I. Problem/Condition.

The electrocardiographic T wave represents ventricular repolarization. Abnormalities of the T wave are associated with a broad differential diagnosis and can be associated with life-threatening disease or provide clues to an otherwise obscure illness.

When abnormalities of the T wave are noted on a 12-lead electrocardiogram, it is important to bring the clinical history of the patient to bear to assist in making the correct diagnosis. For example, tall, peaked T waves in a patient who missed three runs of dialysis are likely to represent hyperkalemia, while tall “hyperacute” T waves in a patient complaining of the acute onset of crushing, sub-sternal chest pain could represent the acute onset of transmural myocardial ischemia. Thus, the clinical history and setting in which the ECG is obtained affects the pre-test probability of particular diagnoses in considering the interpretation of T wave abnormalities.

Finally, when possible, it is important to compare the abnormalities noted on a 12-lead ECG to a prior tracing. This comparison can be invaluable in assessing the chronicity of abnormalities as well as identifying subtle morphologic changes that may not have been otherwise evident.

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II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

The differential diagnosis of T wave abnormalities can be broadly categorized into disease entities associated with tall T waves and those associated with inverted T waves.

Tall T waves

Hyperacute T waves of early ST-elevation myocardial infarction:

Tall T-waves with a characteristic broad-based morphology appear within 0 to 30 minutes after complete coronary artery occlusion and can be the earliest ECG signature of ST elevation myocardial infarction.

Unlike the disease entities discussed below, the T waves are not narrow, not pointed, and are symmetric. The abnormality should be localized to the ECG territory corresponding to the coronary artery that is occluded. Hyperacute T waves without ST segment elevation is usually a transient abnormality, present during the first 30 minutes after the onset of chest pain. Thereafter, the ST segment will begin to rise giving the more typically seen morphology of ST segment MI.


Hyperkalemia is a common cause of tall or peaked T waves. Recall that generation of the myocyte action potential is dependent on establishment of a transmembrane electrical gradient with sodium as the predominant extracellular cation and potassium as the predominant intracellular cation. Hyperkalemia affects this gradient, increases the action of myocardial potassium channels, affecting repolarization and depolarization.

Among the first ECG manifestations of hyperkalemia is the effect on T waves. The T waves become narrow-based, pointed, and tall. Imagine gripping the T wave with your fingers and pulling it upwards. Thus, both morphology and height of the T wave are abnormal. The abnormalities of T waves are diffuse, seen to a degree in all ECG leads, although they may be more prominent in some territories. Associated ECG findings include decreased P wave amplitude, widened QRS duration, progressive PR prolongation and, in a terminal phase, a sinusoidal ECG pattern. These associated features, when present, may illuminate the diagnosis if it is unclear simply on the basis of T wave abnormalities.

Normal variant and overload syndromes:

T waves can appear tall in the setting of an otherwise normal ECG. This typically occurs in young patients and athletes and manifests as a tall T wave in the anterior precordial leads (V2-V4) with an asymmetric base consisting of a gradual upslope and abrupt downslope. Tall T waves in the setting of left ventricular hypertrophy (as well as associated conditions giving rise to LVH such as hypertrophic cardiomyopathy and aortic stenosis) can have similar morphology with the tall, upright T waves present in leads with dominant negative voltage.

Inverted T waves


Myocardial ischemia is a common cause of inverted T waves. Inverted T waves are less specific than ST segment depression for ischemia, and do not in and of themselves convey a poor prognosis (as compared to patients with an acute coronary syndrome and ST segment depression). Despite this fact, inverted T waves in the setting of an appropriate clinical history are very suggestive of ischemia.

Ischemia can be due to an acute coronary syndrome caused by rupture of an atherosclerotic plaque or due to factors increasing oxygen demand or decreasing oxygen supply such as severe anemia or sepsis. The acute coronary syndromes associated with inverted T waves include unstable angina and non-ST elevation myocardial infarction, the prime distinction between the two syndromes being the absence or presence of serum biomarkers of myocyte necrosis such as troponin, CK and CK-MB.

One particularly important ischemic syndrome associated with inverted T waves is Wellens Syndrome. Patients with Wellens syndrome manifest deep, symmetrically inverted T waves in the anterior precordial leads. These T waves are suggestive of a severe stenosis of the proximal left anterior descending coronary artery and, left untreated, can progress to a large anterior ST elevation infarction. Thus, recognition of this syndrome on the ECG is critically important.

Cerebral T waves:

Severe insult to the central nervous system can cause deep, symmetric T wave inversions on the ECG, usually diffuse rather than limited to one ECG territory. Prolongation of the QT interval is also seen. These abnormalities are thought to be due to sympathetic discharge from the central nervous system. Specific disease entities associated with cerebral T waves include subarachnoid hemorrhage, massive ischemic stroke, subdural hematoma, and traumatic brain injury.

Medication effect and electrolyte abnormalities:

Medications such as digoxin, class I, and class III anti-arrhythmics, and psychoactive medications can cause T wave inversion as can severe hypokalemia, hypomagnesemia, and hypocalemia. The abnormalities are diffuse rather than localized to a coronary territory.

Left ventricular hypertrophy:

As noted above in the section on tall T waves, left or right ventricular hypertrophy can cause abnormalities of the T wave. Leads that evince t wave inversion are typically the leads with large positive voltage, and the T wave will deflect opposite that of the QRS complex. As with ST segment depression in the setting of ventricular hypertrophy, these T wave abnormalities are sometimes referred to as a “strain” pattern.

Conduction delay:

Left or right bundle branch block results in abnormal repolarization of the myocardium and can be associated with T wave inversion. In the setting of right bundle branch block, T wave inversions are expected in leads V1-V3. In the setting of left bundle branch block, the T waves should deflect opposite the major deflection of the QRS (for example, one expects T waves to be inverted in leads V6 and 1 if left bundle branch block is present). These T wave inversions are called “secondary” T wave changes, as in secondary to the conduction delay.


Later stages of pericarditis can manfest with diffuse T wave inversions on the 12 lead ECG. The sequence of ECG changes in acute pericarditis evolves over 2-3 weeks. The initial changes include ST segment elevation that is concave upwards. Subsequently, T wave become inverted. The ST segment next returns to baseline, leaving diffuse T wave inversions as the isolated abnormality which normalize thereafter.

Pulmonary embolism:

Acute pulmonary embolism large enough to cause right ventricular pressure overload can cause multiple abnormalities on the 12 lead ECG. The classic “S1Q3T3” pattern consists of a deep S wave in lead I and Q wave with T wave inversion in lead III. This pattern is seen in a minority of pulmonary embolism cases. Septal and anterior T wave inversions can also be associated with large pulmonary embolism and represent an acute right ventricular strain pattern, sometimes with associated right bundle branch block. The most common ECG abnormality seen in pulmonary embolism, however, is simply sinus tachycardia.


Finally, hyperventilation can cause deep, reversible ST segment abnormalities. T wave inversions and T wave flattening are sometimes present for no clear clinical reason, hence are referred to as “non-specific T wave abnormalities.”

B. Describe a diagnostic approach/method to the patient with this problem.

The diagnostic approach to T wave abnormalities identified on the 12 lead ECG includes first considering the indication for performing the ECG in the first place. Was the tracing performed to assist in diagnosis of a chest pain syndrome? In response to electrolyte abnormalities noted on the chemistry panel? As a routine screening tracing prior to initiation of a new medication? Each of these indications influences the pre-test probability of the diseases listed above in the differential diagnosis and will affect interpretation accordingly. Second, comparison of the tracing to a prior tracing will provide valuable information as to the chronicity of the abnormalities.

1. Historical information important in the diagnosis of this problem.

If tall T waves are identified, the presence or absence of chest pain, dyspnea, nausea, diaphoresis, or other symptoms suggestive of an acute myocardial infarction can suggest hyperacute T waves associated with myocardial infarction. The presence of known or suspected renal failure, dialysis dependence, and review of the medication list can service as important clues to the diagnosis of hyperkalemia. Similarly, if T wave inversions are identified, symptoms of cardiac ischemia should be actively delineated if present.

Characteristic history of pleuritic chest pain, or dyspnea, cough, and hemoptysis could suggest pericarditis or pulmonary embolism respectively. Headache or report of new neurologic deficit would implicate cerebral T waves as the cause of the T wave inversions. A review of the medication list and prior serum chemistries, if available, is a valuable diagnostic aid.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

The physical examination may be unrevealing or may provide additional clues to the diagnosis. Acute ischemia may manifest with signs of heart failure such as an S3, elevated jugular venous pressure, or pulmonary rales. Acute ischemia can also cause transient murmur of mitral regurgitation if a papillary muscle is ischemic, or a transient S4 (if sinus rhythm is present) due to impaired ventricular relaxation. Not uncommonly, the examination is normal is the setting of ischemia.

Cerebral T waves may be associated with neurologic deficit or photophobia and impaired consciousness due to the underlying pathology. A friction rub suggests pericarditis and a loud pulmonic component of the second heart sound and murmurs of tricuspid regurgitation and pulmonic insufficiency may be associated with pulmonary embolism.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

Serum chemistries and biomarkers of myocyte necrosis are useful if electrolyte dyscrasia or an acute coronary syndrome is suspected. Cranial imaging is mandatory if cerebral T waves are suspected. Ventilation-perfusion scan or computed tomography (CT) pulmonary angiography can aide in the diagnosis of pulmonary embolism. If the diagnosis of cardiac ischemia is unclear, echocardiography may demonstrate wall-motion abnormalities and provide an adjunct piece of data favoring ischemia.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Making the appropriate diagnosis of a disorder underlying T wave abnormalities identified on the electrocardiogram requires integration of clinical, demographic, electrocardiographic, and laboratory data as well as considering the pretest probability of disease. If it is not possible on this basis to distinguish between T wave changes secondary to a life threatening disorder and T wave changes secondary to a non-life threatening disorder, diagnostic and therapeutic considerations directed towards the suspected life-threatening disorder should be arranged.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.


III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Disorders of T Waves.

If tall T waves are identified, two emergent considerations need be considered: the first is whether the T waves represent the hyperacute T waves of early ST elevation myocardial infarction. This diagnosis is suggested by the recent (within 30 minutes) onset of ischemic symptoms. If in doubt, the diagnosis can sometimes be confirmed by repeating the ECG in 30 minutes; the repeat tracing will often demonstrate ST elevations. If hyperacute T waves of early ST elevation myocardial infarction are diagnosed, management should consist of urgent reperfusion and adjunct pharmacotherapies as outlined in the STEMI section.

The second emergent consideration to be made in the setting of tall T waves is whether hyperkalemia is present. If suspected, intravenous calcium gluconate should be administered which stabilizes the cardiac membrane. Further therapies directed towards hyperkalemia are outlined in the Hyperkalemia section.

If inverted T waves are identified and myocardial ischemia is suspected, appropriate management includes anti-ischemic therapy, anti-thrombotic therapy, and anti-platelet therapy as outlined in the Unstable Angina and Non-ST Elevation MI sections. If Wellens Syndrome is suspected or if the patient has high-risk features such as heart failure, unstable arrhythmias, cardiogenic shock, or a high TIMI or GRACE risk score, consideration should be given to early angiography with PCI as appropriate.

Cerebral T waves due to intracerebral hemorrhage or ischemic stroke mandate appropriate management as outlined in the respective chapters. Likewise, the management of pulmonary embolism and pericarditis are reviewed in respective chapters.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

The most common pitfall associated with interpretation of abnormalities of the T waves is not integrating the ECG findings with findings of history, physical examination, and selected laboratory and imaging studies to identify emergent conditions. For example, a high-risk acute coronary syndrome can be present in the face of a normal ECG, and a flagrantly abnormal ECG with T wave inversions can be present without ischemia, attributable to multiple other diagnoses as above.

IV. What's the evidence?

Morris, F, Brady, WJ.. ” ABC of clinical electrocardiography Acute myocardial infarction”. Part I. BMJ. vol. 324. 2002. pp. 831-34.

Channer, K, Morris, S. “ABC of clinical electrocardiography Myocardial ischemia.”. BMJ. vol. 324. 2002.. pp. 1023-26.

Edhouse, J, Brady, WJ, Morris, F.. “ABC of clinical electrocardiography Acute myocardial infarction – Part II.”. BMJ. vol. 324. 2002. pp. 963-66.

Slovis, C, Jenkins, R.. ” ABC of clinical electrocardiography Conditions not primarily affecting the heart.”. BMJ. vol. 324. 2002.. pp. 1320-23.

Tandy, TK, Bottomy, DP, Lewis, JG.. “Wellens Syndrome”. Ann Em Med. vol. 33. 1999. pp. 347-51.