What are the EKG findings in a patient with hypokalemia?

EKG Findings in Hypokalemia

Hypokalemia produces characteristic EKG changes including prominent U waves (>1 mm), T-wave flattening or broadening, ST-segment depression, and QT interval prolongation, with these findings most visible in the mid-precordial leads V2-V4. 1

Classic EKG Manifestations

The electrocardiographic changes in hypokalemia follow a predictable pattern that correlates with severity:

Primary Features

• Prominent U waves are the hallmark finding, defined as >1 mm in amplitude, particularly in leads V2 and V3 1
• U waves larger than T waves in the same lead, often accompanied by ST-segment depression 1
• T-wave abnormalities including flattening, broadening, or inversion 1, 2
• ST-segment depression occurring alongside the U wave prominence 1, 2
• QT interval prolongation (more accurately QU interval prolongation when U waves are prominent) 1, 2

Specific Diagnostic Criteria

• A U wave >0.5 mm in lead II or >1.0 mm in lead V3 is considered abnormal 1
• A T:U ratio of 1 or less indicates significant hypokalemia 3
• The mid-precordial leads (V2-V4) provide the best visualization of these changes 2

Additional Findings

• PR interval prolongation may occur 2
• Increased P wave amplitude can be present 2
• QRS widening may develop in more severe cases 1

Severity Correlation

The American College of Cardiology classifies hypokalemia severity, with corresponding EKG manifestations 1:

• Mild (3.0-3.5 mEq/L): T-wave flattening and early ST-segment changes 4
• Moderate (2.5-2.9 mEq/L): Prominent U waves, definite ST-depression, QT prolongation 1
• Severe (<2.5 mEq/L): All above findings plus potential for conduction abnormalities 1

Arrhythmia Risk

Beyond the morphologic changes, hypokalemia creates a substrate for dangerous arrhythmias 1:

• Ventricular arrhythmias including premature ventricular contractions, ventricular tachycardia, torsades de pointes, and ventricular fibrillation 4, 3
• Atrial arrhythmias including atrial fibrillation 4
• Conduction disturbances including first or second-degree atrioventricular block 4
• Risk of progression to pulseless electrical activity (PEA) or asystole if untreated 4

Electrophysiologic Mechanisms

The EKG changes reflect specific cellular effects 3, 5:

• Hypokalemia increases resting membrane potential and prolongs action potential duration 3
• The refractory period is prolonged to a greater degree than the action potential, creating conditions for reentrant arrhythmias 3
• Increased automaticity and decreased conductivity further promote arrhythmogenesis 3
• Membrane hyperpolarization and increased excitation threshold contribute to conduction slowing 5

Clinical Context and Prevalence

In a multicenter study of 79,599 patients, EKG abnormalities were present in 40% of hypokalemic patients with potassium <3.5 mmol/L 6:

• T-wave flattening occurred in 27% 6
• ST-segment depression in 16% 6
• QTc prolongation in 14% 6

High-Risk Scenarios Requiring Urgent Monitoring

The American Heart Association recommends continuous cardiac monitoring for 1:

• Moderate to severe hypokalemia with any EKG changes 1
• Patients on digoxin (even mild hypokalemia increases digitalis toxicity risk) 4, 7
• Cardiac disease or heart failure patients (target potassium ≥4.0 mEq/L) 4
• Hypokalemia with ventricular arrhythmias requiring urgent intervention 1

Critical Pitfalls to Avoid

• Concurrent hypomagnesemia frequently coexists and can contribute to QT prolongation and torsades de pointes, requiring simultaneous correction 1, 4
• Rapid potassium shifts may cause symptoms before chronic gradual depletion, even at higher potassium levels 4
• The American Heart Association explicitly states that bolus administration of potassium for cardiac arrest is ill-advised (Class III) 1—slow infusion is mandatory 4
• Individual variability exists in EKG manifestations, requiring careful clinical correlation rather than relying solely on potassium levels 1