Paroxysmal supraventricular tachycardia pathophysiology: Difference between revisions

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==== Abnormal impulse formation <ref>Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London</ref>: ====
==== Abnormal impulse formation <ref>Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London</ref>: ====


# Enhanced or ectopic pacemaker
#'''Enhanced or ectopic pacemaker'''
# Triggered activity
#'''Triggered activity'''
#*Early after-depolarization, which is promoted by:
#*'''Early after-depolarization, which is promoted by:'''
#** Slow heart rate
#** Slow heart rate
#** Decreased or increased outward current
#** Decreased or increased outward current
#*Delayed after-depolarization due to
#*'''Delayed after-depolarization due to'''
#**Intracellular Ca++ overload<br />
#**Intracellular Ca++ overload<br />
==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
Except for [[Wolff-Parkinson-White syndrome|'''Familial WPW syndrome''']] which is autosomal dominant and other underlying [[Congenital heart disease|congenital heart diseases,]] the development of PSVT is not linked to a genetic mutation <ref>Sidhu, Jasvinder, and Robert Roberts. “Genetic basis and pathogenesis of familial WPW syndrome.” ''Indian pacing and electrophysiology journal'' vol. 3,4 197-201. 1 Oct. 2003</ref>.
 
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==
==Associated Conditions==
Conditions associated with [disease name] include:
Conditions associated with PSVT include:


*[Condition 1]
*[[Ebstein anomaly]]
*[Condition 2]
*[[Wolff-Parkinson-White syndrome|Familial WPW syndrome]]
*[Condition 3]
*Structural heart disease
*cardiomyopathy
*Myocardial infarction
*Chronic lung disease
*Chronic lung infection
*Stress
*Anxiety


==Gross Pathology==
==Gross Pathology==

Revision as of 23:46, 16 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 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

Reentry is the most prevalent cause of PSVT. less commonly, abnormal impulse formation [4].

Reentry circuits:

a. About 60% are due to  AVNRT either within

  •  AV node
Peri nodal atrial tissue.

b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT)

  • Extra nodal accessory pathway connecting the atrium and ventricle, e.g. Wolff-Parkinson-White syndrome (WPW).

c. 10% are due to pathways within or around the sinus node:

  • Focal atrial tachycardia
  • Intra atrial reentrant tachycardia (IART)
  • Sinoatrial nodal reentrant tachycardia (SANRT)

d. Other rare causes (Rare in adults, but can represent a larger portion of PSVTs in children) are due to

  • Junctional ectopic tachycardia
  • Non-paroxysmal junctional tachycardia

Abnormal impulse formation [5]:

  1. Enhanced or ectopic pacemaker
  2. Triggered activity
    • Early after-depolarization, which is promoted by:
      • Slow heart rate
      • Decreased or increased outward current
    • Delayed after-depolarization due to
      • Intracellular Ca++ overload

Genetics

Except for Familial WPW syndrome which is autosomal dominant and other underlying congenital heart diseases, the development of PSVT is not linked to a genetic mutation [6].

Associated Conditions

Conditions associated with PSVT include:

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. ↑ 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. ↑ 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
  5. ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London
  6. ↑ Sidhu, Jasvinder, and Robert Roberts. “Genetic basis and pathogenesis of familial WPW syndrome.” Indian pacing and electrophysiology journal vol. 3,4 197-201. 1 Oct. 2003


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