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The critical care management of patients after cardiac arrest is burdened by a lack of high-quality clinical studies and the resultant lack of high-certainty evidence. This results in limited practice guideline recommendations, which may lead to uncertainty and variability in management. Critical care management is crucial in patients after cardiac arrest and affects outcome. Although guidelines address some relevant topics (including temperature control and neurological prognostication of comatose survivors, 2 topics for which there are more robust clinical studies), many important subject areas have limited or nonexistent clinical studies, leading to the absence of guidelines or low-certainty evidence. The American Heart Association Emergency Cardiovascular Care Committee and the Neurocritical Care Society collaborated to address this gap by organizing an expert consensus panel and conference. Twenty-four experienced practitioners (including physicians, nurses, pharmacists, and a respiratory therapist) from multiple medical specialties, levels, institutions, and countries made up the panel. Topics were identified and prioritized by the panel and arranged by organ system to facilitate discussion, debate, and consensus building. Statements related to postarrest management were generated, and 80% agreement was required to approve a statement. Voting was anonymous and web based. Topics addressed include neurological, cardiac, pulmonary, hematological, infectious, gastrointestinal, endocrine, and general critical care management. Areas of uncertainty, areas for which no consensus was reached, and future research directions are also included. Until high-quality studies that inform practice guidelines in these areas are available, the expert panel consensus statements that are provided can advise clinicians on the critical care management of patients after cardiac arrest., (© 2023. The Author(s).)

Purpose: To investigate the effects of the selective NLRP3 inflammasome inhibitor MCC950 on post-resuscitation myocardial function and survival in a rat model of cardiopulmonary resuscitation (CPR)., Methods: Thirty-six Sprague Dawley rats were randomized into three groups: (1) MCC950, (2) control, and (3) sham. Each group consisted of a 6 h non-survival subgroup (n = 6) and a 48 h survival subgroup (n = 6). Ventricular fibrillation (VF) was induced and untreated for 6 min. CPR was initiated and continued for 8 min. Resuscitation was attempted with a 4 J defibrillation. MCC950 (10 mg/kg) or vehicle was administered via intraperitoneal injection immediately after the return of spontaneous circulation (ROSC). Myocardial function and sublingual microcirculation were measured after ROSC in the non-survival subgroups. Plasma levels of interleukin Iβ (IL-1β) and cardiac troponin I (cTnI) were measured at baseline and 6 h in the non-survival subgroups. Heart tissue was harvested to measure the NLRP3 inflammasome constituents, including NLRP3, apoptosis-associated speck-like protein (ASC), Caspase-1, and IL-1β. Survival duration and neurologic deficit score (NDS) were recorded and evaluated among survival groups., Results: Post-resuscitation myocardial function and sublingual microcirculation were improved in MCC950 compared with control (p < 0.05). IL-1β and cTnI were decreased in MCC950 compared to control (p < 0.01). The MCC950 treated groups showed significantly reduced ASC, caspase-1, and IL-1β compared with the control group (p < 0.05). Survival at 48 h after ROSC was greater in MCC950 (p < 0.05) with improved NDS (p < 0.05)., Conclusion: Administration of MCC950 following ROSC mitigates post-resuscitation myocardial dysfunction and improves survival., (© 2021. The Author(s).)

Abstract: Aims: A rapid heart rate (HR) that occurs after cardiopulmonary resuscitation (CPR) is a short-term compensatory mechanism preserving cardiac output. However, if of long duration, it is unfavorable for myocardial function postresuscitation because of disrupted balance between myocardial oxygen supply and demand. This raises the assumption that such a sustained fast HR should be regulated. The present study aimed to investigate the follow-on effect of ivabradine (a specific inhibitor of the I f current of the sinoatrial node)-induced HR reduction (HRR) on postresuscitation myocardial function in a rat model of CPR. Methods and results: Six minutes of ventricular fibrillation and 8 min of CPR were performed on Sprague-Dawley rats. All 32 resuscitated animals were then randomized into saline and ivabradine groups, each group having nonsurvival and survival subgroups (n = 8 each). Saline or ivabradine (0.5 mL/kg) was administered at 1 h postresuscitation. Heart rate, myocardial function as expressed by cardiac output, ejection fraction, and myocardial performance index were assessed at baseline and hourly from 1 to 5 h postresuscitation. Heart rate variability was analyzed at baseline and at 1, 3, and 5 h postresuscitation. Serum epinephrine and cardiac troponin I at baseline and at 1, 3, and 5 h postresuscitation in nonsurvival subgroup were measured. Survival duration in the survival subgroup was observed. The baseline HR was approximately 390 beats/min (bpm). After resuscitation, an average increase of Δ ≈ +15 bpm (relative ratio ≈ +3.8%) with a resultant HR of 405 bpm lasting more than 5 h occurred. Ivabradine group achieved a steady HRR of Δ ≈ -30 bpm (relative ratio ≈ -7.4%) as compared with saline group ( P < 0.01). Postresuscitation myocardial function was significantly worse in the ivabradine group (all P < 0.01). Heart rate variability was significantly impaired in the ivabradine group (all P < 0.05). Serum cardiac troponin I and epinephrine concentration were significantly higher in the ivabradine group (all P < ?0.01). Survival duration was significantly shortened in the ivabradine group as compared with the saline group (388 vs. 526 min, P < ?0.01). Conclusions: Ivabradine-induced HRR increases the severity of postresuscitation myocardial dysfunction and shortens survival duration in a rat model of CPR., Competing Interests: The authors report no conflicts of interest., (Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American College of Sports Medicine.)

The systemic inflammatory response following global myocardial ischemia/reperfusion (I/R) injury is a critical driver of poor outcomes. Both pyroptosis and necroptosis are involved in the systemic inflammatory response and contribute to regional myocardial I/R injury. This study aimed to explore the effect of necrosulfonamide (NSA) on post-resuscitation myocardial dysfunction in a rat model of cardiac arrest. Sprague-Dawley rats were randomly categorized to Sham, CPR and CPR-NSA groups. For rats in the latter two groups, ventricular fibrillation was induced without treatment for 6 min, with cardiopulmonary resuscitation (CPR) being sustained for 8 min. Rats were injected with NSA (10 mg/kg in DMSO) or vehicle at 5 min following return of spontaneous circulation. Myocardial function was measured by echocardiography, survival and neurological deficit score (NDS) were recorded at 24, 48, and 72 h after ROSC. Western blotting was used to assess pyroptosis- and necroptosis-related protein expression. ELISAs were used to measure levels of inflammatory cytokine. Rats in the CPR-NSA group were found to exhibit superior post-resuscitation myocardial function, and better NDS values in the group of CPR-NSA. Rats in the group of CPR-NSA exhibited median survival duration of 68 ± 8 h as compared to 34 ± 21 h in the CPR group. After treatment with NSA, NOD-like receptor 3 (NLRP3), GSDMD-N, phosphorylated-MLKL, and phosphorylated-RIP3 levels in cardiac tissue were reduced with corresponding reductions in inflammatory cytokine levels. Administration of NSA significantly improved myocardial dysfunction succeeding global myocardial I/R injury and enhanced survival outcomes through protective mechanisms potentially related to inhibition of pyroptosis and necroptosis pathways., (Copyright © 2022. Published by Elsevier B.V.)

Abstract: Blocking ferroptosis reduces ischemia-reperfusion injury in some pathological contexts. However, there is no evidence that ferroptosis contributes to post-resuscitation myocardial dysfunction (PRMD). Here, we evaluated the therapeutic performance of ferroptosis inhibitors (UAMC-3203 or/and Deferoxamine) on the PRMD in a rat model of cardiac arrest and surveyed the changes of essential ferroptosis markers in the myocardium. Remarkably, all treatments reduce the severity of cardiac dysfunction and microcirculation hypoperfusion after resuscitation compared with control. Consistently, we observe that the ferroptosis marker Glutathione peroxidase 4, 4-hydroxynonenal and non-heme iron altered (1 ± 0.060 vs. 0.021 ± 0.016, 1 ± 0.145 vs. 3.338 ± 0.221, 52.010 ± 3.587 ug/g vs. 70.500 ± 3.158 ug/g, all P < 0.05) in the myocardium after resuscitation. These changes were significantly suppressed by UAMC-3203 [(0.187 ± 0.043, 2.848 ± 0.169, all P < 0.05), (72.43 ± 4.920 ug/g, P  > 0.05)], or Deferoxamine (0.203 ± 0.025, 2.683 ± 0.273, 55.95 ± 2.497 ug/g, all P < 0.05). Briefly, UAMC-3203 or/and Deferoxamine improve post-resuscitation myocardial dysfunction and provide evidence of ferroptosis involvement, suggesting that ferroptosis inhibitors could potentially provide an innovative therapeutic approach for mitigating the myocardial damage caused by cardiopulmonary resuscitation., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Shock Society.)

Cardiac arrest (CA) remains a major public health issue. Inflammatory responses with overproduction of interleukin-1β regulated by NLRP3 inflammasome activation play a crucial role in cerebral ischemia/reperfusion injury. We investigated the effects of the selective NLRP3-inflammasome inhibitor MCC950 on post-resuscitation cerebral function and neurologic outcome in a rat model of cardiac arrest. Thirty-six male rats were randomized into the MCC950 group, the control group, or the sham group (N = 12 of each group). Each group was divided into a 6 h non-survival subgroup (N = 6) and a 24 h survival subgroup (N = 6). Ventricular fibrillation (VF) was electrically induced and untreated for 6 min, followed by 8 min of precordial compressions and mechanical ventilation. Resuscitation was attempted with a 4J defibrillation. Either MCC950 (10 mg/kg) or vehicle was injected intraperitoneally immediately after the return of spontaneous circulation (ROSC). Rats in the sham group underwent the same surgical procedures without VF and CPR. Brain edema, cerebral microcirculation, plasma interleukin Iβ (IL-1β), and neuron-specific enolase (NSE) concentration were measured at 6 h post-ROSC of non-survival subgroups, while 24 h survival rate, neurological deficits were measured at 24 h post-ROSC of survival subgroups. Post-resuscitation brain edema was significantly reduced in animals treated with MCC950 (p < 0.05). Cerebral perfused vessel density (PVD) and microcirculatory flow index (MFI) values were significantly higher in the MCC950 group compared with the control group (p < 0.05). The plasma concentrations of IL-1β and NSE were significantly decreased in animals treated with MCC950 compared with the control group (p < 0.05). 24 h-survival rate and neurological deficits score (NDS) was also significantly improved in the MCC950 group compared with the control group (p < 0.05). NLRP3 inflammasome blockade with MCC950 at ROSC reduces the circulatory level of IL-1β, preserves cerebral microcirculation, mitigates cerebral edema, improves the 24 h-survival rate, and neurological deficits., (Copyright © 2021. Published by Elsevier Masson SAS.)

Background: Several prospective studies have demonstrated that the echocardiographic detection of any myocardial activity during PEA is strongly associated with higher rates of return of spontaneous circulation (ROSC). We hypothesized that PEA represents a spectrum of disease in which not only the presence of myocardial activity, but more specifically that the degree of left ventricular (LV) function would be a predictor of outcomes. The purpose of this study was to retrospectively assess the association between LV function and outcomes in patients with OHCA., Materials and Methods: Using prospectively obtained data from an observational cohort of patients receiving focused echocardiography during cardiopulmonary resuscitation (CPR) in the Emergency Department (ED) setting, we analyzed 312 consecutive subjects with available echocardiography images with initial rhythm of PEA. We used left ventricular systolic fractional shortening (LVFS), a unidimensional echocardiographic parameter to perform the quantification of LV function during PEA. Regression analyses were performed independently to evaluate for relationships between LVFS and a primary outcome of ROSC and secondary outcome of survival to hospital admission. We analyzed LVFS both as a continuous variable and as a categorial variable using the quartiles and the median to perform multiple different comparisons and to illustrate the relationship of LVFS and outcomes of interest. We performed survival analysis using Cox proportional hazards model to evaluate the hazard corresponding to length of resuscitation., Results: We found a positive association between LVFS and the primary outcome of ROSC (OR 1.04, 95%CI 1.01-1.08), but not with the secondary outcome of survival to hospital admission (OR 1.02, 95%CI 0.96-1.08). Given that the relationship was not linear and that we observed a threshold effect in the relationship between LVFS and outcomes, we performed an analysis using quartiles of LVFS. The predicted probability of ROSC was 75% for LVFS between 23.4-96% (fourth quartile) compared to 47% for LVFS between 0-4.7% (first quartile). The hazard of not achieving ROSC was significantly greater for subjects with LVFS below the median (13.1%) compared to the subgroup with LVFS greater than 13.1% (p < 0.05), with the separation of the survival curves occurring at approximately 40 min of resuscitation duration., Conclusions: Left ventricular function measured by LVFS is positively correlated with higher probability of ROSC and may be associated with higher chances of survival in patients with PEA arrest., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Brain mitochondria are more sensitive to global ischemia compared to heart mitochondria. Complex I in the electron transport chain (ETC) is sensitive to ischemic injury and is a major control point of the rate of ADP stimulated oxygen consumption. The purpose of this study was to explore whether changes in cerebral and myocardial mitochondria differ after cardiac arrest. Animals were randomized into 4 groups (n = 6): 1) Sham 2) VF 3) VF+CPR 4) ROSC 1hr. Ventricular Fibrillation (VF) was induced through a guide wire advanced from the right jugular vein into the ventricle and untreated for 8 min. Resuscitation was attempted with a 4J defibrillation after 8 min of cardiopulmonary resuscitation (CPR). Brain mitochondria and cardiac mitochondrial subpopulations were isolated. Calcium retention capacity was measured to assess susceptibility to mitochondrial permeability transition pore opening. ADP stimulated oxygen consumption and ETC activity assays were performed. Brain mitochondria are far more sensitive to injury during cardiac arrest and resuscitation compared to cardiac mitochondria. Complex I is highly sensitive to injury in brain mitochondria. With markedly decreased calcium retention capacity, mitochondria contribute to cerebral reperfusion injury. Therapeutic preservation of cerebral mitochondrial activity and mitochondrial function during cardiac arrest may improve post-resuscitation neurologic function., (Published by Elsevier Masson SAS.)

Out-of-hospital cardiac arrest (CA) is a leading cause of death in the United States. Severe post-resuscitation cerebral dysfunction is a primary cause of poor outcome. Therefore, we investigate the effects of polyethylene glycol-20k (PEG-20k), a cell impermeant, on post-resuscitation cerebral function. Thirty-two male Sprague-Dawley rats were randomized into four groups: 1) Control; 2) PEG-20k; 3) Sham control; 4) Sham with PEG-20k. To investigate blood brain barrier (BBB) permeability, ten additional rats were randomized into two groups: 1) CPR+Evans Blue (EB); 2) Sham+EB. Ventricular fibrillation was induced and untreated for 8 min, followed by 8 min of CPR, and resuscitation was attempted by defibrillation. Cerebral microcirculation was visualized at baseline, 2, 4 and 6 h after return of spontaneous circulation (ROSC). Brain edema was assessed by comparing wet-to-dry weight ratios after 6 h. S-100β, NSE and EB concentrations were analyzed to determine BBB permeability damage. For results, Post-resuscitation cerebral microcirculation was impaired compared to baseline and sham control (p < 0.05). However, dysfunction was reduced in animals treated with PEG-20k compared to control (p < 0.05). Post-resuscitation cerebral edema as measured by wet-to-dry weight ratio was lower in PEG-20k compared to control (3.23 ± 0.5 vs. 3.36 ± 0.4, p < 0.05). CA and CPR increased BBB permeability and damaged neuronal cell with associated elevation of S-100β sand NSE serum levels. PEG-20k administered during CPR improved cerebral microcirculation and reducing brain edema and injury., (Copyright © 2021. Published by Elsevier Masson SAS.)

Accumulating evidence demonstrated that administration of ω-3 polyunsaturated fatty acid (ω-3 PUFA) or ascorbic acid (AA) following cardiac arrest (CA) improves survival. Therefore, we investigate the effects of ω-3 PUFA combined with AA on myocardial function after CA and cardiopulmonary resuscitation (CPR) in a rat model. Thirty male rats were randomized into 5 groups: (1) sham; (2) control; (3) ω-3 PUFA; (4) AA; (5) ω-3 PUFA + AA. Ventricular fibrillation (VF) was induced and untreated for 6 min followed by defibrillation after 8 min of CPR. Infusion of drug or vehicle occurred at the start of CPR. Myocardial function and sublingual microcirculation were measured at baseline and after return of spontaneous circulation (ROSC). Heart tissues and blood were collected 6 h after ROSC. Myocardial function and sublingual microcirculation improvements were seen with ω-3 PUFA or AA compared to control after ROSC (p < 0.05). ω-3 PUFA + AA shows a better myocardial function than ω-3 PUFA or AA (p < 0.05). ω-3 PUFA or AA decreases pro-inflammatory cytokines, cTnI, myocardium malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) modified proteins compared to control (p < 0.05). ω-3 PUFA and AA combined have lower MDA and 4-HNE modified proteins than alone (p < 0.05). ω-3 PUFA or AA treatment reduces the severity of post-resuscitation myocardial dysfunction, improves sublingual microcirculation, decreases lipid peroxidation and systemic inflammation in the early phase of recovery following CA and resuscitation. A combination of ω-3 PUFA and AA treatment confers an additive effect in suppressing lipid peroxidation and improving myocardial function., (Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The objective of this study was to investigate the effects of pharmacologically induced hypothermia with WIN55, 212-2 (WIN)on postresuscitation myocardial function, microcirculation, and metabolism-specific lipids in a rat cardiac arrest (CA) model. Ventricular fibrillation was electrically induced and untreated for 6 minutes in 24 Sprague-Dawley rats weighing 450-550 g. Cardiopulmonary resuscitation including chest compression and mechanical ventilation was then initiated and continued for 8 minutes, followed by defibrillation. At 5 minutes after restoration of spontaneous circulation (ROSC), animals were randomized into four groups: (1) normothermia with vehicle (NT); (2) physical hypothermia with vehicle (PH); (3) WIN55, 212-2 with normothermia (WN); and (4) WIN55, 212-2 with hypothermia (WH). For groups of WN and WH, WIN was administered by continuous intravenous infusion with a syringe pump for 4 hours. PH started at 5 minutes after resuscitation. NT maintained core temperature at 37°C ± 0.2°C with the aid of a heating blanket. Hypothermia groups maintained temperature at 33°C ± 0.5°C for 4 hours after ROSC. There was a significant improvement in myocardial function as measured by ejection fraction, cardiac output, and myocardial performance index in animals treated with WH and PH beginning at 1 hour after start of infusion. In the WH and PH groups, buccal microcirculation was significantly improved compared with NT and WN. Plasma at pre-CA and ROSC 4 hours was harvested for lipid metabolism. The WH group appeared to be closer to baseline than the other groups in lipid metabolism. lysophosphatidylcholine (LPC) 18:2, free fatty acid (FFA) 22:6, and ceramide (CER) (24:0) changed significantly among the lipidomic data compared with NT ( p  < 0.05). Postresuscitation hypothermia improved myocardial function and microcirculation. WH-mediated lipid metabolism had the best metabolic outcome to bring back the animals to normal metabolism, which may be protective to improve outcomes of CA. LPC 18:2, FFA 22:6, and CER (24:0) may be important predictors of outcomes of CA.

Survival after cardiac arrest requires an integrated system of people, training, equipment, and organizations working together to achieve a common goal. Part 7 of the 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care focuses on systems of care, with an emphasis on elements that are relevant to a broad range of resuscitation situations. Previous systems of care guidelines have identified a Chain of Survival, beginning with prevention and early identification of cardiac arrest and proceeding through resuscitation to post-cardiac arrest care. This concept is reinforced by the addition of recovery as an important stage in cardiac arrest survival. Debriefing and other quality improvement strategies were previously mentioned and are now emphasized. Specific to out-of-hospital cardiac arrest, this Part contains recommendations about community initiatives to promote cardiac arrest recognition, cardiopulmonary resuscitation, public access defibrillation, mobile phone technologies to summon first responders, and an enhanced role for emergency telecommunicators. Germane to in-hospital cardiac arrest are recommendations about the recognition and stabilization of hospital patients at risk for developing cardiac arrest. This Part also includes recommendations about clinical debriefing, transport to specialized cardiac arrest centers, organ donation, and performance measurement across the continuum of resuscitation situations.

Focused transthoracic echocardiography (TTE) during cardiac arrest resuscitation can enable the characterization of myocardial activity, identify potentially treatable pathologies, assist with rhythm interpretation, and provide prognostic information. However, an important limitation of TTE is the difficulty obtaining interpretable images due to external and patient-related limiting factors. Over the last decade, focused transesophageal echocardiography (TEE) has been proposed as a tool that is ideally suited to image patients in extremis-those in cardiac arrest and periarrest states. In addition to the same diagnostic and prognostic role provided by TTE images, TEE provides unique advantages including the potential to optimize the quality of chest compressions, shorten cardiopulmonary resuscitation interruptions, guide resuscitative procedures, and provides a continuous image of myocardial activity. This review discusses the rationale, supporting evidence, opportunities, and challenges, and proposes a research agenda for the use of focused TEE in cardiac arrest with the goal to improve resuscitation outcomes., (Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Neurotensin is an endogenous tridecapeptide that binds to neurotensin receptors in the brain, which induce hypothermia. The aim of this study was to investigate whether the receptor agonist ABS 201 could induce therapeutic hypothermia and improve postresuscitation outcomes in a ventricular fibrillation cardiac arrest (VFCA) rat model. VF was electrically induced in 12 rats. Defibrillation was achieved after 6 min of cardiopulmonary resuscitation. After successful resuscitation, animals were randomized to receive ABS 201 (8 mg/kg/h) or placebo. Postresuscitation myocardial function and neurological deficit scores (NDS) were assessed, and postresuscitation survival duration was observed for up to 72 h. After administration of ABS 201, blood temperature decreased significantly from 37°C to 34°C, and was maintained for 2.5 h. There was a significant improvement of postresuscitation myocardial dysfunction, NDS, and survival duration in animals treated with ABS 201. These results demonstrated that ABS 201 induces therapeutic hypothermia in a VFCA rat model, ameliorates postresuscitation myocardial-neurological dysfunction, and prolongs survival duration. ABS 201 may therefore be an alternative method to induce therapeutic hypothermia with current cooling methods and improve postresuscitation outcomes.

Studies have demonstrated that vagus nerve stimulation (VNS) reduces ischemia/reperfusion injury. In this study, we investigated the protective effects of VNS in a rat model of cardiopulmonary resuscitation (CPR). We further investigated whether the beneficial effects of VNS were dependent on the alpha 7 nicotinic acetylcholine receptor (α7nAChR). Forty animals were randomized into four groups and all underwent CPR (n = 10 each): CPR alone (control); VNS during CPR; α7nAChR antagonist methyllycaconitine citrate (MLA) with VNS; α7nAChR agonist 3-(2, 4-dimethoxybenzylidene) anabaseine (GTS-21 dihydrochloride) without VNS. The right vagus nerve was exteriorized in all animals. Ventricular fibrillation was induced and untreated for 8 min. Defibrillation was attempted after 8 min of CPR. VNS was initiated at the beginning of precordial chest compressions and continued for 4 h after return of spontaneous circulation (ROSC) in both the VNS and MLA groups. Hemodynamic measurements and myocardial function, including ejection fraction and myocardial performance index, were assessed at baseline, 1 and 4 h after ROSC. The neurological deficit score was measured at 24-h intervals for a total of 72 h. The heart rate was reduced in the VNS and MLA groups, while no difference was found in mean arterial pressure between the four groups. Better post-resuscitation myocardial and cerebral function and longer duration of survival were observed in the VNS-treated animals. The protective effects of VNS could be abolished by MLA and imitated by GTS-21. In addition, VNS decreased the number of electrical shocks and the duration of CPR required. VNS improves multiple outcomes after CPR.

Background: Epinephrine administered during cardiopulmonary resuscitation (CPR) is associated with severe post-resuscitation myocardial dysfunction. We previously demonstrated that therapeutic hypothermia reduced the severity of post-resuscitation myocardial dysfunction caused by epinephrine; however, the relationship between myocardial adrenoceptor expression and myocardial protective effects by hypothermia remains unclear., Methods and Results: Rats weighing between 450 and 550 g were randomized into 5 groups: (1) normothermic placebo, (2) normothermic epinephrine, (3) hypothermic placebo, (4) hypothermic epinephrine, and (5) sham (not subject to cardiac arrest and resuscitation). Ventricular fibrillation was induced and untreated for 8 minutes for all other groups. Hypothermia was initiated coincident with the start of CPR and maintained at 33±0.2°C for 4 hours. Placebo or epinephrine was administered 5 minutes after the start of CPR and 3 minutes before defibrillation. Post-resuscitation ejection fraction was measured hourly for 4 hours then hearts were harvested. Epinephrine increased coronary perfusion pressure during CPR (27±6 mm Hg versus 21±2 mm Hg P <0.05). Post-resuscitation myocardial function was impaired in the normothermic epinephrine group compared with other groups. The concentration of myocardial cAMP doubled in the normothermic epinephrine group (655.06±447.63 μmol/L) compared with the hypothermic epinephrine group (302.51±97.98 μmol/L; P <0.05). Myocardial β 1 -adrenoceptor expression decreased with normothermia cardiac arrest but not with hypothermia regardless of epinephrine., Conclusions: Epinephrine, administered during normothermic CPR, increased the severity of post-resuscitation myocardial dysfunction. This adverse effect was inhibited by intra-arrest hypothermia resuscitation. Declined cAMP with more preserved β 1 -adrenoceptors in hypothermia-resuscitated myocardium is associated with improved post-resuscitated myocardial function in vivo., (© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Cardiac arrest in patients on mechanical support is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure. This American Heart Association scientific statement highlights the recognition and treatment of cardiovascular collapse or cardiopulmonary arrest in an adult or pediatric patient who has a ventricular assist device or total artificial heart. Specific, expert consensus recommendations are provided for the role of external chest compressions in such patients., (© 2017 American Heart Association, Inc.)

Aim: The post-cardiac arrest syndrome is a complex set of pathophysiological processes including a systemic inflammatory response. The goal of the current investigation was to test the hypothesis that early inflammatory markers are independently associated with in-hospital mortality and poor neurological outcome in patients initially resuscitated from out-of-hospital cardiac arrest., Methods: This was a preplanned analysis of data collected from a prospective observational multicenter study in adult out-of-hospital cardiac arrest patients. Blood was drawn at baseline, 12 and 24h after return of spontaneous circulation and plasma levels of interleukin (IL)-1β, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α were measured. The primary outcome measure was survival to hospital discharge. We utilized a mixed linear model to compare the levels of cytokines in survivors and non-survivors over time. We used multivariable logistic regression to assess the association between IL-6 levels and mortality., Results: A total of 102 patients were analyzed. Non-survivors and patients with poor functional outcome had statistical significant higher IL-1Ra, IL-6, IL-8, and IL-10 levels (all p<0.001) at all time points (0, 12 and 24h) compared to survivors. Baseline IL-6 levels were a good predictor of mortality (AUC=0.83 [95%CI: 0.75-0.92]). Baseline IL-6 levels were strongly associated with mortality in multivariable analysis (OR: 2.58 [95%CI: 1.93-3.45], p<0.001) but were not associated with neurological outcome in multivariable analysis (OR: 1.33 [95%CI: 0.62-2.86], p=0.47)., Conclusion: Early inflammatory markers, especially IL-6, are higher in patients with a poor outcome after OHCA. IL-6 remained associated with mortality, but not functional outcome, in multivariable analysis adjusting for patient and event characteristics., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Background: The development of advanced life support (ALS) termination of resuscitation (TOR) guidelines for out-of-hospital cardiac arrest (OHCA) seeks to improve the efficiency of scarce pre-hospital resources. However, as pre-hospital treatment for OHCA evolves and survival improves, these TOR guidelines must be reevaluated in the contemporary context of emergency medical services (EMS) providing access to advanced resuscitation care., Methods: Retrospective review of all adult (>18 years old), non-traumatic, OHCA patients (defined as patients with absence of pulse who received either CPR and/or defibrillation) treated by EMS in Richmond, VA, from January 1, 2009 to December 31, 2010. In addition to standard ALS, intra-arrest cold saline, mechanical CPR, and transportation to a comprehensive post-resuscitation center (CPRC) was provided. Patient treatment and outcomes were recorded via prehospital patient care reports and data were evaluated against previously established criteria for termination of resuscitation in an ALS EMS system. According to the aforementioned previously described criteria for TOR, patients meeting a single criterion for transport are recommended to be transported emergently to a comprehensive post-resuscitation care facility. Conversely, patients failing to meet any of the TOR criteria can be presumed to be expired without exception. Survival at 180 days was presumed when death could not be verified from publically reportable sources., Results: Of the 322 OHCA patients enrolled, the majority were male (59%), unwitnessed (52%), received no bystander CPR (67%), and presented in a non-shockable initial rhythm (79%), with an average age of 62.5 years. Overall survival was 17%, 14%, 12%, and 11% at 7, 14, 30, and 180 days, respectively. Of the 75 patients for which TOR guidelines recommended termination, none survived yielding both 100% specificity (95% CI 100-92.8%) and positive predictive value (95% CI 100-94.1%). However, TOR guidelines recommended transport of 208 of the 283 patients who died within 30 days, resulting in a sensitivity of 26.5% (95% CI 34.5-23.4%)., Conclusion: The TOR guidelines continue to have a reliable positive predictive value for death even in the setting of advanced EMS resuscitation methods and access to a CPRC. However, as the potential for survival from OHCA improves, the efficiency gained from their use is impacted greatly., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Both commercial aviation and resuscitation are complex activities in which team members must respond to unexpected emergencies in a consistent, high quality manner. Lives are at stake in both activities and the two disciplines have similar leadership structures, standard setting processes, training methods, and operational tools. Commercial aviation crews operate with remarkable consistency and safety, while resuscitation team performance and outcomes are highly variable. This commentary provides the perspective of two physician-pilots showing how commercial aviation training, operations, and safety principles can be adapted to resuscitation team training and performance., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Objectives: To determine the rate of appropriate documentation of endotracheal tube (ET) position confirmation in the American Heart Association's Get With the Guidelines-Resuscitation (GWTG-R) and to determine whether outcomes of patients who experience in-hospital cardiac arrest differ in relation to documentation rate., Design: Analysis of data from the GWTG-R, a prospective observational registry of in-hospital cardiac arrest and resuscitation., Setting: Database containing clinical information from the 507 hospitals participating in the GWTG-R., Patients: Adults resuscitated after in-hospital cardiac arrest., Measurements: The rate of appropriate documentation of ET position confirmation, defined as the use of capnography or an esophageal detector device (EDD); relationship between appropriate documentation of ET position confirmation and return of spontaneous circulation (ROSC) or survival to hospital discharge. Proportions with 95% CI are reported for prevalence data. Binary logistic regression was used to determine the relationship between appropriate documentation of ET position confirmation and outcome (ROSC, survival to hospital discharge). Adjusted and unadjusted odds ratios are reported., Main Results: Of the 176,054 patients entered into the GWTG-R database, 75,777 had an ET placed. For 13,263 (17.5%) of these patients, ET position confirmation was not documented in the chart. Auscultation alone was documented in 19,480 (25.7%) cases. Confirmation of ET position by capnography or EDD was documented in 43,034 (56.8%) cases. ROSC occurred in 39,063 (51.6%), and 13,474 (17.8%) survived to discharge. Patients whose ET position was confirmed by capnography or EDD were more likely to have ROSC (adjusted OR 1.229 [1.179, 1.282]) and to survive to hospital discharge (adjusted OR 1.093 [1.033, 1.157])., Conclusion: Documentation of ET position confirmation in patients who experience cardiac arrest is suboptimal. Appropriate documentation of ET position confirmation in the GWTG-R is associated with greater likelihood of ROSC and survival to hospital discharge., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Context: In-hospital cardiac arrest is a significant public health problem with a low probability of patient survival to hospital discharge., Objective: We evaluated the survival rates for adults with in-hospital cardiac arrest based on whether the arrest was witnessed and/or monitored. Our hypothesis is that patients with either a witnessed or monitored arrest had improved survival to hospital discharge with intact neurologic function., Design, Setting, and Patients: We studied a cohort study of 74,213 patients who suffered in-hospital cardiac arrest from January 1, 2000 through February 1, 2008 at the 369 hospitals participating in the National Registry of Cardiopulmonary Resuscitation., Interventions: The primary exposure of interest was whether the arrest was witnessed and/or monitored (i.e. electrocardiography, pulse oximetry, apnea, or bradycardia monitoring) at the time of arrest. Events were classified as being both monitored and witnessed, monitored only, witnessed only, or neither witnessed nor monitored., Main Outcome Measures: Survival to hospital discharge and cerebral performance category at time of discharge., Results: A total of 73% of patients suffering in-hospital cardiac arrest were witnessed and monitored; 10% were monitored but not witnessed; 9% were witnessed but not monitored; and 8% were neither witnessed nor monitored. Compared with those who were unmonitored/unwitnessed, each of the three groups of patients who were monitored and/or witnessed were over twice as likely to survive to hospital discharge with a cerebral performance category of 1 or 2 (monitored/witnessed OR=2.40, 95% CI: 2.08, 2.76; monitored-only OR=2.12, 95% CI: 1.81, 2.47; witnessed-only OR=2.43, 95% CI: 2.10, 2.83)., Conclusions: Patients who are witnessed and/or monitored at the time of cardiac arrest demonstrate a significantly higher rate of survival to hospital discharge compared to those patients who are neither monitored nor witnessed. Monitored and/or witnessed cardiac arrest patients were also more likely to be discharged with favorable neurologic outcome. Cardiac monitoring confers no additional outcome benefit over direct observation of patients suffering in-hospital cardiac arrest., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

The goal of immediate post-cardiac arrest care is to optimize systemic perfusion, restore metabolic homeostasis, and support organ system function to increase the likelihood of intact neurological survival. The post-cardiac arrest period is often marked by hemodynamic instability as well as metabolic abnormalities. Support and treatment of acute myocardial dysfunction and acute myocardial ischemia can increase the probability of survival. Interventions to reduce secondary brain injury, such as therapeutic hypothermia, can improve survival and neurological recovery. Every organ system is at risk during this period, and patients are at risk of developing multiorgan dysfunction. The comprehensive treatment of diverse problems after cardiac arrest involves multidisciplinary aspects of critical care, cardiology, and neurology. For this reason, it is important to admit patients to appropriate critical-care units with a prospective plan of care to anticipate, monitor, and treat each of these diverse problems. It is also important to appreciate the relative strengths and weaknesses of different tools for estimating the prognosis of patients after cardiac arrest.

The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

Background: Quality of chest compressions (CC) is an important determinant of resuscitation outcome for cardiac arrest patients., Purpose: To characterize the quality of CC performed by hospital personnel, evaluate for predictors of CC performance, and determine the effects of audiovisual feedback on CC performance., Methods: Seven hundred and fifty four individuals participated in a CPR quality improvement challenge at 30 US hospitals. Participants performed 2min of CC on a manikin with an accelerometer-based system for measuring both rate (CC/min) and depth (in.) of CC (AED Plus:ZOLL Medical). Real-time audiovisual feedback was disabled. A subset of participants performed a second trial of CC with the audiovisual feedback prompts activated., Results: Mean depth of CC was below AHA minimum guidelines (<1.5in.) for 34% (1.30+/-0.14in.) and above maximum guidelines (>2.0in.) for 12% of participants (2.20+/-0.22in.). Depth of CC was greater for male vs. female (p<0.001) and younger vs. older (p=0.009) but did not differ between ACLS, BCLS, and non-certified participants (p=0.6). Predictors of CC depth included CC rate (r(part)=-0.34, p<0.0001), gender (r(part)=0.13, p=0.001), and age (r(part)=-0.09, p=0.02). Mean depth of CC increased, mean rate decreased, and variance in CC depth and rate declined when feedback was used (p< or =0.0001 vs. without feedback). The percentage of CC performed within AHA guidelines (1.5-2in.) improved from 15 to 78% with feedback., Conclusions: The quality of CC performed by personnel at US hospitals as judged by their performance on a manikin is often suboptimal. Quality of CC can be improved with use of CPR feedback technologies.

Study Aims: Hyperglycemia is associated with poor outcomes in critically ill patients. We examined blood glucose values following in-hospital cardiac arrest (IHCA) to (1) characterize post-arrest glucose ranges, (2) develop outcomes-based thresholds of hyperglycemia and hypoglycemia, and (3) identify risk factors associated with post-arrest glucose derangements., Methods: We retrospectively studied 17,800 adult IHCA events reported to the National Registry of Cardiopulmonary Resuscitation (NRCPR) from January 1, 2005 through February 1, 2007., Results: Data were available from 3218 index events. Maximum blood glucose values were elevated in diabetics (median 226 mg/dL [IQR, 165-307 mg/dL], 12.5 mmol/L [IQR 9.2-17.0 mmol/L]) and non-diabetics (median 176 mg/dL [IQR, 135-239 mg/dL], 9.78 mmol/L [IQR 7.5-13.3 mmol/L]). Unadjusted survival to hospital discharge was higher in non-diabetics than diabetics (45.5% [95% CI, 43.3-47.6%] vs. 41.7% [95% CI, 38.9-44.5%], p=0.037). Non-diabetics displayed decreased adjusted survival odds for minimum glucose values outside the range of 71-170 mg/dL (3.9-9.4 mmol/L) and maximum values outside the range of 111-240 mg/dL (6.2-13.3 mmol/L). Diabetic survival odds decreased for minimum glucose greater than 240 mg/dL (13.3 mmol/L). In non-diabetics, arrest duration was identified as a significant factor associated with the development of hypo- and hyperglycemia., Conclusions: Hyperglycemia is common in diabetics and non-diabetics following IHCA. Survival odds in diabetics are relatively insensitive to blood glucose with decreased survival only associated with severe (>240 mg/dL, >13.3 mmol/dL) hyperglycemia. In non-diabetics, survival odds were sensitive to hypoglycemia (<70 mg/dL, <3.9 mmol/L).

The devastating neurologic injury in survivors of cardiac arrest has been recognized since the development of modern resuscitation techniques. After numerous failed clinical trials, two trials showed that induced mild hypothermia can ameliorate brain injury and improve survival and functional neurologic outcome in comatose survivors of out-of-hospital cardiac arrest. This article provides a comprehensive review of the advances in the care of brain injury after cardiac arrest, with updates on the process of prognostication, the use of therapeutic hypothermia and adjunctive intensive care unit care for cardiac arrest survivors.

Context: Occurrence of in-hospital cardiac arrest and survival patterns have not been characterized by time of day or day of week. Patient physiology and process of care for in-hospital cardiac arrest may be different at night and on weekends because of hospital factors unrelated to patient, event, or location variables., Objective: To determine whether outcomes after in-hospital cardiac arrest differ during nights and weekends compared with days/evenings and weekdays., Design and Setting: We examined survival from cardiac arrest in hourly time segments, defining day/evening as 7:00 am to 10:59 pm, night as 11:00 pm to 6:59 am, and weekend as 11:00 pm on Friday to 6:59 am on Monday, in 86,748 adult, consecutive in-hospital cardiac arrest events in the National Registry of Cardiopulmonary Resuscitation obtained from 507 medical/surgical participating hospitals from January 1, 2000, through February 1, 2007., Main Outcome Measures: The primary outcome of survival to discharge and secondary outcomes of survival of the event, 24-hour survival, and favorable neurological outcome were compared using odds ratios and multivariable logistic regression analysis. Point estimates of survival outcomes are reported as percentages with 95% confidence intervals (95% CIs)., Results: A total of 58,593 cases of in-hospital cardiac arrest occurred during day/evening hours (including 43,483 on weekdays and 15,110 on weekends), and 28,155 cases occurred during night hours (including 20,365 on weekdays and 7790 on weekends). Rates of survival to discharge (14.7% [95% CI, 14.3%-15.1%] vs 19.8% [95% CI, 19.5%-20.1%], return of spontaneous circulation for longer than 20 minutes (44.7% [95% CI, 44.1%-45.3%] vs 51.1% [95% CI, 50.7%-51.5%]), survival at 24 hours (28.9% [95% CI, 28.4%-29.4%] vs 35.4% [95% CI, 35.0%-35.8%]), and favorable neurological outcomes (11.0% [95% CI, 10.6%-11.4%] vs 15.2% [95% CI, 14.9%-15.5%]) were substantially lower during the night compared with day/evening (all P values < .001). The first documented rhythm at night was more frequently asystole (39.6% [95% CI, 39.0%-40.2%] vs 33.5% [95% CI, 33.2%-33.9%], P < .001) and less frequently ventricular fibrillation (19.8% [95% CI, 19.3%-20.2%] vs 22.9% [95% CI, 22.6%-23.2%], P < .001). Among in-hospital cardiac arrests occurring during day/evening hours, survival was higher on weekdays (20.6% [95% CI, 20.3%-21%]) than on weekends (17.4% [95% CI, 16.8%-18%]; odds ratio, 1.15 [95% CI, 1.09-1.22]), whereas among in-hospital cardiac arrests occurring during night hours, survival to discharge was similar on weekdays (14.6% [95% CI, 14.1%-15.2%]) and on weekends (14.8% [95% CI, 14.1%-15.2%]; odds ratio, 1.02 [95% CI, 0.94-1.11])., Conclusion: Survival rates from in-hospital cardiac arrest are lower during nights and weekends, even when adjusted for potentially confounding patient, event, and hospital characteristics.

Background: Bystander CPR rates remain low. One reason may be that the thought of responding to an emergency is so stressful that it decreases the willingness of laypersons to respond., Purpose: The purpose of this study was to quantify the amount of stress experienced by lay responders to a medical emergency and to identify barriers that may have impeded their response to the event., Methods: Responses from 1243 laypersons responding to an emergency during the Public Access Defibrillation Trial were analyzed in a mixed methods study. Stress related to the event was recorded using a 0 (none) to 5 (severe) scale. Qualitative responses to the question of "What was most difficult?" about the event were analyzed using content analysis., Results: Reported stress levels were low overall (mean 1.2, median 1.0). Laypersons responding to an emergency presumed to be a cardiac arrest had higher stress than those involved in other events (median 2.0 versus 1.0). Stress levels were higher in residential than in public settings (mean 1.41, median 1.0 versus mean 1.13, median 1.0). Those who fit a certain profile (females, non-native English speakers) reported statistically higher stress levels than others. A total of 614 qualitative responses were studied and aggregated into four major categories of difficulty: practical issues; characteristics of the victim; interpersonal issues; thoughts and feelings of the lay responder. Most difficulties were in the category of practical issues., Conclusions: Among these study volunteer lay responders, low levels of stress were reported. Incorporating descriptions of the difficulties experienced by lay responders in CPR/AED training curricula may make courses more realistic and useful.

Unlabelled: The adverse event (AE) profile of lay volunteer CPR and public access defibrillation (PAD) programs is unknown. We undertook to investigate the frequency, severity, and type of AE's occurring in widespread PAD implementation., Design: A randomized-controlled clinical trial., Setting: One thousand two hundred and sixty public and residential facilities in the US and Canada., Participants: On-site, volunteer, lay personnel trained in CPR only compared to CPR plus automated external defibrillators (AEDs)., Intervention: Persons experiencing possible cardiac arrest receiving lay volunteer first response with CPR+AED compared with CPR alone., Main Outcome Measure: An AE is defined as an event of significance that caused, or had the potential to cause, harm to a patient or volunteer, or a criminal act. AE data were collected prospectively., Results: Twenty thousand three hundred and ninety six lay volunteers were trained in either CPR or CPR+AED. One thousand seven hundred and sixteen AEDs were placed in units randomized to the AED arm. There were 26,389 exposure months. Only 36 AE's were reported. There were two patient-related AEs: both patients experienced rib fractures. There were seven volunteer-related AE's: one had a muscle pull, four experienced significant emotional distress and two reported pressure by their employee to participate. There were 27 AED-related AEs: 17 episodes of theft involving 20 devices, three involved AEDs that were placed in locations inaccessible to the volunteer, four AEDs had mechanical problems not affecting patient safety, and three devices were improperly maintained by the facility. There were no inappropriate shocks and no failures to shock when indicated (95% upper bound for probability of inappropriate shock or failure to shock = 0.0012)., Conclusions: AED use following widespread training of lay-persons in CPR and AED is generally safe for the volunteer and the patient. Lay volunteers may report significant, usually transient, emotional stress following response to a potential cardiac arrest. Within the context of this prospective, randomized multi-center study, AEDs have an exceptionally high safety profile when used by trained lay responders.

Context: Only 1% to 8% of adults with out-of-hospital cardiac arrest survive to hospital discharge., Objective: To compare resuscitation outcomes before and after an urban emergency medical services (EMS) system switched from manual cardiopulmonary resuscitation (CPR) to load-distributing band (LDB) CPR., Design, Setting, and Patients: A phased, observational cohort evaluation with intention-to-treat analysis of 783 adults with out-of-hospital, nontraumatic cardiac arrest. A total of 499 patients were included in the manual CPR phase (January 1, 2001, to March 31, 2003) and 284 patients in the LDB-CPR phase (December 20, 2003, to March 31, 2005); of these patients, the LDB device was applied in 210 patients., Intervention: Urban EMS system change from manual CPR to LDB-CPR., Main Outcome Measures: Return of spontaneous circulation (ROSC), with secondary outcome measures of survival to hospital admission and hospital discharge, and neurological outcome at discharge., Results: Patients in the manual CPR and LDB-CPR phases were comparable except for a faster response time interval (mean difference, 26 seconds) and more EMS-witnessed arrests (18.7% vs 12.6%) with LDB. Rates for ROSC and survival were increased with LDB-CPR compared with manual CPR (for ROSC, 34.5%; 95% confidence interval [CI], 29.2%-40.3% vs 20.2%; 95% CI, 16.9%-24.0%; adjusted odds ratio [OR], 1.94; 95% CI, 1.38-2.72; for survival to hospital admission, 20.9%; 95% CI, 16.6%-26.1% vs 11.1%; 95% CI, 8.6%-14.2%; adjusted OR, 1.88; 95% CI, 1.23-2.86; and for survival to hospital discharge, 9.7%; 95% CI, 6.7%-13.8% vs 2.9%; 95% CI, 1.7%-4.8%; adjusted OR, 2.27; 95% CI, 1.11-4.77). In secondary analysis of the 210 patients in whom the LDB device was applied, 38 patients (18.1%) survived to hospital admission (95% CI, 13.4%-23.9%) and 12 patients (5.7%) survived to hospital discharge (95% CI, 3.0%-9.3%). Among patients in the manual CPR and LDB-CPR groups who survived to hospital discharge, there was no significant difference between groups in Cerebral Performance Category (P = .36) or Overall Performance Category (P = .40). The number needed to treat for the adjusted outcome survival to discharge was 15 (95% CI, 9-33)., Conclusion: Compared with resuscitation using manual CPR, a resuscitation strategy using LDB-CPR on EMS ambulances is associated with improved survival to hospital discharge in adults with out-of-hospital nontraumatic cardiac arrest.

Considerable progress has been made in providing high-quality prehospital and emergency cardiac care for OHCA victims. The use of early CPR, early defibrillation, early ACLS, and state-of-the-art postresuscitation care offers the best promise for improved community survival and neurologic outcome statistics in the future. The NIH-sponsored Resuscitation Outcomes Consortium represents the largest governmentally sponsored effort of its kind that that will test the value of promising pharmacologic and device interventions on improving survival and neurologic outcome in OHCA patients.

The National Registry of Cardiopulmonary Resuscitation (NRCPR) is an American Heart Association (AHA)-sponsored, prospective, multisite, observational study of in-hospital resuscitation. The NRCPR is currently the largest registry of its kind. The purpose of this article is to describe the NRCPR and to provide the first comprehensive, Utstein-based, standardized characterization of in-hospital resuscitation in the United States. All adult (>/=18 years of age) and pediatric (<18 years of age) patients, visitors, employees, and staff within a facility (including ambulatory care areas) who experience a resuscitation event are eligible for inclusion in the NRCPR database. Between January 1, 2000, and June 30, 2002, 14720 cardiac arrests that met inclusion criteria occurred in adults at the 207 participating hospitals. An organized emergency team is available 24 h a day, 7 days a week in 86% of participating institutions. The three most common reasons for cardiac arrest in adults were (1) cardiac arrhythmia, (2) acute respiratory insufficiency, and (3) hypotension. Overall, 44% of adult in-hospital cardiac arrest victims had a return of spontaneous circulation (ROSC); 17% survived to hospital discharge. Despite the fact that a primary arrhythmia was one of the precipitating events in nearly one half of adult cardiac arrests, ventricular fibrillation (VF) was the initial pulseless rhythm in only 16% of in-hospital cardiac arrest victims. ROSC occurred in 58% of VF cases, yielding a survival-to-hospital discharge rate of 34% in this subset of patients. An automated external defibrillator was used to provide initial defibrillation in only 1.4% of patients whose initial cardiac arrest rhythm was VF. Neurological outcome in discharged survivors was generally good. Eighty-six percent of patients with Cerebral Performance Category-1 (CPC-1) at the time of hospital admission had a postarrest CPC-1 at the time of hospital discharge.

Abstract: Background: Patients with heart failure (HF) have abnormal cellular anatomy and myocardial mechanics that may impact the initial rhythm and subsequent outcomes in cardiac arrest (CA). Hypothesis: Patients with pre-existing HF are less likely to have ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) as the first documented rhythm in CA and have poorer survival than patients without pre-existing HF. Purpose: Identify the first documented cardiac arrest rhythm (FDR) in hospitalized patients with and without a pre-existing history of HF. Methods: We evaluated 60,389 consecutive, adult, index, pulseless CA events with documented initial rhythm in the National Registry of Cardiopulmonary Resuscitation. The primary endpoint was the FDR in patients with and without a history of pre-existing HF. Secondary endpoints were return of spontaneous circulation (ROSC), survival to discharge, and neurological outcome. Results: Thirty three percent of patients had a pre-existing diagnosis of HF. HF patients were more likely to have VF/pVT (25.9 vs. 23.2%) and less likely to have asystole (34.4 vs. 35.3%, p =<.0001) than non-HF. There was no difference in survival to discharge (18.3 vs. 18.2%, p =.66), or good neurological outcomes (82.2 vs. 83.2%, p =.23) between the groups. Women were less likely to have VF/pVT as the first documented rhythm in both HF and non-HF groups. Conclusions: Hospitalized patients with HF are more likely than those without HF to have VF/pVT as the FDR in CA, however the clinical magnitude of this difference is small. Overall survival and neurological outcomes are no different than hospitalized arrest patients without HF. [Copyright &y& Elsevier]

The authors comment on the study "Timing of Neuroprognostication in Pot-Cardiac Arrest Therapeutic Hypothermia," by S. M. Perman and colleagues. They express disappointment over the fact that overall survival to discharge remains dismally low. They then note that the study brings forward some important and controversial issues on end-of-life care in critical care in a retrospective study of 55 consecutive patients treated with hypothermia after cardiac arrest resuscitation.

Summary: Background: Little is known about cardiac arrests (CA) in the Emergency Department (ED). The objective of this study was to determine the characteristics of ED CAs. Methods: 60,852 adult, in-patient CA events in the National Registry of Cardiopulmonary Resuscitation were included. Multiple regression analysis compared ED CA with those occurring in the ICU, telemetry, or general floors. Subgroup analysis examined traumatic vs. non-traumatic ED CA and ED CA occurring after a successful pre-hospital resuscitation (recurrent) vs. primary ED event. Results: In multivariate analysis, ED location predicted improved survival to discharge (OR 0.74, 95%CI [0.67–0.82]). ED CAs had higher survival to discharge rates (ED 22.2, ICU 15.5, Tele 19.8, Floor 10.8, p <0.0001), better cerebral performance category scores (ED 1.59, ICU 1.73, Tele 1.96, Floor 1.69, p <0.0001), and shorter post-event length of stays (ED 8.6, ICU 17.5, Tele 16.5, Floor 14.2 days, p <0.0001) than other locations. Recurrent ED CAs were less likely to survive to discharge (10.1% vs. 24.6%, p <0.0001) than primary events. Trauma-related ED CAs had a lower survival to discharge rate (7.5% vs. 23.8%, p <0.0001), were less likely to be caused by an arrhythmia (23.6% vs. 32.5%, p <0.0008), and more likely to be preceded by hypotension or shock (41.6% vs. 29.0%, p <0.0001) than non-trauma ED events. Conclusions: ED CAs have unique characteristics, and better survival and neurologic outcomes compared to other hospital locations. Primary ED CAs have a better chance of survival to discharge than recurrent events. Traumatic ED CAs have worse outcomes than non-traumatic CA. [Copyright &y& Elsevier]

Background: Black patients have worse in-hospital survival than white patients after in-hospital cardiac arrest (IHCA), but less is known about long-term outcomes. We sought to assess among IHCA survivors whether there are additional racial differences in survival after hospital discharge and to explore potential reasons for differences.Methods: This was alongitudinal study of patients ≥65 years of age who had an IHCA and survived until hospital discharge between 2000 and 2011 from the national Get With The Guidelines-Resuscitation registry whose data could be linked to Medicare claims data. Sequential hierarchical modified Poisson regression models evaluated the proportion of racial differences explained by patient, hospital, and unmeasured factors. Our exposure was black or white race. Our outcome was survival at 1, 3, and 5 years.Results: Among 8764 patients who survived to discharge, 7652 (87.3%) were white and 1112 (12.7%) were black. Black patients with IHCA were younger, more frequently female, sicker with more comorbidities, less likely to have a shockable initial cardiac arrest rhythm, and less likely to be evaluated with coronary angiography after initial resuscitation. At discharge, black patients were also more likely to have at least moderate neurological disability and less likely to be discharged home. Compared with white patients and after adjustment only for hospital site, black patients had lower 1-year (43.6% versus 60.2%; relative risk [RR], 0.72), 3-year (31.6% versus 45.3%; RR, 0.71), and 5-year (23.5% versus 35.4%; RR, 0.67; all P<0.001) survival. Adjustment for patient factors explained 29% of racial differences in 1-year survival (RR, 0.80; 95% confidence interval, 0.75-0.86), and further adjustment for hospital treatment factors explained an additional 17% of racial differences (RR, 0.85; 95% confidence interval, 0.80-0.92). Approximately half of the racial difference in 1-year survival remained unexplained, and the degree to which patient and hospital factors explained racial differences in 3-year and 5-year survival was similar.Conclusions: Black survivors of IHCA have lower long-term survival compared with white patients, and about half of this difference is not explained by patient factors or treatments after IHCA. Further investigation is warranted to better understand to what degree unmeasured but modifiable factors such as postdischarge care account for unexplained disparities. [ABSTRACT FROM AUTHOR]