COMPUTED TOMOGRAPHY ASSESSMENT OF POSITIVE END-EXPIRATORY PRESSURE-INDUCED ALVEOLAR RECRUITMENT IN PATIENTS WITH ACUTE RESPIRATORY DISTRESS SYNDROME

To the Editor :

The recent report by Malbouisson and colleagues (1) illustrates the broadness of the term "recruitment," usually associated with the "open lung approach" strategy in acute respiratory distress syndrome (ARDS).

What the authors have measured in a group of 16 ARDS patients by thoracic computed tomography (CT) is the air present in the diseased lung during an apnea period of 15 s, required for CT data acquisition. By stopping expiration at 0 and 15 cm H₂O, they created two different apnea situations, and they found a greater amount of air in the second, by holding a 15 cm H₂O airway pressure. They conclude that PEEP of 15 cm H₂O produced "recruitment." But what Malbouisson and colleagues (1) have actually measured is an increased functional residual capacity produced by an airway pressure of 15 cm H₂O. This result is perfectly expected, and can be easily verified by expiratory flow measurements in mechanically ventilated patients, a less sophisticated approach. To draw a conclusion concerning the specific effect of PEEP, they should have included a third step: CT data acquisition during a prolonged end-inspiratory plateau of 15 cm H₂O. Without this step, their conclusion is debatable. Moreover, because "recruitment" is an inspiratory phenomenon, and PEEP an expiratory procedure, it would be more advisable to characterize PEEP as acting to prevent "de-recruitment," and not to produce "recruitment."

Conversely, a peculiar point that was clearly highlighted by the report of Malbouisson and colleagues (1) is the poor hemodynamic tolerance of a respiratory strategy using a high PEEP. Despite a limited plateau pressure, this strategy produced a sharp increase in pulmonary vascular resistance (+18%), a clear impairment of venous return, and a sharp decrease in cardiac output (24%). These results, also perfectly expected (2), are at variance with the perfect hemodynamic tolerance claimed by the initiators of the "open lung approach" (3).

Hôpital Ambroise Paré, Boulogne, France

1. Malbouisson LM, Muller J-C, Constantin J-M, Lu Q, Puybasset L, Rouby J-J. the CT Scan ARDS Study Group. Computed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 163: 1444-1450 [Abstract/Free Full Text].

2. Schmitt JM, Vieillard-Baron A, Augarde R, Prin S, Page B, Jardin F. PEEP titration in ARDS patients: impact on right ventricular outflow impedance evaluated by pulmonary artery Doppler flow velocity measurements. Crit Care Med 2001; 29: 1154-1158 [Medline].

3. Carvalho C, Parbas C, Meideiros D, Magaldi R, Filho G, Kkairalla R, Deheizelin D, Munhoz C, Kaufmann M, Ferreira M, Takagaki T, Amato M. Temporal hemodynamic effects of permissive hypercapnia associated with ideal PEEP in ARDS. Am J Respir Crit Care Med 1997; 156: 1458-1466 [Abstract/Free Full Text].

From the Author :

Alveolar recruitment can be defined as the re-expansion of lung regions that remain nonventilated throughout the respiratory cycles generated by the mechanical ventilator. In patients with ARDS, alveolar recruitment has two components: a "permanent" recruitment resulting from the effects of PEEP, and a "cyclic" recruitment resulting from the effects of tidal volume (1). PEEP, by preventing the end-expiratory collapse of some lung areas, keeps them fully open throughout the respiratory cycle, whereas each tidal volume recruits some of the lung regions that re-collapse during the following expiration.

It has to be pointed out that the majority of patients with ARDS have a variable proportion of their lungs that remains normally aerated at zero end-expiratory pressure (ZEEP) (2). As a consequence, PEEP-induced increase in functional residual capacity (FRC) is caused by an increase in the volume of lung regions normally aerated at ZEEP and by a true alveolar recruitment resulting from the re-expansion of collapsed lung areas (3). Evidence has recently accumulated showing that PEEP can provoke in the same patient alveolar recruitment in some lung regions and overdistension in some others (3). As a consequence, PEEP-induced alveolar recruitmentor according to Dr. Jardin, "PEEP-induced prevention of de-recruitment"is not equivalent to PEEP-induced increase in FRC, as wrongly stated by Dr. Jardin in his letter. Measurement of expiratory flows during a PEEP-release maneuver will be indicative of alveolar recruitment only in the small proportion of patients with ARDS in whom the lung is entirely collapsed at ZEEP (3, 7).

The aim of our study was to set up a CT method for differentiating PEEP-induced overdistension from PEEP-induced true alveolar recruitment (7). Assessing the differences in alveolar recruitment resulting from PEEP or a prolonged inspiratory pause was not a goal of the study. However, we do not see any reason why a CT method designed for measuring alveolar recruitment should be influenced by the means used for promoting alveolar recruitment.

To go along these lines, our study was not designed to assess or justify the "open lung approach." A marked hemodynamic impairment was mainly observed in patients in whom PEEP induced an important distension of previously aerated lung areas. When PEEP exclusively re-expanded collapsed lung regions without distending already aerated lung areas, the hemodynamic impairment was modest. Therefore, Dr. Jardin's general statement that the "open lung approach" is always associated with deleterious hemodynamic consequences appears questionable.

Hospital Pitié-Salpétrière, Université Paris VI, Paris, France

1. Gattinoni L, Pelosi P, Crotti S, Valenza F. 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 1995;151;1807-1814.

2. Puybasset L, Cluzel P, Gusman P, Grenier P, Preteux F, Rouby J-J. Regional distribution of gas and tissue in acute respiratory distress syndrome. I. Consequences on lung morphology. Intensive Care Med 2000; 26: 847-863 .

3. Puybasset L, Muller JC, Cluzel P, Coriat P, Rouby J-J. Regional distribution of gas and tissue in acute respiratory distress syndrome. III. Consequences on the effects of positive end-expiratory pressure. Intensive Care Med 2000; 26: 1215-1227 [Medline].

4. Dambrosio M, Roupie E, Mollet JJ, Anglade MC, Vasile N, Lemaire F, Brochard I. Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation. Anesthesiology 1997; 87: 495-503 [Medline].

5. Vieira SR, Puybasset L, Lu Q, Richecoeur J, Cluzel P, Coriat P, Rouby J-J. A scanographic assessment of pulmonary morphology in acute lung injury. Significance of the lower inflection point detected on the lung presure-volume curve. Am J Respir Crit Care Med 1999; 159: 1612-1623 [Abstract/Free Full Text].

6. Lichtwark-Aschoff M, Mols G, Hedlund A, Kessler V, Markstrom AM, Guttman J, Hedenstierna G, Sjostrand UH. Compliance is nonlinear over tidal volume irrespective of positive end-expiratory pressure level in surfactant-depleted piglets. Am J Respir Crit Care Med 2000; 162: 2125-2133 [Abstract/Free Full Text].

7. Malbouisson L, Muller J-C, Constantin J-M, Lu Q, Puybasset L, Rouby J-J. the CT Scan ARDS Study Group. Computed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 163: 1444-1450 .