Cardiac arrest is one of the most intense clinical scenarios faced by the emergency clinician. The challenges are twofold: restarting spontaneous circulation and simultaneously attempting to find―and then reverse―the cause of the cardiac arrest. Chaos, confusion, fear, misinformation, and missing information are all common obstacles to managing the patient in cardiac arrest. To assist emergency clinicians in this situation, protocols such as Basic Life Support and Advanced Cardiovascular Life Support (ACLS) have been codified and refined in the past decade.1-3 These protocols have helped clinicians to think in a clear and goal-oriented manner and lead to one of two clinical outcomes: If their efforts are unsuccessful, the patient will be pronounced dead. If their efforts are successful, however, they will oftentimes find themselves facing the question (though perhaps not openly admitting it) of, “Now what?”
With the return of spontaneous circulation (ROSC), one of the emergency clinician’s initial challenges has been met. The heart is spontaneously circulating blood. The second challenge of attempting to find and reverse the cause of the cardiac arrest remains, however; efforts now shift to these investigative ends while the emergency clinician simultaneously attempts to keep the newly resuscitated patient stable. Within the last several years, a more specific continuing treatment plan―beyond that of simple stability―has emerged. This plan is aimed at addressing the patient’s postarrest pathology, which includes the initial disease process that led to the cardiac arrest and the aftermath of the event.4
No organ system is exempt from the insult of cardiac arrest. Cardiac, neurologic, renal, and hepatic functions all suffer, not only from the momentary decrease in perfusion, but also from the massive inflammatory responses/cascades present during reperfusion.5 Historically, hypothermia has appeared to confer some degree of protection from these insults.6 Case reports of victims of cold water drowning who make full neurologic recoveries after having been in arrest for extended periods are well-known.7-10 Brain death—or severe neurologic compromise—is an unfortunate and devastating result of cardiac arrest. This event undermines all prior efforts to save the patient. Although other organ systems can be compensated for, artificially circumscribed, or even replaced (as is the case with renal and liver failure after cardiac arrest), neurologic function must stand on its own. It can determine the extent to which the patient is functional, even despite a perfusing rhythm.
Simple speculation about the practice of inducing hypothermia after cardiac arrest, followed by intense and promising research, has led to its use for the specific purpose of improving neurologic outcomes.11 A growing body of evidence12 suggests that control of body temperature (ie, preventing hyperthermia and, more specifically, inducing hypothermia) should become the standard of care. Many emergency medical services (EMS) providers are also investigating the use of specific guidelines and procedural protocols for inducing hypothermia in postcardiac arrest patients.13 A wide variation still exists in the technical application of hypothermia therapy, however.
The ring of the red notification phone breaks the relative calm of an otherwise typical Monday morning and heralds the arrival of a critically ill patient. The dispatcher announces that EMS is on the way with a 57-year-old man in cardiac arrest, with an ETA of 3 minutes. Shortly after preparations for their arrival are complete, EMS personnel enter with CPR in progress and the patient already intubated. As monitor/defibrillator attachment, ETT placement confirmation, additional IV access, and complete exposure of the patient occur, you hear more about the clinical scenario from EMS. Mr. I.C. is a 57-year-old male who was moving furniture when, as described by witnesses, he complained of difficulty catching his breath and a slight tightness in his chest. He began coughing violently, vomited once, gasped, and collapsed. Emergency medical services personnel state that they arrived approximately 20 minutes after the patient had collapsed, with CPR in progress. The patient was intubated in the field, and EMS reports that the initial rhythm was PEA. Upon the patient’s arrival in the ED, the rhythm is noted to be ventricular fibrillation. Defibrillation is attempted twice over the next 4 minutes, with concomitant administration of medications. During the next rhythm check, QRS complexes are noted on the monitor and a pulse is palpated. The patient has had a return of spontaneous circulation, apparently 50 minutes from onset of the arrest. As you initiate postresuscitation care, you consider the patient’s prognosis and wonder if he qualifies for therapeutic hypothermia; ie, will therapeutic hypothermia make a difference in his outcome?
Early research suggested that at temperatures greater than 30°C (86°F), the benefits of hypothermia outweigh the risks of adverse effects, whereas temperatures less than 30°C (86°F) are associated with a greater incidence of more severe adverse effects.14 The goal temperature for hypothermia used most often in studies showing improvement of outcomes was 32°C (90°F) to 33.9°C (93°F).11,15 The literature has recently proposed that this range be referred to as moderate therapeutic hypothermia.16 The goal of this literature review is to assist the emergency clinician in adapting the known body of evidence and techniques into an easily applicable protocol to maximize outcomes after cardiac arrest. The online version of this issue includes the Mount Sinai Hospital Induced Hypothermia Protocol and Post- ROSC Care Package documents (available at www.ebmedicine.net/MSSMProtocol), which readers may find helpful in establishing institutional protocols.
The MEDLINE® database was searched for articles published from 1950 to October 2010 that used the term hypothermia. This generalized search yielded well over 3000 publications. The effort was narrowed to English publications using 1 or more of the following terms: induced, therapeutic, cardiac arrest, heart, brain, emergency, resuscitation, and central nervous system. This search produced approximately 500 publications, which formed the basis for this review. Within this set, most of the publications involved either animal studies or small, human studies.
The greatest difficulty in searching the literature on hypothermia is the nature of the therapy. It is not a single intervention, but rather a combination of various interventions. Variations in inclusion/exclusion parameters, methodologies of cooling, goal temperatures, timing, and outcome measures are a major limitation to synthesizing the evidence.17-19
The results of 2 landmark prospective randomized clinical trials published in 2002 established the foundation for inducing hypothermia in postcardiac arrest patients.11,15 These 2 studies have been used as the basis for many of the recommendations and guidelines published in the last decade. (See Table 1.)
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available.