The concern with Inderal (Propanolol) is not with amide local anesthetics but with epinephrine.  The interaction is as follows: 

As you know, there are two main classes of beta blockers - cardioselective and non-cardioselective.  The cardioselective beta blockers block only the beta-1 receptors (those responsible for making the heart beat faster and more forcefully) but leave the beta-2 receptors open.  The non-cardioselective beta blockers block both beta-1 and beta-2 receptors (those responsible for peripheral vasodilation and other effects).

Also, as you know, epinephrine is an adrenergic activist, stimulating alpha, beta-1 and beta-2 receptors.

If  someone is taking a cardioselective beta blocker and are given moderate to high doses of epinephrine in the local anesthetic, the epinephrine will want to stimulate both beta receptors but the beta-2 receptors are the only ones that are open.  This is good because the heart will not beat faster and more forcefully (the beta-1 receptors are blocked) but beta-2 mediated activation by the epi will cause vasodilation as usual.  This vasodilation will counteract alpha mediated vasoconstriction. (which is undesirable from a CVS perspective).  So the end result is no major effect on the patients cardiovascular system.

However if the patient is taking a non-cardioselective beta blocker (eg Inderal), both beta-1 and beta-2 receptors are blocked and so if they receive a moderate to high dose of epi, it can not stimulate either beta receptor.  All that happens is the alpha mediated vasoconstriction and this results in a rise in blood pressure (no counteracting beta-2 mediated vasodilation can occur) and to make matters worse, the patient will characteristically have a low pulse due to being on a beta blocker.  Low pulse and rising blood pressure is obviously a bad combination.  Direct comments or e-mail us at localanesthetics@yahoo.ca

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