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A high performance computational study of the cellular processes of ventriculur cardiac tissue exposed to cyanide (CN) is presented. The model used was based on the Luo-Rudy formalism with modifications. To account for the CN-caused changes, the model used ion concentrations based on published metabolic siudies with CN used as a blocking agent. The model included a cell swelling-activated chloride current, and a membrane current activated by the decline in the ATP concentration. The calculations show the rise in the resting voltage and the connection between the abbreviated AP duration and the modulation in the pseudo-ECG. Similariries in the ECG of tissue affected by CN and tissue exhibiting rhe Bruguda syndrome suggest that fundamental mechanism responsible fur the generniion of polymorphic VF observed in both cases share a commonality wirh implications for treatment.