4.6 Article Proceedings Paper

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

Journal

Publisher

WILEY
DOI: 10.1161/JAHA.117.007721

Keywords

CO2 production; cardiopulmonary resuscitation (CPR); metabolism; O-2 consumption; respiratory quotient

Funding

  1. National Heart, Lung, and Blood Institute of the National Institutes of Health [RO 1HL67630]

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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 CO2 production (VCO2) 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 [ FIO2] 1.0), with 30% O-2 (CA-FIO2 0.3), and sham with 30% O-2 (sham-FIO2 0.3). Animals were resuscitated with manual cardiopulmonary resuscitation. The volume of extracted O-2 (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 O-2 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.

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