Vasoactive Agents in Burn Patients: Perspectives on Angiotensin-II

Abstract

Severe burn injury poses significant clinical challenges, often necessitating the use of vasoactive agents to maintain perfusion. This narrative review explores the current landscape of vasoactive agents in acute burn shock resuscitation and in severe burn-injured patients who develop septic shock, with a particular focus on the potential role of the novel vasoactive agent, synthetic angiotensin-II (AT-II), in these settings. While catecholamines and vasopressin remain cornerstone therapies, adverse effects, variable patient responses, and a new understanding of burn injury pathophysiology highlight the potentially evolving role of vasoactive agents in these clinical scenarios. A key system involved in blood pressure regulation, the renin-angiotensin-aldosterone system, is often dysregulated in acute burn and septic shock. Contributory mechanisms and potential benefits of synthetic AT-II are discussed here and form the physiologic rationale behind the exogenous administration of synthetic AT-II in the context of available safety and efficacy data. To date, administration of synthetic AT-II has shown promise in improving hemodynamics and clinical outcomes in distributive shock populations; however, data in acute burn shock and in burn patients who develop septic shock are lacking. In addition, a comprehensive understanding of the potential and future areas of research in burn shock and severe burn-injured patients is provided.

Keywords: angiotensin-II; burn shock; renin-angiotensin-aldosterone system; septic shock; vasopressors.

Figure 1.

Upper Portion of Figure Describes the Classical RAAS Pathway. In the setting of hypotension, renin secretion from the kidney converts liver-synthesized angiotensinogen to angiotensin-I. Angiotensin-converting enzyme, largely located in the lung and renal vasculature facilitates conversion to angiotensin-II, which exerts several effects on angiotensin type 1 receptors. The lower portion of the figure describes the alternative RAAS pathway. Key effector molecules including angiotensin (1-9) and angiotensin (1-7) are synthesized and act on angiotensin type 2, Mas, and MrgD receptors, resulting in various effects. The interplay between these pathways may be dysregulated in the setting of acute/chronic disease, organ dysfunction, medication exposure, etc. Abbreviations: ACE: angiotensin-converting enzyme; AT1R: angiotensin type 1 receptor; AT2R: angiotensin type 2 receptor; NEP/PEP: neprilysin/prolyl-endopeptidase.