Prospective Investigation on The Significance of Carboxyhemoglobin Level in out-of-Hospital Cardiopulmonary Arrest
*Youichi Yanagawa Department Of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Japan
*Corresponding Author: Youichi Yanagawa
Department Of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Japan Email:firstname.lastname@example.org
Published on: 2017-03-19
Purpose: This study prospectively investigated the significance of the level of carboxyhemoglobin following an out of hospital (OH) cardiopulmonary arrest (CPA).
Methods: Patients who were transported to this department due to an OH CPA from April 2013 to March 2014 were included in the study. The subjects were divided into two groups based on their ability to achieve the return of spontaneous circulation and those who were not (ROSC+ vs. ROSC-).
Results: One hundred eight patients were included as subjects in this study (ROSC-, n=64; ROSC+, n=44). There were no significant differences associated with sex, age or the frequency of bystander CPR between the two groups; while the frequency of witnessed collapse, frequency of ventricle fibrillation at the scene, pH level and the base excess were significantly higher in the ROSC+ group than in the ROSC- group. The level of lactate in the ROSC+ group was lower than that in the ROSC- group. While the level of carboxyhemoglobin in the ROSC+ group was higher than that in the ROSC- group, the difference was not significant (p=0.06). The time course of carboxyhemoglobin level changes was investigated in 35 subjects. The average 2nd level of carboxyhemoglobin tended to significantly increase in comparison with the 1st level in the ROSC+ group, while the average 2nd level of carboxyhemoglobin tended to significantly decrease in the ROSC- group (p<0.05).
Conclusion: There might be an association between carboxyhemoglobin level and ROSC, given that the level of carboxyhemoglobin tended to increase after ROSC.
Global cerebral ischemia-reperfusion injury induces the expression of Heme oxygenase 1 (HO-1) . HO-1 is a ubiquitous inducible stress-response protein which serves a major metabolic function in heme turnover. HO-1 activity cleaves heme to form biliverdin-IXα, endogenous carbon monoxide (CO), and iron, which play a concerted role in cytoprotection against oxidative stress and in the modulation of cell proliferation and differentiation [2,3]. At low concentrations, exogenous CO can confer cyto- and tissue-protective effects similar to those associated with endogenous HO-1 expression, including antioxidative, anti-inflammatory, antiproliferative, and antiapoptotic effects .