Cardiovascular failure in sepsis involves a combination of hypovolemia, decreased vascular tone, myocardial
depression and microcirculatory alterations. Fluids represent the first line therapeutic intervention, with controversy regarding
the type of fluid. Recent data indicate that albumin is safe and might even be beneficial in specific subgroups.
Starches may be an alternative, although concerns exist on potential detrimental effects on renal function of old generation
starches. Trials testing new generation starches are ongoing. When fluids fail to correct hypotension, vasopressor agents
are used. Various adrenergic agents increase blood pressure, especially dopamine, noradrenaline and adrenaline, by stimulating
alpha-adrenergic receptors. They also variably stimulate beta-adrenergic receptors, increasing cardiac contractility,
heart rate, and splanchnic perfusion, but with increased risk of arrhythmias, immunomodulation and increased metabolism.
Furthermore, dopamine stimulates dopaminergic receptors, resulting in doubtful effects on splanchnic and renal perfusion,
but also in endocrine alterations. Do these pharmacologic differences among the various alpha-adrenergic agents
translate into clinical differences? Several randomized trials tested the effects of these agents on outcome. Epinephrine
produces more undesired effects than norepinephrine, but no clear cut differences on outcome were observed in underpowered
trials. Norepinephrine should be preferred over dopamine, as suggested in one large trial and confirmed in a
meta-analysis. Vasopressin may be considered as an alternative or in addition to adrenergic agents. In one large trial, no
significant difference in outcome was observed, and the exact role of vasopressin still needs clarification. Finally, various
inotropic agents can counteract septic myocardial depression. So far, no study supports their routine use, but these may be
justified on an individual basis.