Elsevier

Resuscitation

Volume 83, Issue 3, March 2012, Pages 338-342
Resuscitation

Clinical paper
Body temperature regulation and outcome after cardiac arrest and therapeutic hypothermia

https://doi.org/10.1016/j.resuscitation.2011.10.026Get rights and content

Abstract

Objective

Therapeutic temperature modulation is recommended after cardiac arrest (CA). However, body temperature (BT) regulation has not been extensively studied in this setting. We investigated BT variation in CA patients treated with therapeutic hypothermia (TH) and analyzed its impact on outcome.

Methods

A prospective cohort of comatose CA patients treated with TH (32–34 °C, 24 h) at the medical/surgical intensive care unit of the Lausanne University Hospital was studied. Spontaneous BT was recorded on hospital admission. The following variables were measured during and after TH: time to target temperature (TTT = time from hospital admission to induced BT target <34 °C), cooling rate (spontaneous BT  induced BT target/TTT) and time of passive rewarming to normothermia. Associations of spontaneous and induced BT with in-hospital mortality were examined.

Results

A total of 177 patients (median age 61 years; median time to ROSC 25 min) were studied. Non-survivors (N = 90, 51%) had lower spontaneous admission BT than survivors (median 34.5 [interquartile range 33.7–35.9] °C vs. 35.1 [34.4–35.8] °C, p = 0.04). Accordingly, time to target temperature was shorter among non-survivors (200 [25–363] min vs. 270 [158–375] min, p = 0.03); however, when adjusting for admission BT, cooling rates were comparable between the two outcome groups (0.4 [0.2–0.5] °C/h vs. 0.3 [0.2–0.4] °C/h, p = 0.65). Longer duration of passive rewarming (600 [464–744] min vs. 479 [360–600] min, p < 0.001) was associated with mortality.

Conclusions

Lower spontaneous admission BT and longer time of passive rewarming were associated with in-hospital mortality after CA and TH. Impaired thermoregulation may be an important physiologic determinant of post-resuscitation disease and CA prognosis. When assessing the benefit of early cooling on outcome, future trials should adjust for patient admission temperature and use the cooling rate rather than the time to target temperature.

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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    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.

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