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:

Electrical impulses are generated in the sinoatrial (SA) node. These electrical impulses propagate through the right and left atrium. Then travels in an anterograde direction to the ventricles via the atrioventricular (AV) node. The AV node has a physiologic delay in impulse conduction, this delay is essential for synchronized contractions between atria and ventricles .

Pathogenesis

PSVTS are believed to be caused by reentry circuits, less frequently abnormal automaticity .

Abnormal automaticity:

Electrical impulses are affected by the previous action potential.change in the absolute or relative refreactory perios can trigger abnormal automaticity

In PSVT the abnormal impulses are due to:

·        Early after-depolarization, which is promoted by:

·        Slow heart rate

·        Decreased or increased outward current

·        Delayed after-depolarization

·        Intracellular Ca++ overload

• Impulse Abnormalities:

The impulse is affected by the previous action potential. In PSVT the abnormal impulse is due to:

·        Early after-depolarization, which is promoted by:

·        Slow heart rate

·        Decreased or increased outward current

·        Delayed after-depolarization

·        Intracellular Ca++ overload

• Conduction pathways:

Different reentry circuits in the heart.

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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