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


METHODS
Prospective study.


METHODS
Research laboratory.


METHODS
Adult female sheep (n = 5).


METHODS
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 and 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.


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 at 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 H2O. 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.
Tao
W
W
Department of Surgery, University of Texas Medical Branch, Galveston 77555-0528, USA.
Brunston
R L
RL
Bidani
A
A
Pirtle
P
P
Dy
J
J
Cardenas
V J
VJ
Traber
D L
DL
Zwischenberger
J B
JB
D000208:Acute Disease; D000818:Animals; D001166:Arteriovenous Shunt, Surgical; D002245:Carbon Dioxide / Q000032:analysis* / Q000097:blood; D004195:Disease Models, Animal; D015199:Extracorporeal Membrane Oxygenation / Q000295:instrumentation / Q000379:methods*; D005260:Female; D006439:Hemodynamics; D010100:Oxygen / Q000097:blood; D011659:Pulmonary Gas Exchange; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D012131:Respiratory Insufficiency / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D012756:Sheep
D002245:Carbon Dioxide; D010100:Oxygen