<scp>SCAI</scp> expert consensus statement on out of hospital cardiac arrest

Out of hospital cardiac arrest (OHCA) remains a significant public health problem with high mortality and morbidity. (1) The true magnitude of mortality and morbidity from OHCA is unknown due to the lack of mandatory reporting, unified national surveillance systems, difficulty in accounting for cases not attended by emergency medical services (EMS), variability in existing reporting systems and paucity of data regarding long term neurological and functional outcomes (Appendix S1).1 Improving survival rates with good neurological outcomes among OHCA patients requires improved response times and quality of care in the “chain of survival” from early activation of EMS and resuscitation to advanced post admission care.2 Given the high prevalence of coronary artery disease (CAD) as the cause for cardiac arrest in patients with a presenting rhythm of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), interventional cardiologists are often consulted to consider emergent coronary angiography (angiography) and possible percutaneous coronary intervention (PCI) in OHCA patients. While emergent angiography and PCI are indicated in selected OHCA patients when the post resuscitation electrocardiogram (ECG) shows ST-segment elevation myocardial infraction (STEMI), there are significant institutional and individual variations in performance and timing for those patients without STEMI on post resuscitation ECG. The role of the cardiac catheterization laboratory encompasses not only angiography and PCI but also hemodynamic assessment and mechanical circulatory support (MCS) device use in patients with concomitant cardiogenic shock (CS). The purpose of this document is to provide an evidence-based and patient-oriented recommendation for the management of these patients. This document has been developed according to SCAI Publications Committee policies for writing group composition, disclosure and management of relationships with industry (RWI), internal and external review, and organizational approval. The writing group has been organized to ensure diversity of perspectives and demographics, multistakeholder representation, and appropriate balance of RWI. Relevant author disclosures are included in Table S1. Before appointment, members of the writing group were asked to disclose all relevant financial relationships with industry (>$25,000) from the 12 months prior to their nomination. A majority of the writing group disclosed no relevant financial relationships. Disclosures were periodically reviewed during document development and updated as needed. SCAI policy requires that writing group members with a current financial interest are recused from participating in discussions or voting on relevant recommendations. The work of the writing committee was supported exclusively by SCAI, a nonprofit medical specialty society, without commercial support. Writing group members contributed to this effort on a volunteer basis and did not receive payment from SCAI. Literature searches were performed by group members designated to lead each section and initial section drafts were authored by the section leads. Recommendations were discussed by the full writing group on a series of teleconferences until all group members agreed on the text and qualifying remarks. All recommendations are supported by a short summary of the evidence or specific rationale. The draft manuscript was posted for public comment in February 2020 and the document was revised to address pertinent comments. The writing group unanimously approved the final version of the document. The SCAI Publications Committee and Executive Committee endorsed the document as official society guidance in May 2020. SCAI consensus statements are primarily intended to help clinicians make decisions about treatment options. Clinicians also must consider the clinical presentation, setting, and preferences of individual patients to make judgements about optimal approaches. Table 1 summarizes the study characteristics of large studies combining all OHCA patients that compared immediate or early coronary angiography with no or delayed coronary angiography. Table 2 summarizes recently published and ongoing randomized control trials (RCTs). The literature guiding the role and timing of angiography and PCI in resuscitated OHCA patients is predominantly limited to observational studies. (Appendix S2).3 YES HR – 1.27, 95% CI – 1.13 – 1.42) N0 STEMI Patients. Factors associated with favorable prognosis: Younger age, initial shockable rhythm, less time to ROSC, no cardiogenic shock YES OR 0.66, 95% CI 0.58,0.75) YES OR – 2.85, 95% CI. – 2.04 – 4.0) NO HR – 0.69, 95% CI – 0.35 – 1.37 Inc: Comatose OHCA patients + Initial Shockable Rhythm + No STEMI of ECG Ex: Shock/obvious noncardiac cause Immediate: Upon presentation Delayed: After neurological recovery Inc: Comatose OHCA patients + Initial Shockable Rhythm + No STEMI on ECG Ex: STEMI Immediate: Admission to Cath Lab Delayed: Admission to ICU for further assessment Inc: Witnessed OHCA with achieving ROSC >20 min Exc: STEMI/obvious noncardiac cause Immediate: Within 120 min Not Immediate: No angiography or after 3 days Open Label, Multicenter, United States Inc: Comatose OHCA patients with No STEMI Ex: STEMI/obvious noncardiac etiology Interventional Early angiography: Within 120 min Control group: After 6 hr Inc: Comatose OHCA patients Ex: STEMI on ECG/obvious noncardiac etiology Immediate: Upon presentation Delayed: 46–96 hr Open Label, Multicenter, Germany Inc: Comatose OHCA patients Ex: STEMI/Hemodynamic Instablity Immediate: Upon presentation Delayed: After 24 hr/neurological recovery Open Label, Multicenter, Spain Inc: Comatose OHCA patients Ex: STEMI/Hemodynamic Instability Urgent: Upon presentations Deferred: After neurological Recovery Irrespective of initial rhythm or ECG findings, the predominant cause of death in two-thirds of patients with OHCA is due to anoxic brain injury and another one-third is due to a refractory post arrest shock and multi-organ failure.4 The rate of survival to discharge with good neurologic function among OHCA patients is low with wide geographical variation estimated at 0.8–20%.5 Anoxic brain injury and postcardiac arrest shock share common risk factors that are related to the timing and quality of pre hospital care.6 Among OHCA patients who are comatose after return of spontaneous circulation (ROSC), there is no single factor at the time of presentation to reliably prognosticate subsequent neurological outcome. While accurate prognostication is important to avoid pursuing futile treatments or inappropriately withdrawing treatment in patients with a chance of recovery, the quality of existing neurological prognostication studies is insufficient to make any definitive recommendations for long term neurologic outcomes.7 Nevertheless, there are pre and intra arrest factors associated with unfavorable neurological outcomes (Table 3).8, 9 When deciding whether to offer invasive treatments, it is prudent to consider presence of co-morbidities that portend unfavorable short- and long-term prognoses, such as advanced age, severe dementia, chronic advanced respiratory failure, severe frailty or disability, end stage renal or liver disease, and advanced metastatic malignancy.10 Risk stratification scores are often used in medicine for prognostication and decision-making.11 The Cardiac Arrest Hospital Prognosis score (CAHP),12 CREST, and13 C-GRApH are risk stratification tools to assist in decision-making.14 (Table 4). Cardiac Arrest Hospital Prognosis (CAHP)12 1,410 patients 41% with post ROSC STEMI of ECG 69% male Age as continuous variable Non-shockable rhythm Time from collapse to BLS Time from BLS to ROSC Location of cardiac arrest Epinephrine dose Arterial pH CAHP <150 86% had early invasive strategy 61% discharged alive from hospital with 95% with CPC score 1 or 2 CAHP 150–200 66% had early invasive strategy 10% discharged alive from hospital with 88% with CPC score 1 or 2 CAHP >200 47% had early invasive strategy 3% discharged alive from hospital with 86% with CPC score 1 or 2 CREST Model13 638 patients derivation 318 patients Validation No patients with STEMI 18.9% recognized identified as circulatory cause of death History of coronary artery disease Non-shockable rhythm Ejection fraction <30% at time of admission Shock at the time of admission Ischemic time > 25 min CREST score death due to shock 0–7.1% 1–9.5% 2–22.5% 3–32.4% 4–20% 5–50% C-GRApH14 122 patients derivation 344 patients validation History of coronary artery disease Glucose ≥200 mg/dL Non-shockable rhythm Age > 45 pH (arterial) ≤ 7.0 C-GRApH (0–1) 70% with CPC score of 1 or 2 C-GRApH (4, 5) 98% with CPC score 3 to 5 In addition to risk stratification tools, imaging tools are available to provide further information regarding clinical assessment and management.15, 16 (Table 5). Anoxic encephalopathy Intracranial bleeding Subarachnoid hemorrhage Post myocardial infarction complications Pulmonary embolus Pericardial tamponade/effusions Valvular dysfunction Regional wall motion abnormalities Hypertrophic cardiomyopathy Given the heterogeneous nature of OHCA patients, fluidity in evolution of the clinical course, and uncertainty associated with neurological prognostication, we advocate a path of “Situational Awareness and Assessment”17 taking into consideration all the clinical factors available to aid in clinical decision-making along the continuum of care of these patients (Figure 1).17 We advocate confirming all the prehospital and hospital clinical history and data, considering carefully patient's comorbidities, patient's and family wishes if known as well as all of the favorable and unfavorable prognostic factors, synthesizing the data to provide the best possible prediction regarding the etiology of the arrest and anticipated neurological and hemodynamic outcomes to help guide the role and timing of invasive strategy in these patients (Figure 1). We also support the use of terminology such as activation of cardiac cath Lab (CCL) rather than angiography as it encompasses other invasive procedures (angiography, PCI, Right Heart Cath, MCS, and others) that may need to be performed in this patient population. We recommend use of terminology—“Definite” or “Defer” activation of CCL along a decision-making continuum at initial and subsequent encounters based on clinical history, presence of favorable/unfavorable resuscitation factors, initial rhythm, ECG and hemodynamic status (Figure 1). This terminology is subsequently used in all recommendations in this document (Table 6). In selected comatose OHCA patients with ROSC exhibiting STEMI on ECG we recommend a definite invasive strategy. We recommend against the use of prehospital TTM using cold intravenous crystalloids. We recommend initiating TTM inpatient as soon as possible. Among patients with an initial shockable rhythm and diagnostic ST-segment elevations on post ROSC ECG, the prevalence of acute thrombotic coronary occlusion or culprit lesion causing cardiac arrest is greater than 85%.15 Given this observation, conscious survivors of OHCA at presentation with initial ECG showing STEMI should be treated with immediate angiography and primary PCI as is the current standard of care for STEMI patients.18 Among comatose OHCA patients with ROSC and STEMI, there are no RCTs to support favorable neurological outcomes or survival benefit of immediate angiography. In the targeted temperature management (TTM) trial, which evaluated 33 versus 36°C after cardiac arrest, 41% of the 939 patients had acute STEMI on their initial ECG. In this study, lower time to ROSC was the highest predictor of survival with good neurological function.19, 20 In the International Cardiac Arrest (INTCAR) Registry, among 746 comatose post-arrest (79% OHCA) patients, 26.5% presented with STEMI and 73.5% without STEMI on their initial ECG; 91% of STEMI patients had immediate angiography whereas 33% patients without STEMI had an immediate angiography.21 The survival rate was 55.1% in the STEMI group versus 41.3% in the patients without STEMI on their initial ECG. The decision to perform immediate angiography was based on operator preference rather than a predefined protocol targeting certain selected patients who might benefit from immediate angiography. Therefore, the ECG should not be the sole determinant when activating the CCL and instead should be paired with the clinical presentation and the patient's clinical findings when considering invasive assessment and potential therapies. Among OHCA patients with an initial shockable rhythm without STEMI on post-ROSC ECG, the prevalence of an acute thrombotic occlusion is ~3.4–30%.21, 22 The prevalence of significant, stable or thrombotic, non-occlusive lesions on angiography ranges from 24 to 60%.23, 24 While ECG and biomarkers are used in patients with acute coronary syndrome without cardiac arrest, these lack specificity or sensitivity in predicting coronary ischemia as the cause of initial or recurrent cardiac arrest in these patients.25 When ST elevation is not present, current noninvasive methods lack sensitivity to definitely assess ongoing coronary ischemia and tools to prognosticate neurological outcomes at presentation in comatose patients are inadequate as mentioned. As such, the decision of if and when to activate the CCL in these patients is challenging. The existing literature on evaluating the benefit of angiography in these patients is predominantly from observational cohort studies (Table 1) with several limitations (Appendix S2). A meta-analysis of 23 observational studies showed that angiography performed within 24 hr was associated with improved survival (Risk Ratio:1.52, 95% CI: 1.32–1.74, p < .001) and better neurological outcomes (Risk ratio: 1.69, 95% CI: 1.40–2.04, p < .001) compared with angiography performed more than 24 hr later or not at all.26 The only published randomized trial, Coronary Angiography after Cardiac Arrest Trial (COACT), involving 538 patients showed no survival benefit at 90 days for immediate or early angiography in hemodynamically stable OHCA patients without STEMI on ECG compared with delayed angiography after neurological recovery.22 Patients with CS unresponsive to medical therapy, obvious or suspected non-coronary cause of arrest, and STEMI on the ECG were excluded in this trial. TTM was initiated in more than 90% of patients and 87% of patients received norepinephrine. Neurological etiologies were the cause of death in more than 70% of the patients in both groups. In the delayed-angiography group, 14.4% of the patients underwent urgent coronary angiography because of CS, recurrent ventricular arrhythmia, or recurrence of ischemia. In 39.5% of these patients, an unstable lesion was detected, a percentage that was higher than that in the immediate-angiography group (13.6%). PCI was performed in 22 of these patients (57.9%), which is higher than the percentage of patients in the immediate-angiography group (33%), but the rate of survival among these patients was not lower than that in the total cohort (71.1 and 65.4%, respectively).27 While the prevalence of obstructive CAD in patients resuscitated from shockable rhythms including VT or VF, ranges from 25 to 60%,28-30 the prevalence of CAD in OHCA patients with initial non-shockable rhythms, asystole, or pulseless electrical activity (PEA), is not well-defined. In OHCA patients presenting with non-shockable rhythms, noncardiac etiologies of OHCA often need to be considered.31, 32 The overall survival and favorable prognosis is significantly higher with initial shockable rhythm compared to a non-shockable rhythm.21, 33-44 Primary PEA and asystole are more often due to non-coronary etiologies especially in the elderly with multiple co morbidities.45 It is also possible that some patients with initial non-shockable rhythms may develop VF/VT with administration of epinephrine during resuscitation, and they should still be treated as OHCA with non-shockable rhythm.46 Patients with OHCA are at higher risk of bleeding when undergoing PCI due to injuries sustained as a result of loss of consciousness and often there is concern for intracranial bleeding.47 These patients are also at higher risk of thrombotic complications because of potentially delayed bioavailability of oral antiplatelet agents either due to active vomiting or reduced absorption from the gut in the setting of low cardiac output state with concomitant CS.48 The pro-inflammatory state resulting in endogenous changes in coagulation and anticoagulation cascades as part of postresuscitative state, multiorgan dysfunction and therapeutic hypothermia increases the risk of both bleeding and thrombotic complications in OHCA patients.49 Radial access is associated with reduced risk of bleeding complications compared with femoral access among patients undergoing PCI for ACS.50 However, in a large RCT and a retrospective analysis, there was no difference in the primary outcome, including mortality, among patients undergoing primary PCI between radial and femoral access.51, 52 In the setting of OHCA, especially if there is concomitant shock, traditionally the femoral access site has been preferred—due to concerns of vasospasm, increasing procedural time to reperfusion and convenience of restricting the working field to groin area if hemodynamic support is required. Among comatose survivors of OHCA undergoing PCI, postresuscitative state and hypothermia may affect the absorption and metabolism of oral antiplatelets agents.48 Some studies have shown an increased rate of stent thrombosis among post OHCA patients with hypothermia.53 As demonstrated in patients with STEMI without cardiac arrest, the newer oral antiplatelet agents (ticagrelor and prasugrel) in addition to aspirin may be associated with reduced risk of ST even among comatose OHCA patients and are favored over clopidogrel.54-57 In patients with a large thrombus burden, bolus doses of glycoprotein IIb/IIIa inhibitors may be considered after carefully weighing against the increased risk of bleeding.58 Cangrelor, an intravenous P2 Y12 inhibitor may be an option to use in these patients as a bridge during delayed absorption of oral agents.59 Studies among patients with acute coronary syndromes have consistently showed increased risk of acute stent thrombosis with bivalirudin compared with unfractionated heparin.60 OHCA patients undergoing PCI are at high risk for thrombotic events and bleeding complications as described above and the risk of bleeding should be weighed against thrombotic risk. Irrespective of whether a definite versus deferred CCL strategy is employed, post resuscitative support is important to the patient's overall outcome. Although studies have not specifically evaluated optimal cardiac arrest team membership, studies evaluating OHCA care systems, hospital volumes, and receiving hospital characteristics allow us to demonstrate that a multi-disciplinary approach may improve clinical outcomes (Figure 2).61-64 Following the publication of two seminal trials65, 66 demonstrating improved survival with the delivery of in-hospital mild hypothermia for patients with resuscitated VF or VT (Table 7), OHCA patients should be assessed for targeted temperature managament (TTM) on arrival to the hospital. Pre hospital initiation of TTM has not demonstrated improved clinical outcomes and in some situations, it is associated with possible harm (Table 8).67-71 275 Hypothermia: 136 Normothermia: 137 Inc: > 18 to <75 years; Witnessed cardiac arrest, ventricular fibrillation or non-perfusing ventricular tachycardia as the initial cardiac rhythm, presumed cardiac origin of the arrest, estimated interval of 5–15 min from the patients collapse to first attempt at resuscitation, No more than 60 min from collapse to ROSC Ex: Temperature below 300 C on admission, comatose state due to administration of drugs, pregnancy, response to verbal commands after ROSC, evidence of hypotension for more than 30 min after ROSC, evidence of hypoxemia for more than 15 min after ROSC, terminal illness that preceded arrest, pre-existing coagulopathy. Favorable neurological outcomes was significantly higher in hypothermia group (55 vs. 39%). Mortality at six months was significantly lower in hypothermia group (41 vs. 55%) Open labeled, Randomized, Multicenter Trial, Melbourne, Australia 77 Hypothermia: 43 Normothermia: 34 Inc: Ventricular fibrillation, Persistent coma after ROSC Ex: <18 years for men; < 50 years for women (because of possibility of pregnancy), cardiogenic shock, possible causes of shock other than cardiac arrest Basic cooling initiated in ambulance. Core temperature of 33°C was maintained for at 12 hr after arrival to hospital. at 18 active was for 6 Favorable neurologic outcomes were significantly higher in hypothermia group vs. was no significant mortality difference between hypothermia and patients Patients with VF patients pre hospital cooling temperature by No difference in outcomes prehospital in hospital risk 95% interval to p patients in control patients Initial rhythm of asystole and PEA temperature compared to control pre hospital cooling vs. in hospital cooling p < .001) No difference in outcomes pre hospital in hospital p received patients with VF without VF care with VF without VF temperature both patients with VF and in patients without to hospital discharge was among the intervention and control among patients with VF vs. p rates of and with VF received 2 without VF received 2 patients in control Patients with OHCA and shock have higher mortality rates and neurological Patients with shock have an of in response to cardiac This a of pro-inflammatory and The early and of shock in OHCA patients are related to a of clinical of which may be to the cardiac of coronary are an important of care among patients with In the randomized in with and Shock than of the patients had resuscitation prior to and more than of the were related to refractory In patients who underwent PCI of the culprit lesion the risk of death and severe renal was significantly lower compared with those who underwent immediate are no large randomized trials to evaluating the use of among patients with The role of in patients with STEMI by shock, comatose patients with OHCA, is evaluated in the Shock patients be randomized to percutaneous versus In the in Shock vs. mortality in STEMI patients treated with primary PCI in cardiogenic patients, with cardiac arrest prior to were to versus with did not mortality compared to at 30 The use of MCS, specifically has been increasing among patients undergoing PCI with limited evidence of and possible in Therefore, the role of and in patients with OHCA and shock, with a on patient to be evaluated in randomized a that is the of this document. The role of support for refractory OHCA is of interest and in single with the and have demonstrated are ongoing randomized trials to if benefit in carefully selected patients with OHCA (Table this strategy be of and is has not been SCAI has a for assessment of patients with A hospital survivors to a single cardiac ICU over an and associated the SCAI shock with post discharge mortality in patient with acute coronary syndrome and but not cardiac need to appropriate and to that have the to provide acute care for patients (Figure A a and an in Cardiac Arrest Patients 18 years of over years of of more than 5 min without cardiac after that the prognosis for short or survival Cardiac arrest during times Early initiation of support in refractory OHCA Patients for Cardiac Arrest 30 Patients arrival interval within cardiac arrest of patients with emergency arrival less than or to 30 min from cardiac arrest if by EMS initiation interval within 2 hr of cardiac arrest of patients with initiated less than or to 30 min from arrival in Cardiac Arrest patients for Cardiac Arrest Early resuscitation advanced cardiac support resuscitation Primary to hospital discharge reporting of procedural outcomes for PCI and coronary artery is in In the current public reporting noncardiac mortality neurologic is from cardiac mortality and is as related This the clinical outcomes of both the and in high risk OHCA patients be for by current In it is if public reporting of outcomes to risk with patients undergoing PCI or 90 A SCAI on has been of OHCA patients from public reporting of PCI outcomes and of high risk at as In to be to OHCA as the and the have recently significant The data between these two have been for Cath PCI version 5 has recently more regarding cardiac arrest status (Appendix The of more data on cardiac arrest is to develop accurate for and public to the data and used in OHCA to improve outcomes among these Comatose patients with OHCA have a high mortality and morbidity. The management decisions in these patients are and clinical and approach along the continuum of care from pre hospital to post hospital The is not for the or of any information by the than should be to the author for the

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