• George Prinianakis, Maria Plataki, Eumorfia Kondili, Maria Klimathianaki, Katerina Vaporidi, and Dimitris Georgopoulos.
• University Hospital of Heraklion, Medical School, University of Crete, Department of Intensive Care Medicine, Stavrakia, 71110 Heraklion, Crete, Greece.
• Intensive Care Med. 2008 Jan 1; 34 (1): 70-4.

ObjectiveDuring pressure support ventilation (PS), an abrupt increase in ventilator pressure above the pre-set level is considered to signify expiratory muscle activity. However, relaxation of inspiratory muscles may also cause the same phenomenon, and this hypothesis has not been explored. The aim of this study is to examine the cause of this increase in ventilator pressure, during PS, in critically ill patients.DesignRetrospective study.SettingIn a university intensive care unit.MethodsFifteen patients instrumented with esophageal and gastric balloons, and in whom airway pressure (P (aw)) during PS exhibited an acute increase above the pre-set level towards the end of mechanical inspiration were retrospectively analyzed. For each breath, the time of the rapid increase in P (aw) was identified (t (Paw)) and, using the transdiaphragmatic (P (di)) and gastric (P (ga)) pressure waveforms, related to: (1) the end of neural inspiration (peak P (di)) and (2) the time at which P (ga) started to increase rapidly after the end of neural inspiration indicating expiratory muscle recruitment.ResultsThe t (Paw) was observed 32+/-34ms after the end of neural inspiration, well before (323+/-182ms) expiratory muscle recruitment (identified in eight patients). There was a significant linear relationship between the rate of rise of P (aw) after t (Paw) and the rates of decline of P (di) and inspiratory flow.ConclusionWe conclude that, during PS ventilation, the relaxation of inspiratory muscles accounts for the acute increase in P (aw) above the pre-set level, in addition to the contribution made by the occurrence of expiratory muscle activity.

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