Partial liquid ventilation.

Abstract

Correspondence: B. Lachmann, Dept of Anesthesiology (Room Ee 2393), Erasmus University Rotterdam, Postbox 1738, 3000 DR Rotterdam, The Netherlands. There is strong indication that modes of that lead to repeated closure and opening of surfactantdeficient alveoli can induce severe functional and histological lung damage [1]. New modes of are directed at prevention of lung injury due to mechanical by maintaining alveolar at end-expiration, by means of positive end-expiratory pressure (gas PEEP). Recent evidence suggests that such modes may prevent not only lung parenchymal injury but also proinflammatory mediator expression in the lung tissue [2], and bacterial translocation from the lung into the circulation [3]. The incidence of acute respiratory distress syndrome (ARDS) and multiple system organ failure (MSOF), which is still the leading cause of death in ARDS [4], may thus be reduced. An alternative technique to maintain alveolar volume at end-expiration is by instilling perfluorocarbon (PFC) fluids into the lung, thereby providing to the alveoli. Because PFCs dissolve high amounts of oxygen and carbon dioxide at normospheric pressures, gas exchange over the alveolar air-liquid interface is maintained when conventional mechanical gas is superimposed. This technique has become known as partial liquid ventilation (PLV) [5]. In this issue of the European Respiratory Journal, KAISERS et al. [6] show that mean short-term survival time in lung-lavaged pigs treated with PLV with low dose intratracheal PFC can be increased almost fourfold compared to a nontreated control group, when both groups are volume-control ventilated (tidal volume = 12 mL·kg-1; PEEP = 5 cmH2O; inspiratory/expiratory (I/E) ratio = 1:2; fraction of inspired oxygen (FI,O2) = 1.0). The increased survival was attributed to a preserved oxygen delivery with PLV, which deteriorated in the nonPFC-treated control group. The authors also partially confirm previous experiences with PLV in animal models of acute lung injury (ALI), which have shown that: 1) Higher doses of PFC lead to higher levels of oxygenation [7]. This is suggested to result from dose-dependent recruitment of collapsed atelectatic alveoli by PFC fluid. Thereby, gas exchange also continues during the expiratory phase of the respiratory cycle. 2) Oxygenation deteriorates over time if no additional doses of PFC are applied [8]. This is attributed to evaporation of PFC, which will cause affected alveoli to collapse. 3) Lung mechanics and carbon dioxide elimination improve after an initial low dose of PFC and show no further improvements with subsequent higher doses of PFC [7]. This is attributed to the replacement of the alveolar air-liquid interface with a thin air-PFC interface. Evaporating PFC appears to cover the entire lung surface. As PFCs have a low constant surface tension (which is 12 mN·m-1 in the case of FC 3280), pulmonary compliance is increased after a low-dose PFC and CO2 elimination is higher. No further improvement is seen after additional PFC dosing. 4) PLV does not impair any cardiovascular parameter; even in animals with a large anterior-posterior thoracic diameter. Mean pulmonary artery pressure decreases when PFC is applied, due to reversal of hypoxic pulmonary vasoconstriction [9]. 5) PLV does prevent the progress of histologically assessed lung injury [10]. 6) Gas-PEEP has to be applied during PLV to prevent bulk movement of PFC fluids from the alveoli into the airways and to prevent dangerously high airway pressures at the onset of inspiration [7]. 7) PLV can be combined with other ventilatory support techniques in ALI, such as nitric oxide administration and high frequency oscillation [11, 12]. Although preliminary evaluations of phase II and III clinical studies with PLV have shown that PFCs can be safely applied to patients with ALI [13], these trials did not show the tremendous improvement of gas exchange that might have been anticipated from animal studies, nor could they demonstrate improvement in survival of patients treated with PLV compared to those treated with conventional mechanical only. There is a tendency towards an increased number of pneumothoraces in patients treated with PLV. How does one explain such findings?