Fig. 1
A Contributing factors common to both VA and VV-ECMO. B Specific therapies. Vasoplegia, prevalent in both VA and VV-ECMO, can be severe. The primary vasopressor is NE, with vasopressin as a potential addition to reduce NE requirements or in cases of NE failure. In refractory vasodilatory shock, methylene blue and/or angiotensin-2 may be considered as a salvage therapy. During VA-ECMO, inotropes play a specific role. Dobutamine or milrinone are typically employed as the first-line agent to maintain a certain level of contractility, ensuring the opening of the aortic valve. In some instances, levosimendan, a calcium-sensitizing agent with a long half-life may be useful to facilitate both VA-ECMO weaning and transition to alternative supportive therapies. In VV-ECMO, persistent right ventricular failure during VV-ECMO might necessitate inhaled nitric oxide to reduce pulmonary artery pressure, the use of vasopressors to maintain right ventricular perfusion, and the administration of inotropes. Area of research: Long-term and high-dose exposure to catecholamines are associated with serious side effects especially at the heart level. Notably, in VA-ECMO, a strategy of decatecholamination can be explored by employing non-catecholaminergic vasopressors (vasopressin, angiotensin-2) and inotropes (IPDE3, levosimendan), with or without the addition of landiolol. AVP arginine vasopressin; I/R ischemia–reperfusion; iNO inhaled nitric oxide; IPDE3 phosphodiesterase 3 inhibitor