The ECG can be helpful in making the diagnosis of hyperkalemia. Peaked T waves appear as serum potassium levels exceed 5.5 to 6.5 mEq/L; P-wave disappearance and PR prolongation occur with levels above 6.5 to 7.5 mEq/L; and QRS prolongation occurs when levels rise above 7 to 8 mEq/L.^1-3 These ECG changes occur in only half of patients with hyperkalemia, but recognizing these changes, when they are present, is vital to rapid diagnosis and initiation of lifesaving treatment.⁴ A serum potassium level above 5 mEq/L is diagnostic of hyperkalemia, but the value itself does not always predict ECG changes or the degree of cardiotoxicity.⁵

Patients with suspected or known hyperkalemia should have an intravenous line established and should be placed on continuous cardiac monitoring. The treatment of hyperkalemia is based on the clinical scenario combined with the 12-lead ECG and the laboratory potassium value. The treatment strategy consists of three main steps: 1) stabilizing the cardiac membrane, 2) shifting potassium into the cells, and 3) removing potassium from the body.

Critical Decision

When should intravenous calcium be administered in patients with hyperkalemia?

Administration of calcium as either calcium chloride or calcium gluconate for hyperkalemia is controversial.1 Some authors advocate administering calcium for any ECG changes associated with hyperkalemia, including isolated peaked T waves. We believe that there are only three indications for administering calcium in hyperkalemia, as follows: 1) a widening QRS including a sine wave, 2) a cardiac arrest that is believed to be due to hyperkalemia, or 3) signs of rapidly progressing hyperkalemia in the face of tumor lysis syndrome, massive hemolysis, or rhabdomyolysis where a normal ECG has rapidly progressed through tall peaked T waves and loss of the P wave. In this situation, calcium could be given “prophylactically” while other methods are used to stop potassium release, drive already released potassium into the cell, and begin emergent dialysis to remove potassium from the body.

Because intravenous calcium can cause tachycardia, hypertension, and arrhythmias, as well as hypercalcemia, we urge that calcium not be given routinely for hyperkalemia in an otherwise stable patient with a normal QRS or just isolated, peaked T waves. In the context of digitalis toxicity, intravenous calcium should still be used for life-threatening hyperkalemia with a widening QRS while awaiting the administration and effects of digoxin Fab fragments.