Targeted temperature management (TTM) refers to the global practice of controlling temperature after cardiac arrest. Mild therapeutic hypothermia refers to a temperature between 32°C and 34°C.
The positive effects of TTM postarrest are believed to be related to its effects in suppressing the whole body reperfusion injury, and preventing exacerbation of that injury by hyperthermia.
Device therapy for TTM can be divided into surface cooling and invasive technology.
The three phases of TTM are induction, maintenance, and rewarming.
There is no consensus on the optimal rate of rewarming although it is recognized that uncontrolled or rapid rewarming can lead to vasodilation, hemodynamic instability, and dangerous electrolyte shifts.
The lack of pupillary reflexes 3 days postcardiac arrest, the presence of myoclonic status epilepticus (MSE), and the absence of somatosensory-evoked potentials (SSEPs) all very likely portend an extremely poor prognosis.
The implementation of therapeutic hypothermia (TH) and targeted temperature management postcardiac arrest has arguably been one of the most significant contributions to resuscitation care. It should be viewed as the most important intervention in the postresuscitation period.
The modern application of TH had its origins in the 1950s. In 1956, Bigelow pioneered the use of hypothermia for neurologic protection during cardiac surgeries, a practice that has since become standard.1 In 1964 Peter Safar's historic paper “the first ABC's of resuscitation” recommended the use of hypothermia after cardiac arrest in patients who do not regain consciousness after return of spontaneous circulation.2 Physicians hypothesized that hypothermia's ability to suppress metabolic activity would translate into a tissue preservative capacity. Low target temperatures were used to accentuate the reduction in metabolism. However, a core body temperature below 30°C which we now refer to as “deep hypothermia,” exposes patients to the dangers of cardiac instability. Presumably whatever beneficial effects existed at these temperatures were outweighed by harm, and the therapy was abandoned. Then the 1980s and 1990s saw the emergence of animal research on the beneficial effects of “mild hypothermia.” Mild TH, that is a temperature between 32°C and 34°C, has profound effects on stemming reperfusion injury, without the deleterious consequences of cardiac instability.
INTRODUCTION INTO MODERN PRACTICE
The modern framework of TH postcardiac arrest stems from two landmark trials in the New England Journal of Medicine in 2002. The larger study known as the “Hypothermia after Cardiac Arrest (HACA) trial” was a multicenter randomized controlled trial (RCT) in Europe involving 273 postventricular fibrillation (VF)/ventricular tachycardia (VT) cardiac arrest patients who were randomized to either cooling to 32°C to 34°C for 24 hours, or “normothermia.” The normothermia control group did not have any temperature management. The neurologic outcome at 6 months was favorable in 55% of the hypothermia patients versus 39% of the control group.3 The second major trial enrolled 77 patients in Australia with out-of-hospital arrest from VF. At ...