Literature DB >> 24717694

Early neuroprotection after cardiac arrest.

Antonio M Dell'anna1, Sabino Scolletta, Katia Donadello, Fabio S Taccone.   

Abstract

PURPOSE OF REVIEW: Many efforts have been made in the last decades to improve outcome in patients who are successfully resuscitated from sudden cardiac arrest. Despite some advances, postanoxic encephalopathy remains the most common cause of death among those patients and several investigations have focused on early neuroprotection in this setting. RECENT
FINDINGS: Therapeutic hypothermia is the only strategy able to provide effective neuroprotection in clinical practice. Experimental studies showed that therapeutic hypothermia was even more effective when it was started immediately after the ischemic event. In human studies, the use of prehospital hypothermia was able to reduce the time to target temperature but did not result in higher survival rate or neurological recovery in patients with out-of-hospital cardiac arrest, when compared with standard in-hospital therapeutic hypothermia. Thus, intra-arrest hypothermia (i.e., initiated during cardiopulmonary resuscitation) may be a valid alternative to improve the effectiveness of therapeutic hypothermia in this setting; however, more clinical data are needed to demonstrate any potential benefit of such intervention on neurological outcome. Together with cooling, early hemodynamic optimization should be considered to improve cerebral perfusion in cardiac arrest patients and minimize any secondary brain injury. Nevertheless, only scarce data are available on the impact of early hemodynamic optimization on the development of organ dysfunction and neurological recovery in such patients. Some new protective strategies, including inhaled gases (i.e., xenon, argon, nitric oxide) and intravenous drugs (i.e., erythropoietin) are emerging in experimental studies as promising tools to improve neuroprotection, especially when combined with therapeutic hypothermia.
SUMMARY: Early cooling may contribute to enhance neuroprotection after cardiac arrest. Hemodynamic optimization is mandatory to avoid cerebral hypoperfusion in this setting. The combination of such interventions with other promising neuroprotective strategies should be evaluated in future large clinical studies.

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Year:  2014        PMID: 24717694     DOI: 10.1097/MCC.0000000000000086

Source DB:  PubMed          Journal:  Curr Opin Crit Care        ISSN: 1070-5295            Impact factor:   3.687


  8 in total

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2.  Therapeutic hypothermia promotes cerebral blood flow recovery and brain homeostasis after resuscitation from cardiac arrest in a rat model.

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Authors:  Nidia Quillinan; Guiying Deng; Kaori Shimizu; Ivelisse Cruz-Torres; Christian Schroeder; Richard J Traystman; Paco S Herson
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4.  Calcium/Calmodulin-Dependent Kinase (CaMKII) Inhibition Protects Against Purkinje Cell Damage Following CA/CPR in Mice.

Authors:  Nicholas E Chalmers; Joan Yonchek; Kathryn E Steklac; Matthew Ramsey; K Ulrich Bayer; Paco S Herson; Nidia Quillinan
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5.  Evaluation of Cardiopulmonary Resuscitation Conditions in Turkey: Current Status of Code Blue.

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6.  Gynostemma pentaphyllum is neuroprotective in a rat model of cardiopulmonary resuscitation.

Authors:  Gerburg Keilhoff; Torben Esser; Maximilian Titze; Uwe Ebmeyer; Lorenz Schild
Journal:  Exp Ther Med       Date:  2017-10-16       Impact factor: 2.447

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8.  Breakthrough in cardiac arrest: reports from the 4th Paris International Conference.

Authors:  Peter J Kudenchuk; Claudio Sandroni; Hendrik R Drinhaus; Bernd W Böttiger; Alain Cariou; Kjetil Sunde; Martin Dworschak; Fabio Silvio Taccone; Nicolas Deye; Hans Friberg; Steven Laureys; Didier Ledoux; Mauro Oddo; Stéphane Legriel; Philippe Hantson; Jean-Luc Diehl; Pierre-Francois Laterre
Journal:  Ann Intensive Care       Date:  2015-09-17       Impact factor: 6.925

  8 in total

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