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Diagnosis: Hypokalemia

Chan, Theodore MD; Brady, William MD; Harrigan, Richard MD

Cases in Electrocardiography

Dr. Chan is an associate professor of clinical medicine, emergency medicine, the director of CQI, and the associate medical director of the department of emergency medicine at the University of California

San Diego; and Dr. Brady is an associate professor and the program director in the department of emergency medicine at the University of Virginia School of Medicine in Charlottesville.

Dr. Harrigan is an associate professor of emergency medicine and the associate research director in the department of emergency medicine at Temple University Hospital and School of Medicine in Philadelphia

The ECG in Figure 1 demonstrates sinus rhythm with a prominent U wave deflection following the T wave, most conspicuously seen in the precordial leads. The T wave has a diminished amplitude. The U wave deflection appears to overlap both the preceding T wave and following P wave of the next cardiac cycle. The computer reported a remarkably prolonged QTc interval of 0.78 seconds.

Figure 1

Figure 1

Normally, the U wave is a small, rounded deflection with an ascent shorter than descent, though it can appear symmetric in appearance. The height of the normal U wave can vary, but is no more than one-quarter of the T wave height.1 At normal heart rates, the duration from the apex of the T wave to the apex of the U wave is 0.10 seconds. The normal U wave is directed leftward and anterior, similar to the T wave, with an axis of approximately +60 degrees. U waves are usually most prominent in leads II and V2–4, and least prominent in leads I and aVL. U waves with negative deflections can be seen in leads aVR, aVF, and III. The U wave is often inconspicuous in appearance in normal individuals, and can be mistaken as part of the T wave or a prolonged QT interval.

The exact mechanism for the U wave is unknown. Several hypotheses have been proposed to explain this last deflection of ventricular repolarization. Genesis of the U wave has been attributed to delayed repolarization of the Purkinje fibers, afterpotentials generated by mechanico-electrical coupling during ventricular relaxation, longer duration of the action potential of conducting myocytes, and repolarization of the papillary muscle cells or other portion of the ventricular myocardium.2

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Increased Amplitude

Increased amplitude of the U wave can be seen with exercise, pheochromocytoma and certain medications, including inotropic agents, digoxin, amiodarone, and quinidine. In addition, larger U waves may be seen in the cardiac cycle immediately following a long pause as occurs with extrasystole beats, and also can be seen with bradycardia. Young athletes may have U waves with an amplitude of up to 2 mm. Prominent U waves greater than 1.5 mm can be seen in patients with acute CNS events such as strokes. In these cases, however, the U wave can be obscured by a fast heart rate and increased T wave amplitude.

Pathologic U waves on ECG are most commonly associated with hypokalemia. Low serum potassium levels affect the transmembrane gradient across the cardiac cells. These changes result in an elevation in the resting membrane potential, increase in duration of the action potential and refractory period, and prolongation of phase 3 repolarization of the cardiac cycle.

These changes have a pronounced effect on the ECG with a progressive decline in serum potassium levels. The earliest sign of hypokalemia is often a decrease in T wave amplitude. With more severe levels of hypokalemia, ST segment depression and T wave inversion may be seen. With significant drops in serum potassium, prominent U waves appear, particularly in the mid-precordial leads, and are considered a classic ECG finding associated with hypokalemia.3

With severe hypokalemia, large giant U waves can be seen that often mask the smaller preceding T wave. In addition the PR interval and QT interval, or more correctly the QTU interval, can be prolonged. As a result, patients with severe hypokalemia are at risk for life-threatening dysrhythmias including ventricular tachycardia, torsades de pointes, and ventricular fibrillation.4 Treatment focuses primarily on aggressive parenteral as well as oral potassium repletion and identification of the cause of hypokalemia, including inadequate intake or excessive renal or gastrointestinal losses.

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The Case

In this particular case, the patient had a history of chronic episodic hypokalemia as a result of her renal tubular acidosis. She had run out of her potassium supplement four days prior to presentation. In the ED, her serum potassium level was 2.1 mEq/L.

She was admitted to the hospital for intravenous and oral potassium supplementation. On the first day of admission, a repeat ECG was obtained (Figure 2), which demonstrated even more remarkable changes associated with her condition.

Figure 2

Figure 2

Giant U waves were present, easily seen in the precordial leads. The patient's serum potassium level at this time was 1.9 mEq/L. She continued to receive aggressive repletion and electrolyte correction, and by day four of her hospitalization, her condition improved. Prior to discharge, a repeat ECG showed resolution of the changes associated with hypokalemia (Figure 3).

Figure 3

Figure 3

The patient was discharged home in good condition with a potassium level of 3.6 mEq/L.

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References:

1. Yan GX, Lankipalli RS, et al. Ventricular repolarization components in the electrocardiogram. J Amer Coll Card 2003;42(3):401.
2. Surawicz B. U wave: Facts, hypotheses, misconceptions, and misnomers. J Cardiovasc Electrophysiol 1998;9:1117.
3. Surawicz B. Electrolytes and the electrocardiogram. Postgrad Med 1974; 55:123.
4. Helfant RH. Hypokalemia and arrhythmias. Am J Med 1986;80:13.
© 2003 Lippincott Williams & Wilkins, Inc.