ECG changes of hypokalemia and hypomagnesemia during anesthesia and how to treat?

• A. U waves, flattened T waves; torsades de pointes with hypomagnesemia; treat with magnesium sulfate and potassium repletion
• B. ST elevations
• C. Peaked T waves
• D. AV block

Answer: (A)

The key idea is that electrolyte gaps can dramatically alter the heart’s rhythm during anesthesia. Low potassium changes the heart’s repolarization, producing characteristic ECG signs of hypokalemia: the T waves become flattened and U waves appear after the T wave. Low magnesium, even if potassium is not severely low, can prolong the QT interval and raise the risk of torsades de pointes, a specific, potentially dangerous form of polymorphic ventricular tachycardia often triggered by early afterdepolarizations. Because these disturbances increase the risk of dangerous arrhythmias during anesthesia, treating them promptly by correcting the electrolyte deficits is essential.

The best approach is to replete both magnesium and potassium. Administer intravenous magnesium sulfate for any torsades de pointes or QT prolongation; typical use is a bolus of around 1–2 g IV, followed by a maintenance infusion as needed to maintain serum magnesium in the therapeutic range. Correct potassium as well to normalize the level (often targeting roughly 4–5 mEq/L), using IV potassium chloride with careful monitoring for extravasation and arrhythmias. It’s important to correct magnesium first when both are low because magnesium helps potassium repletion work more effectively and reduces the likelihood of recurrent torsades. Throughout, monitor the ECG closely, review perioperative medications that can prolong QT, and be ready to treat any sustained arrhythmia according to ACLS guidelines.