Table 1 Options for the treatment of vasoplegia
Agent | MOA | Dose |
|---|---|---|
Norepinephrine | Significant α1, α2 agonism Moderate β1 agonism | 0.01–3 μg/kg/min |
Epinephrine | Significant α1, α2 agonism Significant β1 agonism | 0.01–1 μg/kg/min |
Phenylephrine | Significant α1, α2 agonism No effect on β1 | 0.1–5 μg/kg/min |
Dopamine | Dose dependent adrenergic agonism α1 agonism as dose increases | 1–20 μg/kg/min |
Vasopressin | Repletion of vasopressin in ADH depleted state V1 agonism | 0.01–0.1 U/min |
Vitamin C Thiamine Hydrocortisone | Cofactor for catecholamine synthesis Cofactor of lactate dehydrogenase (increase in lactate clearance) Aids in vitamin C metabolism Repletion of glucocorticoid and mineralocorticoid activity in cortisol depleted state Inhibition of pro-inflammatory cytokines | 1.5 g every 6 h 100 mg every 6 h 50 mg every 6 h |
Methylene blue | Inhibition of guanylyl cyclase and inducible endothelial NO synthase | 1–2 mg/kg |
Hydroxocobalamin | Inhibition of NO directly and inducible endothelial NO synthase Inhibition of hydrogen sulfide | 5 g |
Angiotensin II | AT1 agonism Stimulation of aldosterone release Increase in ADH synthesis | 10–40 ng/kg/min |