A patient on a non-selective beta-blocker experiences a hypertensive crisis after receiving adrenaline. The mechanism is best explained by:
- A Reflex bradycardia from beta-1 blockade causing baroreceptor-mediated hypertension
- B Beta-2 blockade in peripheral vessels removes vasodilatory tone, leaving unopposed alpha-1 vasoconstriction ✓
- C Beta-blocker inhibiting adrenaline metabolism by MAO
- D Increased alpha-2 sensitivity causing enhanced noradrenaline release
Correct answer: B. Beta-2 blockade in peripheral vessels removes vasodilatory tone, leaving unopposed alpha-1 vasoconstriction
Explanation
Non-selective beta-blockers block both beta-1 (cardiac) and beta-2 (vasodilatory) receptors. When adrenaline is given, its vasodilatory beta-2 effect on blood vessels is blocked, leaving only alpha-1 mediated vasoconstriction unopposed, causing severe hypertension. This is a classic pharmacodynamic interaction seen when adrenaline is used in patients on non-selective beta-blockers. Beta-1 blockade actually tends to lower blood pressure by reducing cardiac output.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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