Table 1.

Current and contemplated uses of Ang II

Disease state	Properties of Ang II providing benefit	Status of use/evidence
High-output shock	Direct vasoconstriction, catecholamine sparing	Approved for clinical use based on two RCTs (Chawla et al, 201627; Khanna et al, 201736)
Cardiogenic shock	Vasoconstriction, inotropy	Use supported by retrospective data (Busse et al, 20176)
Cardiac arrest	Vasopressor effect, improved contractility, increased coronary perfusion, catecholamine potentiation	Use supported by retrospective data (Busse et al, 20176)
Sepsis-induced AKI	Restored glomerular perfusion pressure via efferent vasoconstriction	Evaluated in post hoc analysis of ATHOS-3 RCT (Tumlin, 201834)
Shock and ARDS	Vasopressor effect, replacement of Ang II thought to be deficient due to ACE dysfunction or deficiency	Evaluated in post hoc analysis of ATHOS-3 RCT (Busse et al, 2018121)
ACE inhibitor overdose	Vasopressor effect, replacement of Ang II thought to be deficient due to ACE inhibitors	Use supported by retrospective data (Trilli et al, 199488; Jackson et al, 199386; Newby et al, 199587)
Shock and liver failure	Vasopressor effect, replacement of Ang II thought to be deficient due to reduced angiotensinogen synthesis	Not yet studied
Shock and CPB/ECMO	Vasopressor effect, replacement of Ang II thought to be deficient due to reduced pulmonary circulation	Not yet studied

Abbreviations: ACE, angiotensin converting enzyme; AKI, acute kidney injury; Ang II, angiotensin II; ARDS, acute respiratory distress syndrome; ATHOS-3, Angiotensin II for the Treatment of Vasodilatory Shock; CPB, cardiopulmonary bypass; ECMO, extracorporeal membrane oxygenation; RCT, randomized controlled trial.