Step 1: Ask what epinephrine actually contributes during arrest. Its life-saving effect is vasoconstriction that pushes blood through the coronary and brain circulation. Any replacement must reproduce this pressor effect, not treat the rhythm.
Step 2: Map each choice. Amiodarone treats refractory ventricular fibrillation and pulseless VT as an antiarrhythmic. Atropine blocks vagal tone in bradycardia. Adenosine slows AV nodal conduction to break supraventricular tachycardia. None of these three constrict vessels to support pressure.
Step 3: Vasopressin is the odd one out that does raise pressure. At high doses it stimulates V1 receptors on vascular smooth muscle, driving vasoconstriction through a non-adrenergic pathway, so it works even when adrenergic responsiveness is poor.
Step 4: Guidelines have permitted one 40 unit dose of vasopressin to stand in for an epinephrine dose across asystole, pulseless electrical activity, and shockable arrest, confirming it as the true alternative.
\[\boxed{\text{High dose vasopressin}}\]