This study shows the advantage of using the PRVC mode for ventilation during acute respiratory failure. PIP was lower for all patients using the PRVC mode compared to the VC mode, and alveolar ventilation was unchanged as indicated by the constant PaCO2. The new mode of ventilation did not improve outcome or duration of treatment, despite a statistically significant difference in peak pressures (4 cmH2O). Though this difference in peak pressure is small, it may be more relevant in situations where larger tidal volumes are contemplated.
This study is the only study that has measured the difference between PIP on the two modes of ventilation, PRVC and VC. In contrast to other studies comparing pressure-limited ventilation with various forms of ventilation, our patients had only mild respiratory insufficiency. In the studies by Rappaport et al [9] and Hickling et al [7], the inclusion criterion was a PaO2/FiO2 ratio < 150, whereas < 300 was used in our study. However, two of our patients failed the assigned VC mode, while no patient on PRVC failed (P = 0.24). For this tendency to have achieved statistical significance, 110 patients should have been enrolled in the study. The risk of type 2 error for an overlooked difference of 10% failing VC is only 20% with 1-β = 80%.
Further studies are needed to decide if PRVC improves outcome when compared with VC in patients with acute respiratory failure. Other subgroups, such as acute severe asthma or ARDS, could be a focus for attention.
A recent review recommends pressure-control ventilation in all clinical circumstances requiring artificial ventilation [10]. During PRVC, as with pressure control, there is a maximum pressure difference between the ventilator and the lung at the beginning of the inspiratory cycle. The resulting flow is also maximal. With the increase in intrathoracic pressure this difference diminishes, as does the resulting inspiratory flow. The flow pattern is therefore called decelerating inspiratory flow. In VC ventilation, there is a constant inspiratory flow and the resulting intrathoracic pressure is always increasing. Pressure-regulated ventilation is therefore capable of delivering the same volume at a lower PIP. This fact may play a more significant role when higher tidal volumes are required, and greater differences in peak pressures between PRVC and VC may be expected.
Our conclusion is that, during mechanical ventilation for acute respiratory failure, PIP was significantly lower on PRVC than VC, and thus PRVC may be superior to VC in certain patients.
Our results emphasize one of the basic problems in intensive care research-that therapeutic signals are too weak to be discovered in clinical trials consisting of few patients.