The U Wave

The U wave is the wave that begins with the second heart sound and after the T wave returns to the baseline or close to it.¹

It is a low-amplitude and low-frequency deflection that occurs after the end of the T wave ². It is usually monophasic and positive, and is best visible within a heart rate range of 50 to 100 bpm ³.

U wave is more evident in the leads V2 and V3, and is not usually recorded in the peripheral leads ².

In leads V2 or V3, where the U wave is usually higher, its amplitude is approximately 0.33 mV or 11% of the T wave ^2 4.

The presence of the U wave depends on the heart rate. It is rarely registered at heart rates above 95 bpm, while it is better observed at heart rates less than 65 bpm.

The U wave vector is directed similarly to the T wave vector. U wave is normally positive in precordial leads and is negative in lead aVR. U wave is usually isoelectric in leads I and aVL ^1 4.

Major hypotheses for the origin of the U wave

There are three major theories for the origin of the U wave ^1 3

• Repolarization of the His–Purkinje system.
• Repolarization of the papillary muscle or M cells.
• The mechanoelectrical hypothesis: afterpotential caused by stretching of the left ventricular wall during diastole.

Abnormalities of the U Wave

“AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram ² suggest that the U wave should be included in the EKG interpretation when the U wave is inverted, when it is merged with the T wave, or when its amplitude is greater than that of the T wave” ².

An abnormal U wave is a subtle finding and is rarely an isolated EKG abnormality ⁴.

Increased U Wave Amplitude

Several cardioactive drugs, such as thioridazine, amiodarone, dofetilide, digoxin, quinidine, or sotalol, may cause an increase in the amplitude of the U wave ⁴.

Serum potassium levels below 3 mmol/L (3 mEq/L) may also cause an increase in U wave amplitude in association with progressive depression of the ST-segment, and a decrease in T wave amplitude. With serum potassium levels below 2.7 mmol/L (2.7 mEq/L) the U wave amplitude may exceed the T wave amplitude in the same lead ⁴.

Severe hypokalemia:
Prominent U waves (orange arrows), ST-segment depression and negative T waves (red arrows).

During spontaneous or exercise-induced myocardial ischemia there is occasionally an increase in the amplitude of the U wave in the precordial leads. It is likely to be caused by a compensatory increase in movement of the non-ischaemic myocardial wall and by increased sympathetic stimulation ⁴.

Abnormal prominent U wave in anterior precordial leads without prolongation of the QT interval is a common finding in patients with Andersen-Tawil syndrome ⁵.

U Wave Inversion

During acute myocardial ischemia a transient inversion of the U wave may be observed.

This phenomenon is most common during exercise or coronary spasm, although it may also be observed during PTCA or during an acute coronary syndrome ⁴.

The presence of a negative U wave during exercise in the anterior precordial leads is both sensitive and specific for anterior wall myocardial ischemia, whereas a negative U wave in the inferior leads is specific but not sensitive for acute ischemia of the inferior wall ⁴.

Negative U waves may also appear transiently in the presence of elevated blood pressure ^2 4.

T wave and U wave fusion

In the absence of T wave notching or QT interval prolongation, separation of the T wave from the U wave is not difficult to determine.

The fusion of the U wave and the T wave may occur in the presence of a markedly prolonged QT interval ².

It may also occur with an increase in sympathetic tone ².

In the same situations where there is an increase in the amplitude of the U wave, a fusion of the T wave with the U wave may occur ².

When the T wave is notched, the distant T wave peak can be mistaken for U wave.

Fusion between T wave and U wave may also occur during atrial fibrillation or after a premature impulse ¹.