Clinical paperBody temperature regulation and outcome after cardiac arrest and therapeutic hypothermia☆
Introduction
Therapeutic hypothermia (TH) improves the outcome of comatose patients after cardiac arrest (CA)1, 2 and is recommended by recent post-resuscitation guidelines.3, 4 Although therapeutic temperature modulation is increasingly used, how exactly body temperature (BT) is regulated after CA is only beginning to be elucidated, and the impact of TH on BT regulation has not been extensively studied. Intact central nervous system is required for thermoregulation.5 Altered thermoregulation is thus frequently observed in patients with primary acute brain conditions, mainly due to hypothalamic dysfunction.6, 7 Multiorgan dysfunction and shock states may also cause dysfunction of BT regulation, due to secondary damage of central and peripheral thermoregulatory pathways.8, 9
Recently, it has been suggested that low spontaneous BT early following resuscitation from CA may be associated with increased in-hospital mortality.10, 11 However, to our knowledge, no study has investigated regulation of BT both in the early phase of post-resuscitation care and during the various phases of induced cooling and examined the impact of BT variations on outcome. We examined this issue in a single-center prospective cohort of adult comatose CA patients treated with TH and monitored with core BT for at least 48 h.
Section snippets
Subjects
Patients included in this study were part of a prospective observational database of comatose patients who were successfully resuscitated from CA and were treated with TH at the medical/surgical intensive care unit (ICU) of the University Hospital of Lausanne, Switzerland, over a 6-year period (2003–2009). The approval for the study was obtained by the local Institutional Review Board with waiver of informed consent since all interventions were part of standard patient care. All patients were
Patient characteristics
During the study period, 210 patients with coma after out-of-hospital CA were admitted to our ICU. A total of 33 patients were excluded: 14 patients were not treated with TH, 14 patients died within 48 h and 5 patients had incomplete data. Thus, a total of 177 patients were included in the present study. Baseline patient characteristics are summarized in Table 1.
Associations between in-hospital mortality and spontaneous body temperature on admission
Associations of spontaneous admission BT and in-hospital mortality are summarized in Table 2. Overall, non-survivors had a lower
Discussion
The main findings in this cohort of comatose patients treated with TH after CA can be summarized as follows: (1) spontaneous BT on admission is associated with in-hospital mortality; (2) overall, non-survivors had lower admission BT than survivors; however when accounting for seasonal variations of outdoor temperature, non-survivors had lower admission BT all year round, except during warmer months (June–August), where admission BT was actually higher in non-survivors, (3) because of lower
Conclusions
Impaired BT regulation is a marker of poor outcome after CA and TH. In our cohort, lower spontaneous admission BT and longer time of passive rewarming were associated with in-hospital mortality. Time to target temperature was shorter in non-survivors however we found no correlation between outcome and the rate of cooling. These findings suggest that impaired thermoregulation is an important pathophysiologic determinant of post-resuscitation disease and CA prognosis. Admission body temperature
Funding
Mauro Oddo is supported by a Grant from the Swiss National Science Foundation (Grant 320030_138191) and the European Society of Intensive Care Medicine (ECCRN Clinical Research Award 2010).
Conflict of interest statement
The authors have no conflict of interest to declare.
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2020, ResuscitationCitation Excerpt :The average human BT is between 35.5 and 37.5 °C and is regulated in the hypothalamus8 Failure to adjust to this BT can cause fatalities or serious damage to the patient. Initial spontaneous hypothermia was associated with poor outcomes in cardiac arrest patients.9,10 The lower initial BT might be due to global brain ischaemia, causing dysfunction of temperature regulation in the hypothalamus.9
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A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2011.10.026.