From the EM Model
3.0 Cardiovascular Disorders
3.1 Cardiopulmonary Arrest

An estimated 155,000 cases of EMS-treated sudden cardiac arrest occur each year in the United States.¹ Despite advances in cardiopulmonary resuscitation (CPR) and periodic changes in guidelines, most of these victims do not survive to hospital admission or die of multisystem organ failure within a few days. Among those who survive there is a high incidence of brain damage.^2,3 It has long been noted that patients with cardiac arrest who suffer cold-water drowning or arrest in the cold seem to do better than patients who arrest in a warm environment, and hypothermia has long been used in cardiothoracic surgery. These observations led researchers to investigate intentionally cooling resuscitated victims of cardiac arrest. In Bernard’s two early studies from Australia, mortality rates dropped from 77% to 45% and from 68% to 51%, while good neurologic outcome rose from 14% to 50% and 26% to 49% when cardiac arrest victims were cooled.^4,5 Similar results were seen in the European Hypothermia After Cardiac Arrest (HACA) trial, where 6-month mortality rates dropped from 55% to 41% and good neurologic outcome rose from 39% to 55%.⁶ Since then, additional studies have shown improved survival, although some are small, nonrandomized, with historical controls, and a few demonstrate trends rather than statistically significant differences.^4-20 In the setting of percutaneous coronary intervention (PCI) following a cardiac arrest, cooling also increased survival with good neurologic outcome from 16% to 55% (p=0.001).⁸

Case Presentation

A 55-year-old man collapses in his office. Coworkers call EMS and are instructed in bystander CPR. Paramedics find the patient in ventricular fibrillation and promptly defibrillate. After 2 more minutes of CPR, the patient is defibrillated a second time and shortly regains a palpable radial pulse. The monitor shows sinus rhythm with a rate of 70; blood pressure is 100/70. He is unresponsive to sternal rub and has no gag reflex, so he is intubated. A 12-lead ECG showing an anterolateral ST-segment elevation myocardial infarction (STEMI) is transmitted to the hospital. The emergency physician activates the cardiac catheterization laboratory. As they begin the 20-minute transport to the emergency department, the paramedics ask about hypothermia.

Pathophysiology

It is thought that cooling the body to between 32°C and 34°C (89.6°F and 93.2°F) decreases brain oxygen use and limits brain damage after cardiac arrest.²¹ Cerebral reperfusion injury is caused by a multitude of factors, including free radical production, intracellular calcium influx, pathologic protease cascade, mitochondrial damage, and apoptosis by activation of cell-death signaling pathways.^7,21,22 These reactions begin within the first few hours following a cardiac arrest and continue for several days, providing a window for neuroprotective strategies such as therapeutic hypothermia.²² The cerebral metabolic rate decreases by 6% to 7% for each 1°C (1.8°F) decrease in temperature.²¹ Decreasing metabolic rate and oxygen consumption after the arrest decreases destructive enzymatic reactions and free radical production.^6,21