6Therapeutic hypothermia after cardiac arrest and myocardial infarction
Section snippets
Epidemiology of cardiac arrest
The world leading cause of morbidity and death are cardiovascular diseases. About 17 million people worldwide die from these each year.1 Many of theses deaths are due to sudden cardiac arrest. The incidence of out-of-hospital sudden cardiac arrest lies between 36 and 128 per 100,000 inhabitants per year in industrial countries. Unfortunately, full cerebral recovery after cardiac arrest is still a rare event. Eighty percent of patients after cardiac arrest stay in coma lasting more than one
Non-randomized trials
The first case series of hypothermia after cardiac arrest was published in the late 1950ies.38 Since then, over 20 non-randomized trials of therapeutic hypothermia after cardiac arrest have been published.39, 40, 41, 42, 43, 44, *45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62 The target temperature that has been used in these trials was very consistently a range of 32–34 °C, the rate of patients with ventricular fibrillation was between 35–100%, the time from cardiac
Cooling methods
The optimal timing and technique for the induction of hypothermia after cardiac arrest is not yet defined, and it is currently a major topic of ongoing research. The therapeutic hypothermia therapy consists of three phases: induction, maintenance and rewarming. Extrapolated from animal studies20 the induction of hypothermia should be initiated as early as possible after cardiac arrest. Ideally the maintenance phase should be done with a regulated device such to avoid overshoot of cooling or
Therapeutic hypothermia after cardiac arrest
Induced hypothermia significantly improves outcomes in comatose survivors after resuscitation from out-of-hospital cardiac arrest. As stated in the resuscitation guidelines 2005 of the European Resuscitation Council5 all comatose survivors after ventricular fibrillation out-of-hospital cardiac arrest should be cooled as fast as possible to a temperature of 32–34 °C over 12 to 24 hours. This therapy might also be beneficial in patients with other rhythms or causes or in-hospital cardiac arrest.
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Cited by (25)
Combined analyses of creatine kinase MB, cardiac troponin I and myoglobin in pericardial and cerebrospinal fluids to investigate myocardial and skeletal muscle injury in medicolegal autopsy cases
2011, Legal MedicineCitation Excerpt :In most cases of delayed brain injury death, hypothermia (cold exposure) and pneumonia, each marker was relatively low in both PCF and CSF, suggesting milder damage to the myocardium and skeletal muscles in the death process. Accidental hypothermia due to cold exposure may minimize damage to the viscera, including the myocardium and skeletal muscles, in the death process; it is clinically known that mild-to-moderate therapeutic hypothermia can stabilize hemodynamics, reduce myocardial damage and improve short-term survival [44,45]. In addition, postmortem decomposition is suppressed in a low-temperature environment.
Rapid cooling of the heart with total liquid ventilation prevents transmural myocardial infarction following prolonged ischemia in rabbits
2010, ResuscitationCitation Excerpt :Ultrafast cooling with TLV would therefore afford a greater protection even if technically challenging. It would be even more relevant to protect the heart against myocardial infarction in patients resuscitated from cardiac arrest with underlying coronary disease.7 In this setting, one might predict that TLV would protect both the heart and the brain and would be less challenging than for the treatment of myocardial infarction.
Hypothermia as a cytoprotective strategy in ischemic tissue injury
2010, Ageing Research ReviewsCitation Excerpt :Hypothermia has been widely used by several biomedical disciplines, and recognized as an effective cytoprotectant. It has been studied to improve outcome from myocardial infarction (Holzer and Behringer, 2008; Schefold et al., 2008), organ transplantation (El-Wahsh, 2007; Anaya-Prado and Delgado-Vazquez, 2008), cardiopulmonary bypass (Drinkwater and Laks, 1993), spinal cord injury (SCI) (Yoshitake et al., 2007), intestinal ischemia (Stefanutti et al., 2008), and neonatal hypoxia-ischemia (Wagner et al., 2002; Mishima et al., 2004; Zhu et al., 2004; Edwards and Azzopardi, 2006). At the clinical level, it has been shown from a small number of prospective randomized studies to improve neurological outcome from cardiac arrest (Bernard et al., 2002; HACA, 2002) and neonatal hypoxia-ischemia (Gluckman et al., 2005; Shankaran et al., 2005).
Anesthesia and analgesia protocol during therapeutic hypothermia after cardiac arrest: A systematic review
2010, Anesthesia and AnalgesiaTherapeutic hypothermia for acute myocardial infarction: Past, present, and future
2009, Critical Care Medicine