CO 中毒脑病概要1.ppt

Carbon Monoxide Gavin Greenfield Mark Yarema March 21, 2002 Carbon Monoxide - Overview Sources Pathophysiology (3 effects) Acute Presentation Delayed Neurological Sequelae presentation Co-oximeter – what is it? Treatment – NBO vs HBO CO – What is it? colourless poisonous gas generated through incomplete combustion of carbon containing products – anything that contains carbon and is burned most common cause of fire related death responsible for more morbidity and mortality than any other toxin (in industrialized countries); leading cause of poisonous deaths in the U.S. Examples of Exposurenote smoke from fires smoke from cigarettes indoor burning of charcoal (bbq’s) fossil fuel engine exhaust gas or coal heater emissions formaldehyde producing plants CO also produced from hepatic metabolism of methylene chloride vapour (paint removers and other solvents) Pathophysiology – Carboxyhemoglobinnote CO binds to hemoglobin 240 times as strongly as oxygen amount of oxygen that can be carried by the hemoglobin is inversely related to the number of binding sites occupied by CO Oxygen Dissociation Curve Pathophysiology – Oxygen Dissociation Curvenote Shifted to the left (as does low body temperature and alkalosis) caused by change in structure of the Hb molecule after CO binds it – results in Hb more tightly holding on to remaining oxygen molecules results in hemoglobin being unable to release its bound oxygen to tissues Pathophysiologynote Binding of hemoglobin by CO (with induction of carboxyhemoglobin and shifting of curve to left) does not account for all of the consequences observed animals transfused blood with highly saturated carboxyhemoglobin but minimal free CO do not get symptoms the small free portion that is dissolved in plasma likely has a major role Quick Review of Kreb’s Cycle Pathophysiology – Toxic effects of CO on respiratory pigments and mitochondrial cytochromesnote CO results in the cessation of cytochrome oxidative phosphorylation at a cellular l