Induced Therapeutic Hypothermia
Approximately 300,000 people suffer a sudden cardiac arrest in the United States each year. Historically, 2-8% of these patients will survive to be discharged from the hospital. Recent advances in pre-hospital treatment have increased the number of patients who experience a return of spontaneous circulation (ROSC), but less than half of these patients will survive to be discharged from the hospital. The main cause of death for these patients is due to anoxic brain injury. The use of induced therapeutic hypothermia may prove to be an important advancement in improving patient outcome.
The use of therapeutic hypothermia is not a new concept. Hippocrates, the father of Western medicine, noted the benefits of hypothermia in treating injuries. Napoleon’s surgeons recorded that wounded soldiers who were further from the fire had a higher survival rate that the wounded officers who stayed close to the fire. In the 1950’s, studies showed that inducing hypothermia in dogs decreased oxygen consumption, and that induced hypothermia after cardiac arrest in humans improved survival rates.
In 2002, two studies demonstrated that the induction of mild hypothermia in comatose ROSC patients improved not only survival, but also neurological outcomes. The Hypothermia after Cardiac Arrest Study Group demonstrated that mild hypothermia (32-34o C, 90-93o F) improved functional recovery at hospital discharge for ROSC patients; 55% for hypothermia patients vs. 39% for normothermic patients. A similar study showed good outcomes in 49% of hypothermia patients vs. 26% for normothermic patients. The American Heart Association has made a Class IIa (weight of evidence/opinion is in favor of usefulness/efficacy) recommendation for induced hypothermia for the unconscious ROSC patient after out of hospital V-Fib/Pulseless V-Tach arrest.
These studies have shown that induced therapeutic hypothermia may be beneficial for the comatose ROSC patient, but why does it work? Here is what the evidence points to:
- For every 1 degree Celsius drop in body temperature, cellular metabolism slows by 5-7%, decreasing the body’s need for oxygen.
- Drops in body temperature cause the cell membranes to stabilize during periods of hypoxia; this prevents the influx of harmful ions and disruption of cell function.
- Therapeutic hypothermia may reduce the effects of reperfusion injury due to the body’s inflammatory response during reperfusion. This response can cause increased intracranial pressure and brain cell injury/death.
The goal of induced therapeutic hypothermia is to decrease the patient’s body temperature to 32-34oC, and then maintain that for 24 hours. After that time period, the patient will slowly be re-warmed, over 6-8 hours. Cooling can be achieved several different ways: cooled saline infusions, cooling blankets such as the Arctic Sun, or ice/cold packs.
When are we going to start induced hypothermia?
- The patient must have a return of spontaneous circulation.
- The initial presenting rhythm must be Ventricular Fibrillation, Ventricular Tachycardia, or Asystole (this presumes that the initial rhythm was V-Fib)
- The cardiac arrest must not be due to trauma or hemorrhage.
- The patient’s age must be greater than 12 years old.
- The patient must be comatose, GCS < 5, and have an advance airway placed (ET tube or King Airway). If you are unable to place an advanced airway in the patient, DO NOT initiate therapy.
- The patient’s initial temperature must be above 34oC/93oF
- DO NOT USE IN PREGNANCY
How are we going to start induced hypothermia?
- Remove patient’s clothing.
- Apply chemical cold packs to groin and axilla.
- Notify the hospital that you have started cooling the patient.
- Use Versed, 0.15mg/mg to max of 6mg, to maintain sedation.
- Use Morphine, 4mg IV/IO, repeat in 2mg increments to max of 10mg, to control shivering and pain.
- Use fluids/Dopamine to maintain Systolic BP of 100 mmHg.
- Only use Norcurron if you are unable to maintain the airway. The patient’s neurological status cannot be measured if the patient is paralyzed. Seizures are common post arrest, Norcurron will mask these
Our goal as pre-hospital providers is not to reach the target temperature of 32-34oC but to be the first step in the process. Our job is to restore and support perfusion to the heart, brain, and vital organs, and to provided the visual clues to the ER that the patient needs to be more aggressively cooled. Studies have shown that when cooling is started in the field, even by simple methods, the target temperature is reached 3-4 hours sooner.
Keys To Sucess
- Provided exceptional CPR and early defibrillation during the arrest. High quality CPR and early defibrillation increase the likelihood of return of spontaneous circulation.
- If the patient is a candidate for induced therapeutic hypothermia, begin it early!
- Support the patient’s blood pressure, hypotension leads to cerebral hypoxia and increased intracranial pressure.
- Maintain the airway and ventilations. DO NOT HYPERVENTILATE. Keep end tidal C02 normal, 35-45 mmHg. Hyperventilation leads to decrease cerebral circulation due to vaso-constriction.
- Control shivering and pain by using Versed and Morphine. Shivering uses needed oxygen and generates heat, making it harder to cool the patient.
- Do not paralyze the patient just because you can. The patient’s neurological status cannot be measured if the patient is paralyzed. Seizures are common post arrest, Norcurron will mask these. Treat any seizure activity according to standard protocols.