Condition
Septic Shock
Septic shock is a life-threatening drop in blood pressure after a severe infection, when widened, leaky blood vessels leave organs short of blood flow. Angiotensin II, a hormone that tightens blood vessels, has strong evidence behind it: in one trial, 70% of people reached a target blood pressure within three hours, versus 23% on placebo. Those participants had shock that resisted standard drugs, so results mostly apply to that group.
Sources: PMID 31061651
- Updated
- How we grade
- 37 studies cited
- Supplements studied
- 0
- Medicines and peptides
- 1
- Graded outcomes
- 4
Prescription medicines and peptides studied, for context
| Grade | Outcome | Effect | Size | Studies | People | Studies list |
|---|---|---|---|---|---|---|
| Thromboembolic Events SAFETY CONCERN: ATHOS-3: 13% vs 5% thromboembolic events (DVT, arterial). Major imbalance in DVT. Concurrent DVT prophylaxis required. Systematic review (n=1,461): Similar rates in larger observational data (8.8% vs 9.4% VTE). | Worsens (the measure goes down) | Moderate effect | 51 studies | |||
| Mean Arterial Pressure Response ATHOS-3 (n=321): 70% achieved MAP ≥75 mmHg or ≥10 mmHg increase at 3h vs 23% placebo (P<0.001). 45% absolute increase in responders. Effective in catecholamine-resistant shock. | Improves (the measure goes up) | Large effect | 50 studies | |||
Studies that measured mean arterial pressure response
| ||||||
| Vasopressor Dose Reduction ATHOS-3: Significant reduction in background vasopressor requirements. Catecholamine-sparing effect allows reduction of norepinephrine doses. May reduce catecholamine toxicity. | Improves (the measure goes down) | Moderate effect | 50 studies | |||
Studies that measured vasopressor dose reduction
| ||||||
| 28-Day Mortality ATHOS-3: No significant mortality difference (46% vs 54%, P=0.12). Study not powered for mortality. Post-hoc AKI/RRT subgroup: 53% vs 30% survival (P=0.012). Mortality benefit uncertain. | NoneNo effect | 50 studies | ||||
Studies that measured 28-day mortality
| ||||||
Key findings
- Thromboembolic EventsWorsens (the measure goes down)
- Mean Arterial Pressure ResponseImproves (the measure goes up)
- Vasopressor Dose ReductionImproves (the measure goes down)
Safety notes in the studies
- May reduce catecholamine toxicity.
Studies cited
37 studies from PubMed
- Angiotensin-II and Thromboembolic Events: A Systematic Review
- Angiotensin II Is Involved in MLKL Activation During the Development of Heart Failure Following Myocardial Infarction in Rats.
- The Role of Local Angiotensin II/Angiotensin Type 1-receptor Mechanisms in Adipose Tissue Dysfunction to Promote Pancreatic Cancer.
- Roles of autophagy in angiotensin II-induced cardiomyocyte apoptosis.
- Angiotensin II (Giapreza): A Distinct Mechanism for the Treatment of Vasodilatory Shock
- FDA Approval of Angiotensin II for the Treatment of Hypotension in Adults with Distributive Shock
- Association Between Early Response to Angiotensin-II and Mortality in Septic Shock: A Post Hoc Analysis of the ATHOS-III Clinical Trial
- Renin-Angiotensin System in the Intensive Care Unit
- Outcomes in Patients with Vasodilatory Shock and Renal Replacement Therapy Treated with Intravenous Angiotensin II
- Angiotensin II: a new therapeutic option for vasodilatory shock
- Angiotensin II Brings More Questions Than Answers
- Angiotensin II and Treatment of High-Output Shock in Human Beings: A Matched Case Series
- Vasodilatory shock in the ICU and the role of angiotensin II.
- Angiotensin II for the Treatment of Vasodilatory Shock
- Angiotensin II type 1a receptor-deficient mice develop angiotensin II-induced oxidative stress and DNA damage without blood pressure increase.
- Angiotensin II and skeletal muscle abnormalities.
- Angiotensin (1-7) receptor antagonism equalizes angiotensin II-induced hypertension in male and female spontaneously hypertensive rats.
- Angiotensin II-nitric oxide interaction in the kidney.
- Angiotensin II type 2 receptor decreases ischemia reperfusion induced fluid leak.
- Angiotensin II and renal tubular ion transport.
- Angiotensin II, angiotensin II antagonists and spironolactone and their modulation of cardiac repolarization.
- Angiotensin-II behaves as an endogenous pro-inflammatory molecule.
- Protective effects of angiotensin II interruption: evidence for antiinflammatory actions.
- Cardiac angiotensin II: an intracrine hormone?
- Angiotensin II as a mediator of renal tubular transport.
- Angiotensin II induces phenotype-dependent apoptosis in vascular smooth muscle cells.
- Angiotensin II receptor blockers: review of the binding characteristics.
- Angiotensin II receptors in the kidney.
- Biology and functions of renal receptors for angiotensin II and its active fragments.
- Angiotensin II receptors on colorectal carcinoma cells.
- Regional angiotensin II production in essential hypertension and renal artery stenosis.
- The intrarenal renin-angiotensin system.
- Angiotensin II receptor subtypes in the kidney.
- Angiotensin II is mitogenic in neonatal rat cardiac fibroblasts.
- Angiotensin II and renal hypertension in dog, rat and man: effect of converting enzyme inhibition.
- [Angiotensin II analogue and essential hypertension].
- Angiotensin II in arterial and renal venous plasma and renal lymph in the dog.