In the Australian study, which involved 77 .
patients who remained comatose after the restoration of spontaneous circulation, 49% of .
those treated with hypothermia were discharged home or into a rehabilitation facility .
compared to the 26% of those not treated with hypothermia. There were no significant .
differences between the 2 groups with respect to the frequency of adverse events. The .
out come of the European study, which involved 9 center in 5 countries and had a larger .
number of patients, were similar. Taken together, the findings in these trials are important, .
because in the United States so far, permanent brain damage after cardiopulmonary- .
cerebral resuscitation causes many delayed deaths and is seen in about 10to 30 percent of .
survivors of out-of hospital cardiac arrest. The fact that 2 studies yielded similar results .
makes the important conclusions even more compelling. The rationale for the use of .
therapeutic hypothermia is complex. Spontaneous uncontrolled hypothermia start with .
potential deleterious shivering, thermo genesis , catecholamine release, and .
vasoconstriction, there as controlled hypothermia is potentially beneficial. Therapeutic .
hypothermia after cardiac arrest, as used in the 2 stories above, is directed at mitigating .
neurological injury. Temperature levels are important; mild hypothermia (33°C to 36°C) .
may be most effective, and is simple and safe. Moderate hypothermia (28°C to 32°C) can .
cause arrhythmias or even ventricular fibrillation and if prolonged, can lead to .
coagulopathy and infection. The timing and duration are important; mild hypothermia .
should be initiated as soon as possible after resuscitation, but even when delayed for a few .
.
hours, mild hypothermia has been shown to have some benefits un animal models of .
cardiac arrest. Mild hypothermia induced in patients for 12 hours, as in the Australian .
study, or 24 hours as in the European study, does not appear to have the putative .
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