These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Pathophysiologic mechanisms of cardiac arrhythmias.
    Author: Wit AL, Rosen MR.
    Journal: Am Heart J; 1983 Oct; 106(4 Pt 2):798-811. PubMed ID: 6310978.
    Abstract:
    Arrhythmias result from abnormalities of impulse initiation or impulse conduction or a combination of both. Abnormal impulse initiation results from either automaticity or triggered activity. Automaticity can further be subdivided into (1) automaticity caused by the normal automatic mechanism (a normal property of cardiac cells in the sinus node, in some parts of the atria, in the atrioventricular junctional region, and in the His-Purkinje system) and (2) automaticity caused by an abnormal mechanism (resulting from a decrease in membrane potential of cardiac fibers, which normally have a high level of membrane potential). Triggered activity is caused by afterdepolarizations, which are second depolarizations that occur either during repolarization (referred to as early afterdepolarizations) or after repolarization is complete or nearly complete (referred to as delayed afterdepolarizations). Abnormal impulse conduction results in reentrant excitation. Usually a combination of slowed conduction and unidirectional conduction block provides the conditions necessary for reentry to occur. Slow conduction and block may result from a decrease in the resting potential and velocity of depolarization of the action potential or may be a consequence of the anisotropic structure of cardiac muscle, in which case resting potential and action potential upstroke velocity may be normal.
    [Abstract] [Full Text] [Related] [New Search]