At normal plasma HCO3– (in white spheres) concentration, some HCO3– is reabsorbed from the renal tubules (in yellow tube) through the interstitium (not shown) to the intravascular compartment (in red tube). When plasma HCO3– concentration increases, plasma pH increases resulting in metabolic alkalosis. During metabolic alkalosis, the reabsorption of HCO3– from renal tubules to the intravascular compartment decreases.
In intracellular acidosis, the concentration of H+ (in white) inside the cell increases. Acidosis results in the transcellular shift of intracellular K+ (in green) to the extracellular fluid compartment leading to hyperkalemia. In intracellular alkalosis, the concentration of H+ inside the cell decreases. Alkalosis results in the transcellular shift of extracellular K+ to the intracellular fluid compartment leading to hypokalemia.
Class I antiarrhythmic medications block Na+ channels, preventing the efflux of intracellular Na+ into the cellular space. Blocking Na+ channels prolongs the duration of the cardiac action potential and the effective refractory period. In contrast, Class III antiarrhythmic medications block K+ channels, thus, preventing the influx of extracellular K+ into the intracellular space. Blocking K+ channels delays repolarization, prolonging the duration of the cardiac action potential and the effective refractory period.
The animations show the propagation of electrical impulses from the sino-atrial node through the myocardium, along with corresponding changes in aortic, atrial and ventricular pressures, and in ventricular volume.