Eade potential

Judicious use of the approximations discussed here has the potential to facilitate accurate quasiparticle calculations on molecular systems of unprecedented size. These techniques provide a number of new options for the calculation of EADEs with advantageous compromises between computational cost and reliability. 

It is always best to understand a biological problem before trying to find ways to avoid it. The reason that action potential duration is important is that repolarization is a fragile process. It can fail, and when it does so, the action potential is followed by one or many oscillations. These are called early after-depolarizations (EADs). We will also encounter late after-depolarizations (DADs) later in this chapter. 

Hazard quotient Ratio of the estimated chemical intake (dose) to a reference dose level below which adverse health effects are unlikely. The value is used to evaluate the potential for noncancer health effects, such as organ damage, from chemical exposures (from http //web.ead.anl.gov/uranium/glossacro last accessed July 2010). 

The position of the maximum value of Ead(v,r) depends on v because, although Eei(x) increases toward the potential barrier, iivib(v,x) decreases, and this second contribution to f ad(v,x) assumes increasing importance as v increases. Although the v = 0 adiabatic maximum is usually located at the electronic saddle point, the maxima for higher states of bond-stretching vibration may be displaced into the entrance and exit valley on the potential energy surface. Vibrationally adiabatic motion is then expected up to the first of these maxima (r-AB > r-Bc). Trajectory calculations support this expectation [39-44]. 

Figure 5 Reduction of Irt prolongs action potential duration. Here, the prolongation effects of 25%, 50%, and 75% reduction of h r on APD are shown in a virtual cell model after 1000 paced beats at a cycle length (CL) = 1000 ms. A 75% current reduction results in the development of arrhythmogenic early afterdepolarizations (EADs). [Adapted from (38).]...

Arrhythmias occur within a few seconds after reperfusion, following ischemic periods of 10-30 min long. They start by a spontaneous stimulus in the reperfused zone and change afterward in a re-entry multiple wavelet type of ventricular tachycardia (VT) or ventricular fibrillation (VF). Extremely short action potential, short refractory period and slow conduction are the main contributing factors. Increased hyperpolarization and elevated intracellular calcium that act negatively on gap conductance impair conduction. Unidirectional conduction is favored by the marked heterogeneity in extracellular potassium, action potential and refractory period. The extra stimulus is initiated in the reperfused zone, probably by early (EAD) and late (DAD) afterdepolirizations. 

Triggered automaticity is also a possible mechanism for abnormal impulse generation. Briefly, triggered automaticity refers to transient membrane depolarizations that occur during repolarization (early after-depolarizations [EADs]) or after repolarization (delayed afterdepolarizations [DADs]) but prior to phase 4 of the action potential. After-depolarizations may be related to abnormal calcium and sodium influx during or just after full cellular repolarization. Experimentally, early after-depolarizations may be precipitated by hypokalemia, type la antiarrhythmic drugs, or slow stimulation rates— any factor that blocks the ion channels (e.g., potassium) responsible... 

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