Post-cardiac Arrest Treatment Research Articles

Post Resuscitation Care

After successful resuscitation, further treatment has a decisive influence regarding patient outcome. Not only overall survival, but also the neurological outcome that is crucial for patients' quality of life can be positively influenced by optimized post-cardiac arrest treatment. The management of various consequences of post-cardiac arrest syndrome is discussed in the current version of the ERC-guidelines in the chapter "post resuscitation care". A step-by-step approach based on an algorithm provides the necessary structure. The immediate treatment and stabilization of patients after ROSC is followed by the diagnosis of the triggering pathology in order to initiate adequate therapy. During the subsequent intensive care treatment, the focus is on optimizing neurological recovery.

Association between post-cardiac arrest treatments and clinical outcomes according to scene time interval in out-of-hospital cardiac arrest: Retrospective cross-sectional study

BackgroundPrevious studies have reported that Post-Cardiac arrest (PCA) treatments including targeted temperature management (TTM), coronary reperfusion therapy (CRT), and extracorporeal membrane oxygenation (ECMO) are time-sensitive; however, there are no reports of the clinical outcomes of PCA treatment according to the scene time interval (STI). Our study aimed to investigated the clinical outcomes of PCA treatment according to the STI. MethodsWe used a Korean nationwide OHCA cohort database from January 2017 to December 2020. The inclusion criteria were all adult OHCA patients with a presumed cardiac etiology, bystander-witnessed arrest, and prehospital return of spontaneous circulation (ROSC). The outcomes were survival to discharge and good neurological recovery. The main exposure of interest was PCA treatment. We compared the outcomes using multivariable logistic regression, and interaction terms were included in the final model to assess whether the STI modified the effect of PCA treatment on clinical outcomes of OHCA. ResultsTTM and CRT were associated with high survival to discharge and good neurological recovery. In the interaction analysis, ECMO had an interaction effect with the STI on a good CPC among patients with OHCA [short STI (0 to 11 min) (1.16 (0.77—1.75)), middle STI (12 to 15 min) (0.66 (0.41—1.06)), and long STI (16 to 30 min) (0.59 (0.40—0.88)) (p for interaction <0.05)]. ConclusionIn adult bystander-witnessed patients with OHCA with prehospital ROSC, an STI of >16 min was a risk factor for poor neurological outcome in those patients who underwent ECMO.

Targeted Temperature Management After Cardiac Arrest: A Systematic Review.

Targeted temperature management (TTM) has been the cornerstone of post-cardiac arrest care, but even after therapy, neurological outcomes remain poor. We performed a systematic review to evaluate the influence of TTM in post-cardiac arrest treatment, its effect on the neurological outcome, survival, and the adverse events associated with it. We also aimed to examine any difference between the effect of therapy at various intensities and durations on the prognosis of the patient.A search of two databases was done to find relevant studies, followed by a thorough screening in which the inclusion and exclusion criteria were applied, and a quality appraisal of clinical trials was done. In this systematic review, six randomized clinical trials with a total of 3870 participants were examined. Of these, 2,767 participants were treated with targeted hypothermia to varying degrees (between 31 and 36 degrees Celsius), 931 participants were treated with targeted normothermia (36.5 to 37.5 degrees Celsius), and 172 participants were treated with only normothermia (without any active cooling or interventions).It was concluded that TTM at a lower temperature did not have any benefit regarding the neurological outcome and mortality over targeted normothermia but was superior to no temperature management. TTM was also found to have significantly more negative effects when the intensity or duration was increased.

Repolarization and ventricular arrhythmia during targeted temperature management post cardiac arrest

BackgroundTargeted temperature management (TTM) following out-of-hospital cardiac arrest (OHCA) prolongs the QT-interval but our knowledge of different temperatures and risk of arrhythmia is incomplete. ObjectiveTo assess whether the QTc, QT-peak (QTp) and T-peak to T-end interval (TpTe) may be useful markers of ventricular arrhythmia in contemporary post cardiac arrest treatment. MethodsAn ECG-substudy of the TTM-trial (TTM at 33 °C vs. 36 °C) with serial ECGs from 680 (94%) patients. Bazett’s (B) and Fridericia’s (F) formula were used for heart rate correction of the QT, QTp and TpTe. Ventricular arrhythmia (VT/VF) were registered during the first three days of post cardiac arrest care. ResultsThe QT, QTc and QTp intervals were prolonged more at 33 °C compared to 36 °C and restored to similar and lower levels after rewarming. The TpTe-interval remained between 92–100 ms throughout TTM in both groups.The QTc intervals were associated with ventricular arrhythmia, but not after adjustment for cardiac arrest characteristics. The QTp-interval was not associated with risk of ventricular arrhythmia. Heart rate corrected TpTe-intervals were associated with higher risk of arrhythmia (Odds ratio (OR): TpTe(B): 1.12 (1.02–1.23, p = 0.01 TpTe(F): 1.12 (1.02–1.23, p = 0.02) per 20 ms). Further a prolonged TpTe-interval ≥ 90 ms was consistently associated with higher risk (ORadjusted: TpTe(B): 2.05 (1.25–3.37), p < 0.01, TpTe(F): 2.14 (1.32–3.49), p < 0.01). ConclusionsTTM prolongs the QT-interval by prolongation of the QTp-interval without association to increased risk. The TpTe-interval is not significantly affected by core temperature, but heart rate corrected TpTe intervals are robustly associated with risk of ventricular arrhythmia. Trial registrationThe TTM-trial is registered and accessible at ClinicalTrials.gov (Identifier: NCT01020916).

Immediate postcardiac arrest treatment: coronary catherization or not?

Early coronary angiogram (CAG) remains a cornerstone in postcardiac arrest management as coronary disease (CAD)-related cardiac arrest is the leading cause of sudden death in adults. The opportunity to treat the cause early on with immediate CAG may improve outcome in cardiac arrest patients with AMI. Identifying the patients who will benefit from such an early invasive strategy is an unanswered question. Recent and ongoing trials may improve the level of evidence on this problematic, especially for some subgroup; however, current guidelines remain founded upon a very heterogeneous level of evidence. The key variable to argue for immediate CAD remains the pattern of the ECG monitored after return of spontaneous of circulation (ROSC). ST-segment elevation (STE) on postresuscitation ECG is the strongest argument to rule for an early CAG strategy. In other situations, identifying the best candidates for early CAG is very challenging. Different approaches including elements, such as circumstances of cardiac arrest and expected outcomes. may also drive the strategy. This review aims to provide an overview of these different discussion points. The indication for early CAG should rely on multiple factors and an individual approach.

The role of age in post-cardiac arrest therapy in an elderly patient population.

We investigated the effect of age on post-cardiac arrest treatment outcomes in an elderly population, based on a local database and a systemic review of the literature. Data were collected retrospectively from medical charts and reports. Sixty-one comatose patients, cooled to 32-34 °C for 24 h, were categorized into three groups: younger group (≤65 years), older group (66-75 years), and very old group (>75 years). Circumstances of cardiopulmonary resuscitation (CPR), patients' characteristics, post-resuscitation treatment, hemodynamic monitoring, neurologic outcome and survival were compared across age groups. Kruskal-Wallis test, Chi-square test and binary logistic regression (BLR) were applied. In addition, a literature search of PubMed/Medline database was performed to provide a background. Age was significantly associated with having a cardiac arrest on a monitor and a history of hypertension. No association was found between age and survival or neurologic outcome. Age did not affect hemodynamic parameter changes during target temperature management (TTM), except mean arterial pressure (MAP). Need of catecholamine administration was the highest among very old patients. During the literature review, seven papers were identified. Most studies had a retrospective design and investigated interventions and outcome, but lacked unified age categorization. All studies reported worse survival in the elderly, although old survivors showed a favorable neurologic outcome in most of the cases. There is no evidence to support the limitation of post-cardiac arrest therapy in the aging population. Furthermore, additional prospective studies are needed to investigate the characteristics and outcome of post-cardiac arrest therapy in this patient group.

Targeted Temperature Management for Improved Outcomes: Are We There Yet?

Therapeutic hypothermia, also referred to as targeted temperature management, has been a component of the postcardiac arrest treatment guidelines since 2010. Although almost a decade has passed since its inclusion in the postarrest guidelines, many unanswered questions remain regarding selection of the appropriate patient population, optimal target temperature, ideal window of time in which to initiate therapy after arrest, most efficient, safe, and accurate equipment choice for inducing and maintaining hypothermia, most effective duration of treatment, and rate of cooling or rewarming. On a national and international level, critical care nurses are in a unique position to participate in research that will define targeted temperature management protocols and practices. Nurses are also ideal for standardizing the targeted temperature management policy and protocol locally and nationally based on current available evidence. This review aims to serve 2 purposes: first, to provide a broad update on the current clarifications and limitations per research findings on target temperature management therapy; second, to explain how critical care nurses can use this updated information to improve outcomes for their patients with cardiac arrest.

Intranasal post-cardiac arrest treatment with orexin-A facilitates arousal from coma and ameliorates neuroinflammation.

Cardiac arrest (CA) entails significant risks of coma resulting in poor neurological and behavioral outcomes after resuscitation. Significant subsequent morbidity and mortality in post-CA patients are largely due to the cerebral and cardiac dysfunction that accompanies prolonged whole-body ischemia post-CA syndrome (PCAS). PCAS results in strong inflammatory responses including neuroinflammation response leading to poor outcome. Currently, there are no proven neuroprotective therapies to improve post-CA outcomes apart from therapeutic hypothermia. Furthermore, there are no acceptable approaches to promote cortical or cognitive arousal following successful return of spontaneous circulation (ROSC). Hypothalamic orexinergic pathway is responsible for arousal and it is negatively affected by neuroinflammation. However, whether activation of the orexinergic pathway can curtail neuroinflammation is unknown. We hypothesize that targeting the orexinergic pathway via intranasal orexin-A (ORXA) treatment will enhance arousal from coma and decrease the production of proinflammatory cytokines resulting in improved functional outcome after resuscitation. We used a highly validated CA rat model to determine the effects of intranasal ORXA treatment 30-minute post resuscitation. At 4hrs post-CA, the mRNA levels of proinflammatory markers (IL1β, iNOS, TNF-α, GFAP, CD11b) and orexin receptors (ORX1R and ORX2R) were examined in different brain regions. CA dramatically increased proinflammatory markers in all brain regions particularly in the prefrontal cortex, hippocampus and hypothalamus. Post-CA intranasal ORXA treatment significantly ameliorated the CA-induced neuroinflammatory markers in the hypothalamus. ORXA administration increased production of orexin receptors (ORX1R and ORX2R) particularly in hypothalamus. In addition, ORXA also resulted in early arousal as measured by quantitative electroencephalogram (EEG) markers, and recovery of the associated behavioral neurologic deficit scale score (NDS). Our results indicate that intranasal delivery of ORXA post-CA has an anti-inflammatory effect and accelerates cortical EEG and behavioral recovery. Beneficial outcomes from intranasal ORXA treatment lay the groundwork for therapeutic clinical approach to treating post-CA coma.

Identifying Important Gaps in Randomized Controlled Trials of Adult Cardiac Arrest Treatments: A Systematic Review of the Published Literature.

Cardiac arrest is a major public health concern worldwide. The extent and types of randomized controlled trials (RCT)-our most reliable source of clinical evidence-conducted in these high-risk patients over recent years are largely unknown. We performed a systematic review, identifying all RCTs published in PubMed, EMBASE, Scopus, Web of Science, and the Cochrane Library from 1995 to 2014 that focused on the acute treatment of nontraumatic cardiac arrest in adults. We then extracted data on the setting of study populations, types and timing of interventions studied, risk of bias, outcomes reported, and how these factors have changed over time. Over this 20-year period, 92 RCTs were published containing 64 309 patients (median, 225.5 per trial). Of these, 81 RCTs (88.0%) involved out-of-hospital cardiac arrest, whereas 4 (4.3%) involved in-hospital cardiac arrest and 7 (7.6%) included both. Eighteen RCTs (19.6%) were performed in the United States, 68 (73.9%) were performed outside the United States, and 6 (6.5%) were performed in both settings. Thirty-eight RCTs (41.3%) evaluated drug therapy, 39 (42.4%) evaluated device therapy, and 15 (16.3%) evaluated protocol improvements. Seventy-four RCTs (80.4%) examined interventions during the cardiac arrest, 15 (16.3%) examined post cardiac arrest treatment, and 3 (3.3%) studied both. Overall, reporting of the risk of bias was limited. The most common outcome reported was return of spontaneous circulation: 86 (93.5%) with only 22 (23.9%) reporting survival beyond 6 months. Fifty-three RCTs (57.6%) reported global ordinal outcomes, whereas 15 (16.3%) reported quality-of-life. RCTs in the past 5 years were more likely to be focused on protocol improvements and postcardiac arrest care. Important gaps in RCTs of cardiac arrest treatments exist, especially those examining in-hospital cardiac arrest, protocol improvement, postcardiac arrest care, and long-term or quality-of-life outcomes.

Admission of out-of-hospital cardiac arrest victims to a high volume cardiac arrest center is linked to improved outcome

AimCardiac arrest centers have been associated with improved outcome for patients after cardiac arrest. Aim of this study was to investigate the effect on outcome depending on admission to high-, medium- or low volume centers. MethodsAnalysis from a prospective, multicenter registry for out of hospital cardiac arrest patients treated by the emergency medical service of Vienna, Austria. The frequency of cardiac arrest patients admitted per center/year (low <50; medium 50–100; high >100) was correlated to favorable outcome (30-day survival with cerebral performance category of 1 or 2). ResultsOut of 2238 patients (years 2013–2015) with emergency medical service resuscitation, 861 (32% female, age 64 (51;73) years) were admitted to 7 different centers. Favorable outcome was achieved in 267 patients (31%). Survivors were younger (58 vs. 66 years; p<0.001), showed shockable initial heart rhythm more frequently (72 vs. 35%; p<0.001), had shorter CPR durations (22 vs. 29min; p<0.001) and were more likely to be treated in a high frequency center (OR 1.6; CI: 1.2–2.1; p=0.001).In multivariate analysis, age below 65 years (OR 15; CI: 3.3–271.4; p=0.001), shockable initial heart rhythm (OR 10.1; CI: 2.4–42.6; p=0.002), immediate bystander or emergency medical service CPR (OR 11.2; CI: 1.4–93.3; p=0.025) and admission to a center with a frequency of >100 OHCA patients/year (OR 5.2; CI: 1.2–21.7; p=0.025) was associated with favorable outcome. ConclusionsHigh frequency of post-cardiac arrest treatment in a specialized center seems to be an independent predictor for favorable outcome in an unselected population of patients after out of hospital cardiac arrest.

PD98059 Protects Brain against Cells Death Resulting from ROS/ERK Activation in a Cardiac Arrest Rat Model.

The clinical and experimental postcardiac arrest treatment has not reached therapeutic success. The present study investigated the effect of PD98059 (PD) in rats subjected to cardiac arrest (CA)/cardiopulmonary resuscitation (CPR). Experimental rats were divided randomly into 3 groups: sham, CA, and PD. The rats except for sham group were subjected to CA for 5 min followed by CPR operation. Once spontaneous circulation was restored, saline and PD were injected in CA and PD groups, respectively. The survival rates and neurologic deficit scores (NDS) were observed, and the following indices of brain tissue were evaluated: ROS, MDA, SOD, p-ERK1/2/ERK1/2, caspase-3, Bax, Bcl-2, TUNEL positive cells, and double fluorescent staining of p-ERK/TUNEL. Our results indicated that PD treatment significantly reduced apoptotic neurons and improved the survival rates and NDS. Moreover, PD markedly downregulated the ROS, MDA, p-ERK, and caspase-3, Bax and upregulated SOD and Bcl-2 levels. Double staining p-ERK/TUNEL in choroid plexus and cortex showed that cell death is dependent on ERK activation. The findings in present study demonstrated that PD provides neuroprotection via antioxidant activity and antiapoptosis in rats subjected to CA/CPR.

Abstract 17637: Combination Therapy With Hypothermic Target Temperature Management and Valproic Acid After Cardiac Arrest

Introduction: While hypothermic target temperature management (HTTM) has been regarded as a reliable strategy for post-cardiac arrest treatment, there are no pharmacologic agents proved to be neuroprotective against post-cardiac arrest brain injury. In recent years, many studies have shown that valproic acid (VPA), a well-known antiepileptic drug, is neuroprotective against various brain insults. VPA inhibits histone deacetylase activity and causes hyperacetylation of histones, followed by transcriptional activation of anti-apoptotic genes. In this study we tested the hypothesis that combination therapy of hypothermia and VPA could enhance neuroprotection and improve outcome. Methods: Male Long-Evans rats were instrumented for continuous telemetric EEG recording with video and then subjected to 8-minute asphyxia cardiac arrest. Nine rats that achieved the return of spontaneous circulation (ROSC) were allocated into the following 3 groups. Controlled normothermia (N group, 36.5-37.5 °C, n=3), HTTM (H group, 32-33 °C for 24 hours, n=3) and HTTM with VPA administration (HV group, 32-33 °C for 24 hours, 300 mg/kg, IV, n=3). Three-day survival, best achieved neurologic function score (NFS), the number of seizure event was compared between the 3 groups. Results: The 3-day survival was 33.3% in N group, 33.3 % in H group and 100 % in HV group (p=0.12). The best NFS averaged 263.33 ± 36.67 in N group, 380 ± 64.29 in H group and 468.33 ± 15.90 in HV group (p=0.13). The total number of seizure events in each group averaged 0.33 ± 0.33 in N group, 4.33 ± 2.96 in H group, 0 in HV group (p=0.20). Conclusions: These early results suggest that the combination of HTTM and VPA is a promising strategy that could result in synergistic neuroprotection after cardiac arrest.

Targeted temperature management: a health economic perspective

More and more limited financial resources in the health care sector call for an economic evaluation of potential new therapies. The economic evaluation of a new therapy is complex and depends not only on the perspective of the various stakeholders, but also on the country-specific characteristics of various reimbursement systems. From the patient perspective, the costs for new therapies might not be a concern, as long as the insurance system covers the costs. From the hospital perspective, a new therapy which reduces the length of stay might be worthwhile in a DRG-based reimbursement system, but not in a pay-per-patient-day reimbursement system. To respect the perspective of the society, a cost-effectiveness analysis could be expressed in terms of a ratio where the denominator is a gain in quality-adjusted life years (QALY) and the numerator is the cost associated with the health gain. QALY is a measure of disease burden and takes into account the quality of life measured as the Health Utility Index (HUI, dead = 0 and perfect health = 1) and quantity of life lived measured as survival time: QALY = survival time × HUI (for example, 4 years survival with HUI 0.5 = 2 QALY, or 2 years survival with HUI 1 = 2 QALY). Previous studies reported that mild therapeutic hypothermia improves neurologic recovery and survival in patients resuscitated from cardiac arrest. The estimated number needed to treat is only six patients; nevertheless, target temperature management has hardly been implemented in post-cardiac arrest treatment. The aim of the current study was to evaluate the cost-effectiveness of therapeutic hypothermia in post-cardiac arrest patients. The QALY–cost ratio was chosen as the primary outcome. To assess the cost-effectiveness of temperature management, data from a Cochrane review about mild hypothermia after cardiac arrest including 398 patients were analyzed. The QALY–cost ratio was calculated based on the cerebral performance score and total treatment costs after cardiac arrest. The assumed costs included potential cooling procedure, hospital stay, rehabilitation, and potential defibrillation implantation in Austria. Total treatment costs per 100 patients were €4.1 million for patients treated with mild hypothermia, and €3.7 million for patients with standard care. Post-arrest patients receiving mild hypothermia gained an average of 1.11 QALY compared with conventional care. This resulted in a cost-effectiveness ratio of €3.827 per QALY. Targeted temperature management at 32 to 34°C after cardiac arrest seems to be a very cost-effective treatment, with €3.827 per QALY far below commonly used benchmarks for assessing the cost-effectiveness of an intervention. These results may provide an economic rationale for implementing targeted temperature management as a standard treatment after cardiac arrest.

TTM 2.0

The professional treatment of the reperfusion syndrome following cardiac arrest and successful resuscitation has improved over the past decade. In 2002 and 2003 mild hypothermia treatment was first recommended by international guidelines following remarkable milestone trials. With growing experience and an increasing number of hospitals implementing hypothermia as standard treatment, technical devices also improved to enhance patient safety. The term target temperature management (TTM) has been introduced by several societies indicating that cooling down is not enough [1]. We are supposed to manage temperature therapy as part of a package of interventions after cardiac arrest [2,3]. As intracranial pressure can correlate with brain and body temperature, modern TTM is about precision although the optimal target temperature is still unknown. This has been shown by the current TTM Trial by Nielsen and colleagues comparing 33°C and 36°C as different target levels without a significant difference in outcome variables [4]. As these results have been criticized in several points, the conclusion can only be that obviously different patient characteristics need a more individual TTM following cardiac arrest. As stated, TTM 2.0 indicates we have reached the next step that includes professional TTM in a large bundle of therapy steps such as early coronary intervention, close monitoring of supportive care and precise neurological prognostication. The way to go is still long as TTM is still underused worldwide [5,6]. If TTM would be seen as a medication or drug, it should be adjusted or dosed depending on the severity of the disease or hypoxic brain damage. Especially, a moderate reperfusion injury will respond and benefit from a medication like TTM compared with a severe and long-lasting hypoxia leading to death despite any therapy. Therefore, a key in the near future will be the early grading of the hypoxic brain damage by a combination of clinical data, biomarkers, advanced neurological monitoring and radiological findings. This might lead to a more personalized and adjusted post-cardiac arrest treatment.

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.

Serial Plasma Choline Measurements after Cardiac Arrest in Patients Undergoing Mild Therapeutic Hypothermia: A Prospective Observational Pilot Trial

ObjectiveCholine is related to phospholipid metabolism and is a marker for global ischaemia with a small reference range in healthy volunteers. The aim of our study was to characterize the early kinetics of plasma free choline in patients after cardiac arrest. Additionally, we investigated the potential of plasma free choline to predict neurological outcome.MethodsTwenty patients admitted to our medical intensive care unit were included in this prospective, observational trial. All patients were enrolled between May 2010 and May 2011. They received post cardiac arrest treatment including mild therapeutic hypothermia which was initiated with a combination of cold fluid and a feedback surface cooling device according to current guidelines. Sixteen blood samples per patient were analysed for plasma free choline levels within the first week after resuscitation. Choline was detected by liquid chromatography-tandem mass spectrometry.ResultsMost patients showed elevated choline levels on admission (median 14.8 µmol/L; interquartile range; IQR 9.9-20.1) which subsequently decreased. 48 hours after cardiac arrest choline levels in all patients reached subnormal levels at a median of 4.0 µmol/L (IQR 3-4.9; p = 0.001). Subsequently, choline levels normalized within seven days. There was no significant difference in choline levels when groups were analyzed in relation to neurological outcome.ConclusionsOur data indicate a choline deficiency in the early postresucitation phase. This could potentially result in impaired cell membrane recovery. The detailed characterization of the early choline time course may aid in planning of choline supplementation trials. In a limited number of patients, choline was not promising as a biomarker for outcome prediction.

Abstracts from the 3rd Annual Therapeutic Hypothermia and Temperature Management ConferenceMarch 4–5, 2013Miami, FL

Abstracts from the 3rd Annual Therapeutic Hypothermia and Temperature Management ConferenceMarch 4–5, 2013Miami, FL

In-hospital hypothermia

Mild therapeutic hypothermia after cardiac arrest has become standard in post-resuscitation care in many hospitals as it is recommended by current guidelines. The last update of guidelines by the European Resuscitation Council on post-cardiac arrest treatment in 2010 recommends hypothermia for every patient after cardiac arrest who remains unconscious after cardiac arrest [1]. In addition to milestone trials [2-4], current published retrospective data from the large Finnish registry showed in a large group of patients a significant reduction of hospital mortality of survivors of out-of-hospital cardiac arrest after implementation of hypothermia [5]. The mild therapeutic hypothermia procedure after cardiac arrest can be divided into three phases: introduction, maintenance and rewarming. The cooling techniques and devices to induce cooling of the cardiac arrest survivor can be separated into three main groups: conventional cooling (no device), non-invasive (surface) systems, and invasive (intravascular) systems (Table ​(Table11). Table 1 Cooling techniques Conventional cooling methods The easiest way to induce hypothermia after cardiac arrest is by using cold saline (for example, 0.9% NaCl solution), crushed ice or ice bags. Kim and colleagues reported the safety and efficacy of the administration of up to 2 litres of 4°C cold saline to the patient after hospital admission [6]. Others published data using 30 ml/kg body weight of saline 0.9% NaCl or Ringer's lactate combined sometimes with ice bags, which led to an acceptable reduction of the temperature [7-10]. Furthermore cold saline as well as other methods like cooling caps and helmets have been evaluated for induction mainly in the preclinical setting [4,11,12]. Kliegel and colleagues pointed out that cold infusion alone is effective for induction but not for tight maintenance of the target temperature [13]. However, in at least one trial the combination of cold saline and ice packs was proven to be effective even to maintain temperature [7]. Focusing on the induction in the in-hospital setting, most authors rank cold saline and crushed ice more as effective adjuvant methods to be combined with a computer-controlled cooling device [10]. The big advantage of cold saline is its availability at almost every place in the hospital if provided and the low costs. Following the data available concerning different amounts of saline administered to the patient, a median amount of 1 to 2 litres of saline seems safe after cardiac arrest. To maintain target temperature with cold saline and ice bags seems to require a high binding of personnel method without a very precise influence on the central body temperature.

Advances in post-resuscitation care

#### Key points It is now widely recognised that interventions applied after return of spontaneous circulation (ROSC) impact significantly on the quality of survival, and there is considerable variation in post-cardiac arrest treatment and patient outcome between hospitals.[1][1] This review

Abstract 68: Trends in Postresuscitation Care: A 7-Year Experience After Implementation of Therapeutic Hypothermia

Background: The 2010 AHA guidelines for CPR emphasize the crucial importance of patient care in the early post-resuscitation period. In particular, therapeutic hypothermia and adequate treatment of the post-cardiac arrest syndrome are of utmost importance. Methods: In a single center retrospective registry analysis, the data from all resuscitated patients treated in the cardiology ICU between 2003 and 2009 were evaluated systematically. All data on hemodynamics, respiration, hypothermia, diagnostic and therapeutic procedures and outcome were analyzed. Results: 436 consecutive post-cardiac arrest patients were included. The proportion of patients treated with mild hypothermia could be increased from 56% (2003) to &gt;80% (2006-2009). &gt;90% of the patients with out-of-hospital arrest (OHA) were cooled. Induction of therapeutic hypothermia could be accelerated significantly (time to &lt;34°C, 2003: 13h 59min, 2005: 6h 30min, 2009: 2:15min). The frequency of using cold infusions and intravascular cooling devices correlated directly with the velocity of cooling induction. The PaO2/FiO2 ratio on arrival at the ICU was 242±23 indicating an acute lung injury (ALI). The comparison of cooled and uncooled patients showed no significant differences in the parameters of respiration (in spite of significantly greater fluid intake in the hypothermia group). However, the cooled patients were significantly longer intubated than the uncooled patients (7.0±0.9 vs. 3.7±1.5 days). In patients treated with hypothermia the LVEF improved significantly from 35.4±0.7% at admission to 40.1±1.1% at hospital discharge. In contrast, in patients not treated with hypothermia there was no significant increase in LVEF. In-hospital mortality was 43%. Despite improvement in cooling measures, there was no significant improvement in the survival rates between 2003 and 2009. Conclusion: This registry provides an overview of trends in post-cardiac arrest treatment. By optimizing the post-resuscitation care cooling induction can be accelerated. An acute lung injury is part of the post cardiac arrest syndrome. Hypothermia might improve LVEF recovery in patients with post cardiac arrest syndrome.