Preserved spontaneous breathing in acute lung injury: show me the money?

Excerpt

It is well known that due to the increased intrathoracic pressure mechanical ventilation interacts with hemodynamics, which in most cases leads to a decreased cardiac output, i.e., reduces organ perfusion. For more details, interested readers should refer to the excellent reviews on this topic [1, 2]. In the clinical setting possible harmful effects for mechanically ventilated patients must be of course be taken into consideration. However, a major problem is the fact that conventional hemodynamic monitoring poorly mirrors regional perfusion, especially in conditions of hemorrhagic shock or sepsis [3]. Furthermore, although surrogate techniques are available for monitoring regional blood flow, they are fairly complicated for routine clinical use [4, 5]. Nevertheless, according to available literature, things seem to be “not too bad” with respect to hepatic blood flow: in fact, patient studies showed that the PEEP-induced decrease in hepatic perfusion can be simply reversed by restoring intravascular volume to normalize cardiac output [6‐9]. These data, however, suffer from three major limitations: (a) they do not consider the effects on the microcirculation, which may be still compromised even given normalized cardiac output [10], (b) volume replacement alone may not restore regional perfusion to the same extent in septic as in nonseptic subjects [11, 12], and (c) until now the effects of intrathoracic pressure have been studied mostly by applying different PEEP levels without considering the effects induced by the simultaneous changes in peak airway pressure. Finally, until now only few investigations have focused on the specific effects of common ventilatory modes and/or strategies related to mechanical ventilation [13]. …