RESUMO
BACKGROUND: Despite a continued focus on improved cardiopulmonary resuscitation quality, survival remains low from in-hospital cardiac arrest. Advanced Resuscitation Training has been shown to improve survival to hospital discharge and survival with good neurological outcome following in-hospital cardiac arrest at its home institution. We sought to determine if Advanced Resuscitation Training implementation would improve patient outcomes and cardiopulmonary resuscitation quality at our institution. METHODS: This was a prospective, before-after study of adult in-hospital cardiac arrest victims who had cardiopulmonary resuscitation performed. During phase 1, standard institution cardiopulmonary resuscitation training was provided. During phase 2, providers received the same quantity of training, but with emphasis on Advanced Resuscitation Training principles. Primary outcomes were return of spontaneous circulation, survival to hospital discharge, and neurologically favorable survival. Secondary outcomes were cardiopulmonary resuscitation quality parameters. RESULTS: A total of 156 adult in-hospital cardiac arrests occurred during the study period. Rates of return of spontaneous circulation improved from 58.1 to 86.3% with an adjusted odds ratios of 5.31 (95% CI: 2.23-14.35, P < 0.001). Survival to discharge increased from 26.7 to 41.2%, adjusted odds ratios 2.17 (95% CI: 1.02-4.67, P < 0.05). Survival with a good neurological outcome increased from 24.8 to 35.3%, but was not statistically significant. Target chest compression rate increased from 30.4% of patients in P1 to 65.6% in P2, adjusted odds ratios 4.27 (95% CI: 1.72-11.12, P = 0.002), and target depth increased from 23.2% in P1 to 46.9% in P2, adjusted odds ratios 2.92 (95% CI: 1.16-7.54, P = 0.024). CONCLUSIONS: After Advanced Resuscitation Training implementation, there were significant improvements in cardiopulmonary resuscitation quality and rates of return of spontaneous circulation and survival to discharge.
RESUMO
Altered cellular redox states have been associated with a variety of chronic diseases, especially those correlated with inflammation. One of the primary oxidants generated during the inflammatory response is hydrogen peroxide (H2O2). Macrophages in particular are thought to produce large amounts of H2O2, however they must somehow protect themselves from the potentially lethal concentrations they produce. To investigate how immune cells protect themselves from H2O2 observed in chronic inflammatory diseases, we established an adapted population of macrophages in culture by gradually increasing sub-lethal concentrations of H2O2 in the media to typically lethal concentrations over the course of more than a month. The resulting cells were tolerant to very high concentrations of H2O2. Further investigation revealed that the cells were able to rapidly neutralize the H2O2 added to their culture media due to a dramatic upregulation of catalase. Interestingly, T cells, which are also implicated in chronic inflammation, were unable to adapt to H2O2 under the same procedure, however when T cells were cultured in media from adapted macrophages, they were able to survive typically lethal concentrations of H2O2. These data support the hypothesis that macrophages are able to protect themselves and neighboring cells during states of chronic inflammation from the oxidizing environment they create.
