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Meta-Analysis
. 2016 Feb 15;2(2):CD003709.
doi: 10.1002/14651858.CD003709.pub4.

Vasopressors for hypotensive shock

Gunnar Gamper  1 , Christof Havel, Jasmin Arrich, Heidrun Losert, Nathan Leon Pace, Marcus Müllner, Harald Herkner
Affiliations
Meta-Analysis

Vasopressors for hypotensive shock

Gunnar Gamper et al. Cochrane Database Syst Rev. .

Abstract

Background: Initial goal-directed resuscitation for hypotensive shock usually includes administration of intravenous fluids, followed by initiation of vasopressors. Despite obvious immediate effects of vasopressors on haemodynamics, their effect on patient-relevant outcomes remains controversial. This review was published originally in 2004 and was updated in 2011 and again in 2016.

Objectives: Our objective was to compare the effect of one vasopressor regimen (vasopressor alone, or in combination) versus another vasopressor regimen on mortality in critically ill participants with shock. We further aimed to investigate effects on other patient-relevant outcomes and to assess the influence of bias on the robustness of our effect estimates.

Search methods: We searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2015 Issue 6), MEDLINE, EMBASE, PASCAL BioMed, CINAHL, BIOSIS and PsycINFO (from inception to June 2015). We performed the original search in November 2003. We also asked experts in the field and searched meta-registries to identify ongoing trials.

Selection criteria: Randomized controlled trials (RCTs) comparing various vasopressor regimens for hypotensive shock.

Data collection and analysis: Two review authors abstracted data independently. They discussed disagreements between them and resolved differences by consulting with a third review author. We used a random-effects model to combine quantitative data.

Main results: We identified 28 RCTs (3497 participants) with 1773 mortality outcomes. Six different vasopressors, given alone or in combination, were studied in 12 different comparisons.All 28 studies reported mortality outcomes; 12 studies reported length of stay. Investigators reported other morbidity outcomes in a variable and heterogeneous way. No data were available on quality of life nor on anxiety and depression outcomes. We classified 11 studies as having low risk of bias for the primary outcome of mortality; only four studies fulfilled all trial quality criteria.In summary, researchers reported no differences in total mortality in any comparisons of different vasopressors or combinations in any of the pre-defined analyses (evidence quality ranging from high to very low). More arrhythmias were observed in participants treated with dopamine than in those treated with norepinephrine (high-quality evidence). These findings were consistent among the few large studies and among studies with different levels of within-study bias risk.

Authors' conclusions: We found no evidence of substantial differences in total mortality between several vasopressors. Dopamine increases the risk of arrhythmia compared with norepinephrine and might increase mortality. Otherwise, evidence of any other differences between any of the six vasopressors examined is insufficient. We identified low risk of bias and high-quality evidence for the comparison of norepinephrine versus dopamine and moderate to very low-quality evidence for all other comparisons, mainly because single comparisons occasionally were based on only a few participants. Increasing evidence indicates that the treatment goals most often employed are of limited clinical value. Our findings suggest that major changes in clinical practice are not needed, but that selection of vasopressors could be better individualised and could be based on clinical variables reflecting hypoperfusion.

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Conflict of interest statement

Gunnar Gamper: no conflict of interest.

Christof Havel: no conflict of interest.

Jasmin Arrich: no conflict of interest.

Heidrun Losert: no conflict of interest.

Nathan Leon Pace: no conflict of interest.

Marcus Müllner: no conflict of interest.

Harald Herkner: no conflict of interest.

Figures

1
1
Comparisons including vasopressors identified from the systematic review. The 10 interventions with 31 direct comparisons were derived from 28 studies. Line thickness is proportional to the number of included participants. Boxes indicate the two networks that we formally assessed in our network meta‐analysis. npvd/'placebo' denotes non‐protocol vasoactive drugs or placebo.
2
2
Search flow diagram.
3
3
Risk of bias summary: review authors' judgements about each risk of bias item for each included study.
4
4
Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.
5
5
Funnel plot of comparison: 1 norepinephrine, outcome: 1.1 mortality.
6
6
Forest plot of comparison: 1 Norepinephrine, outcome: 1.1 Total mortality.
7
7
Graphical representation of the evidence network including vasopressors showing available direct comparisons. The lines represent direct comparisons, and line thickness is proportional to precision of the estimates (1/SE).
8
8
Network forest plot comparing seven vasopressor regimens vs norepinephrine (reference) from 22 studies with 24 pair‐wise comparisons. Heterogeneity/inconsistency: tau2 < 0.0001; I2 statistic = 0%. Test of heterogeneity/inconsistency: Q = 8.48 (d.f. 18), P value = 0.97; 'NPVD' denotes non‐protocol vasoactive drugs with or without placebo. RR denotes risk ratio, as calculated by a fixed‐effect model. RR > 1 indicates increased mortality risk; RR < 1 indicates reduced mortality risk vs norepinephrine (reference).
9
9
Graphical representation of the evidence network including vasopressors and combinations with beta‐agonist action showing available direct comparisons. The lines represent direct comparisons, and line thickness is proportional to precision of the estimates (1/SE).
10
10
Network forest plot comparing four vasopressor regimens with a beta‐agonist component vs norepinephrine (reference) from 6 studies with 6 pair‐wise comparisons. Heterogeneity/inconsistency: tau2 < 0.0001; I2 statistic = 0%. Test of heterogeneity/inconsistency: Q = 0.42(d.f. 3), P value = 0.94; 'nor_' denotes norepinephrine added to the other drugs as described. RR denotes risk ratio, as calculated by a fixed‐effect model. RR > 1 indicates increased mortality risk; RR < 1 indicates reduced mortality risk vs norepinephrine (reference).
11
11
Subgroup analysis in patients with septic shock: network forest plot comparing 7 vasopressor regimens vs norepinephrine (reference) from 18 studies with 20 pair‐wise comparisons. Heterogeneity/inconsistency: tau2 < 0.0001; I2 statistic = 0%. Test of heterogeneity/inconsistency: Q = 5.21, d.f. = 14, P value = 0.98; 'NPVD' denotes non‐protocol vasoactive drugs with or without placebo. RR denotes risk ratio, as calculated by a fixed‐effect model. RR > 1 indicates increased mortality risk; RR < 1 indicates reduced mortality risk vs norepinephrine (reference).
1.1
1.1. Analysis
Comparison 1 Norepinephrine, Outcome 1 Total mortality.
1.2
1.2. Analysis
Comparison 1 Norepinephrine, Outcome 2 LOS ICU.
1.3
1.3. Analysis
Comparison 1 Norepinephrine, Outcome 3 LOS hospital.
1.4
1.4. Analysis
Comparison 1 Norepinephrine, Outcome 4 Arrhythmia.
2.1
2.1. Analysis
Comparison 2 Epinephrine, Outcome 1 Total mortality.
3.1
3.1. Analysis
Comparison 3 Vasopressin, Outcome 1 Total mortality.
3.2
3.2. Analysis
Comparison 3 Vasopressin, Outcome 2 LOS ICU.
4.1
4.1. Analysis
Comparison 4 Terlipressin, Outcome 1 Total mortality.
4.2
4.2. Analysis
Comparison 4 Terlipressin, Outcome 2 LOS ICU.
4.3
4.3. Analysis
Comparison 4 Terlipressin, Outcome 3 LOS hospital.
4.4
4.4. Analysis
Comparison 4 Terlipressin, Outcome 4 Duration mechanical ventilation.
4.5
4.5. Analysis
Comparison 4 Terlipressin, Outcome 5 Pressor‐free days.
4.6
4.6. Analysis
Comparison 4 Terlipressin, Outcome 6 Serious adverse events.
5.1
5.1. Analysis
Comparison 5 Dopamine, Outcome 1 Total mortality.
5.2
5.2. Analysis
Comparison 5 Dopamine, Outcome 2 LOS ICU.
5.3
5.3. Analysis
Comparison 5 Dopamine, Outcome 3 LOS hospital.
5.4
5.4. Analysis
Comparison 5 Dopamine, Outcome 4 Pressor‐free days.
5.5
5.5. Analysis
Comparison 5 Dopamine, Outcome 5 Arrhythmia.
6.1
6.1. Analysis
Comparison 6 Sensitivity analysis norepinephrine, Outcome 1 Mortality.
7.1
7.1. Analysis
Comparison 7 Sensitivity analysis epinephrine, Outcome 1 Mortality.
8.1
8.1. Analysis
Comparison 8 Sensitivity analysis vasopressin, Outcome 1 Mortality.
9.1
9.1. Analysis
Comparison 9 Sensitivity analysis terlipressin, Outcome 1 Mortality.
10.1
10.1. Analysis
Comparison 10 Sensitivity analysis dopamine, Outcome 1 Mortality.
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