TY - JOUR
AU - Kern, Karl, B.
AB - Abstract Introduction Sudden cardiac arrest continues to be the leading cause of death in the industrialized world. Sources of data Original papers, reviews and guidelines. Areas of agreement Community programs for lay bystander cardiopulmonary resuscitation (CPR) and automatic external defibrillation improve outcomes. Post-arrest care, including targeted temperature management (TTM) combined with early coronary angiography and percutaneous coronary intervention, is helpful for those suffering cardiac arrest during an ST-segment elevation myocardial infarction. Areas of controversy (1) The optimal approach to encourage lay bystanders to assist with resuscitation efforts. (2) Whether TTM combined with early coronary angiography is cost effective for those without ST elevation on their post-arrest ECG is unknown. Growing points Increasing data show that chest compression-only CPR is preferred by lay rescuers and improves local survival rates. Areas timely for developing research Randomized clinical trials are underway to examine the utility of early coronary angiography in the treatment of post-arrest patients without ST-segment elevation. cardiac arrest, chest compression-only CPR, public access defibrillation, post-arrest coronary angiography, refractory out-of-hospital cardiac arrest Introduction Sudden cardiac death (SCD) is a major public health problem. In the United States, there are approximately 360 000 out-of-hospital cardiac arrests each year.1 Only 10% of OHCA patients of all ages survive to hospital discharge.1 Etiology of SCD Coronary heart disease (CHD) remains the most common cause of SCD. CHD accounts for approximately 80% of all SCDs2 while non-ischemic cardiomyopathies are responsible for another 10–15%. SCD can occur in individuals with structural heart disease (10–15%) such as CHD and in individuals without any structural heart disease such as arrhythmic syndromes, including long-QT syndromes, short-QT syndromes, catecholaminergic polymorphic VT and Burgada syndrome.3,4 Hence, it is important to be familiar with the different conditions that cause SCD (Table 1). For instance, hypertrophic cardiomyopathy (HCM) is the most common cause of SCD in adults younger than 35 years of age. An in-depth knowledge of the etiology and pathophysiology of SCD not only assists in clinical management but also helps to establish prognosis, prevent future recurrence and screen family members at risk for SCD. Table 1 Causes of sudden cardiac arrest ○Coronary artery disease ▪ ST-segment elevation myocardial infarction ▪ Other myocardial infarction ▪ Unstable angina ▪ Silent ischemia ○ Coronary anomalies ○ Congenital heart disorders ○ Hypertrophic cardiomyopathy ○ Dilated cardiomyopathy ○ Valvular heart disease ○ Electrical heart disease ▪ Long-QT syndromes ▪ Brugada syndrome ▪ Drug or medication induced ○Coronary artery disease ▪ ST-segment elevation myocardial infarction ▪ Other myocardial infarction ▪ Unstable angina ▪ Silent ischemia ○ Coronary anomalies ○ Congenital heart disorders ○ Hypertrophic cardiomyopathy ○ Dilated cardiomyopathy ○ Valvular heart disease ○ Electrical heart disease ▪ Long-QT syndromes ▪ Brugada syndrome ▪ Drug or medication induced Table 1 Causes of sudden cardiac arrest ○Coronary artery disease ▪ ST-segment elevation myocardial infarction ▪ Other myocardial infarction ▪ Unstable angina ▪ Silent ischemia ○ Coronary anomalies ○ Congenital heart disorders ○ Hypertrophic cardiomyopathy ○ Dilated cardiomyopathy ○ Valvular heart disease ○ Electrical heart disease ▪ Long-QT syndromes ▪ Brugada syndrome ▪ Drug or medication induced ○Coronary artery disease ▪ ST-segment elevation myocardial infarction ▪ Other myocardial infarction ▪ Unstable angina ▪ Silent ischemia ○ Coronary anomalies ○ Congenital heart disorders ○ Hypertrophic cardiomyopathy ○ Dilated cardiomyopathy ○ Valvular heart disease ○ Electrical heart disease ▪ Long-QT syndromes ▪ Brugada syndrome ▪ Drug or medication induced Coronary heart disease Overt CHD is associated with a marked increase in SCD risk. Generally, SCD occurs in patients with CHD during or after myocardial infarction, secondary to multi-vessel coronary artery disease, previous myocardial infarction with myocardial scarring particularly during the first 30 days post-MI, and in those with ischemic cardiomyopathy and marked left ventricular systolic dysfunction. About two-thirds of all SCD due to CHD occur either as the first clinical manifestation of coronary artery disease or in individuals with known coronary artery disease who were thought to be low risk based on current risk stratification schemes. Four main pathophysiologic substrates contribute to SCD: transient ischemia, acute coronary syndrome, scar-related arrhythmia, and ischemic cardiomyopathies that produce potentially fatal arrhythmias such as ventricular fibrillation, ventricular tachycardia, asystole, and bradycardia. With improvements in primary prevention and revascularization techniques, age-adjusted mortality related to CHD has declined within the last five decades; however, the percentage of SCD associated with CHD has remained unchanged. This association suggests complex interactions between CHD and triggering events such as ischemia, autonomic nervous system dysfunction, electrolyte imbalance or drug toxicity. Furthermore, individual genetic profiles add another layer of complexity.3 Clinical studies have highlighted this complexity. Acute coronary thrombosis has been reported in 25–48% of OHCA survivors who underwent immediate angiography. In a Framingham cohort, 20–34% of SCD occurred in the setting of acute coronary syndrome.5 Detailed pathologic studies have identified pathological features such as plaque fissure, plaque hemorrhage and thrombosis in up to 95% of patients who died suddenly.6 These patients often have ST elevations on their electrocardiograms and immediate angiography with revascularization can be life-saving for this group of patients with SCD. However, the absence of ST elevations does not preclude benefit from immediate angiography, as the ECG has a poor negative predictive value in this setting.7 The presence of coronary artery disease is associated with a better prognosis in patients with SCD. Factors such as the use of appropriate medical therapy and ischemic preconditioning may lead to better outcomes with SCD. The opportunity to find and treat a culprit vessel, may also improve outcomes from cardiac arrest. Non-atherosclerotic coronary artery abnormalities Non-atherosclerotic coronary abnormalities such as congenital lesions, coronary artery embolism, coronary arteritis, spasm and myocardial bridging have all been associated with SCD. Congenital heart disease Congenital coronary anomalies are prevalent in 1% of all patients undergoing coronary angiography and in 0.3% of patients undergoing an autopsy. SCD due to congenital coronary anomalies is exercise related and accounts for 17% of SCD in young athletes. The presence of an anomalous origin of the left coronary artery is frequently associated with SCD. Coronary artery embolism is most commonly associated with aortic valve endocarditis, especially with large vegetations. Coronary arteritis seen with Kawasaki disease, polyarteritis nodosa, and related vasculitis syndromes also carry a risk of SCD. Hypertrophic cardiomyopathy HCM with its estimated prevalence of 1 in 500 is the most common cause of SCD in adults less than 35 years of age. Often such individuals have had no prior cardiac symptoms. The incidence of SCD in selected families with HCM treated at large referral centers was 2–4% per year in adults and 4–6% in children and adolescents. High-risk features associated with SCD in HCM patients are: history of ventricular arrhythmias, family history of SCD, recurrent syncope, exercise-induced hypotension, non-sustained ventricular tachycardia and severe (>30 mm) left ventricular hypertrophy. Initial treatment of SCD with chest compression-only cardiopulmonary resuscitation Chest compressions and early defibrillation remain the foundation of basic life support when encountering the out-of-hospital cardiac arrest (OHCA) patient. The AHA guidelines have evolved to emphasize chest compressions, with a transition from a compression-to-ventilation ratio of 15:2 to 30:2, while teaching lay rescuers and the value of chest compression-only bystander CPR (CCO CPR). Much of the transition from standard CPR to CCO CPR has occurred in the absence of randomized data, though this knowledge gap is slowly being filled. Most experimental, translational work supports the use of CCO CPR. Comparing clinically relevant endpoints in a swine model, Wang et al. demonstrated similar short- and long-term outcomes between standard CPR and CCO CPR.8 In another porcine model of OHCA, Ewy et al. demonstrated greater neurological normal survival with CCO CPR compared to standard CPR.9 Interestingly, Ewy et al. also demonstrated equivalence in 24-h survival in a swine model of CCO CPR with upper airway inspiratory obstruction, compared to standard CPR without upper airway inspiratory obstruction.10 More recently, Xanthos et al. demonstrated higher survival rates and higher 24-h neurologic scores with CCO CPR compared to standard CPR.11 CCO CPR is uniquely suited to successfully treat the second phase of ventricular fibrillation according to the Weisfeldt and Becker model.12 These ‘CPR Giants’ proposed a three-phase model of ventricular fibrillation cardiac arrest (VFCA), including an electrical phase, a hemodynamic phase and a metabolic phase. The early electrical phase readily responds to an electrical shock with successful defibrillation resulting in return spontaneous circulation. This initial few minutes after the onset of VFCA is followed by the hemodynamic phase, during which time the heart's metabolic stores are exhausted and it is less responsive to electrical defibrillation. However, providing reasonable myocardial perfusion with CPR can make the heart much more likely to respond positively to defibrillation. Finally, after extended minutes in VFCA, the heart enters the metabolic phase, during which time neither electrical defibrillation nor continued CPR is likely to be helpful. A clear goal of CCO CPR is to address the hemodynamic phase of ventricular fibrillation. After the initiation of chest compressions, both arterial perfusion pressure and coronary perfusion pressure gradually increase and plateau to reach life-saving perfusion pressures that maintain end organ perfusion. However, interruptions in chest compressions for any reason, including ventilation, can result in a substantial drop in the crucial perfusion pressure ultimately compromising survival.13 Thus, the goal of CCO CPR is to create a physiologic milieu, with the maintenance of life-saving arterial and coronary perfusion pressures during the hemodynamic phase, optimized for not just ROSC but long- term survival with favorable neurological function. In a departure from the AHA guidelines, in 2003, the Sarver Heart Center Cardiopulmonary Research Group at the University of Arizona and, later, Mercy Health System in rural Wisconsin, instituted a different protocol for their OHCA that instituted continuous chest compression and eliminated pauses for ventilation. This protocol resulted in three observational studies that demonstrated improved survival in OHCA in rural Wisconsin and Arizona.14–16 In 2000, Hallstrom et al. effectively demonstrated the equivalency of 911 dispatcher-instructed bystander CCO CPR when compared to standard CPR in survival to hospital discharge.17 Ten years later, Rea et al. and Svennsson et al. re-demonstrated that there was no significant difference in 30-day survival between dispatcher-instructed bystander CCO CPR and standard CPR.18,19 The Resuscitation Outcomes Consortium investigated CCO CPR during EMS provided resuscitation efforts, and demonstrated no difference in outcomes between CCO CPR with asynchronous, simultaneous positive pressure ventilation compared to standard CPR that was interrupted for ventilations at a 30:2 compression-to-ventilation ratio.20 The ease with which CCO CPR can be taught, increased user adoption and secondary training, and equivalency in clinical endpoints has resulted CCO CPR has become the standard of care for the OHCA. Public access automatic external defibrillators Despite the improvements made in resuscitative efforts, only about 10% of patients with OHCA survive. Prompt defibrillation remains the definitive treatment for VFCA. There is a threefold improved survival in patients who have a bystander witnessed, initially shockable rhythm and receive early defibrillation. Layperson administered rapid defibrillation via public automatic external defibrillators (AEDs) have demonstrated improved survival after OHCA in American casinos and airlines.21,22 When the general public is trained in early defibrillation with AEDs, patient survival improves compared to defibrillation by emergency medical services at the time of their arrival.23,24 However, a number of challenges continue to exist: (i) Optimal AED placement location, (ii) public access to AEDs and (iii) layperson utilization of available AEDs. Accordingly, public AED placement has focused on high-risk areas, such as transportation centers, entertainment venues, medical practices and schools, with documented at least one OHCA per 5 years. Targeted AED programs, including training non-medical personnel to respond with AEDs to cardiac arrest emergencies, have also been successful in certain venues like inner city subway systems.25 Actual public usage of AEDs depends on both the spatial and temporal availability and coverage loss may occur whenever a registered AED is not present or is unavailable (locked in building after business hours) at the time of cardiac arrest. In dense population centers, placement of AEDs in high-risk OHCA areas with 24–7 availability can successfully serve to overcome some of these limitations.26 Geo-tagged registered AED maps, in the form of smartphone apps help to easily identify the location of the nearest AED. However, limitations persist in rural areas. One strategy to overcome these limitations include mobile AEDs with trained citizens available to transport and deliver early defibrillation before the arrival of emergency medical personnel.27 The availability of AEDs also requires a general public that is willing to be trained in the appropriate usage of the device. In one survey conducted in the UK only 5.1% of responders knew where find the nearest AED with only 2.1% respond that they would actually retrieve and use the device when needed, despite 26.1% reporting knowledge of how to use an AED.28 This was in stark contrast to the 61.1% who reported that they had been trained in basic life support. Though there is room for improvement, considerable gains have been made. Data from the All-Japan Utstein Registry of the Fire and Disaster Management Agency suggests that from 2001 to 2015, there was an increased availability of AEDs and increased public access defibrillation, resulting in improved survival at one month with minimal neurological deficits.29,30 Successful utilization of AEDs requires placing and maintaining AEDs in high-risk OHCA sites with round-the-clock availability, enrolling a core group at these high-risk sites to respond, clear signage indicating the location of AEDs, widespread public education on how and why to use AEDs, and ongoing assessment of the program itself. Post-cardiac arrest care Management of post-cardiac arrest patients should include multiple simultaneous interventions with a goal to identify and treat the cause of cardiac arrest, minimize cerebral injury, restore and maintain cardiovascular stability, and manage sequela of systemic hypoperfusion. Interventions that have been shown to improve survival are immediate coronary angiography and targeted temperature management (TTM).31 Initial assessment It is important to perform a comprehensive evaluation including a detailed history, a thorough physical examination, and appropriate laboratory and imaging studies. Often OHCA is unwitnessed which limits the extent of information available. Laboratory testing for myonecrosis, electrolytes, metabolic abnormalities and arterial blood gas analysis may be helpful. A 12-lead ECG is perhaps most critical for early risk stratification.32 This should be reviewed with an expert, if needed, and compared to a previous electrocardiogram. Imaging modalities such as echocardiography to assess for structural heart disease often leads to appropriate treatment selection. Coronary angiography and percutaneous coronary intervention The American College of Cardiology Interventional Council recommends an algorithmic approach to risk stratify patients in order identify those who would benefit from early reperfusion therapy (Fig. 1). Recent American and European guidelines recommend immediate coronary angiography in OHCA survivors demonstrating ST-segment elevation myocardial infarction (STEMI).33,34 However, in patients without ST-segment elevation, the guidelines are less clear. Several reports have demonstrated that the absence of post-arrest ST elevations does not eliminate the possibility of an acute occlusion of a major epicardial coronary artery. In a study analyzing data from the INTCAR registry of 746 comatose post-cardiac arrest patients, an occluded coronary vessel was found in 74% of STEMI patients and 23% of those without ST-segment elevation.35 In other words, about one of every four post-arrest patients without ST elevation is found to have an acutely occluded coronary on early cardiac catheterization post resuscitation. Therefore, it is reasonable to offer coronary angiography to comatose post-cardiac arrest patients with and without STEMI. The European Society of Cardiology assigned a class IIA recommendation for coronary angiography in OHCA survivors without diagnostic ST-T changes but with a high suspicion of ongoing infarction.34 American Heart Association cardiopulmonary resuscitation guidelines made a similar recommendation. In addition, regardless of the ECG findings, emergent coronary angiography is needed in patients with ongoing hemodynamic instability due to cardiogenic shock. Comprehensive evaluation, careful risk stratification and ascertaining goals of care with immediate family members will optimize chances of the patient's recovery and health care utilization. Fig. 1 Open in new tabDownload slide Algorithm for risk stratification of comatose cardiac arrest patients. ACT, assessment, consultation, transport; CCL, cardiac catheterization laboratory; CPR, cardiopulmonary resuscitation; ECG, electrocardiography; LV, left ventricular; OHCA, out-of-hospital cardiac arrest; PCI, percutaneous coronary intervention; ROSC, return of spontaneous circulation; STEMI, ST-segment elevation myocardial infarction; TH, therapeutic hypothermia; TTM, targeted temperature management; VF, ventricular fibrillation. Reproduced with permission from the Journal of the American College of Cardiology.32 Fig. 1 Open in new tabDownload slide Algorithm for risk stratification of comatose cardiac arrest patients. ACT, assessment, consultation, transport; CCL, cardiac catheterization laboratory; CPR, cardiopulmonary resuscitation; ECG, electrocardiography; LV, left ventricular; OHCA, out-of-hospital cardiac arrest; PCI, percutaneous coronary intervention; ROSC, return of spontaneous circulation; STEMI, ST-segment elevation myocardial infarction; TH, therapeutic hypothermia; TTM, targeted temperature management; VF, ventricular fibrillation. Reproduced with permission from the Journal of the American College of Cardiology.32 Targeted temperature management Neurologic injury is the most common cause of death in patients with OHCA.36 A recent large randomized controlled trial demonstrated survival rates near 50% when the temperature was maintained at either 33 or 36°C.37 Hyperthermia during TTM is associated with increased risk of death.38 Current guidelines suggest that either temperature goal is acceptable and that all comatose post-arrest patients should maintain hypothermia through actively controlled core temperature in the range of 32–36°C. Neuromuscular blockade and deep sedation are helpful in preventing shivering and resultant hyperthermia. TTM should be initiated with intravascular or surface cooling methods as soon as possible, perhaps in the emergency room or cardiac catheterization laboratory. Cooling should be maintained for 12–48 h following cardiac arrest (most centers select 24 h), with gradual rewarming (0.25–0.5°C/h).39 Hypothermia may help by decreasing cerebral edema, reducing seizure activity and minimizing metabolic demands. Combined TTM and coronary angiography Multiple cohort studies have demonstrated improved survival of post-arrest STEMI patients who are comatose and who received both TTM and coronary angiography. In this group, survival-to-hospital discharge was 60%, with 86% of the survivors having a good neurological outcome. Hence, the International Committee on Resuscitation recommended therapeutic hypothermia in combination with percutaneous coronary intervention (PCI), with cooling begun preferably before PCI. With combined TTM and PCI, there has been a concern for both bleeding risk and stent thrombosis. However, a recent analysis of 49,109 cardiac arrest patients who underwent PCI, the incidence of stent thrombosis in the hypothermia group was comparable to patients not receiving hypothermia.40 Secondary prevention with ICD therapy Survivors of SCD often require the implantation of an internal cardioerter-defibrillator. The recent development of a leadless subcutaneous implanted defibrillator has the advantage of avoiding the increasing problem of failing or infected transvenous leads. These newer subcutaneous ICDs are a good option for younger patients who lead an active lifestyle. Next frontier: out-of-hospital refractory ventricular fibrillation The next likely opportunity to improve long-term outcomes for victims of sudden cardiac arrest is the treatment of those with refractory ventricular fibrillation. A new approach is needed for those who fail to respond to defibrillation. The challenge is that waiting too long to try something new and any therapy will be ineffective. But change too early and some who would have been resuscitated with less invasive means are exposed to the increased morbidity of invasive therapies. Several key advances from the last few years make it possible to change the current paradigm for treating out-of-hospital VFCA. Presently our approach is based on a ‘stay and play’ mentality. Patients are treated in the field with escalating advanced life support measures, including chest compressions, repeated attempts at defibrillation, vasoactive medications and tracheal intubation. Several key advances in resuscitation now make a different approach, a ‘load and go’ scenario, possible. These advances include mechanical CPR devices,41,42 percutaneously inserted systemic circulatory support systems,43,44 PCI during CPR45–47 and target temperature management during resuscitation efforts.37,48,49 Refractory ventricular fibrillation The first practical step in this new paradigm is to define ‘refractory’ ventricular fibrillation. Is it failure to defibrillate after a given number of attempts? If so, how many defibrillation attempts? Saio et al. used three shocks as their cutoff value.50 Yannopoulos et al. used the combination of three unsuccessful shocks and the administration of amiodarone.51 What of those patients whose initial cardiac arrest rhythm was ventricular fibrillation but who defibrillate early into a non-perfusing, non-shockable rhythm (pulseless electrical activity or asystole)? Is ‘refractory’ a certain passage of time without restoration of spontaneous circulation? How long should that time period be? Saio et al. used 10 min of conventional treatment without success,50 Reynolds et al. used a range of 10–15 min52 and Belohlavek et al. used a shorter range of 5–10 min.53 However ‘refractory’ is defined, the optimal candidates for this new approach must be carefully chosen to benefit. Besides merely time in cardiac arrest, other patient and resuscitation characteristics have been identified to alter outcomes. These characteristics must be considered and accounted for if successful outcomes are to be achieved (Table 2). Table 2 Patient and resuscitation characteristics affecting outcome from cardiac arrest ○ Patient ▪ Age ▪ Gender ▪ Co-morbid conditions Renal failure Pneumonia Cardiogenic shock Trauma ○ Resuscitation ▪ Location (public vs. private) ▪ Witnessed arrest ▪ Bystander CPR ▪ Type of bystander CPR (compression-only vs. standard) ▪ Initial cardiac arrest rhythm ▪ Bystander AED usage ▪ Time to ROSC ○ Patient ▪ Age ▪ Gender ▪ Co-morbid conditions Renal failure Pneumonia Cardiogenic shock Trauma ○ Resuscitation ▪ Location (public vs. private) ▪ Witnessed arrest ▪ Bystander CPR ▪ Type of bystander CPR (compression-only vs. standard) ▪ Initial cardiac arrest rhythm ▪ Bystander AED usage ▪ Time to ROSC Table 2 Patient and resuscitation characteristics affecting outcome from cardiac arrest ○ Patient ▪ Age ▪ Gender ▪ Co-morbid conditions Renal failure Pneumonia Cardiogenic shock Trauma ○ Resuscitation ▪ Location (public vs. private) ▪ Witnessed arrest ▪ Bystander CPR ▪ Type of bystander CPR (compression-only vs. standard) ▪ Initial cardiac arrest rhythm ▪ Bystander AED usage ▪ Time to ROSC ○ Patient ▪ Age ▪ Gender ▪ Co-morbid conditions Renal failure Pneumonia Cardiogenic shock Trauma ○ Resuscitation ▪ Location (public vs. private) ▪ Witnessed arrest ▪ Bystander CPR ▪ Type of bystander CPR (compression-only vs. standard) ▪ Initial cardiac arrest rhythm ▪ Bystander AED usage ▪ Time to ROSC Role of mechanical CPR devices The advent of mechanical CPR devices allows for effective chest compressions to be performed during transport, while manual chest compressions have been shown to be difficult to perform and potentially dangerous for the provider in a moving vehicle.54,55 Extracorporeal circulatory support Extracorporeal cardiopulmonary resuscitation (eCPR) has been investigated for decades, but international centers recently have shown significant salvage rates in patients almost certain to die if standard ACLS care is the only option. Long-term survival rates of nearly 30% have been achieved in some centers. Japanese investigators have shown two keys to success are instituting eCPR with full circulatory support within 50 min of collapse,44 and combining temperature management with cooling to 33°C as soon as possible, preferably cooling simultaneously with starting circulatory support.43 PCI during CPR The feasibility of performing PCI during ongoing cardiopulmonary resuscitation is no longer an issue. Numerous case reports now show that such is not only feasible, but often successful and can improve survival. The largest clinical experience to date was reported by Wagner in two sequential publications, one in 2010 and a follow-up in 2016.46,47 These authors showed that in a series of 75 patients suffering cardiac arrest in the catheterization laboratory with mechanical chest compressions providing system perfusion, PCI of the culprit vessel was effective in restoring spontaneous circulation in 32/75 (43%). A total of 19/75 (25%) survived to hospital discharge with favorable neurological status (CPC 1 or 2). Interestingly, those with pulseless electrical activity as the initial cardiac arrest rhythm did not do as well as those with either ventricular fibrillation or asystole (Table 3). Of the 20 survivors to hospital discharge, 19/20 (95%) were neurologically intact, supporting the efficacy of mechanical chest compressions in maintaining adequate blood flow to the brain while angioplasty is being performed to stabilize the ischemic myocardium, promoting return of spontaneous circulation. Table 3 Outcome by initial rhythm for cardiac arrest in the cath lab . n . Survival . VF 11 6 (55%) PEA 50 7 (14%) Asystole 14 7 (50%) Total 75 20 (27%) . n . Survival . VF 11 6 (55%) PEA 50 7 (14%) Asystole 14 7 (50%) Total 75 20 (27%) Data summarized from references 46 and 47. Table 3 Outcome by initial rhythm for cardiac arrest in the cath lab . n . Survival . VF 11 6 (55%) PEA 50 7 (14%) Asystole 14 7 (50%) Total 75 20 (27%) . n . Survival . VF 11 6 (55%) PEA 50 7 (14%) Asystole 14 7 (50%) Total 75 20 (27%) Data summarized from references 46 and 47. TTM, instituted intra-arrest during CPR Nagao et al. in Japan were among the first to systematically cool OHCA victims treated with eCPR.43 They found a significant improvement in neurologically intact survival in such patients compared to those receiving normothermic eCPR. Clinical experience with the new paradigm: ‘Load and Go’ The first report in the modern era of this new approach was from Stub et al. in Australia in 2015 with the CHEER trial.55 The CHEER trial consisted of a coordinated approach to refractory cardiac arrest using mechanical CPR, rapid intravenous administration of ice-cold saline to induce intra-arrest therapeutic hypothermia (33°C), percutaneous cannulation of the femoral artery and vein for initiation of veno-arterial ECMO, and early coronary angiography for patients with suspected coronary artery occlusion. Twenty-six patients were studied, including 11 with OHCA. Five of the 11 (45%) survived and all were neurologically intact at discharge. The mean time from collapse to ECMO was 56 min, including an average of 40 min for survivors and 78 min for non-survivors. Though the numbers are small, these are the best outcomes reported to date for OHCA treated with ECMO. A second report of this comprehensive approach to treating patients with refractory VFCA was published in 2016.51 Yannapolous et al. studied 18 patients between the age of 18 and 75 years, with a body habitus that would accommodate the mechanical CPR automated (LUCAS), and with an estimated transfer time from the scene to the cardiac catheterization laboratory of ≤30 min. Refractory VF/VT arrest was defined as failure to achieve sustained return of spontaneous circulation after treatment with three direct current shocks and administration of 300 mg of amiodarone. Eighteen patients met the inclusion and exclusion criteria. Fourteen patients survived to hospital admission and 10 of 18 (55%) survived to hospital discharge, with 9 of 10 achieving good neurological function (cerebral performance categories 1 and 2). Combining these two studies provides a total experience with this new paradigm of 29 OHCA patients.51,55 Twenty-four hour survival was seen in 15/29 (52%) while 14 of 15 (93%) survivors were neurologically intact. These data, while limited, are encouraging and suggest such an approach for refractory out-of-hospital VFCA can succeed. Conclusions Though a few may disagree, the general consensus is that timely resuscitation efforts save lives. It is now quite clear that chest compression-only CPR performed by lay bystanders is the preferred basic life support technique. Superior hemodynamic support is achieved by interrupting chest compressions less often, and the public is much more willing to perform chest compressions only, than compressions and mouth-to-mouth breathing. Exciting results are being reported where longstanding barriers to early defibrillation by EMS providers are overcome with community Targeted Automated External Defibrillator (AED) Programs. The important role of post-arrest coronary angiography and intervention is becoming more defined, with additional lives benefiting from early coronary reperfusion post resuscitation. Finally, the next frontier in improving outcomes for patients with refractory VFCA is here. Several centers have shown promising results with an aggressive approach utilizing mechanical CPR during early transport to the hospital where extracorporeal circulatory support can be instituted to allow percutaneous reperfusion in the cath lab in a much more timely fashion. Conflict of interest statement The authors have no potential conflicts of interest. References 1 Mozaffarian D , Benjamin EJ, Go AS, et al. . on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics--2016 update: a report from the American Heart Association . Circulation 2016 ; 133 : 447 – 54 . 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TI - Sudden cardiac death
JF - British Medical Bulletin
DO - 10.1093/bmb/ldx011
DA - 2017-06-01
UR - https://www.deepdyve.com/lp/oxford-university-press/sudden-cardiac-death-HSQ1pv5d0d
SP - 5
VL - 122
IS - 1
DP - DeepDyve
ER -