Reentry can even develop in part aided by reduced gap

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: tochondrial oxidaDve metabolism leads to a fall in ATP •  Further, diversion of pyruvate into lacDc acid formaDon causes intracellular acidosis that impairs troponin C binding of Ca2+ •  AlteraDons in acDon potenDal reduce contracDlity and make heart prone to arrhythmia (to be covered in subsequent lectures) •  •  •  •  •  Effects of Ischemia on the Cardiac AcDon PotenDal Reduced membrane potenDal (less negaDve) due to less Na/K ATPase impairs phase 0 of AP (fewer Na channels open) Increased KATP channel acDvaDon (less ATP) reduces phase 2 duraDon Increased intracellular [Na+] (because of reduced Na/K ATPase acDvity and intracellular acidosis sDmulates Na+/H+ exchanger) inhibits Na+/Ca2+ exchanger, hence increases intracellular [Ca2+] SR Ca2+ overload due partly to above, and to compensatory, beta adrenergic sympatheDc ­driven increase in Ca2+ influx Overloaded SR Ca2+ store may release Ca2+ during diastole, in turn sDmulaDng an influx of Na+ due to sDmulaDon of the Na+/Ca2+ exchanger, generaDng an a\er depolarizaDon that might trigger an extra beat. Re ­entry can even develop, in part aided by reduced gap juncDonal communicaDon between cardiomy...
View Full Document

This document was uploaded on 04/09/2014.

Ask a homework question - tutors are online