TOC | Lytes | Hypokalemia
Hyperkalemia (Serum K > 5.0 mEq/L or 5 mmol/L)
|Signs & Symptoms
The symptoms of hyperkalemia are related to impaired neuromuscular transmission
changes: increase T, S ,PR interval, QRS interval;
decreased P, R, ST segment; 2-3 AV block; atrial or vent. arrhythmia
Discontinuance of all medications that adversely
affect potassium balance is mandatory in true hyperkalemia,
particularly when it is severe (plasma [K+] > 6.0 mEq/L).
Algorithmic management of Hyperkalemia
Is life-threatening hyperkalemia present?
A. If No (Life-threatening hyperkalemia is not present) --> Resin exchange with laxative, loop diuretic as furosemide, dialysis
B. If Yes (life-threatening hyperkalemia is present)-->
Step 1: Stabilize the myocardium: (IV Calcium infusion)
Step 2: Shift potassium into cells: (IV glucose +/- insulin +/- Na bicarbonate; Albuterol nebulizer Rx or IV infusion)
Step 3: Enhance elimination of potassium: (Kayexalte, Lasix, Dialysis)
REF: Mayo Clinic Proceedings Dec 2007
* If aldosterone deficiency has been documented in cases of chronic hyperkalemia that are inadequately controlled by diet or diuretics, aldosterone replacement with fludrocortisone acetate may be useful. The combination of fludrocortisone and a loop diuretic may limit the development of hypertension or edema. However, because its onset of action may take several days or longer, this therapy is not sufficiently effective to be used in the treatment of acute, life-threatening hyperkalemia.
A. Pseudohyperkalemia (Factitious hyperkalemia)
1. Improper blood collection (lab error)
2. Hematologic disorder with increased WBC or platelets
B. Exogenous potassium load
C. Decreased renal potassium excreation
D. Cellular shift of K+
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REF: ACP Medicine 6-2008
Treatment of Hyperkalemia
In true hyperkalemia, particularly when it is severe (plasma [K+] > 6.0 mEq/L), discontinuance of all medications that adversely affect potassium balance is mandatory.46 These medications include nonselective beta blockers, ACE inhibitors, potassium-sparing diuretics, NSAIDs, and trimethoprim. Salt substitutes, which contain potassium chloride, should also be avoided. Persons with mild hyperkalemia (plasma [K+] < 6.0 mEq/L) can usually be treated conservatively with reduction of daily intake to less than 2 g and, if indicated, with the addition of a loop diuretic.
Active treatment to lower the plasma [K+] or to antagonize its effects on the cell membrane should be started if the plasma [K+] has risen acutely to 6.0 mEq/L or higher, particularly if ECG manifestations of hyperkalemia are present; several therapeutic options are available [see Table 11].
An infusion of calcium rapidly normalizes the ECG. An increase in the [Ca+] raises the threshold potential, thereby returning membrane excitability to normal. Calcium should be administered, however, in the presence of only those ECG manifestations of hyperkalemia that may precede ventricular fibrillation. Because calcium can exacerbate or precipitate glycoside-induced cardiac arrhythmias, it should be used only when necessary and with great care in patients receiving digoxin or other digitalis preparations.
Calcium is administered intravenously as the gluconate or chloride salt (10 ml of 10% calcium gluconate over 2 to 3 minutes, with ECG monitoring). Normalization of the ECG may persist for less than 60 minutes; furthermore, this treatment does not alter the plasma [K+] or total potassium body stores. Consequently, measures that will lower the plasma level and remove potassium from the body should be initiated simultaneously.
Sodium bicarbonate, glucose (with or without insulin), and beta2-adrenergic receptor stimulation lower the plasma [K+] by promoting the entry of potassium from the extracellular fluid into cells. The administration of sodium bicarbonate reduces the hydrogen ion concentration in the extracellular fluid. Theoretically, if the Na+-H+ exchanger were in an active mode, the administration of sodium bicarbonate would favor the movement of H+ out of cells as Na+ enters. The subsequent exit of sodium by the Na+,K+-ATPase pump would shift potassium into the cell. In the steady state, however, the Na+-H+ exchanger appears to be inactive.47 By comparison, the Na+-H+ exchanger is activated by intracellular acidosis.
Several studies have found sodium bicarbonate therapy to be ineffective in the treatment of acute hyperkalemia, despite a rise in the serum [HCO3-]. Furthermore, bicarbonate does not appear to potentiate the hypokalemic action of beta2-adrenergic agonists or the combination of glucose and insulin, which are more effective in this setting.48 Because of these findings, sodium bicarbonate, if used in the treatment of hyperkalemia, should be used in combination with other agents.47
Beta2-adrenergic agonists can also transiently lower the serum potassium level. Albuterol can be administered at a dosage of 10 to 20 mg in 4 ml of saline by nasal inhalation over 10 minutes or by a 0.5 mg I.V. infusion. The blood potassium level usually falls by 0.5 to 1.5 mEq/L within 30 minutes after the I.V. infusion, but more than 1 hour is required for a peak effect when albuterol is inhaled.49
The hypokalemic effect of insulin is observed within 30 to 60 minutes, and it can be achieved by simply administering 25 g of glucose intravenously, because a glucose infusion rapidly stimulates insulin release. Alternatively, 10 units of regular insulin can be given intravenously with this glucose load to patients with diabetes, although this regimen can cause hypoglycemia in normal persons. Regardless of the method, care must be taken to avoid producing severe hyperglycemia by the glucose infusion, because a high plasma glucose concentration can exacerbate hyperkalemia by causing water, which contains potassium, to shift from the intracellular compartment into the plasma.
Like the administration of calcium, the administration of glucose and insulin, bicarbonate, and beta2-adrenergic agonists is a temporary measure because total body potassium stores are not reduced. Therefore, additional therapy is required to ensure that the plasma [K+] does not return to pretreatment levels. Furthermore, in some patients, lowering the plasma [K+] with these agents shortly before dialysis can lead to reduced dialytic potassium removal, possibly resulting in rebound hyperkalemia after the dialysis treatment has been completed.49
Increasing urine flow with diuretics is sometimes
useful, but renal insufficiency frequently limits the effectiveness of
However, the Na+-K+ cation exchange resin sodium polystyrene sulfonate can be administered in sorbitol (to promote diarrhea) orally or as a retention enema. The use of sodium polystyrene sulfonate can exchange 4 mEq of Na+/g for 4 mEq of K+; therefore, in theory, 30 g of Kayexalate (Na Polystyrene Sulfonate) could remove 120 mEq of potassium. However, because the quantity of gastrointestinal potassium available for exchange may be as little as 5 mEq/day, the effectiveness of sodium polystyrene sulfonate has been questioned.47 In some studies, sodium polystyrene sulfonate was no more effective than the laxative in which it was administered. Some experts no longer recommend use of sodium polystyrene sulfonate in sorbitol; however, the diarrhea this agent induces may in itself be helpful in reducing the serum [K+]. I recommend use of sodium polystyrene sulfonate if the urine output is low and if dialysis is not readily available.
Dialysis should be considered in severe or refractory cases of hyperkalemia, particularly when there is advanced renal failure. When available, hemodialysis is preferable in the acute setting because it removes potassium much more quickly than peritoneal dialysis does.
If aldosterone deficiency has been documented in cases of chronic hyperkalemia that are inadequately controlled by diet or diuretics, aldosterone replacement with fludrocortisone acetate may be useful. The combination of fludrocortisone and a loop diuretic may limit the development of hypertension or edema. However, because its onset of action may take several days or longer, this therapy is not sufficiently effective to be used in the treatment of acute, life-threatening hyperkalemia.