Effectiveness of Angiotensin II for Catecholamine Refractory Septic or Distributive Shock on Mortality: A Propensity Score Weighted Analysis of Real-World Experience in the Medical ICU

Quan, Michele; Cho, Nam Ik; Bushell, Thomas; Mak, Joseph; Nguyen, Nolan; Litwak, Jane; Rockwood, Nicholas; Nguyen, H. Bryant

doi:10.1097/cce.0000000000000623

Cited by 10 publications

(22 citation statements)

References 40 publications

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“…Although treating patients in shock with Ang-2 makes sense pathophysiologically, the study by Quan et al and Bellomo et al showed that patients in shock treated with Ang-2 had higher mortality rate. 3,46 However, in the same study, the mortality rate was significantly lower when Ang-2 is given to patients with elevated renin. 3,46 In vasodilatory shock, renin production is triggered to increase Ang-2 and induce vasoconstriction, but in these patients the mechanism failed.…”

Section: Dovepressmentioning

confidence: 78%

“…3,46 However, in the same study, the mortality rate was significantly lower when Ang-2 is given to patients with elevated renin. 3,46 In vasodilatory shock, renin production is triggered to increase Ang-2 and induce vasoconstriction, but in these patients the mechanism failed. 3 The study by Bellomo et al showed that there was an increase in the levels of Ang-1 and Ang-1/Ang-2 ratio in patients with vasodilatory shock compared to controls, while the levels of Ang-2 in both groups tended to remain.…”

Section: Dovepressmentioning

confidence: 78%

“…34 In 2017, the Food and Drug Administration (FDA) approved Ang-2 as a vasopressor to increase blood pressure in cases of septic shock or distributive shock in adult patients. 3 In ATHOS-3, the patients started receiving Ang-2 after a dose of norepinephrine equivalent dose (NED) 200 ng/kg/minute for more than six hours and was used as a third line vasopressor after norepinephrine and vasopressin. 13 In the latest Surviving Sepsis Campaign guidelines, it is stated that Ang-2 is not the first line but can act as an additional vasopressor therapy.…”

Section: Discussionmentioning

confidence: 99%

“…37 In this systematic review study, we found that Ang-2 was able to increase MAP above 65mmHg. 3,[12][13][14] Ang-2 binds to AT-I causing vasoconstriction in both afferent and efferent glomerular arterioles. The effect is greatest on the efferent side, causing a decrease in renal blood flow and an increase in glomerular filtration pressure.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin-2 (Ang-2) is capable of stimulating vasoconstriction, aldosterone and vasopressin secretion, sodium and water reabsorption, and cardiac contractility. 3 The clinical outcome of the patient with shock is concerning. Compared with patients without shock, patients with shock carry more burden in their clinical outcomes, such as mortality and length of stay.…”

Section: Introductionmentioning

confidence: 99%

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How Effective is Angiotensin II in Decreasing Mortality of Vasodilatory Shock? A Systematic Review

Semedi

Rehatta

Soetjipto

et al. 2023

OAEM

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Background: Patients with severe vasodilation accompanied by refractory hypotension despite high doses of vasopressors were associated with a high mortality rate. The Ang-2 for the Treatment of High-Output Shock (ATHOS) 3 trial demonstrated that angiotensin 2 (Ang-2) could effectively increase MAP and blood pressure in vasodilatory shock patients. This systematic review aims to summarize the impact of Ang-2 for the treatment of vasodilatory shock on clinical outcomes, including length of stay, MAP level (before and after), and mortality also Ang-2 dose needed. Methods: A systematic search in PubMed, Sage, ScienceDirect, Scopus and Gray literature was conducted to obtain studies about the use of Ang-2 in vasodilatory shock patients. Results: In all of the studies that we obtained, there were different results regarding mortality in patients with vasodilatory shock with Ang-2. Mortality was significantly lower when Ang-2 was administered to patients with elevated renin. The initial dose of Ang-2 can be started at 10-20 ng/kg/min, but there is no agreement on the maximum dose. Ang-2 may be considered a third-line vasopressor if the targeted MAP has not been achieved after administration of norepinephrine >200 ng/kg/min for more than 6 hours. Although not statistically significant, the use of Ang-2 can reduce the length of stay in the ICU and in the hospital when compared to patients without Ang-2 therapy, in addition to reducing the dose of vasopressor. Conclusion: Overall, the use of Ang-2 has potential to be a regimen for patients with vasodilatory shock. Further study is needed to obtain more data.

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