Dobutamine drip how to#

How to titrate: typically, against blood pressure.Variceal gastrointestinal hemorrhage (theoretically an attractive agent, but pragmatically it's impossible to titrate adequately).Central diabetes insipidus (only very low doses are needed, e.g.Front-line agent for hepatorenal syndrome (HRS) in countries lacking terlipressin (such as the United States).Typically given in low doses (0-0.06 U/min), either as primary or secondary agent. Vasodilatory shock (particularly sepsis).Its dominant effect on cardiac output is often to cause a reduction (but this may depend on the heart's ability to tolerate increased afterload).It does cause venoconstriction, which may increase preload.It increases systemic vascular resistance (SVR).Mechanism: Stimulates V1 and V2 receptors, causing vasoconstriction and renal water retention.If you don't have it, epinephrine can usually be used as an alternative agent. Its main drawback is pricing & availability: in the United States the price is astronomical and some hospitals don't have it.It doesn't cause vasoconstriction, so it's safe to give peripherally.Isoproterenol is probably the most powerful chronotrope.How to titrate: typically, against heart rate.Clinical use: Bradycardia (will work in some patients who are refractory to epinephrine).Physiologic effect: Very powerful chronotrope, with positive inotropic effects as well.This may be a problem, but it can also help wean the patient off dobutamine once the infusion has been running for a long time (it may be easier to wean off than would be expected). Prolonged infusion of dobutamine may cause desensitization of beta-receptors and reduced efficacy.Dobutamine is easier to titrate due to its short half-life, so it is often a preferred agent if the patient's response to inotropy isn't entirely predictable.However, milrinone is renally eliminated, which can make it difficult to titrate in patients with renal failure. Milrinone causes a bit more vasodilation, so it might be better for cardiogenic shock.

They shouldn't be titrated against blood pressure, because they have no predictable effect on blood pressure.

Ideally, the inodilators should be titrated against cardiac output or a surrogate of cardiac output (e.g.

However, epinephrine could be a superior choice in that situation, if blood pressure is tenuous.

(2) Septic shock with inadequate cardiac output (as an add-on agent).

Care is required for patients with hypotension, since there is a risk of exacerbating hypotension. Overall, the effect on blood pressure is unpredictable. However, if the heart is already working as hard as it can, then the vasodilator effect may be dominant, causing a drop in blood pressure. If the heart responds strongly (with increased stroke volume and heart rate), it is possible for these drugs to increase blood pressure.

Effect on blood pressure is variable, depending on how responsive the heart is to inotropy.

Cardiac output is increased due to both inotropic effect and vasodilation.

Secondary effect is peripheral vasodilation.

Primary effect is positive inotropy, with positive chronotropy as well.

Milrinone inhibits intracellular adenylyl cyclase, thereby increasing intracellular cyclic AMP levels.

Dobutamine stimulates mostly beta-receptors, with very little stimulation of alpha-receptors.

Inopressors (norepinephrine, epinephrine, dopamine)Ĭlassic inodilators (milrinone, dobutamine).

Inodilators (milrinone, dobutamine, isoproterenol).

Dobutamine drip