A post-resuscitation shock occurs in 50–70% of patients who had a cardiac arrest. It is an early and transient complication of the post-resuscitation phase, which frequently leads to multiple-organ failure and high mortality. The pathophysiology of post-resuscitation shock is complex and results from the whole-body ischemia–reperfusion process provoked by the sequence of circulatory arrest, resuscitation manoeuvers and return of spontaneous circulation, combining a myocardial dysfunction and sepsis features, such as vasoplegia, hypovolemia and endothelial dysfunction. Similarly to septic shock, the hemodynamic management of post-resuscitation shock is based on an early and aggressive hemodynamic management, including fluid administration, vasopressors and/or inotropes. Norepinephrine should be considered as the first-line vasopressor in order to avoid arrhythmogenic effects of other catecholamines and dobutamine is the most established inotrope in this situation. Importantly, the optimal mean arterial pressure target during the post-resuscitation shock still remains unknown and may probably vary according to patients. Mechanical circulatory support by extracorporeal membrane oxygenation can be necessary in the most severe patients, when the neurological prognosis is assumed to be favourable. Other symptomatic treatments include protective lung ventilation with a target of normoxia and normocapnia and targeted temperature management by avoiding the lowest temperature targets. Early coronary angiogram and coronary reperfusion must be considered in ST-elevation myocardial infarction (STEMI) patients with preserved neurological prognosis although the timing of coronary angiogram in non-STEMI patients is still a matter of debate. Further clinical research is needed in order to explore new therapeutic opportunities regarding inflammatory, hormonal and vascular dysfunction.