A 56-year-old male with a medical history significant for coronary artery disease complicated by non-ST segment elevation myocardial infarction in 2011 (at which time he received a single stent), hypertension, hyperlipidemia, tobacco use, chronic obstructive pulmonary disease, and ischemic cardiomyopathy presented with worsening angina and exertional dyspnea. He reported increasingly frequent anginal symptoms over a course of approximately 3 weeks. Elective heart catheterization demonstrated

Hyperkalemia is a potentially dangerous electrolyte abnormality that warrants the clinician’s attention whenever it is discovered. Although often asymptomatic, it represents a disturbance in homeostasis that should be investigated. The most important factor in the clinical severity of hyperkalemia is the rate at which potassium elevation occurs. Chronic hyperkalemia, such as seen in renal failure, may be well tolerated at much higher levels than even modest elevations that occur abruptly in

HIH is a known adverse effect of heparin, with a mechanism postulated to be tied, at least in part, to the renin-angiotensin-aldosterone axis. This case report presents a unique example of a patient without significant renal impairment experiencing acute, objectively symptomatic hyperkalemia after a single dose of heparin that resolved fully and immediately following administration of protamine. Correction of HIH with protamine has not been reported previously. Although aldosterone suppression