San Lorenzo I S, Chiesa M, Gamba P, Toniolo A
Cardiologia. 1989 May;34(5):439-46.
Carbon monoxide poisoning causes tissue hypoxia because of reduced transfer and altered release of oxygen by hemoglobin. Considering many case histories, we realized that symptoms and clinical signs of acute poisoning are mostly neurologic: coma, headache, dizziness, vomiting. On the contrary, it seems that myocardium, the other organ which mostly requires O2, is attacked in a "silent way". ECG in 5 patients with accidental carbon monoxide poisoning underlined that cardiac rate increased (3 of them presented tachyarrhythmias by atrial fibrillation) and the presence of more or less important alteration of ventricular repolarization like "subendocardial lesion". Simple hyperbaric oxygen treatment determined the regression of the rhythm disorder and of the abnormalities of ventricular repolarization. The only patient who had not the restoration of sinus rhythm had chronic atrial fibrillation.
一氧化碳中毒会导致组织缺氧，因为血红蛋白转运氧气的能力降低且释放氧气的方式发生改变。考虑到众多病例史，我们发现急性中毒的症状和临床体征大多为神经系统方面的：昏迷、头痛、头晕、呕吐。相反，似乎另一个最需要氧气的器官——心肌，却在以一种“无声的方式”受到攻击。5例意外一氧化碳中毒患者的心电图显示心率加快（其中3例出现房颤所致的快速心律失常），并且存在或多或少明显的心室复极改变，如“心内膜下病变”。单纯高压氧治疗使心律失常和心室复极异常得到缓解。唯一未恢复窦性心律的患者患有慢性房颤。
