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Cooling the body after cardiac arrest

Arrich J, Holzer M, Havel C, Müllner M, Herkner H
Published Online: 
12 September 2012

Sudden cardiac death means that the heart and subsequently the circulation stops. Patients with a structural heart disease like coronary heart disease have a higher risk for sudden cardiac death. Around 30% to 50% of all patients with coronary heart disease suffer sudden cardiac death at some stage of their illness. In cardiac arrest the brain lacks blood and oxygen and the patient loses consciousness. After a few minutes of lack of oxygen brain cells begin to be irreversibly damaged. Although potentially lethal, if a patient in cardiac arrest is found and resuscitated early, they may be saved and brain damage prevented. To date about one tenth to a third of successfully resuscitated patients leave hospital to live an independent life again.

One form of therapy that may help to improve these neurologic deficits is called 'therapeutic hypothermia' or 'resuscitative hypothermia'. It is a form of therapy where patients that have been resuscitated after cardiac arrest and are still unconscious after resuscitation are cooled to 33 °C for several hours. Clinical trials have shown that with therapeutic hypothermia the neurologic damage caused by the cardiac arrest may be attenuated. Pathophysiologic studies discovered that therapeutic hypothermia works in many different ways. One way is that it lowers cell metabolism and prevents the production of harmful substances that form during resuscitation and continuously damage the brain cells. Hypothermia may be initiated by different methods like cold drips, cooling pads or cooling catheters.

We have summarized three randomized trials with conventional cooling methods on a total of 383 patients that evaluated the effects of therapeutic hypothermia in patients resuscitated after cardiac arrest in comparison to resuscitated patients treated without therapeutic hypothermia. With conventional cooling methods like cooling blankets or cooling helmets, patients were 55% more likely to leave the hospital without major brain damage. When the results of two additional studies (one study only published as an abstract and another comparing cooling through haemofiltration) were added, this effect remained unchanged. No cooling specific adverse events were reported. One of the limitations of our review is that the majority of patients had a specific form of cardiac arrest, with ventricular fibrillation and ventricular tachycardia as the underlying cardiac rhythm. In summary, there is current evidence supporting the use of conventional cooling to induce mild hypothermia in cardiac arrest survivors within the first hours of resuscitation.

This record should be cited as: 
Arrich J, Holzer M, Havel C, Müllner M, Herkner H. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database of Systematic Reviews 2012, Issue 9. Art. No.: CD004128. DOI: 10.1002/14651858.CD004128.pub3
Assessed as up to date: 
25 July 2011