text: Short QT syndrome types 1-3 are due to increased activity of outward potassium currents in phases 2 and 3 of the cardiac action potential.  This causes a shortening of the plateau phase of the action potential (phase 2), causing a shortening of the overall action potential, leading to an overall shortening of refractory periods and the QT interval. In the families afflicted by short QT syndrome, two different missense mutations have been described in the human ether-a-go-go gene (HERG).  These mutations result in the expression of the same amino acid change in the cardiac IKr ion channel.  This mutated IKr has increased activity compared to the normal ion channel, and would theoretically explain the above hypothesis.  Short QT syndrome types 4 and 5 are due to abnormalities in the calcium channel.
option_0: Short QT syndrome pathophysiology
option_1: Long QT Syndrome pathophysiology
option_2: Sick sinus syndrome pathophysiology
option_3: Brugada syndrome pathophysiology
option_4: Pacemaker syndrome pathophysiology
option_5: Dextrocardia pathophysiology
option_6: Sinoatrial arrest pathophysiology
option_7: Short QT syndrome risk factors