If the membrane depolarization is sufficiently large, the inward sodium current is activated resulting in a triggered action potential. Delayed afterdepolar- izations are the underlying mechanism for VT in the setting of digoxin toxicity, catecholaminergic polymor- phic VT, and idiopathic outflow tract VA. Delayed af- terdepolarizations are also considered to be an impor- tant trigger of VA in the setting of HF. Purkinje cells are more susceptible to spontaneous sarcoplasmic re- ticulum calcium release than ventricular myocytes sug- gesting that delayed afterdepolarizations may be an important mechanism for some Purkinje fiber-related Reentry is the underlying mechanism for most sustained VA in the presence of structural heart Reentry may occur around a fixed anatomical obstacle, such as scar after an MI or surgically repaired congenital heart disease. In this setting, an excitable gap separates the excitation wave- front from its tail of refractoriness. The existence of structural reentrant substrates provide the rationale for VT ablation in scar-related VTs.S3.4-11,S3.4-12 Functional reentry around areas of functional block without anatomical obstacles can also occur. Two main models of functional reentry have been proposed.S3.4-2,S3.4-3 The leading circle model has a functionally refractory core and no excitable gap. Spiral wave reentry is driven by a rotor with a curved wavefront and wavetail pivoting around an excitable but unexcited core. There remains much debate about the precise mechanism(s) of VF (ro- tor versus multiple wavelet reentry). Both mechanisms may be operational in different phases of VF.S3.4-10 Phase 2 reentry may occur due to heterogeneity of ventricular repolarization. Electrotonic currents may flow from endocardial sites with longer action poten- tial durations to the epicardium with shorter action po- tential durations which can result in reexcitation when these sites have recovered from refractoriness. 