Induction Of Mild Hypothermia Research Articles

Therapeutic Hypothermia for Traumatic Brain Injury

Experimental evidence demonstrates that therapeutic temperature modulation with the use of mild induced hypothermia (MIH, defined as the maintenance of body temperature at 32-35 °C) exerts significant neuroprotection and attenuates secondary cerebral insults after traumatic brain injury (TBI). In adult TBI patients, MIH has been used during the acute "early" phase as prophylactic neuroprotectant and in the sub-acute "late" phase to control brain edema. When used to control brain edema, MIH is effective in reducing elevated intracranial pressure (ICP), and is a valid therapy of refractory intracranial hypertension in TBI patients. Based on the available evidence, we recommend: applying standardized algorithms for the management of induced cooling; paying attention to limit potential side effects (shivering, infections, electrolyte disorders, arrhythmias, reduced cardiac output); and using controlled, slow (0.1-0.2 °C/h) rewarming, to avoid rebound ICP. The optimal temperature target should be titrated to maintain ICP <20 mmHg and to avoid temperatures <35 °C. The duration of cooling should be individualized until the resolution of brain edema, and may be longer than 48 h. Patients with refractory elevated ICP following focal TBI (e.g. hemorrhagic contusions) may respond better to MIH than those with diffuse injury. Randomized controlled trials are underway to evaluate the impact of MIH on neurological outcome in adult TBI patients with elevated ICP. The use of MIH as prophylactic neuroprotectant in the early phase of adult TBI is not supported by clinical evidence and is not recommended.

Induction of Mild Hypothermia by Noninvasive Body Cooling in Healthy, Unanesthetized Subjects: Editorial Commentary on Bandschapp et al., 2011

Induction of Mild Hypothermia by Noninvasive Body Cooling in Healthy, Unanesthetized Subjects: Editorial Commentary on Bandschapp <i>et al.</i>, 2011

A cardiac arrest

Describe the interaction between the use of mild induced hypothermia and acute diffuse coronary spasm. We report the case of a 52-yr-old Caucasian woman resuscitated after initial cardiac arrest, with normal postresuscitation electrocardiogram, sufficient hemodynamic conditions, and decreased level of consciousness, who received mild induced hypothermia to reduce brain damage as suggested by cardiopulmonary resuscitation guidelines. After the beginning of mild therapeutic hypothermia, the patient experienced malignant diffuse coronary artery spasm, so-called Prinzmetal's angina, leading to myocardial ischemia and ventricular tachycardia, which was only resolved by intracoronary vasodilator injection. Mild induced hypothermia was apparently the trigger of a severe and diffuse coronary artery spasm.

Induced mild hypothermia in children

The objective of this study was to measure outcomes and to determine the safety and effectiveness of mild induced hypothermia in children after traumatic and posthypoxic brain injury. Methods. Forty patients, following traumatic or posthypoxic brain injury, were involved in the study. Mean age was 10.7 ± 0.8 years. Median GCS (Glasgow Coma Scale) was 6.0 (4-7) and mean PIM2 (Pediatric Index of Mortality) 14.6 ± 3.8 %. Results. GOS (Glasgow Outcome Scale) of 5 was assigned for 15 (37.5%) patients, GOS 4 for 14 (35.0%), GOS 3 for 7 (17.5%) and GOS 2 for 4 (10%) patients. The average GOS in patients after severe head trauma was 3.6 ± 0.9 points and in patients with posthypoxic brain injury 5 points, (p < 0.05). No life threatening complications occurred. Conclusion. Mild induced hypothermia can be safely used in pediatric patents after severe traumatic or posthypoxic brain injury. This method may be of benefit while improving outcomes in children.

Induction of Mild Hypothermia by Noninvasive Body Cooling in Healthy, Unanesthetized Subjects

The induction of mild hypothermia has been considered as an important means to provide protection against cerebral ischemia. Yet, to date, the relative clinical efficacies of different noninvasive methods for reducing core body temperature have not been thoroughly studied. The aim of the current investigation was to compare the relative effectiveness of several noninvasive cooling techniques for reducing core temperatures in healthy volunteers. Cooling methods included convective/conductive and evaporative/conductive combinations, as well as evaporative cooling alone. Additionally, focal facial warming was employed as a means to suppress involuntary motor activity and thus better enable noninvasive cooling. Core temperatures were measured so to monitor the relative efficiencies of these induced cooling methodologies. With each employed methodology, rectal temperature reductions were induced, with combined evaporative/conductive (n=4, 1.44°C±0.99°C) and convective/conductive (n=4, 1.51°C±0.89°C) approaches yielding the largest decreases: note, that evaporative cooling alone was not as efficient in lowering core body temperature (n=10, 0.56°C±0.20°C; n=16, 0.58°C±0.27°C). In this study on healthy volunteers, the evaporative/conductive and convective/conductive combination methods were more effective in reducing core temperatures as compared with an evaporative approach alone. These therapeutic approaches for the induction of mild hypothermia (including the use of facial warming) could be employed in warranted clinical cases, importantly without the need for administration of anesthetics or paralytics.

Importance of invasive interventional strategies in resuscitated patients following sudden cardiac arrest

Post-resuscitation care has become a major part of the chain of survival for victims of cardiac arrest. Once spontaneous circulation is restored, it is important to consider early coronary angiography and concurrent use of mild therapeutic hypothermia. In those resuscitated from an arrest considered to be cardiac in origin, coronary angiography should be performed inmmediately to identify any culprit coronary occlusion or unstable lesions. If a culprit lesion is found, immediate percutaneous coronary intervention should be performed. Any out-of-hospital cardiac arrest victim successfully resuscitated, but who remain comatose after return of spontaneous circulation, should be cooled to 32–24°C for 24 h. Induction of mild hypothermia can be accomplished without delaying coronary intervention. When these two post-resuscitation therapies are provided concurrently long-term survival is 50–60%, with favorable neurological function achieved in 80–90% of such survivors.

The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation

Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest. In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling). At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH. The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.

Surface cooling for induction of mild hypothermia in conscious healthy volunteers

In 16 healthy male volunteers (range 21-47 years), esophageal temperature decreased from baseline median 36.2°C (IQR 35.9 to 36.6°C) to 35°C within median 53 minutes (IQR 44 to 83 minutes), indicating a median cooling rate of 1.1°C/h (IQR 1.0 to 1.5°C). The minimum temperature reached was median 34.4°C (IQR 34.1 to 34.4°C). No shivering or discomfort of the attending volunteers was observed. Results

Evaluation of Outcomes Among Subsets of Patients Treated With Induced Hypothermia After Cardiac Arrest in a Community Teaching Hospital

PURPOSE: The neuroprotective effects and mortality benefit of mild induced hypothermia (MIH) after cardiac arrest has been demonstrated. The impact of providing this therapy to patients who have relative exclusion criteria remains unclear.

Hypothermia Reduces Perihemorrhagic Edema After Intracerebral Hemorrhage

The prognosis of spontaneous intracerebral hemorrhage (sICH) is poor because of the mass effect arising from the hematoma and the associated peri-hemorrhagic edema, leading to increased intracranial pressure. Because the efficacy of surgical and anti-edematous treatment strategies is limited, we investigated the effects of mild induced hypothermia in patients with large sICH. Twelve patients with supratentorial sICH >25 mL were treated by hypothermia of 35 degrees C for 10 days. Evolution of hematoma volume and perifocal edema was measured by cranial CT. Functional outcome was assessed after 90 days. These patients were compared to patients (n=25; inclusion criteria: sICH volume >25 mL, no acute restriction of medical therapy on admission) from the local hemorrhage data bank (n=312). Side effects of hypothermia were analyzed. All patients from both groups needed mechanical ventilation and were treated in a neurocritical care unit. All hypothermic patients (mean age, 60+/-10 years) survived until day 90, whereas 7 patients died in the control group (mean age, 67+/-7 years). Absolute hematoma size on admission was 58+/-29 mL (hypothermia) compared to 57+/-31 mL (control). In the hypothermia group, edema volume remained stable during 14 days (day 1, 53+/-43 mL; day 14, 57+/-45 mL), whereas edema significantly increased in the control group from 40+/-28 mL (day 1) to 88+/-47 mL (day 14). ICH continuously dissolved in both groups. Pneumonia rate was 100% in the hypothermia group and 76% in controls (P=0.08). No significant side effects of hypothermia were observed. Hypothermia prevented the increase of peri-hemorrhagic edema in patients with large sICH.

Hypothermia after cardiac arrest should be further evaluated—A systematic review of randomised trials with meta-analysis and trial sequential analysis

BackgroundGuidelines recommend mild induced hypothermia (MIH) to reduce mortality and neurological impairment after out-of-hospital cardiac arrest. Our objective was to systematically evaluate the evidence for MIH taking into consideration the risks of systematic and random error and to GRADE the evidence. MethodsSystematic review with meta-analysis and trial sequential analysis of randomised trials evaluating MIH after cardiac arrest in adults. We searched CENTRAL, MEDLINE, and EMBASE databases until May 2009. Retrieved trials were evaluated with Cochrane methodology. Meta-analytic estimates were calculated with random- and fixed-effects models and random errors were evaluated with trial sequential analysis (TSA). ResultsFive randomised trials (478 patients) were included. All trials had substantial risk of bias. The relative risk (RR) for death was 0.84 (95% confidence interval (CI) 0.70 to 1.01) and for poor neurological outcome 0.78 (95% CI 0.64 to 0.95). For the two trials with least risk of bias the RR for death was 0.92 (95% CI 0.56 to 1.51) and for poor neurological outcome 0.92 (95% confidence interval 0.56 to 1.50). TSA indicated lack of firm evidence for a beneficial effect. The substantial risk of bias and concerns with directness rated down the quality of the evidence to low. ConclusionsEvidence regarding MIH after out-of-hospital cardiac arrest is still inconclusive and associated with non-negligible risks of systematic and random errors. Using GRADE-methodology, we conclude that the quality of evidence is low. Our findings demonstrate that clinical equipoise exists and that large well-designed randomised trials with low risk of bias are needed.

Review: Contemporary practices in postcardiac arrest syndrome: the role of mild therapeutic hypothermia

Out-of-hospital cardiac arrest remains a major cause of mortality and morbidity despite progress in resuscitative practices. The number of survivors with severe neurological impairment at hospital discharge is similarly dismal. Recently, much attention has been directed toward the use of mild therapeutic hypothermia in the care of comatose survivors with postcardiac arrest syndrome. Recent research suggests mild hypothermia lowers mortality and improves neurological outcome after successful treatment of cardiac arrest. The current 2005 updated guidelines of International Liaison Committee on Resuscitation and European Resuscitation Council recommend the utilization of mild induced hypothermia in postresuscitation treatment. Hypothermia induction in order to avoid the pathophysiological mechanisms of euthermia and hyperthermia and subsequent complications are briefly discussed. Cooling methods, potential side effects and questions regarding implementation of therapeutic hypothermia recommendations in every day clinical practice and future investigation are also addressed.

The effects of mild induced hypothermia on the myocardium: a systematic review

Mild induced hypothermia improves neurological outcome and reduces mortality among initially comatose survivors of out-of-hospital cardiac arrest. Similar pathological processes occur in the heart and the brain, namely ischaemia followed by reperfusion injury. Animal data indicate that mild induced hypothermia results in improved myocardial salvage, reduced infarct size, reduced left ventricular remodelling and better long-term left ventricular function. Several small human studies suggest that infarct size may be reduced by mild induced hypothermia, although this has not reached significance in any human study to date. There are variable reports of harm to the myocardium caused by mild induced hypothermia, including reduced myocardial contractility and cardiac output, electrocardiographic changes and arrhythmias, especially bradycardia. These harmful effects are reversible with rewarming.

Cardiac function during mild hypothermia in pigs: increased inotropy at the expense of diastolic dysfunction

The induction of mild hypothermia (MH; 33 degrees C) has become the guideline therapy to attenuate hypoxic brain injury after out-of-hospital cardiopulmonary resuscitation. While MH exerts a positive inotropic effect in vitro, MH reduces cardiac output in vivo and is thus discussed critically when severe cardiac dysfunction is present in patients. We thus assessed the effect of MH on the function of the normal heart in an in vivo model closely mimicking the clinical setting. Ten anaesthetized, female human-sized pigs were acutely catheterized for measurement of pressure-volume loops (conductance catheter), cardiac output (Swan-Ganz catheter) and for vena cava inferior occlusion. Controlled MH (from 37 to 33 degrees C) was induced by a vena cava inferior cooling catheter. With MH, heart rate (HR) and whole body oxygen consumption decreased, while lactate levels remained normal. Cardiac output, left ventricular (LV) volumes, peak systolic and end-diastolic pressure and dP/dt(max) did not change significantly. Changes in dP/dt(min) and the time constant of isovolumetric relaxation demonstrated impaired active relaxation. In addition, MH prolonged the systolic and shortened the diastolic time interval. Pressure-volume analysis revealed increased end-systolic and end-diastolic stiffness, indicating positive inotropy and reduced end-diastolic distensibility. Positive inotropy was preserved during pacing, while LV end-diastolic pressure increased and diastolic filling was substantially impaired due to delayed LV relaxation. MH negatively affects diastolic function, which, however, is compensated for by decreased spontaneous HR. Positive inotropy and a decrease in whole body oxygen consumption warrant further studies addressing the potential benefit of MH on the acutely failing heart.

Pre-hospital cardiac arrest and induction of mild hypothermia: studies on epidemiology and feasibility

Acta Anaesthesiologica ScandinavicaVolume 54, Issue 6 p. 789-790 Pre-hospital cardiac arrest and induction of mild hypothermia: studies on epidemiology and feasibility A. Kämäräinen, A. KämäräinenSearch for more papers by this author A. Kämäräinen, A. KämäräinenSearch for more papers by this author First published: 01 June 2010 https://doi.org/10.1111/j.1399-6576.2010.02228.xCitations: 1 Address:Antti KämäräinenTopeliuksenkatu 35a900250 HelsinkiFinlande-mail: antti.kamarainen@uta.fi Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume54, Issue6July 2010Pages 789-790 RelatedInformation

Hypothermia during percutaneous coronary intervention in comatose survivors of cardiac arrest

Urgent invasive coronary strategy including coronary angiography and percutaneous coronary intervention (PCI) is feasible and safe in combination with mild induced hypothermia and may significantly improve survival with good neurological outcome in comatose patients after reestablishment of spontaneous circulation (ROSC). The starting hypothermia already in the prehospital setting or immediately after arrival to the catheterization laboratory to complement urgent coronary angi-ography and PCI seems to be a logical strategy.

Hypothermia and pediatric cardiac arrest

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.

Cardiocerebral resuscitation: facts and prospects

Cardiopulmonary resuscitation in the prehospital setting still has to cope with poor lay-rescuer knowledge of resuscitation techniques, low public availability of automated external defi brillators, many detrimental interruptions of chest compressions during lay and professional resuscitation eff orts and suboptimal postresuscitation care. Th erefore the survival of patients aft er cardiac arrest remains poor. To address those fl aws, cardiopulmonary resuscitation guidelines of 2005 are targeted at improving cardiopulmonary resuscitation by achieving adequate depth, number, and minimal interruptions of chest compressions per minute, and avoiding hyperventilation. But a combination of chest compressions and rescue breathing is still the mainstay of resuscitation ofi n primary and secondary cardiac arrest despite diff erent pathophysiological causes. In the last two decades a concept of cardiocerebral resuscitation emerged, and according to research it is equal to or even better than standard cardiopulmonary resuscitation in terms of patients\' prognosis aft er successful resuscitation of sudden or primary unexpected cardiac arrest. Cardiocerebral resuscitation of patients with primary cardiac arrest consists of layrescuer uninterrupted chest compressions without rescue breathing in the fi rst minutes of resuscitation, advanced life support techniques that do not interrupt chest compressions and thus maintain their positive hemodynamic eff ects. If professional rescuers arrive at the scene within 4 to 5 minutes aft er primary cardiac arrest, defi brillation should be attempted prior to resuscitation techiques, but if professional help arrives later than 4 to 5 minutes aft er primary cardiac arrest, two minutes of resuscitation techniques should be performed prior to the fi rst defi brillation. Post-resuscitation care includes mild induced hypothermia, coronarography and percutaneous coronary intervention.

Mild Hypothermia Delays the Evolution of Early LV Dilatation and Late Stone Heart from Untreated Sustained Ventricular Fibrillation

Introduction: Mild induced hypothermia is now the recommended treatment for persistently comatose adults after resuscitation from out-of-hospital ventricular fibrillation (VF) cardiac arrest. The cardio-protective benefits of induced mild hypothermia are still unclear. Although induced mild hypothermia is a well-established effective therapy for improving neurological outcomes, its effects on early ventricular dilatation or late stone heart development, secondary to untreated VF, are unknown. Hypothesis: Pre-arrest induced mild hypothermia in sustained VF substantially extends the time interval from commencement of cardiac arrest until the development of stone heart, thereby prolonging the limit of rescusitability. Method: Fourteen female swine (27 ± 1 kg) were used in this study. Animals were randomized to 2 groups, normothermia (n=6) and hypothermia (n=8). Mild hypothermia (32-34 °C) was induced by surrounding the swine body with ice packs for prior to imaging. After achieving a rectal temperature of 32-34 °C, routine CMR images in normal sinus rhythm were obtained. A pacing catheter electrode was placed temporarily into the RV to induce VF with 100Hz alternating current. Before fibrillation, a set of short-axis views were acquired. Data collection started immediately after the initiation of VF, every minute for the first 5 minutes, and every 5 minutes thereafter until the development of stone heart (2/3 reduction in the baseline mean LV volume). Results: Time to stone heart occurred at 52 ± 4 minutes in the hypothermia animals compared to 29 ± 3 minutes in the normothermia animals (P<0.001). During the first 5 minutes of untreated VF, mean LV volume increased by 11% in the hypothermia group compared to 34% increase in the normothermia group (P<0.05). Between 10 and 30 minutes of untreated VF, there were no significant changes in LV volumes in the hypothermia group versus 75% decrease in LV volume in the normothermia group. Conclusion: Stone heart, or severe LV myocardial ischemic contracture, is an irreversible phenomenon and marks the limit of myocardial resuscitability. This study demonstrates that in a closed-chest whole animal model of untreated prolonged VF cardiac arrest, pre-arrest induced mild hypothermia substantially delays the development of stone heart. This adds to our current understanding of the beneficial mechanism of mild hypothermia and suggests that morphologic changes are at least in part responsible for or an important by-product of this practice. Introduction: Mild induced hypothermia is now the recommended treatment for persistently comatose adults after resuscitation from out-of-hospital ventricular fibrillation (VF) cardiac arrest. The cardio-protective benefits of induced mild hypothermia are still unclear. Although induced mild hypothermia is a well-established effective therapy for improving neurological outcomes, its effects on early ventricular dilatation or late stone heart development, secondary to untreated VF, are unknown. Hypothesis: Pre-arrest induced mild hypothermia in sustained VF substantially extends the time interval from commencement of cardiac arrest until the development of stone heart, thereby prolonging the limit of rescusitability. Method: Fourteen female swine (27 ± 1 kg) were used in this study. Animals were randomized to 2 groups, normothermia (n=6) and hypothermia (n=8). Mild hypothermia (32-34 °C) was induced by surrounding the swine body with ice packs for prior to imaging. After achieving a rectal temperature of 32-34 °C, routine CMR images in normal sinus rhythm were obtained. A pacing catheter electrode was placed temporarily into the RV to induce VF with 100Hz alternating current. Before fibrillation, a set of short-axis views were acquired. Data collection started immediately after the initiation of VF, every minute for the first 5 minutes, and every 5 minutes thereafter until the development of stone heart (2/3 reduction in the baseline mean LV volume). Results: Time to stone heart occurred at 52 ± 4 minutes in the hypothermia animals compared to 29 ± 3 minutes in the normothermia animals (P<0.001). During the first 5 minutes of untreated VF, mean LV volume increased by 11% in the hypothermia group compared to 34% increase in the normothermia group (P<0.05). Between 10 and 30 minutes of untreated VF, there were no significant changes in LV volumes in the hypothermia group versus 75% decrease in LV volume in the normothermia group. Conclusion: Stone heart, or severe LV myocardial ischemic contracture, is an irreversible phenomenon and marks the limit of myocardial resuscitability. This study demonstrates that in a closed-chest whole animal model of untreated prolonged VF cardiac arrest, pre-arrest induced mild hypothermia substantially delays the development of stone heart. This adds to our current understanding of the beneficial mechanism of mild hypothermia and suggests that morphologic changes are at least in part responsible for or an important by-product of this practice.

Improving the Outcome of In-Hospital Cardiac Arrest: The Importance of Being EARNEST

Cardiopulmonary resuscitation techniques were introduced more than 50 years ago, yet the rate of survival from cardiac arrest, particularly in the hospital setting, remains dismally low. This article reviews the prevalence, etiology, and outcome of in-hospital cardiac arrest, with a focus on the determinants of outcome that are amenable to improvement. These include principally components of basic life support that may be supported by either prompting or mechanical assistance (eg, chest compression, ventilation, and defibrillation). Also reviewed are preevent and postevent effectors such as medical staff skills and recognition of impending arrest, induction of mild hypothermia, and stabilization after return of spontaneous circulation.