Most recent studies from Pubmed:
Organ injury caused by ischaemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35 degrees C) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomised clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischaemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia,will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal "therapeutic window" for gene therapy.
AIM OF THE STUDY: Primarily, to investigate induction of therapeutic hypothermia during prehospital cardiopulmonary resuscitation (CPR) using ice-cold intravenous fluids. Effects on return of spontaneous circulation (ROSC), rate of rearrest, temperature and haemodynamics were assessed. Additionally, the outcome was followed until discharge from hospital. MATERIALS AND METHODS: Seventeen adult prehospital patients without obvious external causes for cardiac arrest were included. During CPR and after ROSC, paramedics infused +4 degrees C Ringer's acetate aiming at a target temperature of 33 degrees C. RESULTS: ROSC was achieved in 13 patients, 11 of whom were admitted to hospital. Their mean initial nasopharyngeal temperature was 35.17+/-0.57 degrees C (95% CI), and their temperature on hospital admission was 33.83+/-0.77 degrees C (-1.34 degrees The mean infused volume of cold fluid was 1571+/-517 ml. The rate of rearrest after ROSC was not increased compared to previous reports. Hypotension was observed in five patients. Of the 17 patients, 1 survived to hospital discharge. CONCLUSION: Induction of therapeutic hypothermia during prehospital CPR and after ROSC using ice-cold Ringer's solution effectively decreased nasopharyngeal temperature. The treatment was easily carried out and well tolerated.
Mild resuscitative hypothermia has been shown to improve neurological outcome after cardiac arrest presenting with ventricular fibrillation (VF) due to cardiac causes. We describe the experience of inducing mild hypothermia in three patients with non-cardiac causes of arrest and long delays before a return of spontaneous circulation (ROSC). In one patient, extreme metabolic acidosis due to inadvertent oesophageal intubation complicated therapy, and the role of point-of-care diagnostics in the prehospital setting is briefly discussed. All patients survived to discharge from hospital, and neuropsychological examinations revealed good recovery. It is concluded that mild resuscitative hypothermia may be beneficial also in patients with obvious non-coronary causes for cardiac arrest.While there is limited research on the topic of induced hypothermia, the research available is heavily in favor of the procedure. When I hear physicians criticize the immaturity of this therapy, I laugh thinking about epinephrine. As RM's last few posts have implied, Epi has been around for quite a while and there is no evidence in support of its use in cardiac arrest protocols. Would those physicians be so critical of Epi?