Functional changes in the hypothalamic-pituitary-adrenal axis after successful cardiopulmonary resuscitation

Abstract Background Cardiac arrest (CA) is a terminal event that results in a range of pathophysiological changes in the body, most notably, systemic ischemia-reperfusion injury. The hypothalamic-pituitary-adrenal (HPA) axis is an important neuroendocrine system that modulates adrenocortical hormone release. This study was designed to investigate the changes in HPA-related hormone levels after successful cardiopulmonary resuscitation (CPR) and to explore possible etiologies to provide a basis for relevant clinical research. Methods We collected the clinical data of 96 patients with CA admitted to the Emergency Department of Beijing Chaoyang Hospital, Capital Medical University, between January 2016 and May 2017. Serum samples were collected 6, 24, and 72 hours after restoring spontaneous circulation (ROSC). The data were compared with those of the healthy control group (n = 50). An enzyme-linked immunosorbent assay (ELISA) was performed to measure copeptin, adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH), and total cortisol. Demographic data were collected for both groups. For the CPR group, clinical data and the end-of-study cerebral performance category (CPC) were analyzed. Patients were followed up through day 28. Death or survival after day 28 was used as the study endpoint. Simple values were expressed as medians and quartiles or ratios (%) for statistical analysis. Continuous variables are expressed as mean ± standard deviation. Categorical variables were expressed as frequencies and percentages. The mean values of normally distributed measurement data were analyzed using 1-way analysis of variance (ANOVA) for among-group comparisons and the least significant difference (LSD) test for between-group comparisons. SPSS v17 (SPSS, Chicago, IL, USA) was used for statistical analysis, and P < 0.05 was considered statistically significant. Results No significant between-group differences were observed in terms of age or sex. The 28-day mortality rate in the CPR group was 71%. ACTH and CRH levels were significantly lower in the CPR group than in the healthy control group (P < 0.001). Copeptin and cortisol levels 6 hours after ROSC were significantly higher in the CPR group than in the healthy control group (P < 0.001). No significant changes in any indicator were observed over time (6, 24, and 72 hours after ROSC) (P > 0.05). The CPC score was 1–2 (good cerebral performance group) in 13 patients, 3–4 (poor cerebral performance group) in 17 patients, and 5 (brain death or clinical death) in 66 patients. Patients with significantly declining ACTH and CRH levels had higher CPC scores (P < 0.05); however, no significant differences were found in other indicators (P > 0.05). Conclusion After post-CA ROSC, ischemia-reperfusion injury may cause brain damage and HPA axis damage and dysfunction, the severity of which is associated with CPC score.