The Intelligent Use of Adrenaline

Abstract Case Report A 52–year–old patient experienced anterior and inferior ST–elevation myocardial infarction, leading to cardiogenic shock necessitating invasive hemodynamic and pharmacological support. During angiography, an intra–aortic balloon pump (IABP) was inserted, and a norepinephrine infusion along with dobutamine was initiated, showing partial clinical and laboratory improvement. Critical disease in all three vessels was detected, prompting angioplasty with stenting of the right coronary artery and left anterior descending artery. Echocardiography revealed severe reduction in left ventricular systolic function (ejection fraction 10%). Despite revascularization and intensive support, the patient‘s hemodynamic status deteriorated (SCAI D), necessitating the addition of adrenaline (0.03 μg/kg/min) to the ongoing dobutamine infusion, suspending noradrenaline. Subsequent days showed gradual improvement, allowing for withdrawal from amine support and discontinuation of the IABP. Follow–up included a cardiac MRI displaying severe systolic dysfunction (EF 21%), extensive ischemic–pattern delayed enhancement across three–vessel distribution. Given the persistent severe left ventricular dysfunction, the patient underwent subcutaneous defibrillator implantation for primary prevention after optimizing anti–remodeling therapy. Despite optimized medical therapy and cycles of levosimendan, the patient experienced heart failure exacerbation, requiring hospitalization (INTERMACS 3). Considering the clinical condition and absence of contraindications, the patient was listed for heart transplantation. Due to refractory hemodynamic instability despite inotropic agents, a left ventricular assist device was implanted as a bridge to transplantation. Roughly 6 months later, the patient successfully underwent heart transplantation without acute complications. Conclusions Very low doses of adrenaline demonstrate increased sensitivity to β2 receptors over α receptors, thereby enhancing mean arterial pressure and peripheral perfusion. At the cardiac level, it induces an increase in both heart rate and coronary blood flow, while peripherally reducing resistances, predominantly due to the prevalence of β2 receptors in skeletal muscle. This improvement contributes to the enhancement of ventricular–arterial coupling. In conditions characterized by a primary pump deficit, such as cardiogenic shock, the use of low–dose adrenaline emerges as a valid therapeutic option.