ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Permissions
Right arrowRequest Permissions
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Zakynthinos, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Zakynthinos, S. G.
Eur Respir J 2005; 25:259-268
Copyright ©ERS Journals Ltd 2005

Prone position improves expiratory airway mechanics in severe chronic bronchitis

S. D. Mentzelopoulos1, C. Roussos2 and S. G. Zakynthinos2

1 University of Athens Medical School, Dept of Intensive Care Medicine, Attikon University Hospital, and 2 University of Athens Medical School, Dept of Intensive Care Medicine, Evaggelismos General Hospital, Athens, Greece

CORRESPONDENCE: S. D. Mentzelopoulos, 12 Ioustinianou Street, GR-11473, Athens, Greece. Fax: 30 2103218493. E-mail: sdm@hol.gr

Keywords: Air flow, airway resistance, chronic obstructive pulmonary disease, compliance, mechanical ventilation

Received: August 12, 2004
Accepted September 30, 2004


   ABSTRACT
TOP
 ABSTRACT
MATERIAL AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
 REFERENCES
 
Based on lung parenchyma-airways' interdependence, the present authors hypothesised that prone positioning may reduce airway resistance in severe chronic bronchitis.

A total of 10 anaesthetised/mechanically ventilated patients were enrolled. Partitioned respiratory system (RS) mechanics during iso-flow experiments (flow = 0.91 L·s–1, tidal volume (VT) varied within 0.2–1.2 L), haemodynamics, gas-exchange, expiratory airway resistance (Raw,exp), functional residual capacity (FRC), change in FRC ({Delta}FRC), end-expiratory lung volume (EELV), expiratory airway resistance at EELV (Raw,exp,EELV), intrinsic positive end-expiratory pressure (PEEPi), and mean end-expiratory flow were determined in baseline semirecumbent (SRBAS), prone, and post-prone semirecumbent (SRPP) postures.

Pronation versus SRBAS resulted in significantly reduced Raw,exp (at VT ≥0.8 L), Raw,exp,EELV (18.3±1.4 versus 31.6±2.6 cm H2O·L–1·s–1), inspiratory airway resistance (at VT ≥1.0 L), static lung elastance (at VT ≤0.6 L), "additional" RS/lung resistance (at a range of VTs), {Delta}FRC (0.35±0.03 versus 0.47±0.03 L), EELV (4.92±0.49 versus 5.65±0.65 L), RS/lung PEEPi (6.7±1.1/5.4±0.6 versus 8.9±1.7/7.8±1.1 cm H2O), mean end-expiratory flow (63.9±4.2 versus 47.9±4.0 mL·s–1), and shunt fraction (0.16±0.03 versus 0.21±0.03); benefits were reversed in SRPP.

In severe chronic bronchitis, prone positioning reduces airway resistance and dynamic hyperinflation.

Pronation of chronic obstructive pulmonary disease (COPD) patients improves lung parenchyma mechanics and arterial oxygenation 1. Lung inflation gradient is attenuated 1, 2 and lung compression by the heart is eliminated 1, 3. Regional alveolar ventilation may become more homogenous 1, 4, suggesting reduction in alveolar atelectasis and hyperinflation 1. Decreased atelectasis and more uniform inflation should result in more homogenous and increased average alveolar septal tension 5; the latter is transmitted to airway walls via connective tissue cables 5, resulting in outward wall traction and airway calibre increase 6. If parenchymal elastic recoil is "maintained" (e.g. chronic bronchitis) 6, 7, pronation might enhance "parenchyma-induced bronchodilation".

In severe chronic bronchitis 8, bronchial wall inflammation/hypertrophy leads to airway stenosis 6; increased mucosal thickness may augment airway obstruction reversibility with "effective bronchodilation" 6. However, severe COPD patients may be unresponsive to brochodilator drugs 9; in such patients, alternative mechanisms of increasing airway calibre may become important. Severe COPD is characterised by increased airway resistance and intrinsic positive end-expiratory pressure (PEEPi) 10, 11.

The present authors theorised that in severe chronic bronchitis, prone position versus semirecumbent may reduce airway resistance. The current authors also sought to determine any pronation benefits on dynamic pulmonary hyperinflation. PEEPi, functional residual capacity (FRC), change in FRC ({Delta}FRC; where {Delta}FRC = increment in FRC reflecting dynamic hyperinflation), end-expiratory lung volume (EELV; where EELV = FRC plus {Delta}FRC), and mean end-expiratory flow (V') were also comparatively assessed in the prone and semirecumbent positions.


   MATERIAL AND METHODS
TOP
 ABSTRACT
 MATERIAL AND METHODS
RESULTS
 DISCUSSION
 APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
 REFERENCES
 
Patients
Institutional Review Board (Evaggelismos General Hospital, Scientific Committee, Athens, Greece) approval and patient/next-of-kin consent were obtained. A total of 10 severe chronic bronchitis patients (table 1Go) 8, 9 were enrolled. Patients were positioned semirecumbent, orotracheally intubated and mechanically ventilated (Siemens 300C ventilator; Siemens AG, Berlin, Germany). All patients were admitted to the intensive care unit because of acute respiratory failure (arterial oxygen tension (Pa,O2)/inspiratory oxygen fraction (FI,O2) , 82–135 mmHg; carbon dioxide arterial tension (Pa,CO2), 72.8–112.6 mmHg) secondary to acute bronchitis, defined as in Dewan et al. 13. There were no patients with an already existing tracheostomy. The duration of mechanical ventilation until study protocol initiation ranged 32.4–46.5 h. Patients were poor responders to bronchodilators 7, 9 during the pre-admission period of clinical stability. Previously published exclusion criteria 1 were applied. During the 7.0–7.5-h study period, patient care was provided by a physician not involved in the present study. Monitoring was as previously described 1. Any enteral nutrition was replaced by parenteral administration, gastric contents were suctioned, and the nasogastric tube was removed. Anaesthesia was induced with propofol/fentanyl and maintained throughout the study period with propofol/fentanyl infusions to achieve respiratory muscle inactivity 14, 15.


View this table:
[in this window]
[in a new window]
  		Table. 1— 1 Individual patient characteristics prior to and after hospital admission and initial in-hospital management

 
Inspiratory V', tidal volume, and tracheal, oesophageal and gastric pressures
Inspiratory V', tidal volume (VT), tracheal, oesophageal and gastric pressures (Paw, Poes and Pga, respectively) were measured with heated pneumotachograph (pneumotachometer; Hans Rudolph Inc., Kansas City, MT, USA) and Validyne pressure-transducers (Validyne, Nortridge, CA, USA) 1, 16. Correct oesophageal and gastric balloon positioning were verified before anaesthesia induction as previously described 17–19. Following analogue-to-digital conversion, variable data were stored on an IBM-type computer for later analysis with Anadat software (RHT-InfoData, Montreal, QC, Canada). During data sampling, variable tracings were displayed on a dedicated monitor and recorded with an eight-channel electrostatic recorder (Gould ES 1000; Gould Electronics Inc., Eastlake, OH, USA). Breathing circuit modifications included removal of humidifier and use of low compliance tubing 16. A manually operated, pneumatically driven valve (Hans-Rudolph 9300) was inserted between the pneumotachograph and ventilator's Y-piece. Care was taken to avoid gas leaks. Equipment dead space (endotracheal tube not included) was 130 mL.

Respiratory mechanics were sequentially assessed with constant V' rapid airway occlusion in baseline semirecumbent (SRBAS, 60° inclination), prone, and post-prone semirecumbent (SRPP, 60° inclination) positions. Patient turning was performed as previously completed 1. Following pronation, abdominal movement restriction was minimised by placing a roll under the upper part of the chest wall and a pillow under the pelvis 1, 2. The reliability of Poes measurements was tested as previously described 1. Figure 1Go presents data originating from a representative study participant.



View larger version (19K):
[in this window]
[in a new window]
  		Fig. 1— Methodology of assessment of respiratory mechanics. a) Tidal volume, b) flow, and c) gastric, d and e) oesophageal and f) tracheal pressures (Pga, Poes and Paw, respectively) data print-out, showing two baseline ventilation breaths separated by a sigh test breath (VT = 1.2 L), an expiratory occlusion tracing of Paw, and three superimposed expiratory occlusion tracings originating from the rest three breaths of the set. f) The Paw tracings of the expiratory occlusions of the three test sighs (– – –, and grey line) at rest were superimposed according to their time lag relative to inflection point (IP). Expiratory occlusion pressure (PEO) 1 is the earliest expiratory occlusion relative to IP. The long dashed lines were drawn from the start of the earliest (dashed line) and latest expiratory occlusion Paw tracings, and enclose an expired tidal volume slice, during which the dynamic deflation compliance of the respiratory system was determined. Deflation compliance was approximately constant during all studied volume slices. Pmax: peak inspiratory pressure; DPEEPi: dynamic intrinsic positive end-expiratory pressure (PEEPi); SPEEPi: static PEEPi; Ppeak: peak pressure; Pplateau: plateau pressure; P1: pressure immediately after end-inspiratory airway occlusion; P2: plateau inspiratory pressure.

 
Figure 1dGo shows a Poes tracing which constitutes the average of Poes tracings of all four sigh-breaths. All other tracings originate from the second of the four test sighs. The Poes tracing in figure 1eGo shows the maximal amplitude of cardiac oscillation = Ppeak–Pplateau; and Poes rise rate during cardiac oscillation = time needed for Poes to rise from Pplateau to Ppeak. For each set of test breaths, cardiac oscillation variables were averaged and compared among study postures, in order to assess the reliability of Poes measurements. The test breath is followed by an expiratory occlusion (continuous black line; fig. 1Go), during which expiratory occlusion pressure 4 was determined. This occlusion was the most delayed in all four test-sighs relative to the expiratory flow inflection point.

Table 2Go displays baseline ventilator settings employed throughout the study period. Interventions (below described) were separated by 15-min periods of baseline ventilation for re-establishment of baseline conditions 20. Within 30–60 min after study-posture assumption, six sets of four test breaths were administered. In the sets of test breaths a constant, square-wave, inspiratory V' (0.91 L·s–1) was employed. For the first, second, third, fourth, fifth and sixth set of test breaths, the respective administered VTs were 0.2, 0.4, 0.6 (baseline), 0.8, 1.0, and 1.2 ("sigh" 21) L. Test breaths were separated by 1-min baseline ventilation. Maximal allowable plateau airway pressure (P2,aw) was 50 cmH2O.


View this table:
[in this window]
[in a new window]
  		Table. 2— 2 Baseline ventilator settings employed throughout the study period

 
Test breaths were preceded by 2-s duration end-expiratory occlusions, enabling determination of static respiratory system (RS) PEEPi, chest wall PEEPi, and abdominal chest wall-component PEEPi (fig. 1Go) 1; the latter was always ~0. For Poes, end-expiratory occlusion-plateaus were obtained by ensemble averaging 22 of Poes tracings of each test breath set (fig. 1Go). Dynamic PEEPi was defined as Paw change generating inspiratory V' and initiating lung inflation 23. Dynamic PEEPi was determined at baseline ventilation breaths that preceded test breaths (fig. 1Go). Expiratory occlusions were followed by 4–6-s duration end-inspiratory occlusions, enabling determination of maximal pressure (Pmax), pressure immediately after initiation of end-inspiratory occlusion (P1), and plateau pressure (P2) on computer-stored Paw tracings, and of Pmax and P2 on computer-stored Pga tracings (fig. 1Go). For Poes, Pmax, P1, and P2 were determined after ensemble averaging of the tracings of each set of test breaths 22 (fig. 1Go). Paw values were referred to atmospheric pressure, and Poes/Pga values were referred to their pre-end-expiratory occlusion values 1. For each set of test breaths, transpulmonary pressure (PL) was determined as difference between average Paw value and averaged Poes.

Haemodynamics and gas exchange
Within 75–90 min of study-posture assumption, thermodilution cardiac output (in triplicate), central venous and pulmonary artery wedge pressures, heart rate, mean arterial and pulmonary artery pressures, and gas exchange variables were determined/recorded as previously described 1. Formula-derived variables included cardiac, systemic, and pulmonary vascular resistance index, oxygen consumption, respiratory quotient, alveolar oxygen partial pressure, and shunt fraction (see Appendix 1).

Inspiratory resistance and elastance
Total respiratory system, chest wall, and lung inspiratory mechanical properties were computed by standard formulas (see Appendix 2) 1.

Expiratory airway resistance
Monitor-displayed expiratory V' waveforms exhibited an inflection point, ~1 s following the release of inspiratory occlusion (fig. 1Go). Inflection point was defined as point of maximum change in curve-slope following expiratory peak V' (fig. 1Go) 15. Expiratory Paw was determined during 2-s duration expiratory occlusions performed with the pneumatically driven valve within 1 s following inflection point's appearance (fig. 1Go). Each expiratory occlusion was followed by a 2-s duration endotracheal tube disconnection from breathing circuit, in order to achieve a nonoccluded expiratory period approximately equal to baseline ventilation's expiration time (table 2Go).

For each set of post-test breath expirations, RS dynamic deflation compliance was assumed as identical at any expiration time point from test VT to EELV. This would mean identical expiratory occlusion pressure at any expiration time point, corresponding to identical RS volume, and should allow superimposition of Paw tracings of each test breath-set (fig. 1Go). The aforementioned assumption was supported by the following facts: 1) test breaths were separated by 1-min periods of baseline ventilation with identical VT and inspiratory V', resulting in identical Paw/Poes changes; thus, pre-test breath VT history and corresponding pressure changes were identical; 2) just prior to inspiratory occlusion release, P2,aw values, representing initial, expiratory driving pressure were identical; and 3) lung emptying pattern was virtually identical, as confirmed by analysis of expiratory V' and expired VT tracings.

For each set of test breaths, the Paw tracing with the most delayed (relative to inflection point) expiratory occlusion (reference Paw tracing) was used for determination of expiratory airway resistance (Raw,exp). Expiratory occlusion portions of the rest three Paw tracings were superimposed on the reference Paw tracing (fig. 1Go). Subsequently, lines were drawn from the onset of the earliest and latest expiratory occlusion towards the expiratory V' VT tracings (fig. 1Go). These lines enclosed expired VT slices of 0.05–0.15 L. For each VT slice, deflation time constant was defined as the time needed for expiration of the initial 63% portion of that particular VT slice. For each VT slice, RS dynamic deflation compliance was determined as VT changes divided by respective Paw changes (fig. 1Go). Raw,exp was computed as VT-slice time constant divided by RS dynamic deflation compliance.

{Delta}FRC, FRC and end-expiratory lung volume
At 105 min following study-posture assumption, baseline ventilation {Delta}FRC was measured by allowing exhalation to FRC (fig. 2Go) 16. Immediately thereafter, FRC was determined with the closed-circuit helium dilution technique 2, 24, 25. An anaesthesia bag filled with 2.0 L of 13% helium in oxygen was connected to the airway opening, and 20 deep manual breaths were administered at a rate of 4 cycles·min–1. Helium concentration in the anaesthesia bag was measured with a helium dilution analyser (PK Morgan Ltd., Kent, UK). FRC was computed as follows:


{erj250259E001}

(001)
where Vi = initial gas volume in the anaesthesia bag, and [He]i and [He]fin are the initial and final helium bag concentrations, respectively. EELV was computed as FRC plus {Delta}FRC. Baseline ventilation was resumed for 15 min, the endotracheal tube was clamped during an end-expiratory occlusion, and baseline ventilation EELV was determined as described above. {Delta}FRC was computed as the helium dilution EELV–FRC difference. The reliability of the helium dilution technique 26 was assessed by comparing measured and computed {Delta}FRC and EELV.



View larger version (12K):
[in this window]
[in a new window]
  		Fig. 2— Methodology of determination of expiratory resistance at end-expiratory lung volume (EELV), and mean end-expiratory flow. Change ({Delta}) in functional residual capacity (FRC) expiration was defined as expiration from EELV to respiratory system relaxation volume (dotted arrow); respiratory system relaxation volume (- - -) coincides with FRC. Mean end-expiratory flow during {Delta}FRC expiration was determined by dividing the grey shaded flow-time surface area (enclosed by the expiratory flow tracing, and the zero flow line: shown in b) by the number of seconds corresponding to the duration of {Delta}FRC expiration. The duration of baseline tidal volume-to-EELV expiration is the time period corresponding to the interval between the first and second vertical arrows. VT: tidal volume.

 
Expiratory airway resistance at EELV (Raw,exp,EELV) and mean end-expiratory V'
Computer-stored tracings of flow and volume during measurement of change in FRC in a representative study participant placed in the SRPP position is shown in figure 2Go. The expiratory flow corresponding to the EELV point of exhaled volume was determined. At this point, the driving pressure was considered as equal to dynamic intrinsic PEEPi. Expiratory resistance at EELV was then determined by dividing dynamic PEEPi by expiratory flow at EELV (fig. 2Go). {Delta}FRC reflects dynamic hyperinflation, and corresponds to the terminal portion of expiration 1, 14, during which expiratory V' limitation is present 15. Thus, during {Delta}FRC expiration, increases in expiratory driving pressure do not affect expiratory V' 27, 28. Expiratory V' limitation is due to excessive expiratory airway narrowing 29. An increase in expiratory V' during the V'-limited portion of expiration and a reduced duration of the latter expiration portion would indicate less expiratory airway narrowing and attenuation of expiratory V' limitation. Mean end-expiratory V' during {Delta}FRC expiration were determined as shown in figure 2Go. The duration of "baseline VT-to-EELV" expiration (initial phase of passive expiration) was also determined (fig. 2Go).

Statistical analysis
For each posture, apart from single measurements (FRC, EELV, {Delta}FRC), only means of obtained sets of measurements were analysed. Variable comparisons were conducted with two-factor univariate ANOVA for repeated measures, followed by the Scheffé test as appropriate. Significance was accepted at p<0.05. Values are presented as mean±SD or grand mean*±SD.


   RESULTS
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
DISCUSSION
 APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
 REFERENCES
 
Full data were obtained from all patients, and no protocol-related complications 1 occurred. Pga was unaffected by posture change (data not shown). Mean maximal amplitude of "cardiac oscillations" in Poes (2.1*±0.8 cmH2O) and mean Poes-rise rate during these oscillations (10.2*±3.7 cmH2O·s–1), and absolute Poes at EELV (11.8*±3.2 cmH2O) were similar in all study postures. Consequently, the initial, correct positioning of the oesophageal balloon relative to the heart was maintained throughout the study period 1. Respiratory cycle-induced changes in Poes were measured as accurately as possible in all study postures, and their comparability among these postures was "adequate" 1, 2, 24, 25, 30.

Inspiratory mechanics
The main results on partitioned inspiratory mechanics are presented in figure 3Go.



View larger version (25K):
[in this window]
[in a new window]
  		Fig. 3— Main results on partitioned inspiratory mechanics. Data are presented as mean±SD for pre-prone semirecument ({blacksquare}), prone ({blacktriangleup}) and post-prone semirecumbent (•) positions (a–f). Rmax,Lung: total (maximal) inspiratory resistance of the lung; Rint,Lung: interrupter (inspiratory airway) resistance of the lung; {Delta}R: additional resistance due to tissue stress relaxation tension and/or time constant inequality within the lung; Estat,cw: static elastance of the chest wall; VT: tidal volume; Estat,Lung: static lung elastance; RS: respiratory system. *: p<0.05 versus baseline semirecumbent; #: p<0.05 versus first value of the same body posture.

 
Additional RS resistance was significantly lower in prone versus SRBAS at all test VTs. Static chest wall elastance (Estat,cw), was higher in prone versus SRBAS at all test VTs. Maximal and interrupter (Rint,Lung) lung resistance were lower in prone versus SRBAS at VTs ≥1.0 L. Additional lung resistance ({Delta}RLung) was lower in prone versus SRBAS at all test VTs. Dynamic and static (Estat,Lung) lung elastance were lower in prone versus SRBAS at VTs ≤0.6 L. All other determined variables were unaffected by posture change. VT dependence of inspiratory mechanics was virtually unaffected by posture change.

Haemodynamics and gas exchange
Haemodynamics and gas exchange during baseline ventilation are shown in table 3Go.


View this table:
[in this window]
[in a new window]
  		Table. 3— 3 Haemodynamics and gas exchange during baseline ventilation

 
Haemodynamic variables were unaffected by posture change. Pronation resulted in higher Pa,O2/inspired O2 fraction (Pa,O2/FI,O2) and lower shunt fraction versus SRBAS.

PEEPi, {Delta}FRC, FRC and EELV
Dynamic pulmonary hyperinflation variables and variables determined during passive expiration are shown in table 4Go.


View this table:
[in this window]
[in a new window]
  		Table. 4— 4 Variables reflecting dynamic pulmonary hyperinflation and variables determined during passive expiration from end-expiratory lung volume (EELV) to functional residual capacity (FRC)

 
Static RS and lung PEEPi, and measured/computed {Delta}FRC were lower in prone versus SRBAS and SRPP. FRC was unaffected by body posture. Measured/computed EELV was lower in prone versus SRBAS. Computed {Delta}FRC and EELV did not differ significantly from measured {Delta}FRC and EELV (p = 0.07–0.9).

Expiratory airway resistance and end-expiratory V'
Raw,exp was lower in prone versus SRBAS (at VTs ≥0.8 L) and SRPP (at VT = 1.0 L), and decreased with increasing VT in all postures (fig. 4Go). Dynamic PEEPi and Raw,exp,EELV, were lower, and mean end-expiratory V' was higher in prone versus SRBAS and SRPP (table 4Go). Duration of {Delta}FRC-expiration was shorter in prone versus SRBAS and SRPP (table 4Go). Duration of the initial passive expiration phase was similar in all postures (2.65*±0.6 s).



View larger version (13K):
[in this window]
[in a new window]
  		Fig. 4— Results on expiratory airway resistance (Raw,exp). Data are presented as mean±SD for pre-prone semirecument ({blacksquare}), prone ({blacktriangleup}) and post-prone semirecumbent (•) positions. #: p<0.05 versus baseline semirecumbent; : p<0.05 versus post-prone semirecumbent; +: p<0.05 versus first sequential value of the same body posture; §: p<0.05 versus second sequential value of the same body posture.

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
 DISCUSSION
APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
 REFERENCES
 
The main findings of the present study were that in severe chronic bronchitis, pronation reduces Raw,exp, Raw,exp,EELV and Rint,Lung, and increases mean end-expiratory V' versus SRBAS (60° inclination). Following return to SRPP, pronation-induced benefits on airway resistance and mean end-expiratory V' are reversed, and dynamic pulmonary hyperinflation is augmented. Favourable effects on airway resistance were observed mainly at traditional, high VTs of ≥0.8 L. However, Raw,exp,EELV during expiration from baseline VT (0.6 L or 7.6±0.7 mL·kg–1 actual body weight) was also reduced, being in concordance with pronation benefits on baseline ventilation PEEPi, {Delta}FRC, and EELV; the latter results indicate attenuation of dynamic hyperinflation. Additional pronation benefits include reductions in {Delta}RLung, Estat,Lung, and shunt fraction, and Pa,O2/FI,O2 increase 1.

In the prone position, Estat,cw increases and lung parenchyma mechanics are improved (Estat,Lung/{Delta}RLung decrease) 1–3. Results on Raw,exp, Raw,exp,EELV, and Rint,Lung, support the hypothesis of the current authors, which was based on mechanical interdependence between airway and parenchyma 5, 6. Prone position's reduced atelectasis and more uniform alveolar inflation 1–4 should result in an overall increased average and more homogenously distributed regional alveolar septal tension during the respiratory cycle. Such tension transmitted to airway walls 5 should result in increased airway calibre and reduced airflow resistance. The return to SRPP resulted in partial reversal of pronation effects on Estat,Lung and {Delta}RLung, and consequently, neutralisation of prone position's favourable parenchyma airway calibre interaction with respect to Raw (figs 3Go and 4Go; table 4Go).

Pronation results are further explained by the airway/parenchymal hysteresis 6. At the same lung volume, the elastic recoil pressures of the airways and parenchyma are less during expiration than during inspiration; this is known as hysteresis, and reflects viscoelastic energy dissipation 6. If bronchial hysteresis exceeds parenchymal hysteresis, the expiratory re-establishment of pre-inspiratory bronchial elastic recoil after high VT administration lags behind the expiratory re-establishment of pre-inspiratory elastic recoil of the lung parenchyma. Thus, parenchymal traction exerted on the airways prevails over airway smooth muscle tone, resulting in bronchodilation 6. In COPD, airway hysteresis increases during high VT breathing. Airway wall viscoelasticity is augmented 6 secondary to increased velocity of hypertophied/hyperplastic 31 airway smooth muscle shortening after high VT stretching 6, 32. As VT increases, parenchymal recoil and traction on airway walls also increases. The increasing VT-induced increase in parenchymal recoil is probably enhanced in the prone position. Significant differences observed in Estat,Lung at low VTs (≤0.6 L), are eliminated at high VTs (≥0.8 L) (fig. 3Go). {Delta}RLung results (fig. 3Go), suggest unchanged lung parenchymal viscoelasticity 16 with increasing VT in all postures, and minimal parenchymal viscoelasticity (i.e. minimal parenchymal hysteresis) 6 in the prone position. Consequently, in the prone position, increasing airway hysteresis and minimised/stable parenchymal hysteresis with increasing VT should result in enhanced parenchyma-induced bronchodilation 6.

Raw,exp was measured by modifying a complex method 15. Raw,exp,EELV was measured by dividing driving pressure by expiratory flow at EELV. Results were comparable to those previously reported 15, 33. In COPD, Todd et al. 33, found lung expiratory resistance of 21.01±2.88 cmH2O·L–1·s–1, being 3.5-fold higher relative to inspiratory resistance. Kondili et al. 15, found RS expiratory resistance of 23.83±8.1 cmH2O·L–1·s–1 during VT slices expired at very similar time intervals of passive expiration as reported herein (fig. 1Go). Raw,exp,EELV values (table 4Go) are comparable to recently determined RS expiratory resistance values (29.02±15.60 cmH2O·L–1·s–1) at 0.4–0.5 L above FRC 15 (compare 0.4–0.5 L with the semirecumbent {Delta}FRC values reported in table 4Go).

EELV and FRC measurements with helium dilution may be affected by airway closure, which may interfere with correct mixing of helium between the anaesthesia bag and lung 26. The current authors employed high VTs (1.0–1.5 L), which resulted in PL >20 cmH2O and probable re-opening of closed airways 26, 34, 35. Low respiratory rates were also used, which resulted in a prolonged expiratory time of ~12 s, in order to augment expiratory helium mixing between anaesthesia bag and lung and minimise helium trapping. This was probably achieved because {Delta}FRC (EELV-portion reflecting trapped volume) 1, 16 was estimated with acceptable accuracy with the helium dilution technique. Indeed, helium dilution-computed and measured {Delta}FRC did not differ significantly (table 4Go). Other limitations of the helium dilution technique are related to FRC reduction during anaesthesia and loss of gas volume due to continuing gas exchange 26.

Implications for clinical practice and further research
Severe COPD is characterised by elevated Raw and PEEPi 10, 11. During controlled mechanical ventilation, adverse effects of PEEPi and dynamic hyperinflation include haemodynamic compromise and risk of barotrauma 36. Ventilatory management goals should include minimisation of dynamic hyperinflation, Raw, and risk of ventilator-associated lung injury. Use of helium oxygen mixtures and external positive end-expiratory pressure not exceeding PEEPi have been advocated 37. Other, recent textbook recommendations include use of low VTs (5–7 mL·kg–1 predicted body weight) at rates of 20–24 cycles·min–138. The importance of adequate expiratory time to allow for effective lung deflation cannot be overemphasised. Recently, Gainnier et al. 39, employed VTs of 7–8 mL·kg–1 actual body weight at rates of 14±2.3 cycles·min–1. The present authors employed similar baseline VT at relatively high rates of 18.0±0.7 cycles·min–1; however, relative to the study by Gainnier et al. 39, the (baseline ventilation) expiratory time was comparable (~3 s) secondary to 40% higher inspiratory flow (similar inspiratory flow has also been recently used 37), whereas Pa,CO2 and pH (table 3Go) were also comparable. Despite this argumentation, it is likely that the baseline ventilation settings in the current study could be further optimised according to the above-mentioned ventilation goals. Therefore, based on the results of the present study, the authors recommend the use of the prone position in severe COPD patients who continue to experience adverse effects of PEEPi and dynamic hyperinflation, even during optimised ventilation in the semirecumbent position.

Reduction in Raw and PEEPi, and attenuation of dynamic hyperinflation, indicate reduced respiratory workload in prone position. Pulmonary hyperinflation and increased EELV result in diminution of the diaphragm's apposition zone, shortened operating length of diaphragmatic muscle fibres, and reduced diaphragmatic mechanical effectiveness during spontaneous inspiration 40. Severe COPD patients failing to wean from mechanical ventilation experience increased respiratory workload 10, 11. Consequently, further investigation is warranted to determine whether pronation benefits demonstrated herein can be maintained during partial ventilatory support and/or spontaneous breathing.

Conclusion
Pronation of anaesthetised, volume-controlled mode ventilated, severe chronic bronchitis patients reduces airway resistance and attenuates dynamic hyperinflation. This is probably attributable to improved parenchyma mechanics inducing an increase in airway calibre during the respiratory cycle.


   APPENDIX 1: FORMULAS USED TO DERIVE HAEMODYNAMIC AND GAS EXCHANGE VARIABLES 41, 42
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: FORMULAS USED...
APPENDIX 2: INSPIRATORY...
 REFERENCES
 

  1. Cardiac index = CO/BSA
  2. Systemic vascular resistance index = (MAP–CVP)x80xCI-1
  3. Pulmonary vascular resistance index = (MPAP–PAWP)x80xCI–1
  4. Oxygen consumption per m2 BSA = CIx1.36xHgbx (SaO2–SvO2)
  5. Respiratory quotient = (FEY of carbohydrate intake) 1.0+(FEY of protein intake)x0.8+(FEY of lipid intake)x0.7 43
  6. Alveolar PO2 = Pi,O2–PA,CO2x[FI,O2–(1–FI,O2)xR–1]; Pi,O2 = FI,O2x(PB–47); PA,CO2~Pa,CO2
  7. O2 content of blood = Hgbx1.36xSO2x10–1+0.003xPO2
  8. Shunt fraction = (Cc,O2–Ca,O2)x(Cc,O2–Cv,O2)–1.

CO: cardiac output (L·min–1); BSA: body surface area (m2); MAP: mean arterial pressure (mmHg); CVP: central venous pressure (mmHg); 80: transformation factor of Wood units (mmHg·L–1·min) to standard metric units (dynes·s·cm–5); CI: cardiac index (L·min–1·m–2); MPAP: mean pulmonary artery pressure (mmHg); PAWP: pulmonary artery wedge pressure (mmHg); Hgb: haemoglobin concentration in g·L–1; 1.36: O2 combining power of 1 g of haemoglobin (mL); Sa,O2: arterial O2 saturation; Sv,O2: mixed venous O2 saturation; FEY: fractional energy yield relative to total of prescribed nutritional support; Si,O2: inspired O2 partial pressure (mmHg); R: respiratory quotient; PB: barometric pressure (mmHg); 47: water saturated vapour pressure at 37°C (mmHg); 0.003: O2 solubility coefficient at 37°C (mL·dL–1·mmHg); PO2: O2 partial pressure (mmHg); Cc,O2/Ca,O2/Cv,O2, O2 content in end-capillary/arterial/mixed-venous blood, respectively.

1 mmHg = 0.133 kPa.


   APPENDIX 2: INSPIRATORY MECHANICAL VARIABLES
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
REFERENCES
 
For the respiratory system, chest wall and lung the following inspiratory mechanical variables were determined: 1) maximal, interrupter, and additional resistances, computed as respective Pmax–P2, Pmax–P1 and P1–P2 differences divided by the preceding inspiratory flow; and 2) dynamic and static elastances, computed as respective P1–static PEEPi and P2–static PEEPi differences divided by the administered VT. Lung interrupter resistance reflects "ohmic" airway resistance; lung additional resistance reflects lung tissue stress relaxation tension and time constant inequality.


   REFERENCES
TOP
 ABSTRACT
 MATERIAL AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: FORMULAS USED...
 APPENDIX 2: INSPIRATORY...
 REFERENCES
 

  1. Mentzelopoulos SD, Zakynthinos SG, Roussos C, Tzoufi MJ, Michalopoulos AS. Prone position improves lung mechanical behaviour and enhances gas exchange efficiency in mechanically ventilated chronic obstructive pulmonary disease patients. Anesth Analg 2003;96:1756–1767.[Abstract/Free Full Text]
  2. Pelosi P, Tubiolo D, Mascheroni D, et al. Effects of the prone position on respiratory mechanics and gas exchange during acute lung injury. Am J Respir Crit Care Med 1998;157:387–393.
  3. Albert RK, Hubmayr RD. The prone position eliminates compression of the lungs by the heart. Am J Respir Crit Care Med 2000;161:1660–1665.[Abstract/Free Full Text]
  4. Mure M, Domino KB, Lindahl SG, Hlastala MP, Altemeier WA, Glenny RW. Regional ventilation-perfusion distribution is more uniform in the prone position. J Appl Physiol 2000;88:1076–1083.[Abstract/Free Full Text]
  5. Hopin FG Jr. Sources of lung recoil. In: Milic-Emili J, ed. Eur Respir Mon 1999; pp. 33–53.
  6. Brusasco V, Pellegrino P, Rodarte JR. Airway mechanics. In: Milic-Emili J, ed. Eur Respir Mon 1999; pp. 68–91.
  7. Mannino DM. COPD: Epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest 2002;121: Suppl. 5 121S–126S.[Abstract/Free Full Text]
  8. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995;152: Suppl. 5 77S–121S.
  9. American Thoracic Society. Lung function testing: selection of reference values and interpretive strategies. Am Rev Respir Dis 1991;144:1208–1218.
  10. Purro A, Appendini L, De Gaetano A, Gudjonsdottir M, Donner CF, Rossi A. Physiologic determinants of ventilator dependence in long-term mechanically ventilated patients. Am J Respir Crit Care Med 2000;161:1115–1123.[Abstract/Free Full Text]
  11. Appendini L, Purro A, Patessio A, et al. Partitioning of inspiratory muscle workload and pressure assistance in ventilator-dependent COPD patients. Am J Respir Crit Care Med 1996;154:1301–1309.[Abstract]
  12. Hankinson JL, Odencrantz JR, Fedan JB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med 1999;159:178–187.
  13. Dewan NA, Rafique S, Kanwar B, et al. Acute exacerbation of COPD: factors associated with poor treatment outcome. Chest 2000;117:662–671.
  14. Prechter GC, Nelson SB, Hubmayr RD. The ventilatory recruitment threshold for carbon dioxide. Am Rev Respir Dis 1990;141:758–764.[Web of Science][Medline] [Order article via Infotrieve]
  15. Kondili E, Alexopoulou C, Prinianakis G, Xirouchaki N, Georgopoulos D. Pattern of lung emptying and expiratory resistance in mechanicaly ventilated patients with chronic obstructive pulmonary disease. Intensive Care Med 2004;30:1311–1318.[Web of Science][Medline] [Order article via Infotrieve]
  16. Guérin C, Coussa ML, Eissa NT, et al. Lung and chest wall mechanics in mechanically ventilated COPD patients. J Appl Physiol 1993;74:1570–1580.[Abstract/Free Full Text]
  17. Baydur A, Behrakis PK, Zin WA, Jaeger M, Milic-Emili J. A simple method for assessing the validity of the esophageal balloon technique. Am Rev Respir Dis 1982;126:788–791.[Web of Science][Medline] [Order article via Infotrieve]
  18. Ranieri VM, Brienza N, Santostasi S, et al. Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome. Role of abdominal distention. Am J Respir Crit Care Med 1997;156:1082–1091.[Abstract/Free Full Text]
  19. Diehl JL, Lofaso F, Deleuze P, Similowski T, Lemaire F, Brochard L. Clinically relevant diaphragmatic dysfunction after cardiac operations. Ann Thorac Surg 1994;107:487–498.
  20. Johnson B, Richard JC, Straus C, Mancebo J, Lemaire F, Brochard L. Presssure-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.[Abstract/Free Full Text]
  21. Suter PM. Does the advent of (new) low tidal volumes bring the (old) sigh back to the intensive care unit? Anesthesiology 2002;96:783–784.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
  22. Tantucci C, Corbeil C, Chasse M, Braidy J, Matar N, Milic-Emili J. Flow resistance in patients with chronic obstructive pulmonary disease in acute respiratory failure. Am Rev Respir Dis 1991;144:384–389.[Web of Science][Medline] [Order article via Infotrieve]
  23. Maltais F, Reissmann H, Navalesi P, et al. Comparison of static and dynamic measurements of intrinsic PEEP in mechanically ventilated patients. Am J Respir Crit Care Med 1994;150:1318–1324.[Abstract]
  24. Pelosi P, Croci M, Callapi E, et al. Prone positioning improves pulmonary function in obese patients during general anesthesia. Anesth Analg 1996;83:578–583.[Abstract]
  25. Pelosi P, Croci M, Calappi E, et al. The prone positioning during general anesthesia minimally affects respiratory mechanics while improving functional residual capacity and increasing oxygen tension. Anesth Analg 1995;80:955–960.[Abstract]
  26. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 1997;83:811–818.
  27. Valta P, Corbeil C, Lavoie R, et al. Detection of expiratory flow limitation during mechanical ventilation. Am J Respir Crit Care Med 1994;50:1311–1317.
  28. Koutsoukou A, Armaganidis A, Stavrakaki-Kallergi C, et al. Expiratory flow limitation and intrinsic positive end-expiratory pressure at zero positive end-expiratory pressure in patients with adult respiratory distress syndrome. Am J Respir Crit Care Med 2000;161:1590–1596.[Abstract/Free Full Text]
  29. West JB. Ventilation. In: West JB, ed. Pulmonary pathophysiology- the essentials. 4th Edn. Baltimore, Williams & Wilkins, 1992; pp. 3–18.
  30. Milic-Emili J, Mead J, Turner JM. Topography of esophageal pressure as a function of posture in man. J Appl Physiol 1964;19:212–216.[Abstract/Free Full Text]
  31. Saetta M, Turato G. Lung structure and function. In: Milic-Emili J, ed. Eur Respir Mon 1999; pp. 1–19.
  32. Mitchell RW, Rabe KF, Magnussen H, Leff AR. Passive sensitization of human airways induces myogenic contractile responses in vitro. J Appl Physiol 1997;83:1276–1281.[Abstract/Free Full Text]
  33. Todd OM, Pellegrino R, Brusasco V, Rodarte JR. Measurement of pulmonary resistance and dynamic compliance with airway obstruction. J Appl Physiol 1998;85:1982–1988.[Abstract/Free Full Text]
  34. Don HF, Wahba WM, Craig DB. Airway closure, gas trapping, and the functional residual capacity during anesthesia. Anesthesiology 1972;36:533–539.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
  35. Glaister DH, Schroter RC, Sudlow MF, Milic-Emili J. Transpulmonary pressure gradient and ventilation distribution in excised lungs. Respir Physiol 1973;17:347–354.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
  36. Tuxen DV. Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction. Am Rev Respir Dis 1989;140:5–9.[Web of Science][Medline] [Order article via Infotrieve]
  37. Jolliet P, Watremez C, Roeseler J, et al. Comparative effects of helium-oxygen and external positive end-expiratory pressure on respiratory mechanics, gas exchange, and ventilation-perfusion relationships in mechanically ventilated patients with chronic obstructive pulmonary disease. Intensive Care Med 2003;29:1442–1450.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
  38. Schmidt GA, Hall JB, Wood LDH. Ventilatory Failure. In: Murray JF, Nadel JA, Mason RJ, Boushey HA, eds. Textbook of Respiratory Medicine. 3rd Edn. Philadelphia, WB Saunders, 2000; pp. 2443–2471.
  39. Gainnier M, Arnal JM, Gerbaux P, Donati S, Papazian L, Sainty JM. Helium-oxygen reduces work of breathing in mechanically ventilated patients with chronic obstructive pulmonary disease. Intensive Care Med 2003;29:1666–1670.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
  40. Vassilakopoulos T, Zakynthinos S, Roussos C. Muscle Function. In: Marini JJ, Slutsky AS, eds. Physiological Basis of Ventilatory Support. New York, Dekker, 1998; pp. 103–153.
  41. Mark JB, Slaughter TF, Reves JG. Cardiovascular monitoring. In: Miller RD, ed. Anaesthesia. 5th Edn. New York, Churchill Livingstone, 2000; pp. 1117–1230.
  42. Moon ME, Camporesi EM. Respiratory monitoring. In: Miller RD, ed. Anaesthesia. 5th Edn. New York, Churchill Livingstone, 2000; pp. 1255–1296.
  43. Marino PL. Nutrient and energy requirements. In: Marino PL, ed. The ICU book. 2nd Edn. Baltimore, Williams & Wilkins, 1997; pp. 721–736.



This article has been cited by other articles:


Home page
 Eur Respir JHome page
S. D. Mentzelopoulos, J. Sigala, C. Roussos, and S. G. Zakynthinos
Static pressure-volume curves and body posture in severe chronic bronchitis
Eur. Respir. J., July 1, 2006; 28(1): 165 - 174.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Permissions
Right arrowRequest Permissions
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Zakynthinos, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Zakynthinos, S. G.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS