Peaked t waves

Peaked t waves DEFAULT

ECG Diagnosis: Hyperacute T Waves

After QT prolongation, hyperacute T waves are the earliest-described electrocardiographic sign of acute ischemia, preceding ST-segment elevation.1 Hyperacute T waves are broad-based and symmetrical, usually with increased amplitude and often associated with a depressed ST take off.1 Hyperacute T waves are most evident in the anterior chest leads and are more apparent when a previous electrocardiogram is available for comparison.2 Hyperacute T waves are noted early after the onset of coronary occlusion and transmural infarction and tend to be a short-lived structure that evolves rapidly into ST-segment elevation.3 The electrocardiographic differential diagnosis of the hyperacute T wave includes both transmural acute myocardial infarction and hyperkalemia as well as early repolarization, left ventricular hypertrophy, and acute myopericarditis.4

The principle entity to exclude is hyperkalemia—this T-wave morphology may be confused with the hyperacute T wave of early transmural myocardial infarction. In contrast to hyperacute T waves associated with myocardial ischemia or infarction, hyperkalemic T waves tend to be narrow and peaked with a prominent or sharp apex.4 For patients presenting with hyperacute T waves in the setting of suspected myocardial ischemia or infarction, treatment includes symptomatic control with nitroglycerin or morphine, oral antiplatelet agents (aspirin), consideration of anticoagulation with unfractionated heparin, and obtaining frequent serial 12-lead electrocardiograms (every 5 to 10 minutes). Prompt consultation with a cardiologist is indicated in these cases.


T wave Overview

The T wave is the positive deflection after each QRS complex. It represents ventricular repolarisation.

ECG basics: waves, segments and intervals LITFL ECG library
Normal T wave characteristics
  • Upright in all leads except aVR and V1
  • Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm males, 8mm females)
  • Duration relates to QT interval

T wave abnormalities

  • Peaked T waves
  • Hyperacute T waves
  • Inverted T waves
  • Biphasic T waves
  • ‘Camel Hump’ T waves
  • Flattened T waves

Peaked T waves

ECG Peaked T waves hyperkalemia

Hyperacute T waves (HATW)

Broad, asymmetrically peaked or ‘hyperacute’ T-waves (HATW) are seen in the early stages of ST-elevation MI (STEMI), and often precede the appearance of ST elevation and Q waves. Particular attention should be paid to their size in relation to the preceding QRS complex, as HATW may appear ‘normal’ in size if the preceding QRS complex is of a small amplitude.

They are also seen with Prinzmetal angina.

Hyperacute T waves due to anterior STEMI
Loss of precordial T-wave balance

Loss of precordial T-wave balance occurs when the upright T wave is larger than that in V6. This is a type of hyperacute T wave.

  • The normal T wave in V1 is inverted. An upright T wave in V1 is considered abnormal — especially if it is tall (TTV1), and especially if it is new (NTTV1).
  • This finding indicates a high likelihood of coronary artery disease, and when new implies acute ischemia

Inverted T waves

Inverted T waves are seen in the following conditions:

  • Normal finding in children
  • Persistent juvenile T wave pattern
  • Myocardial ischaemia and infarction (including Wellens Syndrome)
  • Bundle branch block
  • Ventricular hypertrophy (‘strain’ patterns)
  • Pulmonary embolism
  • Hypertrophic cardiomyopathy
  • Raised intracranial pressure

** T wave inversion in lead III is a normal variant. New T-wave inversion (compared with prior ECGs) is always abnormal. Pathological T wave inversion is usually symmetrical and deep (>3mm).

Paediatric T waves

Paediatric T waves Normal T waves 2 year old boy

Persistent Juvenile T-wave Pattern

Juvenile-T-wave-inversion Persistent Juvenile T-wave Pattern
  • T-wave inversions in the right precordial leads may persist into adulthood and are most commonly seen in young Afro-Caribbean women
  • Persistent juvenile T-waves are asymmetric, shallow (<3mm) and usually limited to leads V1-3

Myocardial Ischaemia and Infarction

T-wave inversions due to myocardial ischaemia or infarction occur in contiguous leads based on the anatomical location of the area of ischaemia/infarction:

  • Inferior = II, III, aVF
  • Lateral = I, aVL, V5-6
  • Anterior = V2-6


  • Dynamic T-wave inversions are seen with acute myocardial ischaemia
  • Fixed T-wave inversions are seen following infarction, usually in association with pathological Q waves
Inferior T wave inversion due to acute ischaemia
Inferior T wave inversion with Q waves
Lateral; leads T wave inversion acute ischaemia
Anterior T wave inversion with Q waves

Bundle Branch Block

In bundle branch block, T-wave inversion is an expected finding, even in the absence of ischaemia:

  • Appropriate discordance refers to the fact that abnormal depolarisation (such as in bundle branch block) should be followed by abnormal repolarisation, which appears discordant to the preceding QRS complex in the form of ST-depression and T-wave inversion
Left Bundle Branch Block
Left bundle branch block with T-wave inversion
Right Bundle Branch Block (RBBB)
Right bundle branch block with T-wave inversion

Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)
Left ventricular hypertrophy with T-wave inversion
  • Left ventricular hypertrophy (LVH) produces T-wave inversion in the lateral leads I, aVL, V5-6 (left ventricular ‘strain’ pattern), with a similar morphology to that seen in LBBB
Right Ventricular Hypertrophy (RVH)
Right ventricular hypertrophy with T-wave inversion
  • Right ventricular hypertrophy produces T-wave inversion in the right precordial leads V1-3 (right ventricular ‘strain’ pattern) and also the inferior leads (II, III, aVF)
Pulmonary Embolism
  • Acute right heart strain (e.g. secondary to massive pulmonary embolism) produces a similar pattern to RVH
  • T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads
massive pulmonary embolism ECG T wave inversion
Acute massive PE with s! Q3 T3 RBBB TWI V1-3
  • Pulmonary embolism may also produce T-wave inversion in lead III as part of the SI QIII TIII pattern
  • S wave in lead I, Q wave in lead III, T-wave inversion in lead III
SI QIII TIII pattern in acute PE
Hypertrophic Cardiomyopathy (HCM)
Hypertrophic Cardiomyopathy (HCM)
Raised intracranial pressure (ICP)
ECG TWI Raised intracranial pressure (ICP) SAH
  • Events causing a sudden rise in intracranial pressure (e.g. subarachnoid haemorrhage) produce widespread deep T-wave inversions with a bizarre morphology

Biphasic T waves

There are two main causes of biphasic T waves:

The two waves go in opposite directions:

Biphasic T waves due to ischaemia – T waves go UP then DOWN

Biphasic T waves due to ischaemia

Biphasic T waves due to Hypokalaemia – T waves go DOWN then UP

Biphasic T waves due to hypokalaemia

Wellens Syndrome

Wellens syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with/following ischaemic sounding chest pain) that is highly specific for critical stenosis of the left anterior descending artery.

There are two patterns of T-wave abnormality in Wellens syndrome:

  • Type A = Biphasic T waves with the initial deflection positive and the terminal deflection negative (25% of cases)
  • Type B = T-waves are deeply and symmetrically inverted (75% of cases)

Note: The T waves evolve over time from a Type A to a Type B pattern

Wellens Type A
  • Wellens Pattern A Type 1 T wave
  • Wellens Pattern A Type 1 T wave 2
Wellens Type B
  • Wellens Pattern B Type 2 T wave 2
  • Wellens Pattern B Type 2 T wave

‘Camel hump’ T waves

Camel hump’ T waves is a term used by Amal Mattu to describe T-waves that have a double peak. There are two causes for camel hump T waves:

  • Prominent U waves fused to the end of the T wave, as seen in severe hypokalaemia
  • Hidden P waves embedded in the T wave, as seen in sinus tachycardia and various types of heart block
Prominent U waves due to severe hypokalaemia
Hidden P waves in sinus tachycardia
Hidden P waves in marked 1st degree heart block
Hidden P waves in 2nd degree

Flattened T waves

Flattened T waves are a non-specific finding, but may represent

  • Ischaemia (if dynamic or in contiguous leads) or
  • Electrolyte abnormality, e.g. hypokalaemia (if generalised)


Dynamic T-wave flattening due to anterior ischaemia (above). T waves return to normal once the ischaemia resolves (below).

Dynamic T wave flattening due to anterior ischaemia
T waves return to normal as ischaemia resolves

Note global T-wave flattening in hypokalaemia associated with prominent U waves in the anterior leads (V2 and V3).

T-wave flattening in hypokalaemia
ECG Library Basics
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Ed Burns

Emergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |

Dr Rob Buttner LITFL Author

Robert Buttner

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner


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68 causes of T wave, ST segment abnormalities

How often do you see an ECG that is just a little off? Maybe the T wave is flat, oddly-shaped or inverted. Maybe the ST segment is coved, very minimally-depressed or shows some J point elevation.

These are referred to as “non-specific” T wave and ST segment changes on the ECG because they are simply not specifically signaling any medical condition. Here, we consider the potentially-underlying reasons for these annoying minimal ECG changes and explore various clinical situations that could cause T waves and ST segments to deviate from normal.

In some instances, T wave changes might suggest specific conditions, such as peaked T waves in hyperkalemia or symmetric T wave inversions during myocardial ischemia. But what about all the other T wave abnormalities, such as flat T waves, biphasic T waves or asymmetric T wave inversions?

Similarly, ST segment abnormalities on the ECG can sometimes be due to a specific cause, such as ST segment elevation myocardial infarction, pericarditis or myocardial ischemia. Other times, there are just subtle abnormalities.

Review the following ECG findings when the ST segment change or T wave change is actually indicative of a specific condition. These are very important not to misinterpret.

After reading the list below in entirety, you will completely understand why the T wave and ST segment changes mentioned above are sometimes called non-specific. Although some in their severe form have a more classic ECG appearance that could help pinpoint a diagnosis, every situation is different. A mild abnormality (i.e. mild hyperkalemia or a very small MI) may only show a mild ECG change and not a full-blown abnormal finding. When a finding may sometimes be classic, it is listed next to the cause.

  1. Hypokalemia (ST segment depression, T-wave flattening)
  2. Hyperkalemia (multiple possible changes; when severe, classic finding is peaked T waves)
  3. Hypomagnesemia (flat, wide T waves; results in prolonged QT)
  4. Hypermagnesemia (increased T-wave amplitude)
  5. Hypercalcemia (short T wave with shortened QT interval; “J wave” when severe)
  6. Hypocalcemia (flat, wide T waves; results in prolonged QT)
  7. Hyponatremia (non-ischemic ST segment elevation)
  8. Memory T-wave abnormality post-pacing
  9. Memory T-wave abnormality post-rate-dependent BBB
  10. ST-T wave abnormalities associated with a LAFB
  11. ST-T wave abnormalities associated with LPFB
  12. ST-T wave abnormalities associated with LBBB
  13. ST-T wave abnormalities associated with RBBB
  14. ST-T wave abnormalities associated with NSIVCD
  15. ST-T wave abnormalities associated with WPW
  16. ST-T wave abnormalities associated with paced beats
  17. ST-T wave abnormalities associated with PVCs
  18. Myocarditis
  19. Myocardial ischemia (classic is significant ST segment depression; when mild, may be just a non-specific change)
  20. Myocardial infarction (non-ST segment elevation MI)
  21. VERY early myocardial injury (classic is “hyperacute T waves”)
  22. Reciprocal ischemic changes
  23. Left ventricular aneurysm (classic is persistent ST segment elevation 6 weeks after MI)
  24. Coronary spasm
  25. Digoxin
  26. Quinidine
  27. Tricyclic antidepressants (T-wave changes; classic is QRS widening)
  28. Many medication overdoses (see the below example of a clonidine overdose; this case looked like hyperacute T waves)

  29. Atrial flutter (flutter waves overlapping T waves)
  30. Infiltrative cardiomyopathy
  31. Takotsubo cardiomyopathy
  32. Hypertrophic obstructive cardiomyopathy
  33. Apical hypertrophic cardiomyopathy
  34. Arrhythmogenic right ventricular dysplasia
  35. Brugada syndrome
  36. Long QT syndromes
  37. LVH with strain
  38. RVH with strain
  39. Stage 3 pericarditis (T waves flattened)
  40. Cocaine toxicity
  41. Cardiac tumor
  42. Loeffler’s endocarditis
  43. Hypothemia
  44. Mitral valve prolapse
  45. Pericardial effusion
  46. Pericardial abscess
  47. Subarachnoid hemorrhage (deep inverted T waves, QT prolonged as well)
  48. Subdural hematoma (deep inverted T waves, QT prolonged as well)
  49. Intracranial hemorrhage (deep inverted T waves, QT prolonged as well)
  50. Stroke (deep inverted T waves, QT prolonged as well)
  51. Post carotid endarterectomy (deep inverted T waves, QT prolonged as well)
  52. Hyperventilation (can cause ST depression)
  53. Limb lead reversal
  54. ECG lead misplacement
  55. Physiologic junctional depression (occurs with sinus tachycardia)
  56. Pseudo ST-depression (wandering baseline from artifact, poor skin-electrode contact)
  57. Heightened adrenergic state (pain, panic attack, etc...)
  58. Early repolarization
  59. Hypothyroidism
  60. Truncal vagotomy
  61. Hypopituitarism
  62. Gallbladder disease
  63. Adrenal insufficiency
  64. Pulmonary embolism
  65. Post-prandial
  66. Persistent juvenile T-wave pattern
  67. Left-sided pleural effusion
  68. Normal variant

Every time you see an ECG with a T wave or ST segment that is not normal, use this list to identify the possible causes. There are likely additional scenarios I did not think to mention here; please use the comment section to add to the list.

- by Steven Lome


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.

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.

Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.

No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.


Waves peaked t

ECG T Wave

Continuing Education Activity

Normally, the T wave on an electrocardiogram (ECG) is representative of ventricular repolarization. Changes in T wave morphology can be indicative of various benign or pathologic conditions affecting the myocardium. Proper knowledge of T wave morphology is essential to successful evaluation and management of several conditions. This activity reviews the definition of an electrocardiographic T wave, explains how different clinical states can cause changes to T wave morphology, and highlights the role of educating interprofessional team members on the significance of T wave changes in order to improve patient care.


  • Outline the physiology associated with the electrocardiographic T wave.

  • Describe normal T wave morphology on a standard electrocardiogram.

  • Review common clinical diseases that cause changes in T wave morphology.

  • Explain the importance of educating interdisciplinary team members regarding the significance of electrocardiographic T wave changes.

Access free multiple choice questions on this topic.


The T wave on an electrocardiogram (ECG) represents typically ventricular repolarization.[1][2] However, various waveform morphologies may present as an indication of benign or clinically significant injury or insult to the myocardium. Understanding the differential diagnosis for T wave discrepancies is crucial to the successful and safe management of various cardiac pathologies. This article summarizes the ECG T wave in its entirety, including how it is defined, measured, and how it may vary.


Normal T-wave Etiology

Normally, the T wave is formed at the end of the last phase of ventricular repolarization. Ventricular repolarization is the process by which the ventricular myocytes return to their negative resting potential so they can depolarize again. While this phase of the cardiac cycle is rapid, an upright low amplitude broad hump following the QRS complex is seen in normal T wave morphology.

Abnormal T-wave Etiology

Abnormalities in the T-wave may represent variations of normal cardiac electrophysiology or signs pathology. Tall T-waves (also called hyper-acute T waves) can be an early sign of ST-elevation myocardial infarction. The morphology of the T waves can begin to broaden and peak within 30 minutes of complete coronary artery occlusion, and thus may be the earliest sign of myocardial infarction on the EKG. The T waves will be broadened and peaked in the leads corresponding to the artery occlusion.[1] Tall T waves can also be signs of ventricular hypertrophy, depending on the distribution in the precordial leads. Additionally, T waves may be tall as a normal variant. Due to this, it is crucial to compare all ECGs with elevations in T-wave morphology to a prior study. Keep in mind elevated T waves may even occur in as normal variation in young patients and athletes, typically in the precordial V2-V4 leads.[3] 

Inverted T waves are associated with myocardial ischemia. The inversion of a T wave is not specific for ischemia, and the inversion itself does not correlate with a specific prognosis. However, if the clinical history is suggestive of ischemia in the setting of inverted T waves, this is correlative.[4] Wellen syndrome is symmetrically inverted T waves in anterior precordial leads; these T waves suggest a severe narrowing of the left anterior descendent coronary artery at a proximal location. Recognition of this condition is vital to prevent a large anterior STEMI.[5] However, Wellens signs can be seen in various other pathologies such as pulmonary disease, so appropriate clinical correlation is imperative.

Hyperkalemia is a condition that can cause peaked T waves. Depending on the degree of hyperkalemia, the peaked T-waves may range from a low amplitude to tall peaks to a sinusoidal pattern on ECG. The mechanism of the T-wave morphologies is through inhibition of the positively charged extracellular potassium on repolarization of the myocardium. In initial ECG changes in hyperkalemia, the T waves become narrow, pointed, and tall; these changes will be seen in all leads on the EKG. As the hyperkalemia progresses, other EKG abnormalities may occur: decreased P wave height, a widened QRS, PR prolongation, and eventually, the ECG may become sinusoidal.[4][6] 

Several medications are indirectly associated with T wave abnormalities. Medications such as antiarrhythmics, digoxin, and diuretics can cause electrolyte abnormalities leading to changes in T wave appearance. A key to differentiating ischemia/infarction from electrolyte-induced T-wave changes is through the distribution of changes on ECG. Electrolyte abnormalities cause diffuse changes in the T-wave morphology throughout the ECG rather than specific to a coronary artery distribution.

Diffuse, deep, symmetrically inverted T waves may be seen in a severe central nervous system trauma or pathology. These are called cerebral T waves. Conditions associated with cerebral T waves are an ischemic stroke, intracranial bleed, and traumatic brain injury.[4] Left bundle branch block innately causes T wave to deflect in the opposite of the major deflection of the QRS. Diffuse T wave inversions on an ECG can be associated with pericarditis. The changes on an ECG for pericarditis take place over 2-3 weeks, initially with ST-elevation, then T wave inversion, with eventual resolution of the ST segment.[7] Massive pulmonary embolism can cause right ventricular strain, which can manifest as the classic S1Q3T3 (deep S wave in lead I, Q wave and T wave inversion in lead III).


Approximately 15.5 million Americans over the age of 20 have coronary heart disease, according to the 2016 Heart Disease and Stroke Statistics update from the American Heart Association (AHA). It is estimated that a myocardial infarction occurs about every 42 seconds in the United States.[8]

A study was done by Sanchis-Gomar et al. to evaluate the prevalence of hyperkalemia, a common cause of T-wave changes in the general population. The study included approximately 2.2 million patients to find the prevalence of hyperkalemia. Sachis-Gomar et al. were able to deduce that approximately 1.55% or 3.7 million Americans have hyperkalemia. The rates were elevated in those with chronic kidney disease, heart failure, diabetes, and hypertension. About 6% of patients with chronic kidney disease and heart failure were found to have hyperkalemia.[9]


Normal T-wave Physiology

Normal T waves are upright in leads I, II, and V3-V6, inverted in AVR. Less than five mm in limb leads, less than ten mm in precordial leads, and variable presentations in III, AVL, AVF, and V1-V2.[2] This graphical depiction on ECG is associated with lead placement and the electrical pathways of the heart. 

Abnormal T-wave Pathophysiology

T wave changes are secondary to electrolyte abnormalities in the myocardium since the ECG is representative of the electricity of the heart. The outflow of potassium from the myocyte during repolarization is necessary to restore resting membrane potential. In disease states such as ischemia, the Na/K-ATPase cannot function to restore this gradient; when there is hyperkalemia, the electrochemical gradient for potassium to flow out of the cell is skewed, altering the repolarization phase. These changes during phase three of the action potential are reflected by abnormalities in the T wave on an ECG.


Ventricular repolarization is depicted on the ECG in the form of a T-wave. Ventricular depolarization (phase zero) is the opening of Na channels, phase one is as these Na channels begin to close and K channels open. Phase two of the ventricular action potential is sustained by the opening of Ca channels. The repolarization (phase three), is caused by the closing of these Ca channels and the opening of K channels. The potassium flows out of the cell due to its electrochemical gradient, to restore the resting membrane potential near -88 to -90 mV.

History and Physical

As there are many different causes of T-wave abnormalities, there are just as many potential presentations. A thorough history and physical, along with a rigorous medication review, can provide essential information to suggest a specific diagnosis. For example, a history of prior episodes of chest pain with recent worsening in symptoms may indicate an ischemia component. A new or recently added medication such as digoxin may point suggest possible drug intoxication.[10] The temporality of the presentation is another essential part to assess the etiology of T-wave abnormalities. Acute onset of dyspnea with tachycardia after a recent surgery may suggest a pulmonary embolism. While the presentations above have clear cut symptoms on performance, it is important to remember that many times T-wave changes are asymptomatic as many causes of T-wave changes are non-pathological, such as normal variants or lead to misplacement. 


An ECG is one aspect of the clinical evaluation of a patient. The assessment of the ECG should always be integrated into a complete diagnostic workup. Metabolic panels and biomarkers of myocardial ischemia are needed in scenarios of suspected ischemia or electrolyte abnormalities. If cerebral T waves are seen, a non-contrast enhanced CT scan is suggested to look for any acute bleeding or trauma to the central nervous system. If a pulmonary embolism is suspected, a CT angiography should be conducted.

Treatment / Management

Treatment options differ depending on the etiology of the T-wave changes. Some T-wave changes require no intervention. However, some causes of T-wave changes are associated with high morbidity and mortality without emergent intervention. 

Ischemia and Infarction

If acute T waves are seen indicative of ischemia in a coronary artery distribution, management should be focused on reperfusion and treatment of the acute coronary syndrome.[11]


In severe hyperkalemia in the presence of peaked T-waves, calcium gluconate should be administered promptly to stabilize the cardiac membrane, in hopes to prevent arrhythmia. Mild hyperkalemia without T-wave abnormalities can be managed with polystyrene sulfonate, a potassium binder, insulin which forces potassium intracellularly, or furosemide, which drives potassium out of the body through the urinary tract.[12] 

Pulmonary Embolism

Pulmonary embolism (PE) is a common cause of T-wave changes. Treatment options for PE vary depending on the size and severity. Acute massive and submassive PEs should be considered for catheter-directed tPA. Smaller pulmonary embolisms in the absence of hemodynamic compromise or right heart strain can be found for systemic anticoagulation.[13] All institutions currently or planning on treating PEs in the future are encouraged to set up a pulmonary embolism response team made up of a cardiologist and pulmonologist. This team is designed to swiftly and accurately triage new PEs for appropriate treatment.[14]


Pericarditis can be managed with ibuprofen and colchicine for at least three months. If recurrent, pericarditis, a longer course of treatment is recommended.[15]

Drug-drug interaction or Intoxication

Serum drug levels may help identify intoxication with a particular medication that may be causing ECG abnormalities. It is recommended to stop the drug if intoxication or drug-drug interaction is suspected while workup is being done. Some drugs have reversal agents. For example, dig immune Fab is the first-line agent for digoxin toxicity. It is an immunoglobulin fragment that binds with digoxin and neutralizes it.[10] 

Differential Diagnosis

T-wave Inversion

  • Normal variant

  • Myocardial ischemia

  • Ventricular strain

  • Cerebrovascular injury

  • Hypertrophic cardiomyopathy

  • Idiopathic

  • Left bundle branch block

  • Right bundle branch block

  • Ventricular beats

Peaked T-waves

  • The hyperacute phase of myocardial infarction

  • Prinzmetal angina

  • Normal variant

  • Hyperkalemia

  • Left ventricular hypertrophy

  • Left bundle branch block

  • Acute pericarditis[4]


Prognosis depends mainly on the underlying etiology. T wave abnormalities seen on the EKG may be benign or represent severe, life-threatening threatening conditions. The ECG, combined with a thorough history and physical, will provide valuable information towards the etiology and prognosis for the patient.


The worst complication of T-wave abnormalities is a misdiagnosis of a serious T-wave pathology or delay in treatment intervention. Other possible complications include cardiomyopathy, myocardial ischemia or infarction, arrhythmia, tamponade, heart failure, and even death. 


Consultations with interventional cardiology would be appropriate in the setting of suspected myocardial infarction. It is recommended that a consult is placed to nephrology in the context of chronic kidney disease or severe hyperkalemia.

Deterrence and Patient Education

Patients must be educated on the signs and symptoms of ischemic heart disease and instructed to seek medical attention when these arise. The American Heart Association along with the American College of Cardiology are avid proponents for heart disease awareness. Millions of dollars go toward educating the public every year on this very topic.[16] However, it is essential that all healthcare providers regularly educate our patients on possible heart disease presentations. So our patient can seek help rapid, appropriate help.

According to the 2018 USRDS report, kidney disease is on the rise in the United States of America.[17] Chronic kidney disease is a common cause of electrolyte abnormalities and therefore may lead to T-wave changes. It is vital to educate our patients on appropriate risk factor modification through tight diabetic and blood pressure control. Primary prevention of kidney disease is essential. In those with previously developed kidney disease should be monitored closely for electrolyte abnormalities. 

Enhancing Healthcare Team Outcomes

When working in an emergent situation, it is essential that communication between providers, on all levels of training, is in sync.[14] There is level I evidence to support maximization of interprofessional communication, and care coordination optimizes healthcare outcomes. [18] While an ECG is a valuable tool, also during the history and physical, it is vital that the appropriate diagnosis and early intervention be addressed. It is highly recommended protocols and algorithms are set in place at all institutions treating cardiac disease. This way the best outcomes for our patient can be achieved. [Level I]

ECG demonstrating the second type of pattern associated with Wellens’ syndrome


ECG demonstrating the second type of pattern associated with Wellens’ syndrome. In leads V2-V3, the T waves are deeply inverted, typical of Type-B T waves. As discussed, Type-A T waves often evolve into Type-B T waves, which is what occurred in (more...)

T-Wave morphology


T-Wave morphology. Image courtesy S Bhimji MD

Figure 1: Normal EKG showing P waves (green arrows), QRS complex (blue arrows), and T waves (red arrows)


Figure 1: Normal EKG showing P waves (green arrows), QRS complex (blue arrows), and T waves (red arrows). Contributed by Yasar Sattar, MD



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EKG/ECG - Hyperkalemia - The EKG Guy -

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