Paroxysmal supraventricular tachycardia pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 41: Line 41:


==== Reentry circuits: ====
==== Reentry circuits: ====
a. About 60% are due to  AVNRT either within
a. 60% are due to  AVNRT either within


*  AV node
*  AV node
Line 47: Line 47:
* Peri nodal atrial tissue.
* Peri nodal atrial tissue.


b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT)
b. 30% are due to Atrioventricular reciprocating tachycardia (AVRT)<ref>{{Cite journal|last=Pablo|first=Denes|date=1978|title=Determinants of atrioventricular reentrant paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome|url=https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.58.3.415|journal=Circulation|volume=58|pages=415-425|via=Am Heart Assoc}}</ref>


* 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).
Line 62: Line 62:
* 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>: ====


#'''Enhanced or ectopic pacemaker'''
#'''Enhanced or ectopic pacemaker'''

Revision as of 05:10, 20 July 2020

Paroxysmal supraventricular tachycardia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Paroxysmal supraventricular tachycardia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Paroxysmal supraventricular tachycardia pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Paroxysmal supraventricular tachycardia pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Paroxysmal supraventricular tachycardia pathophysiology

CDC on Paroxysmal supraventricular tachycardia pathophysiology

Paroxysmal supraventricular tachycardia pathophysiology in the news

Blogs on Paroxysmal supraventricular tachycardia pathophysiology

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Paroxysmal supraventricular tachycardia pathophysiology

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. 60% are due to  AVNRT either within

  •  AV node
  • Peri nodal atrial tissue.

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

  • 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 [6]:

  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 [7].

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. ↑ 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. ↑ Pablo, Denes (1978). "Determinants of atrioventricular reentrant paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome". Circulation. 58: 415–425 – via Am Heart Assoc.
  6. ↑ Friedewald V.E. (2016) Supraventricular Tachycardia: (SVT/Paroxysmal Supraventicular Tachycardia/PSVT). In: Clinical Guide to Cardiovascular Disease. Springer, London
  7. ↑ 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


Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Paroxysmal_supraventricular_tachycardia_pathophysiology&oldid=1629338"