Abstract
BACKGROUND: The concept that resuscitation from cardiac arrest (CA) results in a metabolic injury is broadly accepted, yet patients never receive this diagnosis. We sought to find evidence of metabolic injuries after CA by measuring O(2) consumption and CO(2) production (VCO(2)) in a rodent model. In addition, we tested the effect of inspired 100% O(2) on the metabolism. METHODS AND RESULTS: Rats were anesthetized and randomized into 3 groups: resuscitation from 10-minute asphyxia with inhaled 100% O(2) (CA-fraction of inspired O(2) [FIO(2)] 1.0), with 30% O(2) (CA-FIO(2) 0.3), and sham with 30% O(2) (sham-FIO(2) 0.3). Animals were resuscitated with manual cardiopulmonary resuscitation. The volume of extracted O(2) (VO(2)) and VCO(2) were measured for a 2-hour period after resuscitation. The respiratory quotient (RQ) was RQ=VCO(2)/VO(2). VCO(2) was elevated in CA-FIO(2) 1.0 and CA-FIO(2) 0.3 when compared with sham-FIO(2) 0.3 in minutes 5 to 40 after resuscitation (CA-FIO(2) 1.0: 16.7±2.2, P<0.01; CA-FIO(2) 0.3: 17.4±1.4, P<0.01; versus sham-FIO(2) 0.3: 13.6±1.1 mL/kg per minute), and then returned to normal. VO(2) in CA-FIO(2) 1.0 and CA-FIO(2) 0.3 increased gradually and was significantly higher than sham-FIO(2) 0.3 2 hours after resuscitation (CA-FIO(2) 1.0: 28.7±6.7, P<0.01; CA-FIO(2) 0.3: 24.4±2.3, P<0.01; versus sham-FIO(2) 0.3: 15.8±2.4 mL/kg per minute). The RQ of CA animals persistently decreased (CA-FIO(2) 1.0: 0.54±0.12 versus CA-FIO(2) 0.3: 0.68±0.05 versus sham-FIO(2) 0.3: 0.93±0.11, P<0.01 overall). CONCLUSIONS: CA altered cellular metabolism resulting in increased VO(2) with normal VCO(2). Normal VCO(2) suggests that the postresuscitation Krebs cycle is operating at a presumably healthy rate. Increased VO(2) in the face of normal VCO(2) suggests a significant alteration in O(2) utilization in postresuscitation. Several RQ values fell well outside the normally cited range of 0.7 to 1.0. Higher FIO(2) may increase VO(2), leading to even lower RQ values.