventilation, indicating that the lung remained open and therefore was no longer recruitable. However, time effect of recruitment maneuver could not be evaluated since ventilatory settings were changed to higher PEEP level immediately after measurements.
In conclusion, the most relevant finding of this study was that a ventilatory strategy based on recent recommendations (i.e., limited VT and PEEP at or above Plip) leads to alveolar instability and lung collapse. These results suggest that a specific approach may be needed to prevent alveolar instability in the situation where strategies limiting end-inspiratory pressure and overdistension are used. In our study, increasing PEEP or performing a recruitment maneuver appear as two possible strategies to counteract low VT-induced derecruitment.
| |
Footnotes |
|---|
Correspondence and requests for reprints should be addressed to Dr. Laurent Brochard, Réanimation Médicale, Hôpital Henri Mondor, 94010 Creteil, France. E-mail: laurent.brochard{at}hmn.ap-hop-paris.fr
(Received in original form April 18, 2000 and in revised form February 6, 2001).
This article has an online data supplement, which is accessible from this issue's table of contents online at www.atsjournals.org
Acknowledgments:
The writers thank Richard Medeiros for his help in editing the manuscript, Lucie Breton for technical support during the study, and Florence Picot for her help in typing the manuscript.
| |
References |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Slutsky AS,
Tremblay LN.
Multiple system organ failure: is mechanical
ventilation a contributing factor?
Am J Respir Crit Care Med
1998;
157:
1721-1725
2.
Ranieri VM,
Suter PM,
Tortorella C,
De Tullio R,
Dayer JM,
Brienza A,
Bruno F,
Slutsky AS.
Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a
randomized controlled trial.
JAMA
1999;
282:
54-61
3. Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS. Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model. J Clin Invest 1997; 99: 944-952 [Medline].
4. Dreyfuss D, Saumon G. Ventilation-induced injury. Tobin MJ, editor. In: Principles and practice of mechanical ventilation. New York: MacGraw Hill; 1994. p. 793-811.
5. Taskar V, John J, Evander E, Robertson B, Jonson B. Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion. Am J Respir Crit Care Med 1997; 155: 313-320 [Abstract].
6. Muscedere JG, Mullen JB, Gan K, Bryan AC, Slutsky AS. Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994; 149: 1327-1334 [Abstract].
7. International consensus conferences in intensive care medicine. Ventilator-associated lung injury in ARDS. Am J Respir Crit Care Med 1999; 160:2118-2124.
8.
Brochard L,
Roudot-Thoraval F,
Roupie E,
Delclaux C,
Chastre J,
Fernandez-Mondéjar E,
Clémenti E,
Mancebo J,
Factor P,
Matamis D,
Ranieri M,
Blanch L,
Rodi G,
Mentec H,
Dreyfuss D,
Ferrer M,
Brun-Buisson C,
Tobin M,
Lemaire F.
Tidal volume reduction for
prevention of ventilator-induced lung injury in acute respiratory distress syndrome: The Multicenter Trail Group on Tidal Volume reduction in ARDS.
Am J Respir Crit Care Med
1998;
158:
1831-1838
9. Brower RG, Shanholtz CB, Fessler HE, Shade DM, White Jr. P, Wiener CM, Teeter JG, Dodd-o JM, Almog Y, Piantadosi S. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med 1999;27:1492-1498.
10.
Stewart TE,
Meade MO,
Cook DJ,
Granton JT,
Hodder RV,
Lapinsky SE,
Mazer CD,
McLean RF,
Rogovein TS,
Schouten BD,
Todd TR,
Slutsky AS.
Evaluation of a ventilation strategy to prevent barotrauma
in patients at high risk for acute respiratory distress syndrome: Pressure- and Volume- Limited Ventilation Strategy Group.
N Engl J Med
1998;
338:
355-361
11. The Acute Respiratory Distress Syndrome Network. The Acute Respiratory Distress Syndrome. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301-1308.
12.
Amato MB,
Barbas CS,
Medeiros DM,
Magaldi RB,
Schettino GP,
Lorenzi-Filho G,
Kairalla RA,
Deheinzelin D,
Munoz C,
Oliveira R,
Takagaki TY,
Carvalho CR.
Effect of a protective-ventilation strategy
on mortality in the acute respiratory distress syndrome.
N Engl J Med
1998;
338:
347-354
13. Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988; 138: 720-723 [Medline].
14.
Jonson B,
Richard J-C,
Straus C,
Mancebo J,
Lemaire F,
Brochard L.
Pressure-volume curves and compliance in acute lung injury: evidence
of recruitment above the lower inflection point.
Am J Respir Crit Care
Med
1999;
159:
1172-1178
15. Svantesson C, Drefeldt B, Jonson B. The static pressure-volume relationship of the respiratory system determined with a computer-controlled ventilator. Clin Physiol 1997; 17: 419-430 .
16.
Hickling KG.
The pressure-volume curve is greatly modified by recruitment: a mathematical model of ARDS lungs.
Am J Respir Crit Care
Med
1998;
158:
194-202
17. Dambrosio M, Roupie E, Mollet JJ, Anglade MC, Vasile N, Lemaire F, Brochard L. Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation. Anesthesiology 1997; 87: 495-503 [Medline].
18.
Neumann P,
Berglund JE,
Mondejar EF,
Magnusson A,
Hedenstierna G.
Effect of different pressure levels on the dynamics of lung collapse
and recruitment in oleic-acid-induced lung injury.
Am J Respir Crit
Care Med
1998;
158:
1636-1643
19. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand 1995; 39: 118-125 [Medline].
20.
Rothen HU,
Neumann P,
Berglund JE,
Valtysson J,
Magnusson A,
Hedenstierna G.
Dynamics of re-expansion of atelectasis during general
anaesthesia.
Br J Anaesth
1999;
82:
551-556
21. Suter PM, Fairley HB, Schlobohm RM. Shunt, lung volume and perfusion during short periods of ventilation with oxygen. Anesthesiology 1975; 43: 617-627 [Medline].
22. Dantzker DR, Wagner PD, West JB. Proceedings: instability of poorly ventilated lung units during oxygen breathing. Am J Physiol 1974; 242: 72P .
23.
Santos C,
Ferrer M,
Roca J,
Torres A,
Hernandez C,
Rodriguez-Roisin R.
Pulmonary gas exchange response to oxygen breathing in acute
lung injury.
Am J Respir Crit Care Med
2000;
161:
26-31
24.
Cereda M,
Foti G,
Musch G,
Sparacino ME,
Pesenti A.
Positive end-
expiratory pressure prevents the loss of respiratory compliance during
low tidal volume ventilation in acute lung injury patients.
Chest
1996;
109:
480-485
25. Ranieri VM, Mascia L, Fiore T, Bruno F, Brienza A, Giuliani R. Cardiorespiratory effects of positive end-expiratory pressure during progressive tidal volume reduction (permissive hypercapnia) in patients with acute respiratory distress syndrome. Anesthesiology 1995; 83: 710-720 [Medline].
26. Chelucci GL, Dall'Ava-Santucci J, Dhainaut JF, Chelucci A, Allegra A, Lockhart A, Zin WA, Milic-Emili J. Association of PEEP with two different inflation volumes in ARDS patients: effects on passive lung deflation and alveolar recruitment. Intensive Care Med 2000; 26: 870-877 [Medline].
27.
Carvalho CR,
Barbas CS,
Medeiros DM,
Magaldi RB,
Lorenzi Filho G,
Kairalla RA,
Deheinzelin D,
Munhoz C,
Kaufmann M,
Ferreira M,
Takagaki TY,
Amato MB.
Temporal hemodynamic effects of permissive hypercapnia associated with ideal PEEP in ARDS.
Am J Respir
Crit Care Med
1997;
156:
1458-1466
28. Thorens JB, Jolliet P, Ritz M, Chevrolet JC. Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome. Intensive Care Med 1996; 22: 182-191 [Medline].
29. Zavala E, Mancini M, Mancebo J, Fernandez C, Roca J, Rossi A, Rodriguez-Roisin R. Improvement of pulmonary gas exchange during a "protective ventilatory strategy" in ARDS [abstract]. Am J Respir Crit Care Med 1999; 159: A457 .
30. Blanch L, Fernandez R, Valles J, Sole J, Roussos C, Artigas A. Effect of two tidal volumes on oxygenation and respiratory system mechanics during the early stage of adult respiratory distress syndrome. J Crit Care 1994; 9: 151-158 [Medline].
31. Kiiski R, Takala J, Kari A, Milic-Emili J. Effect of tidal volume on gas exchange and oxygen transport in the adult respiratory distress syndrome. Am Rev Respir Dis 1992; 146: 1131-1135 [Medline].
32. Kiiski R, Kaitainen S, Karppi R, Takala J. Physiological effects of reduced tidal volume at constant minute ventilation and inspiratory flow rate in acute respiratory distress syndrome. Intensive Care Med 1996; 22: 192-198 [Medline].
33.
Pelosi P,
Cadringher P,
Bottino N,
Panigada M,
Carrieri F,
Riva E,
Lissoni A,
Gattinoni L.
Sigh in acute respiratory distress syndrome.
Am J
Respir Crit Care Med
1999;
159:
872-880
34. Foti G, Cereda M, Sparacino ME, De Marchi L, Villa F, Pesenti A. Effects of periodic lung recruitment maneuvers on gas exchange and respiratory mechanics in mechanically ventilated acute respiratory distress syndrome (ARDS) patients. Intensive Care Med 2000; 26: 501-507 [Medline].
This article has been cited by other articles:
 |
|
 |
|
  A. Mercat, J.-C. M. Richard, B. Vielle, S. Jaber, D. Osman, J.-L. Diehl, J.-Y. Lefrant, G. Prat, J. Richecoeur, A. Nieszkowska, et al. Positive End-Expiratory Pressure Setting in Adults With Acute Lung Injury and Acute Respiratory Distress Syndrome: A Randomized Controlled Trial JAMA, February 13, 2008; 299(6): 646 - 655. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. B. Allen, B. T. Suratt, L. Rinaldi, J. M. Petty, and J. H. T. Bates Choosing the frequency of deep inflation in mice: balancing recruitment against ventilator-induced lung injury Am J Physiol Lung Cell Mol Physiol, October 1, 2006; 291(4): L710 - L717. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Luecke, J. P. Meinhardt, P. Herrmann, A. Weiss, M. Quintel, and P. Pelosi Oleic Acid vs Saline Solution Lung Lavage-Induced Acute Lung Injury: Effects on Lung Morphology, Pressure-Volume Relationships, and Response to Positive End-Expiratory Pressure. Chest, August 1, 2006; 130(2): 392 - 401. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Gal Con: low tidal volumes are indicated during one-lung ventilation. Anesth. Analg., August 1, 2006; 103(2): 271 - 273. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Mols, H.-J. Priebe, and J. Guttmann Alveolar recruitment in acute lung injury Br. J. Anaesth., February 1, 2006; 96(2): 156 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. R. Bernard Acute Respiratory Distress Syndrome: A Historical Perspective Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 798 - 806. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. B. Allen, L. A. Pavone, J. D. DiRocco, J. H. T. Bates, and G. F. Nieman Pulmonary impedance and alveolar instability during injurious ventilation in rats J Appl Physiol, August 1, 2005; 99(2): 723 - 730. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Michelet, A. Roch, D. Brousse, X.-B. D'Journo, F. Bregeon, D. Lambert, G. Perrin, L. Papazian, P. Thomas, J.-P. Carpentier, et al. Effects of PEEP on oxygenation and respiratory mechanics during one-lung ventilation Br. J. Anaesth., August 1, 2005; 95(2): 267 - 273. [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]
|
|
|
|
|
|
G. M. Albaiceta, F. Taboada, D. Parra, L. H. Luyando, J. Calvo, R. Menendez, and J. Otero Tomographic Study of the Inflection Points of the Pressure-Volume Curve in Acute Lung Injury Am. J. Respir. Crit. Care Med., November 15, 2004; 170(10): 1066 - 1072. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Johnson Lung recruitment during general anesthesia/Le recrutement alveolaire pendant l'anesthesie generale Can J Anesth, August 1, 2004; 51(7): 649 - 653. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Prodhan and N. Noviski Pediatric Acute Hypoxemic Respiratory Failure: Management of Oxygenation J Intensive Care Med, May 1, 2004; 19(3): 140 - 153. [Abstract] [PDF]
|
|
|
|
|
|
J. M. Downie, A. J. Nam, and B. A. Simon Pressure-Volume Curve Does Not Predict Steady-State Lung Volume in Canine Lavage Lung Injury Am. J. Respir. Crit. Care Med., April 15, 2004; 169(8): 957 - 962. [Abstract] [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]
|
|
|
|
|
|
I. Moran, E. Zavala, R. Fernandez, L. Blanch, and J. Mancebo Recruitment manoeuvres in acute lung injury/acute respiratory distress syndrome Eur. Respir. J., August 1, 2003; 22(42_suppl): 37s - 42s. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Halter, J. M. Steinberg, H. J. Schiller, M. DaSilva, L. A. Gatto, S. Landas, and G. F. Nieman Positive End-Expiratory Pressure after a Recruitment Maneuver Prevents Both Alveolar Collapse and Recruitment/Derecruitment Am. J. Respir. Crit. Care Med., June 15, 2003; 167(12): 1620 - 1626. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Maggiore, F. Lellouche, J. Pigeot, S. Taille, N. Deye, X. Durrmeyer, J.-C. Richard, J. Mancebo, F. Lemaire, and L. Brochard Prevention of Endotracheal Suctioning-induced Alveolar Derecruitment in Acute Lung Injury Am. J. Respir. Crit. Care Med., May 1, 2003; 167(9): 1215 - 1224. [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]
|
|
|
|
|
|
J. E. Baumgardner, K. Markstaller, B. Pfeiffer, M. Doebrich, and C. M. Otto Effects of Respiratory Rate, Plateau Pressure, and Positive End-Expiratory Pressure on PaO2 Oscillations after Saline Lavage Am. J. Respir. Crit. Care Med., December 15, 2002; 166(12): 1556 - 1562. [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]
|
|
|
|
|
|
J. H. T. Bates and C. G. Irvin Time dependence of recruitment and derecruitment in the lung: a theoretical model J Appl Physiol, August 1, 2002; 93(2): 705 - 713. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Sinclair, D. A. Kregenow, W. J. E. Lamm, I. R. Starr, E. Y. Chi, and M. P. Hlastala Hypercapnic Acidosis Is Protective in an In Vivo Model of Ventilator-induced Lung Injury Am. J. Respir. Crit. Care Med., August 1, 2002; 166(3): 403 - 408. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Hubmayr Perspective on Lung Injury and Recruitment: A Skeptical Look at the Opening and Collapse Story Am. J. Respir. Crit. Care Med., June 15, 2002; 165(12): 1647 - 1653. [Full Text] [PDF]
|
|
|
|
|
|
K.-C. Cheng, H. Zhang, C.-Y. Lin, and A. S. Slutsky Ventilation with Negative Airway Pressure Induces a Cytokine Response in Isolated Mouse Lung Anesth. Analg., June 1, 2002; 94(6): 1577 - 1582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. TOBIN Critical Care Medicine in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 565 - 583. [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]
|
|
| ||||||||||||||||||||||||||