Editing Cardiac arrest (section)

==Causes and mechanisms==
[[File:Basic representation of cardiac conduction.gif|thumb|221x221px|[[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 causes. 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 [[Cardiac conduction system|electrical activity]] in the [[heart muscle]], there is inconsistent contraction of the [[ventricle (heart)|ventricle]]s, which prevents the heart from generating adequate [[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 [[ventricular tachycardia]] and [[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 [[pulseless electrical activity]], [[bradycardia]], and [[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]]
[[Coronary artery disease]] (CAD), also known as atherosclerotic cardiovascular disease, involves the deposition of cholesterol and subsequent inflammation-driven formation of [[Atherosclerosis|atherosclerotic plaques]] in the arteries. CAD involves the accumulation and remodeling of the [[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 [[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 [[stenosis]] of at least one segment of a major [[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 [[arteritis]]), [[embolism]], [[vasospasm]], mechanical abnormalities related to connective tissue diseases or trauma, and congenital [[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 [[Kawasaki disease]]. Other types of [[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.
* [[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 [[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: [[cardiomyopathy|cardiomyopathies]] ([[hypertrophic cardiomyopathy|hypertrophic]], [[dilated cardiomyopathy|dilated]], or [[Arrhythmogenic cardiomyopathy|arrhythmogenic]]), [[Cardiac arrhythmia|cardiac rhythm disturbances]], [[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 [[Hypertension|high blood pressure]], or hypertension, which has led to maladaptive overgrowth of muscular tissue of the [[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 [[Echocardiography|echocardiogram]] and [[Electrocardiography|electrocardiogram]] (EKG).<ref name="Katholi-2011" />

Abnormalities of the cardiac conduction system (notably the [[atrioventricular node]] and [[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 [[genetic disorder]]s.<ref name="Walls-2017" /> The genetic [[mutation]]s often affect specialized proteins known as [[ion channel]]s that conduct [[Ion|electrically charged particles]] across the [[cell membrane]], and this group of conditions is therefore often referred to as [[Channelopathy|channelopathies]]. Examples of these inherited arrhythmia syndromes include [[long QT syndrome]] (LQTS), [[Brugada syndrome]] (BrS), [[catecholaminergic polymorphic ventricular tachycardia]] (CPVT), and [[short QT syndrome]] (SQTS). 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 [[Syncope (medicine)|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 antibiotic|quinolone]] or [[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>

Although it is not recognized as an inherited condition, [[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, pre-excited atrial fibrillation, and cardiac arrest.<ref name="Podrid-2016" />  [[Ebstein's anomaly]] has an increased risk of accessory pathways as well.

===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 [[respiratory arrest]], [[diabetes]], certain [[medication]]s, and [[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 [[Bleeding|hemorrhage]], [[aortic rupture]], [[hypovolemic shock]], [[pulmonary embolism]], poisoning such as from the [[Jellyfish#Toxicity|stings of certain jellyfish]], and [[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 [[Hs and Ts]]. The Hs are [[hypovolemia]], [[Hypoxia (medicine)|hypoxia]], hydrogen cation excess ([[acidosis]]), [[hyperkalemia]], [[hypokalemia]], [[hypothermia]], and [[hypoglycemia]]. The Ts are [[toxin]]s, (cardiac) [[Cardiac tamponade|tamponade]], [[Pneumothorax|tension pneumothorax]], thrombosis ([[myocardial infarction]]), [[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" /> [[Ventricular fibrillation]] and pulseless or sustained [[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>

[[Bradycardia|Bradyarrhythmias]] occur following dissociation of spontaneous electrical conduction and the mechanical function of the heart resulting in [[pulseless electrical activity]] (PEA) or through complete absence of electrical activity of the heart resulting in [[asystole]]. Similar to the result of tachyarrhythmias, these conditions lead to an inability to sustain adequate cardiac output.<ref name="Saunders-2015" />