Nothing better epitomizes the emergency physician's role than the excellent evidence-based management of a patient in cardiac arrest. We encounter these patients with startling regularity. We self-identify as master resuscitationists, gurus of the clinical challenge.
It's a well-earned label, and one need only witness the not-so-well-oiled inpatient approach to appreciate the depths of our comfort with cardiac arrest management. The American Board of Emergency Medicine and various emergency medicine organizations recently produced documentation to preempt the American Heart Association merit badges often sought by credentialers, codifying and recognizing the cardiac arrest expertise woven into the fabric of our specialty.
Unfortunately, so little of what we do seems to work.
Study after study has beaten back the advanced and erudite interventions we turn to when patients take a turn for the worse. Epinephrine, lidocaine, amiodarone, bicarbonate—all have failed to show benefit when examined. We often find that even our most seemingly benign tools can cause outright harm. Consider the devastating effects of hyperoxia noted by a study that identified that oxygen—yes, oxygen—can be harmful, and that early hyperoxia exposure after resuscitation from cardiac arrest was independently associated with poor neurological function at discharge. (Circulation. 2018;137:2114; http://bit.ly/31Yr5cG.)
Or the landmark trial (JAMA. 2018;319:779; http://bit.ly/2OS3aWO) that showed, when synthesized with the PART and AIRWAYS-2 trials, that advanced airway management is at best of miniscule value and more likely harmful in all those with cardiac arrest. (EMN. 2018;40:1; http://bit.ly/2SOJ154.) But therein lies the culprit for our effete efforts.
Nearly all of our data and certainly most of our conversation address all comers in cardiac arrest. It's a homogenous approach often necessitated by the difficulty of research in this population, but one that overshadows the intrinsic heterogeneity of the disease process. At best, we dichotomize to in-hospital (IHCA) and out-of-hospital cardiac arrest (OHCA), a subtle nod toward this inharmonious state but one that continues to gloss over the importance of such granularity. Emergency physicians must approach the literature—and the bedside—with a comprehensive understanding of these limitations, and tailor our approach and management accordingly.
The Three-Phase Model
Evidence emerged at the turn of the century that the pathophysiology of cardiac arrest may consist of three time-sensitive phases. Simplified, the model describes a moving resuscitation milieu once the heart has stopped and a different priority set and therapeutic target as time progresses following a flat line or fibrillation: the electrical phase (a window in which ventricular fibrillation dominates), the circulatory phase (when BLS interventions or epinephrine might require prioritization), and the terminal or metabolic phase, an often futile ending. It's likely that the bevy of our data and the source of our shortcoming are due to most encounters and evidence emanating from this final condition when nothing could reasonably be expected to perform with any consistent success. The benefit of our resuscitative interventions is a function of the phase in which they are delivered.
Anecdotally, we know this. It's the unfortunate emergency physician who hasn't had the opportunity to defibrillate a STEMI patient who has slipped into a run of ventricular fibrillation. They almost universally respond immediately, and (let's be honest) we get to bask in the enjoyment of a life saved and a bewildered but hemodynamically bolstered patient. We've even eked out a fairly convincing signal of increased success with earlier epinephrine delivery: a function of less hypoxic time, surely, but perhaps also a verification of the window of opportunity for vasoactives within the circulatory phase of cardiac arrest, a window that resoundingly closes once the metabolic phase begins.
It's with this knowledge of time-sensitive and window-selective response with which we must approach cardiac arrest if we are truly to wear the badge of master resuscitationists. The therapeutic nihilism born from so many negative trials is a tempting trap and absolutely informative in a majority of patients at the end of life, but should likely not be taken as the final word when patients present in the earlier phases of arrest. It is incumbent upon us yet again to know the literature and understand the p-values, but only to interpret such information in concert with our hard-won knowledge base and a mature recognition of the limitations of those data.
The Future of Cardiac Arrest
There are a host of fascinating and potentially revolutionary interventions on the resuscitative horizon. These promising tools are informed by our growing understanding of the complex cardiac arrest disease process. While not yet ready for incorporation into routine practice, it will be important for bedside clinicians and statistical skeptics to remember the difficulty of truly assessing utility in the difficult research environment and inherently dissimilar nature of cardiac arrest.
Stutter CPR is the simplest and perhaps most elegant future possible intervention under study. It calls for a priming course of chest compressions, a rapid series of CPR interspaced with three short intentional 20-second pauses. (Anesth Analg. 2016;122:767.) Theoretically, these compressions build upon the knowledge base where ischemic post-conditioning has shown promise in mitigating ischemia-reperfusion injury. (Circulation. 2015;132[Suppl 3]:A16996; http://bit.ly/31T0yxj.) Certainly, this will be the space to watch as more evidence continues to emerge about the danger of reactive oxygen species and the potential benefit of anti-inflammatory and immunomodulatory therapies (such as the COLCOT and CANTOS trials).
The publication of the ResQ trial brought the concept of augmented negative intrathoracic pressure into focus, and seized upon the preload support promulgated by the thoracic pump theory. In a heroic effort spanning the United States, researchers from the ResQ Trial, funded by the National Institutes of Health, randomized more than 2000 patients with OHCA to standard care or the augmented CPR model and found that six percent of controls survived to hospital discharge with favorable neurological function compared with nine percent of patients in the intervention group (odds ratio 1.58, 95% CI 1.07-2.36; p=0.019).(Lancet. 2011;377:301.)
Exciting stuff, to be sure, but the paper was quickly dismissed by skeptics citing a number of troublesome conflicts, including a failure of the two interventions to show benefit independently in their own trials as well as some perceived bias (the inventor of the ResQPod and ResQPump, the devices studied, was the senior author on the paper). Supporters of the practice cite intervention synergy and patient selection, as well as more difficult-to-quantify benefits (the ResQPod has a metronomic blinking light to guide compression speed, for example), as the reason behind the disparity, but further investigation has been frustratingly limited. Nonetheless, preclinical research examining the combination continues with meta-analyses calling for further studies due to the potential to one day benefit our patients. (Resuscitation. 2017;121:195; Crit Care Med. 2015;43:889.)
On the cutting edge of resuscitation science, sodium nitroprusside-enhanced CPR has shown superior resuscitation rates and neurologic outcomes...in pigs. In keeping with the arguments of ResQ supporters, researchers in one study considered that giving large boluses of nitroprusside to provide afterload reduction to thoracic compressions would be life-saving if administered with a means to maintain adequate coronary and cerebral perfusion pressures (that is, application of compression-decompression CPR and an impedance threshold device).
Fifteen pigs were used, with seven receiving the full intervention bundle. All seven animals in the intervention group achieved ROSC with a single shock compared with just two of eight in the control group and also demonstrated improved diastolic, coronary, carotid, and cerebral pressures over time. (Resuscitation. 2012;83:374; http://bit.ly/2uLeRrA.) Subsequent porcine studies have continued to show similar effect sizes, but large human studies have yet to be mounted.
Managing cardiac arrest is a phenomenal and fundamental task for the emergency physician, one inextricably tied to our resuscitative identity. The importance of competent management has been underlined by ubiquitous ACLS courses and roving “code teams,” but mastery should be claimed by emergency physicians all over the world. As evidence continues to erupt on interventions new and old, we must lend a skeptical but wise eye toward its interpretation, and approach this incredible task with a deep understanding of the three-phase model and the reasoned expertise it requires.
Dr. Pescatoreis the chief physician for the Delaware Division of Public Health and an emergency physician in New Jersey and the host with Ali Raja, MD, of the podcast EMN Live, which focuses on hot topics in emergency medicine:http://bit.ly/EMNLive. Follow him on Twitter @Rick_Pescatore, and read his past columns athttp://bit.ly/EMN-Pescatore.