scholarly journals Post-cardiac arrest syndrome in adult hospitalized patients

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 ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Michael K Levy ◽  
Karl B Kern ◽  
Dana Yost ◽  
Bjarne Madsen Hardig ◽  
Fred W Chapman

Recent observational studies have found associations between poorer outcomes and treatment that included mechanical CPR devices, contradicting findings from randomized trials. Resuscitation time bias is a systematic error occurring in observational studies of interventions applied to pulseless patients later in resuscitation attempts. Previous observational studies lack data on duration of resuscitation, a factor strongly related to outcome. We retrospectively analyzed cardiac arrest data to learn how resuscitation time and device use relate to clinical outcomes, and determine whether resuscitation time bias was present. Methods and Results: We analyzed data from all 49 patients with ventricular fibrillation, out-of-hospital cardiac arrest treated by our emergency medical service in one year. We compared 19 patients who received only standard manual CPR (the sCPR group) to 30 patients who received manual followed by mechanical CPR (the mCPR group). Response to CPR differed between groups even before device application. All sCPR patients achieved return of spontaneous circulation (ROSC), and did so after a median (IQR) of 3.3 (2.2-5.1) minutes of manual CPR. Patients in the mCPR group failed to get ROSC through 6.9 (5.3-11.0) min of manual CPR; mCPR patients that did get ROSC did so after 11.2 (5.7-23.8) additional minutes of CPR, delivered by a mechanical device. mCPR patients also received significantly more defibrillations and ALS drugs. ROSC and survival to hospital discharge were higher in the sCPR than the mCPR group (100% vs. 70%, P = 0.008; 74% vs. 43%, P = 0.045). Conclusion: Only patients remaining pulseless after early resuscitation efforts received mechanical CPR. Consequently, mechanical CPR devices assisted by facilitating prolonged treatment of patients who already had lower chances of survival before device application. Resuscitation time bias was present, and must be considered when interpreting registry reports comparing sCPR and mCPR.


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.


2020 ◽  
pp. 088506662090680
Author(s):  
Natalie Achamallah ◽  
Jeffrey Fried ◽  
Rebecca Love ◽  
Yuri Matusov ◽  
Rohit Sharma

Introduction: Absence of pupillary light reflex (PLR) is a well-studied indicator of poor neurologic recovery after cardiac arrest. Interpretation of absent PLR is difficult in patients with hypothermia or hypotension, or who have electrolyte or acid-base disturbances. Additionally, many studies exclude patients who receive epinephrine or atropine from their analysis on the basis that these drugs are thought to abolish the PLR. This observational cohort study assessed for presence or absence of PLR in in-hospital cardiac arrest patients who received epinephrine with or without atropine during advanced cardiac life support and achieved return of spontaneous circulation (ROSC). Methods: Pupil size and reactivity were assessed in adult patients who had an in-hospital cardiac arrest, received epinephrine with or without atropine, and achieved ROSC. Measurements were taken using a NeurOptics NPi-200 infrared pupillometer. Results: Forty patients had pupillometry performed within 1 hour (median: 6 minutes) after ROSC. Of these only 1 (2.5%) patient had nonreactive pupils at first measurement after ROSC. The remaining 39 (97.5%) had reactive pupils. Of the 19 patients who had pupils checked within 3 minutes of ROSC, 100% had reactive pupils. Degree of pupil responsiveness was not correlated with cumulative dose of epinephrine. Ten patients received atropine in addition to epinephrine, including the sole patient with nonreactive pupils. The remaining 9 (90%) had reactive pupils. Conclusion: Epinephrine and atropine do not abolish the PLR in patients who achieve ROSC after in-hospital cardiac arrest. Lack of pupillary response in the post-arrest patient should not be attributed to these drugs.


Author(s):  
Jerry P Nolan ◽  
Christian Hassager

Cardiac arrest is the most extreme of medical emergencies. If the victim is to have any chance of high-quality neurological recovery, cardiac arrest must be diagnosed quickly, followed by summoning for help as basic life support (chest compressions and ventilations) is started. In most cases, the initial rhythm will be shockable, but this will have often deteriorated to a non-shockable rhythm by the time a monitor and/or defibrillator is applied. While basic life support will sustain some oxygen delivery to the heart and brain and will help to slow the rate of deterioration in these vital organs, it is important to achieve restoration of a spontaneous circulation as soon as possible (by defibrillation if the rhythm is shockable). Once return of spontaneous circulation is achieved, the quality of post-cardiac arrest management will influence the patient's final neurological and cardiological outcome. These interventions aim to restore myocardial function and minimize neurological injury.


Resuscitation ◽  
2016 ◽  
Vol 106 ◽  
pp. e65
Author(s):  
Matthias Treutlein ◽  
Claus-Martin Muth ◽  
Alexander Dinse-Lambracht

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jong Hwan Kim ◽  
Jeong Ho Park ◽  
Sun Young Lee ◽  
Sang Do Shin ◽  
Jieun Pak ◽  
...  

Objectives: Targeted temperature management (TTM) is the core post-resuscitation care to minimize neurologic deficit after out-of-hospital cardiac arrest (OHCA). Uncontrolled body temperature of patients may reflect the thermoregulation ability which can be associated with neurologic damage during arrest. The aim of this study was to investigate the association between initial body temperature (BT) and neurologic outcomes in OHCA patients who underwent TTM. Methods: We used nationwide OHCA database from January 2016 to December 2017. Adult OHCA patients with presumed cardiac etiology who underwent TTM after return-of-spontaneous circulation (ROSC) were included. The main exposure was a BT at initiation of TTM which was categorized into 3 groups: low (-35.5°c), middle(35.6°c-37.4°c), and high BT (37.5°c-). The primary outcome was good neurologic outcome (cerebral performance categories (CPC) 1 or 2). Adjusted ratios (AORs) and 95% confidence intervals (CIs) were estimated to evaluate association between initial BT of TTM and outcome in multivariable logistic regression model. Stratified subgroup analyses were according to the target temperature of TTM (hypothermia vs normothermia). Results: Of a total of 744 patients, 208 (28.0%) patients were low initial BT group and 471 (63.3%) patients were normal initial BT group and 65 (8.7%) patients were high initial BT group. Good neurological recovery rate was 13.9% in low initial BT group, 41.8% in middle initial BT group and 36.9% in high initial BT group. The adjusted odds ratios for good neurologic recovery were 0.281 (95% confidence interval [CI] 0.17-0.47) in low BT group and 0.65 (95% CI 0.34-1.27) in high BT group compared with normal initial BT group. Similar results were also found regardless of target temperature of TTM. Conclusion: Low initial BT of TTM was associated with unfavorable neurologic recovery for OHCA patients who underwent TTM after ROSC.


Author(s):  
Jerry P. Nolan ◽  
Michael J. A. Parr

Systemic ischaemia during cardiac arrest and the reperfusion response after return of spontaneous circulation (ROSC) cause the post-cardiac arrest syndrome (PCAS). The severity and duration of this syndrome is determined by the cause and duration of cardiac arrest, quality of resuscitation, and interventions after ROSC. Four key clinical components are recognized—post-cardiac arrest brain injury, myocardial dysfunction, other organ ischaemia/reperfusion (e.g. liver, kidney), and potential persistence of the precipitating pathology causing the cardiac arrest. The interventions applied after ROSC impact significantly on the quality of survival. All components of the PCAS need to be addressed if outcome is to be optimized; treatment should start immediately after ROSC. An ‘ABCDE’ (Airway, Breathing, Circulation, Disability, Exposure) systems approach is used to identify and treat physiological abnormalities and organ injury. All survivors of out-of-hospital cardiac arrest should be considered for urgent coronary angiography unless the cause of cardiac arrest is clearly non-cardiac or continued treatment is considered futile. Targeted temperature management (mild hypothermia and avoidance of hyperthermia) should be considered for those patients who remain comatose after ROSC. If targeted temperature management has been used, early prognostication on outcome is unreliable and should be delayed until 3 days after return to normothermia; it should not rely on just one modality.


Author(s):  
Marwan F. Jumean ◽  
Mark S. Link

Our understanding of arrhythmias following resuscitated cardiac arrest has evolved over the past two decades to entail complex pathophysiological processes including, in part, ischaemia and ischaemia-reperfusion injury. Electrical instability after the return of spontaneous circulation (ROSC) is common, ranging from atrial fibrillation to recurrent ventricular tachycardia and fibrillation. Electrical instability following out-of-hospital cardiac arrest is most commonly due to myocardial ischaemia and post-arrest myocardial dysfunction. However, electrolyte disturbances, elevated catecholamine levels, the frequent use of vasopressors and inotropes, and underlying structural heart disease or channelopathies also contribute in the acute setting. Limited data exists that specifically address the management of arrhythmias in the immediate post-arrest period. In addition to treating any potential reversible cause, the management in the haemodynamically-stable patient includes beta-blockers, class I (lignocaine and procainamide) and III anti-arrhythmic agents (amiodarone). Defibrillation is often needed for recurrent ventricular arrhythmias.


Author(s):  
Jerry P Nolan

Cardiac arrest is the most extreme of medical emergencies. If the victim is to have any chance of high-quality neurological recovery, cardiac arrest must be diagnosed quickly, followed by summoning for help as basic life support (chest compressions and ventilations) is started. In most cases, the initial rhythm will be shockable, but this will have often deteriorated to a non-shockable rhythm by the time a monitor and/or defibrillator is applied. While basic life support will sustain some oxygen delivery to the heart and brain and will help to slow the rate of deterioration in these vital organs, it is important to achieve restoration of a spontaneous circulation as soon as possible (by defibrillation if the rhythm is shockable). Once return of spontaneous circulation is achieved, the quality of post-cardiac arrest management will influence the patient’s final neurological outcome. These interventions aim to restore myocardial function and minimize neurological injury.


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