I Kr, the potassium current responsible for potassium efflux during repolarization is sensitive to extracellular potassium levels. P wave duration and PR interval also get prolonged due to slowing of conduction. Decrease in the V max of the sodium current causes slowing of impulse conduction within the myocardium resulting in QRS widening. This is because maximum number of sodium channels are available at a resting membrane potential of about -75mV and decreases at lesser negativity. If the intracellular negativity is reduced, the rate of rise of action potential in phase 0 (V max) is reduced. Phase of 0 of the action potential depends on the intracellular negativity. Hyperkalemia decreases the potassium gradient across the cell and reduces the intracellular negativity of the resting membrane potential. 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. Potassium concentration within the cell is much higher than that in the extracellular fluid which includes plasma. But the levels at which ECG changes are seen are quite variable from person to person. 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. ECG changes in hyperkalemia: Mechanism: The classical ECG change in hyperkalemia is tall tented T waves.
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