HYPERKALEMIA is the most dangerous electrolyte abnormality. It may result in sudden arrhythmogenic death because of its effect on the cells’ resting membrane potentials. The most common explanation for hyperkalemia is often referred to as laboratory error. Actually, the laboratory does the right analysis, but the serum sample has hemolyzed after (or while) being drawn.
Other common causes of hyperkalemia are: chronic renal failure, acidosis (K moves out of the cell as the pH falls) and medications including NSAIDs, K-sparing diuretics, digoxin, ACE-inhibitors, and administration of IV potassium chloride. Also, cell death (when comes out of injured muscle or red cells), including burns, crush injuries, rhabdomyolysis, tumor lysis syndrome, and intravascular hemolysis. Much less common causes include adrenal insufficiency, hyperkalemic periodic paralysis, and hematologic malignancies.
An electrocardiogram (ECG) is the most important study to obtain in the setting of suspected hyperkalemia (e.g., a patient with chronic renal failure or an unexplained bradycardic rhythm). The first ECG changes in hyperkalemia are tall peaked T waves which occur as K values rise to 5.5–6.5 mEq/L. Loss of the p wave may follow as K levels rise to 6.5–7.5 mEq/L. The most dangerous ECG finding (typically at levels > 8 mEq/L) is widening of the QRS complex , which may merge with the abnormal T wave and create what appears to be a sine wave of ventricular tachycardia.
MANAGEMENT ― Treatment is based on the presence or absence of ECG changes, serum levels, and the patient’s underlying renal function. If the patient has life-threatening ECG changes of hyperkalemia (widening QRS complex, a sine wave–like rhythm or bradycardia/heart block), 10% calcium chloride should be given (10 mL, preferably through a central line) to temporarily stabilize the myocardial cell membranes (see Table 1). Although calcium is relatively fast-acting, its effect lasts only 30–60 minutes, requiring additional measures to lower K levels. However, most patients with hyperkalemia will not have QRS widening, and only require K moved intracellularly, and then removed from the body.
| Table (1). Medications Used in Acute Treatment of Hyperkalemia | |||||
|---|---|---|---|---|---|
| MEDICATION | DOSAGE | ONSET | LENGTH OF EFFECT | MECHANISM OF ACTION | CAUTIONS |
| Calcium gluconate | 10 to 20 mL of 10 percent solution IV over two to three minutes | Immediate | 30 minutes | Protects myocardium from toxic effects of calcium; no effect on serum potassium level | Can worsen digoxin toxicity |
| Insulin | Regular insulin 10 units IV with 50 mL of 50 percent glucose | 15 to 30 minutes | Two to six hours | Shifts potassium out of the vascular space and into the cells; no effect on total body potassium | Consider 5 percent dextrose solution infusion at 100 mL per hour to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above 250 mg per dL (13.9 mmol per L) |
| Albuterol (Ventolin) | 10 to 20 mg by nebulizer over 10 minutes (use concentrated form, 5 mg per mL) | 15 to 30 minutes | Two to three hours | Shifts potassium into the cells, additive to the effect of insulin; no effect on total body potassium | May cause a brief initial rise in serum potassium |
| Furosemide (Lasix) | 20 to 40 mg IV, give with saline if volume depletion is a concern | 15 minutes to one hour | Four hours | Increases renal excretion of potassium | Only effective if adequate renal response to loop diuretic |
| Sodium polystyrene sulfonate (Kayexalate) | Oral: 50 g in 30 mL of sorbitol solution Rectal: 50 g in a retention enema |
One to two hours (rectal route is faster) | Four to six hours | Removes potassium from the gut in exchange for sodium | Sorbitol may be associated with bowel necrosis. May lead to sodium retention |
How can potassium be moved intracellularly? The most effective way is by giving glucose and insulin. Glucose and insulin work by activating the glucose transport system to move glucose into the cell. As glucose is carried intracellularly, K is carried along. The usual dosage of glucose is two ampules of dextrose 50% in water (D50W; 100 mL) and 10 U of regular insulin (Actrapid). Another excellent first-line method of driving K into the cell is use of inhaled β-agonist bronchodilators. β-Agonists may be especially helpful in a patient who has renal failure with fluid overload, additionally treating bronchospasm from pulmonary edema. HCO3 may also be used to drive K into the cell, but it is effective only in acidotic patients. Usually one to two ampules of HCO3 (50 mEq of HCO3 per ampule) are given over 1–10 minutes, depending on patient acuity.
Hyperkalemia itself is often asymptomatic; check the ECG.
The ECG changes seen as K rises are tall, peaked T waves , followed by loss of P waves, and, finally, widening of the QRS complex.
Administering glucose and insulin, supplemented by an inhaled β-agonist, is the most effective method to drive K into the cell and acutely lower serum K.
HCO3 only works to lower serum K in acidotic patients.
Only give calcium for hyperkalemia if there is a wide QRS complex or life-threatening bradycardia.
REFERENCES
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Hollander-Rodriguez, J.C. and Calvert, J.F. (2013). Hyperkalemia. American Family Physician, [online] 73(2), pp.283–290. Available at: https://www.aafp.org/afp/2006/0115/p283.html
Erin, K. (2017). Updated Treatment Options in the Management of Hyperkalemia. [online] Uspharmacist.com. Available at: https://www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia