Post-cardiac arrest syndrome

Reviewed and revised 15 November 2016

OVERVIEW

aka post-resuscitation syndrome

  • occurs after return of spontaneous circulation (ROSC) following cardiorespiratory arrest and  involves multiple systems
  • Reflects a state of whole-body ischaemia and subsequent reperfusion
  • Often super-imposed on the underlying condition, which caused the cardiac arrest and pre-existing comorbidities, and other complications of resuscitation
  • Severity depends on the duration and cause of cardiac arrest

Mortality and morbidity following cardiac arrest

  • Early mortality due to cardiovascular instability
  • Late mortality and morbidity occurs from brain injury (the most common cause of death after ROSC), multi-organ failure and sepsis

MECHANISM

Postcardiac arrest syndrome was once thought to be largely due to production of free radicals, although the pathophysiology is more complex

  • Hypoperfusion and ischaemia cause a cascade of events
    • disruption of homeostasis
    • free radical formation
    • protease activation
    • a SIRS response resembling severe sepsis
  • The disruption may continue for hours or days
  • Hypothermia may slow down this cascade

MAJOR MANIFESTATIONS

  1. Postcardiac arrest brain injury
    • Disruption on both a micro- and macro- circulatory levels may result in either ischaemia or hyperaemia
  2. Postcardiac arrest myocardial dysfunction
    • Although the heart initially becomes hyperkinetic, likely due to circulating catecholamines, global hypokinesis often follows
    • Usually resolves within 72 hours
  3. Systemic ischaemia/reperfusion response
    • The response of the body is similar to the septic shock with activation of the immune and complement systems, and release of inflammatory cytokines and a wide range of cellular responses
  4. Persistent precipitating pathology
    • The cause of the arrest may continue to impact physiological parameters

CONTRIBUTING FACTORS

Post cardiac arrest brain injury

  • Impaired cerebrovascular autoregulation
  • Cerebral oedema
  • Neurodegeneration

Post cardiac arrest myocardial dysfunction

  • Myocardial stunning – global hypokinesis
  • Poor cardiac output
  • Acute coronary syndromes

Systemic ischaemia / reperfusion response

  • Systemic inflammatory response syndrome (SIRS)
  • Poor vasoregulation
  • Microcirculatory failure
  • Activation of coagulation cascade
  • Adrenal suppression
  • Poor tissue oxygen deliver and utilization
  • Susceptibility to infection

Persistent precipitating pathology

  • Cardiovascular disease (e.g. myocardial ischemia, cardiomyopathy)
  • Pulmonary disease (e.g. pulmonary embolus, asthma)
  • CNS disease (e.g. stroke, subarachnoid hemorrhage)
  • Poisoning
  • Infection / Sepsis
  • Hypovolaemia

Other complications of resuscitation such as injuries (e.g. rib fractures, sternal fractures), medication adverse effects and complications of invasive lines and monitoring.


References and Links

LITFL

Journal articles

  • Mongardon N, Dumas F, Ricome S, Grimaldi D, Hissem T, Pène F, Cariou A. Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome. Ann Intensive Care. 2011 Nov 3;1(1):45. PMC3223497.
  • Neumar RW, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation. Circulation. 2008 Dec 2;118(23):2452-83. PMID: 18948368. [Free Full Text]
  • Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011 Apr 5;123(13):1428-35. doi: 10.1161/CIRCULATIONAHA.110.988725. PMID: 21464058. [Free Full Text]
  • Zia A, Kern KB. Management of postcardiac arrest myocardial dysfunction. Curr Opin Crit Care. 2011 Jun;17(3):241-6. PMID: 21378558.

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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