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Cochrane Database Syst Rev. 2011 May 11;(5):CD003709. doi: 10.1002/14651858.CD003709.pub3.

Vasopressors for hypotensive shock.

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Department of Emergency Medicine, Medical University of Vienna, Vienna General Hospital;, Währinger Gürtel 18-20 / 6D, Vienna, Austria, 1090.

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Initial goal directed resuscitation for shock usually includes the administration of intravenous fluids, followed by initiating vasopressors. Despite obvious immediate effects of vasopressors on haemodynamics their effect on patient relevant outcomes remains controversial. This review was originally published in 2004 and was updated in 2011.


Our primary objective was to assess whether particular vasopressors reduce overall mortality, morbidity, and health-related quality of life.


We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2010, Issue 2), MEDLINE, EMBASE, PASCAL BioMed, CINAHL, BIOSIS, and PsycINFO (from inception to March 2010). The original search was performed in November 2003. We also asked experts in the field and searched meta-registries for ongoing trials.


Randomized controlled trials comparing various vasopressor regimens for hypotensive shock.


Two authors abstracted data independently. Disagreement between the authors was discussed and resolved with a third author. We used a random-effects model for combining quantitative data.


We identified 23 randomized controlled trials involving 3212 patients, with 1629 mortality outcomes. Six different vasopressors, alone or in combination, were studied in 11 different comparisons.All 23 studies reported mortality outcomes; length of stay was reported in nine studies. Other morbidity outcomes were reported in a variable and heterogeneous way. No data were available on quality of life or anxiety and depression outcomes. We classified 10 studies as being at low risk of bias for the primary outcome mortality; only four studies fulfilled all trial quality items.In summary, there was no difference in mortality in any of the comparisons between different vasopressors or combinations. More arrhythmias were observed in patients treated with dopamine compared to norepinephrine. Norepinephrine versus dopamine, as the largest comparison in 1400 patients from six trials, yielded almost equivalence (RR 0.95, 95% confidence interval 0.87 to 1.03). Vasopressors used as add-on therapy in comparison to placebo were not effective either. These findings were consistent among the few large studies as well as in studies with different levels of within-study bias risk.


There is some evidence of no difference in mortality between norepinephrine and dopamine. Dopamine appeared to increase the risk for arrhythmia. There is not sufficient evidence of any difference between any of the six vasopressors examined. Probably the choice of vasopressors in patients with shock does not influence the outcome, rather than any vasoactive effect per se. There is not sufficient evidence that any one of the investigated vasopressors is clearly superior over others.

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