4,200
edits
Early Repolarization: Difference between revisions
Jump to navigation
Jump to search
m
no edit summary
mNo edit summary |
mNo edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
== | {{authors| | ||
|mainauthor= Victor Froelicher, MD | |||
|moderator= Victor Froelicher, MD | |||
|supervisor= | |||
}} | |||
Characterization of standard 12 lead ECG abnormalities can be facilitated by considering the portion of the cardiac ventricular myocytes action potential which influences them. This is only helpful for action potential phenomena originating with the initial wave of activation. Their temporal timing is influenced mainly by transmural dispersion from endo to epicardium. This contrasts with late potentials which are due to phase 0 of the action potentials (depolarization) originating from myocardium isolated by fatty tissue (epsilon waves of ARVD) or by fibrosis (cardiomyopathy) experiencing major delays. These can be arrhythmogenic because they compete with the normal pacemakers. | Characterization of standard 12 lead ECG abnormalities can be facilitated by considering the portion of the cardiac ventricular myocytes action potential which influences them. This is only helpful for action potential phenomena originating with the initial wave of activation. Their temporal timing is influenced mainly by transmural dispersion from endo to epicardium. This contrasts with late potentials which are due to phase 0 of the action potentials (depolarization) originating from myocardium isolated by fatty tissue (epsilon waves of ARVD) or by fibrosis (cardiomyopathy) experiencing major delays. These can be arrhythmogenic because they compete with the normal pacemakers. | ||