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Hypothermia and cardiac arrest: the promise of intra-arrest cooling
Roger A Band, Benjamin S Abella
Critical Care , 2008, DOI: 10.1186/cc6845
Abstract: In the previous issue of Critical Care, Bruel and colleagues report findings from a small, prospective, observational study in which they investigate the feasibility, efficacy and safety of intra-arrest therapeutic hypothermia (TH) for victims of out-of-hospital cardiac arrest (OHCA) [1]. From an initial pool of 412 cardiac arrest victims, the study enrolled 33 patients with a variety of presenting rhythms. This represents the first study of its kind to investigate the feasibility of intra-arrest cooling in the clinical setting, an approach that has shown significant promise in animal models of cardiac arrest and brain injury [2-4].Sudden cardiac arrest, defined as the abrupt loss of mechanical cardiac activity and concomitant global loss of blood flow, is a leading cause of death in the United States and Europe. Approximately 200,000 people suffer OHCA in the United States each year, and over 90% will succumb during resuscitation efforts or during subsequent hospitalization [5,6]. Survival to hospital discharge depends on a number of factors, including prompt delivery of cardiopulmonary resuscitation and defibrillation when indicated, the initial cardiac rhythm of arrest, and the quality of post-resuscitation care including provision of TH.Despite the significant effort that has been invested in this field, few therapeutic or pharmacologic interventions have yielded meaningful increases in overall survival from OHCA over the past 20 years [6,7]. The relatively new and evolving treatment modality of TH, however, has been associated with markedly decreased mortality and neurologic injury among patients who initially survive OHCA [8,9].TH reduces both the cerebral metabolic rate and oxygen demand, and it is thought to attenuate reperfusion injury, global inflammation and endothelial dysfunction – all consequences of cerebral and other organ ischemia [10,11]. Through such mechanisms, TH is thought to improve clinical parameters and outcomes. Two landmark multicenter ra
Hypothermia and pediatric cardiac arrest  [cached]
Schlunt Michelle,Wang Lynn
Journal of Emergencies, Trauma and Shock , 2010,
Abstract: The survival outcome following pediatric cardiac arrest still remains poor. Survival to hospital discharge ranges anywhere from 0 to 38% when considering both out-of-hospital and in-hospital arrests, with up to 50% of the survivors having neurologic injury. The use of mild induced hypothermia has not been definitively proven to improve outcomes following pediatric cardiac arrest. This may be due to the lack of consensus regarding target temperature, best method of cooling, optimal duration of cooling and identifying the patient population who will receive the greatest benefit. We review the current applications of induced hypothermia in pediatric patients following cardiac arrest after searching the current literature through Pubmed and Ovid journal databases. We put forth compiled recommendations/guidelines for initiating hypothermia therapy, its maintenance, associated monitoring and suggested adjunctive therapies to produce favorable neurologic and survival outcomes.
Recent treatment of postischaemic anoxic brain damage after cardiac arrest by using therapeutic hypothermia
An?eli? Sla?ana
Srpski Arhiv za Celokupno Lekarstvo , 2008, DOI: 10.2298/sarh0810549a
Abstract: Organ injury caused by ischemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35oC) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomized clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia, will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal 'therapeutic window' for gene therapy.
Therapeutic hypothermia and neurological outcome after cardiac arrest  [PDF]
Petrovi? Milovan,Pani? Gordana,Joveli? Aleksandra,?anji Tibor
Vojnosanitetski Pregled , 2011, DOI: 10.2298/vsp1106495p
Abstract: Introduction/Aim. The most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation. Methods. The prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days. Results. The study was conducted on 82 patients: 45 patients (age 57.93 ± 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 ± 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003). Conclusion. Mild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.
Out-of-hospital therapeutic hypothermia in cardiac arrest victims
Wilhelm Behringer, Jasmin Arrich, Michael Holzer, Fritz Sterz
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2009, DOI: 10.1186/1757-7241-17-52
Abstract: Sudden cardiac arrest remains a major unresolved public health problem. In Europe and the USA, approximately 425.000 people suffer of sudden cardiac death with very poor survival, usually less than 10% [1,2]. After cardiac arrest and brain ischemia, reperfusion initiates multiple independent chemical cascades and fatal pathways, resulting in neuronal death due to necrosis and apoptosis [3]. Because of the multi-factorial pathogenesis of post-arrest neuronal death, a multifaceted treatment strategy is required to achieve survival without brain damage. Hypothermia, a re-discovered promising treatment strategy, exerts its beneficial effects on brain ischemia by various mechanisms, and perfectly fulfils the requirements of a multifaceted treatment strategy [4].In therapeutic hypothermia, different degrees of cooling can be differentiated, though definition of these temperature levels may differ slightly between authors: mild (34 to 32°C), moderate (31 to 28°C), deep (27 to 11°C), profound (10 to 6°C), and ultra-profound (5 to 0°C) hypothermia. Protective hypothermia, induced before cardiac arrest, has to be differentiated from preservative hypothermia, induced during cardiac arrest treatment, and from resuscitative hypothermia, induced after successful resuscitation. Protective hypothermia is used in cardiac surgery and neurosurgery, but is clinically unrealistic in sudden cardiac death. This review will focus on a) preservative mild hypothermia during cardiac arrest treatment and b) resuscitative mild hypothermia after successful resuscitation in respect to its clinical application in the out-of-hospital setting.Preservative hypothermia can further be differentiated into the induction of hypothermia during ischemia (before initiation of resuscitation - or before reperfusion) and the induction of hypothermia during resuscitation.Research in myocytes showed that injury to cells not only occurs during ischemia itself, but mainly with reperfusion by initiating several casc
Does anesthetic provide similar neuroprotection to therapeutic hypothermia after cardiac arrest?
Hong Zhang
Critical Care , 2010, DOI: 10.1186/cc8923
Abstract: Therapeutic hypothermia has been shown to provide neuroprotection against ischemic injury after cardiac arrest in in vitro and in vivo models. In the previous issue of Critical Care, Meybohm and colleagues [1] demonstrate that cardiac arrest triggers the release of cerebral inflammatory cytokines in pigs' cerebral cortex. Therapeutic hypothermia alters inflammatory response in cardiac arrest and subsequent cardiopulmonary resuscitation. The combination of hypothermia with sevoflurane post-conditioning does not confer additional anti-inflammatory effects compared with hypothermia alone.Cardiac arrest remains the leading cause of death in the US and Europe, with an out-of-hospital cardiac arrest survival-to-discharge rate of less than 10%. In-hospital cardiac arrest presents a dismal prognosis. According to a large in-hospital registry, the survival-to-discharge rate is 18%, whereas that of a developing country is 6.9% [2,3]. Without prompt care, the chance for meaningful survival falls dramatically within minutes of arrest onset. When immediate care is available and victims are successfully resuscitated, the majority of these initial survivors subsequently suffer crippling neurologic injury or die in the few days following the cardiac arrest event. Thus, improving survival and brain function after initial resuscitation from cardiac arrest remains a critical challenge. Therapeutic hypothermia, introduced more than six decades ago, remains an important neuroprotective factor in cardiac arrest. Laboratory studies have demonstrated that cooling after resuscitation from cardiac arrest improves both survival as well as subsequent neurologic and cardiac function and has few side effects. these findings have been reproduced using a variety of cooling techniques in different species, including rats, dogs, and pigs.However, physician use of hypothermia induction in patients resuscitated from cardiac arrest is low. In 2003, Abella and colleagues [4] reported that 87% of US phys
Therapeutic hypothermia post out-of-hospital cardiac arrest - more questions than answers?
Richard Lyon
Critical Care , 2011, DOI: 10.1186/cc10123
Abstract: Patients post out-of-hospital cardiac arrest (OHCA) are common admissions to the ICU. Therapeutic hypothermia has been shown to improve both survival and neurological outcome for OHCA patients surviving to reach the ICU and now forms part of routine post-resuscitation care. The Time to Target Temperature (TTTT) study group presents key observations on the relationship between body temperature and outcome following OHCA [1], yet ultimately are we left with more questions than answers on therapeutic hypothermia?Nearly a decade ago two landmark papers fundamentally changed the practice of post-resuscitation care. The Hypothermia after Cardiac Arrest study group [2] and Bernard and colleagues [3] not only demonstrated the benefit of cooling OHCA patients but also highlighted how hugely effective the therapy was, with a number needed to treat of seven patients and six patients, respectively, for survival. Such impressive therapeutic benefit is rarely seen in medical practice, let alone in critical care medicine. A key difference between these two studies was the time from return of spontaneous circulation (ROSC) to the onset of cooling. The time to reach the target temperature (<34°C) varied greatly from immediately post ROSC to over 16 hours post ROSC and yet the therapeutic benefit of cooling was still evident. The TTTT group demonstrated that the change in body temperature during the period from ROSC to cooling initiation has a direct relationship on survival [1].Since 2002 few studies have examined the optimum method, rate of cooling and timing of initiation. Little is known about the mechanism of action of therapeutic hypothermia. Whilst animal evidence strongly suggests that early cooling, especially intra-arrest, is beneficial, few human studies have demonstrated a benefit from early cooling. Early cooling, in the prehospital or emergency department setting, has significant technical challenges and may distract from the basic principles of resuscitation. Yet emerg
The Practice of Therapeutic Hypothermia after Cardiac Arrest in France: A National Survey  [PDF]
Jean-Christophe Orban, Florian Cattet, Jean-Yves Lefrant, Marc Leone, Samir Jaber, Jean-Michel Constantin, Bernard Allaouchiche, Carole Ichai, for the AzuRéa group
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045284
Abstract: Aims Cardiac arrest is a major health concern worldwide accounting for 375,000 cases per year in Europe with a survival rate of <10%. Therapeutic hypothermia has been shown to improve patients’ neurological outcome and is recommended by scientific societies. Despite these guidelines, different surveys report a heterogeneous application of this treatment. The aim of the present study was to evaluate the clinical practice of therapeutic hypothermia in cardiac arrest patients. Methods This self-declarative web based survey was proposed to all registered French adult intensive care units (ICUs) (n = 357). Paediatrics and neurosurgery ICUs were excluded. The different questions addressed the structure, the practical modalities of therapeutic hypothermia and the use of prognostic factors in patients admitted after cardiac arrest. Results One hundred and thirty-two out of 357 ICUs (37%) answered the questionnaire. Adherence to recommendations regarding the targeted temperature and hypothermia duration were 98% and 94% respectively. Both guidelines were followed in 92% ICUs. During therapeutic hypothermia, sedative drugs were given in 99% ICUs, mostly midazolam (77%) and sufentanil (59%). Neuromuscular blocking agents (NMBA) were used in 97% ICUs, mainly cisatracurium (77%). Numerous prognostic factors were used after cardiac arrest such as clinical factors (95%), biomarkers (53%), electroencephalography (78%) and evoked potentials (35%). Conclusions In France, adherence to recommendations for therapeutic hypothermia after cardiac arrest is higher than those previously reported in other countries. Numerous prognostic factors are widely used even if their reliability remains controversial.
A Comparison of Cooling Techniques to Treat Cardiac Arrest Patients with Hypothermia  [PDF]
Anna Finley Caulfield,Shylaja Rachabattula,Irina Eyngorn,Scott A. Hamilton,Rajalakshmi Kalimuthu,Amie W. Hsia,Maarten G. Lansberg,Chitra Venkatasubramanian,J. J. Baumann,Marion S. Buckwalter,Monisha A. Kumar,James S. Castle,Christine A. C. Wijman
Stroke Research and Treatment , 2011, DOI: 10.4061/2011/690506
Abstract: Introduction. We sought to compare the performance of endovascular cooling to conventional surface cooling after cardiac arrest. Methods. Patients in coma following cardiopulmonary resuscitation were cooled with an endovascular cooling catheter or with ice bags and cold-water-circulating cooling blankets to a target temperature of 32.0–34.0°C for 24 hours. Performance of cooling techniques was compared by (1) number of hourly recordings in target temperature range, (2) time elapsed from the written order to initiate cooling and target temperature, and (3) adverse events during the first week. Results. Median time in target temperature range was 19 hours (interquartile range (IQR), 16–20) in the endovascular group versus. 10 hours (IQR, 7–15) in the surface group ( ). Median time to target temperature was 4 (IQR, 2.8–6.2) and 4.5 (IQR, 3–6.5) hours, respectively ( ). Adverse events were similar. Conclusion. Endovascular cooling maintains target temperatures better than conventional surface cooling. 1. Introduction Each year an estimated 165,000 people in the United States have an out-of-hospital cardiac arrest, and many more undergo in-hospital resuscitation [1–4]. Those that survive may have devastating neurological impairments from global ischemic brain injury. Mild-to-moderate therapeutic hypothermia for 12 to 24 hours has been shown to improve neurological outcome in two randomized clinical trials of comatose survivors following out-of-hospital ventricular fibrillation arrest [5, 6]. Based on the results of these trials, the 2005 American Heart Association guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommended to consider the use of therapeutic hypothermia for unconscious adult patients with return of spontaneous circulation after witnessed out-of-hospital ventricular fibrillation arrest (Class IIA) and nonventricular fibrillation and in-hospital cardiac arrest (Class IIB) [7]. The 2010 guidelines continue to recommend therapeutic hypothermia in these patients, now as Class I and Class IIB recommendations, respectively [8]. In spite of the data and guidelines hospitals in the United States have been slow to adopt therapeutic hypothermia in the routine management of comatose postcardiac arrest patients [9]. This may be in part explained by physician unfamiliarity with therapeutic hypothermia and in part by the labor intensiveness and inaccuracy of surface cooling using ice bags and cooling blankets [10]. Most studies to date have used conventional surface-based cooling techniques (ice bags and cool air or water
Prehospital therapeutic hypothermia in cardiac arrest: will there ever be evidence?
Joerg C Schefold, Christian Storm, Dietrich Hasper
Critical Care , 2008, DOI: 10.1186/cc6844
Abstract: The design of future trials on therapeutic hypothermia, however, seems challenged by the fact that withholding this treatment in a control arm might be considered unjustifiable from an ethical point of view. In the prehospital setting, such a trial would require a large number of study patients to demonstrate an additional benefit. This is due to the fact that both a spontaneous decline in body core temperature occurs, especially in the no-flow and low-flow phase, and that the overall gain of time (typically around 45 min) may be considered marginal against the background of most published data, indicating that target temperatures cannot be reached until about 6 to 8 hours later [2,3]. Given the optimistic view that prehospital cooling increases the number of favourable neurological outcomes from 55% [4] to 60%, about 750 patients would have to be included in a given randomised trial.Nevertheless, although we totally agree with Bruel and colleagues that the intervention is safe and feasible, and that a clear biological rationale for the earliest possible induction of therapeutic hypothermia exists [2-5], we doubt that a prospective randomised trial on additional prehospital cooling is feasible and justifiable. We may have reached another boundary of evidence-based medicine.Cédric Bruel, Jean-Jacques Parienti, William Marie, Xavier Arrot, Cédric Daubin, Damien Du Cheyron, Massimo Massetti and Pierre CharbonneauWe would like to thank Schefold and colleagues for their interest in our article [1]. Two issues are discussed in their correspondence. First, they questioned the ethical rationale of a randomised study in which the control group would not receive out-of-hospital therapeutic hypothermia (which is not yet standard practice) [6]. We believe the findings of our small pilot feasibility study should not be overinterpreted, particularly regarding safety issues, because we presented no control group. For this reason, it is our view that the potential benefit in terms
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