P284 POTENTIAL PROARRHYTHMIC SIDE EFFECT OF HIGH DOSE AND PROLONGED SODIUM NITROPRUSSIDE INFUSION THROUGH CALCIUM ION REDUCTION

Abstract

Abstract Patient presentation. A fifty y/o male patient with a history of congenital aortic stenosis surgically corrected previously and with chronic heart failure due to severe left ventricular dysfunction presented to our emergency department complaining dyspnea. Due to acute decompensated heart failure with ongoing cardiogenic shock, he was admitted to our intensive cardiology unit. Initial work up. The blood exams showed a normal renal and liver function, normal total and free calcium, 9.4 mg/dL and 1.16 mmol/L respectively, lactates were mildly increased. The chest x–ray showed pulmonary congestion. At the echocardiography we found severe biventricular dysfunction, moderate mitral regurgitation, severe pulmonary hypertension. Since the patient was unstable, adrenaline, high–dose sodium nitroprusside (SNP), and intra–aortic balloon pump were started. The right heart catheterization revealed combined pulmonary hypertension reversible with SNP and, therefore, the patient was inserted in the heart transplant list. Diagnosis and Management. One of the side effects of SNP is the thiocyanate toxicity. A high dose of SNP was necessary for this patient (2.2 mcg/kg/min). Thus, thiocyanate levels increased up to 10 mg/100 mL (NV<3). Importantly, the patient was asymptomatic despite these levels. However, the free calcium ion progressively decreased up to 0.94 mmol/L, despite normal total calcium and calcium supplementation iv and orally. Since arrhythmic burden markedly increased, we started lidocaine which was not effective. Follow–up. Since we suspected a possible causative role of thiocyanate, which might bond the double positive charged free calcium ion with its two negatively charged sulfur atoms, explaining the normal total calcium level and the low calcium ion, we carefully reduced SNP dose within days. This allowed us to reduce thiocyanate to 6 mg/100 mL, without compromising patient hemodynamics. Concomitantly, the free calcium ion tended to normalize, lowering the arrhythmic burden. Conclusions We describe for the first time a proarrhythmic side effect of prolonged SNP infusion, likely related to thiocyanate accumulation and free calcium ion binding, which, despite aggressive calcium supplementation, was normalized only after SNP down titration.