The clinical signs and symptoms of cyanide poisoning mimic those of hypoxia, with one exception: Unless respiratory arrest has occurred, patients are not cyanotic. Although small amounts of cyanide bind to the ferrous (Fe2+) form of hemoglobin, there is no significant interference with the ability of hemoglobin to bind oxygen. 15 The clinical manifestations of cyanide poisoning are readily understood based on the effect of cyanide on cytochrome oxidase activity. Blockade of the ability of mitochondria to use oxygen produces a state of severe hypoxia despite the presence of oxygen. The resulting anaerobic metabolism generates large amounts of lactic acid.4!! Unexplained lactic acidosis is an important, albeit nonspecific clinical clue to the timely diagnosis of cyanide poisoning in case of an "unknown" exposure.

The inability to use oxygen leads to decreased oxygen extraction by tissues with a concomitant increase in the oxygen content of venous blood. This results in a decrease in the normal arteriolar-venous oxygen [(A-v) O2] difference, a measure of the amount of oxygen extracted by the tissues.6 Although discussion of these concepts facilitates understanding of the cellular effects of cyanide, it is difficult to detect this underutilization of oxygen in an emergency setting. A reliable estimation of the (A-v) O2 difference requires that the venous sample be taken from the pulmonary artery. This is most practical in the invasively monitored intensive care unit patient who has suspected cyanide toxicity due to a nitroprusside infusion. 616 Anticipated laboratory abnormalities are shown in Tab.l.e... .1.82.-2.

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