The QT interval includes the QRS complex, the ST segment, and the T wave. It encompasses the time from the beginning of ventricular depolarization to the end of ventricular repolarization, and therefore includes all of the electrical events that take place in the ventricles. From the standpoint of time, more of the QT interval is devoted to ventricular repolarization than depolarization (that is, the T wave is wider than the QRS complex).

The duration of the QT interval is proportionate to the heart rate. The faster the heart rate, the faster it must repolarize to prepare for the next contraction; thus, the shorter the QT interval. Conversely, when the heart rate is slow, the QT interval is long. In general, the QT interval composes about 40% of each cardiac cycle (the R-R interval).

Because the QT interval varies normally with the heart rate, a corrected QT interval, or QTc, is used to assess for absolute QT prolongation. The QTc adjusts for differences in heart rate by dividing the QT interval by the square root of the R-R interval (in seconds). The formula is most accurate at heart rates between 50 and 120 beats/minute; at the extremes of heart rate, its usefulness is limited. The normal value for the QTc in men is <=0.44 seconds and in women is <=0.45 to 0.46 seconds.1 The QTc should not exceed 500 milliseconds during therapy with any medication that can prolong the QT interval (550 milliseconds if there is an underlying bundle branch block); adhering to this rule will reduce the risk of ventricular dysrhythmias. A prolonged QT interval is generally the result of prolonged ventricular repolarization (in other words, the T wave is lengthened).

A premature ventricular contraction falling during the elongated T wave can initiate torsade de pointes. Torsade de pointes, meaning "twisting of the points," is a unique form of ventricular tachycardia (VT) that is usually seen in patients with prolonged QT intervals. Torsade de pointes resembles VT, except that the QRS complexes spiral around the baseline, changing their axis and amplitude. A prolonged QT interval can result from various electrolyte disturbances (notably hypocalcemia, hypomagnesemia, and hypokalemia). Alterations in the serum calcium primarily affect the QT interval. Hypocalcemia prolongs it; hypercalcemia shortens it.

Several inherited disorders of cardiac repolarization associated with long QT intervals have been identified and are linked to specific chromosomal abnormalities. The cause in almost half of genotyped individuals is one of various mutations in a gene that encodes pore-forming subunits of the membrane channels that generate a slow K+ current that is adrenergic sensitive. All individuals in these families need to be screened for the presence of the genetic defect with resting and stress ECGs. If the abnormality is found, beta-adrenergic antagonists and sometimes implantable cardioverter defibrillators are recommended because the risk of sudden death from a lethal dysrhythmia is greatly increased, especially when the patient is a child or young adult.

Among the medications that can increase the QT interval are antiarrhythmic agents such as sotalol, quinidine, procainamide, disopyramide, amiodarone, dofetilide, and dronedarone. By increasing the QT interval, these drugs can paradoxically increase the risk of serious ventricular tachydysrhythmias. The QT interval must be carefully monitored in all patients taking these medications, and the drug should be stopped if substantial prolongation (more than 25%) occurs. Other medications that can prolong the QT interval include tricyclic antidepressants, phenothiazines, erythromycin, quinolone antibiotics, and some antifungal medications and antihistamines when taken concurrently with certain antibiotics, particularly erythromycin and quinolones.

REFERENCE