ECG IN HYPERKALEMIA
Potassium is most abundant intracellular cation Most important determinant of resting membrane potential (RMP)
Mild to moderate levels of hyperkalemia Decrease TP(less negative) Decrease RMP (less negative) Decrease RMP more than decrease TP Diminish difference between two and increase excitability
Decrease in slope of upstroke of AP (dV/dT) Major determinants of conduction velocity Counterbalanced by decrease in RMP to TP difference Result in ultimate increase in conduction velocity initially
Disproportional effects of varying levels of hyperkalemia on RMP and the TP Initial increase in excitability and conduction velocity followed by their decrease as potassium level increases further
Severe hyperkalemia Associated with increase in difference between RMP and TP Leading to decrease in excitability Further decrement in AP upstroke (dV/dT) overwhelms positive effect of TP decrease on conduction velocity
Rate of rise of phase 0 of AP (Vmax) is directly proportional to value of RMP at the onset of phase 0 Decrease in V max levels causes a slowing of myocardial conduction manifested by progressive prolongation of P wave, PR interval and QRS complex
Mechanism for early ECG manifestations of hyperkalemia (ST depression, peaked T waves, and short-QT) Ikr is mostly responsible for K+ efflux in phases 2 and 3 Ikr currents are sensitive to extracellular K+ levels As potassium levels increase in extracellular space potassium conductance through these currents is increased Leads to increase in slope of phases 2 and 3 shorten repolarization time
Modulation of potassium currents by electrolyte concentration
Effects of hyperkalemia depend on tissue involved Atrial myocardium most sensitive ventricular myocardium less sensitive Specialized tissue (SA node and His bundle) least sensitive
References 1.Electrolyte disorders and arrhythmogenesis ,Nabil El-Sherif1, Gioia Turitto2, Cardiology Journal 2011, Vol. 18 2.Hyperkalemia Revisited, Walter A. Parham, MD,Ali A. Mehdirad, MD, FACC ,Kurt M. Biermann, BS ,Carey S. Fredman, MD, FACC, Tex Heart Inst J 2006