Abstract

Introduction: Although metabolic problems after cardiac arrest (CA) have been postulated, the actual measurement of metabolic alterations after CA remain undescribed. The measurement of oxygen extraction (VCO2), carbon dioxide excretion (VCO2), and respiratory quotient (RQ), reflect the energy metabolism and may provide insight into the post-arrest metabolism. Objective: To investigate metabolism alterations after CA, which may be detected via changes in VCO2, VO2, and RQ. Secondarily to test whether it is affected by therapeutic temperature management (TTM) Methods: Sixteen male rats underwent a protocol for 10 minutes of asphyxial CA and return of spontaneous circulation (ROSC). Three groups were compared: Group1: controls (no-CA, n=5), group2: CA (n=6), and group3: CA with TTM (n=5). Within the TTM group, the body was cooled to 33 °C. Capnography was recorded and O2 extraction was measured for 120min to measure VCO2 and VO2. RQ was the ratio of VCO2/VO2. Results: The post arrest VCO2 was 1.5 fold higher in the CA group than in the controls (17.3±2.2mL/kg/min versus 11.2±1.0mL/kg/min, p<.01) in minutes 20 through 60. The VCO2 value in CA was normalized after 60min. VCO2 (12.5±1.3 mL/kg/min, p<.01) in TTM-treated CA was significantly lower than untreated CA. The post arrest VO2 was greater in the CA group than in the controls, starting 15min after ROSC, and gradually increased to an extraction rate 2.1 fold higher (29.8±6.0mL/kg/min) than controls (14.1±1.6mL/kg/min, p<.01). There were no differences in VO2 between TTM-treated and untreated CA. RQs in TTM-treated and untreated CA were significantly and persistently lower than controls (0.5±0.1, 0.5±0.1 vs. 0.9±0.1, p<.01). Conclusions: VO2 in rats after CA was markedly elevated after ROSC and RQ decreased to extremely low levels. VCO2 showed some attenuation by TTM, however surprisingly TTM did not affect VO2 or RQ. These results suggest that profound alterations in oxygen extraction occur after CA and may be measured non-invasively in patients. The finding of a lowered RQ has not be described previously, appears to be driven by increased VO2, and may be due to non-CO2 generating oxygen utilization. If true, this may have great importance for mechanism, monitoring, and customized treatment of CA.

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