Post–Cardiac Arrest Syndrome

2020 ◽  
Vol 31 (4) ◽  
pp. 383-393
Author(s):  
Linda Dalessio

More than 356 000 out-of-hospital cardiac arrests occur in the United States annually. Complications involving post–cardiac arrest syndrome occur because of ischemic-reperfusion injury to the brain, lungs, heart, and kidneys. Post–cardiac arrest syndrome is a clinical state that involves global brain injury, myocardial dysfunction, macrocirculatory dysfunction, increased vulnerability to infection, and persistent precipitating pathology (ie, the cause of the arrest). The severity of outcomes varies and depends on precipitating factors, patient health before cardiac arrest, duration of time to return of spontaneous circulation, and underlying comorbidities. In this article, the pathophysiology and treatment of post–cardiac arrest syndrome are reviewed and potential novel therapies are described.

Author(s):  
Estivalis G. Acosta-Gutiérrez ◽  
Andrés M. Alba-Amaya ◽  
Santiago Roncancio-Rodríguez ◽  
José Ricardo Navarro-Vargas

Adult In-hospital Cardiac Arrest (IHCA) is defined as the loss of circulation of an in-patient. Following high-quality cardiopulmonary resuscitation (CPR), if the return of spontaneous circulation (ROSC) is achieved, the post-cardiac arrest syndrome develops (PCAS). This review is intended to discuss the current diagnosis and treatment of PCAS. To approach this topic, a bibliography search was conducted through direct digital access to the scientific literature published in English and Spanish between 2014 and 2020, in MedLine, SciELO, Embase and Cochrane. This search resulted in 248 articles from which original articles, systematic reviews, meta-analyses and clinical practice guidelines were selected for a total of 56 documents. The etiologies may be divided into 56% of in-hospital cardiac, and 44% of non-cardiac arrests. The incidence of this physiological collapse is up to 1.6 cases/1,000 patients admitted, and its frequency is higher in the intensive care units (ICU), with an overall survival rate of 13% at one year. The primary components of PCAS are brain injury, myocardial dysfunction and the persistence of the precipitating pathology. The mainstays for managing PCAS are the prevention of cardiac arrest, ventilation support, control of peri-cardiac arrest arrythmias, and interventions to optimize neurologic recovery. A knowledgeable healthcare staff in PCAS results in improved patient survival and future quality of life. Finally, there is clear need to do further research in the Latin American Population.


Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Joseph M Wider ◽  
Erin Gruley ◽  
Jennifer Mathieu ◽  
Emma Murphy ◽  
Rachel Mount ◽  
...  

Background: Mitochondrial dysfunction contributes to cardiac arrest induced brain injury and has been a target for neuroprotective therapies. An emerging concept suggests that hyperactivation of neuronal mitochondria following resuscitation results in hyperpolarization of the mitochondrial membrane during reperfusion, which drives generation of excess reactive oxygen species. Previous studies from our group demonstrated that limiting mitochondrial hyperactivity by non-invasively modulating mitochondrial function with specific near infrared light (NIR) wavelengths can reduce brain injury in small animal models of global and focal ischemia. Hypothesis: Inhibitory wavelengths of NIR will reduce neuronal injury and improve neurocognitive outcome in a clinically relevant swine model of cardiac arrest. Methods: Twenty-eight male and female adult swine were enrolled (3 groups: Sham, CA/CPR, and CA/CPR + NIR). Cardiac arrest (8 minutes) was induced with a ventricular pacing wire and followed by manual CPR with defibrillation and epinephrine every 30 seconds until return of spontaneous circulation (ROSC), 2 of the 20 swine that underwent CA did not achieve ROSC and were not enrolled. Treatment groups were randomized prior to arrest and blinded to the CPR team. Treatment was applied at onset of ROSC by irradiating the scalp with 750 nm and 950 nm LEDs (5W) for 2 hours. Results: Sham-operated animals all survived (8/8), whereas 22% of untreated animals subjected to cardiac arrest died within 45 min of ROSC (CA/CPR, n= 7/9). All swine treated with NIR survived the duration of the study (CA/CPR + NIR, n=9/9). Four days following cardiac arrest, neurological deficit score was improved in the NIR treatment group (50 ± 21 CA/CPR vs. 0.8 ± 0.8 CA/CPR + NIR, p < 0.05). Additionally, neuronal death in the CA1/CA3 regions of the hippocampus, assessed by counting surviving neurons with stereology, was attenuated by treatment with NIR (17917 ± 5534 neurons/mm 3 CA/CPR vs. 44655 ± 5637 neurons/mm 3 CA/CPR + NIR, p < 0.05). All data is reported as mean ± SEM. Conclusions: These data provide evidence that noninvasive modulation of mitochondria, achieved by transcranial irradiation of the brain with NIR, mitigates post-cardiac arrest brain injury.


2006 ◽  
Vol 21 (6) ◽  
pp. 445-450 ◽  
Author(s):  
Corita Grudzen

AbstractAmericans are living longer and are more likely to be chronically or terminally ill at the time of death. Although surveys indicate that most people prefer to die at home, the majority of people in the United States die in acute care hospitals. Each year, approximately 400,000 persons suffer sudden cardiac arrest in the US, the majority occurring in the out-of-hospital setting. Mortality rates are high and reach almost 100% when prehospital care has failed to restore spontaneous circulation. Nonetheless, patients who receive little benefit or may wish to forgo life-sustaining treatment often are resuscitated. Risk versus harm of resuscitation efforts can be differentiated by various factors, including cardiac rhythm. Emergency medical services policy regarding resuscitation should consider its utility in various clinical scenarios. Patients, family members, emergency medical providers, and physicians all are important stakeholders to consider in decisions about out-of-hospital cardiac arrest. Ideally, future policy will place greater emphasis on patient preferences and quality of life by including all of these viewpoints.


2009 ◽  
Vol 42 (3) ◽  
pp. 338-341 ◽  
Author(s):  
José Roberto Lambertucci ◽  
Silvio Roberto Souza-Pereira ◽  
Tânia Antunes Carvalho

Simultaneous occurrence of brain tumor and myeloradiculopathy in cases of Manson's schistosomiasis have only rarely been described. We report the case of a 38-year-old man who developed seizures during a trip to Puerto Rico and in whom a brain tumor was diagnosed by magnetic resonance imaging: brain biopsy revealed the diagnosis of schistosomiasis. He was transferred to a hospital in the United States and, during hospitalization, he developed sudden paraplegia. The diagnosis of myeloradiculopathy was confirmed at that time. He was administered praziquantel and steroids. The brain tumor disappeared, but the patient was left with paraplegia and fecal and urinary dysfunction. He has now been followed up in Brazil for one year, and his clinical state, imaging examinations and laboratory tests are presented here.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lorissa Lamoureux ◽  
Herbert K Whitehouse ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri

Background: We have reported in rat and swine models of cardiac arrest that sodium hydrogen exchanger isoform-1 (NHE-1) inhibition facilitates resuscitation, ameliorates myocardial dysfunction, and improves survival. Others have reported that α-methylnorepinephrine (α-MNE) - a selective α2-adrenoreceptor agonist - is superior to epinephrine given its lack of β-agonist effects. We examined in a rat model of VF and closed-chest resuscitation the effects of combining the NHE-1 inhibitor zoniporide (ZNP) with α-MNE. Methods: VF was electrically induced in 32 male retired breeder Sprague-Dawley rats and left untreated for 8 minutes after which resuscitation was attempted by an 8 minute interval of chest compression and delivery of electrical shocks. Rats were randomized 1:1:1:1 to receive a 3 mg/kg bolus of ZNP or 0.9% NaCl before starting chest compression and a 100 μg/kg bolus of α-MNE or its vehicle at minute 2 of chest-compressions establishing 4 groups of 8 rats each. Successfully resuscitated rats were monitored for 240 minutes. Results: The number of rats that had return of spontaneous circulation and then survived 240 min were: α-MNE(-)/ZNP(-) 4 and 2; α-MNE(-)/ZNP(+) 5 and 5; α-MNE(+)/ZNP(-) 2 and 1; and α-MNE(+)/ZNP(+) 7 and 7 yielding a statistically significant effect on overall survival times corresponding to 105 ± 114, 150 ± 124, 58 ± 108, and 210 ± 85 min, respectively (p < 0.045). Post-resuscitation lactate levels were attenuated in all treatment groups with the greatest effect by the α-MNE(+)/ZNP(+) combination without major differences in hemodynamic function (Table). Conclusion: We confirm a beneficial effect resulting from the combination of ZNP (given to attenuate myocardial reperfusion injury) and α-MNE (given to augment peripheral vascular resistance during chest compression without the detrimental actions of epinephrine). The proposed combination may prove to be a highly effective novel strategy for resuscitation from cardiac arrest.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Matt Oberdier ◽  
Jing Li ◽  
Dan Ambinder ◽  
Xiangdong Zhu ◽  
Sarah Fink ◽  
...  

Background: Out-of-hospital sudden cardiac arrest is a leading cause of death in the United States, affecting over 350,000 people per year with an overall survival rate around 10%. CPR, defibrillation, and therapeutic hypothermia are common resuscitation strategies, but hypothermia is difficult to implement timely to achieve survival benefit. A cell-permeable peptide TAT-PHLPP9c has been shown to alter metabolic pathways similar to hypothermia, and decreases the release of two biomarkers, taurine and glutamate, during the high osmotic stress of heart stunning and brain injury in a mouse arrest model. Hypothesis: TAT-PHLPP9c, given during CPR, enhances 24-hour survival in a swine ventricular fibrillation (VF) model. Methods: In 14 (8 controls and 6 treated) sedated, intubated, and mechanically ventilated swine, after 5 min of VF, ACLS with vest CPR and periodic defibrillations was performed. Venous blood samples were collected at baseline, after 2 min of CPR, and at 2 and 30 min after return of spontaneous circulation (ROSC). The animals were survived up to 24 hrs and plasma samples were analyzed for glutamate and taurine in 2 controls and 1 animal given peptide. Results: Three of the control animals had ROSC, but none survived for 24 hrs, while 4 of 6 treated animals achieved neurologically intact survival at 24 hrs (p < 0.02). Compared to baseline, both taurine and glutamate plasma concentrations increased in the control group, but the increase was reduced substantially by the peptide treatment at 30 min after ROSC (Figure). Conclusion: The use of the cooling mimicking peptide TAT-PHLPP9c administered during CPR significantly improved 24-hour survival in this swine model of cardiac arrest. It reduced the increase of cerebral and myocardial metabolic biomarkers, which encourages utilizing a strategy of cell-permeable peptides for intravenous administration for more rapid onset of hypothermia-like salutary effects than are possible with current CPR cooling devices.


2019 ◽  
Vol 39 (6) ◽  
pp. 939-958 ◽  
Author(s):  
Nguyen Mai ◽  
Kathleen Miller-Rhodes ◽  
Sara Knowlden ◽  
Marc W Halterman

Systemic inflammation and multi-organ failure represent hallmarks of the post-cardiac arrest syndrome (PCAS) and predict severe neurological injury and often fatal outcomes. Current interventions for cardiac arrest focus on the reversal of precipitating cardiac pathologies and the implementation of supportive measures with the goal of limiting damage to at-risk tissue. Despite the widespread use of targeted temperature management, there remain no proven approaches to manage reperfusion injury in the period following the return of spontaneous circulation. Recent evidence has implicated the lung as a moderator of systemic inflammation following remote somatic injury in part through effects on innate immune priming. In this review, we explore concepts related to lung-dependent innate immune priming and its potential role in PCAS. Specifically, we propose and investigate the conceptual model of lung–brain coupling drawing from the broader literature connecting tissue damage and acute lung injury with cerebral reperfusion injury. Subsequently, we consider the role that interventions designed to short-circuit lung-dependent immune priming might play in improving patient outcomes following cardiac arrest and possibly other acute neurological injuries.


2015 ◽  
Vol 308 (11) ◽  
pp. H1414-H1422 ◽  
Author(s):  
Jing Li ◽  
Huashan Wang ◽  
Qiang Zhong ◽  
Xiangdong Zhu ◽  
Sy-Jou Chen ◽  
...  

Sudden cardiac arrest (SCA) is a leading cause of death in the United States. Despite return of spontaneous circulation, patients die due to post-SCA syndrome that includes myocardial dysfunction, brain injury, impaired metabolism, and inflammation. No medications improve SCA survival. Our prior work suggests that optimal Akt activation is critical for cooling protection and SCA recovery. Here, we investigate a small inhibitor of PTEN, an Akt-related phosphatase present in heart and brain, as a potential therapy in improving cardiac and neurological recovery after SCA. Anesthetized adult female wild-type C57BL/6 mice were randomized to pretreatment of VO-OHpic (VO) 30 min before SCA or vehicle control. Mice underwent 8 min of KCl-induced asystolic arrest followed by CPR. Resuscitated animals were hemodynamically monitored for 2 h and observed for 72 h. Outcomes included heart pressure-volume loops, energetics (phosphocreatine and ATP from 31P NMR), protein phosphorylation of Akt, GSK3β, pyruvate dehydrogenase (PDH) and phospholamban, circulating inflammatory cytokines, plasma lactate, and glucose as measures of systemic metabolic recovery. VO reduced deterioration of left ventricular maximum pressure, maximum rate of change in the left ventricular pressure, and Petco2 and improved 72 h neurological intact survival (50% vs. 10%; P < 0.05). It reduced plasma lactate, glucose, IL-1β, and Pre-B cell colony enhancing factor, while increasing IL-10. VO increased phosphorylation of Akt and GSK3β in both heart and brain, and cardiac phospholamban phosphorylation while reducing p-PDH. Moreover, VO improved cardiac bioenergetic recovery. We concluded that pharmacologic PTEN inhibition enhances Akt activation, improving metabolic, cardiovascular, and neurologic recovery with increased survival after SCA. PTEN inhibitors may be a novel pharmacologic strategy for treating SCA.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jan Harald Nilsen ◽  
Torstein Schanche ◽  
Sergei Valkov ◽  
Rizwan Mohyuddin ◽  
Brage Haaheim ◽  
...  

AbstractWe recently documented that cardiopulmonary resuscitation (CPR) generates the same level of cardiac output (CO) and mean arterial pressure (MAP) during both normothermia (38 °C) and hypothermia (27 °C). Furthermore, continuous CPR at 27 °C provides O2 delivery (ḊO2) to support aerobic metabolism throughout a 3-h period. The aim of the present study was to investigate the effects of extracorporeal membrane oxygenation (ECMO) rewarming to restore ḊO2 and organ blood flow after prolonged hypothermic cardiac arrest. Eight male pigs were anesthetized and immersion cooled to 27 °C. After induction of hypothermic cardiac arrest, CPR was started and continued for a 3-h period. Thereafter, the animals were rewarmed with ECMO. Organ blood flow was measured using microspheres. After cooling with spontaneous circulation to 27 °C, MAP and CO were initially reduced to 66 and 44% of baseline, respectively. By 15 min after the onset of CPR, there was a further reduction in MAP and CO to 42 and 25% of baseline, respectively, which remained unchanged throughout the rest of 3-h CPR. During CPR, ḊO2 and O2 uptake (V̇O2) fell to critical low levels, but the simultaneous small increase in lactate and a modest reduction in pH, indicated the presence of maintained aerobic metabolism. Rewarming with ECMO restored MAP, CO, ḊO2, and blood flow to the heart and to parts of the brain, whereas flow to kidneys, stomach, liver and spleen remained significantly reduced. CPR for 3-h at 27 °C with sustained lower levels of CO and MAP maintained aerobic metabolism sufficient to support ḊO2. Rewarming with ECMO restores blood flow to the heart and brain, and creates a “shockable” cardiac rhythm. Thus, like continuous CPR, ECMO rewarming plays a crucial role in “the chain of survival” when resuscitating victims of hypothermic cardiac arrest.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
David Salcido ◽  
Christian Martin-Gill ◽  
LEONARD WEISS ◽  
David D Salcido

Background: Mobile phone-based dispatch of volunteers to out-of-hospital cardiac arrest (OHCA) has been shown to increase the likelihood of early chest compressions and AED application. In the United States, limited characterization of patients encountered as a result of such systems exists, including PulsePoint Respond, a smartphone-based volunteer dispatch system. Objective: Examine prehospital case characteristics and outcomes from a multi-year deployment of PulsePoint in Pittsburgh, Pennsylvania. Methods: Case data, including PulsePoint determinant triggers and timing, prehospital electronic health records (EHRs), and computer aided dispatch records were obtained for suspected EMS-treated OHCA cases that did and did not generate PulsePoint alerts within the service area of Pittsburgh EMS for the period July 2016 to October 2020. EHRs were reviewed to determine true OHCA status, and OHCA case characteristics were extracted according to the Utstein template. Key characteristics and the outcome of prehospital return of spontaneous circulation (ROSC) were summarized and compared between cases with and without PulsePoint dispatches. Chi-squared tests were used to determine statistical significance of relationships. Results: There were 1229 OHCA cases overall in the capture period, with an estimated 29.6% occurring in public. Of 840 total PulsePoint dispatches, 68 (8.1%) were for true OHCA. Forty-five (66.2%) of these were witnessed, 43 (63.2%) received bystander CPR, and 17 (25%) had an AED applied prior to first responder arrival. Twenty-seven (39.7%) had an initial shockable rhythm, and 34 (50%) achieved ROSC in the field. Compared to non-PulsePoint dispatch generating OHCA, PulsePoint alert-associated patients were significantly more likely to be male (p=0.024), have bystander CPR/AED application performed (p<0.001), have an initial shockable rhythm (p<0.001), and achieve ROSC (p<0.001). EMS response time, age, ALS response time, and witnessed status were not significantly different. Conclusions: A minority of PulsePoint dispatches in Pittsburgh were triggered by true OHCA. Among cases that did generate a PulsePoint dispatch, case characteristics were prognostically favorable.


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