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==Pathophysiology==
==Pathophysiology==
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded [[electrocardiogram|electrocardiograph]]ic deflections continuously change in shape, magnitude and direction".<ref>{{cite journal |author=Robles de Medina EO, Bernard R, Coumel P, ''et al.'' |title=Definition of terms related to cardiac rhythm. WHO/ISFC Task Force |journal=Eur J Cardiol |volume=8 |issue=2 |pages=127–44 |year=1978 |pmid=699945 |doi= |url=}}</ref>
* Ventricular fibrillation has been described as a "chaotic asynchronous fractionated activity of the heart. A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded [[electrocardiogram|electrocardiograph]]ic deflections continuously change in shape, magnitude, and direction".<ref>{{cite journal |author=Robles de Medina EO, Bernard R, Coumel P, ''et al.'' |title=Definition of terms related to cardiac rhythm. WHO/ISFC Task Force |journal=Eur J Cardiol |volume=8 |issue=2 |pages=127–44 |year=1978 |pmid=699945 |doi= |url=}}</ref>
 
Ventricular fibrillation most commonly occurs within [[disease]]d hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with [[cardiomyopathy]], [[myocarditis]], and other heart pathologies. In addition, it is seen with [[electrolyte disturbance]]s and overdoses of cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.
 
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to [[myocardial infarction]], and 14% of all ventricular fibrillation resuscitations in patients under the age of 40.<ref>{{cite journal |author=Viskin S, Belhassen B |title=Idiopathic ventricular fibrillation |journal=Am. Heart J. |volume=120 |issue=3 |pages=661–71 |year=1990 |pmid=2202193 |doi= 10.1016/0002-8703(90)90025-S|url=http://linkinghub.elsevier.com/retrieve/pii/0002-8703(90)90025-S |format=}}</ref> It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently-described syndromes such as the [[Brugada syndrome]] may give clues to the underlying mechanism of ventricular arrhythmias. In the [[Brugada syndrome]], changes may be found in the resting [[ECG]] with evidence of [[right bundle branch block]] (RBBB) and [[ST elevation]] in the chest leads V1-V3, with an underlying propensity to [[sudden cardiac death]].<ref>{{cite journal |author=Brugada P, Brugada J |title=Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report |journal=J. Am. Coll. Cardiol. |volume=20 |issue=6 |pages=1391–6 |year=1992 |pmid=1309182 |doi= 10.1016/0735-1097(92)90253-J|url=}}</ref>
 
The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of [[sudden cardiac death]] in these patients without pathological evidence of underlying heart disease.<ref>{{cite journal |author=Saumarez RC, Heald S, Gill J, ''et al.'' |title=Primary ventricular fibrillation is associated with increased paced right ventricular electrogram fractionation |journal=Circulation |volume=92 |issue=9 |pages=2565–71 |year=1995 |pmid=7586358 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7586358}}</ref>
 
Familial conditions that predispose individuals to developing ventricular fibrillation and [[sudden cardiac death]] are often the result of [[gene mutation]]s that affect cellular transmembrane ion channels. For example, in [[Brugada syndrome]], sodium channels are affected. In certain forms of [[long QT syndrome]], the potassium inward rectifier channel is affected.
===Triggered Activity===
===Triggered Activity===
Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding [[action potential]]s. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.
The triggered activity can occur due to the presence of after-depolarisations. These are depolarising oscillations in the membrane voltage induced by preceding [[action potential]]s. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed after depolarisations (DADs). All after-depolarisations may not reach threshold potential, but if they do, they can trigger another after-depolarisation, and thus self-perpetuate.
===Abnormal Automaticity===
===Abnormal Automaticity===
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a [[Hypoxia (medical)|hypoxic]] myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one [[pacemaker]]. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.
Automaticity is a measure of the propensity of fiber to initiate an impulse spontaneously. The product of a [[Hypoxia (medical)|hypoxic]] myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one [[pacemaker]]. Scar and dying tissue are inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.
 
It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of [[membrane potential]]. That is, the maximum diastolic potential is less negative and therefore exists closer to the [[threshold potential]]. Cellular depolarisation can be due to a raised external concentration of [[potassium]] ions K<sup>+</sup>, a decreased intracellular concentration of [[sodium]] ions Na<sup>+</sup>, increased permeability to Na<sup>+</sup>, or a decreased permeability to K<sup>+</sup>. The ionic basic automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to &ndash;50 to &ndash;60&nbsp;mV.
 
Myocardial cells are exposed to different environments. Normal cells may be exposed to [[hyperkalemia]], abnormal cells may be perfused by normal environment. For example, with a healed [[myocardial infarction]], abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with [[myocardial ischaemia]]. In conditions such as myocardial ischaemia, possible mechanism of [[arrhythmia]] generation include the resulting decreased internal K<sup>+</sup> concentration, the increased external K<sup>+</sup> concentration, [[norepinephrine]] release and [[acidosis]]. When myocardial cell are exposed to [[hyperkalemia]], the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of [[funny current]] even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the in-saturation of automaticity in ischemic tissue.


===Re-entry===
It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of [[membrane potential]]. That is, the maximum diastolic potential is less negative and therefore exists closer to the [[threshold potential]]. Cellular depolarisation can be due to a raised external concentration of [[potassium]] ions K<sup>+</sup>, a decreased intracellular concentration of [[sodium]] ions Na<sup>+</sup>, increased permeability to Na<sup>+</sup>, or a decreased permeability to K<sup>+</sup>. The ionic basis automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to &ndash;50 to &ndash;60&nbsp;mV.
The role of re-entry or '''circus motion''' was demonstrated separately by Mines and Garrey.<ref>Mines GR 1913, Garrey WE 1914</ref> Mines created a ring of excitable tissue by cutting the atria out of the [[ray fish]]. Garrey cut out a similar ring from the [[turtle]] ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a [[refractory period (physiology)|refractory period]] that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of [[ischaemic]] or [[infarct]]ed myocardium, or underlying [[Myocardial scarring|scar tissue]].


It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the [[wavefront]].
Myocardial cells are exposed to different environments. Normal cells may be exposed to [[hyperkalemia]], abnormal cells may be perfused by the normal environment. For example, with a healed [[myocardial infarction]], abnormal cells can be exposed to an abnormal environment such as with myocardial infarction with [[myocardial ischemia]]. In conditions such as myocardial ischaemia, possible mechanism of [[arrhythmia]] generation include the resulting decreased internal K<sup>+</sup> concentration, the increased external K<sup>+</sup> concentration, [[norepinephrine]] release and [[acidosis]]. When myocardial cell are exposed to [[hyperkalemia]], the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. With Ik1 suppressed, a hyperpolarizing effect is lost and therefore there can be activation of [[funny current]] even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the in-saturation of automaticity in ischemic tissue.


In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through [[hypertrophy]] or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
===Re-entry<ref name="pmid11334828">{{cite journal |vauthors=Samie FH, Jalife J |title=Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart |journal=Cardiovasc. Res. |volume=50 |issue=2 |pages=242–50 |date=May 2001 |pmid=11334828 |doi=10.1016/s0008-6363(00)00289-3 |url=}}</ref><ref name="pmid11879868">{{cite journal |vauthors=Haïssaguerre M, Shah DC, Jaïs P, Shoda M, Kautzner J, Arentz T, Kalushe D, Kadish A, Griffith M, Gaïta F, Yamane T, Garrigue S, Hocini M, Clémenty J |title=Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation |journal=Lancet |volume=359 |issue=9307 |pages=677–8 |date=February 2002 |pmid=11879868 |doi=10.1016/S0140-6736(02)07807-8 |url=}}</ref>===
===Characteristics of the Ventricular Fibrillation Waveform===
The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. Mines created a ring of excitable tissue by cutting the [[atria]] out of the ray fish. Garrey cut out a similar ring from the turtle [[ventricle]]. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of [[ischaemic]] or [[infarct]]ed [[myocardium]], or underlying scar tissue.
Ventricular fibrillation can be described in terms of its electrocardiographic waveform appearance. All waveforms can be described in terms of certain features, such as amplitude and frequency. Researchers have looked at the frequency of the ventricular fibrillation waveform to see if it helps to elucidate the underlying mechanism of the arrhythmia or holds any clinically useful information. More recently, Gray has suggested an underlying mechanism for the frequency of the waveform that has puzzled investigators as possibly being a manifestation of the [[Doppler effect]] of rotors of fibrillation.<ref>{{cite journal |author=Jalife J, Gray RA, Morley GE, Davidenko JM |title=Self-organization and the dynamical nature of ventricular fibrillation |journal=Chaos |volume=8 |issue=1 |pages=79–93 |year=1998 |pmid=12779712 |doi=10.1063/1.166289 |url=}}</ref> Analysis of the fibrillation waveform is performed using a mathematical technique known as [[Fourier analysis]].
====Power Spectrum====
The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured. This can be expressed as either the dominant or peak frequency, i.e., the frequency with the greatest power or the median frequency, which divides the spectrum in two halves. Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics.<ref>{{cite journal |author=Shusterman V, Beigel A, Shah SI, ''et al.'' |title=Changes in autonomic activity and ventricular repolarization |journal=J Electrocardiol |volume=Suppl |issue= |pages=185–92 |series=32 |year=1999 |pmid=10688324 |doi= 10.1016/S0022-0736(99)90078-X|url=}}</ref><ref>{{cite journal |author=Kaplan SR, Bashein G, Sheehan FH, ''et al.'' |title=Three-dimensional echocardiographic assessment of annular shape changes in the normal and regurgitant mitral valve |journal=Am. Heart J. |volume=139 |issue=3 |pages=378–87 |year=2000 |pmid=10689248 |doi= 10.1016/S0002-8703(00)90077-2|url=http://linkinghub.elsevier.com/retrieve/pii/S0002-8703(00)90077-2}}</ref>


[[Image:Lead II rhythm generated ventricular fibrilation VF.jpg|400px|center|thumb|Rhythm generated ventricular fibrillation seen in lead II]]
It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of the ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with the continuation of the [[wavefront]].
<br clear="left"/>


[[Image:Vwivfklein.jpg|800px|left|thumb|Continuous 12 lead EKG recording of a patient with ventricular fibrillation and defibrillation]]
In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through [[hypertrophy]] or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of [[myocardium]] for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
<br clear="left"/>
==Genetics==
[[Genes]] involved in the [[pathogenesis]] of ventricular fibrillation include:<ref name="JabbariRisgaard2015">{{cite journal|last1=Jabbari|first1=Reza|last2=Risgaard|first2=Bjarke|last3=Fosbøl|first3=Emil L.|last4=Scheike|first4=Thomas|last5=Philbert|first5=Berit T.|last6=Winkel|first6=Bo G.|last7=Albert|first7=Christine M.|last8=Glinge|first8=Charlotte|last9=Ahtarovski|first9=Kiril A.|last10=Haunsø|first10=Stig|last11=Køber|first11=Lars|last12=Jørgensen|first12=Erik|last13=Pedersen|first13=Frants|last14=Tfelt-Hansen|first14=Jacob|last15=Engstrøm|first15=Thomas|title=Factors Associated With and Outcomes After Ventricular Fibrillation Before and During Primary Angioplasty in Patients With ST-Segment Elevation Myocardial Infarction|journal=The American Journal of Cardiology|volume=116|issue=5|year=2015|pages=678–685|issn=00029149|doi=10.1016/j.amjcard.2015.05.037}}</ref><ref name="AlbertMacRae2010">{{cite journal|last1=Albert|first1=Christine M.|last2=MacRae|first2=Calum A.|last3=Chasman|first3=Daniel I.|last4=VanDenburgh|first4=Martin|last5=Buring|first5=Julie E.|last6=Manson|first6=JoAnn E.|last7=Cook|first7=Nancy R.|last8=Newton-Cheh|first8=Christopher|title=Common Variants in Cardiac Ion Channel Genes Are Associated With Sudden Cardiac Death|journal=Circulation: Arrhythmia and Electrophysiology|volume=3|issue=3|year=2010|pages=222–229|issn=1941-3149|doi=10.1161/CIRCEP.110.944934}}</ref><ref name="WestawayReinier2011">{{cite journal|last1=Westaway|first1=Shawn K.|last2=Reinier|first2=Kyndaron|last3=Huertas-Vazquez|first3=Adriana|last4=Evanado|first4=Audrey|last5=Teodorescu|first5=Carmen|last6=Navarro|first6=Jo|last7=Sinner|first7=Moritz F.|last8=Gunson|first8=Karen|last9=Jui|first9=Jonathan|last10=Spooner|first10=Peter|last11=Kaab|first11=Stefan|last12=Chugh|first12=Sumeet S.|title=
            Common Variants in
            CASQ2
            ,
            GPD1L
            , and
            NOS1AP
            Are Significantly Associated With Risk of Sudden Death in Patients With Coronary Artery Disease
          |journal=Circulation: Cardiovascular Genetics|volume=4|issue=4|year=2011|pages=397–402|issn=1942-325X|doi=10.1161/CIRCGENETICS.111.959916}}</ref><ref name="KronenbergArking2010">{{cite journal|last1=Kronenberg|first1=Florian|last2=Arking|first2=Dan E.|last3=Reinier|first3=Kyndaron|last4=Post|first4=Wendy|last5=Jui|first5=Jonathan|last6=Hilton|first6=Gina|last7=O'Connor|first7=Ashley|last8=Prineas|first8=Ronald J.|last9=Boerwinkle|first9=Eric|last10=Psaty|first10=Bruce M.|last11=Tomaselli|first11=Gordon F.|last12=Rea|first12=Thomas|last13=Sotoodehnia|first13=Nona|last14=Siscovick|first14=David S.|last15=Burke|first15=Gregory L.|last16=Marban|first16=Eduardo|last17=Spooner|first17=Peter M.|last18=Chakravarti|first18=Aravinda|last19=Chugh|first19=Sumeet S.|title=Genome-Wide Association Study Identifies GPC5 as a Novel Genetic Locus Protective against Sudden Cardiac Arrest|journal=PLoS ONE|volume=5|issue=3|year=2010|pages=e9879|issn=1932-6203|doi=10.1371/journal.pone.0009879}}</ref><ref name="AouizeratVittinghoff2011">{{cite journal|last1=Aouizerat|first1=Bradley E|last2=Vittinghoff|first2=Eric|last3=Musone|first3=Stacy L|last4=Pawlikowska|first4=Ludmila|last5=Kwok|first5=Pui-Yan|last6=Olgin|first6=Jeffrey E|last7=Tseng|first7=Zian H|title=GWAS for discovery and replication of genetic loci associated with sudden cardiac arrest in patients with coronary artery disease|journal=BMC Cardiovascular Disorders|volume=11|issue=1|year=2011|issn=1471-2261|doi=10.1186/1471-2261-11-29}}</ref><ref name="RefaatAouizerat2014">{{cite journal|last1=Refaat|first1=Marwan M.|last2=Aouizerat|first2=Bradley E.|last3=Pullinger|first3=Clive R.|last4=Malloy|first4=Mary|last5=Kane|first5=John|last6=Tseng|first6=Zian H.|title=Association of CASQ2 polymorphisms with sudden cardiac arrest and heart failure in patients with coronary artery disease|journal=Heart Rhythm|volume=11|issue=4|year=2014|pages=646–652|issn=15475271|doi=10.1016/j.hrthm.2014.01.015}}</ref>
* [[Gene mutation]]s that affect cellular transmembrane ion channels.
** For example, in [[Brugada syndrome]], sodium channels are affected. In certain forms of [[long QT syndrome]], the potassium inward rectifier channel is affected.
*[[NOS1AP]]
* CASQ2
*[[ACYP2]]
* ZNF385B
*[[RAB3GAP1]]
*[[SCN5A]]
*[[GPD1L]]
* AGTR1
*[[GRIA1]]
*[[ZNF365]]
* GPC5
*[[AP1G2]]
*[[DEGS2]]
* CXADR
* KCTD1
==Associated Conditions==
[[Conditions]] associated with ventricular fibrillation include:<ref> name="pmid27250216">{{cite journal |vauthors=Khairy P |title=Ventricular arrhythmias and sudden cardiac death in adults with congenital heart disease |journal=Heart |volume=102 |issue=21 |pages=1703–1709 |date=November 2016 |pmid=27250216 |doi=10.1136/heartjnl-2015-309069 |url=}}</ref><ref name="pmid28222965">{{cite journal |vauthors=Maury P, Sacher F, Rollin A, Mondoly P, Duparc A, Zeppenfeld K, Hascoet S |title=Ventricular arrhythmias and sudden death in tetralogy of Fallot |journal=Arch Cardiovasc Dis |volume=110 |issue=5 |pages=354–362 |date=May 2017 |pmid=28222965 |doi=10.1016/j.acvd.2016.12.006 |url=}}</ref><ref name="pmid1638716">{{cite journal |vauthors=Saumarez RC, Camm AJ, Panagos A, Gill JS, Stewart JT, de Belder MA, Simpson IA, McKenna WJ |title=Ventricular fibrillation in hypertrophic cardiomyopathy is associated with increased fractionation of paced right ventricular electrograms |journal=Circulation |volume=86 |issue=2 |pages=467–74 |date=August 1992 |pmid=1638716 |doi=10.1161/01.cir.86.2.467 |url=}}</ref><ref name="BektasSoyuncu2012">{{cite journal|last1=Bektas|first1=Firat|last2=Soyuncu|first2=Secgin|title=Hypokalemia-induced Ventricular Fibrillation|journal=The Journal of Emergency Medicine|volume=42|issue=2|year=2012|pages=184–185|issn=07364679|doi=10.1016/j.jemermed.2010.05.079}}</ref><ref name="KlasnerScalzo1996">{{cite journal|last1=Klasner|first1=Ann E|last2=Scalzo|first2=Anthony J|last3=Blume|first3=Carolyn|last4=Johnson|first4=Paul|last5=Thompson|first5=Michael W|title=Marked Hypocalcemia and Ventricular Fibrillation in Two Pediatric Patients Exposed to a Fluoride-Containing Wheel Cleaner|journal=Annals of Emergency Medicine|volume=28|issue=6|year=1996|pages=713–718|issn=01960644|doi=10.1016/S0196-0644(96)70097-5}}</ref><ref name="pmid3181653">{{cite journal |vauthors=Billman GE, Hoskins RS |title=Cocaine-induced ventricular fibrillation: protection afforded by the calcium antagonist verapamil |journal=FASEB J. |volume=2 |issue=14 |pages=2990–5 |date=November 1988 |pmid=3181653 |doi=10.1096/fasebj.2.14.3181653 |url=}}</ref><ref name="HeistRuskin2010">{{cite journal|last1=Heist|first1=E. Kevin|last2=Ruskin|first2=Jeremy N.|title=Drug-Induced Arrhythmia|journal=Circulation|volume=122|issue=14|year=2010|pages=1426–1435|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.109.894725}}</ref>
* Ischemic heart disease.
* [[Cardiomyopathy]]
* [[Myocarditis]]
* [[Brugada syndrome]]
* Other heart pathologies
* [[Electrolyte disturbance]]
* Overdoses of cardiotoxic drugs


==References==
==References==

Latest revision as of 18:52, 3 March 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a coordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood into the arteries and systemic circulation. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, and it is mostly caused by ischemic heart disease. While most episodes occur in diseased hearts, others can afflict normal hearts as well. Despite considerable research, the underlying nature of ventricular fibrillation is still not completely understood.

Pathophysiology

  • Ventricular fibrillation has been described as a "chaotic asynchronous fractionated activity of the heart. A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude, and direction".[1]

Triggered Activity

The triggered activity can occur due to the presence of after-depolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed after depolarisations (DADs). All after-depolarisations may not reach threshold potential, but if they do, they can trigger another after-depolarisation, and thus self-perpetuate.

Abnormal Automaticity

Automaticity is a measure of the propensity of fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue are inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.

It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Cellular depolarisation can be due to a raised external concentration of potassium ions K+, a decreased intracellular concentration of sodium ions Na+, increased permeability to Na+, or a decreased permeability to K+. The ionic basis automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV.

Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalemia, abnormal cells may be perfused by the normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with myocardial infarction with myocardial ischemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration, the increased external K+ concentration, norepinephrine release and acidosis. When myocardial cell are exposed to hyperkalemia, the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. With Ik1 suppressed, a hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the in-saturation of automaticity in ischemic tissue.

Re-entry[2][3]

The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.

It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of the ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with the continuation of the wavefront.

In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.

Genetics

Genes involved in the pathogenesis of ventricular fibrillation include:[4][5][6][7][8][9]

Associated Conditions

Conditions associated with ventricular fibrillation include:[10][11][12][13][14][15][16]

References

  1. ↑ Robles de Medina EO, Bernard R, Coumel P; et al. (1978). "Definition of terms related to cardiac rhythm. WHO/ISFC Task Force". Eur J Cardiol. 8 (2): 127–44. PMID 699945.
  2. ↑ Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  3. ↑ Haïssaguerre M, Shah DC, Jaïs P, Shoda M, Kautzner J, Arentz T, Kalushe D, Kadish A, Griffith M, Gaïta F, Yamane T, Garrigue S, Hocini M, Clémenty J (February 2002). "Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation". Lancet. 359 (9307): 677–8. doi:10.1016/S0140-6736(02)07807-8. PMID 11879868.
  4. ↑ Jabbari, Reza; Risgaard, Bjarke; Fosbøl, Emil L.; Scheike, Thomas; Philbert, Berit T.; Winkel, Bo G.; Albert, Christine M.; Glinge, Charlotte; Ahtarovski, Kiril A.; Haunsø, Stig; Køber, Lars; Jørgensen, Erik; Pedersen, Frants; Tfelt-Hansen, Jacob; Engstrøm, Thomas (2015). "Factors Associated With and Outcomes After Ventricular Fibrillation Before and During Primary Angioplasty in Patients With ST-Segment Elevation Myocardial Infarction". The American Journal of Cardiology. 116 (5): 678–685. doi:10.1016/j.amjcard.2015.05.037. ISSN 0002-9149.
  5. ↑ Albert, Christine M.; MacRae, Calum A.; Chasman, Daniel I.; VanDenburgh, Martin; Buring, Julie E.; Manson, JoAnn E.; Cook, Nancy R.; Newton-Cheh, Christopher (2010). "Common Variants in Cardiac Ion Channel Genes Are Associated With Sudden Cardiac Death". Circulation: Arrhythmia and Electrophysiology. 3 (3): 222–229. doi:10.1161/CIRCEP.110.944934. ISSN 1941-3149.
  6. ↑ Westaway, Shawn K.; Reinier, Kyndaron; Huertas-Vazquez, Adriana; Evanado, Audrey; Teodorescu, Carmen; Navarro, Jo; Sinner, Moritz F.; Gunson, Karen; Jui, Jonathan; Spooner, Peter; Kaab, Stefan; Chugh, Sumeet S. (2011). "Common Variants in CASQ2 , GPD1L , and NOS1AP Are Significantly Associated With Risk of Sudden Death in Patients With Coronary Artery Disease". Circulation: Cardiovascular Genetics. 4 (4): 397–402. doi:10.1161/CIRCGENETICS.111.959916. ISSN 1942-325X. line feed character in |title= at position 19 (help)
  7. ↑ Kronenberg, Florian; Arking, Dan E.; Reinier, Kyndaron; Post, Wendy; Jui, Jonathan; Hilton, Gina; O'Connor, Ashley; Prineas, Ronald J.; Boerwinkle, Eric; Psaty, Bruce M.; Tomaselli, Gordon F.; Rea, Thomas; Sotoodehnia, Nona; Siscovick, David S.; Burke, Gregory L.; Marban, Eduardo; Spooner, Peter M.; Chakravarti, Aravinda; Chugh, Sumeet S. (2010). "Genome-Wide Association Study Identifies GPC5 as a Novel Genetic Locus Protective against Sudden Cardiac Arrest". PLoS ONE. 5 (3): e9879. doi:10.1371/journal.pone.0009879. ISSN 1932-6203.
  8. ↑ Aouizerat, Bradley E; Vittinghoff, Eric; Musone, Stacy L; Pawlikowska, Ludmila; Kwok, Pui-Yan; Olgin, Jeffrey E; Tseng, Zian H (2011). "GWAS for discovery and replication of genetic loci associated with sudden cardiac arrest in patients with coronary artery disease". BMC Cardiovascular Disorders. 11 (1). doi:10.1186/1471-2261-11-29. ISSN 1471-2261.
  9. ↑ Refaat, Marwan M.; Aouizerat, Bradley E.; Pullinger, Clive R.; Malloy, Mary; Kane, John; Tseng, Zian H. (2014). "Association of CASQ2 polymorphisms with sudden cardiac arrest and heart failure in patients with coronary artery disease". Heart Rhythm. 11 (4): 646–652. doi:10.1016/j.hrthm.2014.01.015. ISSN 1547-5271.
  10. ↑ name="pmid27250216">Khairy P (November 2016). "Ventricular arrhythmias and sudden cardiac death in adults with congenital heart disease". Heart. 102 (21): 1703–1709. doi:10.1136/heartjnl-2015-309069. PMID 27250216.
  11. ↑ Maury P, Sacher F, Rollin A, Mondoly P, Duparc A, Zeppenfeld K, Hascoet S (May 2017). "Ventricular arrhythmias and sudden death in tetralogy of Fallot". Arch Cardiovasc Dis. 110 (5): 354–362. doi:10.1016/j.acvd.2016.12.006. PMID 28222965.
  12. ↑ Saumarez RC, Camm AJ, Panagos A, Gill JS, Stewart JT, de Belder MA, Simpson IA, McKenna WJ (August 1992). "Ventricular fibrillation in hypertrophic cardiomyopathy is associated with increased fractionation of paced right ventricular electrograms". Circulation. 86 (2): 467–74. doi:10.1161/01.cir.86.2.467. PMID 1638716.
  13. ↑ Bektas, Firat; Soyuncu, Secgin (2012). "Hypokalemia-induced Ventricular Fibrillation". The Journal of Emergency Medicine. 42 (2): 184–185. doi:10.1016/j.jemermed.2010.05.079. ISSN 0736-4679.
  14. ↑ Klasner, Ann E; Scalzo, Anthony J; Blume, Carolyn; Johnson, Paul; Thompson, Michael W (1996). "Marked Hypocalcemia and Ventricular Fibrillation in Two Pediatric Patients Exposed to a Fluoride-Containing Wheel Cleaner". Annals of Emergency Medicine. 28 (6): 713–718. doi:10.1016/S0196-0644(96)70097-5. ISSN 0196-0644.
  15. ↑ Billman GE, Hoskins RS (November 1988). "Cocaine-induced ventricular fibrillation: protection afforded by the calcium antagonist verapamil". FASEB J. 2 (14): 2990–5. doi:10.1096/fasebj.2.14.3181653. PMID 3181653.
  16. ↑ Heist, E. Kevin; Ruskin, Jeremy N. (2010). "Drug-Induced Arrhythmia". Circulation. 122 (14): 1426–1435. doi:10.1161/CIRCULATIONAHA.109.894725. ISSN 0009-7322.

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