Abnormal T Wave

A wave that includes both an upright (positive) and downward (negative) deflection.

Expect a T wave to follow every QRS complex. The T wave is a graphic representation of the repolarization of the ventricle. The T wave is typically about 0.10 to 0.25 seconds wide with an amplitude less than 5 mm. While ventricular depolarization occurs rapidly producing a tall QRS complex, ventricular repolarization is spread over a longer interval, resulting in a shorter and broader T wave.
The T wave is normally slightly asymmetrical and is usually larger than the P wave (see Figure 4.13). The T wave is normally upright in lead II. Note that as heart rates increase, the P wave (atria) and the T wave (ventricles) begin to share the same space on an ECG. The larger T wave often covers the P wave. Note that the T wave is rarely notched. A notched T wave may also contain a P wave trying to show itself.

If ventricular repolarization returns cell membrane voltage back to its predepolarization resting electrical voltage, then shouldn’t the wave produced by ventricular repolarization be opposite that of ventricular depolarization? In other words, should the QRS complex and the T wave face opposite directions,
upright and inverted. This is usually not the case.
Ventricular depolarization proceeds from the endocardium to the epicardium, essentially depolarizing the ventricles from the inside out. It follows that repolarization also occurs from the inside out, producing inverted T waves opposite in direction to the QRS complex. Instead, repolarization is delayed in endocardial cells, allowing the epicardium to repolarize first. Repolarization normally proceeds
opposite to depolarization, from the outside in. An upright T wave results.

An inverted T wave can point to cardiac ischemia among other causes. Ischemia to the epicardium prolongs ventricular repolarization to this area. This extended repolarization of the epicardium removes the delay between the repolarization of the endocardium and the repolarization of the epicardium, with repolarization now following the sequence of depolarization. An inverted T wave results.

Abnormally shaped T waves can signify acute episodes of cardiac ischemia, electrolyte imbalances, and the influence of cardiac medications. For example, peaked T waves can occur early during periods of myocardial ischemia and infarction. Later, cardiac ischemia may cause the T wave to invert. Electrolyte imbalances can also affect the T wave. Hyperkalemia is often associated with peaked T waves. Hypokalemia can flatten the T wave. Quinidine can widen the T wave while digitalis can flatten the T wave.

Abnormally shaped T waves can also occur following injury to the lungs or the brain. While the physiology is not well understood, T wave inversion can occur with a leftsided tension pneumothorax. Peaked or inverted T waves have also been reported with brain injury, specifically subarachnoid hemorrhage.

Figure 4.13 The QRS Complex, ST Segment and the T Wave | Figure 4.18 Normal and Abnormal T Waves

Figure 4.13 depicts the component parts of the QRS complex…The ST segment begins at the J point and continues to the beginning of the T wave.

Figure 4.18 illustrates a variety of T waves, both normal and abnormal. A normal T wave is upright and slightly asymmetrical. During ischemic episodes, T waves may initially peak, then invert. Electrolyte imbalances such as hyperkalemia can cause the T wave to peak while hypokalemia is associated with flattened T waves. Certain medications such as quinidine can slow repolarization and widen the T wave while digoxin can flatten the T wave.

1. Six Second ECG Guidebook (2012), T Barill, p. 88-90

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