Bühring M, Spies H F
Z Rechtsmed. 1979 Jul 17;83(2):121-7. doi: 10.1007/BF02092268.
In addition to currently known mechanisms of sudden death following water immersion, predominantly vagal cardio-depressive reflexes are discussed. The pronounced circulatory centralization in diving animals as well as following exposure to cold water indicates additional sympathetic activity. In cold water baths of 15 degrees C, our own measurements indicate an increase in plasma catecholamine levels by more than 300%. This may lead to cardiac arrhythmias by the following mechanism: Cold water essentially induces sinus bradycardia. Brady- and tachyarrhythmias may supervene as secondary complications. Sinusbradycardia may be enhanced by sympathetic hypertonus. Furthermore, ectopic dysrhythmias are liable to be induced by the strictly sympathetic innervation of the ventricle. Myocardial ischemia following a rise in peripheral blood pressure constitutes another arrhythmogenic factor. Some of these reactions are enhanced by alcohol intoxication.
除了目前已知的水浸后猝死机制外,主要讨论了迷走神经性心脏抑制反射。潜水动物以及暴露于冷水中后明显的循环集中化表明存在额外的交感神经活动。在15摄氏度的冷水浴中,我们自己的测量表明血浆儿茶酚胺水平增加了300%以上。这可能通过以下机制导致心律失常:冷水主要诱发窦性心动过缓。缓慢性和快速性心律失常可能作为继发性并发症出现。窦性心动过缓可能因交感神经张力过高而加重。此外,心室的严格交感神经支配容易诱发异位心律失常。外周血压升高后心肌缺血是另一个致心律失常因素。其中一些反应会因酒精中毒而增强。