I am going on the assumption that this is a question from a review book and not an actual exam remembered question, which we have been discouraged to post here.
This is from the open anesthesia keyword website, and I think it addresses your confusion.
Heart transplant - autonomic effect
The transplanted heart will not be able to respond to drugs that act by blocking the parasympathetic system because these connections were severed during the transplant. Therefore, treating bradycardia would have to be done with agents such as isoproterenol, glucagon, epinephrine, norepinephrine (drugs that have a direct effect on the heart). Isoproterenol is most commonly used for increasing heart rate in cardiac transplant recipients. Epinephrine/Norepinephrine may have exaggerated beta mimetic effects on the heart rate because the increase in blood pressure will not lead to a reflex slowing of the heart rate via the baroreceptor reflex (i.e., efferent vagus nerve). Implanted mechanical pacemakers work normally in heart transplant recipients since the cardiac leads are placed directly into myocardium.
Transplanted hearts have no baseline parasympathetic innervation and thus don't have the normal tachycardia and increased contractility response to hypotension/hypovolemia. Reflex venous contriction response to hypotension still exists. Thus intravascular volume is even more important. Circulating catecholes will have cause a delayed increase in rate and contractility. Indirect drugs that affect rate will not be effective (antimuscarinics, anticholinesterases, pancuronium, digoxin). Use direct acting agents (isoproterenol, epinephrine). Lack of vagal tone will result in baseline rate of 90-100. Vagal bradycardic reflexes will also be absent (laryngoscopy, hypertension, carotid sinus massage).
About 25% of patients will develop a bradycardia that will require implantation of a permanent pacemaker.
Sources
Barash: Clinical Anesthesia, ed 5, pp 311, 318, 1373.
Hines: stoelting's Anesthesia and Co-Existing Disease, ed 5, pp 21-22.
