The effect of augmented hemodynamics on blood flow during arteriovenous carbon dioxide removal

Arteriovenous carbon dioxide removal (AVCO₂R) as an alter. native treatment for acute respiratory distress syndrome uses a low resistance gas exchanger in a simple arteriovenous shunt to achieve total CO₂ removal and allow lung rest. We have previously shown in our clinically relevant LD₄₀ ovine model of smoke/burn induced acute respiratory distress syndrome that AVCO₂R allows significant decreases in respiratory rate, tidal volume, peak airway pressure, and FiO₂, as compared with standard mechanical ventilation. In addition, we have shown in a prospective randomized outcomes study that AVCO₂R increases ventilator free days, decreases ventilator dependent days, and significantly improves survival. The purpose of this study is to further define the limits of AVCO₂R through hemodynamic augmentation and evaluation of peak end expiratory pressure (PEEP). Administration of an alpha agonist (phenylephrine) and a beta agonist (isoproterenol) increased mean arterial pressure (MAP) and cardiac output (CO), respectively. MAP increases ranged from 2.4% to 94.4% and CO increases ranged from 33% to 146%. Phenylephrine caused elevations in MAP (2.4-94.4%) and AVCO₂R flow (9-67%), and CO never decreased more than 10%. Isoproterenol administration increased CO (33-146%), decreased MAP (9-54%), and decreased AVCO₂R flow (11-42%). In a second group, PEEP was increased stepwise from 0 (baseline) to 20 cm H₂O. Increasing PEEP did not result in significant hemodynamic changes (<10% change from baseline PEEP) for MAP, CO, or AVCO₂R flow. In conclusion, alpha agonist administration increased AVCO₂R blood flow, whereas beta agonist administration decreased MAP and AVCO₂R blood flow, despite CO elevation. Various levels of PEEP are well tolerated and thus allow a range of options during AVCO₂R.