Targeted temperature management (TTM), also known as therapeutic hypothermia (TH), has become standard of care for the management of comatose patients with return of spontaneous circulation (ROSC) after cardiac arrest. The 2010 American Heart Association (AHA) guidelines for management of post–cardiac arrest patients recommend that comatose (i.e., lack of meaningful response to verbal commands) adult patients with ROSC after out-of-hospital ventricular fibrillation (VF) cardiac arrest should be cooled to 32°C to 34°C (89.6°F to 93.2°F) for 12 to 24 hours (Class I, LOE B). Induced hypothermia also may be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of pulseless electric activity or asystole (Class IIb, LOE B).1
Very few recommendations in the AHA guidelines are assigned a Class I recommendation, and, as practitioners at the portal of entry for the majority of cardiac arrest patients, emergency physicians (EPs) need to be familiar with this therapy, understand the rationale for the level of recommendation assigned to TTM, be capable of rapidly identifying appropriate candidates, and have the skills to initiate the therapy.
Why is TTM needed to improve outcomes after cardiac arrest? When a person suffers a cardiac arrest, no effective cardiac contractility occurs, resulting in global hypoperfusion and ischemia. Chest compressions provide some degree of circulation during arrest and high-quality chest compressions can deliver up to 40% of the cardiac output produced by a spontaneously beating heart. The ischemia that occurs during cardiac arrest triggers a number of pathologic processes including the production of reactive oxygen species, initiation of a profound inflammatory cascade, development of metabolic acidosis with accompanying elevated lactate levels, and endothelial and mitochondrial dysfunction, to name some of the dozens of derangements that ensue. When ROSC occurs, ischemic tissues are reperfused with blood, and this reperfusion produces its own injury patterns. Early reperfusion injury occurs immediately after ROSC and lasts for approximately 30 minutes; delayed reperfusion injury begins a few hours later and continues for days.2 The combination of ischemia and reperfusion produces the post–cardiac arrest syndrome (PCAS), a unique disease state requiring specialized care. This was first described by Negovsky in 1972, when he stated that postresuscitation syndrome was a unique disease entity with unique pathophysiology that needed to be understood if it was to be treated appropriately.3 Currently, TTM is the best-studied and most effective therapy for treating patients with PCAS.4 In this chapter, we will discuss the epidemiology of cardiac arrest, the rationale for using TTM, data supporting its use, practical aspects of implementation, and future directions for the therapy.
Although the United States has no standardized, mandatory reporting system, it is estimated that 400,000 cardiac arrests occur each year in the United States, 75% as out-of-hospital cardiac arrests (OHCA) and 25% as in-hospital arrests.5 Viewed from a different ...