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Ventricular fibrillation

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Synonyms and keywords: VF; V-fib

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Ventricular fibrillation (V-fib or VF) is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. As a result, the heart fails to adequately pump blood and hypoxia will occur followed by unconsciousness within 20 – 30 seconds. Ventricular fibrillation is the most commonly identified arrythmia in cardiac arrest patients. While there is some activity, the layperson is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography. Ventricular fibrillation is a medical emergency that requires prompt Basic Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (“flatline”). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain dead due to the effects of cerebral hypoxia. On the other hand, death often occurs if normal sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.

Historical Perspective

Lyman Brewer suggests that the first recorded incident of ventricular fibrillation dates as far back as 1500 BC, and can be found in the Ebers papyrus of ancient Egypt. The extract recorded 3500 years ago may even date from as far back as 3500 BC. It states: “When the heart is diseased, its work is imperfectly performed: the vessels proceeding from the heart become inactive, so that you cannot feel them, if the heart trembles, has little power and sinks, the disease is advanced and death is near.” A book authored by Jo Miles suggests that it may even go back farther. Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least 2500 BC. Whether this is a description of ventricular fibrillation is debatable. The next recorded description occurs 3000 years later and is recorded by Vesalius, who described the appearance of “worm-like” movements of the heart in animals prior to death.

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.

Causes

The heart pumps blood to the lungs, brain, and other organs. Interruption of the heartbeat for only a few seconds can lead to fainting (syncope) or cardiac arrest. Fibrillation is an uncontrolled twitching or quivering of muscle fibers (fibrils). When it occurs in the lower chambers of the heart, it is called ventricular fibrillation. During ventricular fibrillation, blood is not pumped from the heart. Sudden cardiac death results. The most common cause of VF is a heart attack. However, VF can occur whenever the heart muscle does not get enough oxygen.

Epidemiology and Demographics

Sudden cardiac arrest is the leading cause of death in the industrialized world. It exacts significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or “heart attack”. During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

Risk Factors

Most people with VF have no history of heart disease. Yet they often have risk factors for heart disease, such as smoking, high blood pressure, and diabetes.

Natural History, Complications and Prognosis

VF will lead to death within a few minutes unless it is treated quickly and effectively. Even then, long-term survival for people who live through a VF attack outside of the hospital is between 2% and 25%. People who have survived VF may be in a coma or have long-term damage.

Diagnosis

History and Symptoms

A person who has a VF episode can suddenly collapse or become unconscious because the brain and muscles have stopped receiving blood from the heart.

Electrocardiogram

The electrocardiographic findings in ventricular fibrillation comprise of poorly identifiable QRS complexes and absent P waves. The heart rate is >300 beats per minute and it is irregular. The pattern is bizarre with a wandering baseline.

X-ray

There are no x-ray findings associated with ventricular fibrillation.

Electrocardiography and Ultrasound

There are no electrocardiography/ultrasound findings associated with ventricular fibrillation.

CT Scan

There are no CT scan findings associated with ventricular fibrillation.

MRI

There are no MRI findings associated with ventricular fibrillation.

Other Imaging Findings

There are no other imaging findings associated with ventricular fibrillation.

Other Diagnostic Studies

There are no other diagnostic Studies associated with ventricular fibrillation.

Treatment

Medical Therapy

In the event of cardiac arrest due to ventricular fibrillation, the immediate implementation of ACLS guidelines is indicated. When a sudden cardiac arrest occurs, immediate CPR is a vital link in the chain of survival. Another important link is early defibrillation, which has improved greatly with the widespread availability of AEDs. It often starts with analyzing the patient’s heart rhythms with a manual defibrillator.

Surgery

In patients at high risk of ventricular fibrillation, the use of an implantable cardioverter defibrillator has been shown to be beneficial.

Primary Prevention

An implantable cardioverter defibrillator (ICD) is a device that can be implanted in the chest wall of people who are at risk for this serious rhythm disorder. The ICD can help prevent sudden cardiac death by quickly sending an electrical shock when ventricular fibrillation occurs. Template:WH Template:WS

Historical Perspective

Historical Perspective

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

Overview

Lyman Brewer suggests that the first recorded incident of ventricular fibrillation dates as far back as 1500 BC, and can be found in the Ebers papyrus of ancient Egypt. A book authored by Jo Miles suggests that it may even go back farther. Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least 2500 BC. Whether this is a description of ventricular fibrillation is debatable. The next recorded description occurs 3000 years later and is recorded by Vesalius, who described the appearance of “worm-like” movements of the heart in animals prior to death. In 1842, Dr. John Erichsen described ventricular fibrillation following the ligation of a coronary artery (Erichsen JE 1842). In 1850, fibrillation was described by Ludwig and Hoffa when they demonstrated the provocation of ventricular fibrillation in an animal by applying a “Faradic” (electrical) current to the heart. In 1874, Edmé Félix Alfred Vulpian coined the term mouvement fibrillaire, a term that he seems to have used to describe both atrial and ventricular fibrillation. In 1887, Dr. John A. MacWilliam, a physiologist, gave an accurate description of the arrhythmia. Dr. MacWilliam was one of the first to show that ventricular fibrillation could be terminated by a series of induction shocks through the heart. In 1912, the first electrocardiogram recording of ventricular fibrillation was by Dr. August Hoffman. In 1922, Dr. Kerr and Dr. Bender produced an electrocardiogram showing ventricular tachycardia evolving into ventricular fibrillation. The re-entry mechanism was also advocated by DeBoer, who showed that ventricular fibrillation could be induced in late systole with a single shock to a frog heart. In 1928, The concept of “R on T ectopics” was further brought out by Dr. Katz. This was called the “vulnerable period” by Wiggers and Wegria in 1940, who brought to attention the concept of the danger of premature ventricular beats occurring on a T wave. In 1940, another definition of VF was produced by Dr. Wiggers. He described ventricular fibrillation as “an incoordinate type of contraction which, despite a high metabolic rate of the myocardium, produces no useful beats. As a result, the arterial pressure falls abruptly to very low levels, and death results within six to eight minutes from anemia of the brain and spinal cord“.

Historical Perspective

  • Lyman Brewer suggests that the first recorded incident of ventricular fibrillation dates as far back as 1500 BC, and can be found in the Ebers papyrus of ancient Egypt.
  • A book authored by Jo Miles suggests that it may even go back farther. Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least 2500 BC.[1] Whether this is a description of ventricular fibrillation is debatable.[2]
  • The next recorded description occurs 3000 years later and is recorded by Vesalius, who described the appearance of “worm-like” movements of the heart in animals prior to death.
  • In 1842, Dr. John Erichsen described ventricular fibrillation following the ligation of a coronary artery (Erichsen JE 1842).
  • In 1850, fibrillation was described by Ludwig and Hoffa when they demonstrated the provocation of ventricular fibrillation in an animal by applying a “Faradic” (electrical) current to the heart.
  • In 1874, Edmé Félix Alfred Vulpian coined the term mouvement fibrillaire, a term that he seems to have used to describe both atrial and ventricular fibrillation.
  • In 1887, Dr. John A. MacWilliam, a physiologist, gave an accurate description of the arrhythmia. This definition still holds today and is interesting in the fact that his studies and description predate the use of electrocardiography. His description is as follows: “The ventricular muscle is thrown into a state of irregular arrhythmic contraction, whilst there is a great fall in the arterial blood pressure, the ventricles become dilated with blood as the rapid quivering movement of their walls is insufficient to expel their contents; the muscular action partakes of the nature of a rapid incoordinate twitching of the muscular tissue. The cardiac pump is thrown out of gear, and the last of its vital energy is dissipated in the violent and the prolonged turmoil of fruitless activity in the ventricular walls.”
  • Dr. MacWilliam was one of the first to show that ventricular fibrillation could be terminated by a series of induction shocks through the heart.
  • In 1912, the first electrocardiogram recording of ventricular fibrillation was by Dr. August Hoffman.
  • Simultaneously, two other researchers, Mines and Garrey, working separately, produced work demonstrating the phenomenon of circus movement and re-entry as possible substrates for the generation of arrhythmias. This work was also accompanied by Lewis, who performed further outstanding work into the concept of “circus movement”.
  • In 1922, Dr. Kerr and Dr. Bender produced an electrocardiogram showing ventricular tachycardia evolving into ventricular fibrillation.
  • The re-entry mechanism was also advocated by DeBoer, who showed that ventricular fibrillation could be induced in late systole with a single shock to a frog heart.
  • In 1928, The concept of “R on T ectopics” was further brought out by Dr. Katz.
  • This was called the “vulnerable period” by Wiggers and Wegria in 1940, who brought to attention the concept of the danger of premature ventricular beats occurring on a T wave.
  • In 1940, another definition of VF was produced by Dr. Wiggers. He described ventricular fibrillation as “an incoordinate type of contraction which, despite a high metabolic rate of the myocardium, produces no useful beats. As a result, the arterial pressure falls abruptly to very low levels, and death results within six to eight minutes from anemia of the brain and spinal cord“.

References

  1. ↑ Brewer LA (1983). “Sphygmology through the centuries. Historical notes”. Am. J. Surg. 145 (6): 695–701. doi:10.1016/0002-9610(83)90124-1. PMID 6344674.
  2. ↑ Brewer LA (1983). “Sphygmology through the centuries. Historical notes”. Am. J. Surg. 145 (6): 696–702. doi:10.1016/0002-9610(83)90124-1. PMID 6344674.

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Pathophysiology

Pathophysiology

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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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Sahar Memar Montazerin, M.D.[3]

Overview

The heart pumps blood to the lungs, brain, and other organs. Interruption of the heartbeat for only a few seconds can lead to fainting (syncope) or cardiac arrest. Fibrillation is an uncontrolled twitching or quivering of muscle fibers (fibrils). When it occurs in the lower chambers of the heart, it is called ventricular fibrillation. During ventricular fibrillation, blood is not pumped from the heart. Sudden cardiac death results. The most common cause of VF is a heart attack. However, VF can occur whenever the heart muscle does not get enough oxygen.

Causes

Life Threatening Causes

Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Common causes of ventricular fibrillation include:[2][3][4][5][6][7][8]

Causes by Organ System

Cardiovascular Abnormal automaticity, acute myocardial rupture, aortic dissection, aortic stenosis, arrhythmogenic right ventricular dysplasia, Brugada syndrome, cardiomyopathies, commotio cordis, complete heart block, congenital heart disease, coronary artery spasm, dilated cardiomyopathy, heart attack, heart block, heart surgery, hypertrophic cardiomyopathy, hypokalemia, hypoxia, ischemic stroke, myocardial infarction, myocardial ischemia, myocarditis, pericardial tamponade, preexcitation syndrome, prolonged QT syndrome, pulmonary embolism, pulmonary hypertension, re-entry or circus motion, short QT syndrome, sudden cardiac death, sudden infant death syndrome, Sumatriptan, torsade de pointes, unstable angina, valvular heart disease, Wolff-Parkinson-White syndrome
Chemical/Poisoning Belladonna, environmental poisoning
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Amiodarone, calcium chloride, calcium gluconate, Eletriptan, ergotamine tartrate, Fosphenytoin sodium, ibutilide, increased catecholamine levels, medications, Naratriptan, phenobarbital, pramipexole, proarrhythmic drugs
Ear Nose Throat No underlying causes
Endocrine Increased catecholamine levels
Environmental Environmental poisoning
Gastroenterologic No underlying causes
Genetic Brugada syndrome, congenital heart disease
Hematologic Pulmonary embolism
Iatrogenic No underlying causes
Infectious Disease Myocarditis, sepsis
Musculoskeletal/Orthopedic No underlying causes
Neurologic Intracranial hemorrhage, ischemic stroke, Pickwickian syndrome, sleep apnea
Nutritional/Metabolic Acid-base disturbances, electrolyte imbalance
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Aspiration, bronchospasm, hypoxia, Pickwickian syndrome, pulmonary embolism, pulmonary hypertension, sudden infant death syndrome, tension pneumothorax
Renal/Electrolyte Electrolyte imbalance, hypokalemia
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma Electric shock, electrocution
Urologic No underlying causes
Miscellaneous Drowning, hyperthermia, hypothermia, idiopathic,

Causes in Alphabetical Order[8][9][10]

References

  1. ↑ Koplan BA, Stevenson WG (March 2009). “Ventricular tachycardia and sudden cardiac death”. Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 8.0 8.1 Heist, E. Kevin; Ruskin, Jeremy N. (2010). “Drug-Induced Arrhythmia”. Circulation. 122 (14): 1426–1435. doi:10.1161/CIRCULATIONAHA.109.894725. ISSN 0009-7322.
  9. ↑ Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  10. ↑ Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
  11. ↑ Alings, Marco; Wilde, Arthur (1999). ““Brugada” Syndrome”. Circulation. 99 (5): 666–673. doi:10.1161/01.CIR.99.5.666. ISSN 0009-7322.
  12. ↑ Gurabi Z, Koncz I, Patocskai B, Nesterenko VV, Antzelevitch C (February 2014). “Cellular mechanism underlying hypothermia-induced ventricular tachycardia/ventricular fibrillation in the setting of early repolarization and the protective effect of quinidine, cilostazol, and milrinone”. Circ Arrhythm Electrophysiol. 7 (1): 134–42. doi:10.1161/CIRCEP.113.000919. PMC 3951442. PMID 24429494.
  13. ↑ Jain PK, Sharma AK, Agarwal N, Jain PK, Sengar NS, Agarwal N; et al. (2013). “A prospective clinical study of myocarditis in cases of acute ingestion of paraphenylene diamine (hair dye) poisoning in northern India”. J Assoc Physicians India. 61 (9): 633–6, 644. PMID 24772701.

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Differentiating Ventricular Fibrillation from other Diseases

Differentiating Ventricular Fibrillation from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2] Sahar Memar Montazerin, M.D.[3]

Overview

Ventricular fibrillation should be differentiated from other conditions manifesting with a sudden loss of consciousness as well as different cardiac arrhythmias.

Differentiating Ventricular Fibrillation From Other Diseases

Ventricular fibrillation should be differentiated from other conditions causing sudden cardiac death including:

Ventricular fibrillation should also be differentiated from other cardiac arrhythmias that may have similar ECG findings, including:

Ventricular fibrillation should be differentiated from other forms of cardiac arrhythmia including:

Table below compare different characteristics of cardiac arrhythmias:

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[1][2]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[3]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[4][5][6][7]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R’ in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[8][9]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[10][11]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[12][13]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[14][15][16]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[17][18]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

The table below provides information on the differential diagnosis of ventricular fibrillation in terms of ECG appearance:

Disease Name Causes ECG Characteristics ECG view
Ventricular tachycardia [19][20][21][22][23]
[24]
Ventricular fibrillation [17][25][26][27]
[28]
Ventricular flutter [29][30][31]
[32]
Asystole [33][34]
  • There is no electrical activity in the asystole
[35]
Pulseless electrical activity [36][37]
[38]
Torsade de Pointes [39][40][41]
  1. Paroxysms of VT with irregular RR intervals.
  2. A ventricular rate between 200 and 250 beats per minute.
  3. Two or more cycles of QRS complexes with alternating polarity.
  4. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion.
  5. Prolongation of the QT interval.
  6. Is often initiated by a PVC with a long coupling interval, R on T phenomenon.
  7. There are usually 5 to 20 complexes in each cycle.
[42]

References

  1. ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). “The ECG as a tool to determine atrial fibrillation complexity”. Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  2. ↑ Harris K, Edwards D, Mant J (2012). “How can we best detect atrial fibrillation?”. J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  3. ↑ Cosío FG (June 2017). “Atrial Flutter, Typical and Atypical: A Review”. Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  4. ↑ Katritsis DG, Josephson ME (August 2016). “Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia”. Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  5. ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). “Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway”. Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  6. ↑ “Atrioventricular Nodal Reentry Tachycardia (AVNRT) – StatPearls – NCBI Bookshelf”.
  7. ↑ Schernthaner C, Danmayr F, Strohmer B (2014). “Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias”. Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  8. ↑ Scher DL, Arsura EL (September 1989). “Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment”. Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  9. ↑ Goodacre S, Irons R (March 2002). “ABC of clinical electrocardiography: Atrial arrhythmias”. BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  10. ↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). “Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome”. J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  11. ↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). “Perinatal arrhythmias: diagnosis and management”. Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  12. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). “Evaluation and management of wolff-Parkinson-white in athletes”. Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  13. ↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). “Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues”. Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  14. ↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). “Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction”. J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  15. ↑ 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.
  16. ↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). “Sudden cardiac death: epidemiology and risk factors”. Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  17. ↑ 17.0 17.1 Koplan BA, Stevenson WG (March 2009). “Ventricular tachycardia and sudden cardiac death”. Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  18. ↑ Levis JT (2011). “ECG Diagnosis: Monomorphic Ventricular Tachycardia”. Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.
  19. ↑ Ajijola, Olujimi A.; Tung, Roderick; Shivkumar, Kalyanam (2014). “Ventricular tachycardia in ischemic heart disease substrates”. Indian Heart Journal. 66: S24–S34. doi:10.1016/j.ihj.2013.12.039. ISSN 0019-4832.
  20. ↑ Meja Lopez, Eliany; Malhotra, Rohit (2019). “Ventricular Tachycardia in Structural Heart Disease”. Journal of Innovations in Cardiac Rhythm Management. 10 (8): 3762–3773. doi:10.19102/icrm.2019.100801. ISSN 2156-3977.
  21. ↑ Coughtrie, Abigail L; Behr, Elijah R; Layton, Deborah; Marshall, Vanessa; Camm, A John; Shakir, Saad A W (2017). “Drugs and life-threatening ventricular arrhythmia risk: results from the DARE study cohort”. BMJ Open. 7 (10): e016627. doi:10.1136/bmjopen-2017-016627. ISSN 2044-6055.
  22. ↑ El-Sherif, Nabil (2001). “Mechanism of Ventricular Arrhythmias in the Long QT Syndrome: On Hermeneutics”. Journal of Cardiovascular Electrophysiology. 12 (8): 973–976. doi:10.1046/j.1540-8167.2001.00973.x. ISSN 1045-3873.
  23. ↑ de Riva, Marta; Watanabe, Masaya; Zeppenfeld, Katja (2015). “Twelve-Lead ECG of Ventricular Tachycardia in Structural Heart Disease”. Circulation: Arrhythmia and Electrophysiology. 8 (4): 951–962. doi:10.1161/CIRCEP.115.002847. ISSN 1941-3149.
  24. ↑ ECG found in of https://en.ecgpedia.org/index.php?title=Main_Page
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ ECG found in https://en.ecgpedia.org/index.php?title=Main_Page
  29. ↑ Thies, Karl-Christian; Boos, Karin; Müller-Deile, Kai; Ohrdorf, Wolfgang; Beushausen, Thomas; Townsend, Peter (2000). “Ventricular flutter in a neonate—severe electrolyte imbalance caused by urinary tract infection in the presence of urinary tract malformation”. The Journal of Emergency Medicine. 18 (1): 47–50. doi:10.1016/S0736-4679(99)00161-4. ISSN 0736-4679.
  30. ↑ Koster, Rudolph W.; Wellens, Hein J.J. (1976). “Quinidine-induced ventricular flutter and fibrillation without digitalis therapy”. The American Journal of Cardiology. 38 (4): 519–523. doi:10.1016/0002-9149(76)90471-9. ISSN 0002-9149.
  31. ↑ Dhurandhar RW, Nademanee K, Goldman AM (1978). “Ventricular tachycardia-flutter associated with disopyramide therapy: a report of three cases”. Heart Lung. 7 (5): 783–7. PMID 250503.
  32. ↑ ECG found in https://en.ecgpedia.org/index.php?title=Main_Page
  33. ↑ ACLS: Principles and Practice. p. 71-87. Dallas: American Heart Association, 2003. ISBN 0-87493-341-2.
  34. ↑ ACLS for Experienced Providers. p. 3-5. Dallas: American Heart Association, 2003. ISBN 0-87493-424-9.
  35. ↑ ECG found in https://en.ecgpedia.org/index.php?title=Main_Page
  36. ↑ “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 7.2: Management of Cardiac Arrest.” Circulation 2005; 112: IV-58 – IV-66.
  37. ↑ Foster B, Twelve Lead Electrocardiography, 2nd edition, 2007
  38. ↑ ECG found in wikimedia Commons
  39. ↑ Li M, Ramos LG (July 2017). “Drug-Induced QT Prolongation And Torsades de Pointes”. P T. 42 (7): 473–477. PMC 5481298. PMID 28674475.
  40. ↑ Sharain, Korosh; May, Adam M.; Gersh, Bernard J. (2015). “Chronic Alcoholism and the Danger of Profound Hypomagnesemia”. The American Journal of Medicine. 128 (12): e17–e18. doi:10.1016/j.amjmed.2015.06.051. ISSN 0002-9343.
  41. ↑ Khan IA (2001). “Twelve-lead electrocardiogram of torsades de pointes”. Tex Heart Inst J. 28 (1): 69. PMC 101137. PMID 11330748.
  42. ↑ ECG found in https://en.ecgpedia.org/index.php?title=Main_Page

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Epidemiology and Demographics

Epidemiology and Demographics

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

Overview

Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%.[1] The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or “heart attack”. During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

Epidemiology and Demographics

  • Sudden cardiac arrest is the leading cause of death in the industrialised world.
  • It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%.[2]
  • The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or “heart attack”. During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

References

  1. ↑ National Institute for Health and Clinical Excellence Guidelines 2000
  2. ↑ National Institute for Health and Clinical Excellence Guidelines 2000

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Common risk factors associated with the development of ventricular fibrillation include history of myocardial infarction, congenital heart disease, electrolyte abnormalities and etc.

Risk Factors

Risk factors for the development of ventricular fibrillation in general population may include:[1][2][3][4][5][6][7]

Risk factors for the development of ventricular fibrillation especially in the setting of acute myocardial infarction include:[8][9][10]

In one nationwide study, ventricular fibrillation in the setting of acute myocardial infarction was associated with following risk factors:[11]

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ Heist, E. Kevin; Ruskin, Jeremy N. (2010). “Drug-Induced Arrhythmia”. Circulation. 122 (14): 1426–1435. doi:10.1161/CIRCULATIONAHA.109.894725. ISSN 0009-7322.
  8. ↑ Gheeraert PJ, Henriques JP, De Buyzere ML, Voet J, Calle P, Taeymans Y, Zijlstra F (January 2000). “Out-of-hospital ventricular fibrillation in patients with acute myocardial infarction: coronary angiographic determinants”. J. Am. Coll. Cardiol. 35 (1): 144–50. doi:10.1016/s0735-1097(99)00490-8. PMID 10636272.
  9. ↑ Dekker LR, Bezzina CR, Henriques JP, Tanck MW, Koch KT, Alings MW, Arnold AE, de Boer MJ, Gorgels AP, Michels HR, Verkerk A, Verheugt FW, Zijlstra F, Wilde AA (September 2006). “Familial sudden death is an important risk factor for primary ventricular fibrillation: a case-control study in acute myocardial infarction patients”. Circulation. 114 (11): 1140–5. doi:10.1161/CIRCULATIONAHA.105.606145. PMID 16940195.
  10. ↑ Gheeraert PJ, Henriques JP, De Buyzere ML, De Pauw M, Taeymans Y, Zijlstra F (November 2001). “Preinfarction angina protects against out-of-hospital ventricular fibrillation in patients with acute occlusion of the left coronary artery”. J. Am. Coll. Cardiol. 38 (5): 1369–74. doi:10.1016/s0735-1097(01)01561-3. PMID 11691510.
  11. ↑ Jabbari R, Engstrøm T, Glinge C, Risgaard B, Jabbari J, Winkel BG, Terkelsen CJ, Tilsted HH, Jensen LO, Hougaard M, Chiuve SE, Pedersen F, Svendsen JH, Haunsø S, Albert CM, Tfelt-Hansen J (January 2015). “Incidence and risk factors of ventricular fibrillation before primary angioplasty in patients with first ST-elevation myocardial infarction: a nationwide study in Denmark”. J Am Heart Assoc. 4 (1): e001399. doi:10.1161/JAHA.114.001399. PMC 4330064. PMID 25559012.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

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

Overview

VF will lead to death within a few minutes unless it is treated quickly and effectively. Even then, long-term survival for people who live through a VF attack outside of the hospital is between 2% and 25%. People who have survived VF may be in a coma or have long-term damage.

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of ventricular fibrillation include:[1][2]

Prognosis

References

  1. ↑ Holmberg M, Holmberg S, Herlitz J (March 2000). “Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in sweden”. Resuscitation. 44 (1): 7–17. doi:10.1016/s0300-9572(99)00155-0. PMID 10699695.
  2. ↑ Geocadin RG, Koenig MA, Jia X, Stevens RD, Peberdy MA (May 2008). “Management of brain injury after resuscitation from cardiac arrest”. Neurol Clin. 26 (2): 487–506, ix. doi:10.1016/j.ncl.2008.03.015. PMC 3074242. PMID 18514823.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | EKG Examples | | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters

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