BPK 305 Lecture Notes - Lecture 22: Complement Membrane Attack Complex, Tunica Intima, Innate Immune System
Document Summary
Cell damage leads to: hypocontractility, hypo = decreased, leads to decreased co. Increased incidence of arrhythmia: both can be lethal. Intracellular organelles also swell and rupture: mitochondrial rupture, cytosolic ca2+ overload. Ischemia is associated with acidosis: due to increased lactic acid, and unbalanced atp production and breakdown, acidosis decreases contractility (negative inotrope, negative inotrope = loss of contractile force. Increased ca2+ influx causes cell damage due to high ca2+ levels: nhe blockers -> medication travels to tissue through blood. If tissue is ischemic then it will have no blood flow = drug will not work. Injury subendocardium has elevated rmp: due to changes in the k+ channels, persistent flow of charge into neighbouring regions, lv endocardial injury -> elevated t-q segment. 3: left = elevated rmp, right = during diastole there is a difference in vm due to increased. Subendocardial ischemia systolic injury current: diastole is elevated relative to systole, due to changes in na+ channels.