Therapeutic Hypothermia in the Field

This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs. There are two ways to take the CE test that accompanies this article and receive 1.5 hours of CE credit accredited by CECBEMS: 1. Click here to download a PDF of the test. The PDF has instructions for completing the test. 2. Or go to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail editor@EMSWorld.com.

Objectives

• Explain the physiology of post-cardiac arrest syndrome.
• Identify the actions and effects of therapeutic hypothermia.
• Explore various cooling techniques and candidates for therapeutic hypothermia.
• Discuss the physiology of medicine administration for patients receiving therapeutic hypothermia.

On March 18, thousands of participants lined up for the Quintiles Wrightsville Beach Marathon in North Carolina. The race seemed to be going smoothly when 38-year-old James Glasgow collapsed just a few hundred yards from the finish line.¹ Paramedics from New Hanover Regional EMS arrived at his side within moments and found him in ventricular fibrillation. After several minutes of CPR and defibrillation, they restored his pulse. During transport the paramedics performed their routine return-of-spontaneous-circulation (ROSC) care, which included ensuring a patent airway, making sure two IVs were in place and initiating 30 ml/kg of iced normal saline. Upon arrival at New Hanover Regional Medical Center, Glasgow’s core body temperature had been reduced to 32°C. Less than 10 days later, he was released from the hospital neurologically intact, though with no recollection of the marathon.

Knowledge of the potential benefits of therapeutic hypothermia (TH) is actually quite ancient. Hippocrates noted that soldiers with severe head injuries had better survival rates when their injuries occurred in the winter compared to the summer.² In 1938, deep hypothermia was first tested and used to slow cancer cell metabolism and division.² Since then, TH has been used during many thoracic and neurological surgical procedures,³ and since the 1950s has been used to protect the brain during cardiothoracic and neurosurgery.⁴

TH began gaining attention in cardiac arrest care during the first years of this century. Two landmark studies published in the New England Journal of Medicine in 2002^5,6 prompted the International Liaison Committee on Resuscitation (ILCOR) to recommend therapeutic hypothermia for out-of-hospital cardiac arrest due to VF and pulseless ventricular tachycardia in 2003.⁴ These studies observed that cardiac arrest survival with good neurologic outcome increased from 26% to 49% and 39% to 55%, respectively, for out-of-hospital cardiac arrest survivors who were cooled. In 2010, the AHA updated its recommendations and identified therapeutic hypothermia as a Class I recommendation for VF cardiac arrest and a Class IIb recommendation for cardiac arrest with asystole/PEA as the initial presenting rhythm.

Post-Cardiac Arrest Syndrome

It is difficult to understand how TH benefits cardiac arrest patients without understanding what happens within the body when medical providers halt the dying process (i.e., successfully resuscitate a patient). Pre-resuscitation, several organs were exposed to some period of hypoxia. As a result, a constellation of simultaneous events began occurring throughout the body, collectively termed post-cardiac arrest syndrome. These events include post-arrest brain injury, myocardial dysfunction, systemic inflammatory response, and persistence of the precipitating pathology.⁴

Brain injury following cardiac arrest can be either immediate or reperfusion-related. Immediate injury occurs as a result of brain ischemia and neuron, or brain cell, infarction that develops during the initial cardiac arrest as energy stores are consumed. During this time cell swelling develops as a result of the loss of intracellular sodium and potassium ion gradients. The cell’s sodium and potassium pump ceases to function during cardiac arrest, and when ROSC occurs this pump is slow to restart, causing fluid shifts as a result of an osmotic gradient.