Why does ST depression occur in patients with hypokalemia (low potassium levels)?

Why ST Depression Occurs in Hypokalemia

Electrophysiologic Mechanism

ST depression in hypokalemia occurs because low potassium levels alter the plateau phase of the ventricular action potential, creating primary repolarization abnormalities that manifest as ST-segment depression on the ECG. 1

The fundamental mechanism involves several interconnected electrophysiologic changes:

• Hypokalemia prolongs the action potential duration and increases the refractory period (the latter to a greater degree than the former), which creates conditions conducive to both reentrant and automatic arrhythmias 2
• Low potassium increases resting membrane potential and threshold potential, while simultaneously decreasing conductivity and increasing automaticity 2
• These changes in the plateau phase of the ventricular action potential directly produce ST-segment depression as a primary repolarization abnormality, distinct from ischemia-related ST changes 1

Clinical ECG Manifestations

The characteristic ECG findings of hypokalemia include:

• ST-segment depression (often widespread, particularly in leads II, III, aVF, V1-V6) 3, 4, 5, 6
• T-wave flattening or broadening 3, 7
• Prominent U waves (>1 mm, particularly in leads V2-V4) 3, 5, 2
• QT interval prolongation 3, 4
• PR interval prolongation with increased P-wave amplitude 5

The ST-segment depression becomes more evident during increases in heart rate, as demonstrated by Holter monitoring in patients with severe hypokalemia 4

Severity Correlation

The degree of ECG changes correlates with potassium levels:

• Mild hypokalemia (3.0-3.5 mEq/L): T-wave flattening and subtle ST changes 3, 7
• Moderate hypokalemia (2.5-2.9 mEq/L): ST-segment depression, prominent U waves, and increased arrhythmia risk 3, 4
• Severe hypokalemia (<2.5 mEq/L): Marked ST depression, prolonged QT, and life-threatening arrhythmias including ventricular tachycardia, torsades de pointes, and ventricular fibrillation 3, 8, 4

Critical Diagnostic Pitfall

ST depression from hypokalemia can masquerade as myocardial ischemia, particularly when accompanied by chest discomfort 6. The key distinguishing features are:

• Hypokalemia produces widespread ST depression across multiple leads rather than the regional pattern typical of ischemia 6
• Prominent U waves and T-wave changes accompany the ST depression in hypokalemia 3, 5, 2
• ECG abnormalities resolve with potassium correction, confirming the electrolyte etiology 4, 6

Clinical Significance

Even modest hypokalemia increases the risk of serious cardiac arrhythmias, particularly in patients with:

• Cardiac disease or heart failure (target potassium 4.0-5.0 mEq/L) 9, 3
• Digoxin therapy (hypokalemia dramatically increases digitalis toxicity risk) 9, 2
• Concurrent QT-prolonging medications 9

The combination of ST depression with hypokalemia indicates significant cardiac risk and warrants prompt correction, as these ECG changes reflect the arrhythmogenic substrate that can progress to ventricular tachycardia, torsades de pointes, or ventricular fibrillation 3, 8, 4, 2

Concurrent Electrolyte Considerations

Hypomagnesemia frequently coexists with hypokalemia (approximately 40% of cases) and must be corrected first, as magnesium deficiency makes hypokalemia resistant to correction and independently contributes to arrhythmia risk 9, 7