Mixed shock has been identified by the Shock Academic Research Consortium (SHARC) as a “high-risk, understudied population”.¹ It develops in around one-quarter of patients with cardiogenic shock² and has a higher mortality than other shock phenotypes.³ It represents a heterogeneous population, whose unifying feature is a combination of both cardiogenic shock, defined by low cardiac output (CO) due to cardiac pathology, and vasodilatory shock, defined by low systemic vascular resistance. The etiology of mixed shock may be further classified by the sequence of physiological insults: 1) initial vasoplegic shock, most commonly due to sepsis, followed by sepsis- or stress-induced cardiomyopathy and reduced CO; 2) initial cardiogenic shock (eg, due to myocardial infarction or decompensated heart failure), followed by hypoperfusion-induced systemic inflammation and consequent vasoplegia; and 3) simultaneous cardiogenic and inflammatory vasoplegic shock due to global ischemia, which is common following out-of-hospital cardiac arrest.⁴ Crucially, these 3 groups may have differing clinical courses, outcomes, and optimal management strategies.