EFFICACY OF EXPIRATORY TRACHEAL GAS INSUFFLATION IN A CANINE MODEL OF LUNG INJURY

Tracheal gas insufflation (TGI) improves the efficiency of CO2 elimination by reducing the CO2-laden dead space of the airways. The effect of TGI on Pa-CO2 diminishes in the setting of acute lung injury (ALI) because an increased alveolar component dominates the total physiologic dead space. Nevertheless, adopting a strategy of permissive hypercapnia should partially offset the decreased efficacy of TGI by increasing CO2 concentration in the proximal airways. To examine these issues we studied the CO2: removal efficacy of expiratory TGI as an adjunct to conventional mechanical ventilation (CMV) before and after oleic acid-induced lung injury (OAI). We first examined the effect of TGI before and after OAI, keeping tidal volume (VT) and frequency constant, and allowing Pa-CO2 to increase after OAI. We then tested TGI efficiency after matching Pa-CO2 after OAI to its pre-OAI level by increasing VT (post-OA/VT stage). Pa-CO2 was 53 +/- 3,79 +/- 21, and 52 +/- 4 mm Hg in the pre-OAl post-OAl, and post-OA/VT stages of CMV, respectively. The corresponding decrements in Pa-CO2 produced by TGI at a flow rate of in L/min were 16 +/- 3,24 +/- 10, and 10 +/- 2 mm Hg, respectively. TGI decreased total physiologic dead space per breath (VD) by 56, 31, and 28 ml during the pre-OAI, post-OAI, and post-OA/VF stages, respectively. Despite a smaller reduction in VD during the post-OAI stage, the effect of TCI on Pa-CO2 was preserved because of the relatively high Pa-CO2 prior to its initiation. For a similar decrement in VD during the post-OA/Vr stage, TCI was less effective in decreasing Pa-CO2. Our results can be explained by the inverse relationship between Pa-CO2 and the physiologic dead-space fraction (VD/VT), in which at high VD/VT a small decrement in VD causes a relatively large decrease in Pa-CO2. We conclude that application of a permissive hypercapnia strategy during ALI counterbalances the decreased CO2 removal efficacy of TCI caused by increased alveolar dead space.