Guest guest Posted February 29, 2000 Report Share Posted February 29, 2000 Carbon monoxide is very reactive and not only readily binds to hemoglobin it also binds to other metal proteins such as the cytochrome enzymes - in other words it is - to quote Haldane - a tissue poison. It is this latter mechanism which is the problem, not the relative anemia caused by the loss of hemoglobin transport. Goldbaum et al removed blood from dogs exposing it to CO outside the body. When retransfused they achieved a carboxyhaemoglobin level of 60-70% which if it is achieved by allowing the animal to breathe some CO is always fatal. The plasma borne CO is able to poison endothelial mechanisms and alter characteristics of blood elements such as leukocytes altering their adhesion and causing obstruction to blood flow and free radical damage. Because the blood brain barrier is energy dependent it fails becoming very permeable. The resulting edema causes an increase in intracranial pressure reducing blood flow and oxygenation. In patients who recover, the mid brain areas - basal ganglia - are the most damaged because of the dependence of many areas on venous blood for their oxygenation. A wide variety of syndromes may result from spastic cerebral palsy to personality disorders and even short-term memory changes. Because the changes can occur quickly it is essential to treat as an absolute emergency - compare this to anoxia caused by cardiac arrest where we try to restart the heart as quickly as possible. Every hospital should have at least a monoplace chamber. Best wishes to all for the New Year/Century/Millennium. Philip Wolfson Hyperbaric Medicine Unit University of Dundee Reference Goldbaum LR, RG, Absalon KB. Joint Committee on Aviation Pathology. 13. What is the mechanism of carbon monoxide toxicity? Aviat Space Environ Med 1975 46 1289-129. > Quote Link to comment Share on other sites More sharing options...
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