Advancing Clinical Sophistication: The Introduction of Therapeutic Hypothermia Treatment

Advancing Clinical Sophistication: The Introduction of Therapeutic Hypothermia Treatment
A person whose heart suddenly stops beating effectively survives less than 5% of the time; if defibrillated within minutes, immediate survival rates rise to 30-45%. The majority of patients with return of spontaneous circulation (ROSC), however, do not ultimately fare well. Less than half of these patients survive to hospital discharge, and many have residual long-term neurological damage.
Inducing mild hypothermia after ROSC in certain patients has been shown to mitigate the extent of brain damage. In fact, it is the only post-cardiac arrest therapy demonstrated to increase survival rates.
A 2002 European study found that patients who received therapeutic hypothermia after ROSC were living independently and working at least part time more often than those who had not received the treatment (55% vs. 39%).
With a goal of improving cerebral function after a cardiac arrest, the American Heart Association (AHA) in 2005 recommended that therapeutic hypothermia be incorporated into post-resuscitation support. Many hospitals have since instituted relevant protocols.
Now, people who experience an out-of-hospital cardiac arrest in Cambridge, MA, will be able to receive this potentially lifesaving treatment before they even arrive at an emergency department.
Pro EMS plans to implement a therapeutic hypothermia protocol for adult patients with ROSC after out-of-hospital cardiac arrest.
Responding to a call, paramedics will now bring chemical ice packs and chilled intravenous fluids (IVF) to a patient’s bedside along with their equipment and medications.
If a patient remains unconscious, yet hemodynamically stable, after CPR and defibrillation, paramedics may induce mild hypothermia by placing ice packs adjacent to the patient’s neck, groin and axillae. Two liters of chilled IVF will also be infused.
To insure that a patient’s core temperature does not drop below the desired 34ºC, a nasopharyngeal esophageal monitor will be placed.
Once at the hospital, paralytic agents will be administered to prevent shivering and its associated increase in body temperature. While maintained on the hospital’s cooling protocol for a total of 24 hours, patients can undergo diagnostic testing and procedures, including angiography.
Prehospital induction of therapeutic hypothermia is an emerging treatment. Currently, only about 100 of the 24,000 EMS organizations in the United States have begun using it.
Future studies on prehospital therapeutic hypothermia will help clarify which patients will benefit most and what techniques are optimal.
Pro EMS already collects data on patient care as part of its continuous quality improvement. Data collected on this new protocol will help hone procedures so the best possible care can be delivered to patients.
The AHA recommends therapeutic hypothermia for adult patients with ROSC after out-of-hospital cardiac arrest and remaining unconscious when the initial heart rhythm was ventricular fibrillation (class IIa) or non-ventricular fibrillation (class IIb). Their recommendation is for patients to be cooled to 32-34ºC for 12-24 hours
Not all patients with ROSC should receive this treatment, however. Therapeutic hypothermia is not appropriate for cardiac arrest patients who initially presented as hypothermic, remain hypotensive after resuscitation, have had recent major surgery or trauma, or have had a prolonged cardiac arrest.
Other contraindications include patients who are pregnant, have a systemic infection, or were vegetative or comatose prior to the cardiac arrest.
While therapeutic hypothermia can be neuroprotective, it can also be associated with various complications. Thrombocytopenia, infections or arrhythmias may occur. Most complications, however, occur when a patient’s core temperature drops below 32-34ºC or when a patient remains hypothermic for longer than 24 hours.
In a cardiac arrest, brain cells are injured both from the initial injury, when deprived of oxygen and nutrients, as well as with reperfusion, when an increase of free radicals, stimulatory neurotransmitters and other factors causes cell death.
Mild hypothermia causes physiologic changes that counteract brain cell damage and death, including reducing cerebral metabolism, reducing excitatory amino acids, and restoring normal intracellular processes.
Annually, an estimated 250,000 to 450,000 people – men more often than women – experience sudden cardiac arrest.
The immediate cause of a sudden cardiac arrest is a disruption of the heart’s electrical conduction system or arrhythmia, such as ventricular fibrillation. Underlying causes vary; coronary artery disease or coronary heart disease is the most common.
Other cardiac causes of a cardiac arrest include myocardial infarction (MI), cardiomyopathy, valvular disease, congenital heart disease, or a primary heart rhythm abnormality, such as long QT syndrome.
Cardiac arrests also occur from non-cardiac conditions. Some of these include hypovolemia, hypoxemia, pulmonary embolism, sepsis, electrolyte abnormalities (such as hypokalemia or hyperkalemia), tension pneumothorax, intoxication, or severe physical stress to the body.
Before losing consciousness during an arrest, people may subjectively report a variety of symptoms, including feeling dizzy or lightheaded, or experiencing a racing heartbeat, chest pain or nausea.
In addition to its use with ROSC, therapeutic hypothermia is being formally studied for other conditions such as traumatic brain injury with elevated intracranial pressure in adults, acute stroke, traumatic spinal cord injury, and cardiac arrest in newborns due to perinatal asphyxia.
For more information:
American Heart Association Circulation 2008
Post-Cardiac Arrest Syndrome
American College of Emergency Physicians
Focus on: Therapeutic Hypothermia
Medline Plus: Cardiac Arrest

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