Septic shock is an advanced stage of body’s response to an infection and manifests as marked decrease in blood pressure with resulting decrease blood flow (and hence nutrients and oxygen) to the tissues. The decreased blood pressure is due to vasodilatation and increased capillary permeability (leaky capillaries).
The treatment of septic shock includes antibiotics to treat the infection, intravenous fluids to replenish fluid that has seeped out into the tissues from leaky capillaries, and vasopressors (such as norepinephrine) to counter vasodilation. Not uncommonly, norepinephrine is not sufficient to raise blood pressure and increase blood flow to the tissues. Vasopressin, another vasopressor, is sometimes used in addition to norepinephrine to support blood pressure. However, vasopressin has other adverse effects. These adverse effects are due to the fact that vasopressin stimulates three types of vasopressin receptors (V1a, V1b, and V2). Stimulation of V1a has vasopressor effect while stimulation of V1b and V2 results in increased coagulation activity, nitric oxide release, corticosteroid secretion, and excessive water retention.
Selepressin is a selective V1a receptor agonist and has only vasopressor effect. One would assume that selective stimulation of V1a receptors with selepressin will result in beneficial outcome. However, in a clinical trial (N=868), selepressin was not found to be effective in reducing ventilator-free days, norepinephrine-free days, mortality, lower ICU days, or lower need for kidney replacement therapy.
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