Pathophysiology
Clinical meaning
In hyperkalemia, elevated extracellular K⁺ reduces the electrochemical gradient across the cardiac cell membrane, decreasing the resting membrane potential from its normal −90 mV toward −70 to −60 mV. At this partially depolarized state, voltage-gated sodium channels transition from their resting (closed, activatable) state to their inactivated (closed, non-activatable) state. This means that when the cell attempts to depolarize, fewer functional sodium channels are available, producing a slower and lower-amplitude Phase 0 upstroke. The clinical result is slowed impulse conduction velocity, which manifests as progressive QRS widening on the ECG. Simultaneously, the reduced gradient accelerates Phase 3 repolarization (K⁺ efflux), producing the characteristic peaked, narrow T waves that are the earliest ECG sign of hyperkalemia. As K⁺ continues to rise, atrial myocytes - which are more sensitive to hyperkalemia than ventricular myocytes - lose their ability to depolarize, producing P wave flattening and eventual absence (sinoatrial arrest). The final pre-arrest pattern is the sine wave: a smooth, undulating waveform representing extreme QRS widening merging with the T wave, indicating imminent ventricular fibrillation or asystole.