Cardiac Resuscitation
Executive Summary
- High-quality chest compressions are the most important factor in CPR — rate, depth, timing, recoil, and without interruption.
- Advanced airway techniques during cardiac resuscitation do not increase the rate of cardiac recovery and actually worsen neurologic survival.
- No pharmacologic agent given during resuscitation improves the rate of cardiac recovery.
- For witnessed cardiac arrest, rapid defibrillation is very beneficial — this is the principle behind placement of automated external defibrillators in public buildings and spaces.
- Post-resuscitative care using targeted temperature management (a.k.a., therapeutic hypothermia) improves neurologic recovery in patients who remain comatose after restoration of spontaneous circulation.
- Early cardiac catheterization and PCI of obstructive lesions in cardiac arrest survivors appears beneficial — the challenge is patient selection and timing.
Having been in emergency medicine for more than 30 years, I have seen the pendulum of interest in cardiac resuscitation swing back and forth. When it was a new concept, when it was being used for the first time, when it was being taught to and performed by paramedics, when middle-aged adults were surviving, it was exciting. One of my earliest experiences in research was participating in animal studies of cardiac resuscitation. We were using dogs, and after achieving general anesthesia and instrumentation, would induce a cardiac arrest and then perform cardiopulmonary resuscitation (CPR) while monitoring the hemodynamic effects. Now, we well understood that dogs are not a good model for human cardiac arrest. For one, the thoracic anatomy is very different: a V-shaped anterior thorax in dogs versus a flattened ovoid for humans. In addition, human cardiac arrest is often triggered by focal ischemia, whereas we triggered cardiac arrest in dogs by global chemical or electrical means. Despite these differences, we learned a lot about the hemodynamics of chest compression and, from the dog model, lent support to the thoracic pump model of forward blood flow during human chest compression.
Many groups were actively involved in cardiac resuscitation research, but then the field started to go quiet, and a lassitude took over. What happened? My observations note a combination of low success rates and incomplete results. CPR was ideally intended for the heart that was "too good to die" one that had good pre-arrest pump function but was only under the influence of a hiccup, a treatable electrical dysrhythmia. Stop the dysrhythmia, and the nearly normal heart resumes functioning. But as CPR grew in application, not all patients were like this; the chronically ill, the extreme elderly, those with terminal disease, and so on. Successful CPR became unusual, not the high percentage depicted on TV shows. And what about those who did recover cardiac function? Most of them died from global cerebral ischemia during the subsequent days in the intensive care unit (ICU), and if they survived the ICU, were transferred to chronic care facilities with permanent neurologic impairment.
So, we tried getting fancy. Perhaps the low success rate was due to inadequate ventilation, so there was a push for more aggressive airway management by paramedics. Perhaps the ischemic myocardium needed metabolic substrate or was under the influence of harmful endogenous intermediates, so pharmacologic doses of different drugs were tried. Perhaps manual chest compression had limits, so mechanical devices were tried. None of this really budged the needle. Those practicing in the 1990s were often cynical about the effectiveness of CPR; we’d perform it, but our heart (pardon the pun) was just not into it. We’d seen too much, too few patients resuscitated, too many people dying from global brain injury, and too few walking out of the hospital.
Then three factors started to have an effect. Each individually small, but in combination, produced a measurable impact on survival, and even more important, functional neurologic recovery.
The first factor was the automated external defibrillator or AED. As noted in this article, there is a short time after the onset of ventricular fibrillatory cardiac arrest when external defibrillation is likely to be successful restoring a perfusing rhythm. The trick is to have the AED rapidly available within the first few minutes. So, public safety AED programs were created, training police and firefighters to use the devices. AED was expanded to the lay public through public access defibrillation programs; the placement of AEDs in airports and public buildings is a legacy of this effort. Not all AED programs produced measurable success, but they were a start.
The second factor was something that was known from the early studies of CPR physiology: the value of chest compressions done in a consistent manner to maximize hemodynamic benefit. We seemed to have undervalued chest compressions in our efforts to get fancy. There is extensive evidence that high-quality chest compressions — rate of 100 or slightly greater, compression depth of at least 2 inches, equal time devoted to compression and release during each cycle, release with no pressure on the chest wall to allow for maximal chest recoil, continuous compression without pause or interruption, and limiting excessive chest inflation — produce a higher rate of resuscitation and recovery of spontaneous circulation. Like many things simple, high-quality chest compressions are not easy, but the benefits are clear.
The third factor is targeted temperature management (also known as therapeutic hypothermia) in comatose patients resuscitated from cardiac arrest. It is amazing that something as simple as a few degrees in body temperature could make a dramatic difference in neurologic recovery. We are still exploring, and current recommendations will likely be improved to both simplify the treatment and maintain benefit.
There is a fourth factor gaining acceptance: early cardiac catheterization and percutaneous coronary intervention (PCI) of significant lesions. It would make sense that since most cardiac arrests in previously healthy adults are due to coronary artery disease with focal ischemia, opening the blockage and restoring blood flow will prevent a recurrent arrest. The evidence is mounting that this is true. The challenges are patient selection — all survivors or only those with evidence of ST-segment elevation infarction on the ECG —and timing — direct from the ED or within a few days.
The consistent application of targeted temperature management and early cardiac catheterization has prompted the development of cardiac arrest receiving centers, with space, equipment, and personnel to make the commitment to apply the best evidence-based post-arrest care. These centers are modeled after trauma centers, and like trauma centers, demonstrate improved outcomes due to the consistent utilization of proven treatments.
As I enter my 35th year of practicing emergency medicine, I am hopeful once again that we have something substantial to offer, that we can restore a significant number of individuals to their previous functional level after sustaining a cardiac arrest. The authors of this issue have created a concise update of our current best practice and offer ideas of where we might go in the future. I trust this article will give you hope, too.
— J. Stephan Stapczynski, MD, Editor
Introduction
The reversal of cardiac arrest is, in many ways, the holy grail of modern medicine. Prior to the 1960s, cardiac resuscitation was the purview of surgical specialists capable of performing emergent thoracotomy and open cardiac massage, and these attempts primarily involved the perioperative period. This changed dramatically in 1960 when William Kouwenhoven, an electrical engineer by trade, described closed chest compressions as an alternative to open thoracotomy.1 In Dr. Kouwenhoven’s own words, "Anyone, anywhere can initiate cardiac resuscitative procedures ... all that is needed are two hands."1 By that point, electrical cardioversion (defibrillation) had long been recognized as a means of terminating ventricular fibrillation,2,3 and so the two most prominent interventions in cardiac arrest, chest compressions and defibrillation, were already established a decade before Neil Armstrong set foot on the moon.
Even in the modern age, however, outcomes remain poor. A systematic review of the literature between 1980 and 2003 for out-of-hospital cardiac arrest (OHCA) reported an overall survival to hospital discharge of 8.4%,4 and a more recent prospective, observational study from 2006 to 2008 mirrored these data (7.9% for EMS-treated OHCA).5 The latter study indicated significant regional variation in survival rates, from a high of 16.3% in the Seattle area to a low of 3% in Alabama. (See Figure 1.) Outcomes were significantly improved in both studies when only ventricular fibrillation was examined (17.7% and 21% overall, respectively.) Poor overall survivability in cardiac arrest is a reflection of several factors. These include the narrow timeframe in which interventions are likely to be successful, the requirement of bystander involvement, and the need for effective systems to be in place to connect victims to providers.6 Additionally, cardiac arrest seldom afflicts healthy individuals, and these patients often have a host of medical comorbidities.7 Relatively stagnant outcome data raise the question: Have we, as physicians, progressed in the field of cardiac resuscitation during the past 50 years?
Figure 1: Regional Variation in Survival to Hospital Discharge in OHCA
This paper will serve as an overview of cardiac resuscitation, covering mechanical interventions, pharmacotherapy, and post-resuscitative care. An emphasis will be placed on evidence-based approaches and current clinical guidelines. Future directions will also be discussed.
Current Practice: Chest Compressions
The American Heart Association (AHA) published the first clinical guidelines on cardiac resuscitation in 1966,8 and has been updating those guidelines periodically. The latest iteration was released in 2010,6 and several major revisions were included. The most notable change is an emphasis on compressions over airway and breathing (C-A-B replacing the traditional A-B-C mnemonic). The reasoning for this is that, as noted above, arrest secondary to ventricular fibrillation carries the most favorable prognosis, and critical elements of survivability in this group include quality chest compressions and rapid defibrillation.9
The emphasis on chest compressions is also meant to improve bystander participation in witnessed arrest. Rates of bystander CPR increase dramatically when a compression-only strategy (CO-CPR) is used, compared to traditional CPR that involves rescue breathing. In one study, bystander CPR increased from 28.2% to 39.9% over a five-year period following the rollout of a CO-CPR media campaign.10 Outcome data for this approach, however, are mixed. One meta-analysis reported an absolute survival benefit of 2.4% of CO-CPR,11 while a large observational study reported better outcomes for conventional CPR,12 particularly among arrests of younger patients, arrests that were not cardiac in origin, and arrests in which there was a delay in starting CPR. Indeed, the benefits of CO-CPR may stem from minimal interruptions in chest compressions, a variable increasingly recognized as important for successful resuscitation.13-15 Accordingly, CO-CPR may be preferred for bystanders in an out-of-hospital setting, while well-performed conventional CPR (that minimizes interruptions in chest compressions) is likely still ideal for first responders, emergency physicians, and resuscitative teams.
Devices to augment manual chest compressions have gained moderate interest, but none have shown consistent benefit in OHCA.16-18 These include both constrictive band and piston devices, and are aimed at automating quality chest compressions without interruption or the element of rescuer fatigue. Examples include the AutoPulse (ZOLL Medical Corporation) and the LUCAS® (PhysioControl) systems. These devices continue to be used by paramedics and emergency medical technicians, despite reservations about their effectiveness.19,20 Although objective efficacy in the pre-hospital setting is lacking, some success has been reported when automated compression devices have been used by trained personnel in specific in-hospital settings, such as the catheterization lab.21,22
The ideal rate of chest compressions, typically performed at about 100 per minute, is also up for debate. A recent large retrospective study indicated that rates closer to 125/minute may be more likely to produce return of spontaneous circulation (ROSC) for victims of OHCA.23 However, the increased rate was not associated with any increase in survival to hospital discharge.
Finally, it has been proposed that in order to truly minimize interruptions in chest compressions, "hands-on" defibrillation should be considered. In this model, rescuers continue chest compressions during defibrillation, a practice believed by many to be safe utilizing biphasic defibrillators, self-adhesive pads, and standard exam gloves.24,25 The benefits of hands-on defibrillation include maintaining coronary perfusion pressure at the time of shock delivery; coronary perfusion drops significantly when chest compressions are interrupted, and takes some time to return to pre-interruption levels.26 However, some have called the safety of this practice into question, particularly in the case of glove breakdown,27 and the debate is ongoing.
Pharmacotherapy
More than 100 years ago, surgeon George Crile was profiled in The New York Times for "resuscitating persons apparently dead" using "salt and adrenaline solutions."28 More than a century later, little progress has been made in developing effective pharmacotherapies for cardiac resuscitation. Epinephrine continues to be recommended in the current Advanced Cardiac Life Support (ACLS) guidelines,29 despite the dearth of evidence to support its use. Epinephrine is thought to act in a number of ways, including alpha-adrenergic constriction of arterioles and increased pressure in the proximal aorta. This, in turn, increases blood flow into the coronary arteries and improves coronary perfusion pressure, which, itself, is associated with increased rates of ROSC during chest compressions.30 However, epinephrine has many deleterious qualities. Beta-adrenergic activity causes tachycardia, promotes dysrhythmias, and leads to an increase in myocardial oxygen consumption. Extracardiac effects are notable as well; these include systemic vasoconstriction and tissue hypoxia, along with a decrease in cerebral blood flow via excessive alpha agonist activity.31 Additionally, a state of "catecholamine toxicity" has been observed in the post-resuscitation period, in which systemic hypoperfusion related to epinephrine use persists in a dose-related fashion, including decreases in both cardiac index and systemic oxygen delivery.32 Given these untoward effects, achieving ROSC via administration of epinephrine may be a Pyrrhic victory.
In the few randomized trials examining the effects of epinephrine in OHCA, an increase in ROSC has been consistently demonstrated with no concomitant meaningful outcomes. In one large double-blind, placebo-controlled trial — one of the few of its kind in the field of cardiac resuscitation — epinephrine use in OHCA was not associated with any statistically significant improvement in survival to hospital discharge, despite a nearly three-fold increase in ROSC.33 (See Table 1.) Similarly, in a separate OHCA study that compared ACLS with and without intravenous (IV) drug administration, IV interventions were not associated with any significant improvement in survival to hospital discharge or overall one-year survival.34 Finally, in one notable large observational OHCA study, use of epinephrine was actually associated with a significant decrease in both one-month survival and good-to-moderate neurologic function (again, despite a significant increase in pre-hospital ROSC.)35 Even in 2010, prior to publication of two of the three aforementioned studies, the International Liaison Committee on Resuscitation (ILCOR) put it succinctly: "Despite the continued widespread use of epinephrine and increased use of vasopressin during resuscitation in some countries, there is no placebo-controlled study that shows that the routine use of any vasopressor during human cardiac arrest increases survival to hospital discharge."36
Table 1: Epinephrine Use and Survival in OHCA
Study |
Number of Patients |
Study Type |
Odds Ratio (survival to hospital discharge) |
Jacobs et al33 |
534 |
RCT |
OR = 2.2; 95% CI 0.7-6.3 |
Olasveengen et al34 |
851 |
RCT |
OR = 1.15; 95% CI 0.69-1.91 |
Hagihara et al35 |
391,046 |
Prospective, nonrandomized, observational |
OR = 0.46; 95% CI 0.42-0.51* |
* Adjusted OR, survival at 1-month RCT = randomized controlled trial |
|||
Vasopressin, as intimated above, has fared no better, both as a substitute for epinephrine and as an adjunct therapy.37,38 In a similar vein, amiodarone is still recommended for refractory ventricular fibrillation or pulseless ventricular tachycardia, although it has never been shown to improve rates of survival to hospital discharge.29
Vasopressor use in cardiac resuscitation is deeply ingrained in the practice of emergency medicine and critical care, and moving away from such treatments would be a monumental sea change. However, in the face of the evidence, it is unclear how much longer future resuscitation guidelines can continue to tout epinephrine administration as a standard of care. There are now multiple prospective studies indicating that at best, epinephrine has no effect on meaningful outcomes in OHCA, and at worst, may actually impair neurologic recovery — arguably the only outcome that actually matters. However, despite the available evidence, the latest AHA guidelines continue to recommend 1 mg of epinephrine IV/IO every 3 to 5 minutes in cardiac arrest (regardless of setting), with 40 units of vasopressin as an acceptable alternative for the first or second doses.29
Of note, in 2013, a study on in-hospital cardiac arrest in Greece showed the combination of vasopressin, epinephrine, and methylprednisolone during CPR, followed by stress dose hydrocortisone in the post-resuscitative period, resulted in increased survival to hospital discharge with favorable neurological outcomes.39 Although this finding is intriguing, there are several caveats; overall survival, even within the controls, was much lower than typically reported, and significant differences existed within the control and treatment arms in terms of the etiology of arrest. Finally, it is hard to draw conclusions on the efficacy of vasopressors in the treatment group when confounded with both peri-arrest and post-resuscitation corticosteroids. In a separate large retrospective review,40 time to administration of epinephrine for in-hospital cardiac arrest with non-shockable rhythms demonstrated a survival benefit when given less than 3 minutes from arrest, with a gradual decrease in survival for each successive 3-minute interval. These studies are a reminder that cardiac arrest is not a homogenous process, and that there may still be a subset of patients (depending on arrest setting and presenting rhythm) who would benefit from epinephrine administration.
Airway Management
There is little evidence to support any method of advanced airway management during cardiac resuscitation. In the prehospital setting, paramedic attempts at endotracheal intubation during OHCA have been shown to cause repeated and prolonged interruptions in chest compressions,41 and in one large observational study, any method of advanced airway management (including endotracheal intubation and supraglottic airway [SGA] placement) was associated with poorer outcomes compared to traditional bag-valve-mask ventilation.42 These findings were again demonstrated in a recent large retrospective review in which patients who received only bag-valve-mask ventilation were three times more likely to survive to hospital discharge neurologically intact compared to patients who were intubated or received an LMA.43
ILCOR currently proposes (as a IIb recommendation) delaying advanced airway placement until the patient fails to respond to initial CPR and defibrillation attempts if such placement will interrupt chest compressions.36 Bag-valve-mask ventilation is sufficient during this time. If intubation is required before ROSC, it should be performed by experienced personnel and as rapidly as possible. Cricoid pressure is also no longer rountinely recommended during endotracheal intubation.6
Monitoring
The use of continuous end tidal carbon dioxide (ETCO2) measurements has been shown to be an effective adjunct in CPR. Besides confirming endotracheal tube placement, trend capnograms have been demonstrated to be a reliable measure of operator fatigue and the need to change providers of chest compressions.44,45 Other studies have shown this modality to be an accurate index of coronary perfusion pressure46 and cerebral perfusion pressure47 during CPR. When available, use of continuous ETCO2 in the ED may be preferable to simple color capnometry.
Cardiocerebral Resuscitation (CCR)
The emphasis on uninterrupted chest compressions, delayed intubation, early defibrillation, and minimization of overventilation is sometimes collectively referred to as "cardiocerebral resuscitation."48 The distinction between CCR and CPR is intentional, to contrast the practices of traditional CPR that may impair survival, particularly in ventricular fibrillation arrest. In addition to the factors listed above, CCR also emphasizes the three-phase time-sensitive model of cardiac resuscitation.49 (See Figure 2.)
In the three-phase model, the first 4 minutes are termed the electrical phase. This is the point at which immediate defibrillation is the most effective intervention (i.e., an implanted defibrillator that acts within seconds, and with a very high success rate.) This is the basis for the large-scale implementation of defibrillators in public places in recent years, such as airports, sporting events, and casinos, where bystanders and lay rescuers can act within minutes.
The subsequent 6 minutes comprise the circulatory phase, when myocardial energy stores fail. In this phase, defibrillation without replacing energy stores (via quality chest compressions for 1-3 minutes) may actually worsen outcomes, leading to a decrease in both successful defibrillation and ROSC.49 In one observational study, survival increased from 24% to 30% when 90 seconds of CPR was provided prior to defibrillation among patients whose initial response interval was 4 minutes or greater.50 Similar findings were demonstrated in a smaller randomized trial among a subgroup of patients whose response interval was 5 minutes or longer.51 These studies lend some credence to the notion of "priming the pump" prior to defibrillation, and support the concept of the circulatory phase of cardiac arrest.
The final phase is termed the metabolic phase, which is defined as greater than 10 minutes from arrest. From this point onward, the effectiveness of CPR and defibrillation decreases significantly, and overall survival is poor. This last phase is categorized by systemic ischemia, reperfusion injury, translocation of gut bacteria with endotoxin release, and high levels of circulating inflammatory markers (a so-called "sepsis-like syndrome").52
It should be noted that the three-phase model, while important from a theoretical perspective, may be difficult to apply in real-world scenarios. For example, exact downtime is not always known; in the absence of that information, should first responders assume they are in the circulatory phase and delay defibrillation? Are quality chest compressions less important in the electrical phase? These questions highlight the fact that the model provides a theoretical framework and a basis for future research. It should not (at the moment) strictly dictate practice, and the basic tenets of quality chest compressions and early defibrillation remain.
Post-resuscitative Care
Interest in post-resuscitative care has increased during the past decade. Much of this has revolved around the landmark HACA and Bernard et al studies53,54 that demonstrated a significant improvement in neurologic outcomes when therapeutic hypothermia (32 to 34ºC) was instituted after ROSC. Therapeutic hypothermia is thought to mitigate many of the derangements noted in the post-resuscitative period by slowing both cerebral and cardiac metabolism, reducing free radical formation, and attenuating cytokine release.
Recent evidence suggests that more modest temperature goals (36ºC) may be equally beneficial, and that much of the benefit of therapeutic hypothermia may be in aggressively preventing post-resuscitation fevers while balancing the deleterious effects of cooling (such as coagulopathies, arrhythmias, and metabolic disturbances).55 Pre-hospital initiation of cooling has been shown to reach temperature targets faster compared to standard care, although with no improvement in survival or neurologic status at hospital discharge (and is associated with an increased risk of re-arrest and transient pulmonary edema.).56 At present, the AHA guidelines make a Class I recommendation for the induction of hypothermia after a cardiac arrest due to ventricular fibrillation in comatose adult patients, and a Class IIb recommendation in comatose adult survivors of PEA and asystole.57
Other aspects of post-resuscitative care should not be overlooked. These include PCI if necessary (and some might argue, routinely58), early identification and aggressive treatment of seizures, adequate blood glucose control, and hemodynamic optimization. "Bundled" post-resuscitative treatments are becoming standardized in certain centers, with purportedly improved outcomes.59,60
Termination of Efforts
The termination of efforts in CPR is a highly complex subject with regard to the number of factors involved. There should be consideration for patient wishes, age, pre-arrest state, witnessed or unwitnessed arrest, time to CPR, initial rhythm, comorbid disease, length of CPR, potential for organ donation, religion, and family presence, among others.61 Attempts at prognostication and assessment of futility during CPR are difficult. Although some rules exist for both BLS and ALS providers in the pre-hospital setting, there are few data on in-hospital patients. There are some data on the use of ETCO2 as a prognostic marker for ROSC that may be worth considering in tandem with the other issues listed above.62 With the advent of extracorporeal CPR, described below, its availability may challenge conventional ideas on timing, especially in the pediatric and young adult population.
What’s Next? Extracorporeal Membrane Oxygenation (ECMO)
One of the biggest advances in recent years is the use of ECMO in the peri-arrest and post-resuscitative period,63 including the initiation of ECMO in the emergency department.64 (See Figure 3.) This is sometimes referred to as extracorporeal cardiopulmonary resuscitation (ECPR). Although the practice has been described in cardiac arrest for nearly 40 years,65 miniaturized ECMO devices are only now enjoying widespread use (such as the Sorin Lifebox or the Maquet CARDIOHELP). In many ways, the development of smaller and more user-friendly ECMO devices mirrors the historic introduction of closed cardiac massage into clinical practice — what was once the exclusive domain of cardiothoracic surgeons is now becoming available for all providers, including emergency physicians.
Figure 3: Simplified ECMO Schematic
To date, outcomes have been more promising among patients who arrest in-hospital and are started promptly on ECMO, as compared to patients who suffer OHCA and inevitably experience delays prior to ECMO being initiated.66-68 Research suggests that there may be both short- and long-term benefits with ECPR for in-hospital cardiac arrest. In one study, these benefits include a four-fold increase in survival at two years with minimal neurologic impairment.69
Advanced Monitoring
Several methods of advanced monitoring are emerging in the post-resuscitative period. These include bispectral index (BIS),70 a form of simplified non-invasive electroencephalographic monitoring, and cerebral oximetry,71 which utilizes near-infrared spectroscopy to determine regional brain oxygen saturation levels (rSO2). These monitoring devices are meant to both triage post-arrest patients and help guide future therapies. A recent multicenter, prospective trial found that patients who survived OHCA neurologically intact had significantly higher rSO2 compared to those patients who had poor neurologic outcomes.72
Pharmacotherapy
Research into drug therapies that stabilize post-arrest patients, both from a cardiac and a neurologic perspective, is ongoing. Prophylactic lidocaine has shown promise in reducing recurrent ventricular fibrillation following ROSC,72 and there is emerging interest in the use of neurostimulants (such as methylphenidate and amantadine) to promote reawakening in resuscitated comatose patients.72 Other agents that have been studied include sevoflurane, erythropoietin, and delta-opioid compounds, to name a few.73-76 This field is very much in its infancy, and no treatments have been recommended for routine post-resuscitative care.
Future Guidelines
The next version of the AHA and ILCOR guidelines is expected sometime in 2015. It remains to be seen whether any of the evidence-based considerations discussed above — such as a de-emphasis on epinephrine, an increase in the rate of chest compressions, or the notion of providing chest compressions prior to defibrillation in OHCA — will be incorporated into the final recommendations. Only time will tell.
Summary
Among cardiac arrest victims, patients with ventricular fibrillation tend to have the highest survival rates and the greatest possibility of hospital discharge with good neurologic function. Despite our technologic advances, the two most important interventions in this subpopulation remain quality chest compressions and early defibrillation. No vasopressor, including epinephrine, has been shown to improve meaningful outcomes in OHCA, although a subset of undefined patients (particularly in the inpatient setting) may still benefit. Advanced airways, including endotracheal intubation and SGA placement, should be inserted by experienced personnel and should be deferred if they will interrupt chest compressions; bag-valve-mask oxygenation and ventilation is sufficient, at least for the first several minutes. After ROSC, institutional processes should streamline post-resuscitative care, and include not only therapeutic hypothermia, but metabolic and hemodynamic optimization as well. Use of peri-arrest ECMO is increasing as the technology becomes more widespread and easier to implement, and preliminary evidence suggests there may be significant short- and long-term benefits.
References
- Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA 1960;173:1064-1067.
- Beck CS, Pritchard WH, Feil HS. Ventricular fibrillation of long duration abolished by electric shock. J Am Med Assoc 1947;135(15):985.
- Johnson J, Kirby CK, Dripps RD. Defibrillation of the ventricles by electric shock with complete recovery. Ann Surg 1951;134(1):116-118.
- Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence of EMS-treated out-of-hospital cardiac arrest in the United States. Resuscitation 2004;63(1):17-24.
- Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA 2008;300(12):1423-1431.
- Field JM, Hazinski MF, Sayre MR, et al. Part 1: Executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 Suppl 3):
S640-656. - Hallstrom AP, Cobb LA, Yu BH. Influence of comorbidity on the outcome of patients treated for out-of-hospital ventricular fibrillation. Circulation 1996;93(11):2019-2022.
- [No authors listed.] Cardiopulmonary resuscitation. JAMA 1966;198(4):
372-379. - Rea TD, Cook AJ, Stiell IG, et al. Predicting survival after out-of-hospital cardiac arrest: Role of the Utstein data elements. Ann Emerg Med 2010;55(3):249-257.
- Bobrow BJ, Spaite DW, Berg RA, et al. Chest compression-only CPR by lay rescuers and survival from out-of-hospital cardiac arrest. JAMA 2010;304(13):1447-1454.
- Hüpfl M, Selig HF, Nagele P. Chest-compression-only versus standard cardiopulmonary resuscitation: A meta-analysis. Lancet 2010;376(9752):1552-1557.
- Ogawa T, Akahane M, Koike S, Tanabe S, Mizoguchi T, Imamura T. Outcomes of chest compression only CPR versus conventional CPR conducted by lay people in patients with out of hospital cardiopulmonary arrest witnessed by bystanders: Nationwide population based observational study. BMJ 2011;342:c7106.
- Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation 2001;104(20):
2465-2470. - Ornato JP, Peberdy MA. Measuring progress in resuscitation: It’s time for a better tool. Circulation 2006;114(25):
2754-2756. - Bobrow BJ, Clark LL, Ewy GA, et al. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. JAMA 2008;299(10):1158-1165.
- Hallstrom A, Rea TD, Sayre MR, et al. Manual chest compression vs use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest: A randomized trial. JAMA 2006;295(22):2620-2628.
- Axelsson C, Nestin J, Svensson L, Axelsson AB, Herlitz J. Clinical consequences of the introduction of mechanical chest compression in the EMS system for treatment of out-of-hospital cardiac arrest — a pilot study. Resuscitation 2006;71(1):47-55.
- Jennings PA, Harriss L, Bernard S, et al. An automated CPR device compared with standard chest compressions for out-of-hospital resuscitation. BMC Emerg Med 2012;12:8.
- Ewy GA, Zuercher M. Role of manual and mechanical chest compressions during resuscitation efforts throughout cardiac arrest. Future Cardiol 2013;9(6):
863-873. - Giraud R, Siegenthaler N, Schussler O, et al. The LUCAS 2 chest compression device is not always efficient: An echographic confirmation. Ann Emerg Med 2014, Feb. 12 [Epub ahead of print].
- Wagner H, Terkelsen CJ, Friberg H, et al. Cardiac arrest in the catheterisation laboratory: A 5-year experience of using mechanical chest compressions to facilitate PCI during prolonged resuscitation efforts. Resuscitation 2010;81(4):
383-387. - Larsen AI, Hjørnevik AS, Ellingsen CL, Nilsen DW. Cardiac arrest with continuous mechanical chest compression during percutaneous coronary intervention. A report on the use of the LUCAS device. Resuscitation 2007;75(3):454-459.
- Idris AH, Guffey D, Aufderheide TP, et al. Relationship between chest compression rates and outcomes from cardiac arrest. Circulation 2012;125(24):
3004-3012. - Neumann T, Gruenewald M, Lauenstein C, Drews T, Iden T, Meybohm P. Hands-on defibrillation has the potential to improve the quality of cardiopulmonary resuscitation and is safe for rescuers-a preclinical study. J Am Heart Assoc 2012;1(5):e001313.
- Lloyd MS, Heeke B, Walter PF, Langberg JJ. Hands-on defibrillation: An analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 2008;117(19):2510-2514.
- Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation 2001;104(20):
2465-2470. - Sullivan JL, Chapman FW. Will medical examination gloves protect rescuers from defibrillation voltages during hands-on defibrillation? Resuscitation 2012;83(12):1467-1472.
- Surgeon Tells How He Brings Back Life. (1909, Feb 14.) The New York Times.
- Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 Suppl 3):
S729-767. - Callaway CW. Questioning the use of epinephrine to treat cardiac arrest. JAMA 2012;307(11):1198-1200.
- Ristagno G, Tang W, Huang L, et al. Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation. Crit Care Med 2009;37(4):1408-1415.
- Rivers EP, Wortsman J, Rady MY, Blake HC, Mcgeorge FT, Buderer NM. The effect of the total cumulative epinephrine dose administered during human CPR on hemodynamic, oxygen transport, and utilization variables in the postresuscitation period. Chest 1994;106(5):1499-1507.
- Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation 2011;82(9):1138-1143.
- Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L. Intravenous drug administration during out-of-hospital cardiac arrest: A randomized trial. JAMA 2009;302(20):2222-2229.
- Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA 2012;307(11):1161-1168.
- Hazinski MF, Nolan JP, Billi JE, et al. Part 1: Executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2010;122(16 Suppl 2):
S250-275. - Gueugniaud PY, David JS, Chanzy E, et al. Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation. N Engl J Med 2008;359(1):21-30.
- Larabee TM, Liu KY, Campbell JA, Little CM. Vasopressors in cardiac arrest: A systematic review. Resuscitation 2012;83(8):932-939.
- Mentzelopoulos SD, Malachias S, Chamos C, et al. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: A randomized clinical trial. JAMA 2013;310(3):270-279.
- Donnino MW, Salciccioli JD, Howell MD, et al. Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: Retrospective analysis of large in-hospital data registry. BMJ 2014;348:g3028.
- Wang HE, Simeone SJ, Weaver MD, Callaway CW. Interruptions in cardiopulmonary resuscitation from paramedic endotracheal intubation. Ann Emerg Med 2009;54(5):645-652.e1.
- Hasegawa K, Hiraide A, Chang Y, Brown DF. Association of prehospital advanced airway management with neurologic outcome and survival in patients with out-of-hospital cardiac arrest. JAMA 2013;309(3):257-266.
- Mcmullan J, Gerecht R, Bonomo J, et al. Airway management and out-of-hospital cardiac arrest outcome in the CARES registry. Resuscitation 2014;85(5):617-622.
- Kalenda Z. Capnogram as a guide to the efficacy of cardiac massage. Resuscitation 1978;6:259-63.
- Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. New Engl J Med 1988;318:607-611.
- Sanders AB, Atlas M, Ewy GA, et al. Expired PCO2 as an index of coronary perfusion pressure. Am J Emerg Med 1985;3:147-149.
- Lewis LM, Stothert J, Standeven J, et al. Correlation of end-tidal CO2 to cerebral perfusion during CPR. Ann Emerg Med 1992;21:1131-1134.
- Ewy GA. Cardiocerebral resuscitation: The new cardiopulmonary resuscitation. Circulation 2005;111(16):2134-2142.
- Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest: A 3-phase time-sensitive model. JAMA 2002;288(23):
3035-3038. - Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA 1999;281(13):1182-1188.
- Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: A randomized trial. JAMA 2003;289(11):1389-1395.
- Adrie C, Adib-conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a "sepsis-like" syndrome. Circulation 2002;106(5):
562-568. - HACA group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346(8):549-556.
- Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346(8):557-563.
- Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest.
N Engl J Med 2013;369(23):2197-2206. - Kim F, Nichol G, Maynard C, et al. Effect of prehospital induction of mild hypothermia on survival and neurological status among adults with cardiac arrest: A randomized clinical trial. JAMA 2014;311(1):45-52.
- Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: Post−Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S768-S786.
- Chelly J, Mongardon N, Dumas F, et al. Benefit of an early and systematic imaging procedure after cardiac arrest: Insights from the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) registry. Resuscitation 2012;83(12):1444-1450.
- Gaieski DF, Band RA, Abella BS, et al. Early goal-directed hemodynamic optimization combined with therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation 2009;80(4):418-424.
- Sunde K, Pytte M, Jacobsen D, et al. Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest. Resuscitation 2007;73(1):29-39.
- Morrison LJ, Kierzek G, Diekema DS, et al. Part 3: Ethics: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S665-S675
- Callaham M, Barton C. Prediction of outcome of CPR from end-tidal carbon dioxide concentration. Crit Care Med 1990;18;358-362.
- Mégarbane B, Leprince P, Deye N, et al. Emergency feasibility in medical intensive care unit of extracorporeal life support for refractory cardiac arrest. Intensive Care Med 2007;33(5):758-764.
- Bellezzo JM, Shinar Z, Davis DP, et al. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation. Resuscitation 2012;83(8):966-970.
- Mattox KL, Beall AC. Resuscitation of the moribund patient using portable cardiopulmonary bypass. Ann Thorac Surg 1976;22(5):436-442.
- Kagawa E, Inoue I, Kawagoe T, et al. Assessment of outcomes and differences between in- and out-of-hospital cardiac arrest patients treated with cardiopulmonary resuscitation using extracorporeal life support. Resuscitation 2010;81(8):
968-973. - Le guen M, Nicolas-robin A, Carreira S, et al. Extracorporeal life support following out-of-hospital refractory cardiac arrest. Crit Care 2011;15(1):R29.
- Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: An observational study and propensity analysis. Lancet 2008;372(9638):554-561.
- Shin TG, Jo IJ, Sim MS, et al. Two-year survival and neurological outcome of in-hospital cardiac arrest patients rescued by extracorporeal cardiopulmonary resuscitation. Int J Cardiol 2013;168(4):
3424-3430. - Seder DB, Dziodzio J, Smith KA, et al. Feasibility of bispectral index monitoring to guide early post-resuscitation cardiac arrest triage. Resuscitation 2014, April 30 [Epub ahead of print].
- Ahn A, Yang J, Inigo-santiago L, Parnia S. A feasibility study of cerebral oximetry monitoring during the post-resuscitation period in comatose patients following cardiac arrest. Resuscitation 2014;85(4):
522-526. - Ito N, Nishiyama K, Callaway CW, et al. Noninvasive regional cerebral oxygen saturation for neurological prognostication of patients with out-of-hospital cardiac arrest: A prospective multicenter observational study. Resuscitation 2014;85:
778-784. - Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation 2013;84(11):1512-1518.
- Reynolds JC, Rittenberger JC, Callaway CW. Methylphenidate and amantadine to stimulate reawakening in comatose patients resuscitated from cardiac arrest. Resuscitation 2013;84(6):818-824.
- Meybohm P, Gruenewald M, Albrecht M, et al. Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction. Crit Care 2011;15(5):R241.
- Borovnik-lesjak V, Whitehouse K, Baetiong A, Artin B, Radhakrishnan J, Gazmuri RJ. High-dose erythropoietin during cardiac resuscitation lessens postresuscitation myocardial stunning in swine. Transl Res 2013;162(2):110-121.
- Yang L, Zhao X, Sun M, et al. Delta opioid receptor agonist BW373U86 attenuates post-resuscitation brain injury in a rat model of asphyxial cardiac arrest. Resuscitation 2014;85(2):299-305.
- Fang X, Tang W, Sun S, Weil MH. delta-Opioid-induced pharmacologic myocardial hibernation during cardiopulmonary resuscitation. Crit Care Med 2006;34(12 Suppl):S486-489.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content