NURS 3664 Lecture Notes - Lecture 5: Respiratory Sounds, Cardioversion, Endocardium
Document Summary
Unable to conduct impulses (cid:894)ele(cid:272)tri(cid:272)al a(cid:272)ti(cid:448)it(cid:455), a(cid:374)(cid:455)thi(cid:374)g distal does(cid:374)"t get ele(cid:272)tri(cid:272)al a(cid:272)tio(cid:374)(cid:895) Effi(cid:272)ie(cid:374)(cid:272)(cid:455) of the heart as a pu(cid:373)p. Factors that create an extended o2 deprivation to the myocardium: Coronary artery vasospasm less blood delivered to area. Anaerobic a(cid:374)aero(cid:271)i(cid:272) (cid:373)eta(cid:271)olis(cid:373) la(cid:272)ti(cid:272) a(cid:272)id (cid:272)rushi(cid:374)g (cid:272)hest pai(cid:374) 80-90% occur in (l) ventricle (side that does the work) First 12 hours tissue appears normal cellular level cell membranes rupture and enzymes released. 18-24 hours tissue anemia, gray, brown, edema develops. Within 2-3 days - neutrophils & macrophages invade area to remove necrotic tissue transient rise in. Catecholamine mediated lipolysis and glycogenolysis occurs to provide myocardium w/ glucose & free fatty acids for anaerobic metabolism serum glucose levels. 4th 14th - necrotic area very apparent central tissue soft (collagen matrix), may contain hemorrhage (vessels weak and oozy, bleed into sight of necrosis) 10th day 6 wks scar tissue formation continues nonfunctional. 3 6 months collateral circulation continues to develop.
