To the Editor:-We read with interest the report by Kalfon et al. regarding the use of expiratory washout in patients with severe acute respiratory distress syndrome. [1]Although interesting and stimulating, we believe that several points should be discussed.
In our opinion, the indications for the use of expiratory washout (EWO) or tracheal gas insufflation (TGI) can be summarized as situations wherein there is profound hypercarbia, resulting in hemodynamic or acid-base compromise, associated with high airway pressures that cannot be safely increased for fear of barotrauma (e.g., severe ARDS) and secondly wherein there are high airway pressures that cannot be reduced as a result of the contraindication of hypercarbia (e.g., lung injury in association with head injury). In the first situation, the aim of EWO is to reduce PaCO2but at the same airway pressures. In the second situation, the aim is to decrease airway pressures without allowing a resultant increase in PaCO2.
In their study, Kalfon et al. have used EWO for none of the previous indications. Their findings of PaCO2decrease could easily have been reproduced by simply increasing tidal ventilation. This would have provided CO2decrease and would have led to similar airway pressure changes, i.e., increased peak, plateau, and mean tracheal pressure. We are concerned that an uncritical reading of this paper will bias readers against TGI because of the significant increases in airway pressures associated with the mode in which EWO has been used by the authors. To most clinicians, these significant changes in airway pressure would be unacceptable.
Some of these changes in airway pressures could have been avoided by the use of pressure-controlled ventilation (PCV) rather than volume-controlled ventilation. We have recently completed a similar study of EWO, in an animal model, in which we used EWO at a flow of 6 l/min combined with PCV. [2]We observed a 14% reduction in PaCO2but with no increase in peak airway pressure. Mean airway pressure increased by a nonsignificant amount as a result of intrinsic PEEP caused by EWO. We had the capability of measuring this increase in PEEP, unlike Kalfon et al., by the synchronized suppression of EWO and occlusion of the expiratory valve and found a small but significant increment (2 cm H2O above set PEEP of 2 cm H2O). We were also able to measure the increase in FRC induced by EWO and found this to be 79 ml. Not surprisingly, as a result of the increase in PEEP and unchanged peak airway pressure, tidal ventilation decreased from 0.236 l +/- 0.053 to 0.199 l +/- 0.199 l +/- 0.041. Despite this decrease in alveolar ventilation, we were able to demonstrate significant reductions in PaCO2, although less impressive than Kalfon et al.
In summary, we are encouraged by this important study by Kalfon et al., and we believe that TGI holds promise as a means to reduce ventilator-induced lung injury. However, significant increases in airway pressure, as a result of EWO, would be unacceptable to most clinicians, and we believe that better conventional ventilation strategies (i.e., PCV and lowering of set PEEP to compensate for PEEPi) in conjunction with EWO would circumvent this problem.
George P. Findlay, F.R.C.A.
Senior Registrar in Intensive Care Medicine
John Dingley, F.R.C.A.
Consultant in Anaesthesia
Mark N. Smithies, F.R.C.P.
Director of Intensive Care Service; Intensive Care Unit, B3; University Hospital of Wales; Heath Park; Cardiff, CF4 4XW; United Kingdom
(Accepted for publication November 18, 1997.)
