Protamine sulfate
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Acute pulmonary hypertension in an elderly patient, treated with epoprostenol: case report An 81-year-old man developed severe acute pulmonary hypertension during treatment with protamine sulfate for heparin neutralisation during cardiac surgery. He was successfully treated with inhaled epoprostenol [prostacyclin]. The man, who was undergoing coronary artery bypass surgery, underwent tracheal intubation; he received midazolam, fentanyl, propofol and pancuronium bromide. He then received cefazolin, tranexamic acid and heparin, and cardiopulmonary bypass (CPB) was instituted; total CPB time was 56 minutes. He was separated from CPB using low-dose dopamine. He then received a 10mg test dose of protamine sulfate administered over 30 seconds and exhibited no haemodynamic changes. Heparin was then reversed using a dosing ratio of 1mg of protamine sulfate for every 100U of heparin; 340mg administered over 15 minutes. Pericardial closure was initiated. However, 5 minutes after completing the protamine sulfate administration, his pulmonary arterial pressure (PAP) increased from 38/14 to 71/41mm Hg. His PAP increase was associated with a HR of 120 beats/min, a cardiac index (CI) of 1.7 L/min/m2, a systemic systolic BP of 60mm Hg and a central venous pressure of 20mm Hg. The man’s pericardium was reopened and a transoesophageal echocardiogram revealed severe global biventricular hypokinesis and a dilated left ventricle. Protamine sulfate was considered the cause of his haemodynamic instability. He was immediately hyperventilated with 100% oxygen and his PaO2 increased to 320mm Hg, his PaCO2 to 36mm Hg and his pH to 7.47. He was stabilised with epinephrine [adrenaline], norepinephrine [noradrenaline], milrinone and dopamine. However, his PAP remained >70mm Hg and his CI did not change. He received nebulised epoprostenol [Flolan] 50 ng/kg/min within 5–10min. During the first 10 minutes of epoprostenol administration, his PAP decreased to 45/23mm Hg and his CI increased to 2.3 L/min/m2. Two doses of epoprostenol (total dose ≥90 ng/kg/min) were continuously nebulised over the following 2 hours and his PAP remained at baseline levels; he was subsequently weaned off epinephrine and dopamine. His sternum was closed and his haemodynamic state continued to improve. He was extubated 24 hours after surgery. On day 3, he experienced atrial fibrillation. He was subsequently found to be positive for heparin-induced thrombocytopenic syndrome antibody. He was discharged from hospital on postoperative day 9. Author comment: "[O]ur case illustrates the successful management of severe protamine-induced pulmonary hypertension using inhaled [epoprostenol]. Inhaled [epoprostenol] is an alternative therapy with greater simplicity of the delivery system and a potential cost advantage over [nitric oxide] therapy." Jerath A, et al. The successful management of severe protamine-induced pulmonary hypertension using inhaled prostacyclin. Anesthesia and Analgesia 110: 803008083 365-9, No. 2, Feb 2010 - Canada
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