Prognosis after cardiac arrest

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
Matthew Lorincz MD PhD, editor. (

Dr. Lorincz of the University of Michigan received honorariums from Alexion for advisory board service.

Originally released September 19, 2014; last updated April 6, 2020; expires April 6, 2023

This article includes discussion of prognosis after cardiac arrest, cardiopulmonary arrest, circulatory arrest, cardiorespiratory arrest, heart arrest, sudden cardiac death, cardiopulmonary resuscitation, therapeutic hypothermia, and neuroprotection. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Cardiac arrest is defined as the cessation of cardiac activity as confirmed by the absence of signs of circulation. Out-of-hospital cardiac arrest incidence and outcome varies greatly around the globe. During cardiac arrest, basic CPR and early defibrillation are of primary importance. Therapeutic hypothermia increases the chances of survival and reduces the risk of neurologic damage following cardiac arrest. Prognostic determination of patients in coma after resuscitation from cardiac arrest is a common and difficult requirement with significant ethical, social, and legal implications. Several studies have suggested the usefulness of clinical examination, electrophysiologic studies, biochemical markers, and neuroimaging in predicting poor neurologic recovery in comatose survivors. Diffusion tensor magnetic resonance imaging accurately predicted neurologic outcome in patients who were unconscious after cardiac arrest. Five clinical signs were found to strongly predict death or poor neurologic outcome: absent corneal reflexes at 24 hours, absent pupillary response at 24 hours, absent withdrawal response to pain at 24 hours, no motor response at 24 hours, and no motor response at 72 hours. Short latency somatosensory evoked potential N20 is now a well-accepted predictor of poor prognosis. Neuroimaging may reveal extensive cortical and subcortical brain atrophy. The anatomical regions that are more significantly affected include frontal cortex, posterior cingulate cortex, thalamus, putamen, pallidum, caudate, hippocampus, and brain stem. Bystander and first responder resuscitation are crucial. Bystander-initiated cardiopulmonary resuscitation is associated with greater likelihood of survival with good outcome. Prehospital resuscitation efforts should be done for at least 40 minutes in bystander-witnessed out-of-hospital cardiac arrest. Mechanical chest compression devices are satisfactory alternatives. However, mechanical chest compression devices are only to be used when manual chest compressions are impractical, impossible, or unsafe. Chances of favorable neurologic recovery are higher following immediate coronary angiography, with or without percutaneous coronary angioplasty. In this article, the author discusses the various aspects of prognosis after cardiac arrest.

Key points


• Cardiac arrest is the cessation of cardiac activity as confirmed by the absence of signs of circulation.


• Sudden cardiac death from cardiac arrest is the most common cause of death.


• Cardiac disorders like coronary heart disease, cardiomyopathies, cardiac arrhythmias, congenital heart diseases and valvular heart diseases predispose a cardiac arrest.


• Clinical examination, electrophysiologic studies, biochemical markers, and neuroimaging help predict recovery in comatose survivors.


• Five early clinical signs that predict poor outcome include absent corneal reflexes, absent pupillary response, absent withdrawal response to pain, and no motor response.


• Therapeutic hypothermia has considerably improved outcome after adult cardiac arrest.

Historical note and terminology

Sudden cardiac death from cardiac arrest is the most common cause of death worldwide. Efforts are ongoing to find ways to improve ability to revive patients in cardiac arrest and to limit damage following cardiac arrest.

In 1740, The Paris Academy of Sciences officially recommended mouth-to-mouth resuscitation for drowning victims. In 1891, Dr. Friedrich Maass, a German surgeon, performed the first equivocally documented chest compression in humans. George Crile, Chief of Surgery at Western Reserve University was the first to successfully use external chest compression in 1903 and the first to use adrenaline (epinephrine) in resuscitation in 1909. Kouvenhoven and coworkers reported the results of chest compression on 20 patients, of whom14 were successfully revived (Kouwenhoven et al 1960). Dr. Claude Beck, professor of cardiothoracic surgery, performed the first successful human cardiac defibrillation in 1947 (Sternbach et al 2000). In 1956, Peter Safar and James Elam first documented the adequacy of mouth-to-mouth resuscitation (Safar 2001).

Hippocrates had suggested in 450 BC that packing patients in snow might have benefit to survival. In the November 1950 Annals of Surgery, Bigelow and coworkers described the possible role of hypothermia on the basis of their experiments on dogs (Bigelow et al 1950). The New England Journal of Medicine in 2002 published a landmark paper documenting unequivocally the role of hypothermia in cardiac arrest (Bernard et al 2002).

Pennsylvania state legislators passed “House Act 59, Sudden Cardiac Arrest Prevention Act,” in August of 2012; the intent of this law was to educate children, parents, and coaches about the symptoms that are associated with sudden cardiac death.

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