Raising the Dead

     Patients resuscitated from cardiac arrest today are treated with a variety of regimens, including pharmacological therapy, intra-aortic balloon pumps, extracorporeal membrane oxygenation and lengthy stays in state-of-the-art intensive care units. Despite all the treatments available, the success rate for resuscitation to hospital discharge has remained relatively unchanged over the last 50 years. In other words, while all the technological advances have increased survivability of sudden cardiac arrest, patients are not surviving long enough to be discharged from the hospital, and, if they do survive, many have significant neurological impairment.

     Three quarters of cardiac arrests occur in the prehospital setting, with fewer than 5% of those patients surviving to discharge. Of the surviving patients, only 2% will be discharged with minor to no neurological deficits (minor being defined as able to live at home and maintain a part-time job). Many EMS services boast cardiac arrest resuscitation rates nearing 20%; however, many of these patients never survive to discharge from the hospital.1,2 Increasing application of therapeutic hypothermia may help to bridge the gap.

THERAPEUTIC HYPOTHERMIA THROUGH THE AGES
     Therapeutic hypothermia induction is not new; it has actually been well documented throughout medical literature. The use of hypothermia was described by the ancient Egyptians, Greeks and Romans dating back to 2500 B.C. (the Ebers papyrus) and 1600 B.C. (the Smith papyrus). In 450 B.C., Hippocrates hypothesized about packing patients in snow, stating that the cold would be beneficial to them. In 1814, Baron Larrey, a battlefield surgeon in Napoleon's army at the invasion of Russia, found that injured soldiers who were placed next to campfires died sooner than those left in the cold. In the 1930s, Germany experimented with hypothermia in prison camps to learn about the effects of cold water on downed airmen. From the 1950s to 1990s, hypothermia was mentioned sporadically throughout medical literature; however, while benefits seemed clear, there had been an overall hesitation to use therapeutic hypothermia on patients because of numerous documented untoward effects. Research conducted soon found that the majority of detrimental effects were caused by moderate-to-deep hypothermia induction (temperatures ranging from 15°C to 25°C) and were potentiated by extended length of induction (several days at a time, up to 10 days).

     Several studies conducted in 2001 and 2002 demonstrated the efficacy of therapeutic hypothermia induction if mild hypothermia was induced (temperatures ranging from 32°C to 34°C) and maintained for a shorter time (one to two days, with a slow return to normal temperature).3 Considered among the benchmark studies of therapeutic hypothermia, two studies published in 2002 in the New England Journal of Medicine demonstrated that hypothermic patients had a better neurological outcome than the normothermic control group (55% versus 39%).4 The European and Australian Hypothermia After Cardiac Arrest (HACA) trial both showed that survivability nearly doubled with mild, shorter-term hypothermia induction and detrimental effects were limited (see Figure 1).5 Numerous studies from around the world were published shortly after the European and Australian studies that validated the efficacy of therapeutic hypothermia in the hospital setting.

     In 2003, physicians attending the Rocky Mountain Critical Care Conference globally agreed that therapeutic hypothermia should be introduced as a standard of care for post-cardiac arrest patients. Following the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation (ILCOR) meeting in 2005, the American Heart Association (AHA) officially endorsed hypothermia induction for return of spontaneous circulation with adult patients.6 It gave prehospital therapeutic hypothermia induction a Class IIA endorsement for all ventricular fibrillation and ventricular tachycardia arrests, and a Class IIB endorsement for pulseless electrical activity and asystole arrests that were cardiac in origin.

     A tremendous body of literature, backed by growing clinical and in-field application, now supports the use of mild hypothermia induction, and medical providers from paramedic to physician are considering this treatment modality. Several ongoing global meetings, like the Therapeutic and Temperature Management (TTM) Congress (see www.ttmcongress.net), are serving as dynamic and vital resources for the transfer of best-practice protocols, applications and solutions.

POST-CARDIAC ARREST CARE: CEREBRAL RESUSCITATION IS THE GOAL
     An important concept to understand about therapeutic hypothermia is that it acts primarily upon the brain, with some cardiovascular benefits. The concept of post-cardiac arrest care is now aimed toward cerebral resuscitation, not just cardiac resuscitation.

     Ask any EMT or paramedic when cellular damage occurs following cessation of oxygenated blood and you'll get the standard textbook answer: after three to five minutes. For years, we have been under the impression that cellular damage occurs almost immediately when oxygenated blood flow is interrupted, but Dr. Lance Becker at the University of Pennsylvania made a recent discovery that revolutionized the way we think about cardiac arrest resuscitation. "We put oxygen-starved heart cells under a microscope, and after one hour we couldn't see any evidence the cells had died," says Becker. "We thought we had done something wrong. Matter of fact, the cells cut off from the blood supply died hours later."7

     When a cell becomes ischemic, three critical changes occur within the cell, including reactive oxygen species (the formation of oxygen free radicals), mitochondrial dysfunction and cellular inflammatory cascades. Scientists have known for decades that oxygenation starvation in cells will cause damage and, if untreated, will lead to cell death. However, Becker's research helped to explain the theory of radical cell death and, more important, the new concept of reperfusion injury, defined as injury that occurs upon the reintroduction of oxygen into the ischemic cell (see Figure 2).

     In order to further understand the theory of radical cell death, it is important to understand the implication of oxygen free radicals and reactive oxygen species. Mitochondria within the cell require oxygen to produce energy. After the oxygen is used within the mitochondria, an oxygen free radical is released. Normally, within the healthy body, oxygen free radicals are forming; however, our body creates antioxidants that help to combat the oxygen free radicals. The formation of oxygen free radicals is the foundation for aging and one of the primary reasons why the human body fails with age. One reason oxygen free radicals are detrimental is that they contain an unpaired valence electron in the outer shell. These free radicals are highly reactive because the unpaired electrons are seeking to pair up with other electrons. The pairing of electrons causes a chemical chain reaction that uses adenosine triphosphate and causes production of lactic acid.

     During time of major injury or anoxic insult, the body drastically reduces production of the oxygen free radical fighting antioxidants. It is because of this dramatic decrease in antioxidants that oxygen free radicals become a major problem in the comorbid or severely injured patient. Simply put, higher than normal levels of oxygen in the acutely ill or injured patient facilitate production of oxygen free radicals and cause increases in energy use and lactic acid production.

     As previously mentioned, reperfusion injury has several negative physiologic implications. Reperfusion injury causes vascular dysfunction, hypotension, organ dysfunction, cerebral edema and apoptosis (programmed cell death). Hypothermia induction helps to prevent these negative side effects and is beneficial at various stages throughout post-arrest reperfusion injury.

CARDIAC-ARREST SURVIVABILITY: TIME & TEMPERATURE ARE OF THE ESSENCE
     More than 80% of post-cardiac arrest patients will become hyperthermic (temperatures greater than 38°C). The exact mechanism behind this increase in temperature is not known; however, research has proven that an increase in cerebral temperature leads to poor neurological outcome. Cerebral neurons are exquisitely sensitive to changes in temperature. Temperatures above 38°C have been shown to precipitate neuronal death and accelerate death in tissue that is ischemic but not yet dead. Post-cardiac arrest hyperthermia can be seen for days post-insult and needs to be aggressively managed within the hospital.

     So, how does hypothermia help? There are three distinct stages of cerebral damage following anoxic insult: early, intermediate and late. The early stage occurs from the moment of insult to one hour after injury. During this stage, cerebral blood flow decreases while metabolic demand increases. Consumption of oxygen, glucose and adenosine triphosphate is still ongoing, despite a dramatic reduction in supply. During this stage, hypothermia works to significantly decrease the metabolic demands on the brain. By lowering body temperature to 32°C, the metabolic demands of the brain are reduced up to 50%. Hypothermia induction also helps to reduce cerebral edema and intracranial pressure. At rest, the brain uses 20% of the oxygen inhaled and 25% of the glucose ingested. Following hypoxic insult, the oxygen and glucose demands on the brain can double. Studies have shown that some of the most important benefits of therapeutic hypothermia are achieved if therapy is started within 15 minutes of resuscitation. A recent study has demonstrated that the odds of neurological impairment increase 30% for every hour after resuscitation that therapeutic hypothermia is delayed.8 That is why it is so important to consider starting the therapy in the prehospital arena and why EMS' role is so critical in affecting future survivability success.

     The intermediate stage occurs from one to 12 hours post-insult. During this stage, excitatory amino acids and glutamate are released in the brain. Glutamate activates the ion channels in the brain, causing calcium to rush into the intracellular space, which causes neuronal cell death by synergistically activating cytotoxic cascades within cells. Free radicals and nitric oxide are also produced during this stage. Varied levels of nitric oxide in the brain following cardiac arrest can cause vasoconstriction, vasodilatation and vasospasms. Hypothermia induction helps during this stage by decreasing the release of excitatory amino acids and glutamate, as well as decreasing production of nitric oxide.

     The late stage occurs from 12–24 hours post-insult and is accentuated by marked cerebral edema, breakdown of the blood-brain barrier, seizures and irreversible neuronal death. During this stage, hypothermia works by decreasing cerebral edema, thus decreasing intracranial pressure, and by slowing deterioration of the blood brain barrier. It is important to note that if seizures are observed 12–48 hours post-cardiac arrest, it is usually considered an agonal sign and therefore an indicator of irreversible and fatal brain damage.

THERAPY ADOPTION: COMMON OBSTACLES AND HOW TO OVERCOME THEM
     To date, out of 24,000 EMS agencies in the United States, approximately 100 have implemented a therapeutic hypothermia protocol and the number is rapidly increasing, including large agencies like King County EMS (Seattle, WA), Boston EMS, Wake EMS (Raleigh, NC) and Phoenix Fire Department. Outside the United States, there are several large EMS services actively practicing therapeutic hypothermia, including Vienna (Austria) EMS, London EMS, Scottish Ambulance Service and Melbourne (Australia) Ambulance Service. As clinical consultants for several large EMS agencies that have implemented a therapeutic hypothermia protocol, we have been able to view firsthand the reluctance and issues EMS agencies face when they consider protocol implementation.

     Even with full endorsement by the AHA, one of the issues that must frequently be addressed is the efficacy of therapeutic hypothermia induction, which some physicians still consider trial-based rather than evidence-based medicine. Although proof concerning the advantages of mild, shorter-term therapeutic hypothermia is relatively recent, hundreds of articles in peer-reviewed scientific medical journals demonstrate increased survivability with relatively few adverse effects when conducted in hospital. However, it is important to note that relatively few studies have researched the efficacy of therapeutic hypothermia initiated in the prehospital arena.

     Some physicians are hesitant to adopt this protocol for out-of-hospital cardiac arrest simply because there is limited data for prehospital hypothermia application versus the large body of research conducted within the hospital. The European Resuscitation Council stated that prehospital hypothermia is "safe and effective even if there is a lack of experience."9 Several research articles have emphatically concluded that "therapeutic hypothermia is safe and feasible, and a clear biological rationale for the earliest possible induction of therapeutic hypothermia exists; and that a prospective and randomized trial in the prehospital setting is not feasible, nor is it justifiable."10 Articles have also noted that "withholding therapeutic hypothermia in a prehospital control group would be unjustifiable from an ethical point of view."11

     Again, the majority of adverse effects (see Table 1) have generally been seen with moderate-to-deep hypothermia and induction that lasts several days rather than hours. Research has shown few complications associated with mild hypothermia, as long as induction does not exceed 36 to 48 hours.

     Another concern related to pre-hospital hypothermia induction is determining a receiving hospital. Obviously there is very limited benefit to inducing hypothermia in the field only to have the hospital immediately rewarm the patient. Some EMS agencies have wanted to implement a protocol but have not had a receiving hospital that would continue treatment.

     Some EMS agencies have actually implemented the protocol without any receiving hospitals in the immediate area; however, area hospitals later developed a protocol so post-ROSC patients could be transferred to their facility.

     Arizona's Bureau of EMS developed a unique approach when Dr. Ben Bobrow, the state's medical director, implemented a Level I cardiac arrest center. In order to be designated as such, the hospital had to offer some form of therapeutic hypothermia. This is considered so important that the Bureau of EMS has allowed ambulances to bypass the closest hospital to transport patients to a Level I cardiac arrest center, as long as transport time will not exceed 15 minutes. Currently, 13 hospitals in Arizona have achieved this designation and more are expected soon.

     Another EMS option is to utilize the local air medical provider to fly patients to hospitals that support therapeutic hypothermia. Air medical providers in the United States are quickly implementing a therapeutic hypothermia protocol in order to facilitate rapid pre-hospital cooling and rapid transport to hospitals that will continue the cooling.

     How is hypothermia induced in the field? In Seattle's King County Medic One trial (2001), paramedics used two liters of ice-cold saline infusions (3°C) to lower core body temperature in the field. The study found that paramedics were able to lower core temperature by 1.4°C in 30 minutes using ice-cold saline alone. It is important to note that studies have concluded that rapid infusion of two liters of ice-cold saline will not induce pulmonary edema, even in the comorbid post-arrest patient.12–14 However, if the patient arrested because of pulmonary edema, infusion of two liters of fluid is contraindicated.

     At Regional One Air Medical Service in South Carolina (a Med-Trans Corporation flight program), we decided to implement a therapeutic hypothermia protocol in early 2005, when the AHA endorsed the practice. We believed that despite the limited evidence for therapeutic hypothermia in the prehospital arena, we would not selectively choose to adopt parts of the ACLS algorithms while ignoring other recommendations (i.e., the "a la carte" method of resuscitation). A recent study found that 21% of EMS physicians who do not advocate therapeutic hypothermia refrain because of the lack of specific wording within the AHA guidelines advocating that it be started in the prehospital arena.15 Recognizing the benefits of early therapeutic hypothermia, the European Resuscitation Council stated in its guidelines that therapeutic hypothermia "must be initiated as soon as possible," which has led many European EMS agencies to adopt the policy prehospital.16 Because therapeutic hypothermia was researched thoroughly and fully endorsed by the AHA without specific reference to in-hospital versus out-of-hospital initiation, we felt it would be beneficial to adopt the complete resuscitation algorithm at our service. Like many others, we felt it would be unethical to withhold a proven treatment from our patients. To underscore this point, there are now attorneys specializing in lawsuits against medical practitioners who do not use therapeutic hypothermia or who do not offer it as a treatment modality.17

     At Regional One we've implemented a multiple-method cooling approach. The patient is exposed and covered with a saline-soaked sheet, then packed with chemical ice packs (usually four to six strategically placed around the axilla, groin and neck), and the air conditioner is turned on in the aircraft cabin. Next, the patient is infused with the standard two liters of 4°C saline. We found that by actively cooling both internally and externally, patients were cooled an average of 3°C during a 30-minute flight. Several patients have actually reached therapeutic levels (33°C) during a 30-minute flight. A prehospital study published in 2008 from France demonstrated that if therapeutic hypothermia was initiated during resuscitation, patients achieved therapeutic temperature (34°C) in 16 minutes following return of spontaneous circulation.18

     Maintaining chilled intravenous fluids in the aircraft or ambulance has been cited as one of the difficult hurdles to overcome. Wake County (Raleigh, NC) EMS opted to transport chilled saline in coolers in the supervisor's vehicle, freeing up space in the ambulance, yet ensuring materials are available for all cardiac calls. Some agencies are using coolers, while others are choosing to use freezers.

     There is a big difference between a cooler and a freezer. A cooler is able to cool to 40°F less than the ambient air temperature. Hence, a cooler in Las Vegas, where ambient temperature may reach 110°F, will only be able to chill fluids to 70°F, far from therapeutic levels. A freezer can chill regardless of the ambient temperature. Coolers cost as little as $20, whereas freezers start around $300. Some agencies elect to chill fluids in a base freezer, then place them in coolers in the trucks, where they are able to maintain their temperature for a longer period of time. A cooler is much more effective if the fluid is already chilled prior to being placed inside. Most coolers and freezers operate off a 110 DC current or use a standard cigarette lighter plug. Agencies need to consider having fluid in a refrigerator/freezer available for restocking at the hospital so medics can pick up fluid that is already chilled in case they run back-to-back cardiac arrests. Another consideration when purchasing a cooler or freezer is whether you want to purchase a unit that meets FDA approval for intravenous fluids. One EMS agency implemented a hypothermia protocol and quickly purchased 12-volt coolers for all of its ambulances. After a few short months, they realized that the coolers were not designed to run constantly in the trucks and were unable to cool the IV fluids. Many of the coolers failed mechanically after several weeks. After outfitting the entire fleet with coolers, they had to remove them and purchase freezers that could withstand the workload.

ARE YOU READY FOR THE COLD?
     Does therapeutic hypothermia require paramedics to learn new skills? Most times, the answer is no. One aspect of therapeutic hypothermia that has to be addressed is the use of muscle relaxants or neuromuscular blockage to prevent shivering. Allowing the patient to shiver could negate most of the beneficial effects of hypothermia and may actually prove to be detrimental. Shivering increases oxygen and glucose demand, as well as production of lactic acid, and increases metabolic demand by 200%–300%. Most prehospital protocols recommend paralysis or administration of muscle relaxants and/or deep sedatives. Some studies have shown that Demerol (meperidine) can also effectively lower the shiver threshold in patients.

     Tight temperature management is also a critical aspect of therapeutic hypothermia induction. The concern is overshooting the target temperature of 32°C. The deleterious effects of hypothermia are much greater at temperatures lower than 32°C, making the patient at risk for cardiac arrhythmias and coagulopathy disorders in the prehospital setting. Although interaction time is limited, temperature overshoots are possible in the prehospital setting, especially when patient interaction time will exceed 30 minutes.

     Before starting the procedure, an accurate core body temperature must be obtained. If core body temperature is 34°C or less, therapeutic hypothermia is contraindicated, as hypothermia may be the cause of arrest. The easiest and cheapest form of monitoring core body temperature is with a tympanic thermometer; however, it has been found that tympanic temperature monitoring gives the widest variances in actual core temperature. Tympanic temperatures are on average 0.5°–1°C lower than actual core temperatures. Studies have found that temperatures also vary from ear to ear by as much as 0.5°–1°C. Because of these uncontrolled variances, esophageal and rectal temperature monitoring have become the accepted standard for therapeutic hypothermia. One of the big hurdles with prehospital implementation, then, is finding a cost-effective method for monitoring temperature. Obviously, at a cost of approximately $20 per thermometer, the cheapest solution is tympanic monitoring; however, many agencies want to implement core temperature monitoring because it allows for tighter temperature control.

     Although several cardiac monitors used in the critical-care transport setting have core temperature monitoring capabilities, these monitors cost around $25,000 and usually are not an option for EMS. Because of this, EMS providers are looking at stand-alone core temperature monitoring devices that are approximately the size of a pulse oximeter and can monitor both rectal and esophageal temperatures simultaneously. These monitors cost approximately $1,000. Because of the cost involved with outfitting a fleet, some services have looked at staggered purchases and have equipped all ambulances with tympanic thermometers and supervisors' vehicles or chase cars with internal temperature thermometers until they can afford to equip the whole fleet. A stand-alone internal temperature monitoring device with capacity to monitor two probes, as well as capability to download the data, is currently used in Europe and is awaiting FDA approval in the United States. This device is designed to sound an intermittent alarm when the patient reaches 34°C and a continuous alarm for temperatures lower than 33°C.

     Subjects being considered for therapeutic hypothermia and cardiac catheterization treatment are frequently asked for their permission beforehand. It is important to note that approximately 50%–60% of post-cardiac arrest ROSC patients will have to go to the cath lab for emergent treatment to stop an evolving myocardial infarction. Therapeutic hypothermia is not contraindicated in these patients and can be started in the field. It is at the cardiologist's discretion whether therapeutic hypothermia will be continued during the cardiac cath procedure. Some physicians temporarily stop cooling, while others advocate continuation. Hypothermia induction should never be initiated if it will prevent the patient from going to the cath lab. Hypothermia induction will not stop an evolving myocardial infarction, and the treatment of choice is emergent cardiac catheterization.

CONCLUSION      Therapeutic hypothermia offers many proven benefits for the post-cardiac arrest patient if hypothermia is induced within the first 15 minutes following resuscitation and therapeutic temperature is achieved within two hours. It is imperative to note, however, that therapeutic hypothermia will not increase the success of resuscitation. Good resuscitation practices must be employed in tandem with therapeutic hypothermia in order to achieve optimal results. As with all practices of medicine, basic resuscitative techniques must be mastered before advanced techniques are utilized.

     As stated previously, we have had the opportunity to lecture at numerous congresses throughout the world about prehospital therapeutic hypothermia and recognize that there is some resistance to the practice, based mainly on the limited studies that prove efficacy in the prehospital environment. Despite the lack of published data on prehospital applications, we have seen our resuscitation-to-discharge rate triple since the protocol was implemented three years ago. Although there are several hurdles that must be overcome in order to implement a protocol, the ability to increase the survival-to-discharge rate may make the sacrifices well worth it.

Table I: Untoward Effects of Moderate-to-Deep and Prolonged Hypothermia19

  • Increased rates of sepsis
  • Increased rates of bleeding
  • Infection (pneumonia)
  • Coagulopathy
  • Thrombocytopenia
  • Bradycardia
  • Arrhythmias

Resources

     For more information about therapeutic hypothermia and best-practice protocols, other useful sources include:

  • Cold Care: Wake County EMS Develops Protocols for Induced Hypothermia. Emer Med Serv 36(3):56–61, 2007.
  • The Therapeutic Temperature Management (TTM) Congress, www.ttmcongress.net.
  • Therapeutic Hypothermia, www.CodeFreeze.org.

References

  1. Green RS. Hypothermia modulation of anoxic brain injury in adult survivors of cardiac arrest: A review of the literature and an algorithm for emergency physicians. CJEM 7(1), Jan 2005.
  2. Bernard SA. Hypothermia improves outcome from cardiac arrest. Crit Care Resus 7:325–327, 2005.
  3. A practical guide to therapeutic hypothermia. CMAJ 176(6), Mar 13, 2007.
  4. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve neurological outcome after cardiac arrest. N Engl J Med 346(8):549–556, 2002.
  5. Tiainen M. Therapeutic Hypothermia After Cardiac Arrest, University of Helsinki, 2007.
  6. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 112 (suppl 4):IV6–IV11, 2005.
  7. The New Science of Saving Lives. April 2, 2007. Penn University Press Release. www.uphs.upenn.edu/news/News_Releases/apr07/resuscitation-center.html.
  8. Wolff B, et al. Early achievement of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest. Int J Cardiol doi 10.1016/j.icard.2007.12.039, 2008.
  9. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 112 (24 Suppl):IV 1–203, Dec 2005.
  10. Schefold J, et al. Prehospital therapeutic hypothermia in cardiac arrest: Will there ever be evidence? Crit Care 12:413, 2008.
  11. ibid.
  12. Bernard SA. Hypothermia improves outcome from cardiac arrest. Crit Care Resus 7:325–327, 2005.
  13. Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermia using large-volume, ice-cold intravenous fluid in comatose survivors of out-of-hospital cardiac arrest: A preliminary report. Resuscitation 56:9–13, 2003.
  14. Virkkunen I,Yli-Hankala A, Silfvast T. Induction of therapeutic hypothermia after cardiac arrest in prehospital patients using ice-cold Ringer's solution: A pilot study. Resuscitation 62:299–302, 2004.
  15. Suffoletto BP, Salcido DD, Menegazzi JJ. Use of prehospital-induced hypothermia after out-of-hospital cardiac arrest: A survey of the National Association of Emergency Medical Services Physicians. Preh Emerg Care, 12:1, 52–56, 2008.
  16. Wilhelm Behringer, MD. Medical University of Vienna (Austria). E-mail correspondence 1 June 2008.
  17. Retrieved from the law firm of Briggs and Counsel. Available online at http://rockport.injuryboard.com/medical-malpractice/therapeutic-hypothermia-in-maine-when-is-it-malpractice-not-to-offer-the-big-chill.php.
  18. Bruel C, et al. Mild hypothermia during advanced life support: A preliminary study in out-of-hospital cardiac arrest. Crit Care 12:R31, 2008.
  19. Milanovic R, et al. Induced hypothermia after cardiopulmonary resuscitation: Possible adverse side effects. SIGNA VITAE 2(1):15–17, 2007.
Jim Mobley, RN, BSN, CEN, CFRN, NREMT-P, FP-C, is program director/chief flight nurse for Regional One Air Medical Services in Spartanburg, SC. In early 2005, Regional One became the first prehospital provider in the world to implement a non-trial therapeutic hypothermia induction protocol for all adult post-cardiac arrest patients. Jim is a former Army combat medic who served in Operation Desert Storm. He can be reached at FlightNurseJim@aol.com.

Mike Clumpner, AAS, AS, BS, MBA, NREMT-P, CCEMT-P, EMT-T, FP-C, is a firefighter/paramedic for the Charlotte (NC) Fire Department, where he is assigned to the Special Operations Division, and also works as a flight paramedic with Regional One Air Medical Services in Spartanburg, SC. He can be reached at MClumpner@gmail.com.

EMSRESPONDER.com      For additional information on therapeutic hypothermia, visit www.EMSResponder.com/onlineexclusives.

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