scholarly journals Microglial Activation and Neurological Outcomes in a Murine Model of Cardiac Arrest

2021 ◽  
Author(s):  
Alaa Ousta ◽  
Lin Piao ◽  
Yong Hu Fang ◽  
Adrianna Vera ◽  
Thara Nallamothu ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Calcium Binding ◽  
Microglial Activation ◽  
Neuronal Degeneration ◽  
Treatment Options ◽  
Sudden Cardiac Arrest ◽  
Neurological Injury ◽  
Cell Integrity ◽  
Successful Resuscitation

Abstract Background Neurological injury following successful resuscitation from sudden cardiac arrest (CA) is common. The pathophysiological basis of this injury remains poorly understood, and treatment options are limited. Microglial activation and neuroinflammation are established contributors to many neuropathologies, such as Alzheimer disease and traumatic brain injury, but their potential role in post-CA injury has only recently been recognized. Here, we hypothesize that microglial activation that occurs following brief asystolic CA is associated with neurological injury and represents a potential therapeutic target. Methods Adult C57BL/6 male and female mice were randomly assigned to 12-min, KCl-induced asystolic CA, under anesthesia and ventilation, followed by successful cardiopulmonary resuscitation (n = 19) or sham intervention (n = 11). Neurological assessments of mice were performed using standardized neurological scoring, video motion tracking, and sensory/motor testing. Mice were killed at 72 h for histological studies; neuronal degeneration was assessed using Fluoro-Jade C staining. Microglial characteristics were assessed by immunohistochemistry using the marker of ionized calcium binding adaptor molecule 1, followed by ImageJ analyses for cell integrity density and skeletal analyses. Results Neurological injury in post-cardiopulmonary-resuscitation mice vs. sham mice was evident by poorer neurological scores (difference of 3.626 ± 0.4921, 95% confidence interval 2.618–4.634), sensory and motor functions (worsened by sixfold and sevenfold, respectively, compared with baseline), and locomotion (75% slower with a 76% decrease in total distance traveled). Post-CA brains demonstrated evidence of neurodegeneration and neuroinflammatory microglial activation. Conclusions Extensive microglial activation and neurodegeneration in the CA1 region and the dentate gyrus of the hippocampus are evident following brief asystolic CA and are associated with severe neurological injury.

Cardiopulmonary resuscitation: the science behind the hands

Heart ◽  
2018 ◽  
Vol 104 (13) ◽  
pp. 1056-1061 ◽  
Author(s):  
Andrew W Harris ◽  
Peter J Kudenchuk
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Sudden Cardiac Arrest ◽  
Heart Association ◽  
Scientific Basis ◽  
Chest Compressions ◽  
High Quality ◽  
Physiological Basis ◽  
Successful Resuscitation ◽  
External Chest Compressions

Sudden cardiac arrest is a leading cause of death worldwide. Despite significant advances in resuscitation science since the initial use of external chest compressions in humans nearly 60 years ago, there continues to be wide variability in rates of successful resuscitation across communities. The American Heart Association (AHA) and European Resuscitation Council emphasise the importance of high-quality chest compressions as the foundation of resuscitation care. We review the physiological basis for the association between chest compression quality and clinical outcomes and the scientific basis for the AHA’s key metrics for high-quality cardiopulmonary resuscitation. Finally, we highlight that implementation of strategies that promote effective chest compressions can improve outcomes in all patients with cardiac arrest.

scholarly journals Minocycline Reduces Neuronal Death and Attenuates Microglial Response after Pediatric Asphyxial Cardiac Arrest

2009 ◽  
Vol 30 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Minke Tang ◽  
Henry Alexander ◽  
Robert SB Clark ◽  
Patrick M Kochanek ◽  
Valerian E Kagan ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Neuronal Death ◽  
Calcium Binding ◽  
Microglial Activation ◽  
Neuronal Degeneration ◽  
Spontaneous Circulation ◽  
Developing Brain ◽  
Fluoro Jade B ◽  
Microglial Response ◽  
Asphyxial Cardiac Arrest

The mechanisms leading to delayed neuronal death after asphyxial cardiac arrest (ACA) in the developing brain are unknown. This study aimed at investigating the possible role of microglial activation in neuronal death in developing brain after ACA. Postnatal day-17 rats were subjected to 9 mins of ACA followed by resuscitation. Rats were randomized to treatment with minocycline, (90 mg/kg, intraperitoneally (i.p.)) or vehicle (saline, i.p.) at 1 h after return of spontaneous circulation. Thereafter, minocycline (22.5 mg/kg, i.p.) was administrated every 12 h until sacrifice. Microglial activation (evaluated by immunohistochemistry using ionized calcium-binding adapter molecule-1 (Iba1) antibody) coincided with DNA fragmentation and neurodegeneration in CA1 hippocampus and cortex (assessed by deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL), Fluoro-Jade-B and Nissl stain). Minocycline significantly decreased both the microglial response and neuronal degeneration compared with the vehicle. Asphyxial CA significantly enhanced proinflammatory cytokine and chemokine levels in hippocampus versus control (assessed by multiplex bead array assay), specifically tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-1α (MIP-1α), regulated upon activation, normal T-cell expressed and secreted (RANTES), and growth-related oncogene (GRO-KC) ( P<0.05). Minocycline attenuated ACA-induced increases in MIP-1α and RANTES ( P<0.05). These data show that microglial activation and cytokine production are increased in immature brain after ACA. The beneficial effect of minocycline suggests an important role for microglia in selective neuronal death after pediatric ACA, and a possible therapeutic target.

scholarly journals Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

AbstractPrimary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

scholarly journals Right Ventricular Rupture Caused by Prolonged Cardiopulmonary Resuscitation after Sudden Cardiac Arrest

2015 ◽  
Vol 88 (4) ◽  
pp. 434
Author(s):  
Hee Jeong Lee ◽  
Seong Soon Kwon ◽  
Hye Ran Kang ◽  
Duk Won Bang ◽  
Byoung Won Park ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Right Ventricular ◽  
Sudden Cardiac Arrest ◽  
Ventricular Rupture

scholarly journals 4226 Poor provider-patient communication, lack of readiness for discharge, and perceived illness threat are associated with quality of life after survival from cardiac arrest

2020 ◽  
Vol 4 (s1) ◽  
pp. 142-142
Author(s):  
Alex Presciutti ◽  
Jonathan Shaffer ◽  
Mary Newman ◽  
Sarah Perman
Keyword(s):  
Quality Of Life ◽  
Cardiac Arrest ◽  
Online Survey ◽  
Treatment Options ◽  
Illness Perception ◽  
Sudden Cardiac Arrest ◽  
Specific Treatment ◽  
Patient Communication ◽  
Perceived Illness

OBJECTIVES/GOALS: Studies have shown that cardiac arrest survivors have poor quality of life (QoL) secondary to neurologic injury. We hypothesized that poor provider-patient communication, lack of readiness for discharge, and perceived illness threat would be associated with QoL in cardiac arrest survivors. METHODS/STUDY POPULATION: We distributed an online survey to the Sudden Cardiac Arrest Foundation listserv. Survivors completed the Questionnaire for the Quality of Provider-Patient Interactions (QQPPI), Readiness for Hospital Discharge Scale (RHDS), and the Brief Illness Perception Questionnaire (B-IPQ). When completing the QQPPI and RHDS, survivors were asked to think back to their hospitalization and discharge. QoL domains (physical, psychological, social) were measured via the WHO-QOL BREF. Three multiple regression models examined associations between QQPPI, RHDS, and B-IPQ scores with QoL domains, adjusted for age, sex, months since arrest, and understanding of arrest and post-arrest symptoms at discharge. RESULTS/ANTICIPATED RESULTS: A total of 163 survivors (mean age 50.1 years, 50.3% women) provided complete survey data. Greater perceived illness threat (β: −.45, p < .001) and lower readiness for discharge (β: .22, p = .01) were associated with worse physical QoL; greater perceived illness threat (β: −.45, p < .001) was associated with worse psychological QoL; and greater perceived illness threat (β: −.3, p < .001) and poor provider-patient communication (β: .35, p < .001) were associated with worse social QoL. Our models explained 48%, 43%, and 30% of the variance in physical, psychological, and social QoL, respectively (p < .001). DISCUSSION/SIGNIFICANCE OF IMPACT: In-hospital interactions and perceived illness threat have important ramifications for cardiac arrest survivors attempting to return to daily life. Discussions regarding cardiac arrest sequelae, expectations, and specific treatment options during hospitalization could impact future QoL.

scholarly journals The dependence of successful resuscitation on electrocardiographically documented cardiac rhythm in case of out-of-hospital cardiac arrest

Medicina ◽  
2007 ◽  
Vol 43 (10) ◽  
pp. 798 ◽  
Author(s):  
Nedas Jasinskas ◽  
Dinas Vaitkaitis ◽  
Vidas Pilvinis ◽  
Lina Jančaitytė ◽  
Gailutė Bernotienė ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Cardiac Rhythm ◽  
Sudden Cardiac Arrest ◽  
Spontaneous Circulation ◽  
Consensus Conference ◽  
Successful Resuscitation ◽  
Initial Rhythm ◽  
Hospital Deaths ◽  
One Year

Objective. To determine the influence of electrocardiographically documented cardiac rhythm during sudden cardiac arrest on successful resuscitation among out-of-hospital deaths in Kaunas city. Material and methods. An observational prospective study was conducted between 1 January, 2005, and 30 December, 2005, in Kaunas city with a population of 360 627 inhabitants. In this period, all cases of cardiac arrest were analyzed according to the guidelines of the Utstein consensus conference. Cardiac arrest (both of cardiac and noncardiac etiology) was confirmed in 72 patients during one year. Effective cardiopulmonary resuscitation was performed in 18 patients. Results. The total number of deaths from all causes in Kaunas during 1-year study period was 6691. Sixty-two patients due to sudden death of cardiac etiology were resuscitated by emergency medical services personnel. Return of spontaneous circulation was achieved in 11 patients. Ventricular fibrillation was observed in 33 (53.2%) patients. Asystole was present in 11 (17.7%) and other rhythms in 18 (29.1%) cases. Patients with ventricular fibrillation as an initial rhythm were more likely to be successfully resuscitated than patients with asystole. Conclusions. Ventricular fibrillation was the most common electrocardiographically documented cardiac rhythm registered during cardiac arrest in out-of-hospital settings. Ventricular fibrillation as a mechanism of cardiac arrest was associated with major cases of successful resuscitation.

scholarly journals Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest

2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Brad E. Zacharia ◽  
Zachary L. Hickman ◽  
Bartosz T. Grobelny ◽  
Peter A. DeRosa ◽  
Andrew F. Ducruet ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Treatment Strategies ◽  
Disease Process ◽  
Global Cerebral Ischemia ◽  
Neurological Injury ◽  
Successful Resuscitation ◽  
Complement Inhibition ◽  
Neuroprotective Strategy

Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. Emerging preclinical as well as recent human clinical evidence suggests that activation of the complement cascade plays a critical role in the pathogenesis of GCI/R injury following OHCA. In addition, it is well established that complement inhibition improves outcome in both global and focal models of brain ischemia. Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.

Sudden cardiac arrest after minor abdominal trauma: A successful resuscitation in a patient with haemorrhagic phaeochromocytoma

Resuscitation ◽  
2009 ◽  
Vol 80 (11) ◽  
pp. 1323-1324 ◽  
Author(s):  
Chun-Chieh Chiu ◽  
Ying-Cheng Chen ◽  
Tsung-Han Teng ◽  
Li-Heng Yang ◽  
Ya-Pei Chen ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Abdominal Trauma ◽  
Sudden Cardiac Arrest ◽  
Successful Resuscitation

scholarly journals Esmolol during Cardiopulmonary Resuscitation Reduces Neurological Injury in a Porcine Model of Cardiac Arrest

2021 ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

Abstract Background. Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Methods. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 36 pigs and left untreated for 12min. During CPR, animals were randomized to receive epinephrine (30µg/kg) with either esmolol (0.5mg/kg) or saline (control). Pigs were then observed up to 96h. Results. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (p<0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (p<0.05) and hippocampal microglial activation (p<0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (p<0.01). Conclusions. In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

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