Best practice & research. Clinical anaesthesiology
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More than 10 years ago, the randomised studies of therapeutic hypothermia after cardiac arrest showed significant improvement of neurological outcome and survival. Since then, it has become clear that most of the possible adverse events of therapeutic hypothermia are mild and can easily be controlled by proper administration of intensive care. ⋯ Hence, the exact level of target temperature, duration of cooling, rewarming, timing of the therapy and concomitant medication to facilitate therapeutic hypothermia will be important in the future. Additionally, the use of a post-resuscitation treatment bundle (specialised cardiac-arrest centres including intensive post-resuscitation care, appropriate haemodynamic and respiratory management, therapeutic hypothermia and percutaneous coronary intervention) could further improve treatment of cardiac arrest.
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Best Pract Res Clin Anaesthesiol · Sep 2013
Epidemiology and management of cardiac arrest: what registries are revealing.
Major European institutions report cardiovascular disease (CVD) as the first cause of death in adults, with cardiac arrest and sudden death due to coronary ischaemia as the primary single cause. Global incidence of CVD is decreasing in most European countries, due to prevention, lifestyle and treatment. Mortality of acute coronary events inside the hospital decreases more rapidly than outside the hospital. ⋯ There is considerable overlap between both definitions. But this explains that no single method can provide all information. Integrating data from multiple sources (local, national, multinational registries and surveys, death certificates, post-mortem reports, community statistics, medical records) may create a holistic picture of cardiac arrest in the community.
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Best Pract Res Clin Anaesthesiol · Sep 2013
Cardiac aetiology of cardiac arrest: percutaneous coronary interventions during and after cardiopulmonary resuscitation.
Management and prevention of cardiac arrest in the setting of heart disease is a challenge for modern cardiology. After reviewing the aetiology of sudden cardiac death and discussing the way to identify candidates at risk, we emphasise the role of percutaneous coronary interventions during and after cardiopulmonary resuscitation in the treatment of patients with return of spontaneous circulation after cardiac arrest.
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Best Pract Res Clin Anaesthesiol · Sep 2013
ReviewSOPs and the right hospitals to improve outcome after cardiac arrest.
Approximately 400,000 Europeans are yearly resuscitated from out-of-hospital cardiac arrest (OHCA).(1,2) Despite evolving evidence based guidelines for cardiopulmonary resuscitation (CPR), survival rates after OHCA has not improved much in several places around the world. However, a potential for improved survival is absolutely present, based on the huge spread in worldwide survival; some cities with survival over 20-30% and some cities with just a few percent.(1,2) These survival differences can partly be explained by different definitions of OHCA,(2) but mainly due to the overall quality of the local Chain of Survival (COS)(3); early arrest recognition and call for help, early CPR, early defibrillation and early post resuscitation care. By identifying and thereafter improving weak links in the local COS, survival can indeed increase. This review will focus on the quality of the last link in the COS, the hospital treatment after return of spontaneuous circulation (ROSC), and how good quality post resuscitation care can improve not only survival, but survival with neurologically intact outcome.
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The best predictor of good outcome after cardiac arrest is awakening from coma. The longer it takes to regain consciousness, the greater the risk of permanent brain injury. A reliable neurological assessment could previously be performed on day 3 after arrest; absence of or a stereotypic motor reaction to pain and absence of cranial nerve reflexes were reliable predictors of poor outcome, but this has changed. ⋯ This is probably due to increased use of sedative drugs and delayed metabolism during hypothermia but could, in addition, be explained by delayed maturation and recovery processes of brain ischaemia. A clinical neurological assessment should no longer be the sole decisive method for prognostication after cardiac arrest. Instead, a clinical investigation should be used in combination with independent and objective methods, above all neurophysiology (electroencephalography and somatosensory evoked potentials), while biomarkers and brain imaging may be valuable adjuncts.