From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest

OBJECTIVES: Therapeutic hypothermia has been recommended for postcardiac arrest coma due to ventricular fibrillation. However, no studies have evaluated whether therapeutic hypothermia could be effectively implemented in intensive care practice and whether it would improve the outcome of all comatose patients with cardiac arrest, including those with shock or with cardiac arrest due to nonventricular fibrillation rhythms. DESIGN: Retrospective study. SETTING: Fourteen-bed medical intensive care unit in a university hospital. PATIENTS: Patients were 109 comatose patients with out-of-hospital cardiac arrest due to ventricular fibrillation and nonventricular fibrillation rhythms (asystole/pulseless electrical activity). INTERVENTIONS: We analyzed 55 consecutive patients (June 2002 to December 2004) treated with therapeutic hypothermia (to a central target temperature of 33 degrees C, using external cooling). Fifty-four consecutive patients (June 1999 to May 2002) treated with standard resuscitation served as controls. Efficacy, safety, and outcome at hospital discharge were assessed. Good outcome was defined as Glasgow-Pittsburgh Cerebral Performance category 1 or 2. MEASUREMENTS AND MAIN RESULTS: In patients treated with therapeutic hypothermia, the median time to reach the target temperature was 5 hrs, with a progressive reduction over the 18 months of data collection. Therapeutic hypothermia had a major positive impact on the outcome of patients with cardiac arrest due to ventricular fibrillation (good outcome in 24 of 43 patients [55.8%] of the therapeutic hypothermia group vs. 11 of 43 patients [25.6%] of the standard resuscitation group, p = .004). The benefit of therapeutic hypothermia was also maintained in patients with shock (good outcome in five of 17 patients of the therapeutic hypothermia group vs. zero of 14 of the standard resuscitation group, p = .027). The outcome after cardiac arrest due to nonventricular fibrillation rhythms was poor and did not differ significantly between the two groups. Therapeutic hypothermia was of particular benefit in patients with short duration of cardiac arrest (<30 mins). CONCLUSIONS: Therapeutic hypothermia for the treatment of postcardiac arrest coma can be successfully implemented in intensive care practice with a major benefit on patient outcome, which appeared to be related to the type and the duration of initial cardiac arrest and seemed maintained in patients with shock.     

心搏骤停后昏迷患者神经功能预后评估的研究进展

心肺复苏后昏迷患者早期神经功能预后评估作为心搏骤停(CA)后管理的重要组成部分,具有显著的临床意义.本文从神经系统检查、脑电图、诱发电位、神经影像学及血清生物标志物等方面,结合亚低温治疗对神经功能评估的影响,综述了CA后昏迷患者神经功能预后评估的研究进展.     

Anti-arrhythmic and vasopressor medications for the treatment of ventricular fibrillation in severe hypothermia: a systematic review of the literature

OBJECTIVE: To determine the rate of return of spontaneous circulation (ROSC) in animal models performing resuscitation from induced ventricular fibrillation (VF) in severe hypothermia (<30 degrees C). MATERIALS AND METHODS: A medical literature database search from 1966 to present was performed identifying placebo controlled trials using anti-arrhythmic or vasopressor medications to treat ventricular fibrillation in the setting of severe hypothermia. RESULTS: 7 controlled studies were identified (n=117) testing 6 combinations of resuscitative medications. ROSC rates for treatment versus control groups were as follows: amiodarone (6% vs. 18%, p=0.6, n=34), bretylium (35% vs. 35%, p=1.0, n=40), intermediate- and high-dose epinephrine (adrenaline) (36% vs. 27%, p=1.0, n=22), vasopressin (60% vs. 0%, p<0.0001, n=39), vasopressin and amiodarone (0% vs. 0%, p=NS, n=11), low-dose epinephrine and amiodarone (91% vs. 30%, p=0.0075, n=21). Cumulatively, among all studies administering vasopressors, the rate of ROSC was 62% in treatment groups contrasted to 17% in control groups (p<0.0001, n=77). CONCLUSIONS: In controlled animal models of severe hypothermia, ROSC rates for induced ventricular fibrillation are higher with utilization of vasopressor medications. Current guidelines which recommend withholding these medications in the setting of hypothermic cardiac arrest should be re-evaluated.     

The role of hypothermia in post-cardiac arrest patients with return of spontaneous circulation: a systematic review

ObjectivesTo update a comprehensive systematic review of the use of therapeutic hypothermia after cardiac arrest that was undertaken initially as part of the 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. The specific question addressed was: ‘in post-cardiac arrest patients with a return of spontaneous circulation, does the induction of mild hypothermia improve morbidity or mortality when compared with usual care?’MethodsPubmed was searched using (“heart arrest” or “cardiopulmonary resuscitation”) AND “hypothermia, induced” using ‘Clinical Queries’ search strategy; EmBASE was searched using (heart arrest) OR (cardiopulmonary resuscitation) AND hypothermia; The Cochrane database of systematic reviews; ECC EndNote Library for “hypothermia” in abstract OR title. Excluded were animal studies, reviews and editorials, surveys of implementation, analytical models, reports of single cases, pre-arrest or during arrest cooling and group where the intervention was not hypothermia alone.Results77 studies met the criteria for further review. Of these, four were meta-analyses (LOE 1); seven were randomised controlled trials (LOE 1), although six of these were from the same set of patients; nine were non-randomised, concurrent controls (LOE 2); 15 were trials with retrospective controls (LOE 3); 40 had no controls (LOE 4); and one was extrapolated from a non-cardiac arrest group (LOE 5).ConclusionThere is evidence supporting the use of mild therapeutic hypothermia to improve neurological outcome in patients who remain comatose following the return of spontaneous circulation after a cardiac arrest; however, much of the evidence is from low-level, observational studies. Of seven randomised controlled trials, six use data from the same patients.     

Serotonin syndrome after therapeutic hypothermia for cardiac arrest: A case series

Aim

To describe causes, manifestations, and diagnosis of serotonin syndrome following therapeutic hypothermia (TH) after cardiac arrest.

Methods

Retrospective case series from a tertiary academic medical center.

Results

Three male patients suffered witnessed out-of-hospital cardiac arrests and were treated with induced TH. Initial cardiac rhythms included asystole in two and ventricular fibrillation in one. Following completion of rewarming, all three developed neurological signs unexpected for their clinical condition. These included rigidity, hyperreflexia, diffuse tremors, ankle clonus, and marked agitated delirium. Patients also were febrile, hypertensive, and tachycardic. A diagnosis of serotonin syndrome was made in all cases and serotonergic medications were discontinued. All three patients recovered consciousness and two made a full neurological recovery. One patient remained dependent on others for activities of daily living at the time of hospital discharge because of short-term memory impairment.

Conclusions

Unexpected neurologic findings and prolonged high fever following recovery from TH can be manifestations of serotonin syndrome rather than post-cardiac arrest anoxic brain injury.     

Therapeutic hypothermia induced during cardiopulmonary resuscitation using large-volume, ice-cold intravenous fluid

INTRODUCTION: Therapeutic hypothermia after resuscitation improves outcome following prolonged out-of-hospital cardiac arrest. Laboratory studies suggest that this therapy may improve outcome further when induced during cardiopulmonary resuscitation. We report a case where therapeutic hypothermia was induced during cardiopulmonary resuscitation using large-volume (40 mL/kg), ice-cold (4 degrees C) intravenous fluid. DESIGN: Case report. SETTING: A tertiary level hospital in Victoria, Australia. CASE REPORT: The patient suffered a cardiac arrest secondary to pericardial tamponade following right ventricular perforation during cardiac catheterisation. Percutaneous needle drainage was unsuccessful and open drainage via a left emergency thoracotomy was performed. Therapeutic hypothermia during cardiopulmonary resuscitation was induced using of a rapid infusion of large-volume (40 mL/kg), ice-cold (4 degrees C) crystalloid fluid. A spontaneous circulation was restored after 37 min of cardiac arrest. The patient made a satisfactory neurological recovery. CONCLUSION: Treatment with a rapid intravenous infusion of large-volume (40 mL/kg), ice-cold (4 degrees C) fluid during cardiopulmonary resuscitation induces mild hypothermia and may provide neurological protection. Further clinical studies of this approach are warranted.     

A Case of Commotio Cordis Treated with Therapeutic Hypothermia

Background

Therapeutic hypothermia is used as a neuroprotective strategy for patients who have persistent neurologic compromise after return of spontaneous circulation from cardiac arrest. The 2010 American Heart Association Guidelines recommend the use of therapeutic hypothermia in adult cardiac arrest patients when the initial rhythm is ventricular fibrillation. These recommendations are based on primary research in patients with a cardiac cause of their ventricular fibrillation.

Case Report

A 43-year-old male was brought to our emergency department (ED) with commotio cordis. He was struck in the chest with a baseball bat, after which he collapsed at the scene and was pulseless. Return of spontaneous circulation was achieved after defibrillation by treating paramedics, and the patient remained comatose on arrival to the ED. He was transferred to the intensive care unit and treated with therapeutic hypothermia at target temperature of 32−34°C. He was extubated on day 3, and discharged home on day 8 with good neurologic function.

Why Should An Emergency Physician Be Aware of This?

We report a case of commotio cordis in which the adult patient was treated with therapeutic hypothermia and had a favorable outcome. To our knowledge, this is the first reported case of its kind. Evidence for the use of therapeutic hypothermia is incomplete in patients with a traumatic cause of cardiac arrest, such as commotio cordis, despite probable similarities in the pathophysiology of anoxic brain injury. Our case illustrates that there may be benefit from use of therapeutic hypothermia for a broader population than is currently recommended.     

Efficacy of therapeutic hypothermia after out-of-hospital cardiac arrest due to ventricular fibrillation

AIM OF THE STUDY: We investigated implementation and efficacy of mild therapeutic hypothermia in the treatment of out-of-hospital cardiac arrest due to ventricular fibrillation. MATERIALS AND METHODS: Two periods were compared, an historical one (36 patients) between 2000 and 2002 where therapeutic hypothermia was never used, and a recent period (32 patients) between 2003 and 2005 where therapeutic hypothermia (32-34 degrees C) was implemented prospectively in our unit. Cooling was obtained by simply using wet cloths and ice packs. Survival in the two groups and factors associated with survival were analysed, together with the neurological prognosis in discharged patients. RESULTS: Survival was significantly higher in the hypothermia group (56% versus 36%), whereas no significant difference was observed in severity between the two periods. Only age, time from return to spontaneous circulation <20min, and therapeutic hypothermia were independently associated with survival. Therapeutic hypothermia was well tolerated and was associated with a significant improvement in neurological outcome. Whereas only 23% of patients actually reached the target temperature in 2003, 100% did in 2005. CONCLUSION: Therapeutic hypothermia is efficient in significantly improving survival and neurological outcome of out-of-hospital cardiac arrest with ventricular fibrillation. By using a simple method, it can be implemented easily and quickly, without side effects.     

Somatosensory and brainstem auditory evoked potentials in cardiac arrest patients treated with hypothermia

OBJECTIVE: To evaluate the prognostic value of short-latency median nerve somatosensory evoked potentials and brainstem auditory evoked potentials in outcome prediction for comatose cardiac arrest patients treated with hypothermia. DESIGN: Prospective, randomized, controlled trial of mild hypothermia after out-of-hospital cardiac arrest; a substudy of the European Hypothermia After Cardiac Arrest study. SETTING: Intensive care unit of a tertiary referral hospital (Helsinki University Central Hospital). PATIENTS: Sixty consecutive patients (aged 18-75 yrs) resuscitated from out-of-hospital ventricular fibrillation and comatose at 24 hrs after cardiac arrest; all patients were randomly assigned either to therapeutic hypothermia of 33 degrees C or normothermia. INTERVENTIONS: All patients received standard intensive care for at least 2 days. Patients randomized to hypothermia were cooled with an external cooling device for 24 hrs and then allowed to rewarm slowly for 12 hrs. In the normothermia group, the core temperature was kept below 38 degrees C with antipyretics and by physical means. The clinical outcome was assessed 6 months after cardiac arrest. MEASUREMENTS AND MAIN RESULTS: Somatosensory evoked potentials and brainstem auditory evoked potentials were recorded 24-28 hrs after cardiac arrest. All wave latencies were significantly prolonged in the hypothermia group. Bilaterally absent N20 waves predicted permanent coma with a specificity of 100% in both treatment groups. Brainstem auditory evoked potential recordings did not correlate with the outcome in either treatment group. CONCLUSIONS: The prognostic ability of median nerve short-latency somatosensory evoked potentials does not seem to be affected by therapeutic hypothermia. Brainstem auditory evoked potentials had no additional value in outcome prediction.     

Resuscitation from cardiac arrest in cats: influence of epinephrine dosage on brain recovery

The quality of brain recovery after cardiac arrest depends crucially on the speed of cardiac resuscitation because the low cerebral perfusion pressure during the resuscitation procedure facilitates the development of no-reflow. To accelerate return of spontaneous circulation, high dose epinephrine has been recommended but the effect on the dynamics of early brain recovery is still unknown. We, therefore, studied the dynamics of brain resuscitation after cardiopulmonary resuscitation (CPR) with standard and high dose epinephrine using non-invasive NMR techniques. Fifteen min cardiac arrest was induced in normothermic cats by ventricular fibrillation. CPR was performed using an inflatable pneumatic vest for cyclic chest compression. With the beginning of CPR the standard dose group received 0.02 mg/kg epinephrine (n = 6) and the high dose group received 0.2 mg/kg (n = 8). Brain recovery was monitored by magnetic resonance imaging of the apparent diffusion coefficient (ADC) of water for 3 h. Although high dose epinephrine treatment led to a significantly higher blood pressure during early reperfusion, rapidly changing heterogeneities of early brain recovery were observed in both groups. High dose epinephrine thus does not improve the quality of post-cardiac arrest brain recovery during the first 3 h of reperfusion.     

When the Female Heart Stops: Sex and Gender Differences in Out-of-Hospital Cardiac Arrest Epidemiology and Resuscitation

Sex- and gender-based differences are emerging as clinically significant in the epidemiology and resuscitation of patients with out-of-hospital cardiac arrest (OHCA). Female patients tend to be older, experience arrest in private locations, and have fewer initial shockable rhythms (ventricular fibrillation/ventricular tachycardia). Despite standardized algorithms for the management of OHCA, women are less likely to receive evidence-based interventions, including advanced cardiac life support medications, percutaneous coronary intervention, and targeted temperature management. While some data suggest a protective mechanism of estrogen in the heart, brain, and kidney, its role is incompletely understood. Female patients experience higher mortality from OHCA, prompting the need for sex-specific research.     

Protective effects of therapeutic hypothermia in post-resuscitation myocardium

Aim of the study

Post-resuscitation therapeutic hypothermia has been recommended because of its neuroprotective effects. However, a few studies have reported the effects of therapeutic hypothermia on the heart, especially in ventricular fibrillation cardiac arrest. The aim of this study was to determine whether therapeutic hypothermia attenuates post-resuscitation myocardial injury in a swine cardiac arrest model.

Methods

A prospective animal study was performed in the university hospital animal research laboratory. Ventricular fibrillation cardiac arrest was induced in domestic pigs weighing 35–40 kg. After 6 min of no flow time, cardiopulmonary resuscitation was provided to pigs, and the restoration of spontaneous circulation (ROSC) was achieved. The subjects were randomly allocated to a normothermic (NT group, n = 5) or hypothermic (HT group, n = 5) group. In the HT group, therapeutic hypothermia (core temperature 32–34 °C) was maintained for 24 h, and rewarming was performed over a period of 8 h. In the NT group, core temperature was maintained at 37 °C throughout the experiments. Sixty hours after ROSC, blood and myocardial tissues were harvested.

Results

Serum troponin I was not significantly different between the groups. However, myocardial histological damage was attenuated in the HT group. Myocardial ATP contents were higher in the HT group than in the NT group. Immunohistochemistry for apoptosis-related protein showed that survivin expression was higher in the HT group, and XAF1 and cleaved caspase-3 expressions were lower in the HT group than in the NT group.

Conclusions

Therapeutic hypothermia attenuated histological myocardial injury in ventricular fibrillation cardiac arrest model of pigs while preserving more ATP and decreased apoptosis.     

Brain function after resuscitation from cardiac arrest

PURPOSE OF REVIEW: In industrial countries the incidence of cardiac arrest is still increasing. Almost 80% of cardiac arrest survivors remains in coma for varying lengths of time and full cerebral recovery is still a rare event. After successful cardiopulmonary resuscitation, cerebral recirculation disturbances and complex metabolic postreflow derangements lead to death of vulnerable neurons with further deterioration of cerebral outcome. This article discusses recent research efforts on the pathophysiology of brain injury caused by cardiac arrest and reviews the beneficial effect of therapeutic hypothermia on neurologic outcome along with the recent approach to prognosticate long-term outcome by electrophysiologic techniques and molecular markers of brain injury. RECENT FINDINGS: Recent experimental studies have brought new insights to the pathophysiology of secondary postischemic anoxic encephalopathy demonstrating a time-dependent cerebral oxidative injury, increased neuronal expression, and activation of apoptosis-inducing death receptors and altered gene expression with long-term changes in the molecular phenotype of neurons. Recently, nuclear MR imaging and MR spectroscopic studies assessing cerebral circulatory recovery demonstrated the precise time course of cerebral reperfusion after cardiac arrest. Therapeutic hypothermia has been shown to improve brain function after resuscitation from cardiac arrest and has been introduced recently as beneficial therapy in ventricular fibrillation cardiac arrest. SUMMARY: Electrophysiologic techniques and molecular markers of brain injury allow the accurate assessment and prognostication of long-term outcome in cardiac arrest survivors. In particular, somatosensory evoked potentials have been identified as the method with the highest prognostic reliability. A recent systematic review of 18 studies analyzed the predictive ability of somatosensory evoked potentials performed early after onset of coma and found that absence of cortical somatosensory evoked potentials identify patients not returning from anoxic coma with a specificity of 100%.     

Extracorporeal Membrane Oxygenation for Hypokalemia and Refractory Ventricular Fibrillation Associated with Caffeine Intoxication

BackgroundCaffeine has been reported as a cause of cardiac arrest after massive overdose. Here, we report the case of a patient with caffeine intoxication, which can cause fatal dysrhythmias and severe hypokalemia. They were successfully treated with extracorporeal membrane oxygenation (ECMO).Case ReportA 43-year-old woman with a history of bipolar disorder presented to the emergency department after suicidal drug ingestion (caffeine and amitriptyline). Immediately after arrival, she experienced multiple episodes of ventricular fibrillation with severe hypokalemia requiring cardiopulmonary resuscitation and medical therapy. However, conventional treatment was not successful. We instituted ECMO early during resuscitation because prolonged hypokalemia refractory to aggressive potassium replacement precluded the use of antidysrhythmic medications for refractory circulatory compromise with ventricular fibrillation. The use of ECMO provided time to correct hypokalemia (19.3 g potassium) and reduce the caffeine level with hemodialysis. Although she had sustained cardiac arrest, she recovered fully and was discharged home.Why Should an Emergency Physician be Aware of This?Our case indicates the potential effectiveness of ECMO in severely poisoned patients with fatal dysrhythmias. ECMO could provide time for removal of toxic drugs and correction of electrolyte abnormalities.     

Induction of mild hypothermia with infusion of cold (4 degrees C) fluid during ongoing experimental CPR

INTRODUCTION: Therapeutic hypothermia after resuscitation has been shown to improve the outcome regarding neurological state and to reduce mortality. The earlier hypothermia therapy is induced probably the better. We studied the induction of hypothermia with a large volume of intravenous ice-cold fluid after cardiac arrest during ongoing cardiopulmonary resuscitation (CPR). METHODS: Twenty anaesthetised piglets were subjected to 8 min of ventricular fibrillation, followed by CPR. They were randomized into two groups. The hypothermic group was given an infusion of 4 degrees C acetated Ringer's solution 30 ml/kg at an infusion rate of 1.33 ml/kg/min, starting after 1 min of CPR. The control group received the same infusion at room temperature. All pigs received a bolus dose of vasopressin after 3 min of CPR. After 9 min, defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). Core temperature and haemodynamic variables were measured at baseline and repeatedly until 180 min after ROSC. Cortical cerebral blood flow was measured, using Laser-Doppler flowmetry. RESULTS: All pigs had ROSC, except one animal in the hypothermic group. Only one animal in the hypothermic group died during the observation period. The calculated mean temperature reduction was 1.6+/-0.35 degrees C (S.D.) in the hypothermic group and 1.1+/-0.37 degrees C in the control group (p=0.009). There was no difference in cortical cerebral blood flow and haemodynamic variables. CONCLUSION: Inducing hypothermia with a cold infusion seems to be an effective method that can be started even during ongoing CPR. This method might warrant consideration for induction of early therapeutic hypothermia in cardiac arrest victims.     

Reduced effectiveness of hypothermia in patients lacking the wave V in auditory brainstem responses immediately following resuscitation from cardiac arrest

AIMS: Therapeutic hypothermia appears to improve the outcome of pre-hospital cardio-pulmonary arrest (CPA) in patients with an initial cardiac rhythm of ventricular fibrillation or nonperfusing ventricular tachycardia (VF/VT). Notwithstanding, the outcome of this procedure is certainly difficult to predict based solely on the initial rhythm. The aim of the present study was to predict the outcome using auditory brainstem responses (ABRs) in CPA patients treated with therapeutic hypothermia. DESIGN AND SETTING: A prospective observational study in the intensive care unit of a university hospital. PATIENTS: The study included 26 patients resuscitated from out-of-hospital CPA. INTERVENTIONS: Basic and advanced cardiac life support, intensive care and post-resuscitative hypothermia. MEASUREMENT AND RESULTS: ABRs were recorded immediately after the return of spontaneous circulation (ROSC). An ABR wave V was recorded in 16 patients. Among 8 patients with a favourable outcome, the initial rhythms were VF/VT in 6 patients and other rhythms in 2. All 10 patients without a detectable ABR wave V had an unfavourable outcome. The VF/VT as the initial arrest rhythm and the presence of wave V were significantly (p = 0.0095) correlated with a favourable outcome. The presence of wave V had a 100% sensitivity to a favourable outcome. CONCLUSION: The absence of the ABR wave V in the early phase after ROSC wave indicated a reduced effect of therapeutic hypothermia, even in cases that underwent hypothermia promptly after out-of-hospital CPA. Measurement of ABRs appears to be useful as a predictor of effectiveness and as a criterion for determining the indication for therapeutic hypothermia.     

Spontaneous defibrillation after cessation of resuscitation in out-of-hospital cardiac arrest: a case of Lazarus phenomenon

This report describes a case of out-of-hospital cardiac arrest with spontaneous defibrillation and subsequent return of circulation after cessation of resuscitative efforts. A 47-year-old man was found in cardiac arrest and resuscitation was initiated. As no response was achieved, the efforts were withdrawn and final registered cardiac rhythm was ventricular fibrillation. Fifteen minutes later the patient was found to be normotensive and breathing spontaneously. The patient made a poor neurological recovery and died 3 months after the arrest. The authors are unable to give an explanation to the event, but suspect the effect of adrenaline combined with mild hypothermia to have contributed to the self-defibrillation of the myocardium.     

Mild therapeutic hypothermia after cardiac arrest - a nationwide survey on the implementation of the ILCOR guidelines in German intensive care units

AIM: To investigate the implementation of mild therapeutic hypothermia (MTH) after cardiac arrest into clinical practice. METHODS AND RESULTS: A structured evaluation questionnaire was sent to all German hospitals registered to have ICUs; 58% completed the survey. A total of 93 ICUs (24%) reported to use MTH. Of those, 93% started MTH in patients after out-of-hospital resuscitation with observed ventricular fibrillation and 72% when other initial rhythms were observed. Only a minority of ICUs initiate MTH in patients after cardiac arrest with cardiogenic shock (28%), whereas 48% regarded cardiogenic shock as a contra-indication for MTH. On average, target temperature was 33.1+/-0.6 degrees C and duration of cooling 22.9+/-4.9 h. Many centres used economically priced cold packs (82%) and cold infusions (80%) for cooling. The majority of the ICUs considered infection, hypotension and bleeding as relevant complications of hypothermia which was of therapeutic relevance in less than 25% of the cases. CONCLUSIONS: MTH is underused in German ICUs. Centres which use MTH widely follow the recommendations of ILCOR with respect to the indication and timing of cooling. In hospitals that use MTH the technique is considered to be safe and inexpensive. More efforts are needed to promote this therapeutic option and hypothermia since MTH has now been included into European advanced cardiovascular life support protocols.     

Out-of-hospital CPR: better outcome for our patients

Out-of-hospital cardiac arrest is a leading cause of death in developed countries and early resuscitation attempts are crucial to improve survival rates and neurological outcome. Gräsner and colleagues performed an intriguing analysis on the combined approach of mild therapeutic hypothermia (MTH) and immediate percutaneous coronary intervention (PCI) for post-resuscitation care of 584 patients with out-of-hospital cardiac arrest from the German Resuscitation Registry. PCI was independently associated with good neurological outcome at hospital discharge after successful resuscitation, and MTH was associated as an independent factor with increased chance of 24-hour survival. Moreover, a binary logistic regression analysis did not show statistical significance for MTH, in addition to PCI, as an independent predictor for good neurological outcome. The present study supports the evidence that post-resuscitation care based on standardized protocols is beneficial after successful resuscitation. Further prospective and randomized studies are warranted to elucidate criteria for a better selection of candidates for those strategies and to evaluate the potential, in terms of neurological outcome at hospital discharge, of a prehospital cooling strategy in patients who cannot be referred to immediate PCI.     

In-hospital cardiac arrest: incidence,prognosis and possible measures to improve survival

Design Review. Objective Medical literature on in-hospital cardiac arrest (IHCA) was reviewed to summarise: (a) the incidence of and survival after IHCA, (b) major prognostic factors, (c) possible interventions to improve survival. Results and conclusions The incidence of IHCA is rarely reported in the literature. Values range between 1 and 5 events per 1,000 hospital admissions, or 0.175 events/bed annually. Reported survival to hospital discharge varies from 0% to 42%, the most common range being between 15% and 20%. Pre-arrest prognostic factors: the prognostic value of age is controversial. Among comorbidities, sepsis, cancer, renal failure and homebound lifestyle are significantly associated with poor survival. However, pre-arrest morbidity scores have not yet been prospectively validated as instruments to predict failure to survive after IHCA. Intra-arrest factors: ventricular fibrillation/ventricular tachycardia (VF/VT) as the first recorded rhythm and a shorter interval between IHCA and cardiopulmonary resuscitation or defibrillation are associated with higher survival. However, VF/VT is present in only 25–35% of IHCAs. Short-term survival is also higher in patients resuscitated with chest compression rates above 80/min. Interventions likely to improve survival include: early recognition and stabilisation of patients at risk of IHCA to enable prevention, faster and better in-hospital resuscitation and early defibrillation. Mild therapeutic hypothermia is effective as post-arrest treatment of out-of-hospital cardiac arrest due to VF/VT, but its benefit after IHCA and after cardiac arrest with non-VF/VT rhythms has not been clearly demonstrated.