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The following are medications commonly prescribed cardiac pharmaceutical agents. The specificity of the following medications is highly variable, and often are not particularly specific to a given class. As such, they are listed as are commonly accepted.
Antiarrhythmic agents, also known as cardiac dysrhythmia medications, are a class of drugs that are used to suppress abnormally fast rhythms (tachycardias), such as atrial fibrillation, supraventricular tachycardia and ventricular tachycardia. Many attempts have been made to classify antiarrhythmic agents.
Supraventricular tachycardia (SVT) is an umbrella term for fast heart rhythms arising from the upper part of the heart. [2] This is in contrast to the other group of fast heart rhythms – ventricular tachycardia , which start within the lower chambers of the heart . [ 2 ]
AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medications, or, rarely, synchronized cardioversion.
Drugs listed on the Beers List are categorized according to risks for negative outcomes. The tables include medications that have cautions, should be avoided, should be avoided with concomitant medical conditions, and are contraindicated and relatively contraindicated in the elderly population.
The list below describes some of the more common medications used to prevent blood clots. [25] Note that generally since blood clotting is inhibited, a side effect typically is increased bleeding, though it can be reversed by administering a medication that stops the bleeding or by discontinuation of the medication itself.
Besides, the patient should avoid receiving external effects that cause or increase tachycardia. The same measures than in unstable tachycardia can also be taken, with medications and the type of cardioversion that is appropriate for the patient's tachycardia. [10]
A number of drugs that cause QT prolongation does not directly block hERG, but reduces the trafficking of the mature protein to the surface of the cell. This includes probucol , which appears to enhance the intercellular degradation of hERG; and several cardiac glycosides , which reduces trafficking due to decreased intracellular potassium.