Pulseless ventricular tachycardia overview: Difference between revisions
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==Classification== | ==Classification== | ||
[[Pulseless ventricular tachycardia]] may as a [[ventricular tachycardia]] be classified based on the [[morphology]] of the [[QRS complexes]] into two subtypes/groups: [[monomorphic ventricular tachycardia]], and [[polymorphic ventricular tachycardia]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 18:17, 31 May 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]
Overview
Pulseless ventricular tachycardia is an often fatal cardiac dysrhythmia where the regular rhythmic contraction of the heart is replaced by non-rhythmic, faster, yet inadequate contractions. In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation, pulselessness and sudden death. In 1909,Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia. It was also first implied in 1921 that coronary occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia do not appropriately perfuse the organ, leading to ischemia as well as heart failure. This condition requires immediate medical attention as it is an emergency and can lead to ventricular fibrillation and sudden death.[1] As a result of markedly rapid ventricular contractions, diastole is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in cardiac output, and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, wide QRS complexes above 120 milliseconds, the dissociation between the atria and ventricles, presence of fusion beats, and an electrical axis between -90 to -180.[1] Because majority of wide complex tachycardia cases will be ventricular tachycardia, any wide complex tachycardia should always be assumed to be due to ventricular tachycardia until proven otherwise.
Historical Perspective
Classification
Pulseless ventricular tachycardia may as a ventricular tachycardia be classified based on the morphology of the QRS complexes into two subtypes/groups: monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia.
Pathophysiology
Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity.[2] Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.[3]
In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.[1]
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Differentiating Xyz from Other Diseases
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References
- ↑ 1.0 1.1 1.2 Foglesong A, Mathew D. PMID 32119354 Check
|pmid=value (help). Missing or empty|title=(help) - ↑ Armendares S, Pérez Treviño C (1968). "[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)]". Arch Inst Cardiol Mex (in Spanish; Castilian). 38 (6): 779–91. PMID 4237287.
- ↑ Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A (August 1991). "Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7". Cancer Res. 51 (15): 4097–101. PMID 1855225.