REBREATHING IMPROVES ACCURACY OF VENTILATORY MONITORING

Objective. Our objective was to determine if rebreathing would reduce the gradient between arterial and end-tidal CO2 tension during positiv e-pressure ventilation. Methods. Design: Experimental investigation. S etting: Anesthesiology laboratory. Subjects: A total of 10 dogs of eit her sex. Interventions: Anesthesia (sodium pentobarbital) and muscle r elaxation (pancuronium) were induced and animals were tracheally intub ated and ventilated with a standard anesthesia ventilator and breathin g circuit with CO2 absorber and then with a Mapleson D circuit with a fresh gas flow rate (VF) equal to alveolar ventilation plus the sampli ng flow rate of two capnometers. Rebreathing was varied by adjusting t he respiratory rate (RR) so that minute ventilation (VE) to VF ratio w as 1:1, 2:1, 3:1, and 4:1. Results. CO2 production (ATPD) was determin ed as the product of expired concentration of CO2 and V-E (BTPS). Alve olar ventilation (VA) was calculated by dividing the product of CO2 pr oduction and barometric pressure corrected for ambient temperature and water vapor pressure at body temperature by PaCO2. Tidal volume, RR, airway gas temperature, concentration of CO2 in gas at the tracheal tu be and inlet/outlet of the mechanical ventilator, body temperature, ar terial gas tensions and pH, heart rate, arterial blood pressure, and c ardiac output were measured. Minute ventilation, mean arterial blood p ressure and end-expiratory CO2 tension (PECO(2))(BTPS) were calculated . During positive-pressure ventilation, concentration of inspired CO2 was zero with standard circuitry, and significantly increased with Map leson D when VE:VF ratio was 1:1 (0.56 +/- 0.19%), 2:1 (1.97 +/- 1.30% ), 3:1 (2.56 +/- 1.05%), and 4:1 (3.01 +/- 1.45%) (p < 0.05). PECO(2) was 34.8 +/- 3.2 mm Hg during ventilation with the standard circuit, a nd significantly increased during ventilation with Mapleson D when VE: VF ratio was increased from 1:1 (35.4 +/- 2.5 mm Hg) to 2:1 (40.2 +/- 3.6 mm Hg) and was not further increased at a VE:VF ratio of 3:1 (41.8 +/- 2.7 mm Hg) or 4:1 (41.3 +/- 2.4 mm Hg). The selected fresh gas fl ow rate was appropriate, because PaCO2 remained unchanged regardless o f VE:VF ratio, indicating PaCO2 was dependent on VF, not on VE. The gr adient between PaCO2 and PECO(2) during ventilation with the standard circuit was 6.6 +/- 3.0 mm Hg; during ventilation with Mapleson D, it decreased significantly when VE:VF ratio was increased from 1:1 (6.5 /- 3.6 mm Hg) to 2:1 (2.9 +/- 1.5 mm Hg), but was not significantly re duced further at 3:1 (1.7 +/- 1.1 mm Hg) or 4:1 (1.8 +/- 0.5 mm Hg) (p < 0.05). Conclusions, Rebreathing with a Mapleson D circuit and a VF equal to VA permitted normal CO2 elimination. Arterial PCO2 to PECO(2) gradient decreased significantly during rebreathing, thus improving t he reliability of capnography for estimating arterial PCO2. Considerat ion should be given to using the Mapleson D as a rebreathing circuit.