T wave Overview
- The T wave is the positive deflection after each QRS complex.
- It represents ventricular repolarisation.
Characteristics of the normal T wave
- Upright in all leads except aVR and V1
- Amplitude < 5mm in limb leads, < 15mm in precordial leads
- Duration (see 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
- Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia.
Hyperacute T waves
- Broad, asymmetrically peaked or ‘hyperacute’ T-waves are seen in the early stages of ST-elevation MI (STEMI) and often precede the appearance of ST elevation and Q waves.
- They are also seen with Prinzmetal angina.
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
- 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
- Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces.
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 – prior myocardial infarction
- T wave inversion in the lateral leads due to acute ischaemia
- Anterior T wave inversion with Q waves due to recent MI
Bundle Branch Block
Left Bundle Branch Block
- Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.
Right Bundle Branch Block
- Right bundle branch block produces T-wave inversion in the right precordial leads V1-3.
Left Ventricular Hypertrophy
- 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
- 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).
- 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.
- T wave inversion in the inferior and right precordial leads
- Acute massive PE with SI QIII TIII RBBB TWI V1-3
SI QIII TIII
- 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 is associated with deep T wave inversions in all the precordial leads.
Raised intracranial pressure (ICP)
- 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 Hypokalaemia – T waves go DOWN then UP
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 Type B
‘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 heart block with 2:1 conduction
Flattened T waves
Flattened T waves are a non-specific finding, but may represent
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 generalised T-wave flattening in hypokalaemia associated with prominent U waves in the anterior leads (V2 and V3).
LITFL Further Reading
- ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
- ECG A to Z by diagnosis – ECG interpretation in clinical context
- ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
- 100 ECG Quiz – Self-assessment tool for examination practice
- ECG Reference SITES and BOOKS – the best of the rest
- Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric
- Wagner GS. Marriott’s Practical Electrocardiography 12e
- Chan TC. ECG in Emergency Medicine and Acute Care
- Dubin D. Rapid Interpretation of EKG’s
- Mattu A. ECG’s for the Emergency Physician
- Hampton JR. The ECG In Practice, 6e