Premortal changes in the concentration of the serum electrolytes.
Premortal changes in the concentration of the serum electrolytes.
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血清电解质浓度的生前变化。
DOI：
10.1111/j.0954-6820.1948.tb03403.x
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发表时间：
2009
影响因子：
--
通讯作者：
O. Broch
中科院分区：
文献类型：
--
作者：
O. Broch
毫无疑问，产生这些生前电解性变化的必要条件是相当程度的脱水，同时导致血液中的氮质血症和病理性酸。液体的供应量很少，利尿无法测量，可以理解的是，这些变化将在中风的情况下最为明显，患者躺在那里昏迷，没有接受任何营养，考虑到预后无望，通常省略了静脉输液。原因肯定是选择性地失去了水分，同时也保留了一些盐分。从血液浓缩的角度来看，失水的百分比远远大于总碱基的增加。患者一直高烧，失去知觉的失水肯定是相当严重的。有些人出了很多汗，汗水中的盐分相对较少。一名患者(5号)在两天内接受了一升2.6%碳酸氢钠溶液的静脉注射。他得了脑血栓，神志不清，第二天就昏迷了。他在四天后去世了。总碱基增加的条件，就像在第一批患者中看到的那样，在这里应该是存在的。尽管静脉注射的EQ约为620米。小苏打形式的钠，大约相当于血液中全部钠的含量，在这种情况下，血清钠的减少。也没有任何血液浓缩，这可能解释了为什么在这种情况下，总碱基没有出现死亡前的上升。很大程度的脱水和活力受损可能是通过减少滤过，使肾脏部分失灵。尿素和病理性酸的滞留也可以说指向这个方向。也许有一种通过小管对钠的重吸收增加。水肿组(12号、13号、14号)电解质无明显增加。可以合理地认为，细胞外液的充足供应是一个储藏库，可以随时处置，防止脱水和血容量的减少。
Discussion.It can hardly be doubted that the necessary requirement for the production of these premortal electrolytic changes is a considerable degree of dehydration, leading at the same time to azotemia and pathological acids in the blood. The supply of liquids was minimal and the diuresis was impossible to measure, It is understandable that these changes will be most pronounced in case of apoplexy, where the patients are lying unconscious and receive no nourishment and where parenteral administration of liquids is usually omitted in view of the hopeless prognosis. The cause must be supposed to be a selective loss of water, together with some retention of salt. Judging from the hemoconcentration the loss of water is percentually far greater than the increase in the total bases. The patients have been highly febrile and the insensible loss of water has certainly been considerable. Some have perspired very profusely and the sweat contained relatively little salt. One patient (No. 5) was given one litre of a 2.6 per cent sodium bicarbonate solution intravenously in two days. He got a cerebral thrombosis, became soporous and on the next day comatose. He died after four days. The conditions for an increase of the total bases, such as was seen in the first patients, should here be supposed to exist. In spite of intravenous injection of about 620 m. eq. of Na in the form of bicarbonate, which about corresponds to the whole content of Na in the blood, there came in this case a reduction of the serum Na. Neither was there any hemoconcentration, which probably explains why no premortal rise in the total bases occurred in this case. The great degree of dehydration and the impaired vitality must be supposed probably through reduced filtration, to put the kidney partly out of action. The retention of urea and pathological acids may also be said to point in that direction. Perhaps there may be an increased reabsorption of Na through the tubules. No increase of electrolytes was noted in patients with edema (Nos. 12, 13, 14). It is reasonable to suppose that the abundant supply of extracellular fluid serves as a depot which stands at disposal and prevents dehydration and reduction of the blood volume.