Materiały źródłowe

• #1 Ventricular fibrillation pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Ventricular_fibrillation_pathophysiology

  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. […] 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”.

• #2 Ventricular fibrillation – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/ventricular-fibrillation/symptoms-causes/syc-20364523

  Ventricular fibrillation is a type of irregular heart rhythm (arrhythmia). During ventricular fibrillation, the lower heart chambers contract in a very rapid and uncoordinated manner. As a result, the heart doesn’t pump blood to the rest of the body. […] Ventricular fibrillation is caused by either: A problem in the heart’s electrical properties […] A disruption of the blood supply to the heart muscle. […] In ventricular fibrillation, rapid, irregular electrical signals cause the ventricles to quiver uselessly instead of pumping blood. […] The typical heart has four chambers two upper chambers (atria) and two lower chambers (ventricles). […] In a typical heart, this heart signaling process usually goes smoothly, resulting in a typical resting heart rate of 60 to 100 beats a minute. But in ventricular fibrillation, rapid, irregular electrical signals cause the lower heart chambers to quiver uselessly instead of pumping blood.

• #3 Ventricular fibrillation – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/ventricular-fibrillation/symptoms-causes/syc-20364523

  Without immediate treatment, ventricular fibrillation can cause death within minutes. The condition’s rapid, erratic heartbeats cause the heart to abruptly stop pumping blood to the body. Blood pressure drops suddenly and significantly. The longer the body lacks blood, the greater the risk of damage to the brain and other organs.

• #4 Ventricular fibrillation pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Ventricular_fibrillation_pathophysiology

  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. […] 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”.

• #5 Ventricular Fibrillation – ECG book

  https://www.ecgbook.com/ventricular-fibrillation/

  Ventricular fibrillation is an electrical chaos of ventricular impulses. The ventricles (QRS complexes) quiver at a rate of 300-450/min. The ventricles contract in a disorganized manner and the heart does not function as a pump. This is the fundamental difference from polymorphic ventricular tachycardia. During ventricular fibrillation: Syncope within 10 seconds (loss of consciousness). Irreversible brain damage in 3-5 minutes. Often progresses to asystole within 2 minutes. It is the most common cause of sudden cardiac death. Requires urgent treatment – electrical defibrillation. Almost always occurs in structurally or electrically damaged ventricles. Most commonly during myocardial infarction. The mechanism of ventricular fibrillation is not clear, but the most likely are 2 mechanisms: Multiple Micro Re-entries. In the ventricles, there are numerous micro re-entries which generate impulses independently of each other. The ventricles quiver at a frequency of 300 – 450/min. Mother Rotor Re-entry Circuit. In the ventricles, there is a mother macro re-entry from which additional micro re-entries arise. Micro re-entries generate impulses independently of each other. The ventricles quiver at a frequency of 300 – 450/min. Most often triggered by ventricular extrasystole. Which occurs during the vulnerable period of the cycle (corresponding to the T wave on the ECG). Referred to as R-on-T phenomenon. These extrasystoles most commonly arise in the myocardium after a myocardial infarction. The R-on-T phenomenon can induce ventricular fibrillation in 3 situations: During acute myocardial infarction, In cases of extreme hypokalemia, In the presence of prolonged QT interval. The heart does not function as a pump. At such a high frequency, diastole is ineffective. This is a key difference from polymorphic VT. QRS complexes decrease in amplitude and after about 2 minutes, asystole occurs.

• #6 Ventricular Fibrillation – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537120/

  Arrhythmias originating from the ventricular myocardium or His-Purkinje system are grouped under ventricular arrhythmia (VA). This includes a subset of arrhythmias such as ventricular tachycardia (VT), ventricular fibrillation (VF), premature ventricular contractions (PVC), and ventricular flutter. Wide complex tachycardia (WCT) is used to define all tachyarrhythmia with QRS complex duration greater than 0.12 seconds. VF is a WCT caused by irregular electrical activity and characterized by a ventricular rate of usually greater than 300 with discrete QRS complexes on the electrocardiogram (ECG). This activity reviews the causes, pathophysiology, and presentation of VF and highlights the role of the interprofessional team in its management. […] VF occurs when parts of ventricular myocardium depolarize erratically in an uncoordinated manner. VF results from the following:

• #7 Ventricular Fibrillation – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537120/

  Abnormal Impulse Formation […] Increased automaticity: Purkinje cells around ischemic areas during MI can initiate ventricular tachycardia. […] Triggered activity: Early and late after depolarization can overcome refractory threshold and generate triggered potential causing extrasystoles. […] Impulse Conduction […] Functional and anatomical reentry circuits help sustain ventricular arrhythmia.

• #8 Ventricular Fibrillation (VF) • LITFL • ECG Library Diagnosis

  https://litfl.com/ventricular-fibrillation-vf-ecg-library/

  Ventricular fibrillation (VF) is the most important shockable cardiac arrest rhythm. It is invariably fatal unless advanced life support is rapidly instituted. […] The underlying mechanism of VF is not fully understood. Several mechanisms have been hypothesised: […] Multiple wavelet mechanism: Multiple small wandering wavelets are formed, and the fibrillation is maintained by re-entry circuits formed by some of these wavelets […] Mother rotor mechanism: A stable re-entry circuit is formed, the mother rotor. The mother rotor then gives rise to propagating unstable daughter wavefronts, which results in the chaotic electrical activity seen on the ECG. Animal models suggest in any instance of VF there may be one or multiple mother rotors.

• #9 Ventricular fibrillation: mechanisms of initiation and maintenance – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10845083/

  Ventricular fibrillation (VF) is the major immediate cause of sudden cardiac death. Traditionally, VF has been defined as turbulent cardiac electrical activity, which implies a large amount of irregularity in the electrical waves that underlie ventricular excitation. During VF, the heart rate is too high ( 550 excitations/minute) to allow adequate pumping of blood. In the electrocardiogram (ECG), ventricular complexes that are ever-changing in frequency, contour, and amplitude characterize VF. This article reviews prevailing theories for the initiation and maintenance of VF, as well as its spatio-temporal organization. Particular attention is given to recent experiments and computer simulations suggesting that VF may be explained in terms of highly periodic three-dimensional rotors that activate the ventricles at exceedingly high frequency. Such rotors may show at least two different behaviors: (a) At one extreme, they may drift throughout the heart at high speeds producing beat-to-beat changes in the activation sequence. (b) At the other extreme, rotors may be relatively stationary, activating the ventricles at such high frequencies that the wave fronts emanating from them breakup at varying distances, resulting in complex spatio-temporal patterns of fibrillatory conduction. In either case, the recorded ECG patterns are indistinguishable from VF. The data discussed have paved the way for a better understanding of the mechanisms of VF in the normal, as well as the diseased, human heart.

• #10 Mechanism of Ventricular Fibrillation: Current Status and Problems Advanced Biomedical Engineering

  https://abe-journal.org/issues/2022/06/22/688

  Ventricular fibrillation (VF) causes failure of synchronous contraction of the heart ventricles, resulting in cardiac collapse. Currently, VF is still the major cause of sudden cardiac death, and strategies such as prevention, prediction, and immediate termination are not yet established. This article reviews the progress of research on VF mechanism and proposes a future direction to elucidate it. Historical hypotheses proposed for VF mechanism were wandering wavelets, mother rotors, and multiple foci. Current concept is a combination of these hypotheses, but remains to be explicated. Rotor, a spiral shape of the excitation wavefront, plays a major role in VF. The mother rotor eventually breaks up and creates multiple unstable rotors by pathological and electrophysiological abnormalities, terminating as irreversible VF. The dynamics of rotors are influenced by many factors such as ion channel modification, alternance of intracellular calcium, and restitution characteristics of the repolarization duration. The break-up of a rotor is created by headtail interaction of the rotor, or the area of the ischemic tissue zone.

• #11 Ventricular Fibrillation | Thoracic Key

  https://thoracickey.com/ventricular-fibrillation/

  The conduction system has been carefully studied in several young persons who were living a normal life and died suddenly. […] Despite such pathologic findings in and around the conduction system, these persons were considered to be asymptomatic, and SCD was the first manifestation of the disorder. […] Clinically, in almost all, VF was the only common denominator observed by the paramedics at the time of resuscitation. […] VF is generated by self-sustained re-entrant circuits that turn around regions of conduction block. […] Re-entrant excitation is the fundamental mechanism responsible for VF. […] VF is commonly caused by acute myocardial ischemia. […] The process of tissue healing and scar formation after an episode of acute myocardial ischemia involves necrosis of the infarcted region as well as swelling and hypertrophy of the noninfarcted region as it attempts to compensate for the loss of cardiac muscle.

• #12 Reentry and the development of cardiac arrhythmias – UpToDate

  https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print

  Cardiac arrhythmias are generally produced by one of three mechanisms: enhanced automaticity, triggered activity, or reentry. The most common mechanism is reentry. […] Reentry occurs when a propagating impulse persists as a result of continuous activity around a circuit within the myocardium and reexcites the heart after the refractory period has ended. It is the electrophysiologic mechanism responsible for the majority of clinically important arrhythmias. […] Ventricular fibrillation (which, like atrial fibrillation, involves multiple reentrant circuits in the ventricular myocardium, each circuit activating small areas of the ventricular myocardium, and, hence, there is no organized ventricular activation or contraction).

• #13 Ventricular fibrillation pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Ventricular_fibrillation_pathophysiology

  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. […] The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. […] 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.

• #14 Ventricular fibrillation – Wikipedia

  https://en.wikipedia.org/wiki/Ventricular_fibrillation

  Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations 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. […] The role of re-entry or circus motion was demonstrated separately by G. R. Mines and W. E. Garrey. 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. […] Triggered activity can occur due to the presence of afterdepolarisations. 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 afterdepolarizations (DADs).

• #15 Ventricular fibrillation pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Ventricular_fibrillation_pathophysiology

  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. […] 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.

• #16 Idiopathic Ventricular Fibrillation: Diagnosis, Ablation of Triggers, Gaps in Knowledge, and Future Directions

  https://www.innovationsincrm.com/cardiac-rhythm-management/articles-2020/june/1605-idiopathic-ventricular-fibrillation

  A meticulous inspection of the 12-lead ECG should be done to exclude any pathologic ECG findings including the early-repolarization J-wave syndrome phenotypes or QT syndromes. […] The use of provocation tests to survey for concealed sodium or potassium channel mutation should be considered when no apparent structural [normal two-dimensional echo, coronary angiogram, and cardiac magnetic resonance imaging (MRI)] or molecular mechanism is identified. […] The Purkinje system is an endocardial structure in humans and constitutes 1% to 2% of the myocardium mass. […] Given that the distal Purkinje system is overwhelmingly the source of PVC-VF triggers in patients with and without structural or molecular abnormalities, one should suspect distal Purkinje arrhythmogenic disease (DPAD), diffuse or focal and idiopathic or organic, as the common pathway for the initiation of VF.

• #17 Idiopathic Ventricular Fibrillation: Diagnosis, Ablation of Triggers, Gaps in Knowledge, and Future Directions

  https://www.innovationsincrm.com/cardiac-rhythm-management/articles-2020/june/1605-idiopathic-ventricular-fibrillation

  The distal Purkinje arborization-ventricular muscle junction has dual perfusion through the systemic and cavital blood. […] Therefore, Purkinje cells can survive in an anaerobic environment. […] Further investigations are needed to better understand the functional, molecular, or anatomic substrate underlying these fatal rhythm phenotypes.

• #18 Ventricular Fibrillation: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/158712-overview

  Ventricular fibrillation (VF) occurs in a variety of clinical situations but is most often associated with coronary artery disease (CAD). VF can result from acute myocardial infarction (MI) or ischemia, or from myocardial scarring from an old infarct. […] Initiation of VF can occur in several ways. For example, if the myocardium is stimulated by a ventricular premature complex (VPC) during the ascending limb of the T wave, the impulse can propagate erratically through the variably refractory myocardial cells and establish reentrant patterns that result in chaotic ventricular depolarization. Consequently, coordinated myocardial contraction becomes disrupted. […] The reentrant patterns break up into multiple smaller wavelets and the level of disorganization increases, with reentrant circuits producing high-frequency activation of cardiac muscle fibers. As the heart loses its ability to pump blood, myocardial ischemia worsens and a self-perpetuating vicious cycle ensues, leading to death if not corrected.

• #19 Premature Ventricular Complexes as a Trigger for Ventricular Fibrillation – Revista Española de Cardiología (English Edition)

  https://www.revespcardiol.org/en-premature-ventricular-complexes-as-trigger-articulo-13154106

  Spontaneous VF in the form of an arrhythmic storm or an isolated episode were triggered by PVCs. […] The mechanisms that trigger ventricular fibrillation (VF) are poorly understood. […] To study the mechanism underlying the initiation of isolated VF or VF recurrence in arrhythmic storm, we analyzed ICD-recorded data of patients experiencing spontaneous VF episodes. […] The PVC that precedes VF initiation has been known for some time and instances of primary VF in acute myocardial infarction have been described. […] More recently, this has been believed to be the mechanism that triggers VF episodes in arrhythmic storm, and VF recurrence has been avoided by using ablation to eliminate it. […] We do not know why some premature beats trigger VF and others, with no obvious electrophysiological differences, do not. […] This could be of interest in targeted VF ablation procedures, if we assume that it could be induced. […] Spontaneous VF is triggered by PVCs both in cases of arrhythmic storm and in isolated episodes.

• #20 Dynamic mechanism for initiation of ventricular fibrillation in vivo.

  https://vivo.weill.cornell.edu/display/pubid18725487

  Dynamically induced heterogeneities of repolarization may lead to wave-front destabilizations and initiation of ventricular fibrillation (VF). […] The purpose of this study was to determine whether the computer model results pertained to the initiation of VF in dogs in vivo. […] Delivery of CL(VF) was associated with discordant action potential duration alternans and induction of VF in all dogs. […] Maximizing dynamically induced spatial dispersion of repolarization appears to be an effective method for inducing VF. […] Reducing spatial dispersion of refractoriness by modulating restitution parameters can have an antifibrillatory effect in vivo.

• #21 Genetic basis and molecular mechanism for idiopathic ventricular fibrillation | Nature

  https://www.nature.com/articles/32675

  Ventricular fibrillation causes more than 300, 000 sudden deaths each year in the USA alone. In approximately 5-12% of these cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation (IVF). Because IVF causes cardiac rhythm disturbance, we investigated whether malfunction of ion channels could cause the disorder by studying mutations in the cardiac sodium channel gene SCN5A. We have now identified a missense mutation, a splice-donor mutation, and a frameshift mutation in the coding region of SCN5A in three IVF families. We show that sodium channels with the missense mutation recover from inactivation more rapidly than normal and that the frameshift mutation causes the sodium channel to be non-functional. Our results indicate that mutations in cardiac ion-channel genes contribute to the risk of developing IVF.

• #22 Rotors and Turbulence in Ventricular Fibrillation – Role of Inward Rectifier Potassium Channels | USC Journal

  https://www.uscjournal.com/articles/rotors-and-turbulence-ventricular-fibrillation-role-inward-rectifier-potassium-channels?language_content_entity=en

  The anchoring of the rotor in the LV and the subsequent regional difference in frequency between the LV and RV have been attributed to differences in IK1 density between the two chambers. […] Taken together, experimental data in isolated guinea pig and transgenic mouse hearts as well as computer simulations strongly argue that IK1 is a stabilizer of re-entry because of its ability to shorten APD and reduce CV near the center of rotation. Increased IK1 should prevent wave front/wave tail interactions and thus prevent rotor destabilization and break-up. […] As such, the interplay between IK1 and the rapid sodium inward current (INa) is a major factor in the control of cardiac excitability and therefore the stability and frequency of re-entry and VF.

• #23 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20231127/New-signaling-mechanism-implicated-in-the-development-of-ventricular-fibrillation.aspx

  A study led by Guadalupe Sabio and Jos Jalife at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Madrid has identified a new signaling mechanism implicated in the development of ventricular fibrillation, a type of arrhythmia, or irregular heartbeat. […] Working with animal models, the CNIC team discovered a connection between the development of ventricular fibrillation and the activation of two key signaling proteins, the stress kinases p38 and p38. […] Together, these results suggest that stress signaling via p38 and p38 likely plays an important role in the development of this condition. […] An in-depth analysis of this signaling pathway revealed that when these protein kinases are activated they alter the electrical properties of cardiomyocytes (the heart’s muscle cells), triggering the appearance of arrhythmias.

• #24 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20231127/New-signaling-mechanism-implicated-in-the-development-of-ventricular-fibrillation.aspx

  The scientists found that p38 and p38 phosphorylate a receptor called ryanodine receptor 2 and another protein called SAP97, resulting in a mislocalization of the potassium ion channel Kv4.3. These molecular changes lead to premature ventricular activation and an increased susceptibility to ventricular fibrillation. […] The study findings identify a promising therapeutic target for the development of new strategies to prevent sustained ventricular fibrillation and provide protection against this serious condition.

• #25 Potential therapeutic target for ventricular fibrillation found

  https://www.drugtargetreview.com/news/112871/potential-therapeutic-target-for-ventricular-fibrillation-found/

  The team observed that p38 and p38 phosphorylate a receptor called ryanodine receptor 2 and another protein called SAP97, culminating in a mislocalisation of the potassium ion channel Kv4.3. […] These molecular changes lead to premature ventricular activation and an increased susceptibility to ventricular fibrillation. […] These findings offer a possible therapeutic target for the development of new strategies to prevent sustained ventricular fibrillation and provide protection against it.

• #26

  https://journals.lww.com/jtrauma/fulltext/9900/pad2_disturbs_cardiomyocyte_calcium_homeostasis_by.974.aspx

  PAD2 protein levels were significantly elevated in the peripheral blood of patients with hemorrhagic shock. […] Pad2 knockout improved calcium homeostasis in the sarcoplasmic reticulum of cardiomyocytes and alleviated post-shock arrhythmia in mice. […] During myocardial hypoxia occurs in hemorrhagic shock, PAD2 reduces SERCA2a enzyme activity by citrullination, disrupting myocardial calcium homeostasis. […] Peptidylarginine deiminase 2 gene deficiency or inhibition improves ventricular arrhythmias and increases survival following hemorrhagic shock. […] In this study, we first show that PAD2 induced lethal arrhythmia after hemorrhagic shock by disturb cardiomyocyte calcium homeostasis. And PAD2 inactivate SERCA2a by citrullination. […] These findings suggest PAD2 deficiency increases SR calcium content and accelerates SR calcium reuptake, protecting cardiomyocytes from Ca2+ disturbance-related arrhythmias.

• #27

  https://journals.lww.com/jtrauma/fulltext/9900/pad2_disturbs_cardiomyocyte_calcium_homeostasis_by.974.aspx

  We here provide novel evidence that PAD2 induces the citrullination of SERCA2a, a modification that inhibits its enzymatic activity. This represents the first report of citrullination as a regulatory mechanism for SERCA2a, offering new insights into the inactivation of SERCA2a during acute ischemic conditions. […] Collectively, hypoxia enhances PAD2-SERCA2a interaction, promoting citrullination-mediated inhibition of SERCA2a activity through Ca2+-dependent PAD2 activation.

• #28 Ventricular fibrillation, ventricular tachycardia and defibrillation | Deranged Physiology

  https://derangedphysiology.com/main/required-reading/cardiovascular-intensive-care/Chapter-214/ventricular-fibrillation-ventricular-tachycardia-and-defibrillation

  The ARC literature review did not identify any consistent evidence for an improved in-hospital mortality with either shock-first or CPR-first approaches. […] Extreme hypothermia has been traditionally said to make one refractory to defibrillation, but numerous animal trials and human case studies have demonstrated that defibrillation is possible and may even be facilitated by profound hypothermia (eg. Boddicker et al, 2005). […] Acute cardiac ischaemia: the leakage of potassium out of dead myocytes leads to increased extracellular potassium that depolarizes myocytes in the ischemic border zone and leads to electrical heterogeneity of conduction and refractoriness that provide a substrate for reentry, resulting in polymorphic VT and/or VF. […] By definition, VT which occurs in the absence of structural heart disease, genetic conditions such as long QT syndrome, or metabolic/electrolyte abnormalities.

• #29 Ventricular Fibrillation: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/158712-overview

  The predominant mechanism is ventricular arrhythmia. In patients with tetralogy of Fallot, up to 10% have VT after surgical correction of the anomaly, and the incidence of sudden death is 2%-3%. […] Patients with nonischemic cardiomyopathies are the second largest group of patients who experience VF, accounting for approximately 10% of VF cases. Nonischemic myopathies, for the purposes of this article, can be divided into dilated, hypertrophic, and other, rarer, forms. These cardiomyopathies can predispose to both VT and VF. […] The genetic causes of DCM are myriad, with many genes, including those that encode actin, myosin, and troponin proteins, being implicated in its causation. Most familial DCMs are inherited in an autosomal dominant fashion, with mutations typically occurring in the proteins found in the cardiac sarcomere.

• #30 Ventricular Fibrillation: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/158712-overview

  The mechanism of SCD in patients with uncorrected aortic stenosis is unclear, although malignant tachyarrhythmias and bradyarrhythmias have been documented. VF accounts for up to 20% of deaths after aortic valve replacement and remains the second most common cause of postoperative death in this population. […] The presence of multiple accessory pathways, posteroseptal accessory pathways, and a preexcited R-R interval of less than 220 msec during atrial fibrillation is associated with higher risk for VF. […] Brugada syndrome can be caused by mutations in many genes. The principal gene associated with the syndrome is SCN5A, over 400 mutations of which have been described.

• #31 Ventricular fibrillation – Wikipedia

  https://en.wikipedia.org/wiki/Ventricular_fibrillation

  Ventricular fibrillation (V-fib or VF) is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, electric shock, or intracranial hemorrhage. Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves. […] Ventricular fibrillation has been described as „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”. Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease.

• #32 Ventricular Fibrillation: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/158712-overview

  On the electrocardiogram (ECG), VF manifests as a chaotically irregular pattern. This pattern is coarse initially but becomes finer as ventricular disorganization increases. As the ECG waveform flattens, the likelihood of successful defibrillation decreases. […] Even though many individuals have anatomic and functional cardiac substrates that predispose them to ventricular arrhythmias, only a small percentage develop VF. The interplay among regional ischemia, left ventricular (LV) dysfunction, and transient inciting events (eg, worsened ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic disturbances) has been proposed to be the precipitator of VF. […] The mechanism of VF in HCM is not entirely understood. Ventricular arrhythmias in HCM are probably a result of a substrate of electrical instability and disorganized electrophysiologic (EP) transmission due to abnormal LV myocardial architecture. Intramural CAD leading to episodic myocardial ischemia and the resulting necrosis and fibrosis has also been implicated as a potential substrate for VT/VF.

• #33 Mechanism of Ventricular Fibrillation: Current Status and Problems Advanced Biomedical Engineering

  https://abe-journal.org/issues/2022/06/22/688

  Many cardiac and non-cardiac factors induce or reduce the VF characteristics. Cardiac factors include Purkinje fiber, intracellular calcium dynamics, ion channels, and gap junction. Interventions of these parameters have the potential to prevent or induce VF. Optimal control of cardiac factor(s) may be used as VF control therapy, but a clinically useful method is yet to be developed. Non-cardiac factors influencing VF include hypokalemia, hypothermia, heart failure, cardiac ischemia, and autonomic nerve. The detailed mechanisms of VF modification for each factor have been clarified; however, no universal mechanism related to VF is established. The mechanism of VF remains to be determined in order to accomplish VF therapy.

• #34 Idiopathic Ventricular Fibrillation: Diagnosis, Ablation of Triggers, Gaps in Knowledge, and Future Directions

  https://www.innovationsincrm.com/cardiac-rhythm-management/articles-2020/june/1605-idiopathic-ventricular-fibrillation

  Idiopathic ventricular fibrillation (IVF) is a diagnosis of exclusion made when no underlying cause is identified in a cardiac arrest survivor. […] Although ischemic cardiomyopathy still accounts for the majority of SCA, advances in the treatment of coronary disease have reduced the proportion of SCA occurring as a result of ischemia. […] Even so, an important minority of patients with ventricular fibrillation (VF) have no detectable structural heart disease nor an established molecular mechanism and are considered to have idiopathic ventricular fibrillation (IVF). […] The recurrent arrhythmic event rate and appropriate ICD shock rate is very high among IVF patients, estimated to be 31% in the meta-analysis by Ozaydin et al., with a 3.1% mortality rate during an average of five years of follow-up.

• #35 Ventricular Flutter and Fibrillation | SpringerLink

  https://link.springer.com/10.1007%2F978-3-540-29676-8_1829

  Ventricular fibrillation (VF) is a very rapid (150500 bpm) irregularly irregular disorganized ventricular rhythm of varying configuration; with time, the amplitude of the fibrillation wave becomes progressively smaller, particularly immediately before death. […] In both VF and VFL the separation of QRS complex from ST segment and T wave is not possible, and is always associated with a fall in or lack or cardiac output, blood pressure and pulse. […] VFL and VF are usually preceded by ventricular tachycardia (VT). […] Idiopathic (primary) VF occurs in patients with normal cardiac structure. Primary VF has been estimated to account for 5% of cases of sudden cardiac death (SCD) with the mean age 36 years, and the male to female ratio of 2.5:1.

• #36 Ventricular Fibrillation (V-Fib): Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/21878-ventricular-fibrillation

  A provider can confirm a ventricular fibrillation rhythm with an electrocardiogram (EKG), especially after resuscitating you from cardiac arrest. They can also diagnose it during cardiac arrest if you have a cardiac monitor on or an implanted cardiac device. […] This condition is a life-threatening medical emergency. Every minute counts. Ventricular fibrillation treatment starts with calling your local emergency number. […] Ventricular fibrillation is one of the shockable arrhythmias, meaning an AED can help return your hearts rhythm to a normal one. […] If you survive a ventricular fibrillation rhythm, youre at a higher risk of it happening again. Your healthcare provider will run tests to find out what caused it and what follow-up options will work best to keep it from happening again.

• #37 Idiopathic Ventricular Fibrillation: Diagnosis, Ablation of Triggers, Gaps in Knowledge, and Future Directions

  https://www.innovationsincrm.com/cardiac-rhythm-management/articles-2020/june/1605-idiopathic-ventricular-fibrillation

  Although ICDs reduce mortality in survivors of IVF, they do not address the IVF substrate; hence, in the absence of substrate modification, recurrent VF, syncope, cardiac arrest, and ICD shocks occur. […] In this review, we will discuss the proposed criteria for IVF diagnosis, previous reports of premature ventricular complex (PVC)-triggered IVF (PVC-VF) or short-coupled torsades de pointes (sc-Tdp), diagnostic strategies to identify potential candidate PVC-VF triggers for radiofrequency ablation, and future directions on screening for IVF substrate in SCA survivors. […] The consensus statement acknowledges that the frequency of diagnosis of IVF has declined over the last four decades due to improvements in diagnostic techniques that can unmask an underlying structural or molecular etiology in cases previously considered to be IVF.

• #38 Ventricular fibrillation pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Ventricular_fibrillation_pathophysiology

  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. […] 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”.

• #39 Ventricular fibrillation, ventricular tachycardia and defibrillation | Deranged Physiology

  https://derangedphysiology.com/main/required-reading/cardiovascular-intensive-care/Chapter-214/ventricular-fibrillation-ventricular-tachycardia-and-defibrillation

  These tend to originate from a few locations, most commonly the RVOT. […] Polymorphic VT is not torsades de pointes, but torsades des pointes is one form of polymorphic VT, specifically associated with QT prolongation. […] A good article (Koplan & Stevenson, 2009) lists the following: Acute coronary ischaemia, Long QT (congenital or acquired), Brugada syndrome, Catecholaminergic polymorphic VT, Arrhythmogenic right ventricular dysplasia (ARVD), Cardiomyopathy of any cause, Hypokalemia, Hypomagnesemia.

• #40 Ventricular Fibrillation | American Heart Association

  https://www.heart.org/en/health-topics/arrhythmia/about-arrhythmia/ventricular-fibrillation

  Ventricular fibrillation, or VF, is considered the most serious abnormal heart rhythm. VF is extremely dangerous and can lead to sudden cardiac death. Without treatment, the condition is fatal within minutes. […] Disordered electrical activity causes the heart’s lower chambers (ventricles) to quiver instead of contracting (or beating) normally. This prohibits the heart from pumping blood, causing collapse and cardiac arrest. […] VF can have several causes, including: Insufficient blood flow to the heart muscle, Damage to the heart muscle (from a heart attack, for example), Cardiomyopathy (a disease of the heart muscle), Problems with the aorta, Drug toxicity, Sepsis (severe body infection), Electrocution accidents or injury to the heart, Heart attack or angina, Congenital heart disease, Heart surgery, Sudden cardiac death from a sudden blow to the area directly over the heart, Very high or very low potassium levels in the blood.

• #41 Rotors and Turbulence in Ventricular Fibrillation – Role of Inward Rectifier Potassium Channels | USC Journal

  https://www.uscjournal.com/articles/rotors-and-turbulence-ventricular-fibrillation-role-inward-rectifier-potassium-channels?language_content_entity=en

  Ventricular fibrillation (VF) is by far the most important immediate cause of sudden cardiac death (SCD). Every year, VF is responsible for an estimated 300,000 deaths annually in the US alone. Owing to its highly complex electrocardiographic (ECG) appearance, VF is commonly thought of as an exceptionally complex and disorganized cardiac activation in which electrical waves propagate through the ventricles chaotically and unpredictably. In fact, during VF the ventricular activation sequence is profoundly abnormal; electrical wave fronts do not follow the usual paths. The heart rate accelerates to the extreme, and the electrical waves assume a complex vortex-like behavior that looks a lot like eddy formation and turbulence in water. Such turmoil renders the heart unable to pump blood. Thus, the blood pressure drops and immediate loss of consciousness follows. Unfortunately, despite many years of research and speculation, the mechanism underlying VF continues to be a matter of speculation and debate.

• #42 Ventricular fibrillation – Wikipedia

  https://en.wikipedia.org/wiki/Ventricular_fibrillation

  Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Histomorphologically, MFB is characterized by fractures of the cardiac myofibres perpendicular to their long axis, with squaring of the myofibre nuclei. […] Defibrillation is the definitive treatment of ventricular fibrillation, whereby an electrical current is applied to the ventricular mass either directly or externally through pads or paddles, with the aim of depolarising enough of the myocardium for coordinated contractions to occur again.

• #43 Effect of Global Cardiac Ischemia on Human Ventricular Fibrillation: Insights from a Multi-scale Mechanistic Model of the Human Heart | PLOS Computational Biology

  https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003891

  Acute regional ischemia in the heart can lead to cardiac arrhythmias such as ventricular fibrillation (VF), which in turn compromise cardiac output and result in secondary global cardiac ischemia. […] The effect of this secondary ischemia on electrical activity during VF is important clinically, because defibrillation typically occurs several minutes after the onset of VF, and thus the mechanism is likely to have been modified by ischemia. […] It is known that ischemia profoundly affects the electrophysiological properties of cardiac cells and tissue. […] The question of how ischemia influences the behaviour of re-entrant activity during VF is important, and has been addressed by clinical, experimental and modeling studies. […] Two important characteristics of VF are the frequency and spatiotemporal complexity of activation patterns, and these have been studied in animal heart experiments.

• #44 Effect of Global Cardiac Ischemia on Human Ventricular Fibrillation: Insights from a Multi-scale Mechanistic Model of the Human Heart | PLOS Computational Biology

  https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003891

  In spite of the significance of these animal studies, the most valuable question for clinical practice is how global ischemia modulates the mechanism of VF in the human heart. […] The effect of hyperkalemia on the period of spiral wave rotation was studied by [29] who obtained similar dependency but only for concentrations of larger than 8 mM. […] The dependence of activation rate on ischemic factors could be predicted by looking at our APD restitution curves. […] The main part of the present study deals with simulations in a 3D anatomically accurate model of the ventricles of the human heart for situations that resemble the clinical set up used in [13]. […] We found that acidosis had almost no effect on the activation rate, while hyperkalemia decreased and hypoxia increased the frequency of VF.

• #45 Effect of Global Cardiac Ischemia on Human Ventricular Fibrillation: Insights from a Multi-scale Mechanistic Model of the Human Heart | PLOS Computational Biology

  https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003891

  The results obtained in their experiments are in accordance with our simulations. […] Flattening of the restitution curves just prevents the onset of VF, however, this process is not directly related to the elimination of multiple existing spirals. […] The tendency for a fibrillation pattern to become more organized due to global ischemia was first demonstrated experimentally by [37] on rabbit hearts.

• #46 Ventricular Fibrillation (VF) – AF-ABLATION

  https://af-ablation.org/en/arrhythmological-disorders/ventricular-arrhythmias/ventricular-fibrillation-vf/

  However, there are cases in which VF occurs in the absence of other evident pathologies or causes, and in these cases, is called idiopathic ventricular fibrillation. […] The importance of these observations is that the theories that try to explain the pathophysiology and electrophysiology of these disorders must take into account the cases of ventricular fibrillation in subjects with an apparently healthy heart. […] New technologies are being tested to advance our understanding.

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