Revisiting Electrophysiological Mechanisms of VF/VT Arrest During Early Ischemia and Spontaneous Electrical Activity After Defibrillation: From Cell to ACLS

K+ conductance and [K+]o increase during early (<10 min) regional and global ischemia. Early ischemia depolarizes the RMP and decreases INa (that is, residual INa) causing slow conduction, and shortens APD and ERP with dispersion. All of these factors contribute to the reentry mechanisms of VF/VT. While IK, ATP has a pivotal role in the increase in [K+]o, other currents such as IK, Na, IK, Ca, IK, FAA have simultaneously important effects on the increase in [K+]o. Up regulation of IK1, with an increase in inward-rectification, can also contribute to the increase in [K+]o in very early ischemia. VT is induced by ordered reentry of spiral waves, whereas VF is caused by random reentry of the spiral wavelets’ breakup. A biphasic waveform is more effective to defibrillate VF than a monophonic waveform, because, in the biphasic waveform the first hyper polarization resets every state of Na+ channels to prepare for reopening, and the subsequent depolarization simultaneously and uniformly inactivates almost all of the Na+ channels. Pacemaker restoration with spontaneous electrical activity can originate from either the SAN, AVN or Purkinje cells. Ischemia suppresses pacemaker activity, because pacemaker currents are sensitive to the ischemia, especially in the SAN, which has the fastest firing rate. Post ischemic early reperfusion injury induces a stunned myocardium and contractile disturbance, which can cause post-defibrillation pseudo PEA. After at least 5 min of an induced VF arrest, the reduction of PO2 was statistically significant, but that change was not remarkable; therefore, the estimated SaO2 does not decrease remarkably. High-quality CPR prevents global ischemia of the heart and brain due to VF/pulse less VT arrest. Therefore, it is essential to restore the organized electrical activity of pace making, to facilitate effective contraction of the ventricular muscle (that is, ROSC), and to minimize ischemic and post ischemic injury of these important organs.