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'''The normal physiology of PSVT can be understood as follows:'''
'''The normal physiology of PSVT can be understood as follows:'''


'''Electrical impulses are generated in the [[Sinoatrial node|sinoatrial (SA) node]]. These electrical impulses propagate through the right and left [[Atrium (heart)|atrium]]. Then travels in an [[anterograde direction]] to the [[ventricles]] via the [[Atrioventricular|atrioventricular (AV) node.]] The [[Atrioventricular|AV]] node has a physiologic delay in impulse conduction, 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 [[Sinoatrial node|sinoatrial (SA) node]] generates electrical impulses. These electrical impulses propagate through the right and left [[Atrium (heart)|atrium]]. Then travels in an [[Anterograde direction|ِAnterograde direction]] to the [[ventricles]] via the [[Atrioventricular nodes|atrioventricular (AV) node]]. The electrical impulse stimulate contraction of the myocardium.The [[Atrioventricular|AV]] node has a 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> '''.'''


===Pathogenesis===
===Pathogenesis===
PSVTS are believed to be caused by reentry circuits, less frequently abnormal automaticity <ref>Hafeez Y, Grossman SA. Paroxysmal Supraventricular (PSVT) [Updated 2020 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK507699/</nowiki></ref>.
PSVTS are caused by reentry circuits, less frequently abnormal automaticity <ref name=":0">Hafeez Y, Grossman SA. Paroxysmal Supraventricular (PSVT) [Updated 2019 Dec 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK507699</nowiki></ref>


=== Reentry circuits: ===
=== 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 <ref name=":0" />.


=== Abnormal automaticity: ===
=== Abnormal automaticity ===
Electrical impulses are affected by the previous action potential.change in the absolute or relative refreactory perios can trigger abnormal automaticity
Abnormal generation of impulses in PSVT is due to early or delayed after-depolarization of the preceding impulse creating an abnormal focus <ref>Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London</ref>.
 
<br />
In PSVT the abnormal impulses are due to:
 
·        Early after-depolarization, which is promoted by:
 
·        Slow heart rate
 
·        Decreased or increased outward current
 
·        Delayed after-depolarization
 
·        Intracellular Ca++ overload
 
* '''Impulse Abnormalities:'''
 
The impulse is affected by the previous action potential. In PSVT the abnormal impulse is due to:
 
·        Early after-depolarization, which is promoted by:
 
·        Slow heart rate
 
·        Decreased or increased outward current
 
·        Delayed after-depolarization
 
·        Intracellular Ca++ overload
 
* '''Conduction pathways:'''
 
Different reentry circuits in the heart.
 
==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
[Disease name] is transmitted in [mode of genetic transmission] pattern.

Revision as of 21:34, 14 July 2020

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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 right and left atrium. Then travels in an ِAnterograde direction to the ventricles via the atrioventricular (AV) node. The electrical impulse stimulate contraction of the myocardium.The AV node has a physiologic delay in impulse conduction, and this delay is essential for synchronized contractions between atria and ventricles [1][2] .

Pathogenesis

PSVTS are caused by reentry circuits, less frequently abnormal automaticity [3]

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 [3].

Abnormal automaticity

Abnormal generation of impulses in PSVT is due to early or delayed after-depolarization of the preceding impulse creating an abnormal focus [4].

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

  1. ↑ 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
  2. ↑ Anderson, R. H., & Mori, S. (2016). Wilhelm His Junior and his bundle. Journal of Electrocardiology, 49(5), 637–643
  3. ↑ 3.0 3.1 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
  4. ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London


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