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 O consumption and CO production (VCO) in a rodent model. In addition, we tested the effect of inspired 100% O on the metabolism.

METHODS AND RESULTS

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

CONCLUSIONS

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