Which medication is unlikely to be effective and should be avoided in patients who have had a heart transplant?

• A. Atropine
• B. Epinephrine
• C. Dopamine
• D. Adenosine

Answer: (A)

In a heart transplant patient, the donor heart is denervated, meaning the autonomic nerves to the heart are cut. Atropine works by blocking parasympathetic (vagal) input to the SA and AV nodes to raise heart rate. If there’s no vagal input to begin with, blocking it doesn’t produce a meaningful increase in rate. That’s why atropine is unlikely to be effective in this setting.

Other drugs can still raise heart rate because their effects come from direct receptor stimulation rather than relying on nerve input. Epinephrine or dopamine act on beta-1 receptors to increase rate and contractility via circulating drug levels, which remains effective even without innervation. Adenosine has different uses (mainly for certain tachyarrhythmias via AV node effects) and isn’t the first choice for bradycardia in this scenario, but atropine specifically lacks effect due to denervation.