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More environmental prevention of gram-negative infections needed.

syndrome (ARDS). Implicit in his comment is that, in the context of the results of the ARDS Network trial,2 which showed that a VT of 6 mL/kg was associated with better survival in patients with ARDS, decreasing the VT in response to decreasing compliance is beneficial and recommended. We believe that that contention, though broadly correct, overlooks the essential finding of the ARDS Network (in which our institution participated), that a specific VT of 6 mL/kg is recommended, not a varying VT, and not a VT that exceeds 6 mL/kg, even if VT decreases as the lung stiffens. Furthermore, in endorsing a maximum inspiratory pressure up to 50 cm H2O, the “clarification” overlooks the target of a plateau pressure of 30 cm H2O in the ARDS Network trial,2 which would probably be exceeded by a maximum inspiratory pressure of 50 cm H2O in the absence of increased airway resistance (depending, of course, on the inspiratory flow rate). Furthermore, Mr Piper’s comment about the device’s automatic adjustment seems to imply that there is some intelligence in the adjustment process, which, of course, there is not. The adjustment is simply a mechanical response to a changing respiratory-system time constant. The only ventilators that make “intelligent” changes to the delivered VT are much more sophisticated devices.3 The most important issue regarding “automatic” changes in ventilatory parameters is that, unlike any other ventilatory device, setting a “rate” on the Vortran device does not guarantee a preset number of mandatory breaths per minute, because the breaths are not time-triggered independent of the patient’s respiratory-system mechanics (ie, resistance, compliance, and muscle activity). On the contrary, spontaneous breaths are pressure-triggered according to the interaction of the Vortran’s internal leak flow (set by the “rate” knob) and the patient’s inspired VT and expiratory time constant. Indeed, the “rate” knob should be thought of not as a frequency control but rather as a trigger-sensitivity control. What the operator is really doing (with a passive patient) is setting the device to auto-trigger, much like a standard ventilator will do when there is a leak in the system. The second contention is that our choosing a compliance of 14 mL/cm H2O as a working condition in the study1 was imprudent and cast the device’s performance in an unfavorable light. As we stated, our goal was to examine the device’s performance under 2 mass-casualty conditions that would simulate those in which a portable, inexpensive device might be considered desirable, such as poisoning causing neuromuscular paralysis (in which the lung compliance would be expected to be normal) and acute lung injury/ARDS (in which the lung compliance would be decreased). Still, patients with ARDS have been reported to have average compliances as low as 37 mL/cm H2O, with a standard deviation of 23 mL/cm H2O, so compliance values in the teens would be expected in perhaps 30% of patients.4 In that context ourchoiceofcompliancevaluesunderwhich to simulate the use of the device seems defensible and appropriate. Finally, Mr Piper found our statement about calculated PCO2 misleading. We absolutely agree that only actual blood gas data from patients will settle the issue and allay concerns, but our experience in this study makes us reluctant to undertake actual clinical testing to resolve this. Overall, we stand by our suggestions that, “The variable performance under changing load along with the lack of alarms should prompt caution in using the Vortran Automatic Resuscitator for emergency ventilatory support in situations where patients cannot be constantly monitored by trained and experienced operators.”1 As evidence that truth in science is replication of findings, we point out that conclusions from other groups echo our concerns about the device.5