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The Chest Pain Patient with Prominent T Waves

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

Cases in Electrocardiography

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

The T wave is the electrocardiographic representation of the ventricular repolarization period. Abnormalities of the T wave can provide valuable evidence of underlying events, whether it is a cardiac (e.g., ST segment elevation AMI) or systemic event (e.g., hyperkalemia). The electrocardiographic differential diagnosis of the prominent T wave is broad, including early ST segment elevation AMI (STEMI), hyperkalemia, benign early repolarization, left ventricular hypertrophy, acute pericarditis, bundle branch block, and pre-excitation syndromes. These syndromes can cause increased T wave amplitude and duration, often described in the literature as tall, peaked, prominent, tented, or hyperacute, depending upon the associated event.

Perhaps the most ominous cause of the prominent T wave is early STEMI (Figure 2). In the STEMI patient, the ECG demonstrates a well-established temporal evolution following the onset of coronary artery occlusion. The initial electrocardiographic finding resulting from the STEMI is the prominent T wave, termed “hyperacute” in this context, and can appear as early as 30 minutes after the onset of infarction; this structure evolves rapidly on to obvious ST segment elevation if the infarction continues.

Figure 2

Figure 2

The hyperacute T wave is most often replaced within a few minutes to a few hours by the characteristic QRS complex and ST segment-T wave changes of AMI, namely, ST segment elevation with variable presence of Q waves. (Wagner: Marriott's Practical Electrocardiography, 10th ed., 2001 Lippincott Williams & Wilkins; Heart & Lung 1984;13:168; Rosen's Emergency Medicine: Concepts and Clinical Practice, 4th ed., 1998 Mosby Year Book, Inc.) Recent opinion indicates that, unlike ST segment changes and pathologic Q waves, hyperacute T waves are not associated with abnormal elevations in cardiac serum markers. (Acad Emerg Med 2001;8:551 [abstract].)

Such AMI T wave abnormalities can be termed primary (direct, initial manifestation of AMI) or secondary (consequence of the degree of ST segment abnormality). In certain cases, there is greater positive deviation of the T wave than is characteristic of the prominent T wave without established ST segment elevation; this description applies to the hyperacute T wave of early AMI. (Wagner: Marriott's Practical Electrocardiography, 10th ed., 2001 Lippincott Williams & Wilkins.) In other instances of AMI, the degree of T wave deviation may reflect only the degree of associated ST segment elevation, and should be considered a secondary T wave abnormality.

T wave morphology of early AMI is variable and can be symmetric or asymmetric. (Rosen's Emergency Medicine: Concepts and Clinical Practice, 4th ed., 1998 Mosby Year Book, Inc.) In most instances, hyperacute T waves of AMI are asymmetric with a broad base. (Figures 2 and 3.) In addition, the J point, which marks the end of the QRS and the beginning of the ST segment, also may be elevated, indicating impending ST segment elevation. The R wave also increases in amplitude at this stage. As the J point elevates, the giant R wave is formed, which then progresses to typical ST segment elevation of AMI.

Figure 3

Figure 3

Perhaps the next ominous electrocardiographic entity manifested by the prominent T wave is hyperkalemia. T waves of large magnitude are seen in patients with hyperkalemia with a morphology described as “tall and peaked,” and may be confused with the hyperacute T wave of early STEMI. These T waves tend to be tall, narrow, and peaked with a prominent apex, resembling the tall, vaulting appearance of a church steeple. (Figures 1 and 3.) Also, these T waves tend to be symmetric in morphology; if “split down the middle,” the resulting portions would be mirror images.

As the serum potassium level increases, the T waves tend to become taller, more peaked, and increasingly narrowed in a symmetric fashion. These T waves most often are seen in the anterior distribution. (Figure 1.) With further progression of the metabolic abnormality, the QRS complex widens, advancing to the sinoventricular rhythm and ultimately to ventricular fibrillation.

Although there is no exact correlation between serum potassium levels and the onset of ECG changes, 80 percent of patients exhibit ECG changes with serum potassium of 6.8 mEq. (Heart & Lung 1984;13:168.) In general, sudden or rapid increases in the serum potassium will cause more pronounced electrocardiographic changes at relatively lower concentrations; in contrast, gradual increases in the serum potassium will require higher values to manifest electrocardiographic abnormality.

Early repolarization, also known as benign early repolarization (BER), is a variant of the normal ECG. This syndrome has been reported in men and women of all age groups and varying ethnicities; BER, however, is most often seen in young adult males. The electrocardiographic definition of BER includes ST segment elevation, upward concavity of the initial portion of the ST segment, notching or slurring of the terminal QRS complex, symmetric, concordant T waves of large amplitude (Figure 4, left), widespread or diffuse distribution of ST segment elevation on the ECG, and relative temporal stability. (Am J Emerg Med 1998;16;592; Am J Cardiol 1961;8:184.)

Figure 4

Figure 4

Prominent T waves of large amplitude and slightly asymmetric morphology are encountered; the T waves may appear “peaked” and broad, suggestive of the hyperacute T wave encountered in patients with AMI. The T waves are concordant with the QRS complex and are usually found in the precordial leads. The height of the T waves in BER ranges from approximately 6.5 mm in the precordial distribution to 5 mm in the limb leads. (Am J Cardiol 1961;8:184; Electrocardiography in the patient with myocardial ischemia or infarction, in Emergency Cardiac Care, 1st edition, St. Louis, Mosby, 1994, pp. 169–216; Am J Med Sci 1995;309:305.)

Electrocardiographic LVH is frequently encountered in the ED chest pain patient. LVH is identified on the ECG by voltage criteria (cumulative voltage of the S wave in lead V1 and the R wave in lead V5 or V6 greater than 35 millimeters); ST segment-T wave changes resulting from altered repolarization of the hypertrophied myocardium, the so-called “strain” pattern, are noted in approximately 70 percent of patients with LVH. (Br Heart J 1992;67:304.) Isolated, tall T waves may appear in the right precordial leads of patients with LVH. (Figure 4, right.)

Single, prominent T waves in this rather specific setting are therefore easily discernible from the hyperacute T waves of STEMI. Nonetheless, the prominent T waves associated with electrocardiographic LVH may be misinterpreted as hyperacute T waves of early AMI, particularly when the T wave changes are not accompanied by pronounced ST segment elevation, i.e. when the predominant electrocardiographic manifestation of the altered repolarization is the prominent T wave. (Am J Emerg Med 1998;16:692.)

The interpretation of the ECG in this setting is best performed in a systematic fashion, focusing not only on the rhythm but also the morphologic appearance of the various structures; this interpretation also must be performed within the context of the clinical presentation. Considering the ECG in our case (Figure 1), the rhythm is normal sinus without ectopy. The most prominent feature is the T wave; in leads V2 to V5, the T wave is very prominent. Its morphology is tall, narrow, symmetric, and peaked. The J point is minimally elevated. With further inspection, the QRS complex is widened to approximately 0.11 seconds.

These T waves (Figure 1) most closely resemble prominent T waves of hyperkalemia. Recall that with early STEMI, prominent T waves are often broad and asymmetric, in significant contrast to the narrow, peaked, symmetric T waves of hyperkalemia. Furthermore, with essentially normal ST segments including the position of the J point, these T waves are likely not transition structures on to STEMI. With an abnormal QRS complex in the same leads (i.e., increased duration), additional evidence supporting hyperkalemia is found.

Regarding the other possible entities, BER and LVH, both are excluded based upon the absence of related electrocardiographic findings — diffuse ST segment elevation and J point elevation as well as prominent QRS complexes, respectively. When considered within the clinical parameters of this presentation, chronic renal insufficiency certainly suggests hyperkalemia. Ultimately, the serum potassium was elevated, providing biochemical evidence of hyperkalemia.

The ECG in Figure 1 demonstrates normal sinus rhythm with prominent T waves in leads V2 to V5; the QRS complex also is widened minimally in this distribution. The most striking structure on this ECG, the prominent T waves, represents the feature about which to construct a differential diagnosis. As discussed above, the differential includes early STEMI, hyperkalemia, benign early repolarization, left ventricular hypertrophy, acute myopericarditis, and bundle branch block.

The T waves are tall, narrow, and symmetric. The base is slender with a tapering to a narrow peak, much like a church's steeple. The QRS complex is minimally widened. These two findings, when considered together, suggest hyperkalemia as the ultimate cause of the electrocardiographic abnormality.

The repeat ECG did not demonstrate change; the T waves and ST segments were static. Further examination of the patient revealed palpable chest discomfort. The serum potassium was 7.2 mEq/dl, and the serum troponin was within normal limits. The patient urgently received intravenous calcium gluconate, sodium bicarbonate, regular insulin, and dextrose 50%; Kayexalate was administered orally; and albuterol was given via nebulizer.

He underwent hemodialysis later that evening with an uneventful course. It was later discovered that the patient had recently switched to a dietary salt substitute. With the increased potassium intake, the already dysfunctional kidneys were unable to excrete the excess cation, resulting in hyperkalemia.

© 2005 Lippincott Williams & Wilkins, Inc.