Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)☆,☆☆,☆☆☆
Section snippets
Consensus process
The contributors of this statement were selected to ensure expertise in all the disciplines relevant to post-cardiac arrest care. In an attempt to make this document universally applicable and generalisable, the authorship comprised clinicians and scientists who represent many specialties in many regions of the world. Several major professional groups whose practice is relevant to post-cardiac arrest care were asked and agreed to provide representative contributors. Planning and invitations
Background
This scientific statement outlines current understanding and identifies knowledge gaps in the pathophysiology, treatment, and prognosis of patients who regain spontaneous circulation after cardiac arrest. The purpose is to provide a resource for optimizing post-cardiac arrest care and pinpointing the need for research focused on gaps in knowledge that would potentially improve outcomes of patients resuscitated from cardiac arrest.
Resumption of spontaneous circulation after prolonged complete
Epidemiology of the post-cardiac arrest syndrome
The tradition in cardiac arrest epidemiology, based largely on the Utstein consensus guidelines, has been to report percentages of patients who survive to sequential end points such as ROSC, hospital admission, hospital discharge, and various points thereafter (Jacobs et al., 2004, Langhelle et al., 2005) Once ROSC is achieved, however, the patient is technically alive. A more useful approach to studying post-cardiac arrest syndrome is to report deaths during various phases of post-cardiac
Pathophysiology of the post-cardiac arrest syndrome
The high mortality rate of patients who initially achieve ROSC after cardiac arrest can be attributed to a unique pathophysiological process involving multiple organs. Although prolonged whole-body ischaemia initially causes global tissue and organ injury, additional damage occurs during and after reperfusion (Opie, 1989, White et al., 1993). The unique features of post-cardiac arrest pathophysiology are often superimposed on the disease or injury that caused the cardiac arrest as well as
Post-cardiac arrest brain injury
Post-cardiac arrest brain injury is a common cause of morbidity and mortality. In one study of patients who survived to ICU admission but subsequently died in the hospital, brain injury was the cause of death in 68% after out-of hospital cardiac arrest and in 23% after in-hospital cardiac arrest (Laver et al., 2004). The unique vulnerability of the brain is attributed to its limited tolerance of ischaemia as well as its unique response to reperfusion. The mechanisms of brain injury triggered by
Post-cardiac arrest myocardial dysfunction
Post-cardiac arrest myocardial dysfunction also contributes to the low survival rate after in- and out-of-hospital cardiac arrest (Laver et al., 2004, Herlitz et al., 1995, Laurent et al., 2002). A significant body of preclinical and clinical evidence, however, indicates that this phenomenon is both responsive to therapy and reversible (Laurent et al., 2002, Huang et al., 2005, Ruiz-Bailen et al., 2005, Cerchiari et al., 1993, Kern et al., 1997, Kern et al., 1996). Immediately after ROSC, heart
Systemic ischaemia/reperfusion response
Cardiac arrest represents the most severe shock state, during which delivery of oxygen and metabolic substrates is abruptly halted and metabolites are no longer removed. CPR only partially reverses this process, achieving cardiac output and systemic oxygen delivery (DO2) that is much less than normal. During CPR a compensatory increase in systemic oxygen extraction occurs, leading to significantly decreased central (ScvO2) or mixed venous oxygen saturation (Rivers et al., 1992). Inadequate
Persistent precipitating pathology
The pathophysiology of post-cardiac arrest syndrome is commonly complicated by persisting acute pathology that caused or contributed to the cardiac arrest itself. Diagnosis and management of persistent precipitating pathologies such as acute coronary syndrome (ACS), pulmonary diseases, haemorrhage, sepsis, and various toxidromes can complicate and be complicated by the simultaneous pathophysiology of the post-cardiac arrest syndrome.
There is a high probability of identifying an ACS in the
Therapeutic strategies
Care of the post-cardiac arrest patient is time-sensitive, occurs both in- and out-of-hospital, and is sequentially provided by multiple diverse teams of healthcare providers. Given the complex nature of post-cardiac arrest care, it is optimal to have a multidisciplinary team develop and execute a comprehensive clinical pathway tailored to available resources. Treatment plans for post-cardiac arrest care must accommodate a spectrum of patients, ranging from the awake, haemodynamically stable
General measures
The general management of post-cardiac arrest patients should follow the standards of care for most critically ill patients in the ICU setting. This statement focuses on the components of care that specifically impact the post-cardiac arrest syndrome. The time-sensitive nature of therapeutic strategies will be highlighted, as well as the differential impact of therapeutic strategies on individual components of the syndrome.
Monitoring
Post-cardiac arrest patients generally require intensive care monitoring; this can be divided into 3 categories (Table 2): general intensive care monitoring, more advanced haemodynamic monitoring, and cerebral monitoring. General intensive care monitoring (Table 2) is the minimum requirement; additional monitoring should be added depending on the status of the patient and local resources and experience. The impact of specific monitoring techniques on post-cardiac arrest outcome, however, has
Early haemodynamic optimization
Early haemodynamic optimization or early goal-directed therapy (EGDT) is an algorithmic approach to restoring and maintaining the balance between systemic oxygen delivery and demands. The key to the success of this approach is initiation of monitoring and therapy as early as possible and achievement of goals within hours of presentation. This approach focuses on optimization of preload, arterial oxygen content, afterload, contractility, and systemic oxygen utilisation. EGDT has been studied in
Oxygenation
Existing guidelines emphasize the use of an Fio2 of 1.0 during CPR, and clinicians will frequently maintain ventilation with 100% oxygen for variable periods after ROSC. Although it is important to ensure that patients are not hypoxemic, a growing body of preclinical evidence suggests that hyperoxia during the early stages of reperfusion harms postischaemic neurons by causing excessive oxidative stress (Vereczki et al., 2006, Richards et al., 2007, Zwemer et al., 1994, Liu et al., 1998). Most
Ventilation
Although cerebral autoregulation is either absent or dysfunctional in most patients in the acute phase after cardiac arrest (Sundgreen et al., 2001), cerebrovascular reactivity to changes in arterial carbon dioxide tension seems to be preserved (Beckstead et al., 1978, Buunk et al., 1996, Roine et al., 1991, Buunk et al., 1997). Cerebrovascular resistance may be elevated for at least 24 h in comatose survivors of cardiac arrest (Buunk et al., 1996). There are no data to support the targeting of
Circulatory support
Haemodynamic instability is common after cardiac arrest and manifests as dysrhythmias, hypotension, and low cardiac index (Laurent et al., 2002). Underlying mechanisms include intravascular volume depletion, impaired vasoregulation, and myocardial dysfunction.
Dysrhythmias can be treated by maintaining normal electrolyte concentrations and using standard drug and electrical therapies. There is no evidence to support the prophylactic use of anti-arrhythmic drugs after cardiac arrest. Dysrhythmias
Management of acute coronary syndrome
Coronary artery disease is present in the majority of out-of-hospital cardiac arrest patients (Zheng et al., 2001, Pell et al., 2003, Huikuri et al., 2001), and AMI is the most common cause of sudden cardiac death (Huikuri et al., 2001). One autopsy study reported coronary artery thrombi in 74 of 100 subjects who died of ischaemic heart disease within 6 h of symptom onset, and plaque fissuring in 21 of 26 subjects in the absence of thrombus (Davies and Thomas, 1984). A more recent review
Other persistent precipitating pathologies
Other causes of out-of-hospital cardiac arrest include pulmonary embolism, sepsis, hypoxaemia, hypovolaemia, hypokalaemia, hyperkalaemia, metabolic disorders, accidental hypothermia, tension pneumothorax, cardiac tamponade, toxins, intoxication or cerebrovascular catastrophes. The incidence of these causes is potentially higher for in-hospital cardiac arrest (Nadkarni et al., 2006). These potential causes of cardiac arrest that persist after ROSC should be diagnosed promptly and treated.
Acknowledgments
This paper was originally co-published in Resuscitation and Circulation. This article is republished with permission from Circulation. 2008; 118:2452-2483 © 2008, American Heart Association, Inc. and Resuscitation. 79/3: 350-379 © 2008 Elsevier Ireland Ltd. With the permission of the authors the paper has been divided into two parts and the second part will be published in issue 18/1. The reference section is published in full in both parts.
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A Spanish translated version of the summary of this article appears as Appendix in the online version at doi:10.1016/j.resuscitation.2008.09.17.
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Endorsed by the American College of Emergency Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, and Neurocritical Care Society.
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This article was originally co-published in Resuscitation and Circulation. This article is republished with permission from Circulation. 2008; 118:2452-2483 © 2008, American Heart Association, Inc. and Resuscitation. 79/3: 350-379 © 2008 Elsevier Ireland Ltd.