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Anaphylaxis and cardiovascular collapse: case report An 84-year-old man developed anaphylaxis and cardiovascular collapse during treatment with protamine sulfate for anticoagulation reversal. The man, who had a history of symptomatic paroxysmal atrial fibrillation (AF) and coronary artery disease, was referred to a hospital for a repeat AF ablation. At that time, he underwent successful electrical cardioversion and was initiated on dofetilide. He underwent radiofrequency ablation with successful bilateral pulmonary vein and left atrial posterior wall isolation. He received heparin for anticoagulation. His anticoagulation was later reversed with protamine sulfate infusion. At the time of reversal, activated clotting time was found to be 364ms. He was administered a 5mg test dose, and after a 5-minute waiting period, an additional 65mg was administered over 10 minutes. Near the end of the infusion, he developed anaphylaxis and a profound cardiovascular collapse. The man required haemodynamic support with boluses of phenylephrine and epinephrine and a continuous infusion of vasopressin and dopamine. A transthoracic echocardiogram (TTE) performed during this event revealed a newly reduced ejection fraction (EF) with global hypokinesis. He was administered diphenhydramine, methylthioninium chloride [methylene blue] and hydrocortisone. Before this instance, he had received protamine sulfate infusion 3 separate times (3 months, 5 years and 14 years ago), without symptoms. While necessitating ionotropic support, he developed sustained atrial tachycardia, for which cardioversion was attempted twice. Later, he developed sustained ventricular tachycardia. He was administered amiodarone and was successfully cardioverted. In the following 24 hours, norepinephrine was weaned off, and he continued amiodarone treatment because of continued AF while on inotropes. Twenty four hours later, his ejection fraction normalised. On post-procedure day 3, he underwent cardioversion again and was discharged on the same day. The TTE revealed no cardiac tamponade or effusion. It demonstrated global hypokinesis with no regional wall motion abnormalities to indicate acute coronary syndrome. ECG during the event initially showed normal sinus rhythm with no evidence of T- or ST-wave abnormalities, before the development of ventricular and atrial tachycardia. Given cardiac decompensation on TTE, neurogenic shock secondary to air embolus or intracranial haemorrhage were unlikely. His haemoglobin was stable without any clinical signs of haemorrhage. Given the temporal association of global hypokinesis seen on TTE with protamine sulfate administration, protamine reaction was assumed to be the most likely aetiology of the acute decompensation. At a 2-month follow-up, he was feeling well, with no symptomatic AF, fatigue or chest pain, as noted at previous visits. Treatment with amiodarone was discontinued. Geurink KR, et al. A reversal of fortune: A case of cardiovascular collapse following protamine sulfate infusion. HeartRhythm Case Reports 6: 322