 這一篇是由UP TO DATE 文章中摘錄下來
"Clinical manifestations and treatment of hyperkalemia"
Author--Burton D Rose, MD
Section Editor--Richard H Sterns, MD
Deputy Editor--Theodore W Post, MD
This topic last updated: 二月 15, 2008
因為是英文，我無法一字一句翻譯，有些話翻成中文不太好翻，就趁這個機會大家練練英文吧~不過我會盡量幫忙翻譯，希望對大家有用!
TREATMENT-------
Calcium —Calcium directly antagonizes the membrane actions of hyperkalemia. As mentioned above, hyperkalemia-induced depolarization of the resting membrane potential leads to inactivation of sodium channels and decreased membrane excitability. Calcium antagonizes this membrane effect of hyperkalemia, although how this is achieved is not well understood [7] .
(Calcium能直接作用在對抗Hyperkalemia細胞膜上的動作電位。Hyperkalemia會引發靜止膜電位的去極化，導致sodium channels不活化，減少細胞膜上的興奮性。Calcium可以對抗這個Hyperkalemia細胞膜作用，至於如何達到這個作用上不清楚。***說明白一點呢，就是Calcium可以促進Potassium與sodium之間離子的交換，維持Na-K-ATPase pump，減少Potassium在血液中的量。****)
Insulin and glucose —Increasing the availability of insulin lowers the plasma potassium concentration by driving potassium into the cells, apparently by enhancing the activity of the Na-K-ATPase pump in skeletal muscle . Hyperinsulinemia can be induced in either by giving insulin (10 U plus 50 mL of a 50 percent glucose solution as a intravenous bolus followed by a glucose infusion to prevent hypoglycemia) or by the intravenous administration of glucose alone (50 mL of a 50 percent glucose solution), which will rapidly enhance endogenous insulin secretion.
(***說明白一點呢，就是Insulin可以促進Potassium進入到細胞內，降低血液中的Potassium，然而你給Insulin會造成低血糖阿，所以要給glucose，預防Hypoglycemia*****)
Sodium bicarbonate —Raising the systemic pH with sodium bicarbonate results in hydrogen ion release from the cells (as part of the buffering reaction); this change is accompanied by potassium movement into the cells to maintain electroneutrality. In addition, the elevation in the plasma bicarbonate concentration appears to have a direct effect (via an unknown mechanism) that is independent of pH [18] . The potassium-lowering action of sodium bicarbonate is most prominent in patients with metabolic acidosis; it begins within 30 to 60 minutes and persists for several hours.
(***說明白一點呢，就是Sodium bicarbonate會提升身體的PH值，造成hydrogen ion被釋放到細胞外，這個改變也會伴隨著potassium 進入到細胞內，來維持電位的平衡；使用sodium bicarbonate使Potassium降低的作用，用在病人有metabolic acidosis時最為顯著。******)
Beta-2-adrenergic agonists —Like insulin, the beta-2-adrenergic agonists drive potassium into the cells by increasing Na-K-ATPase activity [21] .
(說明白一點呢，就是作用像給Insulin一樣，會促進Potassium進入到細胞，讓血液中的Potassium。****)
Loop or thiazide diuretics —The above modalities only transiently lower the plasma potassium concentration; as a result, additional therapy is required to remove potassium from the body. Although this can easily be achieved in normal subjects with loop and thiazide diuretics, patients with persistent hyperkalemia typically have an abnormality in renal potassium secretion and are unlikely to have a good response to diuretic therapy.
(***說明白一點呢，以上所說的治療形式只能短暫的降低血漿中Potassium的濃度，因此，額外的治療是需要去移除身體中的Potassium離開人體；雖然在正常情況下使用利尿劑排除Potassium很容易被達成，然而當病人持續hyperkalemia，典型的情況下都會有renal排除Potassium異常的現象，如此使用diuretic therapy的效果就不是很好了。****)
Cation exchange resin —The major available cation exchange resin is sodium polystyrene sulfonate (SPS, Kayexalate®), prepared in the sodium phase. In the gut, this resin takes up potassium (and calcium and magnesium to lesser degrees) and releases sodium. Each gram of resin may bind as much as 1 meq of potassium and release 1 to 2 meq of sodium. Thus, a potential side effect is exacerbation of edema due to sodium retention. Calcium polystyrene sulfonate, available outside the United States, does not have significant sodium content.
(說明白一點呢，在內臟，這個resin會跟Potassium結合在一起，然後釋放sodium；一般來說，Kayexalate®的作用較慢，因為它會與Potassium binding然後由糞便排出來，如果很緊急的情況下，這個效果不是這麼快就見效，基本上，會希望病人一天至少大三次；不過這個藥物有個副作用，就是它會造成鈉滯留，如果有水腫的個案，可能會變嚴重；不過每個產品不同，有興趣的話可以詢問醫院用的Kayexalate®是否含有Sodium。***** )
Dialysis —如果以上的情況都沒辦法解決，那就要洗腎啦!!!
 終於完畢了~ ~ |
