Carbon monoxide poisoning and its effect on QTc prolongation

Carbon monoxide (CO) poisoning has been associated with direct toxicity to the cardiovascular system by causing arrhythmias through prolongation of QTc. It has been reported to have arrhythmogenic potential likely due to its action on the cardiac membranes. We present a case of a 69-year-old man who presented to the emergency department for evaluation of a syncopal episode after exposure to CO. His carboxyhemoglobin level was elevated at 10.5% on admission, electrocardiogram revealed QTc interval of 622 msec. He was treated with hyperbaric oxygen and a repeat electrocardiogram 15 h after hyperbaric oxygen initiation showed improvement in QTc to 490 msec and his carboxyhemoglobin level decreased to 1.8%. There is a direct association between acute CO poisoning and QTc prolongation as reported in patient cases and evidence of it was seen by investigators who worked on rats and found that this phenomenon occurs due to the action of nitric oxide on the late Na + channels affecting repolarization. The resolution after hyperbaric oxygen could be due to decrease in the CO concentration and the absence of nitric oxide synthase activation further propagating the QT prolongation, however, further research would have to be performed to consolidate this.