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Schematic representation of normal ECG

In electrocardiography, the T wave represents the repolarization, or recovery, of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period or vulnerable period. The T wave contains more information than the QT interval. The T wave can be described by its symmetry, skewness, slope of ascending and descending limbs, amplitude and subintervals like the Tpeak–Tend interval.[1]

In most leads, the T wave is positive. This is due to the repolarization of the membrane. During ventricle contraction (QRS complex), the heart depolarizes. Repolarization of the ventricle happens in the opposite direction of depolarization and is negative current, signifying the relaxation of the cardiac muscle of the ventricles. This double negative of direction and charge is why the T wave is positive; although the cell becomes more negatively charged, the net effect is in the positive direction, and the ECG reports this as a positive spike.[2] However, a negative T wave is normal in lead aVR. Lead V1 may have a T wave with positive, negative, or biphasic where positive is followed by negative, or vice versa. In addition, it is not uncommon to have an isolated negative T wave in lead III, aVL, or aVF. A periodic beat-to-beat variation in the amplitude or shape of the T wave may be termed T wave alternans.


Cardiac physiologyEdit

The refractory period of cardiac muscle is distinct from skeletal muscle. Nerves that innervate skeletal muscle have an extremely short refractory period after being subjected to an action potential (1 ms). This can lead to sustained or tetanic contraction. In the heart, contractions must be spaced to maintain a rhythm. Unlike in muscle, repolarization occurs at a slow rate (100 ms). This prevents the heart from undergoing sustained contractions because it forces the refractory period and cardiac action potential firing to be of the same length of time.

Repolarization depends on the charges of ions and their flow across membranes. In skeletal muscle cells, repolarization is simple. Sodium ions flowed into the cell earlier to depolarize it and cause skeletal muscle contraction. Once the action potential is over, potassium ions flow out of the cell due to increased cell membrane permeability to those ions. This high permeability contributes to the rapid repolarization of the membrane potential. This repolarization occurs quickly enough that another action potential can cause depolarization, even before the last action potential has dissipated. The cardiac muscle differs in that there are more calcium channels that counteract the potassium channels. While potassium quickly flows out of the cell, calcium slowly flows into the cell. This causes the repolarization to occur more slowly, making the refractory period as long as the action potential, preventing sustained contractions.

The T wave is representative of the repolarization of the membrane. In an EKG reading, the T wave is notable because it must be present before the next depolarization. An absent or strangely shaped T wave may signify disruption in repolarization or another segment of the heartbeat. [3]


The complex electrical activity of the heart must be extremely constant for survival. In general, each heartbeat should produce the same waves on an EKG. The T wave is referred to as the repolarization period of the ventricles because it represents the period in which the cardiac muscle cells of the heart can relax and prepare for the next contraction. It is essential for correct heart function and rhythm. Abnormalities in the T wave, even when minor, can be indicative of seriously impaired physiological functioning. Various types of T wave abnormalities can be observed on an EKG, each stemming from different bodily malfunction.


Inverted T waveEdit

T wave inversion is characterized by an opposite orientation of the T wave. The T wave is therefore reported as negative instead of positive in EKG. T-wave inversions that appear suddenly and are new compared to prior EKGs are always considered to be abnormal. Symmetrical and deep T wave inversions are generally pathological. T-wave inversion (negative T waves) can be a sign of coronary ischemia, Wellens' syndrome, left ventricular hypertrophy, or CNS disorder.

  • Pediatric inverted T waves: normally found in the right precordial leads. They are not harmful and signify more dominant right ventricle force. These inversions may lead into adulthood and are commonly seen in young Afro-Caribbean women.
  • Myocardial ischemia or infarction cause inverted T waves that occur in contiguous leads based on the anatomical location of the ischemia or infarction. Inferior: II, III, aVF Lateral: I, aVL, V5-6 Anterior: V2-6
    • Dynamic T-wave inversions occur with acute myocardial ischemia
    • Fixed T-wave Inversions follow infarction
  • Left Bundle Branch Block: T-wave inversion in lateral leads I, V5-6, aVL
  • Right Bundle Branch Block: T-wave inversion in the right precordial leads V1-3.
    • When a bundle branch block is present, the T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance.
  • Left ventricular hypertrophy: T-wave inversion in lateral leads aVL, V5-6, and I
  • Right ventricular hypertrophy: T-wave inversion in the inferior leads II, III, aVF and right precordial leads V1-3
  • Pulmonary Embolism: Produces a pattern similar to right ventricular hypertrophy. T-wave inversions in inferior leads II, III, aVF and right precordial V1-3
  • Hypertrophic Cardiomyopathy: commonly seen in patients displaying deep T wave inversions in all precordial leads
  • Raised intracranial pressure: events leading to this create deep T-wave inversions with extremely abnormal morphology [4]
Frequency of inverted T-wavesEdit

Numbers from Lepeschkin E in [5]

Age (ethnicity) n V1 V2 V3 V4 V5 V6
1 week - 1 y 210 92% 74% 27% 20% 0.5% 0%
1 y - 2 y 154 96% 85% 39% 10% 0.7% 0%
2 y - 5 y 202 98% 50% 22% 7% 1% 0%
5 y - 8 y 94 91% 25% 14% 5% 1% 1%
8 y - 16 y 90 62% 7% 2% 0% 0% 0%
12 y - 13 y 209 47% 7% 0% 0% 0% 0%
13 y - 14 y 260 35% 4.6% 0.8% 0% 0% 0%
16 y - 19 y (whites) 50 32% 0% 0% 0% 0% 0%
16 y - 19 y (blacks) 310 46% 7% 2.9% 1.3% 0% 0%
20 - 30 y (whites) 285 41% 0% 0% 0% 0% 0%
20 - 30 y (blacks) 295 37% 0% 0% 0% 0% 0%
12 y - 13 y 174 69% 11% 1.2% 0% 0% 0%
13 y - 14 y 154 52% 8.4% 1.4% 0% 0% 0%
16 y - 19 y (whites) 50 66% 0% 0% 0% 0% 0%
16 - 19 y (blacks) 310 73% 9% 1.3% 0.6% 0% 0%
20 - 30 y (whites) 280 55% 0% 0% 0% 0% 0%
20 - 30 y (blacks) 330 55% 2.4% 1% 0% 0% 0%

Biphasic T waveEdit

As the name suggests, Biphasic T waves move in opposite directions. The two main causes of these waves are myocardial ischemia and hypokalemia.

  • Ischemic T waves rise and then fall below the cardiac resting membrane potential
  • Hypokalemic T waves fall and then rise above the cardiac resting membrane potential

Wellens' Syndrome is a pattern of biphasic T waves in V2-3. It is generally present in patients with ischemic chest pain.

  • Type 1: T-waves are symmetrically and deeply inverted
  • Type 2: T-waves are biphasic with negative terminal deflection and positive initial deflection [4]

Flattened T waveEdit

Flat T waves (less than 0.1 mV in the limb leads and less than 0.2 mV in the precordial leads)[6] may indicate coronary ischemia or hypokalemia[6]

Hyperacute T waveEdit

These T waves may be seen in patients displaying Prinzmetal angina. Additionally, patients exhibiting the early stages of STEMI may display these broad and disproportional waves.[7]

'Camel hump' T waveEdit

The name of these T waves suggests the shape it exhibits (double peaks). Since these T wave abnormalities may arise from different events, ie hypothermia and severe brain damage, they have been deemed as nonspecific, making them much more difficult to interpret. [8]

See alsoEdit


  1. ^ Haarmark C, Graff C, Andersen MP, et al. (2010). "Reference values of electrocardiogram repolarization variables in a healthy population". Journal of Electrocardiology. 43 (1): 31–9. doi:10.1016/j.jelectrocard.2009.08.001. PMID 19740481. 
  2. ^
  3. ^ 1953-, Raff, Hershel,; T., Strang, Kevin; 1933-, Vander, Arthur J.,. Human physiology : the mechanisms of body function. ISBN 1259294099. OCLC 914339346. 
  4. ^ a b HANNA, E. B.; GLANCY, D. L. "ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats". Cleveland Clinic Journal of Medicine. 78 (6): 404–414. doi:10.3949/ccjm.78a.10077. 
  5. ^ Antaloczy, Z (1979). Modern Electrocardiology. Amsterdam: Excerpta Medica. p. 401. 
  6. ^ a b Loyola University Chicago Stritch School of Medicine. > EKG Interpretive skills Retrieved on April 22, 2010
  7. ^ Verouden, N. J.; Koch, K. T.; Peters, R. J.; Henriques, J. P.; Baan, J.; Schaaf, R. J. van der; Vis, M. M.; Tijssen, J. G.; Piek, J. J. (2009-10-15). "Persistent precordial "hyperacute" T-waves signify proximal left anterior descending artery occlusion". Heart. 95 (20): 1701–1706. doi:10.1136/hrt.2009.174557. ISSN 1355-6037. PMID 19620137. 
  8. ^ Abbott, Joseph A.; Cheitlin, Melvin D. (1976-01-26). "The Nonspecific Camel-Hump Sign". JAMA. 235 (4): 413–414. doi:10.1001/jama.1976.03260300039030. ISSN 0098-7484.