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dc.contributor.authorRiggins, John
dc.contributor.authorDouglas, Taylor
dc.contributor.authordeSouza, Ian S
dc.date.accessioned2023-01-27T18:11:18Z
dc.date.available2023-01-27T18:11:18Z
dc.date.issued2020-11-07
dc.identifier.citationRiggins J Jr, Douglas T, deSouza IS. Ventricular tachycardia as a consequence of triggered activity. Am J Emerg Med. 2021 Jun;44:480.e5-480.e7. doi: 10.1016/j.ajem.2020.11.008. Epub 2020 Nov 7. PMID: 33221113.en_US
dc.identifier.eissn1532-8171
dc.identifier.doi10.1016/j.ajem.2020.11.008
dc.identifier.pmid33221113
dc.identifier.urihttp://hdl.handle.net/20.500.12648/8159
dc.description.abstractOne of the less frequent underlying mechanisms of ventricular tachycardia (VT) is triggered activity. Triggered activity refers to an extrasystole due to a premature depolarization that occurs when the amplitude of an early or delayed afterdepolarization brings the cardiac membrane to its threshold potential. Hydrochlorothiazide and hydroxyzine can prolong repolarization and QT interval and are associated with early afterdepolarizations. Cyclic AMP-mediated, delayed afterdepolarizations can occur as a result of catecholaminergic surge. Delayed afterdepolarization is classically associated with outflow tract (OT) tachycardia, a type of VT that is uniquely defined by its termination with adenosine. We present a case of triggered OT tachycardia for which intravenous amiodarone through its antiadrenergic effect may have been effective. Infusions of magnesium and a cardioselective, β-receptor antagonist that does not prolong repolarization may have been more appropriate given the concurrent, acquired prolonged QT syndrome. After initial stabilization, considering the underlying VT mechanism may prompt the clinician to select the most appropriate, further treatment.
dc.language.isoenen_US
dc.relation.urlhttps://www.sciencedirect.com/science/article/abs/pii/S0735675720310160?via%3Dihuben_US
dc.rightsCopyright © 2020 Elsevier Inc. All rights reserved.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAfterdepolarizationen_US
dc.subjectOutflow tract tachycardiaen_US
dc.subjectProlonged QTen_US
dc.subjectTriggered activityen_US
dc.subjectVentricular tachycardiaen_US
dc.titleVentricular tachycardia as a consequence of triggered activity.en_US
dc.typeArticle/Reviewen_US
dc.source.journaltitleThe American journal of emergency medicineen_US
dc.source.volume44
dc.source.beginpage480.e5
dc.source.endpage480.e7
dc.source.countryUnited States
dc.description.versionAMen_US
refterms.dateFOA2023-01-27T18:11:18Z
html.description.abstractOne of the less frequent underlying mechanisms of ventricular tachycardia (VT) is triggered activity. Triggered activity refers to an extrasystole due to a premature depolarization that occurs when the amplitude of an early or delayed afterdepolarization brings the cardiac membrane to its threshold potential. Hydrochlorothiazide and hydroxyzine can prolong repolarization and QT interval and are associated with early afterdepolarizations. Cyclic AMP-mediated, delayed afterdepolarizations can occur as a result of catecholaminergic surge. Delayed afterdepolarization is classically associated with outflow tract (OT) tachycardia, a type of VT that is uniquely defined by its termination with adenosine. We present a case of triggered OT tachycardia for which intravenous amiodarone through its antiadrenergic effect may have been effective. Infusions of magnesium and a cardioselective, β-receptor antagonist that does not prolong repolarization may have been more appropriate given the concurrent, acquired prolonged QT syndrome. After initial stabilization, considering the underlying VT mechanism may prompt the clinician to select the most appropriate, further treatment.
dc.description.institutionSUNY Downstateen_US
dc.description.departmentEmergency Medicineen_US
dc.description.degreelevelN/Aen_US
dc.identifier.journalThe American journal of emergency medicine


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Copyright © 2020 Elsevier Inc. All rights reserved.
Except where otherwise noted, this item's license is described as Copyright © 2020 Elsevier Inc. All rights reserved.