Beta Blockers

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Brucelaa67

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AV nodal repolarization is mediated primarily by K+, so how do Beta blockers prolong AV nodal repolarization? (And CCBs too)
Any help, its melting away my brain?

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Sympathetic beta receptors increase heart rate by increasing rate of of phase 4 depolarization(increased If), and increases conduction velocity through through av node, by increased inward ca current. (From Costanzo Physio review)
So if you use beta blockers, rate and conduction will decrease
So I understand the increase in slope of phase 4, and phase 0. But how does repolarization at Av node is prolonged (FA 2017), how does phase 3 (K efflux) get affected?
Thank you. I'll appreciate any input.
 
Activation of beta-2 causes insulin release and also hypokalemia through the up regulation of the Na+/K+ antiporter. Therefore, beta-2 activation will cause a hypokalemia environment. Beta-2 blocker will cause a hyperkalemia environment. The repolarization at phase 3 is more of a passive mechanism in which K+ is being leaked from inside the cell to outside the cell. A hyperkalemia environment will slow down the leaking of K+ and thereby prolong phase 3.
 
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