Ventricular tachycardia pathophysiology: Difference between revisions

Jump to navigation Jump to search
Avirupguha (talk | contribs)
No edit summary
WikiBot (talk | contribs)
m Robot: Automated text replacement (-{{SIB}} +, -{{EH}} +, -{{EJ}} +, -{{Editor Help}} +, -{{Editor Join}} +)
Line 5: Line 5:
'''Associate Editor-In-Chief:''' {{CZ}}
'''Associate Editor-In-Chief:''' {{CZ}}


{{EH}}
 


==Pathophysiology of ventricular tachycardia==  
==Pathophysiology of ventricular tachycardia==  

Revision as of 17:21, 20 August 2012

Ventricular tachycardia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Ventricular Tachycardia from other Disorders

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

Echocardiography

Cardiac MRI

Other Diagnostic Tests

Treatment

Medical Therapy

Electrical Cardioversion

Ablation

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Ventricular tachycardia pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Ventricular tachycardia pathophysiology

CDC onVentricular tachycardia pathophysiology

Ventricular tachycardia pathophysiology in the news

Blogs on Ventricular tachycardia pathophysiology

to Hospitals Treating Ventricular tachycardia pathophysiology

Risk calculators and risk factors for Ventricular tachycardia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]


Pathophysiology of ventricular tachycardia

The morphology of the tachycardia depends on its cause.

In monomorphic ventricular tachycardia, the reason all the beats look the same is because the impulse is being generated from either increased automaticity of a single point in either the left or right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is damaged or dead (scar) tissue from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.

Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the EKG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include Long QT syndrome and Catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischaemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, particularly in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High dose magnesium is often used as an antidote in cardiac arrest protocols.

Monomorphic ventricular tachycardia

References

Template:WH Template:WS