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The T Wave
The T Wave
The T wave represents Phase 3 repolarization of the ventricular myocardium. It is the deflection formed by ventricular repolarization waves due to potassium efflux from cardiomyocytes.
Notice that, halfway through Phase 3, we switch from the absolute refractory period to the relative refractory period. This halfway point tends to roughly correspond to the peak of the T wave.
The Normal T Wave
The Normal T Wave
Here are the features of a normal T wave:
Concave upstroke
Asymmetric with a slow upstroke and rapid downstroke
Concordant with QRS complex (typically 🡪 there are some exceptions)
Lower in amplitude than the QRS complex (<25% of R wave height)
Amplitude <5 mm in limb leads, <10 mm in precordial leads
Abnormal T Waves
Abnormal T Waves
The following are some abnormal T waves. This section will only consist of definitions. A description of the pathologic conditions that lead to these abnormal T waves will be explored in future modules.
A peaked T wave refers to a T wave that is narrow, symmetric, and tall (>5 mm in limb leads, >10 mm in precordial leads, or >25% of the QRS complex)
A hyperacute T wave refers to a T wave that is broad, asymmetric, and tall.
A flat T wave refers to a T wave that is <1 mm in height.
A T wave inversion (TWI) refers to a T wave with a negative polarity. In contrast, a positive T wave is referred to as an upright T wave.
A deep T wave is an inverted T wave that is >3 mm deep and is also usually more symmetric.
Biphasic T waves, as pictured to the right, refer to T waves that switch polarity. They can be further classified into up-down and down-up biphasic T waves.
Up-down biphasic T wave
Down-up biphasic T wave
Some additional T wave terminology:
A concordant T wave goes in the same direction as the QRS complex.
A discordant T wave goes in the opposite direction as the QRS complex.
A primary T wave inversion is caused by abnormal repolarization secondary to ischemic damage to the myocardium.
A secondary T wave inversion is abnormal repolarization that occurs secondary to abnormal depolarization — see below in the section about “Transmural dispersion of repolarization (TDR)”.
T Wave: Polarity and Concordance
T Wave: Polarity and Concordance
The ventricles repolarize from apex to base and epicardium to endocardium. The net repolarization vector ends up pointing upward and rightward.
Note: the direction of the net repolarization vector is also referred to as the “T wave axis”.
A visual of ventricular repolarization.
The net repolarization vector, a.k.a. the T wave axis.
Since repolarization occurs towards the upper right, positive charges are moving towards the bottom left. Since the ECG picks up the movement of positive charges, this would tend to make the T wave positive in I, III, aVF, and aVL. This would also make the T wave negative in aVR.
Depending on anatomic variation and concurrent variation in the T wave axis, it may be a normal variant to have an isolated T wave inversion in lead III.
It is also possible to get an isolated T wave inversion in lead aVL as a normal variant.
By “isolated” TWI, it means there should be no TWI in any other adjacent leads. In the above example, it is only really a normal variant if EITHER lead III or aVL have a TWI, but NOT BOTH. Note that the amplitude of the inverted T wave should be greater in aVR than in either lead III or lead aVL also.
In the precordial leads, since the net repolarization vector points rightward, it is common to have T wave inversions in the more rightmost precordial leads (V1 and V2). In the other leads from V3 to V6, the T wave should typically be upright.
Even in leads that exhibit physiologic TWI, you tend to see QRS concordance of the T waves.
The above is a normal variant of the QRS and T wave morphology in Lead V1.
Transmural dispersion of repolarization (TDR)
Transmural dispersion of repolarization (TDR)
Understanding transmural dispersion of repolarization (TDR) helps explain normal repolarization.
Recall that normal depolarization of the ventricles occurs from endocardium to epicardium, but normal repolarization occurs from epicardium to endocardium. But why does repolarization occur in the opposite direction?
It has to do with the differences in action potential duration (APD) in the different layers of the heart wall; this gradient is known as the TDR.
The graph on the left roughly compares the APDs of the various ventricular wall layers.
Notice that, even though the midmyocardium has the longest APD, the APD generally gets longer as you go from epicardium to endocardium.
Why does the TDR exist?
The coronary arteries permeate the ventricular walls from the pericardium towards the endocardium, making the endocardium the watershed area of the heart. Oxygen (and therefore ATP) is important for running the Na-K-ATPase pumps, which are indirectly responsible for resetting the intracellular Ca ion concentration via the sodium-calcium exchanger (NCX). Since the endocardium receives less oxygen than the epicardium, the intracellular Ca concentration is allowed to build up more in comparison, prolonging phase 2 of the action potential, and thereby the APD.
Even though the endocardial action potential begins first, the epicardial APD is short enough that it begins phase 3 repolarization first. Therefore, a repolarization current is initiated in the epicardium and moves towards the endocardium.
What is the significance of understanding how the TDR and heart repolarizes?
Various heart pathologies can affect the normal sequence of ventricular repolarization, which can manifest as TWI on the ECG. As such, a good understanding of normal TDR is valuable in understanding pathology.
A good way to think about it: any pathology that disrupts normal ventricular depolarization (leading to a widened QRS) leads to disruption of ventricular repolarization in effect, causing so-called “secondary” TWI. As we cover the different pathologies that can exhibit this phenomenon, we will explain the mechanism of the secondary TWI in those cases.
Cardiac memory
Cardiac memory
Whenever there’s a pathology that prolongs QRS, essentially referring to processes that exhibit abnormal ventricular depolarization, this pathology tends to lead to abnormal repolarization due to disruption of the normal TDR. However, there exists an interesting phenomenon whereby the repolarization abnormality persists despite resolution of this depolarization abnormality. This phenomenon is termed “cardiac memory”.
For example, transient LBBB (for example, during ischemia that eventually undergoes timely reperfusion) can cause TWI in left lateral leads, and even on elimination of the conduction block, the TWI can persist despite normalization of the QRS and ventricular conduction. This is thought to be related to electrical remodelling of the myocardium after exposure to abnormal repolarization.
T waves in pediatric ECGs
T waves in pediatric ECGs
It is normal to have TWI in V1-V4 in pediatric ECGs due to the physiologic right ventricular dominance in young children up to the age of ~4. This is known as the juvenile T wave pattern. Sometimes, these early precordial TWI can persist into adulthood, and is called persistent juvenile T wave pattern.
Summary of Normal T Waves
Summary of Normal T Waves
A normal T wave, in terms of morphology, is:
asymmetric with a slow, concave upstroke and a rapid downstroke
QRS-concordant
Not too short (>1 mm) but not too tall either (<5 mm in limb leads, <10 mm in precordial leads, and <25% of the QRS height)
Normally, the polarity of the T wave is:
U Wave
U Wave
The U wave is a small bump that follows the T wave on an ECG, with the peak of the U wave occurring ~90-110 ms after the end of the T wave.
Oftentimes, the U wave is too flat to be perceived.
It is unclear what causes the U wave. It used to be thought of as late repolarization of the Purkinje fibres, but this is losing favour nowadays. Now, it is thought to be the result of mechanical forces in the ventricles causing afterpotentials (i.e. new depolarization, and not late repolarization).
The features of the normal U wave:
Typically concordant with the T wave
Becomes more visible with slower heart rates (usually visible when HR < 65 bpm)
Low in amplitude (<1-2mm in height and proportionately small compared to the T wave, typically <25% of the height of the T wave).
Typically most easily visible in V2-V3
So, what's not normal for a U wave?
A prominent U wave, where the height is >1-2 mm or >25% the height of the T wave. Caused by inotropic agents like digoxin or ventricular hypertrophy.
A camel hump appearance, with apparent fusion of T wave and U wave. Can happen in hypokalemia as a result of QT prolongation.
An inverted U wave, where the wave is discordant with the T wave. Worrisome for acute ischemia.
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