| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
ABSTRACT |
|---|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We studied 16 patients with acute lung injury receiving volume-controlled ventilation to assess the relationships between gas exchange and respiratory mechanics before, during, and after 2 h in the prone position. We measured the end-expiratory lung volume (EELV, helium dilution), the total respiratory system (Cst,rs), the lung (Cst,L) and the thoracoabdominal cage (Cst,w) compliances (end- inspiratory occlusion technique and esophageal balloon), the hemodynamics, and gas exchange. In the prone position, PaO2 increased from 103.2 ± 23.8 to 129.3 ± 32.9 mm Hg (p < 0.05) without significant changes of Cst,rs and EELV. However, Cst,w decreased from 204.8 ± 97.4 to 135.9 ± 52.5 ml/ cm H2O (p < 0.01) and the decrease was correlated with the oxygenation increase (r = 0.62, p < 0.05). Furthermore, the greater the baseline supine Cst,w, the greater its decrease in the prone position (r = 0.82, p < 0.01). Consequently, the oxygenation changes in the prone position were predictable from baseline supine Cst,w (r = 0.80, p < 0.01). Returning to the supine position, Cst,rs increased compared with baseline (42.3 ± 14.4 versus 38.4 ± 13.7 ml/cm H2O; p < 0.01), mainly because of the lung component (57.5 ± 25.1 versus 52.4 ± 23.3 ml/cm H2O; p < 0.01). Thus, (1) baseline Cst,w and its changes may play a role in determining the oxygenation response in the prone position; (2) the prone position improves Cst,rs and Cst,L when the supine position is resumed.
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Patients with acute lung injury (ALI) may be characterized by various degrees of hypoxemia, alterations in respiratory mechanics, and reduction in end-expiratory lung volume (EELV). The prone position has been proposed as a relatively simple maneuver to improve oxygenation (1), and an increased EELV was originally suggested as the main mechanism for oxygenation improvement (2). More recently, experimental studies in animal model of ALI found that the prone position causes a venous admixture reduction and a more even ventilation distribution, without affecting EELV (3, 4).
In the adult respiratory distress syndrome (ARDS), the most severe form of ALI, similar improvement in oxygenation, decrease in venous admixture (5), and more homogeneous regional lung inflation (6) have been reported. However, no data are available on the EELV change, which is still considered a possible mechanism to explain the oxygenation improvement in the prone position (7, 8). Furthermore, oxygenation improvement is not a constant finding during prone positioning, and no evidence is available so far to explain why the majority of the patients improve, whereas others remain unchanged or deteriorate. In a small sample of patients with ALI studied with computed tomography, we previously observed that changes in oxygenation were somewhat related to the lung and thoracic cage shape (9).
In this study we investigated the effects of the prone position on EELV, lung and chest wall mechanics, and the relationships between the changes in oxygenation and in respiratory mechanics.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Study Population
We studied 16 consecutive patients with ALI. Eleven of the 16 met the ARDS criteria of the American European Consensus Conference on ARDS (10). None of them had asthma or chronic lung diseases or cardiogenic pulmonary edema. The main clinical characteristics, the time from onset, the ventilatory settings, and the gas exchange at the moment of the study, as well as the outcome, are summarized in Table 1. Thirteen patients were nasotracheally intubated with a cuffed endotracheal tube (7.5 to 8 mm inner diameter) and three had tracheostomies (8 to 10 mm inner diameter). In five of the 16 patients, prone positioning had been already used before performing the study, whereas the remaining 11 patients were studied at the first time of prone positioning.
|
Ventilatory Setting
All patients were studied while sedated with fentanyl (1.5 to 5.5 µg/kg/h) and diazepam (0.03 to 0.18 mg/kg/h), paralyzed with pancuronium bromide (0.05 to 0.1 mg/kg/h), and ventilated in the volume control mode with constant inspiratory flow. Mechanical ventilation was provided with a Servo Ventilator 900 C (Siemens-Elema, Solna, Sweden). The ventilatory setting, positive end-expiratory pressure (PEEP), and inspired oxygen fraction (FIO2) were set according to the clinical needs and kept constant throughout the study. Tidal volume was 0.682 ± 0.144 L, respiratory rate was 13.5 ± 2.5 breaths/min, TI/Ttot was 0.39 ± 0.08, inspiratory flow was 0.386 ± 0.077 L/s, PEEP was 12.3 ± 3.5 cm H2O, FIO2 was 0.68 ± 0.20, and peak inspiratory pressure was 37.8 ± 6.3 cm H2O.
Protocol and Measurements
Change of position was manually performed by four or five attendants (usually three nurses and two doctors). In the prone position the head was turned laterally and the arms were parallel to the body. A roll under the upper part of the chest wall and a pillow under the pelvis were positioned in an effort to minimize restriction of abdominal movements.
Measurements were obtained in the supine position (baseline) after 30 and 120 min in the prone position and 30 min after returning to the supine position. In 13 patients additional measurements were obtained at 120 min after returning to the supine position.
Gas exchange and hemodynamics. All of the patients already had
an arterial and pulmonary artery thermodilution catheter inserted at
the time of the study. Arterial and mixed venous samples were analyzed for gas tensions and pH immediately after sampling (IL BGM,
1312; Instrumentation Laboratory, Spa, Italy). The right to left intrapulmonary shunt (
S/T) was computed by the shunt equation, assuming a respiratory quotient equal to 1. Mean arterial, pulmonary artery, pulmonary wedge, and central venous pressures were measured
with pressure transducers (Transpac IV L974; Abbott Ireland, Sligo,
Republic of Ireland). Zero level was set at the midaxillary line in both
positions. Cardiac output (CO) was measured in triplicate by the thermodilution method, and the cardiac index (CI) was computed normalizing the CO for the body surface area.
Physiologic dead space. Expired gases were collected over a 2-min period in a Douglas bag at the same time as blood gas samples were collected. Expired gas was analyzed for mixed expired CO2 concentration (Model 760 Capnograph; Teledyne Electronic Devices, Bellmafiok, Mirandola, Italy). The physiologic dead space fraction (VD/VT) was computed according to the standard formulas.
End-expiratory lung volume. EELV was measured using a simplified closed-circuit helium dilution method (11) at PEEP during an end-expiratory pause. An anesthesia bag filled with 1.5 L of a known gas mixture (13% helium in oxygen) was connected to the airway opening previously clamped at end-expiration to maintain the PEEP level, and 10 deep manual breaths were performed. The helium concentration in the anesthesia bag was then measured with a helium analyzer (PK Morgan Ltd, Chatham, Kent, UK), and EELV was computed according to the following formula:
![EELV=Vi[He]<SUB>i</SUB>/[He]<SUB>fin</SUB>−Vi](/content/vol157/issue2/fulltext/387/img001.gif)
|
where Vi is the initial gas volume in the anesthesia bag and [He]i and [He]fin are the initial and final helium concentrations in the bag. The limitations of this method have been fully discussed elsewhere (12).
Intra-abdominal pressure. Average intra-abdominal pressure was measured through a transurethral bladder catheter (13). Using a sterile technique, an average of 100 ml of normal saline were infused through the urinary catheter to fill the catheter tubing. The catheter was then clamped distally to the sampling port. A 20-gauge needle was inserted through the catheter sampling membrane, and the bladder catheter pressures were measured using a water manometer zeroed at the pubis level.
Intra-abdominal pressure was measured only at the baseline, at the end of prone position period, and 120 min after returning to the supine position. The intra-abdominal pressure data were not collected in the first four patients.
Respiratory mechanics. Airway pressure (Paw) and gas flow were measured by a self-calibrating flow transducer (Varflex; Bicore Monitoring System, Irvine, CA) connected at the endotracheal or tracheostomy tube opening. Esophageal pressure (Pes) was measured by an esophageal balloon (Bicore Monitoring System) automatically inflated with 0.5 to 1 ml of air and positioned at the lower third of the esophagus as shown by chest roentgenograph. All the signals were acquired on a CP100 Pulmonary Monitor (Bicore Monitoring System), converted to digital form and processed separately for subsequent analysis with a dedicated computerized program.
To measure the compliance of the respiratory system and to partition it into its pulmonary and chest wall components the occlusion method was used. The end-inspiratory hold button of the Servo 900 C
was pressed for brief (7 to 8 s) airway occlusion (14). Occlusion was
maintained until both Paw and Pes decreased from the maximal value
(Pawmax and Pesmax, respectively) to an apparent plateau (Paw2 and
Pes2, respectively). Similarly the end-expiratory airway pressure (PEaw)
and the end-expiratory esophageal pressure (PEes) were recorded
after a brief end-expiratory hold maneuver. The static respiratory system (Cst,rs) and thoracoabdominal (Cst,w) compliances were obtained dividing the tidal volume, respectively, by the difference between Paw2 
PEaw and Pes2 PEes. The static lung compliance
(Cst,L) was obtained with the following formula:
![Cst,L=V<SC>t</SC>/[(Paw<SUB>2</SUB>−Pes<SUB>2</SUB>)−(P<SC>e</SC>aw−P<SC>e</SC>es)].](/content/vol157/issue2/fulltext/387/img002.gif)
|
One could question the comparison of esophageal balloon measurements in the supine and the prone positions. In fact, it is possible that the transmission of the alveolar pressure to the pleural space is different in the two conditions because of the different relative position of the heart, which moves ventrally on turning prone. However, no alternative methods are available in humans, and this method was considered adequate also in the prone position, and it was adopted to perform lung-volume curves in both awake (15) and paralyzed subjects (11, 16). Moreover, if the change of position would result in artefacts when measuring the esophageal pressure, this would lead to systematic changes in the same direction (false increase or false decrease), but this was not the case in our study (see RESULTS).
Total resistance of the respiratory system (Rtot,rs) and of the chest
wall (Rtot,w) were computed as (Pawmax Paw2)/
i and (Pesmax Pes2)/i, respectively, where i is the flow immediately before the
occlusion. Total lung resistance (Rtot,L) was obtained as the difference between Rtot,rs and Rtot,w. Rtot,rs and Rtot,L include the endotracheal or tracheostomy tube resistance.
All respiratory mechanics data (except the EELV) were obtained as an average of three measurements.
Statistics
All data are expressed as mean ± 1 standard deviation. Comparisons
between the different periods were performed using Friedman's nonparametric analysis of variance. Individual comparison with baseline
were performed with a nonparametric paired t test; Bonferroni's correction was applied for multiple comparisons. The least-squares method
was used to perform linear regression analysis; p 
0.05 was considered
statistically significant.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Gas Exchange and Hemodynamics
In this series of patients the prone position resulted in a significant increase in oxygenation within 120 min (Table 2), even if
there was considerable individual variation in oxygenation response in the prone position. Indeed in 12 patients, PaO2 increased (range, 9 to 73 mm Hg), whereas in four patients it decreased (range, 7 to 16 mm Hg) compared with baseline.
When the patients were repositioned supine the oxygenation
was not significantly different from that in the prone position
or that at baseline. Shunt fraction, PaCO2, and dead space did
not significantly change when the patients were turned prone
and when they were repositioned supine. These responses
were similar both in the patients with ALI and in those with
ARDS. We could not find any relationship between the oxygenation response and the time elapsed from disease onset.
|
As shown in Table 3, mean pulmonary artery pressure, wedge pressure, and central venous pressure slightly, but significantly, increased during the prone position and returned to baseline values after returning to the supine position. However, since we kept the midaxillary line as a zero reference level, these minimal changes could be due to a shift of the real zero pressure level because of ventral movement of the heart. Other hemodynamic variables remained unchanged during the prone position.
|
Respiratory Mechanics
Overall results are shown in Table 4. No significant EELV differences were observed between supine and prone positions despite a trend toward increases while prone. Similarly, the intra-abdominal pressure was not significantly affected by the positional changes. The prone position did not significantly affect Cst,rs and Cst,L (Figure 1), but it resulted in a significant reduction in Cst,w. Thirty minutes after returning to the supine position, Cst,rs increased compared with either baseline or prone position values (p < 0.01). This improvement was mainly due to the lung component (p < 0.01), but the Cst,w returned to baseline levels. The improvement in total respiratory system and lung compliance was consistent in the majority of our patient population. Indeed, in 14 of the 16 patients, plateau pressure was reduced after returning supine compared with that at baseline, with a range of 1.3 to 4.2 cm H2O (average, 2.32 ± 0.92 cm H2O) (p < 0.01). This effect also persisted 120 min after returning supine. Airway resistances were not significantly affected by postural changes.
|
|
Oxygenation-Respiratory Mechanics Relationships
The changes in oxygenation induced by the prone position
were not related to changes in EELV or total respiratory system or lung compliance. However, the oxygenation changes in
the prone position were predictable from the baseline supine
Cst,w. As shown in Figure 2, higher Cst,w were associated
with greater PaO2 improvements in the prone position (
PaO2 =
32.4 + 0.24 * Cst,r; r = 0.80, p < 0.01). Moreover, Cst,w
changes in the prone position were correlated with the baseline Cst,w values (Cst,w = 88.5 0.72 * Cst,w; r = 0.82, p < 0.01) (Figure 3).
|
|
Furthermore, we found a fair correlation between the early
changes of oxygenation (30 min after prone positioning) and
the changes in the compliance of the thoracoabdominal cage.
(PaO2 = 3.9 0.2 * Cst,w; r = 0.62, p < 0.05). The greater
the decrease of thoracoabdominal compliance, the greater the
improvement in oxygenation (Figure 4). At 120 min the PaO2
further increased, and the Cst,w further decreased. However,
the correlation between the thoracoabdominal compliance
changes and oxygenation changes was only close to statistical
significance (r = 0.45; p = 0.07).
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
As previously shown by other studies (5, 17, 18), in this series of patients we observed a great variability of individual responses in oxygenation. On average, however, the PaO2 after 120 min in the prone position was significantly higher than that at baseline. This improvement was not due to EELV changes. At the same time, the compliance of the thoracoabdominal cage was significantly lower than that at baseline. When returning to the supine position, the total respiratory system and lung compliance values were significantly higher than baseline values.
Supine to Prone Shifting
Oxygenation. An increase in EELV was originally proposed by Douglas and colleagues (2) to explain the improvement in oxygenation observed in their pioneering study on the prone position in ALI, and it has since been considered a possible explanation for the improvement in gas exchange associated with the prone position (7, 8, 17). This hypothesis seems unlikely in adult patients with ALI since no significantly EELV changes were observed during prone positioning, and the EELV variations were not related to the changes in oxygenation. The lack of correlation between improvement in oxygenation and changes in EELV is in keeping with previous findings in oleic-acid-injured dogs (3), in normal (16) and in obese (11) anesthetized subjects, and in pediatric patients with ALI (19). Moreover, in a previous study using computed tomography, we did not find any difference in the average slice densities between the prone and the supine positions, suggesting an unmodified total gas volume (6). However, because of the relatively small patient population, we cannot safely exclude a possible marginal increase in EELV during prone positioning; in fact, a trend towards increased EELV was present in this study and in a previous one on animals (3). Nonetheless, this study clearly shows that an increase in global EELV is not necessary to obtain improved gas exchange in the prone position.
Therefore, the rise in oxygenation during prone positioning may only be explained by regional changes of inflation/ventilation or perfusion with an unmodified global EELV. Indeed, data obtained in experimental animal settings attributed the improvement in oxygenation primarily to a regional variation of ventilation, which was found more evenly distributed between the dorsal and the ventral lung regions in the prone position (20). Moreover, in patients with ALI we found, with the CT scan, a more homogeneous regional inflation in the prone position than in the supine position (6), which was actually associated with better oxygenation (9). In summary, the available human and experimental data suggest that the main determinant of the improvement in oxygenation in the prone position is the redistribution of the inflation gradient from dorsal to ventral regions (6), resulting in more even regional inflation/ventilation along the vertical axis, in the absence of a gravitary perfusion distribution (4). However, the regional assessment of perfusion in patients is technically difficult, and this hypothesis remains to be proved.
Respiratory mechanics. Shifting from the supine to the prone position resulted in a significant reduction in the compliance of the thoracoabdominal cage. This decrease could be explained by a decrease of the compliance of either the rib cage or diaphragmatic component of the chest wall or both. We can reasonably assume that the diaphragmatic wall compliance as a whole (notwithstanding differences in regional distribution) remained substantially unchanged in the prone position because the intra-abdominal pressure was not significantly different in the prone and supine positions. The decrease of thoraco-abdominal compliance should therefore be explained by a greater rigidity of the rib cage component of the chest wall in the prone position when compared with the supine position.
Indeed, the compliance of the rib cage component of the chest wall is known to be nonhomogeneous, the ventral part (sternal) presenting a "larger freedom to move," than the dorsal part (vertebral) (21). The dishomogeneity is further enhanced in the supine position where movement remains unimpeded in only the ventral part (the dorsal part of the chest lies on the bed). This is one of the possible mechanisms causing the preferential distribution of ventilation to ventral lung areas in supine, paralyzed subjects with ALI (22). In the prone position, the stiffer component of the rib cage (dorsal part) is free to move, whereas movement of the more compliant (ventral part) becomes impeded by lying on the bed. This results in a decrease in net rib cage compliance. However, because of this rearrangement, at least during volume-controlled ventilation, the prone position should partly redistribute the tidal ventilation towards the dependent ventral regions, resulting in an overall more even regional distribution than that in the supine position.
Returning Supine after the Prone Position
Oxygenation. When returning to the supine position oxygenation slightly declined, but no significant differences were observed when compared with baseline or the prone position. However, because of the small population, we cannot exclude a type II error. Once again, these average values were derived from variable individual responses. Different oxygenation responses when returning to the supine position have been previously described, including both a reversal of oxygenation improvement (5) and a maintenance of improved oxygenation (17, 18). We were unable to find any relationship between respiratory mechanics and oxygenation when the supine position was resumed.
Respiratory mechanics. A main finding of this study was the significant increase of the compliance of the total respiratory system above baseline values when returning to the supine position. This improvement was mainly due to an increase of the lung compliance. It is somewhat surprising to find that the changes in lung compliance were not associated with changes in EELV, which did not significantly change. It is worth considering, however, that the way we measured the compliance included a possible intratidal recruitment (i.e., recruitment during the inspiratory phase of tidal ventilation) (22). In fact the substantial redistribution of regional lung collapse observed during the prone position (6) could well have resulted in an increased portion of the lung becoming recruitable during tidal insufflation when returning to the supine position (22), thus explaining the increase in lung compliance associated with an unmodified lung volume. An alternative explanation could be a change of specific compliance.
Relationships between Changes in Oxygenation and Changes in the Mechanical Properties of the Respiratory System
We submit an integrated interpretation of the findings obtained in this and in other studies of ALI.
Paralyzed patients with ALI in the supine position at end-expiration exhibit an inflation gradient (i.e., relative difference of regional inflation) much greater than that in normal subjects; this is due to the increase in lung weight. The progressive decrease of regional inflation along the vertical axis results in regional collapse of the most dorsal regions (6, 23). At PEEP levels usually applied when these lungs are insufflated, the tidal volume preferentially distributes to the ventral lung regions, causing higher regional Cst,rs than in the dorsal regions (22). When shifting from the supine to the prone position, the pattern is almost completely reverted. At end-expiration, the regional inflation decreases from dorsal to ventral, and the most dependent ventral regions collapse.
It must be noted, however, that the inflation gradient is decreased compared with that in the supine position, i.e., the differences of regional inflation are less pronounced, resulting in an overall more homogenous regional inflation. The decrease of the inflation gradient in the prone position could be due to the changed position of the heart, which no longer compresses the dorsal lung regions (24, 25). The more even regional inflation per se could result in better oxygenation. In fact, we previously found by CT scan at end-expiration a correlation between the increased homogeneity of lung inflation induced by the prone position and the increase of oxygenation (9).
In the present study we found, in addition, that the decrease of the thoracoabdominal compliance in the prone position when compared with the supine position was associated with improvement of oxygenation. We hypothesize a different distribution of tidal volume compared with that in the supine position as a possible mechanism. Indeed, in the prone position, because of the greater stiffness of the dorsal part of the thoracic cage, the insufflated gases should distribute more towards the ventral and diaphragmatic regions (now dependent) where minimal inflation or collapse are present at end-expiration. The greater the stiffness of the dorsal part of the thoracic cage, the greater should be insufflation of the less aerated ventral regions, and the greater the improvement in oxygenation.
Although a thorough understanding of the mechanisms underlying the changes in oxygenation also requires knowledge of regional perfusion, this study showed that the mechanical properties of the thoracoabdominal cage and its variations play an important role in dictating the oxygenation response in the prone position.
Long-term Effects of Prone Position
In recent years a very large number of studies have reported an improvement in oxygenation in patients with ALI when placed in the prone position (7). Indeed, this manuever is now widely accepted as a useful tool to improve oxygenation in patients with severe ALI.
However, besides the improvement in oxygenation associated with prone positioning, some of these studies reported other interesting observations such as the persistent improvement above baseline values when returning to the supine position (17, 18), a dramatic redistribution of CT-lung densities in the prone position (6), and a decrease of densities when returning supine after 4 h in the prone position, compared with baseline (26). More recently, Broccard and colleagues (27) showed that the prone position may decrease the damaging effect of large tidal volume ventilation in dogs with preinjured lungs. In the present study, we have shown that the prone position leads, independent of gas exchange, to an improvement in the mechanical properties of the respiratory system when returning to the supine position, thus adding another piece of evidence to the hypothesis that the prone position, besides improving gas exchange, induces modifications in underlying lung conditions that persist after returning to the supine position.
We believe that these findings taken together, represent a solid base to justify a prospective trial evaluating whether the prone position may affect the clinical course of acute lung injury.
| |
Footnotes |
|---|
Correspondence and requests for reprints should be addressed to Dr. Luciano Gattinoni, Istituto de Anestesia e Rianimazione, Ospedale Maggiore, IRCCS, via F. Sforza 35, 20122, Milan, Italy.
(Received in original form April 3, 1997 and in revised form July 16, 1997).
Acknowledgments: The writers wish to thank the physicians and the nursing staff of the Intensive Care Unit of the Ospedale Maggiore for their cooperation in the management of patients during the study, and Prof. Antonio Pesenti and Prof. Lawrence R. Goodman for their helpful suggestions in preparing the manuscript.
| |
References |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1. Piehl, M. A., and R. S. Brown. 1976. Use of extreme position changes in acute respiratory failure. Crit. Care Med. 4: 13-14 [Medline].
2. Douglas, W. W., K. Rheder, F. M. Beynen, A. D. Sessler, and H. M. Marsh. 1977. Improved oxygenation in patients with acute respiratory failure: the prone position. Am. Rev. Respir. Dis. 115: 559-566 [Medline].
3. Albert, R. K., D. Leasa, M. Sanderson, H. T. Robertson, and M. P. Hlastala. 1987. The prone position improves arterial oxygenation and reduces shunt in oleic-acid-induced acute lung injury. Am. Rev. Respir. Dis. 135: 628-633 [Medline].
4. Lamm, W. J. E., M. M. Graham, and R. K. Albert. 1994. Mechanism by which the prone position improves oxygenation in acute lung injury. Am. J. Respir. Crit. Care Med. 150: 184-193 [Abstract].
5.
Pappert, D.,
R. Rossaint,
K. Slama,
T. Gruning, and
K. J. Falke.
1994.
Influence of positioning on ventilation-perfusion relationships in severe adult respiratory distress syndrome.
Chest
106:
1511-1516
6. Gattinoni, L., P. Pelosi, G. Vitale, A. Pesenti, L. D'Andrea, and D. Mascheroni. 1991. Body position changes redistribute lung computed-tomographic density in patients with acute respiratory failure. Anesthesiology 74: 15-23 [Medline].
7. Broccard, A., and J. J. Marini. 1995. Effect of position and posture on the respiratory system. In J. L. Vincent, editor. Yearbook of Intensive Care and Emergency Medicine, 1st ed. Springer-Verlag, Berlin. 165- 184.
8. Joliet, P., P. Bulpa, and J. C. Chevrolet. 1996. Ventilation en decubitus ventral lors du syndrome de detresse respiratorie aigue (SDRA). Schweiz. Med. Wochenschr. 126: 879-882 [Medline].
9. Gattinoni, L., P. Pelosi, F. Valenza, and D. Mascheroni. 1994. Patient positioning in acute respiratory failure. In M. J. Tobin, editor. Principles and Practice of Mechanical Ventilation, 1st ed. McGraw-Hill, New York. 1067-1076.
10. Bernard, G. R., A. Artigas, K. L. Brigham, J. Carlet, K. Falke, L. Hudson, M. Lamy, J. R. Legall, A. Morris, R. Spragg, and the Consensus Committee. 1994. The American-European consensus conference on ARDS: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am. J. Respir. Crit. Care Med. 149: 818-824 [Abstract].
11. Pelosi, P., M. Croci, E. Calappi, D. Mulazzi, M. Cerisara, P. Vercesi, P. Vicardi, and L. Gattinoni. 1996. Prone positioning improves pulmonary function in obese patients during general anesthesia. Anesth. Analg. 83: 578-583 [Abstract].
12. Pelosi, P., M. Croci, I. Ravagnan, M. Cerisara, P. Vicardi, A. Lissoni, and L. Gattinoni. 1997. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J. Appl. Physiol. 83: 811-818 .
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. 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].
15.
Milic-Emili, J.,
J. Mead, and
J. M. Turner.
1964.
Topography of esophageal pressure as a function of posture in man.
J. Appl. Physiol.
19:
212-216
16. Pelosi, P., M. Croci, E. Calappi, M. Cerisara, D. Mulazzi, P. Vicardi, and L. Gattinoni. 1995. The prone positioning during general anesthesia minimally affects respiratory mechanics while improving functional residual capacity and increasing oxygen tension. Anesth. Analg. 80: 955-960 [Abstract].
17.
Langer, M.,
D. Mascheroni,
R. Marcolin, and
L. Gattinoni.
1988.
The prone position in ARDS patients: a clinical study.
Chest
94:
103-107
18. Chatte, G., J. M. Sab, J. M. Dubois, M. Sirodot, P. Gaussorgues, and D. Robert. 1997. Prone position in mechanically ventilated patients with severe acute respiratory failure. Am. J. Respir. Crit. Care Med. 155: 473-478 [Abstract].
19. Wagaman, M. J., J. G. Shutack, A. S. MoomJian, J. G. Schwartz, T. H. Shaffer, and W. W. Fox. 1979. Improved oxygenation and lung compliance with prone positioning of neonates. J. Pediatr. 94: 787-791 [Medline].
20. Mutoh, T., R. J. Guest, W. J. E. Lamm, and R. K. Albert. 1992. Prone position alters the effect of volume overload on regional pleural pressures and improves hypoxemia in pigs in vivo. Am. Rev. Respir. Dis. 146: 300-306 [Medline].
21. Osmon, G. O. 1995. Functional anatomay of the chest wall. In Ch. Roussos, editor. The Thorax, 2nd ed. Marcel Dekker, New York. 413-443.
22. 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].
23. Pelosi, P., L. D'Andrea, G. Vitale, A. Pesenti, and L. Gattinoni. 1994. Vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am. J. Respir. Crit. Care Med. 149: 8-13 [Abstract].
24.
Liu, S.,
S. S. Margulies, and
T. A. Wilson.
1990.
Deformation of the dog lung in the chest wall.
J. Appl. Physiol.
68:
1979-1987
25.
Hyatt, R. E.,
E. Bar-Yishay, and
M. D. Abel.
1985.
Influence of the heart on the vertical gradient of transpulmonary pressure in dogs.
J. Appl.
Physiol.
58:
52-57
26. Priolet, B., G. Tempelhoff, J. Miller, A. Cannamela, and M. J. Carton. 1993. Ventilation assiste' en decubitus ventral: evaluation tomodensitometrique de son efficacite' dans le traitment des condensations pulmonaires. Rean. Urg. 2: 81-85 .
27. Broccard, A. F., R. S. Shapiro, L. L. Schmitz, S. A. Ravenscraft, and J. J. Marini. 1997. Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model of acute respiratory distress syndrome. Crit. Care Med. 25: 16-27 [Medline].
This article has been cited by other articles:
 |
|
 |
|
  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]
|
|
|
|
|
|
C. Guerin, S. Gaillard, S. Lemasson, L. Ayzac, R. Girard, P. Beuret, B. Palmier, Q. V. Le, M. Sirodot, S. Rosselli, et al. Effects of Systematic Prone Positioning in Hypoxemic Acute Respiratory Failure: A Randomized Controlled Trial JAMA, November 17, 2004; 292(19): 2379 - 2387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. O'Neill, J. G. Venegas, T. Richter, R. S. Harris, J. D. H. Layfield, G. Musch, T. Winkler, and M. F. V. Melo Modeling kinetics of infused 13NN-saline in acute lung injury J Appl Physiol, December 1, 2003; 95(6): 2471 - 2484. [Abstract] [Full Text]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 L. Gattinoni, G. Tognoni, A. Pesenti, P. Taccone, D. Mascheroni, V. Labarta, R. Malacrida, P. Di Giulio, R. Fumagalli, P. Pelosi, et al. Effect of Prone Positioning on the Survival of Patients with Acute Respiratory Failure N. Engl. J. Med., August 23, 2001; 345(8): 568 - 573. [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. 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]
|
|
|
|
|
|
A. T. Jones, D. M. Hansell, and T. W. Evans Pulmonary perfusion in supine and prone positions: an electron-beam computed tomography study J Appl Physiol, April 1, 2001; 90(4): 1342 - 1348. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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. INGIMARSSON, A. THORSTEINSSON, A. LARSSON, and O. WERNER Lung and Chest Wall Mechanics in Anesthetized Children . Influence of Body Position Am. J. Respir. Crit. Care Med., August 1, 2000; 162(2): 412 - 417. [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]
|
|
|
|
|
|
N. CAKAR, T. V. d. KLOOT, M. YOUNGBLOOD, A. ADAMS, and A. NAHUM Oxygenation Response to a Recruitment Maneuver during Supine and Prone Positions in an Oleic Acid-Induced Lung Injury Model Am. J. Respir. Crit. Care Med., June 1, 2000; 161(6): 1949 - 1956. [Abstract] [Full Text]
|
|
|
|
|
|
G. NAKOS, I. TSANGARIS, E. KOSTANTI, C. NATHANAIL, A. LACHANA, V. KOULOURAS, and D. KASTANI Effect of the Prone Position on Patients with Hydrostatic Pulmonary Edema Compared with Patients with Acute Respiratory Distress Syndrome and Pulmonary Fibrosis Am. J. Respir. Crit. Care Med., February 1, 2000; 161(2): 360 - 368. [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]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||