Discussion:
The two main objectives were to test the influence of the two ventilatory modes and simultaneously two different modern heater-humidifiers on humidification measured at the Y-piece. The two main results of this study were that humidity was lower during HFOV than during conventional ventilation and differed according to the heater-humidifier model. Results for the two ventilatory modes were consistent for the in-vitro study, with strictly controlled ventilatory settings and ambient conditions, and the in-vivo study, with its various ventilatory settings and ambient conditions. Several hypotheses may explain these results. The first and most intuitive explanation for this difference is that HFOV flow rates are much higher than IPPV flow rates.13 At the same time, both the inlet and outlet chamber temperatures were found to be higher in HFOV than IPPV. This finding suggests that the heater-humidifier increases the heat of the plate in order to increase the energy delivered by the heater-humidifier, which should be proportional to the air volume delivered by the ventilator. However, the heater-humidifier regulation tends to stop the heater plate when the inlet chamber temperature is high.13 In this situation, the water may be partially heated and the gas insufficiently humidified and heated. Nonetheless, the HFOV and IPPV chamber temperatures did not differ all that much clinically, although they were statistically different. This difference does not seem adequate to explain the temperature reduction of the heating plate.13 A second explanation might be the frequency difference. For the same duct diameter, the thermal losses of the oscillatory flow increase with its frequency.14Thus we can expect that this increasing loss will decrease temperature and AH. However, Nagaya et al. showed that the temperature change in the ETT did not depend on the oscillatory frequency when the oscillatory volume was fixed; but, the temperature did depend on the oscillatory volume when the oscillatory frequency was fixed.15 It is also interesting to note the previous observation during IPPV that AH decreases linearly with the value of VT,16 although the reasons for this phenomenon remain unclear.
Recommendations to target a RH of inspired gas between 75% and 100% come from recommendations for adults, but ventilation in ELBW patients is very different from that in adults, due to the use of low tidal volumes and high instrumental dead space. Because of these particularities, humidity at the tip of the ETT is different from that at the Y-piece.15 Thus, it might not be possible to extrapolate adult recommendations on humidification to preterm neonates, who might even need higher levels of humidity.
It is important to note that the mean RH during HFOV in our study was below the recommended 75%. Poor humidification may have a deleterious effect on inflammation10 17 and on water movements18 at the respiratory tract level as well as at the cellular level. It may thus impair lung development as it can induce such adverse events as atelectasis or plugged ETT and unplanned extubations. The incidence of inadequate humidity as an associated risk factor of pulmonary inflammation and consequently part of ventilator-induced lung injury is poorly documented. The principal reason for the lack of literature on this subject may well be the lack of routine monitoring of humidity and temperature of inspired gases. This study presents a method for exploring humidity and temperature at the Y-piece during tracheal ventilation that could be routinely used for in-vitro and in-vivo studies. Monitoring humidity at the Y-piece is a first approach and is not yet sufficient to extrapolate the real humidity level in the trachea.
The superiority of HFOV over IPPV for lung protection has not yet been proven,19 although we might expect superiority due to the use of lower tidal volumes6 in this ventilatory mode in preterm patients.20 IPPV with volume guarantee mode induces lower expression of early inflammation markers than HFOV,21 which is contradictory to the expected protective effect of HFOV. Our study suggest that inadequate humidification could be a factor explaining potential excess inflammation during HFOV. Another important result of this study is that humidification is not easily predictable and depends not only on ventilation mode but also on the type of circuit and the specific heater-humidifier used.
Our study has several limitations. First, it is an observational study. An interventional study, however, appears difficult to conduct, given the variety of factors involved in determining the humidity level: the medical devices used, the ventilatory settings, and ambient conditions. In this in-vitro and in-vivo study, the only ventilator used was the Drager VN500. One advantage of using a single ventilator is the homogeneity of the study conditions, but its negative aspect is that we cannot extrapolate these results to other ventilators. The specific flow management of the VN500 during HFOV may influence the hygrometric results as the flow is quadrupled during HFOV compared to conventional IPPV. Nevertheless, because other ventilators do not systematically provide flow rates, it seems difficult not to remain vague for the moment. While waiting for humidity monitoring which is technically more difficult, we think that flow rate monitoring should be systematically reported for ventilators.
In conclusion, we found that during mechanical ventilation, humidity measured in-vitro and in-vivo in ELBW preterm infants was lower with HFOV than with IPPV and did not reach recommended values during HFOV. Moreover, humidification values differed significantly according to the humidifier device used. These results suggest that humidification depends on ventilatory mode and heating devices and that HFOV requires a specific humidification management. It is suggested that the systematic control of humidity, temperature, and flow rate during mechanical ventilation may optimize lung protection strategies.