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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 [[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> '''.'''
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===
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 is the most prevalent cause of PSVT. less commonly, abnormal impulse formation '''<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>'''<ref name=":1" />'''.'''


=== 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" />.
a. 60% are due to  AVNRT either within <ref name=":1">{{Cite book|title=Current Medical Diagnosis and Treatment|last=Thomas M. Bashore; Christopher B. Granger;|first=Kevin P. Jackson; Manesh R. Patel|publisher=McGraw-Hill Education|year=2019|isbn=9781260455298|location=|pages=954-956}}</ref>


=== Abnormal automaticity ===
*  AV node
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 />
* Peri nodal atrial tissue.
==Genetics==
 
[Disease name] is transmitted in [mode of genetic transmission] pattern.
b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT) <ref name=":1" /><ref>Pablo Denes, Wu, Delon, Amat-Y-Leon Fernando, Dhingra, Ramesh, Bauernfeind, Robert, Kehoe, Richard, Rosen, Kenneth M.(1978). "Determinants of atrioventricular reentrant paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome". ''Circulation''. '''58''': 415–425 – via Am Heart Assoc</ref>
 
* 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 <ref name=":0" />:
 
* Focal atrial tachycardia
* Intra atrial reentrant tachycardia (IART)
* Sinoatrial nodal reentrant tachycardia (SANRT)


OR
d. Other rare causes (Rare in adults, but can represent a larger portion of PSVTs in children) are due to <ref>Paola Neroni, Giovanni Ottonello, Danila Manus, Alessandra Atzei, Elisabetta Trudu, Susanna Floris, Vassilios Fanos. Paroxysmal supraventricular tachycardia: physiopathology and management. Journal of Pediatric and Neonatal Individualized Medicine 2014;3(2):e030243 doi: 10.7363/030243</ref>


Genes involved in the pathogenesis of [disease name] include:
* Junctional ectopic tachycardia
*[Gene1]
* Non-paroxysmal junctional tachycardia
*[Gene2]
*[Gene3]


OR
==== Abnormal impulse formation <ref>Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London</ref><ref>Antzelevitch, C., & Burashnikov, A. (2011). Overview of Basic Mechanisms of Cardiac Arrhythmia. ''Cardiac electrophysiology clinics'', ''3''(1), 23–45. <nowiki>https://doi.org/10.1016/j.ccep.2010.10.012</nowiki></ref>: ====


The development of [disease name] is the result of multiple genetic mutations such as:
#'''Enhanced or ectopic pacemaker'''
#'''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 <ref>Shah, C., Jiwani, S., Limbu, B., Weinberg, S., & Deo, M. (2019). Delayed afterdepolarization-induced triggered activity in cardiac purkinje cells mediated through cytosolic calcium diffusion waves. ''Physiological reports'', ''7''(24), e14296. <nowiki>https://doi.org/10.14814/phy2.14296</nowiki></ref>


*[Mutation 1]
==Genetics==
*[Mutation 2]
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>.
*[Mutation 3]


==Associated Conditions==
==Associated Conditions==
Conditions associated with [disease name] include:
Conditions associated with PSVT include:


*[Condition 1]
*[[Ebstein anomaly]]<ref>Sylvain M. Chauvaud, MD, Gianluca Brancaccio, MD, and Alain F. Carpentier (2001): Cardiac Arrhythmia in Patients Undergoing Surgical Repair of Ebstein’s Anomaly,Ann thorac surg,  2001:71-1547-52</ref>
*[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==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
No gross pathology findings for PSVT


==Microscopic Pathology==
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
No gross microscopic histopathological findings for PSVT


==References==
==References==

Latest revision as of 21:00, 23 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.

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[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].

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The progression to [disease name] usually involves the [molecular pathway].

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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][5].

Reentry circuits:

a. 60% are due to  AVNRT either within [5]

  •  AV node
  • Peri nodal atrial tissue.

b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT) [5][6]

  • 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 [4]:

  • 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 [7]

  • Junctional ectopic tachycardia
  • Non-paroxysmal junctional tachycardia

Abnormal impulse formation [8][9]:

  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 [10]

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 [11].

Associated Conditions

Conditions associated with PSVT include:

Gross Pathology

No gross pathology findings for PSVT

Microscopic Pathology

No gross microscopic histopathological findings for PSVT

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. ↑ 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
  5. ↑ 5.0 5.1 5.2 Thomas M. Bashore; Christopher B. Granger;, Kevin P. Jackson; Manesh R. Patel (2019). Current Medical Diagnosis and Treatment. McGraw-Hill Education. pp. 954–956. ISBN 9781260455298.
  6. ↑ Pablo Denes, Wu, Delon, Amat-Y-Leon Fernando, Dhingra, Ramesh, Bauernfeind, Robert, Kehoe, Richard, Rosen, Kenneth M.(1978). "Determinants of atrioventricular reentrant paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome". Circulation. 58: 415–425 – via Am Heart Assoc
  7. ↑ Paola Neroni, Giovanni Ottonello, Danila Manus, Alessandra Atzei, Elisabetta Trudu, Susanna Floris, Vassilios Fanos. Paroxysmal supraventricular tachycardia: physiopathology and management. Journal of Pediatric and Neonatal Individualized Medicine 2014;3(2):e030243 doi: 10.7363/030243
  8. ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London
  9. ↑ Antzelevitch, C., & Burashnikov, A. (2011). Overview of Basic Mechanisms of Cardiac Arrhythmia. Cardiac electrophysiology clinics, 3(1), 23–45. https://doi.org/10.1016/j.ccep.2010.10.012
  10. ↑ Shah, C., Jiwani, S., Limbu, B., Weinberg, S., & Deo, M. (2019). Delayed afterdepolarization-induced triggered activity in cardiac purkinje cells mediated through cytosolic calcium diffusion waves. Physiological reports, 7(24), e14296. https://doi.org/10.14814/phy2.14296
  11. ↑ 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
  12. ↑ Sylvain M. Chauvaud, MD, Gianluca Brancaccio, MD, and Alain F. Carpentier (2001): Cardiac Arrhythmia in Patients Undergoing Surgical Repair of Ebstein’s Anomaly,Ann thorac surg, 2001:71-1547-52


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