A 38-year-old woman without diabetes developed hyperglycemic ketoacidosis after five months of tirzepatide therapy for weight management, presenting with high anion gap metabolic acidosis, elevated ketones, and significant hyperglycemia. This represents the first documented case of tirzepatide-induced hyperglycemic ketoacidosis in a non-diabetic patient, contrasting with two previous reports that involved euglycemic ketoacidosis with normal glucose levels. The patient recovered fully with standard treatment including IV fluids, insulin, and electrolyte replacement. This finding reveals a potentially serious but underrecognized metabolic complication of tirzepatide beyond its well-known gastrointestinal effects. The mechanism likely involves the drug's complex effects on glucose metabolism and ketone production through GLP-1 and GIP receptor pathways. Given tirzepatide's expanding use for weight management in non-diabetic individuals, this case suggests clinicians should maintain heightened awareness for ketoacidosis symptoms even in patients without diabetes risk factors. The patient's underlying congenital heart disease may have contributed to metabolic vulnerability, though the exact interplay remains unclear. This represents an important safety signal requiring broader surveillance as tirzepatide use increases.