The diagnostic strategy here is to weigh the speed of onset against the metal-specific signs. The patient deteriorates within an hour of swallowing the poison, showing a fast heart rate and a falling blood pressure, which signals an acute toxic insult driving the patient toward circulatory shock, alongside a striking bluish tint of the conjunctiva, mucosae and nail beds.
Acute arsenic ingestion fits this profile. It is rapidly absorbed and provokes intense gastrointestinal and vascular toxicity, with increased capillary permeability leading to fluid loss, compensatory tachycardia and hypotension, and a bluish discoloration of mucous membranes and nails. This combination of immediate cardiovascular collapse with the described pigmentation is the recognised acute arsenic presentation.
The competing metals behave differently. Lead and mercury intoxication are typically chronic, dominated by neurological, renal and gingival changes rather than a one-hour shock state, and copper poisoning is marked by a metallic taste, blue-green vomiting, hemolysis and liver damage. Therefore, the most likely agent is arsenic.\[\boxed{\text{Arsenic}}\]