What are the EKG changes associated with hypokalemia (low potassium levels) and how are they managed?

EKG Changes in Hypokalemia

Primary EKG Manifestations

Hypokalemia produces characteristic EKG changes including T-wave flattening, ST-segment depression, prominent U waves (particularly in leads V2-V4), and QT interval prolongation, with these findings increasing the risk of life-threatening ventricular arrhythmias. 1, 2

The specific EKG abnormalities include:

• T-wave changes: Flattening and broadening of T waves, progressing to T-wave inversion in severe cases 1, 2, 3
• ST-segment depression: Non-specific ST depression that can mimic ischemia 1, 2, 4
• Prominent U waves: U waves >1 mm in leads V2 and V3, or >0.5 mm in lead II, are considered abnormal and characteristic of hypokalemia 1, 2, 5
• U wave larger than T wave: When the U wave exceeds the T wave amplitude in the same lead, this strongly suggests hypokalemia 5
• QT interval prolongation: Actually represents QU interval prolongation, increasing torsades de pointes risk 1
• PR interval prolongation: Can occur with increasing severity 3
• Increased P wave amplitude: May be observed in moderate to severe cases 3

Arrhythmia Risk

The American Heart Association and American College of Cardiology classify hypokalemia severity as mild (3.0-3.5 mEq/L), moderate (2.5-2.9 mEq/L), and severe (<2.5 mEq/L), with corresponding escalation in arrhythmia risk. 1, 6, 2

Associated arrhythmias include:

• Ventricular arrhythmias: Premature ventricular contractions (PVCs), ventricular tachycardia, torsades de pointes, and ventricular fibrillation 2, 7, 5
• Supraventricular arrhythmias: Atrial fibrillation and supraventricular tachycardia 2
• Conduction abnormalities: First or second-degree atrioventricular block 6, 2
• Cardiac arrest: Progression to pulseless electrical activity (PEA) or asystole in untreated severe cases 6, 2

High-Risk Populations Requiring Urgent Evaluation

Patients with the following characteristics require emergency room evaluation even with mild hypokalemia: 6

• Digoxin therapy: Hypokalemia dramatically increases digitalis toxicity risk, even at mild levels 6, 2, 8
• Cardiac disease or heart failure: These patients should maintain potassium ≥4.0 mEq/L to prevent arrhythmias and mortality 1, 6, 2
• Any EKG abnormalities: Including T-wave flattening, ST depression, prominent U waves, or any arrhythmias 6
• Rapid potassium loss: Patients with acute losses become symptomatic sooner than those with chronic gradual depletion 6

Management Approach

Continuous cardiac monitoring is recommended for patients with moderate to severe hypokalemia (<3.0 mEq/L) and those with any degree of hypokalemia showing EKG abnormalities. 1, 2

Treatment Algorithm:

• Verify hypokalemia: Confirm with blood sample to rule out pseudohypokalemia from hemolysis 2
• Check magnesium levels: Hypomagnesemia frequently coexists and must be corrected concurrently, as it causes renal potassium wasting and makes potassium repletion difficult 1, 6, 2
• Potassium replacement: Use slow intravenous infusion for symptomatic or severe cases; oral replacement for mild cases 6, 8, 7
• AVOID bolus potassium: IV bolus administration for cardiac arrest is Class III (Harm) and should NOT be done 6, 2
• Address underlying cause: Eliminate sources of potassium loss (diuretics, GI losses) and treat metabolic alkalosis if present 6, 8, 7

Target Potassium Levels:

• General hospitalized patients: ≥3.5 mEq/L 2
• Heart failure patients: ≥4.0 mEq/L to reduce arrhythmia and mortality risk 1, 6, 2
• Post-cardiac arrest: 4.0-4.5 mmol/L to prevent recurrent ventricular arrhythmias 6

Critical Pitfalls to Avoid

• Failing to check magnesium: This is the most common error, as hypomagnesemia prevents successful potassium repletion and independently prolongs QT interval 1, 6, 2
• Bolus potassium administration: This is dangerous and contraindicated, even in cardiac arrest scenarios 6, 2
• Inadequate monitoring: Patients with EKG changes require continuous telemetry during correction 1, 2
• Overlooking digoxin toxicity: Even mild hypokalemia significantly increases digoxin toxicity risk 6, 2, 8
• Ignoring clinical context: Rapid potassium losses require more aggressive intervention than chronic depletion, even at similar serum levels 6

Electrophysiologic Mechanism

Hypokalemia increases resting membrane potential, prolongs action potential duration and refractory period (the latter more than the former), increases threshold potential and automaticity, and decreases conductivity—all of which create conditions favorable for both reentrant and automatic arrhythmias 5.