Therapeutic Hypothermia Induction Research Articles

Targeting focal ischemic and hemorrhagic stroke neuroprotection: Current prospects for local hypothermia.

Therapeutic hypothermia (TH) has applications dating back millennia. In modern history, however, TH saw its importation into medical practice where investigations have demonstrated that TH is efficacious in ischemic insults, notably cardiac arrest and hypoxic-ischemic encephalopathy. As well, studies have been undertaken to investigate whether TH can provide benefit in focal stroke (i.e., focal ischemia and intracerebral hemorrhage). However, clinical studies have encountered various challenges with induction and maintenance of post-stroke TH. Most clinical studies have attempted to use body-wide cooling protocols, commonly hindered by side effects that can worsen post-stroke outcomes. Some of the complications and difficulties with systemic TH can be circumvented by using local hypothermia (LH) methods. Additional advantages include the potential for lower target temperatures to be achieved and faster TH induction rates with LH. This systematic review summarizes the body of clinical and preclinical LH focal stroke studies and raises key points to consider for future LH research. We conclude with an overview of LH neuroprotective mechanisms and a comparison of LH mechanisms with those observed with systemic TH. Overall, whereas many LH studies have been conducted preclinically in the context of focal ischemia, insufficient work has been done in intracerebral hemorrhage. Furthermore, key translational studies have yet to be done in either stroke subtype (e.g., varied models and time-to-treat, studies considering aged animals or animals with co-morbidities). Few clinical LH investigations have been performed and the optimal LH parameters to achieve neuroprotection are unknown.

Plasma Glycoproteomic Study of Therapeutic Hypothermia Reveals Novel Markers Predicting Neurologic Outcome Post-cardiac Arrest

Therapeutic hypothermia (TH) is a neuroprotective treatment post-cardiac arrest but is grossly underutilized. After TH induction, traditional biomarkers and parameters can no long predict clinical outcome due to a lack of understanding of hypothermic response. Innovative approaches to better understand the clinical effect of TH will help to prognosticate outcome and expand beneficial population. Protein glycosylation is an important extracellular post-translational modification, regulating various extracellular signaling pathways. Here, we used glycoproteomics to investigate the association of plasma glycoproteins with the prognosis of TH-treated cardiac arrest patients. Using lectin affinity chromatography and mass spectrometry, we identified 640 glycoproteins in the plasma of cardiac arrest patients undergoing TH treatment, of which 23 were up-regulated and 14 were down-regulated in good outcome patients as compared with poor outcome ones. Notably, two glycoproteins with antioxidant activity, ceruloplasmin (CP) and haptoglobin (HP), were found to be associated with favorable neurologic outcome. This was further supported by ELISA assay in a large patients cohort, in which glycosylated CP and HP enriched by concanavilin A (ConA) and wheat germ agglutinin (WGA) lectins were significantly increased in patients developing good outcome (ConA-CP: p=0.033; ConA-HP: p=0.04; WGA-HP: p=0.021). Furthermore, ROC analysis demonstrated the predictive potential of ConA-CP, ConA-HP, and WGA-HP (ConA-CP: AUC=0.732, p=0.031; ConA-HP: AUC=0.746, p=0.022; WGA-HP: AUC=0.714, p=0.046) and combination of them improved the predictive power (AUC=0.830, p=0.002). Our results suggested that glycosylated CP and HP as well as other glycoproteins may play critical roles in neuroprotection and serve as sensitive prognostic markers for TH treatments.

Optimal Control of Inspired Perfluorocarbon Temperature for Ultrafast Hypothermia Induction by Total Liquid Ventilation in an Adult Patient Model.

Recent preclinical studies have shown that therapeutic hypothermia induced in less than 30min by total liquid ventilation (TLV) strongly improves the survival rate after cardiac arrest. When the lung is ventilated with a breathable perfluorocarbon liquid, the inspired perfluorocarbon allows us to control efficiently the cooling process of the organs. While TLV can rapidly cool animals, the cooling speed in humans remains unknown. The objective is to predict the efficiency and safety of ultrafast cooling by TLV in adult humans. It is based on a previously published thermal model of ovines in TLV and the design of a direct optimal controller to compute the inspired perfluorocarbon temperature profile. The experimental results in an adult sheep are presented. The thermal model of sheep is subsequently projected to a human model to simulate the optimal hypothermia induction and its sensitivity to physiological parameter uncertainties. The results in the sheep showed that the computed inspired perfluorocarbon temperature command can avoid arterial temperature undershoot. The projection to humans revealed that mild hypothermia should be ultrafast (reached in fewer than 3min (-72°C/h) for the brain and 20min (-10°C/h) for the entire body). The projection to human model allows concluding that therapeutic hypothermia induction by TLV can be ultrafast and safe. This study is the first to simulate ultrafast cooling by TLV in a human model and is a strong motivation to translate TLV to humans to improve the quality of life of postcardiac arrest patients.

A survey-based study on the protocols for therapeutic hypothermia in cardiac arrest patients in Korea: focusing on the differences between level 1 and 2 centers.

ObjectiveWe aimed to summarize the therapeutic hypothermia (TH) protocols used in emergency departments (EDs) in Korea and to investigate the differences between level 1 and 2 centers.MethodsThe chief residents from 56 EDs were given a structured survey containing questions on the indications for TH, methods for TH induction, maintaining, and finalizing TH treatments. The participants were divided into 2 groups based on their work place (level 1 vs. level 2 centers).ResultsWe received 36 responses to the survey. The majority of the participants (94.4%) reported that they routinely used TH. An average of 5.9 (standard deviation, 3.4) and 3.3 (standard deviation, 2.9) TH procedures were performed monthly in level 1 and 2 centers, respectively (P=0.01). The majority of level 1 and 2 centers (80.0% and 73.1%, respectively) had written TH protocols. Rectal (50.0%) and esophageal probes (38.9%) were most commonly used to monitor the patients’ body temperatures. Midazolam (80.6%) and remifentanyl (47.2%) were the most commonly used sedatives. For TH induction, external cooling devices (77.8%) and cold saline infusion (66.1%) were predominant. Between level 1 and 2 centers, only the number of TH, the usage of remifentanyl, and application of external cooling device showed significant differences (P<0.05).ConclusionOur study summarizes the TH protocols used in 36 EDs. The majority of study participants performed TH using a written protocol. We observed small number of differences in TH induction and maintenance methods between level 1 and 2 centers.

Application of a novel rectal cooling device in hypothermia therapy after cerebral hypoxia-ischemia in rats.

BackgroundA new rectal cooling device for therapeutic hypothermia (TH) therapy is designed and is applied in TH treatment of SD rats with ischemic-hypoxic brain damage.MethodsHealthy adult SD rats (n = 45) were randomly assigned into four groups: the healthy control group (n = 5), the ischemia and hypoxia group (n = 10), the rectal TH cooling group (n = 18), and the ice blanket TH cooling group (n = 11). The rats in the rectal cooling and ice blanket TH groups received 12 h treatment after hypoxic-ischemic brain damage had been established, while those in the ischemia and hypoxia group did not. Taking the start of TH as the zero point, rats were sacrificed after 24 h and the brain and rectum tissues were sampled for histological analysis.ResultsThe TH induction time (37.3 ± 14.7 min) in the rectal cooling group was significantly shorter (F = 4.937, P < 0.05) than that in the ice blanket cooling group (75.6 ± 27.2 min). The HE and NISSL staining results showed that rats in the rectal TH cooling group had significantly decreased (P < 0.01) positive neurons cell count compared to those in ischemia and hypoxia group. In addition, TUNEL staining indicated that the number of apoptotic cells (3.9 ± 1.8 cells / × 400 field) and the apoptosis index (4.4 % ± 1.5) were significantly lower in rectal TH cooling group (P < 0.05) than in ischemia and hypoxia group (23.2 ± 12.1 cells / × 400 field, 26.6 % ± 12.1). Also, no rectal frostbite or inflammatory infiltration was observed in rats in the rectal TH treatment groups.ConclusionOur new cooling device realized rapid TH induction in SD rats with ischemic-hypoxic brain damage, inhibited the apoptosis of cells in the hippocampal CAl region, and did not cause histological damage to the rectal tissues.Electronic supplementary materialThe online version of this article (doi:10.1186/s12871-016-0239-5) contains supplementary material, which is available to authorized users.

Early targeted brain COOLing in the cardiac CATHeterisation laboratory following cardiac arrest (COOLCATH).

Trials demonstrate significant clinical benefit in patients receiving therapeutic hypothermia (TH) after cardiac arrest. However, incidence of mortality and morbidity remains high in this patient group. Rapid targeted brain hypothermia induction, together with prompt correction of the underlying cause may improve outcomes in these patients. This study investigates the efficacy of Rhinochill, an intranasal cooling device over Blanketrol, a surface cooling device in inducing TH in cardiac arrest patients within the cardiac catheter laboratory. 70 patients were randomized to TH induction with either Rhinochill or Blanketrol. Primary outcome measures were time to reach tympanic ≤34 °C from randomisation as a surrogate for brain temperature and oesophageal ≤34 °C from randomisation as a measurement of core body temperature. Secondary outcomes included first hour temperature drop, length of stay in intensive care unit, hospital stay, neurological recovery and all-cause mortality at hospital discharge. There was no difference in time to reach ≤34 °C between Rhinochill and Blanketrol (Tympanic ≤34 °C, 75 vs. 107 mins; p=0.101; Oesophageal ≤34 °C, 85 vs. 115 mins; p=0.151). Tympanic temperature dropped significantly with Rhinochill in the first hour (1.75 vs. 0.94 °C; p<0.001). No difference was detected in any other secondary outcome measures. Catheter laboratory-based TH induction resulted in a survival to hospital discharge of 67.1%. In this study, Rhinochill was not found to be more efficient than Blanketrol for TH induction, although there was a non-significant trend in favour of Rhinochill that potentially warrants further investigation with a larger trial.

Urine Output Changes During Postcardiac Arrest Therapeutic Hypothermia

While commonly described, no studies have characterized cold-induced diuresis or rewarm anti-diuresis occurring during the delivery of therapeutic hypothermia (TH). We sought to determine urine output changes during the provision of postcardiac arrest TH. We analyzed clinical data on patients receiving postcardiac arrest TH at an urban tertiary care center. TH measures included cooling by cold intravenous fluid, external ice packs, and a commercial external temperature management system. TH treatment was divided into phases: (1) induction, (2) maintenance, (3) rewarm, and (4) post-rewarm. The primary outcome measure was the mean urine output rate (mL/hour). We compared urine output rates between TH phases using a Generalized Estimating Equations model, defining urine output rate (mL/hour) as the dependent variable and TH phase (induction, maintenance, rewarm, and post-rewarm) as the primary exposure variable. We adjusted for age, sex, initial ECG rhythm, location of arrest, shock, acute kidney injury, rate of intravenous fluid input, and body mass index. Complete urine output data were available on 33 patients. Mean urine output rates during induction, maintenance, rewarm, and post-rewarm phases were 157 mL/hour (95% CI: 104-210), 103 mL/hour (95% CI: 82-125), 70 mL/hour (95% CI: 51-88), and 91 mL/hour (95% CI: 65-117), respectively. Compared with the post-rewarm phase, adjusted urine output was higher during the TH induction phase (output rate difference +51 mL/hour; 95% CI: 3-99). Adjusted urine output during the maintenance and rewarm phases did not differ from the post-rewarm phase. In this preliminary study, we observed modest increases in urine output during TH induction. We did not observe urine output changes during TH maintenance or rewarming.

Lactate levels remain significantly higher in non-survivors compared with survivors during therapeutic hypothermia after cardiac arrest

Purpose: Previous studies reported that lactate levels may be a reliable prognostic factor of outcome during the first hours after return of spontaneous circulation. However, implementation of a neuroprotective protocol with therapeutic hypothermia (TH) makes prognostication even more difficult. Furthermore, the prognostic value of lactate could be different in patients treated with hypothermia. In this study, we evaluated the effect of TH on lactate levels during the first 36 hours after CA. Methods: After IRB approval and with informed consent, data were collected from 43 consecutive patients admitted to the hospital after cardiac arrest. Cold saline (30 ml/kg) was administered at admission to emergency department. After PCI, therapeutic hypothermia (33°C) was induced by endovascular or surface cooling and maintained for 24 hours. All patients were sedated (propofol/remifentanil) for the duration of TH. Lactate was measured every hour. The threshold for hyperlactatemia was set for values exceeding 2 mmol/l. Data are presented as medians and interquartile ranges. Lactate was compared with the Mann Whitney U test. Results: Of 43 patients, 18 did not survived to hospital discharge due to post-ischemic brain damage. Temperature at CCU-admission was 34.7°C (34.1-35.4). Patients reached the target temperature of 33°C within 2 hours after TH induction. Median lactate levels at the start of TH were significantly different between survivors (2.22 mmol/l (1.7-3.3)) and non-survivors (4.65 mmol/l (3-6.7) p = 0.000). Lactate levels returned to normal values only after 24 hours of TH in survivors. In non-survivors, lactate levels remained higher than the threshold level throughout the maintenance of TH and re-warming. However, they were only significant different compared to survivors during the first 12 hours of TH. There was no difference in start values between survivors and non-survivors for pH, mean arterial pressure, cardiac output or dose of norepinephrine. Dose of norepinephrine increased during the first 5 hours in survivors and non-survivors and remained stable during the maintenance of TH. During re-warming, non-survivors had an increasing need of norepinephrine. There was no correlation between dose of norepinephrine and lactate levels. Conclusion: During therapeutic hypothermia after cardiac arrest, lactate levels are significant different between survivors and non-survivors during the first 12 hours. Lactate levels remain above the threshold for hyperlactatemia during TH and rewarming in non-survivors of cardiac arrest.

Implementation of therapeutic hypothermia after cardiac arrest in intensive care units in Poland

Therapeutic hypothermia (TH) is one of few interventions that improve survival after a cardiac arrest with good neurological outcome. Current guidelines for cardiopulmonary resuscitation recommend TH in comatose adult patients after return of spontaneous circulation (ROSC) regardless of cardiac arrest location and cardiac rhythm during the event. To evaluate level of TH implementation in intensive care units (ICUs) in Poland and identify barriers to the implementation process. A telephone survey was carried out to determine how many Polish ICUs were using TH in the management of comatose patients after a cardiac arrest. The survey was conducted from October to December 2010. The survey also included questions on the number of patients cooled, method of TH induction and maintenance, target temperature, duration of cooling, and cardiac arrest rhythm in patients treated with TH. We have also collected data on pre-hospital use of TH and potential barriers to implementation of TH. We obtained information from 263 of 464 ICUs (56.8%) in Poland. At the time of the survey, 57 ICUs (21.7%) were using TH in comatose patients after ROSC. There was a significant increase in the number of ICUs using TH as compared with the 2005 survey. Most ICUs did not use any sophisticated equipment to induce and maintain TH. Ninety six percent of ICUs were using TH regardless of the cardiac arrest rhythm. In 65% of ICUs (37 units), target temperature was 32-34°C and 63% of ICUs (36 units) maintained TH for 12-24 hours. An increase in ICU experience in TH can be noted: 61% of ICUs (35 units) declared TH use in more than 10 patients during the last year. We found the following barriers to implementation of TH: lack of knowledge, lack of local protocols, lack of equipment, and economic issues. The number of ICUs using TH in Poland increased threefold in the 5 year period of 2005-2010. However, the proportion of ICUs using TH is still low (21.7%) compared to other European countries. Further efforts should be undertaken to reduce barriers to implementation of current resuscitation guidelines.

568

Introduction: Therapeutic hypothermia (TH) is an important treatment for survivors of cardiac arrest. While anecdotally described, no studies have characterized urine output increases during TH induction (“cold diuresis”), nor urine output decreases during TH re-warming (“re-warming anti-diuresis”). An understanding of urine output changes during TH is essential since these patients may exhibit hypovolemia, shock, pulmonary edema or electrolyte abnormalities. Hypothesis: Urine output increases during TH induction and decreases during TH re-warming. Methods: We studied consecutive patients receiving post-cardiac arrest TH at an urban tertiary care center. Using cold intravenous saline, external cooling pads (Arctic Sun) and ice packs, TH was provided to comatose adult survivors of out-of-hospital or in-hospital cardiac arrest as soon as possible after restoration of pulses. We excluded patients <18 years old, with end stage renal disease, who received hemodialysis, or those who died before completing?12 hours of TH. For each TH treatment phase (induction, maintenance, re-warm, and post-TH), we determined fluid input and urine output rates (mL/hr). Using Generalized Estimating Equations and defining post-TH urine output as the baseline, we examined the differences in urine output rates between TH phases, adjusting for fluid input rate, age, sex, location of cardiac arrest, initial arrest ECG rhythm, and vasospressor use. Results: Among 33 patients with complete fluid input and urine output data, mean treatment phase durations were: 1) induction 4.9 hrs (95% CI 4.5-5.4), 2) maintenance 23.1 hrs (22.5-23.6), 3) re-warm 11.1 hrs (10.5-11.7), and 4) post-rewarm 12 hrs (12-12). Mean urine output rates were: 1) induction 162 mL/hr (95% CI: 106-218), 2) maintenance 100 mL/hr (79-121), 3) re-warm 66 mL/hr (50-83), and post-TH 97 mL/hr (70-123). Urine output rate was higher for TH induction than post-TH (p=0.004). There were no significant differences in urine output rates between TH maintenance and post-TH (p=0.88), or TH re-warm and post-TH (p=0.19). Conclusions: Compared with baseline, urine output rate increases during TH induction. Urine output rates do not significantly change during TH maintenance or re-warming.

Abstract 63: Time to Target Temperature and Neurological Outcome in Survivors of Cardiac Arrest

Introduction: Substantial variability exists in time to target temperature for patients who undergo therapeutic hypothermia (TH) after cardiac arrest. How this variability may affect or predict neurologic outcomes is unknown. Hypothesis: Prolonged pre-induction time, or shorter times to target temperature will be associated with poor neurologic outcomes compared to shorter pre-induction times and a more gradual decline to target temperature. Methods: We conducted a retrospective chart review of TH patients from three institutions with identical TH protocols (PATH Database). Demographic variables were collected and analyzed using chi square and Student’s t-tests. We examined the association between time from arrest to return of spontaneous circulation (ROSC) (downtime), time from ROSC to initiation of TH (pre-induction) and time from initiation of TH to arrival at target temperature (induction) and Cerebral Performance Category (CPC) using logistic regression. Results: We enrolled 180 patients with mean age 59.1 ± 15.5 yrs, 56% male, and 26.1% with VF/VT as an initial rhythm. At discharge, 26% (47/180) of the cohort had CPC category 1 or 2 (good neurologic outcome). Mean downtime for survivors with a good outcome was 21.5 ± 13.7 mins vs. 32.6 ± 21.7 mins (p=0.004) for those with poor outcome. Mean pre-induction time for good outcome (CPC 1 or 2) was 144.5 ± 205.4 mins compared to 145.5 ± 171.1 mins for bad outcome (p=ns). Mean induction time for good outcome (CPC 1 or 2) was 270.8 ± 160.8 mins compared to 252.3 ± 151.3 mins for bad outcome (p=ns). In analyses adjusting for gender, initial rhythm, and downtime, there was no association between pre-induction time (OR 1.00, 95% CI 0.99-1.0, p=ns) or induction time (OR 0.99, 95% CI 0.99-1.0, p=ns), and neurologic outcome. Conclusion: In this cohort of post-arrest TH patients, pre-induction time and induction time do not appear to be associated with poor neurologic outcome. Further analysis is necessary to examine this phenomenon.

Therapeutic hypothermia and vasopressor dependency after cardiac arrest

ObjectiveClinical trials of therapeutic hypothermia (TH) after cardiac arrest excluded patients with persistent hemodynamic instability after return of spontaneous circulation (ROSC), and thus equipoise may exist regarding use of TH in these patients. Our objective was to determine if TH is associated with worsening hemodynamic instability among patients who are vasopressor-dependent after ROSC. MethodsWe performed a prospective observational study in vasopressor-dependent post-cardiac arrest patients. Inclusion criteria were age >17, non-trauma cardiac arrest, comatose after ROSC, and persistent vasopressor dependence. The decision to initiate TH (33–34°C) was made by the treating physician. We measured cumulative vasopressor index (CVI) and mean arterial pressure (MAP) every 15min during the first 6h after ROSC. The outcome measures were change in CVI (primary outcome) and MAP (secondary outcome) over time. We graphed median CVI and MAP over time for the treated and not treated cohorts, and used propensity adjusted repeated measures mixed models to test for an association between TH induction and change in CVI or MAP over time. ResultsSeventy-five post-cardiac arrest patients were included (35 treated; 40 not treated). We observed no major differences in CVI or MAP over time between the treated and not treated cohorts. In the mixed models we found no statistically significant association between TH induction and changes in CVI or MAP. ConclusionIn patients with vasopressor-dependency after cardiac arrest, the induction of hypothermia was not associated with a decrease in mean arterial pressure or increase in vasopressor requirement.

Therapeutic hypothermia for acute neurological injuries.

Therapeutic hypothermia (TH) is the intentional reduction of core body temperature to 32°C to 35°C, and is increasingly applied by intensivists for a variety of acute neurological injuries to achieve neuroprotection and reduction of elevated intracranial pressure. TH improves outcomes in comatose patients after a cardiac arrest with a shockable rhythm, but other off-label applications exist and are likely to increase in the future. This comprehensive review summarizes the physiology and cellular mechanism of action of TH, as well as different means of TH induction and maintenance with potential side effects. Indications of TH are critically reviewed by disease entity, as reported in the most recent literature, and evidence-based recommendations are provided.

315 EMFTherapeutic Hypothermia and Vasopressor Dependency After Cardiac Arrest

Objective: Clinical trials of therapeutic hypothermia (TH) after cardiac arrest excluded patients with persistent hemodynamic instability after return of spontaneous circulation (ROSC), and thus equipoise may exist regarding use of TH in these patients. Our objective was to determine if TH is associated with worsening hemodynamic instability among patients who are vasopressor-dependent after ROSC. Methods: We performed a prospective observational study in vasopressor-dependent post-cardiac arrest patients. Inclusion criteria were age >17, non-trauma cardiac arrest, comatose after ROSC, and persistent vasopressor dependence. The decision to initiate TH (33–34 ◦ C) was made by the treating physician. We measured cumulative vasopressor index (CVI) and mean arterial pressure (MAP) every 15 min during the first 6 h after ROSC. The outcome measures were change in CVI (primary outcome) and MAP (secondary outcome) over time. We graphed median CVI and MAP over time for the treated and not treated cohorts, and used propensity adjusted repeated measures mixed models to test for an association between TH induction and change in CVI or MAP over time. Results: Seventy-five post-cardiac arrest patients were included (35 treated; 40 not treated). We observed no major differences in CVI or MAP over time between the treated and not treated cohorts. In the mixed models we found no statistically significant association between TH induction and changes in CVI or MAP. Conclusion: In patients with vasopressor-dependency after cardiac arrest, the induction of hypothermia was not associated with a decrease in mean arterial pressure or increase in vasopressor requirement. © 2012 Elsevier Ireland Ltd. All rights reserved.

Therapeutic hypothermia induction via an esophageal route—a computer simulation

ObjectivesMild therapeutic hypothermia has been shown to improve outcomes after adult cardiac arrest but remains underused. Development of easier methods than currently exist to induce therapeutic hypothermia may help increase use of this treatment. We developed a mathematical model to evaluate the potential to induce mild therapeutic hypothermia through the esophagus. MethodsUsing a finite element mathematical modeling software package incorporating Pennes Bioheat equation, we predicted the changes in body temperature that would occur with placement of an esophageal cooling device containing recirculating chilled water at 10°C. ResultsPatient temperature under the simulated conditions decreased from 37°C to 33°C in approximately 40 minutes. Distribution of body temperature was not uniform in our model, with the skin surface and extremities showing a greater temperature decrease than in the patient's core. ConclusionsOur computer simulations suggest that inducing mild therapeutic hypothermia via an esophageal route is feasible.

Prehospital Use of Therapeutic Hypothermia After Resuscitation from Cardiac Arrest

The use of therapeutic hypothermia (TH) in the care of patients after resuscitation from sudden cardiac arrest (SCA) has been shown to improve both survival and neurologic outcomes in randomized, controlled trials and a growing number of cohort studies with historical controls. The robust nature of the data supporting postarrest TH is reflected in the wide variety of clinical investigations that have confirmed outcome benefits of similar magnitude. A number of important questions remain surrounding the implementation of postarrest TH, including the timing of cooling induction and how rapidly providers need to initiate cooling therapy. Several investigations have suggested that earlier cooling may maximize the benefit from TH and that, conversely, increasing delays to TH induction may lead to worse patient outcomes. Prehospital initiation of TH has been proposed as a means to address time barriers inherent in out-of-hospital SCA. In this paradigm, emergency medical service (EMS) personnel are able to start cooling therapies immediately after resuscitation, which can then be continued during transport. Newer technologies may provide other opportunities for rapid cooling in the field; however, the risks and benefits of prehospital cooling remain poorly understood. This review will describe the growing literature and future directions pertaining to prehospital induction of TH after SCA.