Lowering body temperature in cardiac arrest patients with “non-shockable” heart rhythms increases survival rates and brain function, according to new research in the journal Circulation.

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Reducing the body’s core temperature can help prevent neurologic damage after cardiac arrest.

Therapeutic hypothermia intentionally lowers the body’s core temperature to a range of about 32° to 34° C (89.6° to 93.2° F) to protect the body following a period of insufficient blood flow due to such events as a cardiac arrest, blood clot or stroke.

It is typically used for patients who fail to regain consciousness after return of spontaneous circulation following a cardiac arrest. Previous studies have shown improved survival and neurological function in patients with “shockable” rhythms such as ventricular fibrillation, a condition where the lower chambers quiver and the heart is unable to pump any blood, causing cardiac arrest.

Cardiac arrest occurs when the heart malfunctions and stops beating, causing blood to stop pumping to the body. Death can result in minutes without treatment.

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Neurologic injury results when circulatory collapse impairs oxygen flow to the brain, causing mitochondrial and cellular death and cerebral edema; this is worsened by disruption to the blood-brain barrier in the initial injury.

Once circulation is restored, cell death triggers an inflammatory response in which the immune system releases neutrophils and macrophages to eliminate the dead cells, which produces free radicals that cause continued cell damage, worsening the inflammatory response and the cerebral edema in a vicious cycle.

Hypothermia counters neuroexcitation and reduces cell death by stabilizing the release of calcium and glutamate. It also stabilizes the blood-brain barrier and suppresses the inflammatory process, decreasing cerebral edema. Cerebral metabolism drops 6-10% for every degree Celsius that body temperature drops. As cerebral metabolism declines, the brain needs less oxygen.

Now, a new study shows that therapeutic hypothermia may also benefit comatose cardiac arrest patients with “non-shockable” heart rhythms – those that will not respond to the defibrillation because there is no pulse or electrical activity in the heart.

Researchers, led by Dr. Sarah Perman, assistant professor of emergency medicine at the University of Colorado in Aurora, examined data from 519 patients who had a cardiac arrest due to a non-shockable heart rhythm in the Penn Alliance for Therapeutic Hypothermia (PATH) registry between 2000-13.

Those who received therapeutic hypothermia were 2.8 times more likely to survive after cardiac arrest and 3.5 times more likely to have better neurologic recovery compared with those who were not cooled.

Dr. Perman explains that neurologic injury after cardiac arrest is devastating; the only chance doctors have to give some form of neuroprotection is immediately after the arrest.

She adds:

Our resources right now are not extensive and our outcomes are still fairly grim. Therapeutic hypothermia is one therapy we do have in our arsenal, and if a patient is comatose after arrest, it’s very important to consider applying this therapy, specifically in patients who are neurologically injured.”

Although the American Heart Association (AHA) have included guidelines for the use of therapeutic hypothermia in patients who suffer cardiac arrest since 2005, adoption of this practice has been low, especially for in-hospital cardiac arrest patients and those who arrest with initial non-shockable rhythms.

Unwillingness to apply the procedure is due to the perception that there is no benefit to patients who have an initial non-shockable rhythm.

The researchers would like to see more investigation into the use of neuroprotective strategies such as therapeutic hypothermia for cardiac arrest patients with non-shockable rhythms.

Earlier this year Medical News Today reported that therapeutic hypothermia can also help in the process of kidney transplantation.