View source for Medicine:Cardiac arrest

{{Short description|Sudden stop in effective blood flow due to the failure of the heart to beat}}
{{Infobox medical condition (new)
| name          = Cardiac arrest
| image         = US Navy 040421-N-8090G-001 Hospital Corpsman 3rd Class Flowers administers chest compressions to a simulated cardiac arrest victim.jpg
| caption       = CPR being administered during a simulation of cardiac arrest
| synonyms      = Cardiopulmonary arrest, circulatory arrest, sudden cardiac arrest (SCA)<ref name="Field-2009"/>
| field         = [[Medicine:Cardiology|Cardiology]], [[Medicine:Emergency medicine|emergency medicine]]
| symptoms      = [[Medicine:Altered level of consciousness|Decreased level]] or [[Medicine:Unconsciousness|total loss of consciousness]], [[Medicine:Respiratory arrest|abnormal or no breathing]], no pulse<ref name="Field-2009"/><ref name="NIH2022Symptoms">{{cite web |title=Cardiac Arrest - Symptoms {{!}} NHLBI, NIH |url=https://www.nhlbi.nih.gov/health/cardiac-arrest/symptoms |website=www.nhlbi.nih.gov |access-date=20 September 2023 |language=en |date=27 May 2022}}</ref>
| complications = If reversed, [[Medicine:Coma|coma]], [[Medicine:Persistent vegetative state|persistent vegetative state]], [[Medicine:Post-cardiac arrest syndrome|post-cardiac arrest syndrome]]; if not reversed, [[Biology:Death|death]]
| onset         = The risk of onset increases with age<ref name="NIH2022Causes">{{cite web |title=Cardiac Arrest - Causes and Risk Factors {{!}} NHLBI, NIH |url=https://www.nhlbi.nih.gov/health/cardiac-arrest/causes |website=www.nhlbi.nih.gov |access-date=30 September 2023 |language=en |date=19 May 2022}}</ref>
| duration      = 
| causes        = [[Medicine:Coronary artery disease|Coronary artery disease]], [[Medicine:Congenital heart defect|congenital heart defect]], major [[Medicine:Bleeding|blood loss]], lack of oxygen, [[Engineering:Electrical injury|electrical injury]], [[Medicine:Hypokalemia|very low potassium]], [[Medicine:Heart failure|heart failure]], [[Medicine:Myocardial infarction|myocardial infarction]]
| risks         = 
| diagnosis     = Finding no pulse,<ref name="Field-2009"/> 
ECG (EKG)<ref name="NIH2022Diagnosis">{{cite web |title=Cardiac Arrest - Diagnosis {{!}} NHLBI, NIH |date=19 May 2022 |url=https://www.nhlbi.nih.gov/health/cardiac-arrest/diagnosis|publisher=National Heart, Lung, and Blood Institute, US National Institutes of Health|access-date=3 October 2022}}</ref>
| differential  = 
| prevention    = Not smoking, physical activity, maintaining a healthy weight, healthy eating<ref name="NHLBI-2016"/>
| treatment     = Cardiopulmonary resuscitation (CPR), [[Engineering:Defibrillation|defibrillation]]<ref name="NIH2022Treatment">{{cite web |title=Cardiac Arrest - Treatment |date=19 May 2022 |url=https://www.nhlbi.nih.gov/health/cardiac-arrest/treatment|publisher=National Heart, Lung, and Blood Institute, US National Institutes of Health |access-date=24 July 2022}}</ref>
| medication    = 
| prognosis     = Overall survival rate ≈10% (outside of hospital) 25% (in hospital);<ref name="Adams-2012">{{cite book| vauthors = Adams JG |url= https://books.google.com/books?id=rpoH-KYE93IC&pg=PA1771 |title=Emergency Medicine: Clinical Essentials (Expert Consult – Online) |date=2012 |publisher= Elsevier Health Sciences |isbn=978-1455733941 |page=1771 |language=en|archive-url= https://web.archive.org/web/20170905133735/https://books.google.com/books?id=rpoH-KYE93IC&pg=PA1771|archive-date=2017-09-05|url-status=live }}</ref><ref name="Andersen-2019">{{cite journal | vauthors = Andersen LW, Holmberg MJ, Berg KM, Donnino MW, Granfeldt A | title = In-Hospital Cardiac Arrest: A Review | journal = JAMA | volume = 321 | issue = 12 | pages = 1200–1210 | date = March 2019 | pmid = 30912843 | pmc = 6482460 | doi = 10.1001/jama.2019.1696 }}</ref> depends strongly on type and cause
| frequency     = 13 per 10,000 people per year (outside hospital in the US)<ref name="Kronick-2015"/>
| deaths        = > 425,000 per year (U.S.)<ref>{{cite journal | vauthors = Meaney PA, Bobrow BJ, Mancini ME, Christenson J, de Caen AR, Bhanji F, Abella BS, Kleinman ME, Edelson DP, Berg RA, Aufderheide TP, Menon V, Leary M | display-authors = 6 | title = Cardiopulmonary resuscitation quality: [corrected] improving cardiac resuscitation outcomes both inside and outside the hospital: a consensus statement from the American Heart Association | journal = Circulation | volume = 128 | issue = 4 | pages = 417–435 | date = July 2013 | pmid = 23801105 | doi = 10.1161/CIR.0b013e31829d8654 | doi-access = free }}</ref>
}}
<!-- Definition and symptoms -->

'''Cardiac arrest''', also known as '''sudden cardiac arrest''', is when the heart suddenly and unexpectedly stops beating.<ref name="NIH2022Def">{{cite web |title=Cardiac Arrest - What Is Cardiac Arrest? {{!}} NHLBI, NIH |url=https://www.nhlbi.nih.gov/health/cardiac-arrest |website=www.nhlbi.nih.gov |access-date=20 September 2023 |language=en |date=19 May 2022}}</ref><ref name="Field-2009"/> As a result, blood cannot properly [[Biology:Circulatory system|circulate]] around the body and there is diminished blood flow to the brain and other organs. When the brain does not receive enough blood, this can cause a person to pass out and become unresponsive. Cardiac arrest is also identified by a lack of [[Medicine:Pulse|central pulses]] and [[Medicine:Respiratory arrest|abnormal or absent]] breathing.<ref name="Field-2009">{{cite book| vauthors = Field JM |title=The Textbook of Emergency Cardiovascular Care and CPR|date=2009|publisher=Lippincott Williams & Wilkins|isbn=9780781788991|page=11|url=https://books.google.com/books?id=JaOoXdSlT9sC&pg=PA11|language=en|url-status=live|archive-url=https://web.archive.org/web/20170905133735/https://books.google.com/books?id=JaOoXdSlT9sC&pg=PA11|archive-date=2017-09-05}}</ref>

<!-- Cause and diagnosis -->
Cardiac arrest and resultant hemodynamic collapse often occur due to [[Medicine:Arrhythmia|arrhythmia]]s (irregular heart rhythms). [[Medicine:Ventricular fibrillation|Ventricular fibrillation]] and [[Medicine:Ventricular tachycardia|ventricular tachycardia]] are most commonly recorded.<ref>{{cite journal | vauthors = Bayés de Luna A, Coumel P, Leclercq JF | title = Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases | journal = American Heart Journal | volume = 117 | issue = 1 | pages = 151–159 | date = January 1989 | pmid = 2911968 | doi = 10.1016/0002-8703(89)90670-4 }}</ref> However, as many incidents of cardiac arrest occur out-of-hospital or when a patient is not having their cardiac activity monitored, it is difficult to identify the specific mechanism in each case.

[[Medicine:Structural heart disease|Structural heart disease]], such as [[Medicine:Coronary artery disease|coronary artery disease]], is a common underlying condition in patients who experience cardiac arrest. The most common risk factors include age and cardiovascular disease.<ref name="Goldenberg_2003" /> Additional underlying cardiac conditions include [[Medicine:Heart failure|heart failure]] and inherited arrhythmias. Additional factors that may contribute to cardiac arrest include major [[Medicine:Bleeding|blood loss]], [[Medicine:Hypoxia (medical)|lack of oxygen]], electrolyte disturbance (such as [[Medicine:Hypokalemia|very low potassium]]), [[Engineering:Electrical injury|electrical injury]], and [[Medicine:Anaerobic exercise|intense physical exercise]].<ref name="Zheng-2001-2">{{cite journal |vauthors=Zheng ZJ, Croft JB, Giles WH, Mensah GA |date=October 2001 |title=Sudden cardiac death in the United States, 1989 to 1998 |journal=Circulation |volume=104 |issue=18 |pages=2158–2163 |doi=10.1161/hc4301.098254 |pmid=11684624 |doi-access=free}}</ref>

<!-- Treatment and prognosis -->
Cardiac arrest is diagnosed by the inability to find a pulse in an unresponsive patient.<ref name="NIH2022Diagnosis" /><ref name="Field-2009" /> The goal of treatment for cardiac arrest is to rapidly achieve [[Medicine:Return of spontaneous circulation|return of spontaneous circulation]] using a variety of interventions including CPR, [[Engineering:Defibrillation|defibrillation]], and/or cardiac pacing. Two protocols have been established for CPR: basic life support (BLS) and [[Medicine:Advanced cardiac life support|advanced cardiac life support]] (ACLS).<ref name="AHA-2005">{{cite journal |author=ECC Committee, Subcommittees and Task Forces of the American Heart Association |date=December 2005 |title=2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=112 |issue=24 Suppl |pages=IV1-203 |doi=10.1161/CIRCULATIONAHA.105.166550 |pmid=16314375 |doi-access=free}}</ref>

If return of spontaneous circulation is achieved with these interventions, then sudden cardiac arrest has occurred. By contrast, if the patient does not survive the event, this is referred to as sudden cardiac death. Among those whose pulses are re-established, the care team may initiate measures to protect the patient from brain injury and preserve neurological function.<ref>{{cite journal |display-authors=6 |vauthors=Neumar RW, Nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark RS, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Vanden Hoek T |date=December 2008 |title=Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); 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; and the Stroke Council |journal=Circulation |volume=118 |issue=23 |pages=2452–2483 |doi=10.1161/CIRCULATIONAHA.108.190652 |pmid=18948368 |doi-access=free}}</ref> Some methods may include airway management and mechanical ventilation, maintenance of blood pressure and end-organ perfusion via fluid resuscitation and vasopressor support, correction of electrolyte imbalance, EKG monitoring and management of reversible causes, and temperature management. [[Biology:Targeted temperature management|Targeted temperature management]] may improve outcomes.<ref name="Schenone-2016">{{cite journal|display-authors=6|vauthors=Schenone AL, Cohen A, Patarroyo G, Harper L, Wang X, Shishehbor MH, Menon V, Duggal A|date=November 2016|title=Therapeutic hypothermia after cardiac arrest: A systematic review/meta-analysis exploring the impact of expanded criteria and targeted temperature|journal=Resuscitation|volume=108|pages=102–110|doi=10.1016/j.resuscitation.2016.07.238|pmid=27521472}}</ref><ref name="Arrich_2023">{{cite journal | vauthors = Arrich J, Schütz N, Oppenauer J, Vendt J, Holzer M, Havel C, Herkner H | title = Hypothermia for neuroprotection in adults after cardiac arrest | journal = The Cochrane Database of Systematic Reviews | volume = 5 | issue = 5 | pages = CD004128 | date = May 2023 | pmid = 37217440 | pmc = 10202224 | doi = 10.1002/14651858.CD004128.pub5 | pmc-embargo-date = May 22, 2024 }}</ref> In post-resuscitation care, an implantable cardiac defibrillator may be considered to reduce the chance of death from recurrence.<ref name="NHLBI-2016">{{cite web|title=How Can Death Due to Sudden Cardiac Arrest Be Prevented?|url=http://www.nhlbi.nih.gov/health/health-topics/topics/scda/prevention|website=NHLBI|access-date=16 August 2016|date=June 22, 2016|url-status=live|archive-url=https://web.archive.org/web/20160827200432/http://www.nhlbi.nih.gov/health/health-topics/topics/scda/prevention|archive-date=27 August 2016}}</ref>

<!-- Epidemiology and history -->
Per the 2015 American Heart Association Guidelines, there are approximately 535,000 incidents of cardiac arrest annually (about 13 per 10,000 people).<ref name="Kronick-2015"/> Of these, 326,000 (61%) experience cardiac arrest outside of a hospital setting, while 209,000 (39%) occur within a hospital.<ref name="Kronick-2015">{{cite journal | vauthors = Kronick SL, Kurz MC, Lin S, Edelson DP, Berg RA, Billi JE, Cabanas JG, Cone DC, Diercks DB, Foster JJ, Meeks RA, Travers AH, Welsford M | display-authors = 6 | title = Part 4: Systems of Care and Continuous Quality Improvement: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 132 | issue = 18 Suppl 2 | pages = S397–S413 | date = November 2015 | pmid = 26472992 | doi = 10.1161/cir.0000000000000258 | s2cid = 10073267 | doi-access = free }}</ref>

Cardiac arrest becomes more common with age and affects males more often than females.<ref name="NIH2022Def" /> Twice as many black men die from a cardiac arrest than white men. Asian and Hispanic people are not as frequently affected as white people.<ref name="NIH2022Def" />

==Signs and symptoms==
Cardiac arrest is not preceded by any warning symptoms in approximately 50 percent of people.<ref name="Lilly-2015">{{cite book|title=Braunwald's heart disease: a textbook of cardiovascular medicine | publisher=Saunders| vauthors = Lilly LS, Braunwald E, Mann DL, Zipes DP, Libby P, Bonow RO, Braunwald E |year=2015 |isbn=9781455751341 | veditors = Myerburg RJ |edition=Tenth|location=Philadelphia, PA|pages=821–860|chapter=Cardiac Arrest and Sudden Cardiac Death|oclc=890409638}}</ref> For individuals who do experience symptoms, the symptoms are usually nonspecific to the cardiac arrest.<ref name="National Heart, Lung and Blood Institute-2011">{{cite web |date=1 April 2011 |title=What Are the Signs and Symptoms of Sudden Cardiac Arrest? |url=https://www.nhlbi.nih.gov/health/health-topics/topics/scda/signs |url-status=live |archive-url=https://web.archive.org/web/20150621171145/https://www.nhlbi.nih.gov/health/health-topics/topics/scda/signs |archive-date=21 June 2015 |access-date=2015-06-21 |publisher=National Heart, Lung and Blood Institute}}</ref> For example, new or worsening [[Medicine:Chest pain|chest pain]], fatigue, [[Medicine:Syncope|blackout]]s, [[Medicine:Dizziness|dizziness]], shortness of breath, [[Medicine:Weakness|weakness]], or [[Medicine:Vomiting|vomiting]].<ref name="National Heart, Lung and Blood Institute-2011" /><ref name="NIH2022Def" />

When cardiac arrest is suspected by a layperson (due to signs of unconsciousness, abnormal breathing, and/or no pulse) it should be assumed that the victim is in cardiac arrest. Bystanders should call 911 or emergency medical services and initiate CPR.

== Risk factors ==
Major risk factors for cardiac arrest include age and underlying [[Medicine:Cardiovascular disease|cardiovascular disease]]. A prior episode of sudden cardiac arrest increases the likelihood of future episodes.<ref>{{cite book |title=Harrison's principles of internal medicine. |vauthors=Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J |publisher=Mcgraw-Hill |year=2014 |isbn=9780071802154 |edition=19th |location=New York |chapter=327. Cardiovascular Collapse, Cardiac Arrest, and Sudden Cardiac Death |oclc=893557976}}</ref> A 2021 meta-analysis assessing the recurrence of cardiac arrest in out-of-hospital cardiac arrest survivors identified that 15% of survivors experienced a second event, most often in the first year.<ref name="Lam 30–41">{{cite journal | vauthors = Lam TJ, Yang J, Poh JE, Ong ME, Liu N, Yeo JW, Gräsner JT, Masuda Y, Ho AF | display-authors = 6 | title = Long term risk of recurrence among survivors of sudden cardiac arrest: A systematic review and meta-analysis | journal = Resuscitation | volume = 176 | pages = 30–41 | date = July 2022 | pmid = 35526728 | doi = 10.1016/j.resuscitation.2022.04.027 | s2cid = 248569642 }}</ref> Furthermore, of those who experienced recurrence, 35% had a third episode.<ref name="Lam 30–41"/>

Additional significant risk factors include [[Chemistry:Tobacco smoking|cigarette smoking]], [[Medicine:Hypertension|high blood pressure]], high cholesterol, history of [[Medicine:Arrhythmia|arrhythmia]], lack of physical exercise, obesity, [[Medicine:Diabetes|diabetes]], [[Medicine:Family history|family history]], [[Medicine:Cardiomyopathy|cardiomyopathy]], alcohol use, and possibly caffeine intake.<ref>{{cite journal | vauthors = Friedlander Y, Siscovick DS, Weinmann S, Austin MA, Psaty BM, Lemaitre RN, Arbogast P, Raghunathan TE, Cobb LA | display-authors = 6 | title = Family history as a risk factor for primary cardiac arrest | journal = Circulation | volume = 97 | issue = 2 | pages = 155–160 | date = January 1998 | pmid = 9445167 | doi = 10.1161/01.cir.97.2.155 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Ha AC, Doumouras BS, Wang CN, Tranmer J, Lee DS | title = Prediction of Sudden Cardiac Arrest in the General Population: Review of Traditional and Emerging Risk Factors | journal = The Canadian Journal of Cardiology | volume = 38 | issue = 4 | pages = 465–478 | date = April 2022 | pmid = 35041932 | doi = 10.1016/j.cjca.2022.01.007 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Weinmann S, Siscovick DS, Raghunathan TE, Arbogast P, Smith H, Bovbjerg VE, Cobb LA, Psaty BM | display-authors = 6 | title = Caffeine intake in relation to the risk of primary cardiac arrest | journal = Epidemiology | volume = 8 | issue = 5 | pages = 505–508 | date = September 1997 | pmid = 9270951 | doi = 10.1097/00001648-199709000-00006 }}</ref><ref>{{cite journal | vauthors = Tu SJ, Gallagher C, Elliott AD, Linz D, Pitman BM, Hendriks JM, Lau DH, Sanders P, Wong CX | display-authors = 6 | title = Alcohol consumption and risk of ventricular arrhythmias and sudden cardiac death: An observational study of 408,712 individuals | journal = Heart Rhythm | volume = 19 | issue = 2 | pages = 177–184 | date = February 2022 | pmid = 35101186 | doi = 10.1016/j.hrthm.2021.09.040 | s2cid = 245422237 }}</ref> Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers' risk was closer to that of those who had never smoked.<ref name="Lilly-2015" /><ref name="Goldenberg_2003">{{cite journal | vauthors = Goldenberg I, Jonas M, Tenenbaum A, Boyko V, Matetzky S, Shotan A, Behar S, Reicher-Reiss H | display-authors = 6 | title = Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease | journal = Archives of Internal Medicine | volume = 163 | issue = 19 | pages = 2301–2305 | date = October 2003 | pmid = 14581249 | doi = 10.1001/archinte.163.19.2301 | doi-access = free }}</ref> A statistical analysis of many of these risk factors determined that approximately 50% of all cardiac arrests occur in 10% of the population perceived to be at greatest risk, due to aggregate harm of multiple risk factors, demonstrating that cumulative risk of multiple comorbidities exceeds the sum of each risk individually.<ref name="Saunders-2015">{{cite book |title=Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine |date=2015 | veditors = Mann DL, Zipes PL, Libby P, Bonow RO, Braunwald E |isbn=978-1-4557-5134-1|edition=Tenth |location=Philadelphia, PA | publisher=Saunders |page=826|oclc=881838985 }}</ref>

==Causes and mechanisms==
[[File:Basic representation of cardiac conduction.gif|thumb|221x221px|[[Medicine:Cardiac conduction system|Conduction of the heart]]. Changes in this pattern can result from injury to the cardiac muscle and lead to non-conducted beats and ultimately cardiac arrest.]]
[[File:Ventricular fibrillation.png|thumb|EKG depiction of ventricular fibrillation (no organized rhythm)]]
The underlying causes of sudden cardiac arrest can result from cardiac and non-cardiac etiologies. The most common underlying causes are different, depending on the patient's age. Common cardiac causes include coronary artery disease, non-atherosclerotic coronary artery abnormalities, structural heart damage, and inherited arrhythmias. Common non-cardiac causes include respiratory arrest, diabetes, medications, and trauma.

The most common mechanism underlying sudden cardiac arrest is an arrhythmia (an irregular rhythm).<ref name="Walls-2017" /> Without organized [[Medicine:Cardiac conduction system|electrical activity]] in the heart muscle, there is inconsistent contraction of the [[Medicine:Ventricle (heart)|ventricle]]s, which prevents the heart from generating adequate [[Medicine:Cardiac output|cardiac output]] (forward pumping of blood from the heart to the rest of the body).<ref name="Podrid-2016">{{cite web|url=https://www.uptodate.com/contents/pathophysiology-and-etiology-of-sudden-cardiac-arrest|title=Pathophysiology and etiology of sudden cardiac arrest| vauthors = Podrid PJ |date=2016-08-22|website=www.uptodate.com|access-date=2017-12-03}}</ref> This hemodynamic collapse results in poor blood flow to the brain and other organs, which if prolonged causes persistent damage.

There are many different types of arrhythmias, but the ones most frequently recorded in sudden cardiac arrest are [[Medicine:Ventricular tachycardia|ventricular tachycardia]] and [[Medicine:Ventricular fibrillation|ventricular fibrillation]].<ref>{{cite journal | vauthors = Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C, Smith SC, Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA, Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B, Blanc JJ, Budaj A, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL | display-authors = 6 | title = ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society | journal = Circulation | volume = 114 | issue = 10 | pages = e385–e484 | date = September 2006 | pmid = 16935995 | doi = 10.1161/CIRCULATIONAHA.106.178233 | doi-access = free | author-link9 = Arthur J. Moss }}</ref><ref>{{cite journal | vauthors = Landaw J, Yuan X, Chen PS, Qu Z | title = The transient outward potassium current plays a key role in spiral wave breakup in ventricular tissue | journal = American Journal of Physiology. Heart and Circulatory Physiology | volume = 320 | issue = 2 | pages = H826–H837 | date = February 2021 | pmid = 33385322 | pmc = 8082802 | doi = 10.1152/ajpheart.00608.2020 }}</ref> Both ventricular tachycardia and ventricular fibrillation can prevent the heart from generating coordinated ventricular contractions, thereby failing to sustain adequate blood circulation.

Less common types of arrhythmias occurring in cardiac arrest include [[Medicine:Pulseless electrical activity|pulseless electrical activity]], [[Medicine:Bradycardia|bradycardia]], and [[Medicine:Asystole|asystole]].<ref name="Walls-2017" /> These rhythms are seen when there is prolonged cardiac arrest, progression of ventricular fibrillation, or efforts like defibrillation executed to resuscitate the person.<ref name="Walls-2017" />

=== Cardiac causes ===

==== Coronary artery disease ====
[[File:Coronary Artery Disease.png|thumb|Normal vs blocked coronary artery]]
[[Medicine:Coronary artery disease|Coronary artery disease]] (CAD), also known as atherosclerotic cardiovascular disease, involves the deposition of cholesterol and subsequent inflammation-driven formation of [[Medicine:Atherosclerosis|atherosclerotic plaques]] in the arteries. CAD involves the accumulation and remodeling of the [[Medicine:Coronary circulation|coronary vessels]] along with other systemic blood vessels.<ref>{{cite book |title=StatPearls |vauthors=Pahwa R, Jialal I |date=2021 |publisher=StatPearls Publishing |place=Treasure Island (FL) |chapter=Atherosclerosis |pmid=29939576 |access-date=2021-11-05 |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK507799/}}</ref> When an atherosclerotic plaque dislodges, it can block the flow of blood and oxygen through small arteries, such as the coronary arteries, resulting in [[Medicine:Ischemia|ischemic]] injury. In the heart, this results in myocardial tissue damage which can lead to structural and functional changes that disrupt normal conduction patterns and alter heart rate and contraction.<ref name="Saunders-2015" />

CAD underlies 68 percent of sudden cardiac deaths in the United States.<ref name="Zheng-2001">{{cite journal |vauthors=Zheng ZJ, Croft JB, Giles WH, Mensah GA |date=October 2001 |title=Sudden cardiac death in the United States, 1989 to 1998 |journal=Circulation |volume=104 |issue=18 |pages=2158–2163 |doi=10.1161/hc4301.098254 |pmid=11684624 |doi-access=free}}</ref> Indeed, postmortem examinations have shown that the most common finding in cases of sudden cardiac death is chronic, high-grade [[Medicine:Stenosis|stenosis]] of at least one segment of a major [[Biology:Coronary arteries|coronary artery]].<ref>{{cite book | vauthors = Falk E, Shah PK | chapter = Pathogenesis of atherothrombosis. Role of vulnerable, ruptured, and eroded plaques | chapter-url= https://books.google.com/books?id=1WifwPEsKQMC&pg=PA460 |title=Atherothrombosis and Coronary Artery Disease | veditors = Fuster V, Topol EJ, Nabel EG |date=2005|publisher=Lippincott Williams & Wilkins|isbn=9780781735834|language=en|archive-url=https://web.archive.org/web/20160603002043/https://books.google.com/books?id=1WifwPEsKQMC&pg=PA460&lpg=PA460|archive-date=2016-06-03|url-status=live}}</ref>

While CAD is a leading contributing factor, this is an age-dependent factor, with CAD being a less common cause of sudden cardiac death in people under the age of 40.<ref name="CDC-2002">{{cite journal |author1=Centers for Disease Control Prevention (CDC) |date=February 2002 |title=State-specific mortality from sudden cardiac death--United States, 1999 |journal=MMWR. Morbidity and Mortality Weekly Report |volume=51 |issue=6 |pages=123–126 |pmid=11898927}}</ref>

==== Non-atherosclerotic coronary artery abnormalities ====

Abnormalities of the coronary arteries not related to atherosclerosis include inflammation (known as coronary [[Medicine:Arteritis|arteritis]]), [[Medicine:Embolism|embolism]], [[Medicine:Vasospasm|vasospasm]], mechanical abnormalities related to connective tissue diseases or trauma, and congenital [[Medicine:Coronary artery anomaly|coronary artery anomalies]] (most commonly anomalous origin of the left coronary artery from the pulmonary artery). These conditions account for 10-15% of cardiac arrest and sudden cardiac death.<ref name="Saunders-2015" />
* Coronary arteritis commonly results from a pediatric febrile inflammatory condition known as [[Medicine:Kawasaki disease|Kawasaki disease]]. Other types of [[Medicine:Vasculitis|vasculitis]] can also contribute to an increased risk of sudden cardiac death.
* Embolism, or clotting, of the coronary arteries most commonly occurs from septic emboli secondary to endocarditis with involvement of the aortic valve, tricuspid valve, or prosthetic valves.
* [[Medicine:Coronary vasospasm|Coronary vasospasm]] may result in cardiac arrhythmias, altering the heart's electrical conduction with a risk of complete cardiac arrest from severe or prolonged rhythm changes.
* Mechanical abnormalities with an associated risk of cardiac arrest may arise from coronary artery dissection, which can be attributed to [[Medicine:Marfan syndrome|Marfan Syndrome]] or trauma.<ref name="Saunders-2015" />

====Structural heart disease====
[[File:Heart left ventricular hypertrophy sa.jpg|thumb|Short axis view of the heart demonstrating wall thickening in left ventricular hypertrophy]]
Examples of structural heart diseases include: [[Medicine:Cardiomyopathy|cardiomyopathies]] ([[Medicine:Hypertrophic cardiomyopathy|hypertrophic]], [[Medicine:Dilated cardiomyopathy|dilated]], or arrhythmogenic), cardiac rhythm disturbances, [[Medicine:Myocarditis|myocarditis]], and congestive heart failure.<ref name="Kannel-1998">{{cite journal | vauthors = Kannel WB, Wilson PW, D'Agostino RB, Cobb J | title = Sudden coronary death in women | journal = American Heart Journal | volume = 136 | issue = 2 | pages = 205–212 | date = August 1998 | pmid = 9704680 | doi = 10.1053/hj.1998.v136.90226 }}</ref>
[[File:Left Ventricular Hypertrophy Unlabeled.jpg|thumb|EKG depiction of left ventricular hypertrophy]]
Left ventricular hypertrophy is a leading cause of sudden cardiac deaths in the adult population.<ref>{{cite journal | vauthors = Stevens SM, Reinier K, Chugh SS | title = Increased left ventricular mass as a predictor of sudden cardiac death: is it time to put it to the test? | journal = Circulation: Arrhythmia and Electrophysiology | volume = 6 | issue = 1 | pages = 212–217 | date = February 2013 | pmid = 23424223 | pmc = 3596001 | doi = 10.1161/CIRCEP.112.974931 }}</ref><ref name="Walls-2017" /> This is most commonly the result of longstanding [[Medicine:Hypertension|high blood pressure]], or hypertension, which has led to maladaptive overgrowth of muscular tissue of the [[Medicine:Ventricle (heart)|left ventricle]], the heart's main pumping chamber.<ref name="Katholi-2011">{{cite journal | vauthors = Katholi RE, Couri DM | title = Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications | journal = International Journal of Hypertension | volume = 2011 | pages = 495349 | year = 2011 | pmid = 21755036 | pmc = 3132610 | doi = 10.4061/2011/495349 | doi-access = free }}</ref> This is because elevated blood pressure over the course of several years requires the heart to adapt to the requirement of pumping harder to adequately circulate blood throughout the body. If the heart does this for a prolonged period of time, the left ventricle can experience hypertrophy (grow larger) in a way that decreases the heart's effectiveness.<ref>{{cite book | vauthors = Bornstein AB, Rao SS, Marwaha K | chapter = Left Ventricular Hypertrophy |date=2021| chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK557534/ | title = StatPearls|place=Treasure Island (FL) |publisher= StatPearls Publishing|pmid=32491466|access-date=2021-11-05 }}</ref> Left ventricular hypertrophy can be demonstrated on an [[Medicine:Echocardiography|echocardiogram]] and [[Biology:Electrocardiography|electrocardiogram]] (EKG).<ref name="Katholi-2011" />

Abnormalities of the cardiac conduction system (notably the Atrioventricular Node and [[Medicine:Purkinje fibers|His-Purkinje]] system) may predispose an individual to arrhythmias with a risk of progressing to sudden cardiac arrest, albeit this risk remains low. Many of these conduction blocks can be treated with internal cardiac defibrillators for those determined to be at high risk due to severity of fibrosis or severe electrophysiologic disturbances.<ref name="Saunders-2015" />

Structural heart diseases unrelated to coronary artery disease account for 10% of all sudden cardiac deaths.<ref name="Podrid-2016" /><ref name="Zheng-2001" /> A 1999 review of sudden cardiac deaths in the United States found that structural heart diseases accounted for over 30% of sudden cardiac arrests for those under 30 years.<ref name="CDC-2002" /><ref name="Zheng-2001" />

==== Inherited arrhythmia syndromes ====
Arrhythmias not due to structural heart disease account for 5 to 10% of sudden cardiac arrests.<ref>{{cite journal | vauthors = Chugh SS, Kelly KL, Titus JL | title = Sudden cardiac death with apparently normal heart | journal = Circulation | volume = 102 | issue = 6 | pages = 649–654 | date = August 2000 | pmid = 10931805 | doi = 10.1161/01.cir.102.6.649 | doi-access = free }}</ref><ref>{{cite journal | vauthors =  | title = Survivors of out-of-hospital cardiac arrest with apparently normal heart. Need for definition and standardized clinical evaluation. Consensus Statement of the Joint Steering Committees of the Unexplained Cardiac Arrest Registry of Europe and of the Idiopathic Ventricular Fibrillation Registry of the United States | journal = Circulation | volume = 95 | issue = 1 | pages = 265–272 | date = January 1997 | pmid = 8994445 | doi = 10.1161/01.cir.95.1.265 }}</ref><ref name="Drory-1991">{{cite journal | vauthors = Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, Kramer MR | title = Sudden unexpected death in persons less than 40 years of age | journal = The American Journal of Cardiology | volume = 68 | issue = 13 | pages = 1388–1392 | date = November 1991 | pmid = 1951130 | doi = 10.1016/0002-9149(91)90251-f }}</ref> These are frequently caused by [[Medicine:Genetic disorder|genetic disorder]]s.<ref name="Walls-2017" /> The genetic [[Biology:Mutation|mutation]]s often affect specialized proteins known as [[Biology:Ion channel|ion channel]]s that conduct [[Physics:Ion|electrically charged particles]] across the [[Biology:Cell membrane|cell membrane]], and this group of conditions is therefore often referred to as [[Medicine:Channelopathy|channelopathies]]. Examples of these inherited arrhythmia syndromes include [[Medicine:Long QT syndrome|Long QT syndrome]] (LQTS), Brugada Syndrome, [[Medicine:Catecholaminergic polymorphic ventricular tachycardia|Catecholaminergic polymorphic ventricular tachycardia]], and [[Medicine:Short QT syndrome|Short QT syndrome]]. Many are also associated with environmental or neurogenic triggers such as response to loud sounds that can initiate lethal arrhythmias.<ref name="Saunders-2015" />

LQTS, a condition often mentioned in young people's deaths, occurs in one of every 5000 to 7000 newborns and is estimated to be responsible for 3000 deaths annually compared to the approximately 300,000 cardiac arrests seen by emergency services.<ref name="American Heart Association">{{cite web | url = http://www.americanheart.org/presenter.jhtml?identifier=4741 | title = Sudden Cardiac Death | archive-url = https://web.archive.org/web/20100325174959/http://www.americanheart.org/presenter.jhtml?identifier=4741| archive-date=2010-03-25 | publisher = American Heart Association }}</ref> These conditions are a fraction of the overall deaths related to cardiac arrest but represent conditions that may be detected prior to arrest and may be treatable. The symptomatic expression of LQTS is quite broad and more often presents with [[Medicine:Syncope|syncope]] rather than cardiac arrest. The risk of cardiac arrest is still present, and people with family histories of sudden cardiac arrests should be screened for LQTS and other treatable causes of lethal arrhythmia. Higher levels of risk for cardiac arrest are associated with female sex, more significant QT prolongation, history of unexplained syncope (fainting spells), or premature sudden cardiac death.<ref name="Saunders-2015" /> Additionally, individuals with LQTS should avoid certain medications that carry the risk of increasing the severity of this conduction abnormality, such as certain anti-arrhythmics, anti-depressants, and quinolone or [[Chemistry:Macrolide|macrolide]] antibiotics.<ref>{{cite journal | vauthors = Fazio G, Vernuccio F, Grutta G, Re GL | title = Drugs to be avoided in patients with long QT syndrome: Focus on the anaesthesiological management | journal = World Journal of Cardiology | volume = 5 | issue = 4 | pages = 87–93 | date = April 2013 | pmid = 23675554 | pmc = 3653016 | doi = 10.4330/wjc.v5.i4.87 | doi-access = free }}</ref>

Another condition that promotes arrhythmias is [[Medicine:Wolff–Parkinson–White syndrome|Wolff-Parkinson-White syndrome]], in which an accessory conduction pathway bypassing the atrioventricular node is present and can cause abnormal conduction patterns leading to supraventricular tachycardia and cardiac arrest.<ref name="Podrid-2016" />

===Non-cardiac causes===
Non-cardiac causes account for 15 to 25% of cardiac arrests.<ref name="Drory-1991" /><ref name="Kuisma-1997">{{cite journal | vauthors = Kuisma M, Alaspää A | title = Out-of-hospital cardiac arrests of non-cardiac origin. Epidemiology and outcome | journal = European Heart Journal | volume = 18 | issue = 7 | pages = 1122–1128 | date = July 1997 | pmid = 9243146 | doi = 10.1093/oxfordjournals.eurheartj.a015407 | doi-access = free }}</ref> Common non-cardiac causes include [[Medicine:Respiratory arrest|respiratory arrest]], [[Medicine:Diabetes|diabetes]], certain [[Chemistry:Medication|medication]]s, and [[Medicine:Blunt trauma|blunt trauma]] (especially to the chest).<ref name="NIH2022Causes"/><ref>{{cite journal | vauthors = Smith JE, Rickard A, Wise D | title = Traumatic cardiac arrest | journal = Journal of the Royal Society of Medicine | volume = 108 | issue = 1 | pages = 11–16 | date = January 2015 | pmid = 25572990 | pmc = 4291327 | doi = 10.1177/0141076814560837 }}</ref><ref name="Chen_2018">{{cite journal | vauthors = Chen N, Callaway CW, Guyette FX, Rittenberger JC, Doshi AA, Dezfulian C, Elmer J | title = Arrest etiology among patients resuscitated from cardiac arrest | journal = Resuscitation | volume = 130 | pages = 33–40 | date = September 2018 | pmid = 29940296 | doi = 10.1016/j.resuscitation.2018.06.024 | pmc = 6092216 }}</ref>

* Respiratory arrest will be followed by cardiac arrest unless promptly treated.<ref name="Chen_2018" /> Respiratory arrest can be caused by pulmonary embolus, choking, drowning, trauma, drug overdose, and poisoning.<ref name="NIH2022Causes" /> Pulmonary embolus carries a high mortality rate and may be the triggering cause for up to 5% of cardiac arrests, according to a retrospective study from an urban tertiary care emergency department.<ref>{{cite journal | vauthors = Kürkciyan I, Meron G, Sterz F, Janata K, Domanovits H, Holzer M, Berzlanovich A, Bankl HC, Laggner AN | display-authors = 6 | title = Pulmonary embolism as a cause of cardiac arrest: presentation and outcome | journal = Archives of Internal Medicine | volume = 160 | issue = 10 | pages = 1529–1535 | date = May 2000 | pmid = 10826469 | doi = 10.1001/archinte.160.10.1529 }}</ref> 
* Diabetes-related factors contributing to cardiac arrest include silent myocardial ischemia, nervous system dysfunction, and electrolyte disturbances leading to abnormal cardiac repolarization.<ref>{{cite journal | vauthors = Bergner DW, Goldberger JJ | title = Diabetes mellitus and sudden cardiac death: what are the data? | journal = Cardiology Journal | volume = 17 | issue = 2 | pages = 117–129 | date = 2010 | pmid = 20544609 | url = https://journals.viamedica.pl/cardiology_journal/article/view/21390 }}</ref>
* Certain medications can worsen an existing arrhythmia. Some examples include antibiotics like macrolides, diuretics, and heart medications such as anti-arrhythmic medications.<ref name="NIH2022Causes" />

Additional non-cardiac causes include [[Medicine:Bleeding|hemorrhage]], aortic rupture, [[Medicine:Hypovolemic shock|hypovolemic shock]], [[Medicine:Pulmonary embolism|pulmonary embolism]], poisoning such as from the [[Biology:Jellyfish#Toxicity|stings of certain jellyfish]], and [[Engineering:Electrical injury|electrical injury]].<ref name="Walls-2017" /><ref name="Raab-2008">{{cite journal | vauthors = Raab H, Lindner KH, Wenzel V | title = Preventing cardiac arrest during hemorrhagic shock with vasopressin | journal = Critical Care Medicine | volume = 36 | issue = 11 Suppl | pages = S474–S480 | date = November 2008 | pmid = 20449913 | doi = 10.1097/ccm.0b013e31818a8d7e | publisher = Ovid Technologies (Wolters Kluwer Health) }}</ref><ref name="Voelckel-2000">{{cite journal | vauthors = Voelckel WG, Lurie KG, Lindner KH, Zielinski T, McKnite S, Krismer AC, Wenzel V | title = Vasopressin improves survival after cardiac arrest in hypovolemic shock | journal = Anesthesia and Analgesia | volume = 91 | issue = 3 | pages = 627–634 | date = September 2000 | pmid = 10960389 | doi = 10.1097/00000539-200009000-00024 | publisher = Ovid Technologies (Wolters Kluwer Health) }}</ref><ref name="pmid28444167">{{cite journal | vauthors = Waldmann V, Narayanan K, Combes N, Jost D, Jouven X, Marijon E | title = Electrical cardiac injuries: current concepts and management | journal = European Heart Journal | volume = 39 | issue = 16 | pages = 1459–1465 | date = April 2018 | pmid = 28444167 | doi = 10.1093/eurheartj/ehx142 }}</ref>

Circadian patterns are also recognized as triggering factors in cardiac arrest.<ref>{{cite journal | vauthors = Willich SN, Levy D, Rocco MB, Tofler GH, Stone PH, Muller JE | title = Circadian variation in the incidence of sudden cardiac death in the Framingham Heart Study population | journal = The American Journal of Cardiology | volume = 60 | issue = 10 | pages = 801–806 | date = October 1987 | pmid = 3661393 | doi = 10.1016/0002-9149(87)91027-7 }}</ref> Per a 2021 systematic review, throughout the day there are two main peak times in which cardiac arrest occurs. The first is in the morning hours and the second is in the afternoon.<ref>{{cite journal | vauthors = Tran DT, St Pierre Schneider B, McGinnis GR | title = Circadian Rhythms in Sudden Cardiac Arrest: A Review | journal = Nursing Research | volume = 70 | issue = 4 | pages = 298–309 | date = July 2021 | pmid = 33883500 | doi = 10.1097/NNR.0000000000000512 | s2cid = 233349757 }}</ref> Moreover, survival rates following cardiac arrest were lowest when occurring between midnight and 6am.<ref>{{cite journal | vauthors = Tran DT, St Pierre Schneider B, McGinnis GR | title = Circadian Rhythms in Sudden Cardiac Arrest: A Review | language = en-US | journal = Nursing Research | volume = 70 | issue = 4 | pages = 298–309 | date = July–August 2021 | pmid = 33883500 | doi = 10.1097/NNR.0000000000000512 | s2cid = 233349757 }}</ref>

Many of these non-cardiac causes of cardiac arrest are reversible. A common mnemonic used to recall the reversible causes of cardiac arrest is referred to as the [[Medicine:Hs and Ts|Hs and Ts]]. The Hs are [[Medicine:Hypovolemia|hypovolemia]], [[Medicine:Hypoxia|hypoxia]], hydrogen cation excess (acidosis), [[Medicine:Hyperkalemia|hyperkalemia]], [[Medicine:Hypokalemia|hypokalemia]], [[Physics:Hypothermia|hypothermia]], and [[Medicine:Hypoglycemia|hypoglycemia]]. The Ts are [[Biology:Toxin|toxin]]s, (cardiac) [[Medicine:Cardiac tamponade|tamponade]], [[Medicine:Pneumothorax|tension pneumothorax]], thrombosis ([[Medicine:Myocardial infarction|myocardial infarction]]), [[Medicine:Thrombosis|thromboembolism]], and trauma.

===Mechanism===
[[File:Ventricular fibrillation.png|thumb|upright=1.3|Ventricular fibrillation]]
The definitive electrical mechanisms of cardiac arrest, which may arise from any of the functional, structural, or physiologic abnormalities mentioned above, are characterized by arrhythmias.<ref name="Saunders-2015" /> [[Medicine:Ventricular fibrillation|Ventricular fibrillation]] and pulseless or sustained [[Medicine:Ventricular tachycardia|ventricular tachycardia]] are the most commonly recorded arrhythmias preceding cardiac arrest. These are rapid and erratic arrhythmias that alter the circulatory pathway such that adequate blood flow cannot be sustained and is inadequate to meet the body's needs.<ref name="Saunders-2015" />

The mechanism responsible for the majority of sudden cardiac deaths is ventricular fibrillation. Ventricular fibrillation is a tachyarrhythmia characterized by turbulent electrical activity in the ventricular myocardium leading to a heart rate too disorganized and rapid to produce any meaningful cardiac output, thus resulting in insufficient perfusion of the brain and essential organs.<ref>{{Cite web|title=Ventricular tachycardia - Symptoms and causes|url=https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/symptoms-causes/syc-20355138|access-date=2021-11-29|website=Mayo Clinic|language=en}}</ref> Some of the electrophysiologic mechanisms underpinning ventricular fibrillations include ectopic automaticity, re-entry, and triggered activity.<ref>{{cite journal |vauthors=Szabó Z, Ujvárosy D, Ötvös T, Sebestyén V, Nánási PP |date=2020-01-29 |title=Handling of Ventricular Fibrillation in the Emergency Setting |journal=Frontiers in Pharmacology |volume=10 |pages=1640 |doi=10.3389/fphar.2019.01640 |pmc=7043313 |pmid=32140103 |doi-access=free}}</ref> However, structural changes in the diseased heart as a result of inherited factors (mutations in ion-channel coding genes, for example) cannot explain the sudden onset of cardiac arrest.<ref>{{cite journal |vauthors=Rubart M, Zipes DP |date=September 2005 |title=Mechanisms of sudden cardiac death |journal=The Journal of Clinical Investigation |volume=115 |issue=9 |pages=2305–2315 |doi=10.1172/JCI26381 |pmc=1193893 |pmid=16138184}}</ref>

In ventricular tachycardia, the heart also beats faster than normal, which may prevent the heart chambers from properly filling with blood.<ref>{{Cite web|title=Ventricular fibrillation - Symptoms and causes|url=https://www.mayoclinic.org/diseases-conditions/ventricular-fibrillation/symptoms-causes/syc-20364523|access-date=2021-11-29|website=Mayo Clinic|language=en}}</ref> Ventricular tachycardia is characterized by an altered QRS complex and a heart rate greater than 100 beats per minute.<ref>{{cite journal | vauthors = AlMahameed ST, Ziv O | title = Ventricular Arrhythmias | journal = The Medical Clinics of North America | volume = 103 | issue = 5 | pages = 881–895 | date = September 2019 | pmid = 31378332 | doi = 10.1016/j.mcna.2019.05.008 | s2cid = 199437558 }}</ref> When V-tach is sustained (lasts for at least 30 seconds), inadequate blood flow to heart tissue can lead to cardiac arrest.<ref>{{cite journal | vauthors = Baldzizhar A, Manuylova E, Marchenko R, Kryvalap Y, Carey MG | title = Ventricular Tachycardias: Characteristics and Management | journal = Critical Care Nursing Clinics of North America | volume = 28 | issue = 3 | pages = 317–329 | date = September 2016 | pmid = 27484660 | doi = 10.1016/j.cnc.2016.04.004 }}</ref>

[[Medicine:Bradycardia|Bradyarrhythmias]] occur following dissociation of spontaneous electrical conduction and the mechanical function of the heart resulting in [[Medicine:Pulseless electrical activity|pulseless electrical activity]] (PEA) or through complete absence of electrical activity of the heart resulting in [[Medicine:Asystole|asystole]]. Similar to the result of tachyarrhythmias, these conditions lead to an inability to sustain adequate blood flow as well, though in the case of bradyarrhythmias, the underlying cause is an absence of mechanical activity rather than rapid beats leading to disorganization.<ref name="Saunders-2015" />

==Diagnosis==
[[File:Carotidian pulse and recovery position.jpg|thumb|Medical personnel checking the carotid pulse of a simulated patient]]
Cardiac arrest is synonymous with [[Medicine:Clinical death|clinical death]].<ref name="AHA-2005" /> The physical examination to diagnose cardiac arrest focuses on the absence of a pulse.<ref name="Walls-2017" /> In many cases, lack of a [[Medicine:Pulse|central pulse]] (carotid arteries or subclavian arteries) is the [[Medicine:Gold standard (test)|gold standard]]. Lack of a pulse in the periphery (radial/pedal) may also result from other conditions (e.g. [[Medicine:Shock (circulatory)|shock]]) or be the rescuer's misinterpretation.

Obtaining a thorough history can help inform the potential cause and prognosis.<ref name="Walls-2017" /> The provider taking the person's clinical history should try to learn whether the episode was observed by anyone else, when it happened, what the patient was doing (in particular whether there was any trauma), and whether drugs were involved.<ref name="Walls-2017" />

During resuscitation efforts, continuous monitoring equipment including EKG leads should be attached to the patient so that providers can analyze the electrical activity of the cardiac cycle and use this information to guide the management efforts. EKG readings will help to identify the arrhythmia present and allow the team to monitor any changes that occur with the administration of CPR and defibrillation. Clinicians classify cardiac arrest into "shockable" versus "non-shockable", as determined by the EKG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using [[Engineering:Defibrillation|defibrillation]].<ref name="Resuscitation Council" /> The two "shockable" rhythms are [[Medicine:Ventricular fibrillation|ventricular fibrillation]] and pulseless ventricular tachycardia, while the two "non-shockable" rhythms are [[Medicine:Asystole|asystole]] and [[Medicine:Pulseless electrical activity|pulseless electrical activity]].<ref>{{cite book |url=https://books.google.com/books?id=vNgrOsHjIKEC&pg=PA43 |title=ABC of resuscitation |publisher=Wiley-Blackwell |year=2012 |isbn=9781118474853 |veditors=Soar J, Perkins JD, Nolan J |edition=6th |location=Chichester, West Sussex |page=43 |archive-url=https://web.archive.org/web/20170905133735/https://books.google.com/books?id=vNgrOsHjIKEC&pg=PA43 |archive-date=2017-09-05 |url-status=live}}</ref> Moreover, in the post-resuscitation patient, a 12-lead EKG can help identify some causes of cardiac arrest, such as STEMI which may require specific treatments.

[[Medicine:Emergency ultrasound|Point-of-care ultrasound (POCUS)]] is a tool that can be used to examine the movement of the heart and its force of contraction at the patient's bedside.<ref name="Long-2018">{{cite journal | vauthors = Long B, Alerhand S, Maliel K, Koyfman A | title = Echocardiography in cardiac arrest: An emergency medicine review | journal = The American Journal of Emergency Medicine | volume = 36 | issue = 3 | pages = 488–493 | date = March 2018 | pmid = 29269162 | doi = 10.1016/j.ajem.2017.12.031 | s2cid = 3874849 | doi-access = free }}</ref> POCUS can accurately diagnose cardiac arrest in hospital settings, as well as visualize cardiac wall motion contractions.<ref name="Long-2018" /> Using POCUS, clinicians can have limited, two-dimensional views of different parts of the heart during arrest.<ref name="Paul-2021">{{cite journal | vauthors = Paul JA, Panzer OP | title = Point-of-care Ultrasound in Cardiac Arrest | journal = Anesthesiology | volume = 135 | issue = 3 | pages = 508–519 | date = September 2021 | pmid = 33979442 | doi = 10.1097/ALN.0000000000003811 | s2cid = 234486749 | doi-access = free }}</ref> These images can help clinicians determine whether electrical activity within the heart is pulseless or pseudo-pulseless, as well as help them diagnose the potentially reversible causes of an arrest.<ref name="Paul-2021" /> Published guidelines from the [[Organization:American Society of Echocardiography|American Society of Echocardiography]], American College of Emergency Physicians, European Resuscitation Council, and the [[Organization:American Heart Association|American Heart Association]], as well as the 2018 preoperative [[Medicine:Advanced cardiac life support|Advanced Cardiac Life Support]] guidelines, have recognized the potential benefits of using POCUS in diagnosing and managing cardiac arrest.<ref name="Paul-2021" />

POCUS can help predict outcomes in resuscitation efforts. Specifically, use of transthoracic ultrasound can be a helpful tool in predicting mortality in cases of cardiac arrest, with a systematic review from 2020 finding that there is a significant positive correlation between presence of cardiac motion and short term survival with CPR.<ref>{{cite journal | vauthors = Kedan I, Ciozda W, Palatinus JA, Palatinus HN, Kimchi A | title = Prognostic value of point-of-care ultrasound during cardiac arrest: a systematic review | journal = Cardiovascular Ultrasound | volume = 18 | issue = 1 | pages = 1 | date = January 2020 | pmid = 31931808 | pmc = 6958750 | doi = 10.1186/s12947-020-0185-8 | doi-access = free }}</ref>

Owing to the inaccuracy diagnosis solely based off central pulse detection, some bodies like the European Resuscitation Council have de-emphasized its importance. Instead, the current guidelines prompt individuals to begin CPR on any unconscious person with absent or abnormal breathing.<ref name="Resuscitation Council" /> The Resuscitation Council in the United Kingdom stands in line with the European Resuscitation Council's recommendations and those of the American Heart Association.<ref name="AHA-2005" /> They have suggested that the technique to check carotid pulses should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators like [[Medicine:Agonal respiration|agonal respiration]].<ref name="Resuscitation Council">{{cite web |url=http://www.resus.org.uk/pages/guide.htm |title=Resuscitation Council (UK) Guidelines 2005 |url-status=live |archive-url=https://web.archive.org/web/20091215230632/http://www.resus.org.uk/pages/guide.htm |archive-date=2009-12-15 }}</ref>

Various other methods for detecting circulation and therefore diagnosing cardiac arrest have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation recommendations were for rescuers to look for "signs of circulation" but not specifically the pulse.<ref name="AHA-2005" /> These signs included coughing, gasping, color, twitching, and movement.<ref>{{cite book |author=British Red Cross |author2=St Andrew's Ambulance Association |author3=St John Ambulance |title=First Aid Manual: The Authorised Manual of St. John Ambulance, St. Andrew's Ambulance Association, and the British Red Cross |publisher=Dorling Kindersley |year=2006 |isbn=978-1-4053-1573-9 |url-access=registration |url=https://archive.org/details/firstaidmanualau0000unse }}</ref> Per evidence that these guidelines were ineffective, the current International Liaison Committee on Resuscitation recommendation is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally, a similar protocol to that which the European Resuscitation Council has adopted.<ref name="AHA-2005" /> In a non-acute setting where the patient is expired, diagnosis of cardiac arrest can be done via molecular autopsy or postmortem molecular testing, which uses a set of molecular techniques to find the ion channels that are cardiac defective.<ref>{{Citation| vauthors = Glatter KA, Chiamvimonvat N, He Y, Chevalier P, Turillazzi E |title=Postmortem Analysis for Inherited Ion Channelopathies|date=2006|work=Essentials of Autopsy Practice: Current Methods and Modern Trends|pages=15–37| veditors = Rutty GN |publisher=Springer|language=en|doi=10.1007/1-84628-026-5_2|isbn=978-1-84628-026-9 }}</ref> This could help elucidate the cause of death in the patient.

Other physical signs or symptoms can help determine the potential cause of the cardiac arrest.<ref name="Walls-2017" /> Below is a chart of the clinical findings and signs/symptoms a person may have and potential causes associated with them.
{|
|+Physical findings related to potential causes<ref name="Walls-2017" />
!Location
!Findings
!Possible Causes
|-
|General
|[[Medicine:Pallor|Pale skin]]
|[[Medicine:Bleeding|Hemorrhage]]
|-
|
|Decreased body temperature
|[[Physics:Hypothermia|Hypothermia]]
|-
|Airway
|Presence of secretions, vomit, blood
|[[Medicine:Pulmonary aspiration|Aspiration]]
|-
|
|Inability to provide [[Medicine:Modes of mechanical ventilation|positive pressure ventilation]]
|[[Medicine:Pneumothorax|Tension pneumothorax]]
Airway obstruction
|-
|Neck
|[[Medicine:Jugular venous pressure|Distension of the neck veins]]
|Tension pneumothorax
[[Medicine:Cardiac tamponade|Cardiac tamponade]]

[[Medicine:Pulmonary embolism|Pulmonary embolism]]
|-
|
|Trachea shifted to one side
|Tension pneumothorax
|-
|Chest
|Scar in the middle of the sternum
|Cardiac disease
|-
|Lungs
|Breath sounds only on one side
|Tension pneumothorax
[[Medicine:Tracheal intubation|Right mainstem intubation]]

Aspiration
|-
|
|No breath sounds or distant breath sounds
|Esophageal intubation

Airway obstruction
|-
|
|Wheezing
|Aspiration

Bronchospasm

[[Medicine:Pulmonary edema|Pulmonary edema]]
|-
|
|Rales
|Aspiration

Pulmonary edema

Pneumonia
|-
|Heart
|Decreased heart sounds
|[[Medicine:Hypovolemia|Hypovolemia]]

Cardiac tamponade

Tension pneumothorax

Pulmonary embolus
|-
|Abdomen
|Distended and dull
|Ruptured [[Medicine:Abdominal aortic aneurysm|abdominal aortic aneurysm]]

Ruptured [[Medicine:Ectopic pregnancy|ectopic pregnancy]]
|-
|
|Distended and tympanic
|Esophageal intubation
|-
|Rectal
|Blood present
|[[Medicine:Gastrointestinal bleeding|Gastrointestinal hemorrhage]]
|-
|Extremities
|Asymmetrical pulses
|[[Medicine:Aortic dissection|Aortic dissection]]
|-
|Skin
|Needle tracks
|Drug abuse
|}

== Prevention ==

=== Primary Prevention ===
With the lack of positive outcomes following cardiac arrest, efforts have been spent finding effective strategies to prevent cardiac arrest events. The approach to primary prevention promotes a healthy diet, exercise, limited alcohol consumption, and smoking cessation.<ref name="NHLBI-2016" />

Exercise is an effective preventative measure for cardiac arrest in the general population but may be risky for those with pre-existing conditions.<ref name="Fanous-2019">{{cite journal |vauthors=Fanous Y, Dorian P |date=July 2019 |title=The prevention and management of sudden cardiac arrest in athletes |journal=CMAJ |volume=191 |issue=28 |pages=E787–E791 |doi=10.1503/cmaj.190166 |pmc=6629536 |pmid=31308007}}</ref> The risk of a transient catastrophic cardiac event increases in individuals with heart disease during and immediately after exercise.<ref name="Fanous-2019" /> The lifetime and acute risks of cardiac arrest are decreased in people with heart disease who perform regular exercise, perhaps suggesting the benefits of exercise outweigh the risks.<ref name="Fanous-2019" />

According to a study published in the Journal of the American Heart Association in 2021, diet may be a modifiable risk factor that leads to a lower incidence of sudden cardiac death.<ref name="Shikany-2021">{{cite journal | vauthors = Shikany JM, Safford MM, Soroka O, Brown TM, Newby PK, Durant RW, Judd SE | title = Mediterranean Diet Score, Dietary Patterns, and Risk of Sudden Cardiac Death in the REGARDS Study | journal = Journal of the American Heart Association | volume = 10 | issue = 13 | pages = e019158 | date = July 2021 | pmid = 34189926 | pmc = 8403280 | doi = 10.1161/JAHA.120.019158 }}</ref> The study found that those who fell under the category of having "Southern diets" representing those of "added fats, fried food, eggs, organ and processed meats, and sugar‐sweetened beverages" had a positive association with an increased risk of cardiac arrest, while those deemed following the "Mediterranean diets" had an inverse relationship regarding the risk of cardiac arrest.<ref name="Shikany-2021"/> The American Heart Association also has [https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/nutrition-basics/aha-diet-and-lifestyle-recommendations diet recommendations] aimed at preventing cardiovascular disease.<ref name="www.heart.org">{{Cite web|title=The American Heart Association Diet and Lifestyle Recommendations|url=https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/nutrition-basics/aha-diet-and-lifestyle-recommendations|access-date=2021-11-12|website=www.heart.org|language=en}}</ref>

Additionally, marine-derived omega-3 polyunsaturated fatty acids (PUFAs) have been promoted for preventing sudden cardiac death due to their postulated ability to lower [[Chemistry:Triglyceride|triglyceride]] levels, prevent [[Medicine:Heart arrhythmia|arrhythmia]]s, decrease platelet aggregation, and lower blood pressure.<ref>{{cite encyclopedia|title=Omega-3 fatty acids|encyclopedia=MedlinePlus Medical Encyclopedia|url=https://www.nlm.nih.gov/medlineplus/ency/imagepages/19302.htm|access-date=2015-06-21|date=2 August 2011|archive-url=https://web.archive.org/web/20150621170015/http://www.nlm.nih.gov/medlineplus/ency/imagepages/19302.htm|archive-date=21 June 2015|vauthors=Kaneshiro NK|url-status=live}}</ref> According to a systematic review published in 2012, omega-3 PUFA supplementation is not associated with a lower risk of sudden cardiac death.<ref name="Rizos-2012">{{cite journal|vauthors=Rizos EC, Ntzani EE, Bika E, Kostapanos MS, Elisaf MS|date=September 2012|title=Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis|journal=JAMA|volume=308|issue=10|pages=1024–1033|doi=10.1001/2012.jama.11374|pmid=22968891}}</ref>

There are no specific screening tests, however for people at risk of heart disease, measures such as [[Physics:Blood pressure|blood pressure]] control, [[Chemistry:Cholesterol|cholesterol]] lowering, and other medico-therapeutic interventions are used. A Cochrane review published in 2016 found moderate-quality evidence to show that blood pressure-lowering drugs do not reduce the risk of sudden cardiac death.<ref>{{cite journal |vauthors=Taverny G, Mimouni Y, LeDigarcher A, Chevalier P, Thijs L, Wright JM, Gueyffier F |date=March 2016 |title=Antihypertensive pharmacotherapy for prevention of sudden cardiac death in hypertensive individuals |journal=The Cochrane Database of Systematic Reviews |volume=2016 |issue=3 |pages=CD011745 |doi=10.1002/14651858.CD011745.pub2 |pmc=8665834 |pmid=26961575}}</ref>

===Secondary Prevention===
[[File:Blausen 0543 ImplantableCardioverterDefibrillator.svg|upright=1.3|thumb|Illustration of an implantable cardioverter-defibrillator (ICD)]]
An [[Biology:Implantable cardioverter-defibrillator|implantable cardioverter-defibrillator]] (ICD) is a battery-powered device that monitors electrical activity in the heart, and when an arrhythmia is detected, can deliver an electrical shock to terminate the abnormal rhythm. ICDs are used to prevent sudden cardiac death (SCD) in those who have survived a prior episode of sudden cardiac arrest (SCA) due to ventricular fibrillation or ventricular tachycardia.<ref name="Epstein-2008">{{cite journal|display-authors=6|vauthors=Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Smith SC, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Page RL, Riegel B, Tarkington LG, Yancy CW|date=May 2008|title=ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons|journal=Circulation|volume=117|issue=21|pages=e350–e408|doi=10.1161/CIRCUALTIONAHA.108.189742|pmid=18483207|doi-access=free}}</ref>

Numerous studies have been conducted on the use of ICDs for the secondary prevention of SCD. These studies have shown improved survival with ICDs compared to the use of anti-arrhythmic drugs.<ref name="Epstein-2008" /> ICD therapy is associated with a 50% [[Relative risk reduction|relative risk reduction]] in death caused by an arrhythmia and a 25% relative risk reduction in all-cause mortality.<ref>{{cite journal|display-authors=6|vauthors=Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, Greene HL, Boczor S, Domanski M, Follmann D, Gent M, Roberts RS|date=December 2000|title=Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg . Canadian Implantable Defibrillator Study|journal=European Heart Journal|volume=21|issue=24|pages=2071–2078|doi=10.1053/euhj.2000.2476|pmid=11102258|doi-access=free}}</ref>

Primary prevention of SCD with ICD therapy for high-risk patient populations has similarly shown improved survival rates in several large studies. The high-risk patient populations in these studies were defined as those with severe ischemic cardiomyopathy (determined by a reduced [[Medicine:Ejection fraction|left ventricular ejection fraction]] (LVEF)). The LVEF criteria used in these trials ranged from less than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT.<ref name="Epstein-2008" /><ref name="Shun-Shin-2017">{{cite journal |vauthors=Shun-Shin MJ, Zheng SL, Cole GD, Howard JP, Whinnett ZI, Francis DP |date=June 2017 |title=Implantable cardioverter defibrillators for primary prevention of death in left ventricular dysfunction with and without ischaemic heart disease: a meta-analysis of 8567 patients in the 11 trials |journal=European Heart Journal |volume=38 |issue=22 |pages=1738–1746 |doi=10.1093/eurheartj/ehx028 |pmc=5461475 |pmid=28329280}}</ref>

In certain high-risk patient populations (such as patients with LQTS), ICDs are also used to prevent sudden cardiac death ([[Medicine:Preventive healthcare|primary prevention]]).<ref name="Shun-Shin-2017" />

===Crash teams===
In hospital, a cardiac arrest is referred to as a "crash", or a "code". This typically refers to code blue on the [[Medicine:Hospital emergency codes|hospital emergency codes]]. A dramatic drop in vital sign measurements is referred to as "coding" or "crashing", though coding is usually used when it results in cardiac arrest, while crashing might not. Treatment for cardiac arrest is sometimes referred to as "calling a code".

Patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs.<ref name="Resuscitation Council" /><ref name="Kause-2004">{{cite journal |vauthors=Kause J, Smith G, Prytherch D, Parr M, Flabouris A, Hillman K |date=September 2004 |title=A comparison of antecedents to cardiac arrests, deaths and emergency intensive care admissions in Australia and New Zealand, and the United Kingdom--the ACADEMIA study |journal=Resuscitation |volume=62 |issue=3 |pages=275–282 |doi=10.1016/j.resuscitation.2004.05.016 |pmid=15325446}}</ref> This has been attributed to a lack of knowledge and skill amongst ward-based staff, in particular, a failure to measure the [[Respiratory rate|respiratory rate]], which is often the major predictor of a deterioration<ref name="Resuscitation Council" /> and can often change up to 48 hours prior to a cardiac arrest. In response, many hospitals now have increased training for ward-based staff. A number of "early warning" systems also exist that aim to quantify the person's risk of deterioration based on their [[Medicine:Vital signs|vital signs]] and thus provide a guide to staff. In addition, specialist staff are being used more effectively to augment the work already being done at the ward level. These include:
* Crash teams (or code teams) – These are designated staff members with particular expertise in resuscitation who are called to the scene of all arrests within the hospital. This usually involves a specialized cart of equipment (including a [[Engineering:Defibrillation|defibrillator]]) and drugs called a "[[Medicine:Crash cart|crash cart]]" or "crash trolley".
* Medical emergency teams – These teams respond to all emergencies with the aim of treating people in the acute phase of their illness in order to prevent a cardiac arrest. These teams have been found to decrease the rates of in-hospital cardiac arrest (IHCA) and improve survival.<ref name="Kronick-2015" />
* Critical care outreach – In addition to providing the services of the other two types of teams, these teams are responsible for educating non-specialist staff. In addition, they help to facilitate transfers between [[Medicine:Intensive care unit|intensive care/high dependency units]] and the general hospital wards. This is particularly important as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted; the outreach team offers support to ward staff to prevent this from happening.{{citation needed|date=December 2017}}

==Management==
Sudden cardiac arrest may be treated via attempts at [[Medicine:Resuscitation|resuscitation]]. This is usually carried out based on basic life support, [[Medicine:Advanced cardiac life support|advanced cardiac life support]] (ACLS), [[Medicine:Pediatric advanced life support|pediatric advanced life support]] (PALS), or neonatal resuscitation program (NRP) guidelines.<ref name="AHA-2005"/><ref>{{cite journal | title = 2005 American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and neonatal patients: pediatric advanced life support | journal = Pediatrics | volume = 117 | issue = 5 | pages = e1005–e1028 | date = May 2006 | pmid = 16651281 | doi = 10.1542/peds.2006-0346 | s2cid = 46720891 | author1 = American Heart Association }}</ref>
[[File:CPR training-04.jpg|thumb|CPR training on a mannequin]]

===Cardiopulmonary resuscitation===
Early cardiopulmonary resuscitation (CPR) is essential to surviving cardiac arrest with good neurological function.<ref>{{cite web |title=AHA Releases 2015 Heart and Stroke Statistics {{!}} Sudden Cardiac Arrest Foundation |url=https://www.sca-aware.org/sca-news/aha-releases-2015-heart-and-stroke-statistics |website=www.sca-aware.org |access-date=21 September 2019}}</ref><ref name="Walls-2017">{{Cite book|title=Rosen's emergency medicine : concepts and clinical practice| veditors = Walls RM, Hockberger RS, Gausche-Hill M |isbn=9780323390163|oclc=989157341|date = 2017-03-09| vauthors = Walls R, Hockberger R, Gausche-Hill M | publisher = Elsevier Health Sciences }}</ref> It is recommended that it be started as soon as possible with minimal interruptions once begun. The components of CPR that make the greatest difference in survival are chest compressions and defibrillating shockable rhythms.<ref name="Wang-2017">{{Cite book|title=Tintinalli's emergency medicine manual|veditors = Cydulka RK |isbn= 9780071837026 |oclc=957505642|date = 2017-08-28| vauthors = Wang VJ, Joing SA, Fitch MT, Cline DM, John Ma O, Cydulka RK |publisher = McGraw-Hill Education }}</ref> After defibrillation, chest compressions should be continued for two minutes before another rhythm check.<ref name="Walls-2017" /> This is based on a compression rate of 100-120 compressions per minute, a compression depth of 5–6 centimeters into the chest, full chest recoil, and a ventilation rate of 10 breath ventilations per minute.<ref name="Walls-2017" /> Mechanical chest compressions (as performed by a machine) are no better than chest compressions performed by hand.<ref name="Neumar-2015">{{cite journal |display-authors=6 |vauthors=Neumar RW, Shuster M, Callaway CW, Gent LM, Atkins DL, Bhanji F, Brooks SC, de Caen AR, Donnino MW, Ferrer JM, Kleinman ME, Kronick SL, Lavonas EJ, Link MS, Mancini ME, Morrison LJ, O'Connor RE, Samson RA, Schexnayder SM, Singletary EM, Sinz EH, Travers AH, Wyckoff MH, Hazinski MF |date=November 2015 |title=Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S315–S367 |doi=10.1161/cir.0000000000000252 |pmid=26472989 |doi-access=free}}</ref> It is unclear if a few minutes of CPR before defibrillation results in different outcomes than immediate defibrillation.<ref>{{cite journal |vauthors=Huang Y, He Q, Yang LJ, Liu GJ, Jones A |date=September 2014 |title=Cardiopulmonary resuscitation (CPR) plus delayed defibrillation versus immediate defibrillation for out-of-hospital cardiac arrest |journal=The Cochrane Database of Systematic Reviews |volume=9 |issue=9 |pages=CD009803 |doi=10.1002/14651858.CD009803.pub2 |pmc=6516832 |pmid=25212112}}</ref>

Correctly performed bystander CPR has been shown to increase survival, however it is performed in fewer than 30% of out-of-hospital cardiac arrests (OHCAs) {{as of|2007|lc=y}}.<ref name="Mutchner-2007" /> A 2019 meta-analysis found that use of dispatcher-assisted CPR improved outcomes, including survival, when compared with undirected bystander CPR.<ref>{{cite journal | vauthors = Nikolaou N, Dainty KN, Couper K, Morley P, Tijssen J, Vaillancourt C | title = A systematic review and meta-analysis of the effect of dispatcher-assisted CPR on outcomes from sudden cardiac arrest in adults and children | journal = Resuscitation | volume = 138 | pages = 82–105 | date = May 2019 | pmid = 30853623 | doi = 10.1016/j.resuscitation.2019.02.035 | s2cid = 73727100 | url = http://wrap.warwick.ac.uk/114478/1/WRAP-systematic-review-meta-analysis-effect-dispatcher-assisted-CPR-Couper-2019.pdf }}</ref> Likewise, a 2022 systematic review on exercise-related cardiac arrests supported early intervention of bystander CPR and AED use (for shockable rhythms) as they improve survival outcomes.<ref>{{cite journal | vauthors = Grubic N, Hill B, Phelan D, Baggish A, Dorian P, Johri AM | title = Bystander interventions and survival after exercise-related sudden cardiac arrest: a systematic review | journal = British Journal of Sports Medicine | volume = 56 | issue = 7 | pages = 410–416 | date = April 2022 | pmid = 34853034 | doi = 10.1136/bjsports-2021-104623 | s2cid = 244800392 }}</ref>

If high-quality CPR has not resulted in return of spontaneous circulation and the person's heart rhythm is in [[Medicine:Asystole|asystole]], stopping CPR and pronouncing the person's death is generally reasonable after 20 minutes.<ref name="Resuscitation Council (UK)" /> Exceptions to this include certain cases with [[Physics:Hypothermia|hypothermia]] or [[Medicine:Drowning|drowning]] victims.<ref name="Wang-2017" /><ref name="Resuscitation Council (UK)">{{cite web|author1=Resuscitation Council (UK)|title=Pre-hospital cardiac arrest|url=https://www.resus.org.uk/pages/prehosca.pdf|website=www.resus.org.uk|access-date=3 September 2014|page=41|url-status=live|archive-url=https://web.archive.org/web/20150513032323/http://www.resus.org.uk/pages/prehosca.pdf|archive-date=13 May 2015}}</ref> Some of these cases should have longer and more sustained CPR until they are nearly normothermic.<ref name="Wang-2017" />

If cardiac arrest occurs after 20 weeks of pregnancy, the uterus should be pulled or pushed to the left during CPR.<ref name="Lavonas-2015" /> If a pulse has not returned by four minutes, an emergency Cesarean section is recommended.<ref name="Lavonas-2015" />

=== Airway Management ===
High levels of oxygen are generally given during CPR.<ref name="Neumar-2015" /> Either a [[Medicine:Bag valve mask|bag valve mask]] or an [[Medicine:Advanced airway|advanced airway]] may be used to help with breathing particularly since vomiting and regurgitation are common, especially in OHCA.<ref name="Neumar-2015" /><ref>{{cite journal | vauthors = Simons RW, Rea TD, Becker LJ, Eisenberg MS | title = The incidence and significance of emesis associated with out-of-hospital cardiac arrest | journal = Resuscitation | volume = 74 | issue = 3 | pages = 427–431 | date = September 2007 | pmid = 17433526 | doi = 10.1016/j.resuscitation.2007.01.038 }}</ref><ref>
{{cite journal | vauthors = Voss S, Rhys M, Coates D, Greenwood R, Nolan JP, Thomas M, Benger J | title = How do paramedics manage the airway during out of hospital cardiac arrest? | journal = Resuscitation | volume = 85 | issue = 12 | pages = 1662–1666 | date = December 2014 | pmid = 25260723 | pmc = 4265730 | doi = 10.1016/j.resuscitation.2014.09.008 | eissn = 1873-1570 }}</ref> If this occurs, then modification to existing oropharyngeal suction may be required, such as the use of Suction Assisted Laryngoscopy Airway Decontamination.<ref>
{{cite journal | vauthors = Root CW, Mitchell OJ, Brown R, Evers CB, Boyle J, Griffin C, West FM, Gomm E, Miles E, McGuire B, Swaminathan A, St George J, Horowitz JM, DuCanto J | display-authors = 6 | title = Suction Assisted Laryngoscopy and Airway Decontamination (SALAD): A technique for improved emergency airway management | journal = Resuscitation Plus | volume = 1-2 | pages = 100005 | date = 2020-03-01 | pmid = 34223292 | pmc = 8244406 | doi = 10.1016/j.resplu.2020.100005 | doi-access = free }}</ref> 
[[Medicine:Tracheal intubation|Tracheal intubation]] has not been found to improve survival rates or neurological outcomes in cardiac arrest<ref name="Mutchner-2007">{{cite journal | vauthors = Mutchner L | title = The ABCs of CPR--again | journal = The American Journal of Nursing | volume = 107 | issue = 1 | pages = 60–9; quiz 69–70 | date = January 2007 | pmid = 17200636 | doi = 10.1097/00000446-200701000-00024 }}</ref><ref name="White-2018">{{cite journal | vauthors = White L, Melhuish T, Holyoak R, Ryan T, Kempton H, Vlok R | title = Advanced airway management in out of hospital cardiac arrest: A systematic review and meta-analysis | journal = The American Journal of Emergency Medicine | volume = 36 | issue = 12 | pages = 2298–2306 | date = December 2018 | pmid = 30293843 | doi = 10.1016/j.ajem.2018.09.045 | s2cid = 52931036 | url = https://espace.library.uq.edu.au/view/UQ:4f65350/UQ4f65350_OA.pdf }}</ref> and in the prehospital environment, may worsen it.<ref>{{cite journal | vauthors = Studnek JR, Thestrup L, Vandeventer S, Ward SR, Staley K, Garvey L, Blackwell T | title = The association between prehospital endotracheal intubation attempts and survival to hospital discharge among out-of-hospital cardiac arrest patients | journal = Academic Emergency Medicine | volume = 17 | issue = 9 | pages = 918–925 | date = September 2010 | pmid = 20836771 | doi = 10.1111/j.1553-2712.2010.00827.x | doi-access = free }}</ref> Endotracheal tubes and supraglottic airways appear equally useful.<ref name="White-2018" />

Mouth-to-mouth as a means of providing respirations to the patient has been phased out due to the risk of contracting infectious diseases from the patient.<ref>{{cite journal |vauthors=Hallstrom A, Cobb L, Johnson E, Copass M |date=May 2000 |title=Cardiopulmonary resuscitation by chest compression alone or with mouth-to-mouth ventilation |journal=The New England Journal of Medicine |volume=342 |issue=21 |pages=1546–1553 |doi=10.1056/NEJM200005253422101 |pmid=10824072 |doi-access=free}}</ref>

When done by EMS, 30 compressions followed by two breaths appear better than continuous chest compressions and breaths being given while compressions are ongoing.<ref name="Zhan-2017" /> For bystanders, CPR that involves only chest compressions results in better outcomes as compared to standard CPR for those who have gone into cardiac arrest due to heart issues.<ref name="Zhan-2017">{{cite journal | vauthors = Zhan L, Yang LJ, Huang Y, He Q, Liu GJ | title = Continuous chest compression versus interrupted chest compression for cardiopulmonary resuscitation of non-asphyxial out-of-hospital cardiac arrest | journal = The Cochrane Database of Systematic Reviews | volume = 3 | issue = 12 | pages = CD010134 | date = March 2017 | pmid = 28349529 | pmc = 6464160 | doi = 10.1002/14651858.CD010134.pub2 }}</ref>

===Defibrillation===
[[File:Defibrillator-809447 1920.jpg|thumb|upright=1.3|An automated external defibrillator stored in a visible orange mural support]]
Defibrillation is indicated if an electric-shockable heart rhythm is present. The two shockable rhythms are [[Medicine:Ventricular fibrillation|ventricular fibrillation]] and pulseless ventricular tachycardia. These shockable rhythms have a 25-40% likelihood of survival, compared with a significantly lower rate (<5%) in non-shockable rhythms.<ref>{{cite journal | vauthors = Woolcott OO, Reinier K, Uy-Evanado A, Nichols GA, Stecker EC, Jui J, Chugh SS | title = Sudden cardiac arrest with shockable rhythm in patients with heart failure | journal = Heart Rhythm | volume = 17 | issue = 10 | pages = 1672–1678 | date = October 2020 | pmid = 32504821 | pmc = 7541513 | doi = 10.1016/j.hrthm.2020.05.038 }}</ref> The non-shockable rhythms include asystole and pulseless electrical activity (PEA).

Ventricular fibrillation involves the ventricles of the heart (lower chambers responsible for pumping blood) rapidly contracting in an disorganized pattern and thereby limiting blood flow from the heart. This can be due to uncoordinated electrical activity.<ref>{{Cite web |date=2022-03-24 |title=Arrhythmias - What Is an Arrhythmia? {{!}} NHLBI, NIH |url=https://www.nhlbi.nih.gov/health/arrhythmias |access-date=2024-01-31 |website=www.nhlbi.nih.gov |language=en}}</ref> EKG generally shows irregular QRS complexes without P-waves.<ref>{{cite book | vauthors = Ludhwani D, Goayal A, Jagtap M | chapter = Ventricular Fibrillation |date=2024 | title = StatPearls | chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK537120/ |access-date=2024-01-31 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30725805 }}</ref> By contrast, EKG for ventricular tachycardia will generally show a wide complex QRS with >100 beats occurring per minute.<ref>{{cite book | vauthors = Foth C, Gangwani MK, Ahmed I, Alvey H | chapter = Ventricular Tachycardia |date=2024 | title = StatPearls | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK532954/ |access-date=2024-01-31 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30422549 }}</ref> If sustained, ventricular tachycardia can also lead hemodynamic instability and compromise, resulting in pulselessness and poor perfusion to vital organs.
[[File:Defibrillation Electrode Position.jpg|thumb|Demonstration of electrode pad placement for defibrillation.]]
A defibrillator will deliver an electrical current through a pair of electrodes which are placed onto the patient's chest. This is thought to depolarize myocardial tissue thereby stopping the arrhythmia.<ref>{{Cite web | vauthors = Knight BP | date = 23 January 2023 | veditors = Page RL, Dardas TF | title = Basic principles and technique of external electrical cardioversion and defibrillation | work = UpToDate |url=https://www.uptodate.com/contents/basic-principles-and-technique-of-external-electrical-cardioversion-and-defibrillation |access-date=2024-01-18 }}</ref> Defibrillators can deliver energy as monophasic or biphasic waveforms, although biphasic defibrillators are the most common.<ref>{{cite journal | vauthors = Leng CT, Paradis NA, Calkins H, Berger RD, Lardo AC, Rent KC, Halperin HR | title = Resuscitation after prolonged ventricular fibrillation with use of monophasic and biphasic waveform pulses for external defibrillation | journal = Circulation | volume = 101 | issue = 25 | pages = 2968–2974 | date = June 2000 | pmid = 10869271 | doi = 10.1161/01.CIR.101.25.2968 }}</ref><ref name="Schneider 1780–1787">{{cite journal | vauthors = Schneider T, Martens PR, Paschen H, Kuisma M, Wolcke B, Gliner BE, Russell JK, Weaver WD, Bossaert L, Chamberlain D | display-authors = 6 | title = Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Optimized Response to Cardiac Arrest (ORCA) Investigators | journal = Circulation | volume = 102 | issue = 15 | pages = 1780–1787 | date = October 2000 | pmid = 11023932 | doi = 10.1161/01.CIR.102.15.1780 }}</ref>

For ventricular fibrillation, defibrillation techniques may utilized either monophasic or biphasic waveforms. Prior studies suggest that biphasic shock is more likely to produce successful defibrillation after a single shock, however rate of survival is comparable between the methods.<ref name="Schneider 1780–1787"/>

In out-of-hospital arrests, the defibrillation is made by an [[Medicine:Automated external defibrillator|automated external defibrillator]] (AED), a portable machine that can be used by any user. The AED provides voice instructions that guide the process, automatically checks the victim's condition, and applies the appropriate electric shocks. Some defibrillators even provide feedback on the quality of CPR compressions, encouraging the lay rescuer to press the person's chest hard enough to circulate blood.<ref>{{cite web|title=Zoll Automated External Defibrillator (AED) Plus|url=http://www.lifeassisttraining.com/zollaedplus.html|archive-url=https://web.archive.org/web/20110621004342/http://www.lifeassisttraining.com/zollaedplus.html|archive-date=2011-06-21|work=Life Assistance Training}}</ref>

In addition, there is increasing use of public access defibrillation. This involves placing AEDs in public places and training staff in these areas on how to use them. This allows defibrillation to occur prior to the arrival of emergency services, which has been shown to increase chances of survival. It has been shown that those who have arrests in remote locations have worse outcomes following cardiac arrest.<ref name="Lyon-2004">{{cite journal | vauthors = Lyon RM, Cobbe SM, Bradley JM, Grubb NR | title = Surviving out of hospital cardiac arrest at home: a postcode lottery? | journal = Emergency Medicine Journal | volume = 21 | issue = 5 | pages = 619–624 | date = September 2004 | pmid = 15333549 | pmc = 1726412 | doi = 10.1136/emj.2003.010363 }}</ref>

Defibrillation is applied to certain arrhythmias such as ventricular fibrillation and pulseless ventricular tachycardia. Defibrillation cannot be applied to [[Medicine:Asystole|asystole]], and CPR must be initiated first in this case. Moreover, defibrillation is different than [[Medicine:Cardioversion|synchronized cardioversion]]. In synchronized cardioversion, a similar approach is utilized in that electrical current is applied to correct an arrhythmia, however this is used in cases where a pulse is present but the patient is hemodynamically unstable, such as [[Medicine:Supraventricular tachycardia|supraventricular tachycardia]].

Defibrillators may also be used as part of post-cardiac arrest management. These defibrillators include [[Medicine:Wearable cardioverter defibrillator|wearable defibrillator]] (such as LifeVest), subcutaneous cardiac defibrillator, and [[Biology:Implantable cardioverter-defibrillator|implantable cardiac defibrillator]] (ICD).<ref>{{cite journal | vauthors = Chieng D, Paul V, Denman R | title = Current Device Therapies for Sudden Cardiac Death Prevention - the ICD, Subcutaneous ICD and Wearable ICD | journal = Heart, Lung & Circulation | volume = 28 | issue = 1 | pages = 65–75 | date = January 2019 | pmid = 30389367 | doi = 10.1016/j.hlc.2018.09.011 | s2cid = 53272603 }}</ref>

===Medications===
Medications recommended in the ACLS protocol include epinephrine, amiodarone, and lidocaine.<ref name="Kronick-2015" />  The timing and administration of these medications depends on the underlying arrhythmia of the arrest.

* '''Epinephrine:''' Epinephrine acts on the alpha-1 receptor, which in turn increases the blood flow that supplies the heart.<ref>{{Cite web |title=Deep Dive into the Evidence: Epinephrine in Cardiac Arrest |url=http://www.emra.org/emresident/article/deep-dive-epi/ |access-date=2021-11-12 |website=www.emra.org |language=en}}</ref> Epinephrine in adults improves survival<ref>{{cite journal |vauthors=Vargas M, Buonanno P, Iacovazzo C, Servillo G |date=March 2019 |title=Epinephrine for out of hospital cardiac arrest: A systematic review and meta-analysis of randomized controlled trials |journal=Resuscitation |volume=136 |pages=54–60 |doi=10.1016/j.resuscitation.2019.10.026 |pmid=30685547 |s2cid=207940828}}</ref> but does not appear to improve neurologically normal survival.<ref>{{cite journal |vauthors=Aves T, Chopra A, Patel M, Lin S |date=27 November 2019 |title=Epinephrine for Out-of-Hospital Cardiac Arrest: An Updated Systematic Review and Meta-Analysis. |journal=Critical Care Medicine |volume=48 |issue=2 |pages=225–229 |doi=10.1097/CCM.0000000000004130 |pmid=31789700 |s2cid=208537959}}</ref> 
* '''Anti-Arrhythmic Medications:''' [[Chemistry:Amiodarone|Amiodarone]] and [[Chemistry:Lidocaine|lidocaine]] are anti-arrhythmic medications. Amiodarone is a class III anti-arrhythmic. Amiodarone may be used in cases of [[Medicine:Ventricular fibrillation|ventricular fibrillation]], pulseless ventricular tachycardia, and wide complex tachycardia.<ref>{{cite book | vauthors = Florek JB, Lucas A, Girzadas D | chapter = Amiodarone |date=2024 | title = StatPearls | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK482154/ |access-date=2024-01-31 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29489285 }}</ref> Lidocaine is a class Ib anti-arrhythmic, also used to manage acute arrhythmias.<ref>{{cite book | vauthors = Beecham GB, Nessel TA, Goyal A | chapter = Lidocaine |date=2024 | title = StatPearls | chapter-url = http://www.ncbi.nlm.nih.gov/books/NBK539881/ |access-date=2024-01-31 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30969703 }}</ref> Anti-arrhythmic medications may be used after an unsuccessful defibrillation attempt. However, neither lidocaine nor amiodarone, in those who continue in [[Medicine:Ventricular tachycardia|ventricular tachycardia]] or [[Medicine:Ventricular fibrillation|ventricular fibrillation]] despite defibrillation, improves survival to hospital discharge, despite both equally improving survival to hospital admission.<ref>{{cite journal |vauthors=Sanfilippo F, Corredor C, Santonocito C, Panarello G, Arcadipane A, Ristagno G, Pellis T |date=October 2016 |title=Amiodarone or lidocaine for cardiac arrest: A systematic review and meta-analysis |journal=Resuscitation |volume=107 |pages=31–37 |doi=10.1016/j.resuscitation.2016.07.235 |pmid=27496262 |doi-access=free}}</ref>

In ventricular fibrillation and pulseless ventricular tachycardia, 1&nbsp;mg of epinephrine is given every 3–5 minutes, following an initial round of CPR and defibrillation.<ref name="Neumar-2015" /> Doses higher than 1&nbsp;mg of epinephrine are not recommended for routine use in cardiac arrest. Following an additional round of CPR and defibrillation, amiodarone can also be administered. The first dose is given as a 300&nbsp;mg bolus. The second dose is given as a 600&nbsp;mg bolus.<ref name="Neumar-2015" />

If the patient has a non-shockable rhythm (i.e., asystole or PEA), following an initial round of CPR, 1&nbsp;mg of epinephrine should be given every 3–5 minutes, with the goal of obtaining a shockable rhythm.<ref>{{cite journal | vauthors = Panchal AR, Berg KM, Hirsch KG, Kudenchuk PJ, Del Rios M, Cabañas JG, Link MS, Kurz MC, Chan PS, Morley PT, Hazinski MF, Donnino MW | display-authors = 6 | title = 2019 American Heart Association Focused Update on Advanced Cardiovascular Life Support: Use of Advanced Airways, Vasopressors, and Extracorporeal Cardiopulmonary Resuscitation During Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 140 | issue = 24 | pages = e881–e894 | date = December 2019 | pmid = 31722552 | doi = 10.1161/CIR.0000000000000732 | s2cid = 208019248 | doi-access = free }}</ref>

=== Additional medications ===

* '''Bicarbonate:''' [[Chemistry:Sodium bicarbonate|Bicarbonate]], given as sodium bicarbonate, works to stabilize acidosis and [[Medicine:Hyperkalemia|hyperkalemia]], both of which can contribute to and exacerbate cardiac arrest. If acid-base or electrolyte disturbance is evident, bicarbonate may be used. However, if there is little suspicion that these imbalances are occurring and contributing to the arrest, routine use of bicarbonate is not recommended as it does not provide additional benefit.<ref>{{cite journal | vauthors = Xu T, Wu C, Shen Q, Xu H, Huang H | title = The effect of sodium bicarbonate on OHCA patients: A systematic review and meta-analysis of RCT and propensity score studies | journal = The American Journal of Emergency Medicine | volume = 73 | pages = 40–46 | date = November 2023 | pmid = 37611525 | doi = 10.1016/j.ajem.2023.08.020 | s2cid = 260893519 }}</ref>
* '''Calcium:''' [[Chemistry:Calcium chloride|Calcium]], given as calcium chloride, works as an [[Medicine:Inotrope|inotrope]] and vasopressor. Calcium is used in specific circumstances such as electrolyte disturbances (hyperkalemia) and [[Medicine:Calcium channel blocker toxicity|calcium-channel blocker toxicity]]. Overall, calcium is not routinely used during cardiac arrest as it does not provide additional benefit (compared to non-use) and may even cause harm (poor neurologic outcomes).<ref>{{cite journal | vauthors = Messias Hirano Padrao E, Bustos B, Mahesh A, de Almeida Castro M, Randhawa R, John Dipollina C, Cardoso R, Grover P, Adler Maccagnan Pinheiro Besen B | display-authors = 6 | title = Calcium use during cardiac arrest: A systematic review | journal = Resuscitation Plus | volume = 12 | pages = 100315 | date = December 2022 | pmid = 36238582 | pmc = 9550532 | doi = 10.1016/j.resplu.2022.100315 }}</ref>
* '''Vasopressin:''' [[Biology:Vasopressin|Vasopressin]] overall does not improve or worsen outcomes compared to epinephrine.<ref name="Neumar-2015" /> The combination of epinephrine, vasopressin, and [[Chemistry:Methylprednisolone|methylprednisolone]] appears to improve outcomes.<ref>{{cite journal | vauthors = Belletti A, Benedetto U, Putzu A, Martino EA, Biondi-Zoccai G, Angelini GD, Zangrillo A, Landoni G | display-authors = 6 | title = Vasopressors During Cardiopulmonary Resuscitation. A Network Meta-Analysis of Randomized Trials | journal = Critical Care Medicine | volume = 46 | issue = 5 | pages = e443–e451 | date = May 2018 | pmid = 29652719 | doi = 10.1097/CCM.0000000000003049 | url = https://www.zora.uzh.ch/id/eprint/162689/1/document%282%29.pdf | url-status = live | s2cid = 4851288 | archive-date = 5 March 2020 | archive-url = https://web.archive.org/web/20200305002245/https://www.zora.uzh.ch/id/eprint/162689/1/document%282%29.pdf | hdl = 1983/d002beb9-1298-4134-b062-c617f3df43f2 }}</ref> The use of [[Chemistry:Atropine|atropine]], [[Chemistry:Lidocaine|lidocaine]], and [[Chemistry:Amiodarone|amiodarone]] have not been shown to improve survival to hospital discharge following OHCAs.<ref>{{cite journal | vauthors = Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L | title = Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial | journal = JAMA | volume = 302 | issue = 20 | pages = 2222–2229 | date = November 2009 | pmid = 19934423 | doi = 10.1001/jama.2009.1729 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Lin S, Callaway CW, Shah PS, Wagner JD, Beyene J, Ziegler CP, Morrison LJ | title = Adrenaline for out-of-hospital cardiac arrest resuscitation: a systematic review and meta-analysis of randomized controlled trials | journal = Resuscitation | volume = 85 | issue = 6 | pages = 732–740 | date = June 2014 | pmid = 24642404 | doi = 10.1016/j.resuscitation.2014.03.008 }}</ref><ref>{{cite journal | vauthors = Laina A, Karlis G, Liakos A, Georgiopoulos G, Oikonomou D, Kouskouni E, Chalkias A, Xanthos T | display-authors = 6 | title = Amiodarone and cardiac arrest: Systematic review and meta-analysis | journal = International Journal of Cardiology | volume = 221 | pages = 780–788 | date = October 2016 | pmid = 27434349 | doi = 10.1016/j.ijcard.2016.07.138 }}</ref><ref>{{cite journal | vauthors = McLeod SL, Brignardello-Petersen R, Worster A, You J, Iansavichene A, Guyatt G, Cheskes S | title = Comparative effectiveness of antiarrhythmics for out-of-hospital cardiac arrest: A systematic review and network meta-analysis | journal = Resuscitation | volume = 121 | pages = 90–97 | date = December 2017 | pmid = 29037886 | doi = 10.1016/j.resuscitation.2017.10.012 }}</ref><ref>{{cite journal | vauthors = Ali MU, Fitzpatrick-Lewis D, Kenny M, Raina P, Atkins DL, Soar J, Nolan J, Ristagno G, Sherifali D | display-authors = 6 | title = Effectiveness of antiarrhythmic drugs for shockable cardiac arrest: A systematic review | journal = Resuscitation | volume = 132 | pages = 63–72 | date = November 2018 | pmid = 30179691 | doi = 10.1016/j.resuscitation.2018.08.025 | url = http://wrap.warwick.ac.uk/113491/1/WRAP-effectiveness-antiarrhythmic-drugs-cardiac-review-Nolan-2018.pdf | url-status = live | s2cid = 52154562 | archive-url = https://web.archive.org/web/20200305122730/http://wrap.warwick.ac.uk/113491/1/WRAP-effectiveness-antiarrhythmic-drugs-cardiac-review-Nolan-2018.pdf | archive-date = 5 March 2020 }}</ref><ref name="Wang-2017" />
* '''Atropine:''' [[Chemistry:Atropine|Atropine]] is used for symptomatic [[Medicine:Bradycardia|bradycardia]]. It is given at a does of 1&nbsp;mg (IV), and additional 1&nbsp;mg (IV) doses can be given every 3–5 minutes for a total of 3&nbsp;mg. However, the 2010 guidelines from the [[Organization:American Heart Association|American Heart Association]] removed the recommendation for atropine use in [[Medicine:Pulseless electrical activity|pulseless electrical activity]] and [[Medicine:Asystole|asystole]] for lack of evidence supporting its use.<ref>{{cite journal | vauthors = Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ | display-authors = 6 | title = Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 122 | issue = 18 Suppl 3 | pages = S729–S767 | date = November 2010 | pmid = 20956224 | doi = 10.1161/CIRCULATIONAHA.110.970988 | doi-access = free }}</ref><ref name="Wang-2017" />

=== Special Considerations ===

* '''Dialysis patients:''' Hemodialysis patients carry a greater risk of cardiac arrest events. Multiple factors contribute including increased cardiovascular risk factors, electrolyte disturbances (calcium and potassium, caused by accumulation and aggressive removal), and acid-base disturbances.<ref>{{cite journal | vauthors = Makar MS, Pun PH | title = Sudden Cardiac Death Among Hemodialysis Patients | journal = American Journal of Kidney Diseases | volume = 69 | issue = 5 | pages = 684–695 | date = May 2017 | pmid = 28223004 | pmc = 5457912 | doi = 10.1053/j.ajkd.2016.12.006 }}</ref> Indeed, calcium levels are considered a key factor contributing to cardiac arrests in this population.<ref>{{cite journal | vauthors = Kim ED, Parekh RS | title = Calcium and Sudden Cardiac Death in End-Stage Renal Disease | journal = Seminars in Dialysis | volume = 28 | issue = 6 | pages = 624–635 | date = November 2015 | pmid = 26257009 | doi = 10.1111/sdi.12419 | s2cid = 5503149 }}</ref>
* '''TCA overdoses:''' [[Medicine:Tricyclic antidepressant overdose|Tricyclic antidepressant (TCA) overdose]] can lead to cardiac arrest with classic EKG findings including wide QRS and prolonged QTc. Treatment for this condition includes [[Physics:Activated carbon|activated charcoal]] and [[Chemistry:Sodium bicarbonate|sodium bicarbonate]].<ref>{{cite journal | vauthors = Woolf AD, Erdman AR, Nelson LS, Caravati EM, Cobaugh DJ, Booze LL, Wax PM, Manoguerra AS, Scharman EJ, Olson KR, Chyka PA, Christianson G, Troutman WG | display-authors = 6 | title = Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management | journal = Clinical Toxicology | volume = 45 | issue = 3 | pages = 203–233 | date = January 2007 | pmid = 17453872 | doi = 10.1080/15563650701226192 }}</ref>
* '''Torsades de points:''' Magnesium can be given at a does of 2 g (IV or IO bolus) to manage [[Medicine:Torsades de pointes|torsades de points]]. However, without specific indication, magnesium is not generally given in cardiac arrest.<ref>{{Cite journal | vauthors = Ludwin K, Smereka J, Jaguszewski MJ, Filipiak KJ, Ladny JR, Szarpak L, Wozniak S, Evrin T |date=2020-10-28 |title=Place of magnesium sulfate in cardiopulmonary resuscitation. A systematic review and meta-analysis |url=https://journals.viamedica.pl/disaster_and_emergency_medicine/article/view/70952 |journal=Disaster and Emergency Medicine Journal |volume=5 |issue=4 |pages=182–189 |doi=10.5603/DEMJ.a2020.0041 |issn=2543-5957}}</ref> 
* '''Pulmonary embolism:''' In those with a confirmed [[Medicine:Pulmonary embolism|pulmonary embolism]] as the cause of arrest, thrombolytics may be of benefit .<ref>{{cite journal | vauthors = Perrott J, Henneberry RJ, Zed PJ | title = Thrombolytics for cardiac arrest: case report and systematic review of controlled trials | journal = The Annals of Pharmacotherapy | volume = 44 | issue = 12 | pages = 2007–2013 | date = December 2010 | pmid = 21119096 | doi = 10.1345/aph.1P364 | s2cid = 11006778 }}</ref><ref name="Lavonas-2015" /> 
* '''Opioid use:''' Evidence for use of [[Chemistry:Naloxone|naloxone]] in those with cardiac arrest due to [[Chemistry:Opioid|opioid]]s is unclear, but it may still be used.<ref name="Lavonas-2015" /> 
* '''Local anesthetics:''' In those with cardiac arrest due to local anesthetic, [[Chemistry:Lipid emulsion|lipid emulsion]] may be used.<ref name="Lavonas-2015" />

===Targeted temperature management===
Current international guidelines suggest cooling adults after cardiac arrest using [[Biology:Targeted temperature management|targeted temperature management]] (TTM) with the goal of improving neurological outcomes.<ref name="Lindsay-2018">{{cite journal | vauthors = Lindsay PJ, Buell D, Scales DC | title = The efficacy and safety of pre-hospital cooling after out-of-hospital cardiac arrest: a systematic review and meta-analysis | journal = Critical Care | volume = 22 | issue = 1 | pages = 66 | date = March 2018 | pmid = 29534742 | pmc = 5850970 | doi = 10.1186/s13054-018-1984-2 | doi-access = free }}</ref> The process involves cooling for a 24-hour period, with a target temperature of {{convert|32|-|36|C|F|abbr=}}, followed by gradual rewarming over the next 12 to 24 hrs.<ref name="Neumar-2015-3">{{cite journal | vauthors = Neumar RW, Shuster M, Callaway CW, Gent LM, Atkins DL, Bhanji F, Brooks SC, de Caen AR, Donnino MW, Ferrer JM, Kleinman ME, Kronick SL, Lavonas EJ, Link MS, Mancini ME, Morrison LJ, O'Connor RE, Samson RA, Schexnayder SM, Singletary EM, Sinz EH, Travers AH, Wyckoff MH, Hazinski MF | display-authors = 6 | title = Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 132 | issue = 18 Suppl 2 | pages = S315–S367 | date = November 2015 | pmid = 26472989 | doi = 10.1161/cir.0000000000000252 | doi-access = free }}</ref><ref>{{cite book |title=Therapeutic hypothermia after cardiac arrest : clinical application and management |vauthors=Lundbye JB |date=2012 |publisher=Springer |isbn=9781447129509 |location=London |oclc=802346256}}</ref> There are several methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body or infusing cold saline.

The effectiveness of TTM after OHCA is an area of ongoing study. Several recent reviews have found that patients treated with TTM have more favorable neurological outcomes.<ref name="Arrich_2023" /><ref name="Schenone-2016" /> However, pre-hospital TTM after OHCA has been shown to increase the risk of adverse outcomes.<ref name="Lindsay-2018" /> The rates of re-arrest may be higher in people who were treated with pre-hospital TTM.<ref name="Lindsay-2018" /> Moreover, TTM may have adverse neurological effects in people who survive post-cardiac arrest''.''<ref>{{cite journal | vauthors = Kalra R, Arora G, Patel N, Doshi R, Berra L, Arora P, Bajaj NS | title = Targeted Temperature Management After Cardiac Arrest: Systematic Review and Meta-analyses | language = en-US | journal = Anesthesia and Analgesia | volume = 126 | issue = 3 | pages = 867–875 | date = March 2018 | pmid = 29239942 | doi = 10.1213/ANE.0000000000002646 | pmc = 5820193 }}</ref>

===Do not resuscitate===
Some people choose to avoid aggressive measures at the end of life. A do not resuscitate order (DNR) in the form of an advance health care directive makes it clear that in the event of cardiac arrest, the person does not wish to receive cardiopulmonary resuscitation.<ref>{{cite journal | vauthors = Loertscher L, Reed DA, Bannon MP, Mueller PS | title = Cardiopulmonary resuscitation and do-not-resuscitate orders: a guide for clinicians | journal = The American Journal of Medicine | volume = 123 | issue = 1 | pages = 4–9 | date = January 2010 | pmid = 20102982 | doi = 10.1016/j.amjmed.2009.05.029 }}</ref> Other directives may be made to stipulate the desire for [[Medicine:Intubation|intubation]] in the event of [[Medicine:Respiratory failure|respiratory failure]] or, if comfort measures are all that are desired, by stipulating that healthcare providers should "allow natural death".<ref>{{cite journal | vauthors = Knox C, Vereb JA | title = Allow natural death: a more humane approach to discussing end-of-life directives | journal = Journal of Emergency Nursing | volume = 31 | issue = 6 | pages = 560–561 | date = December 2005 | pmid = 16308044 | doi = 10.1016/j.jen.2005.06.020 }}</ref>

===Chain of survival===
Several organizations promote the idea of a [[Medicine:Chain of survival|chain of survival]]. The chain consists of the following "links":
* Early recognition. If possible, recognition of illness before the person develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival, for every minute a patient stays in cardiac arrest, their chances of survival drop by roughly 10%.<ref name="Resuscitation Council"/>
* Early CPR improves the flow of blood and of oxygen to vital organs, an essential component of treating a cardiac arrest. In particular, by keeping the brain supplied with oxygenated blood, the chances of neurological damage are decreased.
* Early defibrillation is effective for the management of [[Medicine:Ventricular fibrillation|ventricular fibrillation]] and pulseless [[Medicine:Ventricular tachycardia|ventricular tachycardia]].<ref name="Resuscitation Council"/>
* Early advanced care.
* Early post-resuscitation care, which may include [[Medicine:Percutaneous coronary intervention|percutaneous coronary intervention]].<ref>{{cite journal | vauthors = Millin MG, Comer AC, Nable JV, Johnston PV, Lawner BJ, Woltman N, Levy MJ, Seaman KG, Hirshon JM | display-authors = 6 | title = Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis | journal = Resuscitation | volume = 108 | pages = 54–60 | date = November 2016 | pmid = 27640933 | doi = 10.1016/j.resuscitation.2016.09.004 }}</ref>

If one or more links in the chain are missing or delayed, then the chances of survival drop significantly.

These protocols are often initiated by a code blue, which usually denotes impending or acute onset of cardiac arrest or [[Medicine:Respiratory failure|respiratory failure]].<ref>{{cite journal | vauthors = Eroglu SE, Onur O, Urgan O, Denizbasi A, Akoglu H | title = Blue code: Is it a real emergency? | journal = World Journal of Emergency Medicine | volume = 5 | issue = 1 | pages = 20–23 | date = 2014 | pmid = 25215142 | pmc = 4129865 | doi = 10.5847/wjem.j.issn.1920-8642.2014.01.003 }}</ref>

===Other===
Resuscitation with [[Engineering:Extracorporeal membrane oxygenation|extracorporeal membrane oxygenation]] devices has been attempted with better results for in-hospital cardiac arrest (29% survival) than OHCA (4% survival) in populations selected to benefit most.<ref>{{cite journal | vauthors = Lehot JJ, Long-Him-Nam N, Bastien O | title = [Extracorporeal life support for treating cardiac arrest] | journal = Bulletin de l'Académie Nationale de Médecine | volume = 195 | issue = 9 | pages = 2025–33; discussion 2033–6 | date = December 2011 | pmid = 22930866 | doi = 10.1016/S0001-4079(19)31894-1 | doi-access = free }}</ref>

[[Medicine:Cardiac catheterization|Cardiac catheterization]] in those who have survived an OHCA appears to improve outcomes, although high-quality evidence is lacking.<ref>{{cite journal | vauthors = Camuglia AC, Randhawa VK, Lavi S, Walters DL | title = Cardiac catheterization is associated with superior outcomes for survivors of out of hospital cardiac arrest: review and meta-analysis | journal = Resuscitation | volume = 85 | issue = 11 | pages = 1533–1540 | date = November 2014 | pmid = 25195073 | doi = 10.1016/j.resuscitation.2014.08.025 | s2cid = 207517242 }}</ref> It is recommended to be done as soon as possible in those who have had a cardiac arrest with [[Medicine:ST elevation|ST elevation]] due to underlying heart problems.<ref name="Neumar-2015" />

The [[Medicine:Precordial thump|precordial thump]] may be considered in those with witnessed, monitored, unstable ventricular tachycardia (including pulseless VT) if a defibrillator is not immediately ready for use, but it should not delay CPR and shock delivery or be used in those with unwitnessed OHCA.<ref>{{cite journal | vauthors = Cave DM, Gazmuri RJ, Otto CW, Nadkarni VM, Cheng A, Brooks SC, Daya M, Sutton RM, Branson R, Hazinski MF | display-authors = 6 | title = Part 7: CPR techniques and devices: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 122 | issue = 18 Suppl 3 | pages = S720–S728 | date = November 2010 | pmid = 20956223 | pmc = 3741663 | doi = 10.1161/CIRCULATIONAHA.110.970970 }}</ref>

==Prognosis==
The overall rate of survival among those who have OHCA is 10%.<ref>{{cite journal | vauthors = Benjamin EJ, Blaha MJ, Chiuve SE, Cushman M, Das SR, Deo R, de Ferranti SD, Floyd J, Fornage M, Gillespie C, Isasi CR, Jiménez MC, Jordan LC, Judd SE, Lackland D, Lichtman JH, Lisabeth L, Liu S, Longenecker CT, Mackey RH, Matsushita K, Mozaffarian D, Mussolino ME, Nasir K, Neumar RW, Palaniappan L, Pandey DK, Thiagarajan RR, Reeves MJ, Ritchey M, Rodriguez CJ, Roth GA, Rosamond WD, Sasson C, Towfighi A, Tsao CW, Turner MB, Virani SS, Voeks JH, Willey JZ, Wilkins JT, Wu JH, Alger HM, Wong SS, Muntner P | display-authors = 6 | title = Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association | journal = Circulation | volume = 135 | issue = 10 | pages = e146–e603 | date = March 2017 | pmid = 28122885 | pmc = 5408160 | doi = 10.1161/CIR.0000000000000485 }}</ref><ref>{{cite journal | vauthors = Kusumoto FM, Bailey KR, Chaouki AS, Deshmukh AJ, Gautam S, Kim RJ, Kramer DB, Lambrakos LK, Nasser NH, Sorajja D | display-authors = 6 | title = Systematic Review for the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society | journal = Circulation | volume = 138 | issue = 13 | pages = e392–e414 | date = September 2018 | pmid = 29084732 | doi = 10.1161/CIR.0000000000000550 | doi-access = free }}</ref> Among those who have an OHCA, 70% occur at home, and their survival rate is 6%.<ref>{{cite book|title=Strategies to Improve Cardiac Arrest Survival: A Time to Act | author = Institute of Medicine |date=2015-06-30|isbn=9780309371995 |doi=10.17226/21723|pmid = 26225413}}</ref><ref>{{cite journal | vauthors = Jollis JG, Granger CB | title = Improving Care of Out-of-Hospital Cardiac Arrest: Next Steps | journal = Circulation | volume = 134 | issue = 25 | pages = 2040–2042 | date = December 2016 | pmid = 27994023 | doi = 10.1161/CIRCULATIONAHA.116.025818 | doi-access = free }}</ref> For those who have an in-hospital cardiac arrest (IHCA), the survival rate one year from at least the occurrence of cardiac arrest is estimated to be 13%.<ref name="Schluep-2018">{{cite journal | vauthors = Schluep M, Gravesteijn BY, Stolker RJ, Endeman H, Hoeks SE | title = One-year survival after in-hospital cardiac arrest: A systematic review and meta-analysis | journal = Resuscitation | volume = 132 | pages = 90–100 | date = November 2018 | pmid = 30213495 | doi = 10.1016/j.resuscitation.2018.09.001 | s2cid = 52270938 | doi-access = free }}</ref> For IHCA, survival to discharge is around 22%.<ref name="Kronick-2015-2">{{cite journal |display-authors=6 |vauthors=Kronick SL, Kurz MC, Lin S, Edelson DP, Berg RA, Billi JE, Cabanas JG, Cone DC, Diercks DB, Foster JJ, Meeks RA, Travers AH, Welsford M |date=November 2015 |title=Part 4: Systems of Care and Continuous Quality Improvement: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S397–S413 |doi=10.1161/cir.0000000000000258 |pmid=26472992 |s2cid=10073267 |doi-access=free}}</ref><ref name="Wang-2017" /> Those who survive to return of spontaneous circulation and hospital admission frequently present with [[Medicine:Post-cardiac arrest syndrome|post-cardiac arrest syndrome]], which usually presents with neurological injury that can range from [[Medicine:Amnesia|mild memory problems]] to [[Medicine:Coma|coma]].<ref name="Wang-2017" /> One-year survival is estimated to be higher in people with cardiac admission diagnoses (39%) when compared to those with non-cardiac admission diagnoses (11%).<ref name="Schluep-2018" />

A 1997 review found rates of survival to discharge of 14%, although different studies varied from 0 to 28%.<ref name="Ballew-1997">{{cite journal |vauthors=Ballew KA |date=May 1997 |title=Cardiopulmonary resuscitation |journal=BMJ |volume=314 |issue=7092 |pages=1462–1465 |doi=10.1136/bmj.314.7092.1462 |pmc=2126720 |pmid=9167565}}</ref> In those over the age of 70 who have a cardiac arrest while in hospital, survival to hospital discharge is less than 20%.<ref name="van Gijn-2014">{{cite journal |vauthors=van Gijn MS, Frijns D, van de Glind EM, C van Munster B, Hamaker ME |date=July 2014 |title=The chance of survival and the functional outcome after in-hospital cardiopulmonary resuscitation in older people: a systematic review |journal=Age and Ageing |volume=43 |issue=4 |pages=456–463 |doi=10.1093/ageing/afu035 |pmid=24760957 |doi-access=free}}</ref> How well these individuals manage after leaving the hospital is not clear.<ref name="van Gijn-2014" />

The global rate of people who were able to recover from OHCA after receiving CPR has been found to be approximately 30%, and the rate of survival to discharge from the hospital has been estimated at 9%.<ref name="Yan-2020">{{cite journal |display-authors=6 |vauthors=Yan S, Gan Y, Jiang N, Wang R, Chen Y, Luo Z, Zong Q, Chen S, Lv C |date=February 2020 |title=The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis |journal=Critical Care |volume=24 |issue=1 |pages=61 |doi=10.1186/s13054-020-2773-2 |pmc=7036236 |pmid=32087741 |doi-access=free}}</ref> Survival to discharge from the hospital is more likely among people whose cardiac arrest was witnessed by a bystander or emergency medical services, who received bystander CPR, and who live in Europe and North America.<ref name="Yan-2020" /> Relatively lower survival to hospital discharge rates have been observed in Asian countries.<ref name="Yan-2020" />

Prognosis is typically assessed 72 hours or more after cardiac arrest.<ref name="Neumar-2015-2">{{cite journal | vauthors = Neumar RW, Shuster M, Callaway CW, Gent LM, Atkins DL, Bhanji F, Brooks SC, de Caen AR, Donnino MW, Ferrer JM, Kleinman ME, Kronick SL, Lavonas EJ, Link MS, Mancini ME, Morrison LJ, O'Connor RE, Samson RA, Schexnayder SM, Singletary EM, Sinz EH, Travers AH, Wyckoff MH, Hazinski MF | display-authors = 6 | title = Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 132 | issue = 18 Suppl 2 | pages = S315–S367 | date = November 2015 | pmid = 26472989 | doi = 10.1161/cir.0000000000000252 | doi-access = free }}</ref> Rates of survival are better in those who had someone witness their collapse, received bystander CPR, and/or had either [[Medicine:Ventricular fibrillation|V-fib]] or [[Medicine:Ventricular tachycardia|V-tach]] when assessed.<ref name="Sasson-2010">{{cite journal | vauthors = Sasson C, Rogers MA, Dahl J, Kellermann AL | title = Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis | journal = Circulation: Cardiovascular Quality and Outcomes | volume = 3 | issue = 1 | pages = 63–81 | date = January 2010 | pmid = 20123673 | doi = 10.1161/circoutcomes.109.889576 | doi-access = free }}</ref> Survival among those with V-fib or V-tach is 15 to 23%.<ref name="Sasson-2010" /> Women are more likely to survive cardiac arrest and leave the hospital than men.<ref>{{cite journal | vauthors = Bougouin W, Mustafic H, Marijon E, Murad MH, Dumas F, Barbouttis A, Jabre P, Beganton F, Empana JP, Celermajer DS, Cariou A, Jouven X | display-authors = 6 | title = Gender and survival after sudden cardiac arrest: A systematic review and meta-analysis | journal = Resuscitation | volume = 94 | pages = 55–60 | date = September 2015 | pmid = 26143159 | doi = 10.1016/j.resuscitation.2015.06.018 }}</ref> [[Medicine:Cerebral hypoxia|Hypoxic ischemic brain injury]] is a concerning outcome for people suffering a cardiac arrest.<ref name="Gräsner-2021">{{cite journal |display-authors=6 |vauthors=Gräsner JT, Herlitz J, Tjelmeland IB, Wnent J, Masterson S, Lilja G, Bein B, Böttiger BW, Rosell-Ortiz F, Nolan JP, Bossaert L, Perkins GD |date=April 2021 |title=European Resuscitation Council Guidelines 2021: Epidemiology of cardiac arrest in Europe |journal=Resuscitation |volume=161 |pages=61–79 |doi=10.1016/j.resuscitation.2021.02.007 |pmid=33773833 |s2cid=232408830 |doi-access=free}}</ref> Most improvements in cognition occur during the first three months following cardiac arrest, with some individuals reporting improvement up to one year post-cardiac arrest.<ref name="Gräsner-2021" /> 50 – 70% of cardiac arrest survivors report fatigue as a symptom.<ref name="Gräsner-2021" />

==Epidemiology==
=== North America ===
The risk of cardiac arrest varies with geographical region, age, and gender. The lifetime risk is three times greater in men (12.3%) than women (4.2%) based on analysis of the [[Framingham Heart Study]].<ref>{{cite journal |vauthors=Lloyd-Jones DM, Berry JD, Ning H, Cai X, Goldberger JJ |date=2009 |title=Lifetime risk for sudden cardiac death at selected index ages and by risk factor strata and race: cardiovascular lifetime risk pooling project |url=https://www.ahajournals.org/doi/abs/10.1161/circ.120.suppl_18.S416-c |journal=Circulation |volume=120 |pages=S416–S417 |doi=10.1161/circ.120.suppl_18.S416-c |doi-broken-date=31 January 2024}}</ref> This gender difference disappeared beyond 85 years of age.<ref name="Zheng-2001-3">{{cite journal |vauthors=Zheng ZJ, Croft JB, Giles WH, Mensah GA |date=October 2001 |title=Sudden cardiac death in the United States, 1989 to 1998 |journal=Circulation |volume=104 |issue=18 |pages=2158–2163 |doi=10.1161/hc4301.098254 |pmid=11684624 |doi-access=free}}</ref> Around half of these individuals are younger than 65 years of age.<ref name="Wang-2017-2">{{Cite book |title=Tintinalli's emergency medicine manual |vauthors=Wang VJ, Joing SA, Fitch MT, Cline DM, John Ma O, Cydulka RK |date=2017-08-28 |publisher=McGraw-Hill Education |isbn=9780071837026 |veditors=Cydulka RK |oclc=957505642}}</ref>

Based on death certificates, sudden cardiac death accounts for about 20% of all deaths in the United States.<ref name="Wong-2019">{{cite journal | vauthors = Wong CX, Brown A, Lau DH, Chugh SS, Albert CM, Kalman JM, Sanders P | title = Epidemiology of Sudden Cardiac Death: Global and Regional Perspectives | language = English | journal = Heart, Lung & Circulation | volume = 28 | issue = 1 | pages = 6–14 | date = January 2019 | pmid = 30482683 | doi = 10.1016/j.hlc.2018.08.026 | s2cid = 53744984 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Zimmerman DS, Tan HL | title = Epidemiology and risk factors of sudden cardiac arrest | language = en-US | journal = Current Opinion in Critical Care | volume = 27 | issue = 6 | pages = 613–616 | date = December 2021 | pmid = 34629421 | doi = 10.1097/MCC.0000000000000896 | s2cid = 238581415 }}</ref> In the United States, approximately 326,000 cases of out-of-hospital and 209,000 cases of IHCA occur among adults annually, which works out to be an incidence of approximately 110.8 per 100,000 adults per year.<ref name="Kronick-2015" /><ref name="Wang-2017" /><ref name="Wong-2019" />

In the United States, during-pregnancy cardiac arrest occurs in about one in twelve-thousand deliveries or 1.8 per 10,000 live births.<ref name="Lavonas-2015">{{cite journal | vauthors = Lavonas EJ, Drennan IR, Gabrielli A, Heffner AC, Hoyte CO, Orkin AM, Sawyer KN, Donnino MW | display-authors = 6 | title = Part 10: Special Circumstances of Resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care | journal = Circulation | volume = 132 | issue = 18 Suppl 2 | pages = S501–S518 | date = November 2015 | pmid = 26472998 | doi = 10.1161/cir.0000000000000264 | doi-access = free }}</ref> Rates are lower in Canada.<ref name="Lavonas-2015" />

=== Other regions ===
Non-Western regions of the world have differing incidences. The incidence of sudden cardiac death in China is 41.8 per 100,000 and in South India is 39.7 per 100,000.<ref name="Wong-2019" />

==Society and culture==
===Names===
In many publications, the stated or implicit meaning of "sudden cardiac death" is sudden [[Biology:Death|death]] from cardiac causes.<ref name="Dorland-2019">{{Cite book| vauthors = Dorland WA |url=http://worldcat.org/oclc/1134470998|title=Dorland's illustrated medical dictionary.|date=9 December 2019|publisher=Elsevier |isbn=978-1-4557-5643-8|oclc=1134470998}}</ref> Some physicians call cardiac arrest "sudden cardiac death" even if the person survives. Thus one can hear mentions of "prior episodes of sudden cardiac death" in a living person.<ref name="Porter-2008">{{cite journal | vauthors = Porter I, Vacek J | title = Single ventricle with persistent truncus arteriosus as two rare entities in an adult patient: a case report | journal = Journal of Medical Case Reports | volume = 2 | pages = 184 | date = May 2008 | pmid = 18513397 | pmc = 2424060 | doi = 10.1186/1752-1947-2-184 | doi-access = free }}</ref>

In 2021, the American Heart Association clarified that "heart attack" is often mistakenly used to describe cardiac arrest. While a heart attack refers to death of heart muscle tissue as a result of blood supply loss, cardiac arrest is caused when the [[Medicine:Electrical conduction system of the heart|heart's electrical system]] malfunctions. Furthermore, the American Heart Association explains that "if corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by CPR and/or [[Engineering:Defibrillation|defibrillation]] or [[Medicine:Cardioversion|cardioversion]], or [[Artificial cardiac pacemaker|cardiac pacing]]. Sudden cardiac death should not be used to describe events that are not fatal".<ref>{{cite journal | vauthors = Virani SS, Alonso A, Aparicio HJ, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Cheng S, Delling FN, Elkind MS, Evenson KR, Ferguson JF, Gupta DK, Khan SS, Kissela BM, Knutson KL, Lee CD, Lewis TT, Liu J, Loop MS, Lutsey PL, Ma J, Mackey J, Martin SS, Matchar DB, Mussolino ME, Navaneethan SD, Perak AM, Roth GA, Samad Z, Satou GM, Schroeder EB, Shah SH, Shay CM, Stokes A, VanWagner LB, Wang NY, Tsao CW | display-authors = 6 | title = Heart Disease and Stroke Statistics-2021 Update: A Report From the American Heart Association | journal = Circulation | volume = 143 | issue = 8 | pages = e254–e743 | date = February 2021 | pmid = 33501848 | doi = 10.1161/CIR.0000000000000950 | s2cid = 231762900 | doi-access = free }}</ref>

===Slow code===
A "slow code" is a slang term for the practice of deceptively delivering sub-optimal CPR to a person in cardiac arrest, when CPR is considered to have no medical benefit.<ref name="Primož">{{Cite book| vauthors = Primož P, Gräsner GD, Semeraro JT, Olasveengen F, Soar T, Lott J, Van de Voorde C, Madar P, Zideman J, Mentzelopoulos DA, Gradišek S |url=http://worldcat.org/oclc/1258336024|title=European Resuscitation Council Guidelines 2021 : executive summary|oclc=1258336024}}</ref> A "show code" is the practice of faking the response altogether for the sake of the person's family.<ref>{{cite news|date=22 August 1987|title=Slow Codes, Show Codes and Death|newspaper={{wipe|The New York Times}}|url=https://www.nytimes.com/1987/08/22/opinion/slow-codes-show-codes-and-death.html|url-status=live|access-date=2013-04-06|archive-url=https://web.archive.org/web/20130518042545/http://www.nytimes.com/1987/08/22/opinion/slow-codes-show-codes-and-death.html|archive-date=18 May 2013}}</ref>

Such practices are ethically controversial<ref>{{cite journal | vauthors = DePalma JA, Ozanich E, Miller S, Yancich LM | title = "Slow" code: perspectives of a physician and critical care nurse | journal = Critical Care Nursing Quarterly | volume = 22 | issue = 3 | pages = 89–97 | date = November 1999 | pmid = 10646457 | doi = 10.1097/00002727-199911000-00014 | url = http://www.nursingcenter.com/lnc/journalarticle?Article_ID=437848 | url-status = dead | publisher = Lippincott Williams and Wilkins | access-date = 2013-04-07 | archive-url = https://web.archive.org/web/20130328192748/http://www.nursingcenter.com/lnc/journalarticle?Article_ID=437848 | archive-date = 2013-03-28 }}</ref> and are banned in some jurisdictions. The European Resuscitation Council Guidelines released a statement in 2021 that clinicians are not suggested to participate/take part in "slow codes".<ref name="Primož" /> According to the American College of Physicians, half-hearted resuscitation efforts are deceptive and should not be performed by physicians or nurses.<ref>{{cite journal | vauthors = Sulmasy LS, Bledsoe TA | title = American College of Physicians Ethics Manual: Seventh Edition | journal = Annals of Internal Medicine | volume = 170 | issue = 2_Suppl | pages = S1–S32 | date = January 2019 | pmid = 30641552 | doi = 10.7326/M18-2160 | s2cid = 58004782 }}</ref>

==Special Populations==
===Children===
In children, the most common cause of cardiac arrest is [[Medicine:Shock (circulatory)|shock]] or [[Medicine:Respiratory failure|respiratory failure]] that has not been treated.<ref name="Walls-2017" /> Cardiac arrhythmias are another possible cause. [[Medicine:Arrhythmia|Arrhythmia]]s such as [[Medicine:Asystole|asystole]] or [[Medicine:Bradycardia|bradycardia]] are more likely in children, in contrast to [[Medicine:Ventricular fibrillation|ventricular fibrillation]] or [[Medicine:Ventricular tachycardia|tachycardia]] as seen in adults.<ref name="Walls-2017" /> Additional causes of sudden unexplained cardiac arrest in children include [[Medicine:Hypertrophic cardiomyopathy|hypertrophic cardiomyopathy]] and coronary artery abnormalities.<ref>{{cite journal |display-authors=6 |vauthors=Topjian AA, Raymond TT, Atkins D, Chan M, Duff JP, Joyner BL, Lasa JJ, Lavonas EJ, Levy A, Mahgoub M, Meckler GD, Roberts KE, Sutton RM, Schexnayder SM |date=January 2021 |title=Part 4: Pediatric Basic and Advanced Life Support 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Pediatrics |volume=147 |issue=Suppl 1 |pages=e2020038505D |doi=10.1542/peds.2020-038505D |pmid=33087552 |s2cid=224826594}}</ref> In childhood hypertrophic cardiomyopathy, previous adverse cardiac events, non-sustained ventricular tachycardia (NSVT), [[Medicine:Syncope|syncope]], and left ventricular hypertrophy (LVT) have been shown to predict sudden cardiac death.<ref>{{cite journal |vauthors=Norrish G, Cantarutti N, Pissaridou E, Ridout DA, Limongelli G, Elliott PM, Kaski JP |date=July 2017 |title=Risk factors for sudden cardiac death in childhood hypertrophic cardiomyopathy: A systematic review and meta-analysis |url=https://discovery.ucl.ac.uk/id/eprint/1556078/ |journal=European Journal of Preventive Cardiology |volume=24 |issue=11 |pages=1220–1230 |doi=10.1177/2047487317702519 |pmid=28482693 |s2cid=206821305 |doi-access=free}}</ref> Other causes can include drugs such as cocaine and [[Chemistry:Methamphetamine|methamphetamine]] or overdose of medications such as antidepressants.<ref name="Walls-2017" />

For management of pediatric cardiac arrest, CPR should be initiated if suspected. PALS guidelines provide algorithms for pediatric cardiac arrest management. Recommended medications during pediatric resuscitation include epinephrine, [[Chemistry:Lidocaine|lidocaine]], and [[Chemistry:Amiodarone|amiodarone]].<ref name="de Caen-2015">{{cite journal |display-authors=6 |vauthors=de Caen AR, Berg MD, Chameides L, Gooden CK, Hickey RW, Scott HF, Sutton RM, Tijssen JA, Topjian A, van der Jagt ÉW, Schexnayder SM, Samson RA |date=November 2015 |title=Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S526–S542 |doi=10.1161/cir.0000000000000266 |pmc=6191296 |pmid=26473000}}</ref><ref name="Wang-2017" /><ref name="Neumar-2015" /> However, the use of [[Chemistry:Sodium bicarbonate|sodium bicarbonate]] or [[Chemistry:Calcium|calcium]] is not recommended.<ref name="Neumar-2015" /><ref>{{cite journal |vauthors=Velissaris D, Karamouzos V, Pierrakos C, Koniari I, Apostolopoulou C, Karanikolas M |date=April 2016 |title=Use of Sodium Bicarbonate in Cardiac Arrest: Current Guidelines and Literature Review |journal=Journal of Clinical Medicine Research |volume=8 |issue=4 |pages=277–283 |doi=10.14740/jocmr2456w |pmc=4780490 |pmid=26985247}}</ref> The use of [[Chemistry:Calcium|calcium]] in children has been associated with poor neurological function as well as decreased survival.<ref name="Walls-2017" /> Correct dosing of medications in children is dependent on weight, and to minimize time spent calculating medication doses, the use of a [[Medicine:Broselow tape|Broselow tape]] is recommended.<ref name="Walls-2017" />

Rates of survival in children are 3 to 16% in North America.<ref name="de Caen-2015-2">{{cite journal |display-authors=6 |vauthors=de Caen AR, Berg MD, Chameides L, Gooden CK, Hickey RW, Scott HF, Sutton RM, Tijssen JA, Topjian A, van der Jagt ÉW, Schexnayder SM, Samson RA |date=November 2015 |title=Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |journal=Circulation |volume=132 |issue=18 Suppl 2 |pages=S526–S542 |doi=10.1161/cir.0000000000000266 |pmc=6191296 |pmid=26473000}}</ref>

== See also ==
* [[Medicine:Chain of survival|Chain of survival]]
* [[Medicine:Post-cardiac arrest syndrome|Post-cardiac arrest syndrome]]
* [[Medicine:Rearrest|Rearrest]]
* [[Biography:Sam Parnia|Sam Parnia]]
* [[Medicine:Sudden cardiac death of athletes|Sudden cardiac death of athletes]]

== References ==
{{Reflist}}

== External links ==
* [http://www.med.upenn.edu/resuscitation/ The Center for Resuscitation Science at the Hospital of the University of Pennsylvania]

{{Medical condition classification and resources
| DiseasesDB      = 2095
| ICD11           = {{ICD11|MC82}}
| ICD10           = {{ICD10|I46}}
| ICD9            = {{ICD9|427.5}}
| ICDO            =
| OMIM            =
| MedlinePlus     =
| eMedicineSubj   =
| eMedicineTopic  =
| MeshID          = D006323
| SNOMED CT       = 410429000
}}
{{Circulatory system pathology}}

{{DEFAULTSORT:Cardiac Arrest}}
[[Category:Cardiac arrhythmia]]
[[Category:Medical emergencies]]
[[Category:Wikipedia medicine articles ready to translate]]

{{Sourceattribution|Cardiac arrest}}