Paroxysmal supraventricular tachycardia pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
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>.''' | 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: ==== | ||
| Line 51: | Line 51: | ||
* Extra nodal accessory pathway connecting the atrium and ventricle, e.g. Wolff-Parkinson-White syndrome (WPW). | * 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: | c. 10% are due to pathways within or around the sinus node <ref name=":0" />: | ||
* Focal atrial tachycardia | * Focal atrial tachycardia | ||
| Line 57: | Line 57: | ||
* Sinoatrial nodal reentrant tachycardia (SANRT) | * 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 | 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> | ||
* Junctional ectopic tachycardia | * Junctional ectopic tachycardia | ||
* Non-paroxysmal junctional tachycardia | * Non-paroxysmal junctional tachycardia | ||
==== 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><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>: ==== | ||
#'''Enhanced or ectopic pacemaker''' | #'''Enhanced or ectopic pacemaker''' | ||
| Line 70: | Line 70: | ||
#** Decreased or increased outward current | #** Decreased or increased outward current | ||
#*'''Delayed after-depolarization due to''' | #*'''Delayed after-depolarization due to''' | ||
#**Intracellular Ca++ overload< | #**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> | ||
==Genetics== | ==Genetics== | ||
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>. | 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>. | ||
| Line 77: | Line 78: | ||
Conditions associated with PSVT include: | Conditions associated with PSVT include: | ||
*[[Ebstein anomaly]] | *[[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> | ||
*[[Wolff-Parkinson-White syndrome|Familial WPW syndrome]] | *[[Wolff-Parkinson-White syndrome|Familial WPW syndrome]] | ||
*Structural heart disease | *Structural heart disease | ||
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.
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][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]:
- 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 [10]
- Early after-depolarization, which is promoted by:
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:
- Ebstein anomaly[12]
- Familial WPW syndrome
- Structural heart disease
- cardiomyopathy
- Myocardial infarction
- Chronic lung disease
- Chronic lung infection
- Stress
- Anxiety
Gross Pathology
No gross pathology findings for PSVT
Microscopic Pathology
No gross microscopic histopathological findings for PSVT
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
- ↑ 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.
- ↑ 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
- ↑ 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
- ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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