Paroxysmal supraventricular tachycardia pathophysiology: Difference between revisions
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'''The normal physiology of PSVT can be understood as follows:''' | '''The normal physiology of PSVT can be understood as follows:''' | ||
The [[SA node|sinoatrial (SA) node]] generates electrical impulses. These electrical impulses propagate through the [[Atrium (heart)|atria]]. The electrical impulse travels in an [[Electrical conduction system of the heart|ِAnterograde direction]] to the [[ventricles]] via the [[Atrioventricular nodes|atrioventricular (AV) node]]. The [[AV node]] has a [[Electrical conduction system of the heart|physiologic delay]] in impulse conduction, and this delay is essential for synchronized contractions between atria and ventricles <ref>Al-Zaiti, S. S., & Magdic, K. S. (2016). ''Paroxysmal Supraventricular Tachycardia. Critical Care Nursing Clinics of North America, 28(3), 309–316.'' doi:10.1016/j.cnc.2016.04.005</ref><ref>Anderson, R. H., & Mori, S. (2016). ''Wilhelm His Junior and his bundle. Journal of Electrocardiology, 49(5), 637–643''</ref> '''.''' The fact that adjacent conduction pathways have the same [[Refractory period (cardiac)|refractory periods]], ensures normal impulse propagation at optimum speed for synchronous [[Atrioventricular|AV]] contraction. Any change in the [[Refractory period (cardiac)|refractory period]] between adjacent [[Electrical conduction system of the heart|conduction pathways]] creates a [[Reentry Supraventricular Tachycardias|reentry circuit]] composed of one pathway for [[Electrical conduction system of the heart|anterograde conduction]] and the other pathway for retrograde conduction. | The [[SA node|sinoatrial (SA) node]] generates electrical impulses. These electrical impulses propagate through the [[Atrium (heart)|atria]]. The electrical impulse travels in an [[Electrical conduction system of the heart|ِAnterograde direction]] to the [[ventricles]] via the [[Atrioventricular nodes|atrioventricular (AV) node]]. The [[AV node]] has a [[Electrical conduction system of the heart|physiologic delay]] in impulse conduction, and this delay is essential for synchronized contractions between atria and ventricles <ref>Al-Zaiti, S. S., & Magdic, K. S. (2016). ''Paroxysmal Supraventricular Tachycardia. Critical Care Nursing Clinics of North America, 28(3), 309–316.'' doi:10.1016/j.cnc.2016.04.005</ref><ref>Anderson, R. H., & Mori, S. (2016). ''Wilhelm His Junior and his bundle. Journal of Electrocardiology, 49(5), 637–643''</ref> '''.''' The fact that adjacent conduction pathways have the same [[Refractory period (cardiac)|refractory periods]], ensures normal impulse propagation at optimum speed for synchronous [[Atrioventricular|AV]] contraction. Any change in the [[Refractory period (cardiac)|refractory period]] between adjacent [[Electrical conduction system of the heart|conduction pathways]] creates a [[Reentry Supraventricular Tachycardias|reentry circuit]] composed of one pathway for [[Electrical conduction system of the heart|anterograde conduction]] and the other pathway for retrograde conduction<ref>Ferguson JD, DiMarco JP. Contemporary management of paroxysmal supraventricular tachycardia. ''Circulation''. 2003;107(8):1096-1099. doi:10.1161/01.cir.0000059743.36226.e8</ref>. | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Noha Elzeiny, M.B.B.Ch, M.Sc.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
The normal physiology of PSVT can be understood as follows:
The sinoatrial (SA) node generates electrical impulses. These electrical impulses propagate through the atria. The electrical impulse travels in an ِAnterograde direction to the ventricles via the atrioventricular (AV) node. The AV node has a physiologic delay in impulse conduction, and this delay is essential for synchronized contractions between atria and ventricles [1][2] . The fact that adjacent conduction pathways have the same refractory periods, ensures normal impulse propagation at optimum speed for synchronous AV contraction. Any change in the refractory period between adjacent conduction pathways creates a reentry circuit composed of one pathway for anterograde conduction and the other pathway for retrograde conduction[3].
Pathogenesis
PSVTS are caused by reentry circuits, less frequently abnormal automaticity [4]
Reentry circuits
Different pathways resulting in reentry, including pathways within or around the SA node, within the atrial myocardium, within the AV node, or an accessory pathway involving the AV node [4].
Abnormal automaticity
Abnormal generation of impulses in PSVT is due to early or delayed after-depolarization of the preceding impulse creating an abnormal focus [5].
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Al-Zaiti, S. S., & Magdic, K. S. (2016). Paroxysmal Supraventricular Tachycardia. Critical Care Nursing Clinics of North America, 28(3), 309–316. doi:10.1016/j.cnc.2016.04.005
- ↑ Anderson, R. H., & Mori, S. (2016). Wilhelm His Junior and his bundle. Journal of Electrocardiology, 49(5), 637–643
- ↑ Ferguson JD, DiMarco JP. Contemporary management of paroxysmal supraventricular tachycardia. Circulation. 2003;107(8):1096-1099. doi:10.1161/01.cir.0000059743.36226.e8
- ↑ 4.0 4.1 Hafeez Y, Grossman SA. Paroxysmal Supraventricular (PSVT) [Updated 2019 Dec 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507699
- ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London