Induction Of Mild Hypothermia Research Articles

Does induction time of mild hypothermia influence the survival duration of septic rats?

The relationship between hypothermia induction time and survival duration following sepsis was studied on 31 male Sprague-Dawley rats (median weight 311 g, range 260-356 g). After anesthesia and when the target temperature was reached (normothermia: 38°C or mild induced hypothermia: 34°C), sepsis was induced by cecal ligation and perforation. Five experimental groups were used. In groups 1 and 2, temperature of septic rats was maintained throughout the experiment at 38°C (seven rats) or 34°C (six rats), respectively. In groups 3, 4, and 5, septic rats (six per group) were maintained at 38°C for 1, 2, and 3 hours, respectively, and then placed in mild hypothermia (34°C). For each group, the survival duration was determined and blood samples were performed at the tail to measure tumor necrosis factor-α (TNF-α) plasma concentration. Whatever the experimental group, a decrease in temperature from 38°C to 34°C significantly increased the survival duration of septic rats compared with those maintained at 38°C throughout the experiment. The delay between the onset of sepsis and induction of hypothermia was also crucial. Thus, hypothermia induced after 1 hour of sepsis at 38°C significantly increased the survival duration of septic rats (12 hours 37 minutes±1 hour 4 minutes; group 3) compared with hypothermia induced after 3 hours of sepsis (8 hours 56 minutes±1 h 20 minutes; group 5). Moreover, except for group 5, survival duration improvement of septic rats observed in hypothermia was related to a lower increase of TNF-α plasma concentration compared with septic rats in normothermia. During sepsis, mild induced hypothermia significantly increased the survival duration of septic rats. The earlier hypothermia was applied, the longer the septic rats survived. According to these results, hypothermia may therefore provide the necessary time to apply a proper treatment.

Combining therapeutic hypothermia and primary coronary intervention in comatose survivors of ventricular fibrillation due to ST-elevation myocardial infarction

Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion strategy for ST-elevation acute myocardial infarction (STEMI). In comatose survivors of cardiac arrest, mild induced hypothermia (MIH) improves neurological recovery.

Aspects of bleeding complications and hemostasis at central line insertion and mild induced hypothermia

Bleeding complications range from 0.5 to 1.6% in connection with central venous catheter insertions but are more frequent in patients with bone marrow failure and severe thrombocytopenia. Although supportive evidence is scarce, prophylactic platelet transfusion is sometimes performed in these patients before catheter insertion. Furthermore, the ideal threshold platelet count and timing of transfusion remain controversial among clinical studies. Hypothermia is generally considered to reduce coagulation and platelet function. However, studies performed in animals, healthy volunteers, and patients have shown conflicting results. Paper I, a retrospective study in non-intensive care unit patients, showed that serious bleeding complications in association with central line insertions were uncommon and that insertion of a large bore catheter may be an independent risk factor for mild bleeding complications in this population. Paper II, a prospective observational study, evaluated the efficacy of prophylactic platelet transfusions in thrombocytopenic patients with bone marrow failure. Transfusion improved hemostatic parameters in ROTEM and Multiplate tests by increasing the number of platelets and not by enhancing platelet function. Improved clotting parameters persisted between 1 and 4 hours after transfusion. Paper III demonstrated increased platelet aggregation and strengthened clot formation over time in out-of-hospital cardiac arrest patients treated with hypothermia. In patients with dual platelet inhibition, including ticagrelor and aspirin, this effect was offset by powerful P2Y12 blockade, confirmed by analysis of vasodilator-stimulated phosphoprotein. The effect of ticagrelor was delayed in survivors of cardiac arrest, probably due to slow gastric emptying. Paper IV demonstrated prolonged clot initiation and decreased clot propagation in ROTEM testing (EXTEM, FIBTEM, and APTEM assays) in whole blood from out-of-hospital cardiac arrest patients treated with mild induced hypothermia. Paper V investigated whole blood from acute coronary syndrome patients treated with ticagrelor and aspirin. In vitro applied hypothermia to 33 degrees C markedly increased platelet activity measured by flow cytometry, whereas a viscoelastic coagulation test (Sonoclot) revealed a hypocoagulative response.

Safety, feasibility, and outcomes of induced hypothermia therapy following in-hospital cardiac arrest-evaluation of a large prospective registry*.

Despite a lack of randomized trials, practice guidelines recommend that mild induced hypothermia be considered for comatose survivors of in-hospital cardiac arrest. This study describes the safety, feasibility, and outcomes of mild induced hypothermia treatment following in-hospital cardiac arrest. Prospective, observational, registry-based study. Forty-six critical care facilities in eight countries in Europe and the United States reporting in the Hypothermia Network Registry and the International Cardiac Arrest Registry. A total of 663 patients with in-hospital cardiac arrest and treated with mild induced hypothermia were included between January 2004 and February 2012. None. A cerebral performance category of 1 or 2 was considered a good outcome. At hospital discharge 41% of patients had a good outcome. At median 6-month follow-up, 34% had a good outcome. Among in-hospital deaths, 52% were of cardiac causes and 44% of cerebral cause. A higher initial body temperature was associated with reduced odds of a good outcome (odds ratio, 0.79; 95% CI, 0.68-0.92). Adverse events were common; bleeding requiring transfusion (odds ratio, 0.56; 95% CI, 0.31-1.00) and sepsis (odds ratio, 0.52; 95% CI, 0.30-0.91) were associated with reduced odds for a good outcome. In this registry study of an in-hospital cardiac arrest population treated with mild induced hypothermia, we found a 41% good outcome at hospital discharge and 34% at follow-up. Infectious complications occurred in 43% of cases, and 11% of patients required a transfusion for bleeding. The majority of deaths were of cardiac origin.

Effects of mild induced hypothermia on hippocampal connexin 43 and glutamate transporter 1 expression following traumatic brain injury in rats.

Traumatic brain injury (TBI) is a common cause of worldwide disability and mortality. Currently, the incidence and prevalence of TBI is markedly increasing and an effective therapy is lacking. Therapeutic hypothermia (32‑35˚C) has been reported to reduce intracranial pressure and induce putative neuroprotective effects. However, the underlying molecular mechanisms remain to be elucidated. The aim of the present study was to investigate the effects of mild induced hypothermia (MIH) on the expression of connexin 43 (Cx43) and glutamate transporter 1 (GLT‑1) in the hippocampus following TBI in rats. A rat model of TBI was created using a modified weight‑drop device, followed by 4 h of hypothermia (33˚C) or normothermia (37˚C). A wet‑dry weight method was used to assess brain edema and spatial learning ability was evaluated using a Morris water maze. The levels of Cx43 and GLT‑1 were detected by immunohistochemical and western blot analysis, respectively. The results demonstrated that MIH treatment improved TBI‑induced brain edema and neurological function deficits. In addition, therapeutic MIH significantly downregulated Cx43 expression and upregulated the levels of GLT‑1 in the hippocampus post‑TBI. These findings suggested that treatment with MIH may provide a novel neuroprotective therapeutic strategy for TBI through reversing the increase in Cx43 protein and the decrease in GLT‑1.

Mild induced hypothermia: Effects on sepsis-related coagulopathy -results from a randomized controlled trial

IntroductionCoagulopathy associates with poor outcome in sepsis. Mild induced hypothermia has been proposed as treatment in sepsis but it is not known whether this intervention worsens functional coagulopathy. Materials and methodsInterim analysis data from an ongoing randomized controlled trial; The Cooling And Surviving Septic shock (CASS) study. Patients suffering severe sepsis/septic shock are allocated to either mild induced hypothermia (cooling to 32-34°C for 24hours) or control (uncontrolled temperature). Trial registration: NCT01455116. Thrombelastography (TEG) is performed three times during the first day after study enrollment in all patients. Reaction time (R), maximum amplitude (MA) and patients’ characteristics are here reported. ResultsOne hundred patients (control n=50 and intervention n=50; male n=59; median age 68years) with complete TEG during follow-up were included. At enrollment, 3%, 38%, and 59% had a hypocoagulable, normocoagulable, and hypercoagulable TEG clot strength (MA), respectively.In the hypothermia group, functional coagulopathy improved during the hypothermia phase, measured by R and MA, in patients with hypercoagulation as well as in patients with hypocoagulation (correlation between ΔR and initial R: rho=-0.60, p<0.0001 and correlation between ΔMA and initial MA: rho=-0.50, p=0.0002). Similar results were not observed in the control group neither for R (rho=-0.03, p=0.8247) nor MA (rho=-0.15, p=0.3115). ConclusionMild induced hypothermia did seem to improve functional coagulopathy in septic patients. This improvement of functional coagulopathy parameters during the hypothermia intervention persisted after rewarming. Randomized trials are warranted to determine whether the positive effect on sepsis-related coagulopathy can be transformed to improved survival.

Temperature effects on haemostasis in whole blood from ticagrelor- and aspirin-treated patients with acute coronary syndrome

Background. Comatose survivors after cardiac arrest are treated with mild induced hypothermia and potent platelet- inhibiting drugs after coronary stenting. Previous studies have shown an increased incidence of stent thrombosis during clopidogrel and aspirin treatment in conjunction with induced hypothermia. The aim of this study was to investigate the in vitro effect of induced hypo- and hyperthermia on blood from patients undergoing ticagrelor- and aspirin-mediated platelet inhibition. Methods. Whole blood from 15 patients with acute coronary syndrome who were treated with ticagrelor and aspirin and from eight healthy volunteers was incubated for 1 hour at 28, 33, 37, and 39°C. Results. In blood from patients with acute coronary syndrome, the activated clotting time (Sonoclot) was prolonged in mild hypothermic (33°C) compared to normothermic (37°C) samples. Sonoclot, clotting rate and platelet function were decreased in hypothermic compared to normothermic samples. Platelet-induced activation and aggregation (Multiplate®) was unchanged in mild hypothermic compared to normothermic samples. In contrast, mild hypothermia supported increased platelet activation as measured with flow cytometry with up-regulation of PAC-1 and P-selectin on the platelet surface. Conclusion. In acute coronary syndrome patients treated with ticagrelor and aspirin, in vitro hypothermia to 33°C markedly increased platelet activity measured with flow cytometry, whereas viscoelastic coagulation test (Sonoclot) revealed a hypocoagulative response. Prospective clinical trials studying platelet inhibition at different temperatures and correlating changes in platelet function to bleeding or stent occlusion are needed.

Evolution of insulin sensitivity and its variability in out-of-hospital cardiac arrest (OHCA) patients treated with hypothermia.

IntroductionTherapeutic hypothermia (TH) is often used to treat out-of-hospital cardiac arrest (OHCA) patients who also often simultaneously receive insulin for stress-induced hyperglycaemia. However, the impact of TH on systemic metabolism and insulin resistance in critical illness is unknown. This study analyses the impact of TH on metabolism, including the evolution of insulin sensitivity (SI) and its variability, in patients with coma after OHCA.MethodsThis study uses a clinically validated, model-based measure of SI. Insulin sensitivity was identified hourly using retrospective data from 200 post-cardiac arrest patients (8,522 hours) treated with TH, shortly after admission to the intensive care unit (ICU). Blood glucose and body temperature readings were taken every one to two hours. Data were divided into three periods: 1) cool (T <35°C); 2) an idle period of two hours as normothermia was re-established; and 3) warm (T >37°C). A maximum of 24 hours each for the cool and warm periods was considered. The impact of each condition on SI is analysed per cohort and per patient for both level and hour-to-hour variability, between periods and in six-hour blocks.ResultsCohort and per-patient median SI levels increase consistently by 35% to 70% and 26% to 59% (P <0.001) respectively from cool to warm. Conversely, cohort and per-patient SI variability decreased by 11.1% to 33.6% (P <0.001) for the first 12 hours of treatment. However, SI variability increases between the 18th and 30th hours over the cool to warm transition, before continuing to decrease afterward.ConclusionsOCHA patients treated with TH have significantly lower and more variable SI during the cool period, compared to the later warm period. As treatment continues, SI level rises, and variability decreases consistently except for a large, significant increase during the cool to warm transition. These results demonstrate increased resistance to insulin during mild induced hypothermia. Our study might have important implications for glycaemic control during targeted temperature management.

Platelet aggregation and clot formation in comatose survivors of cardiac arrest treated with induced hypothermia and dual platelet inhibition with aspirin and ticagrelor; a prospective observational study

IntroductionWe conducted a prospective observational study in cardiac arrest survivors treated with mild induced hypothermia, evaluating different platelet function tests at hypo- and normothermia. We also investigated the relation between gastric emptying and vasodilator stimulated phosphoprotein (VASP).MethodsComatose survivors of out of hospital cardiac arrest were included and divided into two groups, depending on whether dual platelet inhibition with peroral ticagrelor and aspirin was given or not. The first blood samples (T1) were collected 12–24 hours after reaching target temperature (33°C) and were compared to blood samples collected 12–28 hours after reaching normothermia (37°C) (T2) within each group. All samples were analysed by Sonoclot viscoelasticity, flow cytometry based VASP and with multiple electrode aggregometry, Multiplate®; adenosine diphosphate (ADP), collagen (COL), thrombin receptor agonist peptide (TRAP) and arachidonic acid (ASPI). Sonoclot and Multiplate® instruments were set on in vivo temperatures. Gastric secretion from the nasogastric tube was measured to assess absorption of per orally administered antiplatelet drugs. Differences between T1 and T2 within each group were calculated using Wilcoxon matched pairs signed test. Significance levels were set at P <0.01.ResultsIn total, 23 patients were included. In patients with dual platelet inhibition (n =14) Multiplate®-analyses showed no changes in ADP stimulated platelets. COL, TRAP and ASPI aggregations were higher at T2 compared to T1. Sonoclot-analyses showed that activated clotting time (ACT) was unchanged but both clot rate (CR) and platelet function (PF) were higher at T2 compared to T1. VASP decreased from 53 ± 28(T1) to 24 ± 22(T2), (P <0.001). The average volume of gastric secretion aspirated before T1 correlated well with VASP (T1), r =0.81 (P <0.001). In patients with no platelet inhibition, (n =9) similar changes between T1 and T2 were seen as in patients with dual platelet inhibition while VASP was unchanged.ConclusionsWe have demonstrated increased platelet aggregation and strengthened clot formation over time in out of hospital cardiac arrest patients treated with hypothermia. In patients on oral dual platelet inhibition, the effect of ticagrelor was delayed, probably due to slow gastric emptying.

Hypothermia after cardiac arrest as a novel approach to increase survival in cardiopulmonary cerebral resuscitation: a review.

Context:The aim of this review study was to evaluate therapeutic mild hypothermia, its complications and various methods for induced mild hypothermia in patients following resuscitation after out-of-hospital cardiac arrest.Evidence Acquisition:Studies conducted on post-cardiac arrest cares, history of induced hypothermia, and therapeutic hypothermia for patients with cardiac arrest were included in this study. We used the valid databases (PubMed and Cochrane library) to collect relevant articles.Results:According to the studies reviewed, induction of mild hypothermia in patients after cardiopulmonary resuscitation would lead to increased survival and better neurological outcome; however, studies on the complications of hypothermia or different methods of inducing hypothermia were limited and needed to be studied further.Conclusions:This study provides strategic issues concerning the induction of mild hypothermia, its complications, and different ways of performing it on patients; using this method helps to increase patients’ neurological survival rate.

Wide temperature range testing with ROTEM coagulation analyses.

Mild induced hypothermia is used for neuroprotection in patients successfully resuscitated after cardiac arrest. Temperature-dependent effects on rotational thromboelastometry (ROTEM(®)) assays with EXTEM(®), FIBTEM(®), or APTEM(®) in cardiac arrest patients have not previously been studied. Ten patients with out-of-hospital cardiac arrest who underwent induced hypothermia were studied during stable hypothermia at 33°C. ROTEM temperature effects on EXTEM, FIBTEM, and APTEM assays were studied at temperatures set between 30°C and 42°C. Citrated whole blood test tubes were incubated in temperature-adjusted heating blocks and then investigated at respective temperature in the temperature-adjusted ROTEM. The following variables were determined: clotting time (CT), clot formation time (CFT), α-angle, and maximum clot firmness (MCF). The results from hypo- and hyperthermia samples were compared with the samples incubated at 37°C using the Wilcoxon matched-pairs signed-rank test. A p-value of <0.05 was considered significant. CT-EXTEM(®) and CT-APTEM(®) were prolonged by hypothermia at 30°C (p<0.01 for both) and 33°C (p<0.05 for both). Hyperthermia at 42°C shortened CT-EXTEM (p<0.05) and CT-APTEM (p<0.01). CFT-EXTEM(®) and CFT-APTEM(®) were markedly prolonged by hypothermia at 30°C, 33°C, and 35°C (p<0.01 for all except CFT-EXTEM, 35°C [p<0.05]). The α-angle-EXTEM was markedly decreased at 30°C, 33°C, and 35°C (p<0.01) but increased at 40°C (p<0.05) and 42°C (p<0.01); α-angle-APTEM showed similar results. MCF was unchanged at different temperatures for all tests. ROTEM (EXTEM, FIBTEM, and APTEM assays) revealed a hypocoagulative response to in vitro-applied hypothermia in the blood of cardiac arrest patients reflected in the prolonged clot initiation and decreased clot propagation. Hyperthermia showed the opposite effects. Clot firmness was not affected by temperature.

30-day mortality and neurological outcome in survivors of out-of-hospital cardiac arrest

E-mail: andreja.sinkovic@guest.arnes.si Purpose: Mortality is high in survivors of out-of-hospital cardiac arrest (OHCA) — it is even up to 86% and it strongly correlates with ischemic brain damage. In the last decade, quality of cardiopulmonary resuscitation by emergency medical services (EMS) enormously improved as well as the postcardiac arrest treatment of survivors of OHCA in intensive care units, in particular by introducing mild induced therapeutic hypothermia to prevent ischemic brain injury. Our purpose was to evaluate 30-day mortality and neurological outcome in survivors of OHCA. Methods: We retrospectively studied 119 survivors of OHCA (73.1% men, mean age 64.1±13.5), admitted from 2011 to 2013. On admission, they were comatose with palpable pulse, breathing either spontaneously or mechanically ventilated. Postcardiac arrest treatment included iv. infusion of fluids, vasopressors and inotropes if necessary, percutaneous coronary interventions (PCI) in case of acute coronary syndromes (ACS), mild induced hypothermia of 34°C for the first 24 hours. Neurological evaluation by cerebral performance category (CPC) scale 1-5 was performed. Mild to moderate neurological disability was registered as CPC scale 1-2, severe cerebral disability, vegetative state and brain death as CPC scale 3-5. Results: OHCA was witnessed in 45.4%. It was the consequence of ventricular fibrillation or pulseless ventricular tachicardia (VF/VT) in 54.6% and of asystole or pulseless electrical activity (PEA) in 45.6%. Mean time from OHCA to EMS arrival was 8.6±4.5 minutes, mean time from EMS arrival to return of spontaneous circulation (ROSC) due to resuscitation by EMS 17.6±17 minutes. On arrival to intensive care, the patients were comatose, 92.4% mechanically ventilated. Mild therapeutic hypothermia was performed in 82.4% during the first 24 hours. Mean admission troponin I level was 6.5±20.8 μg/l, admission lactate 6.5±4.2 mmol/l and peak troponin I 35.3±4.8 μg/l. ACS were the cause for 41.1% of OHCA. PCIs were performed in 40.3% after emergency coronary angiography. Mean ejection fraction within the first few hours was 33.7±15%. Vasopressors were administered in 75.6%, inotropes in 57.1%, intraaortic baloon pump in 6.7%. 30-day mortality was 46.2% and 6-month mortality 52.9%. CPC scale 1-2 was achieved in 35.3%, CPC scale 3-5 in 64.7%. Conclusion: Improvements in resuscitation and postresuscitation care resulted in an increased survival and better neurological outcome of successfully resuscitated patients due to OHCA.

Main complications of mild induced hypothermia after cardiac arrest: a review article.

The aim of the present study is to assess the complications of mild induced hypothermia (MIH) in patients with cardiac arrest. Presently, based on the guidelines of the American heart Association, MIH following successful cardiopulmonary resuscitation (CPR) in unconscious adult patients due to ventricular fibrillation (VF) with out-of-hospital cardiac arrest (OOHCA) is essential and required. However, MIH could be associated with complications in Patients with cardiac arrest. Studies conducted on the precautions and care following cardiac arrest and MIH were included. Valid scientific data bases were used for data collection. The obtained results from different studies revealed that mild MIH could be associated with numerous complications and the knowledge and awareness of the medical staff from the complications is required to guarantee successful therapeutic approaches in MIH following cardiac arrest which is a novel medical facility with different styles and complications. Overall, further future studies are required to improve the quality of MIH, to increase survival and to decrease complications rates.

Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury

Previous studies have reported that mild induced hypothermia (MIH) treatment has positive effects on traumatic brain injury (TBI) outcomes, which have recently been linked to β-amyloid (Aβ)-induced secondary brain injury (SBI) extent in hippocampal tissues. We therefore investigate the relationship between MIH treatment and expression of Aβ and related proteins following TBI. Adult Sprague-Dawley rats were randomly divided into three equal groups (S: sham-operated, N: normothermia, and H: mild hypothermia). After TBI induced by fluid percussion, group N remained at normal temperature, and group H underwent MIH (32°C) for 6 hours. Behavioral scale scores were then assessed. All rats were sacrificed 24 hours and hippocampal tissues were harvested, stained with hematoxylin and eosin. mRNA and protein expressions of Aβ, β-amyloid protein precursor (APP), and β-secretase (BACE) were analyzed. Our results revealed significantly improved behavioral scale scores and the surviving neuron numbers were observed in group H compared to group N (p<0.05). Additionally, group N increased APP, Aβ, and BACE levels compared to group S (all p<0.05). Reduced expression of APP-, Aβ-, and BACE were apparent in group H compared to group N (all p<0.05). However, no statistically significant difference was observed between groups H and S in behavioral scale scores and the expression of APP-, Aβ-, and BACE (p>0.05). In conclusion, MIH treatment significantly improves the survival of neuron and reduced Aβ, BACE, and APP upregulation after TBI, which may provide a better understanding of the mechanisms by which hypothermia reduces SBI in TBI patients.

Invasive versus non-invasive cooling after in- and out-of-hospital cardiac arrest: a randomized trial

Mild induced hypothermia (MIH) is indicated for comatose survivors of sudden cardiac arrest (SCA) to improve clinical outcome. In this study, we compared the efficacy of two different cooling devices for temperature management in SCA survivors. Between April 2008 and August 2009, 80 patients after survived in-hospital (IHCA) and out-of-hospital cardiac arrest (OHCA) were included in this prospective, randomized, single center study. Hypothermia was induced after randomization by either invasive Coolgard(®) cooling or non-invasive ArcticSun(®) surface cooling at 33.0 °C core body temperature for 24 h followed by active rewarming. The primary endpoint was defined as the efficacy of both cooling systems, measured by neuron-specific enolase (NSE) levels as a surrogate parameter for brain damage. Secondary efficacy endpoints were the clinical and neurological outcome, time to start of cooling and reaching the target temperature, target temperature-maintenance and hypothermia-associated complications. NSE at 72 h did not differ significantly between the 2 groups with 16.5 ng/ml, interquartile range 11.8-46.5 in surface-cooled patients versus 19.0 ng/ml, interquartile range 11.0-42.0 in invasive-cooled patients, p = 0.99. Neurological and clinical outcome was similar in both groups. Target temperature of 33.0 °C was maintained more stable in the invasive group (33.0 versus 32.7 °C, p < 0.001). Bleeding complications were more frequent with invasive cooling (n = 17 [43.6 %] versus n = 7 [17.9 %]; p = 0.03). Invasive cooling has advantages with respect to temperature management over surface cooling; however, did not result in different outcome as measured by NSE release in SCA survivors. Bleeding complications were more frequently encountered by invasive cooling.

Mild induced hypothermia in patient with acute myocardial infarction after cardiac arrest

Mild induced hypothermia is recommended by both European and American cardiological associations as well as European and Polish Recuscitation Council as a standard therapy in comatose patients resuscitated from cardiac arrest. We report a case of a 60 year-old male patient resuscitated from out-of-hospital cardiac arrest treated with mild hypothermia. The use of hypothermia improved patient's neurological prognosis and outcome by preventing severe brain injury.

Urgent invasive coronary strategy and mild induced hypothermia in patients with resuscitated sudden cardiac arrest

Copyright © Polskie Towarzystwo Kardiologiczne INTRODUCTION Sudden cardiac arrest (SCA) remains the leading cause of death in developed countries, with an annual incidence ranging from 36 to 81 events per 100,000 inhabitants. According to the findings of post mortems and immediate coronary angiography, significant coronary artery disease may be documented in more than 70% of patients suffering from SCA [1, 2]. Following initial cardiocerebral resuscitation in the field, the re-establishment of spontaneous circulation (ROSC) is achieved in 40% to 60% of patients who are subsequently transferred to the emergency department. Because of typical delays in the ‘chain of survival’, up to 80% of patients remain comatose despite ROSC which pinpoints post-resuscitation brain injury. Its severity may ultimately vary from mild disability to permanent vegetative state and cannot be accurately prognosticated on hospital admission. Only a minority of ‘lucky losers’ with prompt initiation of chest compression and defibrillation, which is usually the case if emergency medical personnel are already present when cardiac arrest occurs, regain consciousness immediately after ROSC.

The benign nature of mild induced therapeutic hypothermia—Induced long QTc

The post cardiac arrest syndrome is a constellation of cardiac, metabolic and neurological dysfunction that adversely affects the prognosis in cardiac arrest survivors. Mild induced therapeutic hypothermia (TH) has been shown to improve neurological recovery and mortality [1]. Although TH can prolong the QT interval, it has not been generally associated with Torsade de pointes (TdP) [2].

Mild-induced hypothermia and neuroprognostication following cardiac arrest

Mild-induced hypothermia and neuroprognostication following cardiac arrest

Mild-induced hypothermia and neuroprognostication following cardiac arrest

Department of Emergency Medicine, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA Dr. Merchant was supported, in part, by grant/research support from NIH, K23 grant 10714038, and pilot funding from Physio-Control, Seattle, WA; Zoll Medical, Boston, MA; Cardiac Science, Bothell, WA; and Philips Medical, Seattle, WA. Dr. Perman has not disclosed any potential conflicts of interest.