Final answer:
Abnormal activity of K+ channels in the heart delays repolarization, leading to long QT syndrome, because these channels are responsible for the outflow of K+ that returns the cell to its resting state. Potassium channel blockers like amiodarone and procainamide impede K+ movement, prolonging the QT interval on an ECG and potentially causing cardiac dysrhythmias.
Step-by-step explanation:
Effect of Abnormal K+ Channel Activity on Cardiac Repolarization
Abnormal activity of K+ channels in the heart can significantly impact the repolarization phase of the cardiac action potential, potentially leading to long QT syndrome. The action potential in cardiac cells consists of rapid depolarization, followed by a plateau phase, and concluding with repolarization. During repolarization, voltage-gated K+ channels open, allowing K+ to exit the cardiac myocytes. This outflow of K+ ions returns the cell to its resting membrane potential.
When there is a disturbance, such as the use of potassium channel blockers like amiodarone and procainamide, the movement of K+ through these channels is impeded. Consequently, the repolarization phase of the cardiac action potential is prolonged, which can be observed as a lengthened QT interval on an electrocardiogram (ECG). This extended QT interval reflects the delayed repolarization and can increase the risk of cardiac dysrhythmias, such as torsades de pointes, which can be life-threatening.
The activity of potassium channel blockers and their effects not only extend the QT interval but may also affect the heart rate or pulse by altering the overall rhythm of the heart's electrical activity. For example, an abnormal electrical pattern and an increased frequency between QRS complexes could result in increased heart rate. In cases where there is an extracellular increase in K+ concentration, it can further exacerbate the transmission of action potentials, affecting the contraction and overall function of the heart.