During induction of anesthesia, an anesthetist injects a bolus of a vasoconstrictor agent intravenously to correct hypotension. Heart rate promptly falls from 92 to 58 beats per minute despite the agent having no direct cardiac chronotropic effect. The mechanism of the bradycardia is:

• A Stimulation of presynaptic alpha-2 autoreceptors reducing norepinephrine release
• B Baroreceptor-mediated increase in vagal outflow secondary to the rise in blood pressure ✓
• C Reflex activation of chemoreceptors in the carotid body
• D Direct depression of the sinoatrial node by the drug

Explanation

Pure alpha agonists such as phenylephrine raise blood pressure without directly affecting cardiac receptors. The rise in arterial pressure stretches carotid sinus and aortic baroreceptors, increasing afferent firing through the glossopharyngeal and vagus nerves, which raises parasympathetic outflow to the sinoatrial node and slows the heart. This reflex is preserved even under anesthesia, which is why phenylephrine commonly causes reflex bradycardia in clinical practice.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

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Written and medically reviewed by the StethoPrep medical team.