Byline: Rahul. Kumar, Chaitra. Ramachandraiah, Pratap. Chokka, Vikram. Yeragani The QT interval conceptually represents the duration from the onset of depolarization to the completion of repolarization of the cardiac cycle. On a standard ECG, it is measured from the beginning of the QRS complex (or RS complex if there is no Q wave) to the end of the T wave. This interval has been considered as a surrogate of action potential duration. The QT interval is slightly longer in women than in men, is affected by autonomic tone as well as catecholamines, and it shows circadian variations. The most important aspect of this interval is its relation with heart rate (the reciprocal of inter-beat-interval).[sup] A large number of formulae have been proposed to establish a rule allowing conversion of a pair of QT and R-R durations into a standardized QTc value corresponding to a basal R-R interval of 1 second. Bazett's formula is the most commonly used. Normally the QTc is between 350 to 430 milliseconds. Now there is substantial amount of evidence as to the electrophysiology and how changes in autonomic function can affect the function of the heart. [sup] [1],[2],[3],[4],[5],[6] The main myocardial cell type that determines the QT interval is the 'M' cell type. The cardiac action potential is generated by the changing transmembrane permeability to ion currents such as Na[sup] + , Ca[sup] 2 + and K[sup] + . Like all living cells, the potential inside a myocyte is negative compared to the outside. However, cardiac cells are excitable and when appropriately stimulated, the ion channels within the cell membrane open and close sequentially. This changes the transmembrane ion permeability and leads to the sequential development of the transmembrane potential that is called the action potential. The initial depolarization (phase 0) is triggered by the rapid inward sodium (INa) and the L- and T-type calcium currents (ICa-L and ICa-T), which change the cell potential from - 90 to 30 mV. The transient outward Ito potassium current is responsible for the slight repolarization immediately after the overshoot (phase 1). During the following plateau phase (phase 2), the cell potential is maintained by a balance between the inward L-type calcium current (ICa-L) and the electrogenic sodium-calcium exchange current (INaCa), and the outward Ito current. The repolarization phase (phase 3) of the myocyte is driven predominantly by outward movement of potassium ions, carried as the rapid (IKr) and slow (IKs) components of the delayed rectifier potassium current. The diastolic depolarization (phase 4) results from a combination of the decay of the outward delayed rectifier IKr and IKs currents, which maintains the resting potential at approximately - 90 mV, and the activation of the inward pacemaker current (If) and the inward sodium background leak current (INa-B). A variety of other different potassium channel subtypes are also present in the heart. Cardiac arrhythmias reflect disturbances of impulse initiation or impulse propagation. These consist of conduction blocks, reentrant rhythms and dysfunction of sino-atrial (SA) node and disturbances that originate from various ectopic foci. Paroxysmal ventricular tachycardia is the result of an ectopic focus in the ventricles and can be associated with bizarre QRS complexes in the ECG. This is much more serious than a paroxysmal supraventricular tachycardia as paroxysmal ventricular tachycardia could lead to ventricular fibrillation. Fibrillation is an irregular contraction and is ineffectual in propelling blood. In the ventricles, the vulnerable period coincides with the down slope of the T wave, and when a premature impulse arrives during the vulnerable period, this may lead to fibrillation. This may become self-sustaining due to reentrant process of cardiac excitability. Tricyclic antidepressants (TCAs) have profound effects on cardiovascular system due to their strong autonomic effects and also a quinidine-like effect on cardiac conduction. …