Article Archive
EMS Corner
Hypothermia as a treatment?
Vol. 26 Fall 2011

From EMT Basic training all the way through to full Paramedic, we have been trained to fight the battle of thermal effect problems, both Hypothermia and Hyperthermia.  We have passively warmed patients that were too cold and actively cooled patients that were too warm.  We have also fought since the beginning of EMS — cardiology was intimately involved in the early years — sudden cardiac death with Chain of Survival outlined by the American Heart Association.  With the incidence of out-of-hospital cardiac arrest consistently ranging from 350,000 to 450,000 per year and with only approximately 100,000 of those arresting subject to resuscitation, we are still only “saving” 40,000 of those to successful hospital admission. Of those 40k, the longer term outcome is very uncertain. Many of these will manifest what has come to be called “post-cardiac arrest syndrome” with effects such as brain and heart dysfunction and other systemic alterations.

The major problem seems to be neurological.  While we may be proficient (if you want to call 40 percent proficient) in restoring the cardiac function in many pre-hospital sudden cardiac deaths, in our resilient efforts to restore circulation, brain function seems to fall into a serious syndrome called “reperfusion injury”.  This occurs from hours to days after circulatory restoration and a complex chemical cascade causes the microcirculation within the cerebrum (as well as other factors common after cardiac arrest such as hypotension, hypoxemia, and cerebral swelling) and other target areas of the brain to fail causing neurological damage.

We all remember the treatment protocols for cold water drowning, or patients who have sustained substantial immersion below the thermocline (the dense layer of water that is near freezing, varying in depth depending on location).  We also understand the concept of the Mammalian Diving Reflex for cold water immersion that slows the body’s metabolic processes causing some cold water resuscitations to be effective at 30-40 minutes (+) of submersion.  We get the concept of “nothing is dead until it’s warm and dead." 

One can remember little “Jimmy T.” who spent 40 minutes under the ice, was fished out by Chicago Fire Department divers, rushed to the hospital and successfully resuscitated.  They then placed this child in a barbiturate coma (designed to reduce cerebral oxygen demands and swelling) for two weeks and when they weaned him off the powerful drugs they were found to have a healthy and un-afflicted child running around the pediatric unit. The fact the water was so cold and his body temperature dropped so low is a major contributing factor in his ability to survive.  Here is where some of the Therapeutic Hypothermia comes into play.

Targeted temperature management, also known as therapeutic hypothermia, is a therapeutic intervention that is intended to limit neurologic injury after a patient’s resuscitation from cardiac arrest.1The related drop in body temperature is designed to reduce cerebral oxygen demands due to a decrease in the metabolic rate.  Of course the placement of a patient into a therapeutic hypothermia regime requires certain ‘criteria’ such as coma from related cardiac induced arrest.  Patient criteria are outlined in table 1. 2

It is recommended that no delay in the administration of the therapeutic hypothermia be undertaken as the resultant delay may eliminate or decrease the benefit.  It is further recommended that an appropriate analgesic or paralyzing agent also be administered to prevent natural systemic reactions such a shivering which will increase body temperature and rescind the therapeutic effects.  Remember the caution when treating hyperthermia patients to NOT cool them to the point of shivering?

Field units will not have all of the fancy cooling methods available within the definitive care environment (water circulated cooling pads, etc.).  Therefore, we are reduced to more traditional applications such as cold IV fluids and applying cold packs at key points similar to treatment for hyperthermia.

Therapeutically induced hypothermia is not without its own set of complications.  Shivering (eliminated with paralytics), arrhythmia (bradycardia is most common), severe electrolyte disturbances which need serious monitoring to abate the first hint of a problem, and some related longer-term pneumonia are some that have been identified in various studies.  None of which, except for the shivering, are really a pre-hospital issue and will fall to the definitive environment to halt and correct when problems are detected.

Pre-hospital management is basically to maintain advanced airway therapeutics with CO2 monitoring seeking to maintain normal CO2 levels (35 – 40 mmHg, with care taken to not hyperventilate), perform a baseline neurological exam and record, and then bolus the patient with up to two liters of cold normal saline (0.9% NaCl).  Remember, this is for non-traumatic cardiac arrest patients that have return of spontaneous circulation (ROSC).  Hospitals follow with continued cooling and monitoring of electrolytes and systemic responses.  Rewarming takes place some 24-28 hours later.

This of course presented a problem that EMS had not come across before but one that was relatively simple to solve.  IV fluids, having to be chilled in the field in anticipation of utilization during a ROSC cardiac save, could not just be packed into ice chests.  We had to step up and go to 12V continuous temperature refrigerators (or 110v if there is an inverter in the rig) small enough to fit in available space and keep the beer, uh…, IV fluids, cold enough for use.  These were readily procured through commercial channels and will probably become smaller as space needs and commercial manufacturers step up to the plate to develop suitable ambulance devices.  (See Fig 2, photos)

For many of the same reasons that the CPR protocols have changed in recent years (rapid compressions seeking to establish and maintain perfusion pressures), science has now determined that cerebral perfusion, so dramatically decreased in post arrest patients, must now be allowed to be re-established before catastrophic damage takes place due to chemical and electrolyte changes disrupting the brain’s microcirculation.   So, as we have always tried to get our patients to “chill out” after a major event, now we can help by truly chilling them down.

Many thanks to AMR and Medic West of Las Vegas, Centennial Hills Hospital staff, and Dr. Ross Berkeley, Medical Director at CSN for their thoughtful assistance and consultation for this article.

1.  New England Journal of Medicine; 363;13 September 23, 2010

2. Ibid.


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