Significant reduction in minute ventilation and peak inspiratory pressures with arteriovenous CO₂ removal during severe respiratory failure

Objectives: To quantify CO₂ removal using an extracorporeal low- resistance membrane gas exchanger placed in an arteriovenous shunt and evaluate its effects on the reduction of ventilatory volumes and airway pressures during severe respiratory failure induced by smoke inhalation injury. Design: Prospective study. Setting: Research laboratory. Subjects: Adult female sheep (n = 5). Interventions: Animals were instrumented with femoral and pulmonary arterial catheters and underwent an LD₅₀ cotton smoke inhalation injury via a tracheostomy under halothane anesthesia. Twenty-four hours after smoke inhalation injury, the animals were reanesthetized and systemically heparinized for cannulation of the left carotid artery end common jugular vein to construct a simple arteriovenous shunt. A membrane gas exchanger was interposed within the arteriovenous shunt, and blood flow produced by the arteriovenous pressure gradient was unrestricted at the time of complete recovery from anesthesia. CO₂ removal by the gas exchanger was measured as the product of the sweep gas flow (FIO₂ of 1.0 at 2.5 to 3.0 L/min) and the exhaust CO₂ content measured with an inline capnometer. CO₂ removed by the animal's lungs was determined by the expired gas CO₂ content in a Douglas bag. We made stepwise, 20% reductions in ventilator support hourly. We first reduced the tidal volume to achieve a peak inspiratory pressure of <30 cm H₂O, and then we reduced the respiratory rate while maintaining normocapnia. Pao₂ was maintained by adjusting the FIO₂ and the level of positive end-expiratory pressure. Measurements and Main Results: Mean blood flow through the arteriovenous shunt ranged from 1154 ± 82 mL/min (25% cardiac output) to 1277 ± 38 mL/min (29% cardiac output) over the 6-hr study period. The pressure gradient across the gas exchanger was always <10 mm Hg. Maximum arteriovenous CO₂ removal was 102.0 ± 9.5 mL/min (96% of total CO₂ production), allowing minute ventilation to be reduced from 10.3 ± 1.4 L/min (baseline) to 0.5 ± 0.0 L/min st 6 hrs of arteriovenous CO₂ removal while maintaining normocapnia. Similarly, peak inspiratory pressure decreased from 40.8 ± 2.1 to 19.7 ± 7.5 cm H₂0. Pao₂ was maintained at >100 torr (>13.3 kPa) at maximally reduced ventilator support. Mean arterial pressure and cardiac output did not change significantly as a result of arteriovenous shunting. Conclusions: Extracorporeal CO₂ removal using a low- resistance gas exchanger in a simple arteriovenous shunt allows significant reduction in minute ventilation and peak inspiratory pressure without hypercapnia or the complex circuitry and monitoring required for conventional extracorporeal membrane oxygenation. Arteriovenous CO₂ removal can be applied as an easy and cost-effective treatment to minimize ventilator- induced barotrauma and volutrauma during severe respiratory failure.