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.