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Multiple Choice

Which electrolyte disturbances contribute to QT prolongation and torsades risk?

QT prolongation and the risk of torsades de pointes arise when ventricular repolarization is delayed, and this is driven by disturbances in electrolytes that control the repolarizing currents. Low potassium reduces the outward potassium currents (IKr/IKs) that move the cell toward repolarization, so the action potential lasts longer and the QT interval widens. Low magnesium removes a stabilizing influence on several ion channels and makes early afterdepolarizations more likely, which can trigger torsades in the setting of a long QT. Low calcium lengthens the plateau phase of the action potential, further delaying repolarization and extending the QT interval; high calcium does the opposite, shortening QT. So disturbances of potassium, magnesium, and calcium in the low range all contribute to QT prolongation and torsades risk. Hyperkalemia and hypermagnesemia tend to shorten or not prolong QT, hypercalcemia shortens QT, and hyponatremia does not directly cause QT prolongation.

QT prolongation and the risk of torsades de pointes arise when ventricular repolarization is delayed, and this is driven by disturbances in electrolytes that control the repolarizing currents. Low potassium reduces the outward potassium currents (IKr/IKs) that move the cell toward repolarization, so the action potential lasts longer and the QT interval widens. Low magnesium removes a stabilizing influence on several ion channels and makes early afterdepolarizations more likely, which can trigger torsades in the setting of a long QT. Low calcium lengthens the plateau phase of the action potential, further delaying repolarization and extending the QT interval; high calcium does the opposite, shortening QT.

So disturbances of potassium, magnesium, and calcium in the low range all contribute to QT prolongation and torsades risk. Hyperkalemia and hypermagnesemia tend to shorten or not prolong QT, hypercalcemia shortens QT, and hyponatremia does not directly cause QT prolongation.