Pathophysiology
Clinical meaning
In hyperkalemia, elevated extracellular Kโบ reduces the electrochemical gradient across the cardiac cell membrane, decreasing the resting membrane potential from its normal โ90 mV toward โ70 to โ60 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 (Kโบ efflux), producing the characteristic peaked, narrow T waves that are the earliest ECG sign of hyperkalemia. As Kโบ 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.