Re: [問題] 高血鉀的靜脈注射用藥`急急急
以下節錄自內科學聖經:Harrison's Principles of Internal Medicine
Chapter 41. Fluid and Electrolyte Disturbances
重點我都畫起來了,裡面該有的都有。
真正用來排鉀的東西... 後面有寫。
Severe hyperkalemia requires emergent treatment directed at minimizing
membrane depolarization, shifting K+ into cells, and promoting K+ loss. In
addition, exogenous K+ intake and antikaliuretic drugs should be
discontinued. Administration of calcium gluconate decreases membrane
excitability. The usual dose is 10 mL of a 10% solution infused over 2 to 3
min. The effect begins within minutes but is short-lived (30 to 60 min), and
the dose can be repeated if no change in the electrocardiogram is seen after
5 to 10 min. Insulin causes K+ to shift into cells by mechanisms described
previously and will temporarily lower the plasma K+ concentration. Although
glucose alone will stimulate insulin release from normal pancreatic cells, a
more rapid response generally occurs when exogenous insulin is administered
(with glucose to prevent hypoglycemia). A commonly recommended combination is
10 to 20 units of regular insulin and 25 to 50 g of glucose. Obviously,
hyperglycemic patients should not be given glucose. If effective, the plasma
K+ concentration will fall by 0.5 to 1.5 mmol/L in 15 to 30 min and the
effect will last for several hours. Alkali therapy with intravenous NaHCO3
can also shift K+ into cells. This is safest when administered as an isotonic
solution of 3 ampules per liter (134 mmol/L NaHCO3) and ideally should be
reserved for severe hyperkalemia associated with metabolic acidosis. Patients
with end-stage renal disease seldom respond to this intervention and may not
tolerate the Na+ load and resultant volume expansion. When administered
parenterally or in nebulized form, 2-adrenergic agonists promote cellular
uptake of K+ (see above). The onset of action is 30 min, lowering the plasma
K+ concentration by 0.5 to 1.5 mmol/L, and the effect lasts 2 to 4 h.
Removal of K+ can be achieved using diuretics, cation-exchange resin, or
dialysis. Loop and thiazide diuretics, often in combination, may enhance K+
excretion if renal function is adequate. Sodium polystyrene sulfonate is a
cation-exchange resin that promotes the exchange of Na+ for K+ in the
gastrointestinal tract. Each gram binds 1 mmol of K+ and releases 2 to 3 mmol
of Na+. When given by mouth, the usual dose is 25 to 50 g mixed with 100 mL
of 20% sorbitol to prevent constipation. This will generally lower the plasma
K+ concentration by 0.5 to 1.0 mmol/L within 1 to 2 h and last for 4 to 6 h.
Sodium polystyrene sulfonate can also be administered as a retention enema
consisting of 50 g of resin and 50 mL of 70% sorbitol mixed in 150 mL of tap
water. The sorbitol should be omitted from the enema in postoperative
patients due to the increased incidence of sorbitol-induced colonic necrosis,
especially following renal transplantation. The most rapid and effective way
of lowering the plasma K+ concentration is hemodialysis. This should be
reserved for patients with renal failure and those with severe
life-threatening hyperkalemia unresponsive to more conservative measures.
Peritoneal dialysis also removes K+ but is only 15 to 20% as effective as
hemodialysis. Finally, the underlying cause of the hyperkalemia should be
treated. This may involve dietary modification, correction of metabolic
acidosis, cautious volume expansion, and administration of exogenous
mineralocorticoid.
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