Several clinical conditions [1][2][3] and research protocols [4][5][6][7] require increases in minute ventilation (V 'E) at constant (or nearly constant) arterial carbon dioxide tension (Pa,CO 2 ). At a constant CO 2 production, Pa,CO 2 is inversely related to alveolar ventilation (V 'A), which is a function of V 'E. When V 'E increases, Pa,CO 2 falls unless CO 2 is added to the inspired gas. Maintaining a constant Pa,CO 2 despite an irregular breathing pattern requires continuous and proportional adjustment of the fractional concentration of inspired CO 2 (FI,CO 2 ). Manual adjustments of FI,CO 2 may be adequate if changes in V 'E are slow or if wide variations in V 'A are acceptable. Automated feedback systems provide finer control of V 'A but can result in phase delays, unstable responses or overdamping, despite the use of expensive equipment and complex algorithms. A simple breathing circuit was developed and tested that minimizes the effect of V 'E on V 'A by passively and continuously matching the inspired CO 2 to V 'E regardless of the extent or pattern of breathing. MethodsThe basic concept underlying this approach is that the flow of fresh gas (FI,CO 2 =0) contributing to alveolar CO 2 exchange is kept constant. When V 'E is less than or equal to the fresh gas flow (FGF), the subject inhales only fresh gas. Therefore:When V 'E exceeds FGF, the balance of inhaled gas is drawn from a reservoir containing a reserve gas with a carbon dioxide tension (PCO 2 ) equal to that of mixed venous blood and thus does not participate in CO 2 exchange, ensuring that V 'A is limited by FGF, as indicated by the following equation:where Pv,CO 2 is the oxygenated mixed venous PCO 2 . When the PCO 2 of the mixed venous and reserve gas are not equal, the V 'A depends on both this difference and the difference between V 'E and FGF. Circuit descriptionThe circuit ( fig. 1) A simple, passive circuit that minimizes changes in V 'A during hyperpnoea was devised. It is comprised of a manifold, with two gas inlets, attached to the intake port of a nonrebreathing circuit or ventilator. The first inlet receives a flow of fresh gas (CO 2 =0%) equal to the subject's minute ventilation (V 'E). During hyperpnoea, the balance of V 'E is drawn (inlet 2) from a reservoir containing gas, the carbon dioxide tension (PCO 2 ) approximates that of mixed venous blood and therefore contributes minimally to V 'A.Nine normal subjects breathed through the circuit for 4 min at 15-31 times resting levels. End-tidal PCO 2 (Pet,CO 2 ) at rest, 0, 1.5 and 3.0 min were ( In conclusion, this circuit effectively minimizes changes in alveolar ventilation and therefore arterial carbon dioxide tension during hyperpnoea. Eur Respir J 1998; 12: 698-701.

The currently recommended prehospital treatment for carbon monoxide (CO) poisoning is administration of 100% O(2). We have shown in dogs that normocapnic hyperpnea with O(2) further accelerates CO elimination. The purpose of this study was to examine the relation between minute ventilation (V E) and the rate of elimination of CO in humans. Seven healthy male volunteers were exposed to CO (400 to 1,000 ppm) in air until their carboxyhemoglobin (COHb) levels reached 10 to 12%. They then breathed either 100% O(2) at resting V E (4.3 to 9.0 L min) for 60 min or O(2) containing 4.5 to 4.8% CO(2) (to maintain normocapnia) at two to six times resting V E for 90 min. The half-time of the decrease in COHb fell from 78 +/- 24 min (mean +/- SD) during resting V E with 100% O(2) to 31 +/- 6 min (p < 0. 001) during normocapnic hyperpnea with O(2). The relation between V E and the half-time of COHb reduction approximated a rectangular hyperbola. Because both the method and circuit are simple, this approach may enhance the first-aid treatment of CO poisoning.