Therapeutic Hypothermia in the Field

Neurons also benefit during TH by a stabilization of the cellular membranes. Exactly how this happens is not well understood, but the resulting benefit is that there is a limited calcium influx. An influx of calcium normally excites the cell-speeding metabolism. With less calcium, metabolism remains reduced, enhancing healing.⁴

Cooling Methods

There is no single cooling method shown to be superior to others in regards to patient outcomes.^2,8 Regardless of how cooling is performed, target temperature needs to be obtained within 300 minutes.³ Prior to initiating cooling, it is essential to carefully document a neurological examination.⁴ This baseline examination is essential for neurologists who later evaluate the patients so they can look for improvements from the baseline.

There are many cooling techniques, including ice packs along the axilla, groin and sides of the neck; ice baths; cooling blankets with circulating water; iced normal saline and other fluids; gel-coated cooling pads along the torso; cooling helmets and caps; and invasive lines. Once cooling is initiated, the goal is to achieve the temperature, most commonly 32°C, as rapidly as possible. This is important because slow cooling can exacerbate hypovolemia and electrolyte disorders, including hypokalemia, hypomagnesemia and hyperglycemia.⁴

For prehospital providers, the use of normal saline and lactated Ringer’s chilled to 4°C has become a standard for cooling. Administering 30 ml/kg over 30 minutes has been shown to cool patients 1.4°C.⁴ Additionally, a feasibility study administering 30 ml/kg of 4°C saline at 100 ml/min reduced temperatures by an average of 1.9°C.¹¹ In theory, administering 30 ml/kg of saline to any patient could push them into heart failure, but multiple case studies have demonstrated that saline can be used to induce hypothermia safely, effectively and without significant complications, including pulmonary edema.⁸ Preliminary data from New York City EMS has found that 7.7% of patients receiving prehospital intra-arrest iced saline develop some symptoms of pulmonary edema, but that these patients actually have better outcomes than those who don’t.¹²

There are several devices that target cerebral cooling following cardiac arrest. The benefit of cerebral cooling for brain injuries is discussed later, but isolated cerebral cooling has not been well researched in cardiac arrest patients. All research is on systemic cooling. One study that reviewed targeted cranial cooling found no significant systemic cooling was achieved.¹¹

Temperatures and Times

While the ideal target temperature has not been determined, nearly all studies cool patients to 33°–34°C.³ Cooling patients to 27°C has been shown to cause adverse effects and complications.² Currently most protocols aim for 32°–33°C.

When cooling patients it is essential to monitor temperatures continuously.³ This can be done with esophageal, rectal or Foley thermometers. The AHA says temperature monitoring is best done via esophageal or bladder catheter, and that axillary and oral thermometers are inadequate for ongoing monitoring.⁸ However, a study that compared tympanic to bladder and esophageal temperatures during management of therapeutic hypothermia found that an accurately obtained tympanic temperature reliably reflects esophageal and core body temperature.¹³

Once cooling is initiated it is essential to prevent premature rewarming. Maintain cooling until physicians can control the rewarming process. While the optimal cooling period has not been determined, most protocols maintain it for at least 24 hours.⁴ Some studies keep patients cool for as long as 48 hours.³ Additionally, cerebral edema can persist for up to 72 hours, so it is reasonable to suspect that down the road, the cooling time period may be extended.⁴

Shivering

Shivering, the rhythmic tremoring of skeletal muscle, is the most frequent side effect of therapeutic hypothermia. It is activated when a certain temperature is reached in the hypothalamus, most often between 36°–37°C.¹⁴ Effective shivering increases basal metabolic rate to 2–5 times normal, and is also associated with an increase in energy and oxygen consumption, as well as carbon dioxide elimination. Subclinical shivering may be as subtle as increased muscle tone and will also slow cooling.⁴ Shivering also increases blood pressure, heart rate, respiratory rate and intracranial pressure.