A patient taking propranolol and hydrochlorothiazide has blood pressure rise to 200/100 after four cartridges of local anesthetic with epinephrine. What is the MOST likely explanation?

Correct answer: A. A drug interaction between epinephrine and the non-selective beta blocker

• A. CORRECT. PROPRANOLOL is a NON-SELECTIVE beta blocker — it blocks beta-1 (cardiac) AND beta-2 (vascular smooth muscle) receptors. When epinephrine is administered, its beta-2 mediated VASODILATION is blocked, leaving UNOPPOSED ALPHA-1 vasoconstriction. The result is a marked rise in peripheral resistance and severe hypertension, with a REFLEX BRADYCARDIA. This is a recognized and potentially dangerous interaction. Limit epinephrine to about 0.04 mg (roughly two cartridges of 1:100,000) in patients on non-selective beta blockers, aspirate carefully, and inject slowly.
• B. Lidocaine toxicity produces CNS excitation then depression (perioral tingling, tinnitus, tremor, seizures) and cardiovascular DEPRESSION — not hypertension.
• C. Allergy to amide local anesthetics is exceedingly rare and would present with urticaria, angioedema, or bronchospasm — not isolated hypertension.
• D. Anxiety can raise blood pressure, but not typically to 200/100 in a medicated patient, and the temporal relationship to the epinephrine dose points to the interaction.

Note: SELECTIVE beta blockers (metoprolol, atenolol) do not produce this interaction because beta-2 receptors remain available to mediate vasodilation.