The T wave is the ECG manifestation of ventricular repolarization of the cardiac electrical cycle.
The interval from the beginning of the QRS complex to the apex of the T wave is ref2242ed to as the absolute refractory period.
The last half of the T wave is ref2242ed to as the relative refractory period, or vulnerable period.
T waves can be described by its symmetry, slope of ascending and descending limbs, amplitude and subintervals.
In most leads, the T wave is positive due to the repolarization of the membrane.
Following ventricle contraction, QRS wave, the action of the Na+/K+ pump repolarizes the heart muscle to a state receptive to further conduction, and is why the T wave is positive.
Normally upright in leads I, II, and V3 to V6; inverted in lead aVR; and variable in leads III, aVL, aVF, V1, and V2.
T-wave inversions in leads V1 and V2 may be normal.
T-wave inversions seen in many disease states, but as related to coronary artery disease they may be a result of subendocardial ischemia, acute coronary artery syndrome, or past myocardial infarction so.
Deep or biphasic T waves in the precordial leads are associated with high-grade proximal stenosis of the left anterior descending coronary artery.
T-wave inversion pattern has a wide differential beyond coronary ischemia and includes pulmonary embolism, myocarditis, cerebral vascular accident, let ventricular hypertrophy, and pericarditis.
Lead V1 may have a positive, negative, or biphasic phase.
It is not uncommon to have an isolated negative T wave in lead III, aVL, or aVF.
A variety of clinical processes can cause T-wave inversions; ranging from life-threatening events, such as acute coronary ischemia, pulmonary embolism, and CNS injury, to benign conditions.
A periodic beat-to-beat variation in the amplitude or shape of the T wave is ref2242ed to as T wave alternans.
Tall and narrow, peaked or tented symmetrical T waves may indicate hyperkalemia.
Flat T waves that are less than 1 mV in the limb leads and less than 2 mV in the precordial leads may indicate the presence of coronary ischemia or hypokalemia.
The earliest electrocardiographic finding of ST-elevation MI (STEMI) acute myocardial infarction is sometimes the hyperacute T wave.
Hyperacute T waves may be seen in Prinzmetal angina.
In the presence of a bundle branch block T waves should be deflected opposite the terminal deflection of the QRS complex, and is known as appropriate T wave discordance.
T-wave changes ref2242ed to as primary T-wave changes and secondary T-wave changes.
Primary T-wave changes refer to alterations in the duration or morphology of the action potential, without concurrent changes in the orderly sequence of activation.
Primary T-wave inversion changes are associated with benign syndromes, such as the persistent juvenile T-wave pattern, digitalis effect, acute coronary ischemic events and CNS disease.
Secondary T-wave changes result from ab2242ant ventricular activation of normal action potential characteristics, as seen with bundle branch blocks, preexcitation states, and ventricular ectopic unstable angina present with significantly abnormal T-wave inversions—either symmetric, deeply inverted T waves or biphasic T waves in the precordial leads.
T wave changes in the precordial leads without evidence of acute myocardial infarction imply structural heart disease or metabolic derangements.
Unstable angina and these ECG findings ref2242ed to as Wellen syndrome, is frequently associated with proximal left anterior descending coronary artery critical stenosis.
Neurogenic causes of primary T-wave inversions include patients who have sustained a cerebrovascular accident with deep, widely splayed appearance with an outward bulge of the ascending limb with asymmetry: CVA T-wave pattern.
T-wave changes also associated with CNS hemorrhage and status epilepticus.
With pulmonary embolism T-wave abnormalities, including shallow T-wave inversions in the inferior leads may occur.
Also deep T-wave inversions due to acute right ventricular strain and occasionally seen in patients with massive pulmonary embolism.
Right bundle branch block, with its associated depolarization- repolarization changes, may produce marked ST-segment–T-wave changes.
The expected ST-segment–T-wave configurations are discordant, directed opposite from the terminal portion of the QRS complex; this pattern is called QRS-complex–T-wave axis.
Leads with largely positive QRS complexes demonstrate depressed ST segments and/or inverted T waves.
The right precordial leads, which have predominantly positive forces, are usually associated with ST-segment depression and T-wave inversion.
Patients with Wolff-Parkinson-White syndrome present at times with ST-segment and T-wave changes as well as abnormalities of the QRS complex— the so-called pseudo-infarction findings.
Benign changes include the digitalis effect and the persistent juvenile T-wave pattern.
Digitalis compounds can cause of T-wave inversions in otherwise healthy persons: include T-wave inversions, flattened T waves, an increased U wave, a prolonged PR interval, ST-segment depression with a distinct scooped appearance, and a shortened QTc interval.
Juvenile T-wave inversions may be noted in the precordial leads with an early repolarization pattern, and in some patients T-wave inversions persist into adulthood.