Table 2.
Characteristic of included studies
Study | Study design | N | Patient population | Vasopressors | Dose | Outcomes | Side effects |
---|---|---|---|---|---|---|---|
Septic shock | |||||||
Memis 2002 [27] | Prospective, randomized, double-blind, placebo-controlled study | 30 | Severe sepsis | 0.5 mg/kg/h over 6 h | MAP was significantly increased from baseline immediately after infusion, no difference at 24 h; mortality rate was similar in both groups | Blue coloration of urine, increased methemoglobin concentration | |
Kirov 2001 [28] | Prospective, open-label, randomized, placebo-controlled | 20 | Severe sepsis and/or septic shock | NE > 0.05 μg/kg/min and EPI > 0.05 μg/kg/min to maintain MAP 70–90 mmHg | 2 mg/kg follow by a stepwise infusion until 0.5 mg/kg/h for 6 h | MAP increased significantly immediately after infusion; requirement of vasopressors reduced significantly; no difference in in-hospital mortality rate | Resolving blue coloration of urine and skin |
Weingartner 1999 [29] | Prospective, open-label, non-randomized | 10 | Severe septic shock | NE 0.7 μg/kg/min | 4 mg/kg for 4 h | Significant increase of MAP and SVRI | PaO2/FiO2 ratio significantly decreased at 40 min, remained lower during the infusion period |
Donati 2002 [30] | Prospective, open-label, non-randomized | Unresponsive septic shock | NE and/or DOPA (1.5–3 μg/kg/min) | Immediate increase of MAP and SVRI | Slight increase in plasma osmolarity | ||
Brown 1996 [31] | Case report | 1 | Septic shock | DOPA 10 μg/kg/min and NE 15 μg/min | 100 mg bolus followed by 17 mg/h for 44 h | Increase of MAP reduced vasopressor, alive | Resolving blue coloration of urine and skin |
Park 2005 [32] | Prospective, open-label, non-randomized | 20 | Refractory septic shock | DOPA > 20 μg/kg/min | 1 mg/kg in 15 min | Significant increase of MAP and SVRI till 2 h; 65% mortality | |
Andresen 1998 [33] | Prospective, open-label, non-randomized | 10 | Severe septic shock | NE > 0.2 μg/kg/min, EPI > 0.1 μg/kg/min | 1 mg/kg for 15 min | Significant increase of MAP and SVRI | |
Gachot 1995 [34] | Prospective, open-label, non-randomized | 6 | Severe septic shock | NE 4 μg/kg/h and/or EPI 2 μg/kg/h | 3 mg/kg in 10 min | Significant increase of MAP and SVRI; all but one died | PaO2/FiO2 ratio significantly decreased |
Dumbarton 2011 [35] | Case report | 1 | Septic shock | NE 1 μg/g/kg/min, VASO 0.04 U/min, EPI 1 μg/kg/min to maintain MAP > 65 mmHg | 100 mg bolus and continuous infusion at 0.5 mg/kg/h till 120 h | Increase in blood pressure, allowing for a decrease in NE and EPI; alive | Blue/green discoloration of the skin and mucosa, particularly noticeable in his extremities |
Other types of shock | |||||||
Porizka 2020 [40] | Retrospective study | 20 | Refractory distributive shock: 9 patients (45%) responded positively to MB administration and 11 patients (55%) were non-responders | NE > 0.5 μg/kg/min and CI > 2.4 L/min/m2 | 1.3 ± 0.5 vs. 1.3 ± 0.4 mg/kg respectively | Lower NE requirements in 12 post infusion, lower mortality, and lower hypoxic state in responders | |
Manjii 2017 [41] | Case report | 1 | Undifferentiated shock | NE 0.9 μg/kg/min and 0.04 unit/min of VASO to maintain MAP > 60 mmHg | 2 mg/kg for a total dose of 190 mg once | NE was halved in 2 h, vasopressors weaned in 15 h; alive | |
Oliveira Neto 2003 [42] | Case report | 3 | Anaphylactic shock induced by radiocontrast injection during coronary angiography | Refractory hypotension despite DOPA | 1.5–2 mg/kg | Increase of MAP, all alive | Transient nodal cardiac rhythm, chest pain |
Fisher 2014 [43] | Case report | 1 | Refractory distributive shock following a mixed drug poisoning (carbamazepine, quetiapine, fluoxetine, valproate, oxazepam) | NE 100 μg/min, VASO 0.06 units/min, metaraminol 133 μg/min DOPA 5 μg/kg/min | 1.5 mg/kg and continuous infusion (1.5 mg/kg/h for 12 h, then 0.75 mg/kg/h for 12 h) |
Improvement in hemodynamic parameters and weaning of vasopressors in the following hours; alive |
|
Graham 2015 [44] | Case report | 1 | Vasodilatory shock following overdose of metformin and gliclazide | NE 1.7 mg/kg/min and VASO at 0.06 units/min to maintain MAP of 50–55 mmHg | 2 mg/kg followed by an infusion at 0.25 mg/kg/h for approximately 20 h | Over the following 24 h, the vasopressors were slowly weaned; alive | Blue discoloration of urine |
Aggarwal 2013 [45] | Case report | 1 | Vasodilatory shock following calcium channel blocker and a β-blocker overdose | NE 1 μg/kg/min and DOPA 20 μg/kg/min VASO 0.8 U/min | 1 mg/kg over a 10 min period and then for 10 h | MAP stabilization in 8 h, vasopressor de-escalation; alive | Transient bluish discoloration of the urine, tears, saliva, and skin |
Laes 2015 [46] | Case report | 1 | Vasodilatory shock following ingestion of atenolol, amlodipine, and valsartan | NE 0.1 μg/kg/min, EPI titrated to 0.1 μg/kg/min, and VASO 0.04 units/min to maintain MAP 60 mmHg | 2 mg/kg IV over 30 min and after infusion of 0.75 mg/kg/h | SVRI increased and MAP unchanged; vasopressor requirements decreased within 2 h; alive | None |
N number of patients, MAP mean arterial pressure, NE norepinephrine, DOPA dopamine, VASO vasopressin, SVRI systemic vascular resistance index, EPI epinephrine, CI cardiac index, PaO2 oxygen arterial pressure, FiO2 fraction of inspired oxygen