Vol. 7, Issue 2, Part C (2025)

A 67-year-old man with long-standing diabetes, hypertension, chronic kidney disease, and heavy alcohol use presented with fever, flank pain, dysuria and myalgia. He was diagnosed with acute pyelonephritis and treated with intravenous antibiotics. Initial vitals were stable, but nine hours later he developed profound bradycardia (30 bpm) and severe hypoxemia (SpO₂ 47% on room air). ECG revealed marked ST-segment depression in leads V4-V6, consistent with a posterior wall infarction. Laboratory tests showed severe uremia (BUN 66.2 mg/dL, creatinine 8.74 mg/dL) and hyperkalemia. He was managed with IV atropine, sodium bicarbonate and BiPAP, and subsequently stabilized. This case highlights how uremic metabolic derangements and sepsis from pyelonephritis can precipitate type 2 myocardial infarction by creating an acute imbalance of myocardial oxygen supply and demand [1]. We review the diagnostic considerations and pathophysiological mechanisms linking uremia, systemic infection and posterior wall infarction.