Acute respiratory distress syndrome (ARDS) is a common disease entity in critical care medicine and is still associated with a high mortality. Because of the heterogeneous character of ARDS, animal models are an insturment to study pathology in relatively standardized conditions. Rodent models can bridge the gap from in vitro investigations to large animal and clinical trials by facilitating large sample sizes under physiological conditions at comparatively low costs. One of the most commonly used rodent models of acute lung inflammation and ARDS is administration of lipopolysaccharide (LPS), either into the airways (direct, pulmonary insult) or systemically (indirect, extra-pulmonary insult). This narrative review discusses the dynamics of important pathophysiological pathways contributing to the physiological response to LPS-induced injury. Pathophysiological pathways of LPS-induced lung injury are not only influenced by the type of the primary insult (e.g., pulmonary or extra-pulmonary) and presence of additional stimuli (e.g., mechanical ventilation), but also by time. As such, findings in animal models of LPS-induced lung injury may depend on the time point at which samples are obtained and physiological data are captured. This review summarizes the current evidence and highlights uncertainties on the molecular dynamics of LPS-induced lung injury in rodent models, encouraging researchers to take accurate timing of LPS-induced injury into account when designing experimental trials.

Respiratory sinus arrhythmia (RSA) is a fluctuation of heart period that occurs during a respiratory cycle. It has been suggested that inspiratory heart period acceleration and expiratory deceleration during spontaneous ventilation (henceforth named positive RSA) improve the efficiency of gas exchange compared to the absence or the inversion of such a pattern (negative RSA). During mechanical ventilation (MV), for which maximizing the efficiency of gas exchange is of critical importance, the pattern of RSA is still the object of debate. In order to gain a better insight into this matter, we compared five different methods of RSA classification using the data of five mechanically ventilated piglets. The comparison was repeated using the data of 15 volunteers undergoing a protocol of paced spontaneous breathing, which is expected to result in a positive RSA pattern. The results showed that the agreement between the employed methods is limited, suggesting that the lack of a consensus about the RSA pattern during MV is, at least in part, of methodological origin. However, independently of the method used, the pattern of RSA within the respiratory cycle was not consistent among the subjects and conditions of MV considered. Also, the outcomes showed that even during paced spontaneous breathing a negative RSA pattern might be present, when a low respiratory frequency is imposed.

PEEPminE1 better identifies the open-lung PEEP independently of the adjusted Vt, and may be a practical, more individualized approach for PEEP titration.

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