The Big Chill: Therapeutic Hypothermia

Arthur Hsieh // February 23, 2011

Actively cooling the body's core temperature during cardiac bypass surgery has been a mainstay procedure since the 1950s. However, in the early 2000s, researchers began applying the concept of rapidly inducing hypothermia after a sudden cardiac arrest.

The first interventions used ice packs and cold saline to chill the body; today's resuscitation teams use cooling blankets and other technologies to also control the rate of cooling, maintain a constant temperature, and control the temperature rise, too.

Why does it work?
It's been medical dogma that the brain cannot survive without oxygen for only 4 to 6 minutes before its cells start to die. The entire modern history of cardiac resuscitation is virtually based on this theory.

However, it is possible that the brain goes into an essentially "fail safe" mode, where metabolism dramatically slows when experiencing a sudden "no flow" state, severely reducing its need to nutrients and oxygen.

Perhaps even more dramatic, when the brain is subjected to a sudden onslaught of blood, i.e., immediately after cardiac arrest is reversed, a series of inflammatory reactions begin to destroy brain cells, rather than help them to survive.

This adverse response takes place in normal operating body temperatures; chilling the environment can minimize or perhaps even eliminate this event. Hence, therapeutic hypothermia is a real breakthrough concept in cardiac resuscitation, helping to "save the brain" after we save the heart.

How does it work?
While the optimal approach for applying cooling measures is not yet known, recommendations are to achieve a core body temperature of 32 – 34 degrees C (89.6 – 93.2 F) within 3 to 4 hours of initiating the procedure. The goal is to maintain this temperature for about 24 hours before rewarming the patient through a very controlled process.

It appears crucial that the rate of dropping the temperature is as important as the goal temperature itself. If the body is chilled too slowly, the body will attempt to generate heat through shivering, which may interfere with the cooling process.

There are newer technologies that wrap the patient with a cooling blanket, or the use of invasive cooling catheters that are inserted into the femoral vein and chilled with cold saline. Using these types of devices not only cool the patient rapidly but work more predictably than just ice packs.

Once cooling has been achieved, the patient is kept at the lower temperature for the remaining 24 hours. The patient is kept sedated and sometimes paralyzed to minimize agitation and unnecessary metabolic demands.

Critical care teams work to maintain an adequate blood pressure, normal gas levels, and minimize cardiac dysrhythmias. Toward the end of this period, the process of bringing the core temperature back to normal begins slowly. The rate of temperature rise is about 0.3 to 0.5 degrees C (0.5 to 0.9 degrees F) per hour, to about 36 degrees C (96.8 F). This process may take 8 hours or longer to complete.

There are a few side effects associated with therapeutic hypothermia; these can include bleeding as well as small risk of infection from a depressed immune system.

However, there appears to be significant benefit that outweighs the risks associated with the procedure; many cardiac centers are adopting the technique and equipment. EMS systems are working in conjunction with hospitals to begin the process in the field environment and accelerate the cooling rate.

Are there other uses?
There are current studies examining the use of therapeutic hypothermia with traumatic brain injuries, stroke, and spinal cord injuries.

In the past 50 years, resuscitation science has been fine tuning the art of resuscitation. Researchers have begun focusing on the post resuscitation phase, where procedures such as therapeutic hypothermia hold real promise in increasing survival from sudden cardiac arrest.


1. Jess Arcure BS, MSC; Eric E Harrison MD. (2009). "Review Article of the Use of Early Hypothermia in the Treatment of Traumatic Brain Injuries." JSOM Summer 2009 Volume 10 Edition 1 10.

2. Schwab, S. et al. "Moderate Hypothermia in the Treatment of Patients with Severe Middle Cerebral Artery Infarction." American Heart Association. July 31, 1998, pg. 2461-2466.

3. Florian B, et al. (2008). "Long-term hypothermia reduces infarct volume in aged rats after focal ischemia." Neuroscience Letters 438 (2): 180–18.

4. The Prophylactic Hypothermia Trial to Lessen Traumatic Brain Injury (POLAR-RCT). Ongoing Clinical trial by the Australia and New Zealand Intensive Care Society, Clinical Trials Group. Retrieved 1 February 2011

5. Dietrich, WD. (2009) Therapeutic hypothermia for spinal cord injury. Critical Care Medicine 37(7 Suppl):S238-42.

6. Science Daily. Optimizing Patient Outcomes After Therapeutic Hypothermia for Traumatic Brain Injury. Retrieved 12 February 2011.

7. Yenari, MA and Hemmen, TM. (2010) Therapeutic Hypothermia for Brain Ischemia: Where Have We Come and Where Do We Go? Stroke 41:S72-S74.


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