P242 Cardiogenic Shock With Ischemic Phenotype Secondary to Incessant Ventricular Tachycardia: A Call for Implementation of Hub–and–spoke Model

Abstract

A 55–years–old patient presents to emergency room with extensive anterior STEMI, complicated by acute pulmonary edema. The ECG showed sinusal tachycardia, Q waves in V1–V3, ST elevation >2mm V2–V6. The echocardiogram showed akinesia of the apex and anterolateral wall with severe reduction of contractile function (LVEF 30%). The patient was treated with CPAP, dual antiplatelet therapy and diuretics; the urgent coronary angiography showed three–vessel disease with occlusion of the proximal LAD, treated with PCI and two drug–eluting stents implantation. 48 after admission to ICU, the patient developed "combined" shock (IC↓ RVS↓ WP↑), sustained by both severe cardiac dysfunction and a septic complication, requiring inotropes and targeted antibiotic therapy (noradrenaline 0.02 gamma/Kg/min and piperacillin/tazobactam i.v). At 96 hours there was a recovery of contractile function and haemodynamics (CI from 1.8 to 2.7). Weaned from inotropes, he began therapy with low doses of ACE inhibitor, beta blocker, antialdosteronic. On the 7th day of hospitalization, without ischemic and/or electrolyte "triggers", the patient developed "arrhythmic storm" with incessant sustained ventricular tachycardias. Arrhythmias persisted despite antiarrhythmics (magnesium sulfate, amiodarone, lidocaine), IOT, sedation, mechanical ventilation. The temporary pacemaker for overdrive pacing was placed in. After placement of IABP, the patient underwent revascularization of residual coronary artery stenosis. Despite 1 hour of assistance (ABLS), incessant ventricular tachycardia persisted; a third–level center for VA–ECMO inside support was called. After positioning VA–ECMO there was progressive clinical stabilization and –concomitantly– a progressive reduction of ventricular tachycardias. ECMO support was needed for over 7 days due to persistence of arrhythmic storm; it was slowly weaned with stabilization of the patient; an AICD was implanted. Residual function of the left ventricle was mild reduced (LVEF40%) despite protracted CPR. There wasn’t residual cognitive impairment. Implementation of multidisciplinary teams in the spoke centers would improve protocols and early treatments in patients with cardiogenic shock; spoke centers would provide early access to life–saving therapies and safe transfer to hub centers.