ECG changes in hyperkalemia: Mechanism

ECG changes in hyperkalemia: Mechanism

ECG changes in hyperkalemia: Mechanism: The classical ECG change in hyperkalemia is tall tented T waves. As the severity of hyperkalemia increases, the QRS complex widens and the merging together of the widened QRS complex with the T wave produces the ‘sine wave’ pattern of severe hyperkalemia. But the levels at which ECG changes are seen are quite variable from person to person.

Potassium concentration within the cell is much higher than that in the extracellular fluid which includes plasma. The concentration gradient is maintained by the action of sodium potassium adenosine triphosphatase pump (Na-K pump) which pumps sodium out of the cell and potassium into the cell. Hyperkalemia decreases the potassium gradient across the cell and reduces the intracellular negativity of the resting membrane potential. Phase of 0 of the action potential depends on the intracellular negativity. If the intracellular negativity is reduced, the rate of rise of action potential in phase 0 (V_max) is reduced. This is because maximum number of sodium channels are available at a resting membrane potential of about -75mV and decreases at lesser negativity. Decrease in the V_max of the sodium current causes slowing of impulse conduction within the myocardium resulting in QRS widening. P wave duration and PR interval also get prolonged due to slowing of conduction.

I_Kr, the potassium current responsible for potassium efflux during repolarization is sensitive to extracellular potassium levels. Function of I_Kr increases with hyperkalemia, increasing the potassium conductance in phase 2 and 3 of the action potential. This leads to faster and shorter repolarization, manifest in surface electrocardiogram as tall peaked T waves, the reciprocal of what occurs in hypokalemia.

In severe hyperkalemia there is absence of P waves, sometimes referred to as atrial paralysis. At the same time sinus node still controls the ventricular rhythm and this is known as sinoventricular conduction. This is because sinus node is thought to be more resistant to the effect of hyperkalemia than the atrial tissue. Theoretically the existence of the sinus node activity controlling the ventricular rhythm in the absence of P waves can be inferred from the respiratory sinus arrhythmia – inspiratory increase and expiratory decrease in the rate.