Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post-Cardiac Arrest Rat: A Novel Metabolic Phenotype

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 O₂ consumption and CO₂ production (VCO₂) in a rodent model. In addition, we tested the effect of inspired 100% O₂ on the metabolism.

Methods and results: Rats were anesthetized and randomized into 3 groups: resuscitation from 10-minute asphyxia with inhaled 100% O₂ (CA-fraction of inspired O₂ [FIO₂] 1.0), with 30% O₂ (CA-FIO₂ 0.3), and sham with 30% O₂ (sham-FIO₂ 0.3). Animals were resuscitated with manual cardiopulmonary resuscitation. The volume of extracted O₂ (VO₂) and VCO₂ were measured for a 2-hour period after resuscitation. The respiratory quotient (RQ) was RQ=VCO₂/VO₂. VCO₂ was elevated in CA-FIO₂ 1.0 and CA-FIO₂ 0.3 when compared with sham-FIO₂ 0.3 in minutes 5 to 40 after resuscitation (CA-FIO₂ 1.0: 16.7±2.2, P<0.01; CA-FIO₂ 0.3: 17.4±1.4, P<0.01; versus sham-FIO₂ 0.3: 13.6±1.1 mL/kg per minute), and then returned to normal. VO₂ in CA-FIO₂ 1.0 and CA-FIO₂ 0.3 increased gradually and was significantly higher than sham-FIO₂ 0.3 2 hours after resuscitation (CA-FIO₂ 1.0: 28.7±6.7, P<0.01; CA-FIO₂ 0.3: 24.4±2.3, P<0.01; versus sham-FIO₂ 0.3: 15.8±2.4 mL/kg per minute). The RQ of CA animals persistently decreased (CA-FIO₂ 1.0: 0.54±0.12 versus CA-FIO₂ 0.3: 0.68±0.05 versus sham-FIO₂ 0.3: 0.93±0.11, P<0.01 overall).

Conclusions: CA altered cellular metabolism resulting in increased VO₂ with normal VCO₂. Normal VCO₂ suggests that the postresuscitation Krebs cycle is operating at a presumably healthy rate. Increased VO₂ in the face of normal VCO₂ suggests a significant alteration in O₂ utilization in postresuscitation. Several RQ values fell well outside the normally cited range of 0.7 to 1.0. Higher FIO₂ may increase VO₂, leading to even lower RQ values.