Pulseless ventricular tachycardia pathophysiology: Difference between revisions
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{{Pulseless ventricular tachycardia}} | {{Pulseless ventricular tachycardia}} | ||
{{CMG}}; {{AE}}{{Aisha | {{CMG}}; {{AE}}{{Aisha}} | ||
==Overview== | ==Overview== | ||
Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]]. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal [[resting membrane potential]]. The higher the reduction in [[membrane potential]], the faster and more rapid the already abnormal [[automaticity]].<ref name="pmid4237287">{{cite journal |vauthors=Armendares S, Pérez Treviño C |title=[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)] |language=Spanish; Castilian |journal=Arch Inst Cardiol Mex |volume=38 |issue=6 |pages=779–91 |date=1968 |pmid=4237287 |doi= |url=}}</ref> Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on [[afterdepolarizations]] (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: [[Early afterdepolarizations]](EAD) and [[Delayed afterdepolarizations]] (DAD). When either of these afterdepolarizations become high enough to reach the [[membrane threshold]], they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.<ref name="pmid1855225">{{cite journal |vauthors=Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A |title=Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7 |journal=Cancer Res. |volume=51 |issue=15 |pages=4097–101 |date=August 1991 |pmid=1855225 |doi= |url=}}</ref> | Rapid abnormal [[automaticity]] and [[triggered activity]] are thought to be the main [[electrophysiological]] mechanisms of [[pulseless ventricular tachycardia]]. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal [[resting membrane potential]]. The higher the reduction in [[membrane potential]], the faster and more rapid the already abnormal [[automaticity]].<ref name="pmid4237287">{{cite journal |vauthors=Armendares S, Pérez Treviño C |title=[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)] |language=Spanish; Castilian |journal=Arch Inst Cardiol Mex |volume=38 |issue=6 |pages=779–91 |date=1968 |pmid=4237287 |doi= |url=}}</ref> Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on [[afterdepolarizations]] (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: [[Early afterdepolarizations]](EAD) and [[Delayed afterdepolarizations]] (DAD). When either of these afterdepolarizations become high enough to reach the [[membrane threshold]], they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.<ref name="pmid1855225">{{cite journal |vauthors=Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A |title=Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7 |journal=Cancer Res. |volume=51 |issue=15 |pages=4097–101 |date=August 1991 |pmid=1855225 |doi= |url=}}</ref> | ||
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The exact pathogenesis of [disease name] is not completely understood. | |||
OR | |||
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. | |||
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | |||
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. | |||
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. | |||
*The progression to [disease name] usually involves the [molecular pathway]. | |||
*The pathophysiology of [disease/malignancy] depends on the histological subtype. | |||
== | ==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== | ==Associated Conditions== | ||
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*[Condition 3] | *[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== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]
Overview
Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity.[1] Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.[2]
In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.[3]
Pathophysiology
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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
- ↑ Armendares S, Pérez Treviño C (1968). "[Congenital heart diseases in chromosome abnormalities. I. In Down's syndrome (mongolism)]". Arch Inst Cardiol Mex (in Spanish; Castilian). 38 (6): 779–91. PMID 4237287.
- ↑ Buchmann A, Ruggeri B, Klein-Szanto AJ, Balmain A (August 1991). "Progression of squamous carcinoma cells to spindle carcinomas of mouse skin is associated with an imbalance of H-ras alleles on chromosome 7". Cancer Res. 51 (15): 4097–101. PMID 1855225.
- ↑ Foglesong A, Mathew D. PMID 32119354 Check
|pmid=value (help). Missing or empty|title=(help)