Journal of Intensive Care Medicine

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Year in review in intensive care medicine. 2005. I. Acute respiratory failure and acute lung injury, ventilation, hemodynamics, education, renal failure

Peter Andrews  1, Elie Azoulay  2, Massimo Antonelli  3, Laurent Brochard  4 Contact information, Christian Brun-Buisson  5, Daniel de Backer  6, Geoffrey Dobb  7, Jean-Yves Fagon  8, Herwig Gerlach  9, Johan Groeneveld  10, Jordi Mancebo  11, Philipp Metnitz  12, Stefano Nava  13, Jerome Pugin  14, Michael Pinsky  15, Peter Radermacher  16, Christian Richard  17 Robert Tasker  18

(1) Intensive Care Medicine Unit, Western General Hospital, Edinburgh, UK

(2) Intensive Care Medicine Unit, Saint Louis Hospital, Paris, France

(3) Department of Intensive Care and Anesthesiology, Universita Cattolica del Sacro Cuore, Rome, Italy

(4) Réanimation Médicale, AP-HP, Hôpital Henri Mondor, INSERM U 615, Université, Paris 12, France

(5) Medical Intensive Care Unit, University Hospital Henri Mondor, 51 avenue du Marechal de Lattre de Tassigny, 94000 Creteil, France

(6) Service des Soins Intensifs, Hôpital Erasme, 808 route de Lennick, 1070 Bruxelles, Belgium

(7) Intensive Care Medicine Unit, Royal Perth Hospital, Perth, Australia

(8) Intensive Care Medicine Unit, European Georges Pompidou Hospital, Paris, France

(9) Department of Anesthesiology, Vivantes-Klinikum Neukoelln, Berlin, Germany

(10) Intensive Care Medicine Unit, VUMC, Amsterdam, The Netherlands

(11) Intensive Care Medicine Unit, Hospital Sant Pau, Barcelona, Spain

(12) Department of Anesthesia and General Intensive Care Medicine, University Hospital of Vienna, Vienna, Austria

(13) Intensive Care Medicine Unit, Fondazione S. Maugeri, Pavia, Italy

(14) Intensive Care Medicine Unit, University Hospital of Geneva, Geneva, Switzerland

(15) Intensive Care Medicine Unit, University of Pittsburgh Medical Center, Pittsburgh, Pa., USA

(16) Department of Anesthesia, University Medical School of Ulm, Ulm, Germany

(17) Intensive Care Medicine Unit, University Hospital of Le Kremlin-Bicetre, Le Kremlin Bicetre, France

(18) Pediatric Intensive Care Unit, Addenbrooke's Hospital, Cambridge, UK

LaurentBrochard
Email:
laurent.brochard@hmn.aphp.fr

Received: 8 December  2005   Accepted: 8 December  2005   Published Online: 1 February  2006


Acute Respiratory Failure

Acute lung injury

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have been the subjects of several important studies which address the issues of biological markers, respiratory monitoring tools to guide ventilatory settings, and risk factors for developing ARDS.

Fibroproliferation in ARDS seems to have important prognostic implications. Because fibroproliferation markers, such as procollagen I, predict mortality in patients with ALI and ARDS, Budinger et al. examined whether bronchoalveolar lavage fluid (BALF) from patients with lung injury contains mediators that would activate procollagen-I promoter, and if this activation predicts important clinical outcomes [1]. The BALF was also collected from patients with pulmonary fibrosis and cardiogenic pulmonary edema. The BALF active TGF-beta 1 levels were measured in 29 ARDS patients, with nine negative and six positive controls being enrolled also. The BALF from ARDS patients induced 41% greater procollagen-I promoter activation than that from negative controls (p < 0.05), and a TGF-beta-1 blocking antibody significantly reduced this activation in ARDS patients. The authors conclude that bronchoalveolar lavage fluid from ALI/ARDS patients activates procollagen-I promoter, which is due partly to TGF-beta 1. Activated TGF-beta 1 may impact ARDS outcome independent of its effect on procollagen-I activation.

The role of the pressure-volume (PV) curve to guide the ventilatory settings is still debated. In particular, the expiratory part of the whole loop could be more useful than the inspiratory part, because PEEP is indeed an expiratory setting. Albaiceta et al. studied the effects of two levels of positive end-expiratory pressure (PEEP), 2 cmH2O above the lower inflection point of the inspiratory limb (15 ± 3 cmH2O) and equal to the point of maximum curvature on the expiratory limb of the pressure – volume curve (23.5 ± 4 cmH2O), on gas exchange, respiratory mechanics, and lung aeration in eight patients with early acute lung injury [2]. The PEEP, according to the expiratory point of maximum curvature, induced an improvement in oxygenation, an increase in normally aerated and a decrease in nonaerated lung volumes, and greater alveolar stability. There was also an increase in PaCO2, airway pressures, and hyperaerated lung volume; therefore, high PEEP levels according to the point of maximum curvature of the deflation limb of the pressure-volume curve have both benefits and drawbacks.

Another potential bedside monitoring technique is electrical impedance tomography (EIT). Riedel et al. applied functional EIT to measure relative changes of lung tissue during tidal breathing and create images of local ventilation distribution [3]. Change of body position from supine to prone, left and right lateral, during spontaneous breathing and positive pressure support ventilation, allows interindividual comparison. The article by Riedel et al. [3] is accompanied by an editorial by Calzia et al. who emphasize that this technique has now reached a level of robustness and user-friendliness which permits bedside application, even in an ICU setting [4].

Two articles have explored the physiological effects of prone position and how they could explain clinical benefits. Vieillard-Baron et al. studied the improvement provided by prone position in terms of mechanics and alveolar ventilation in ARDS [5]. They stated that prone position improves homogenization of tidal ventilation by reducing time-constant inequalities, thus improving alveolar ventilation. They previously reported in patients with ARDS that these inequalities are responsible for the presence of a “slow compartment,” which is excluded from tidal ventilation at supportive respiratory rate. In 11 ARDS patients treated by ventilation in the prone position because of a major oxygenation impairment (PaO2/FIO2 < 100 mm Hg), the prone position significantly reduced the expiratory time constant from 1.98 ± 0.53 s at baseline with ZEEP to 1.53 ± 0.34 s, and significantly decreased PaCO2 from 55 ± 11 mm Hg at baseline with ZEEP to 50 ± 7 mm Hg.

In an editorial, Koutsoukou discussed that dynamic hyperinflation and PEEPi was presumably due to tidal expiratory flow limitation with sequential dynamic compression of the peripheral airways during expiration and consequent inhomogeneous regional lung emptying [6]. The reduction of dynamic hyperinflation and PEEPi with proning was probably due largely to abolishment or reduction of the extent of tidal flow limitation. It should be stressed that tidal flow limitation is a risk factor for low-volume lung injury during mechanical ventilation.

Finally, Mentzelopoulos et al. studied static pressure volume curves and body posture in 13 patients with early ARDS [7]. Prone position vs preprone semirecumbent position resulted in significantly reduced pressure at lower inflection point of lung PV curve (2.2 ± 0.2 vs 3.7 ± 0.5 cmH2O) and increased volume at upper inflection point (0.87 ± 0.03 vs 0.69 ± 0.05). Postural reduction in lower inflection point pressure of lung PV curve was the sole independent predictor of pronation-induced increases in PaO2/FIO2, which is also significantly related to increases in functional residual capacity.

Moran et al. provided a detailed and complex meta-analysis of controlled trials of ventilator therapy in acute lung injury and ARDS, a subject of considerable debate in the literature [8]. Overall treatment-effect estimate favored protective ventilation but did not achieve st