Paroxysmal supraventricular tachycardia pathophysiology

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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 . 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.

Pathogenesis

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

Reentry circuts:

Abnormal impulse formation .:

Enhanced or ectopic pace maker

Trigere 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

[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

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