Question from a student - DOBUTAMINE

Dobutamine is well known for it's B1 effects on the heart; however, it can also act on B2 and Alpha 1 receptors. We commonly see decreased PVR with patients on dobutamine. In some cases precipitous drops in blood pressure occur. Dobutamine is a medication that fills a few specific roles and can have disastrous side effects if used improperly.

I don't know why this would happen. It must be pretty rare, because a drop in blood pressure isn't even listed as a possible side effect in any of my drug guides, but perhaps this might help you.

http://www.theannals.com/cgi/content/abstract/33/12/1266

Is it possible that with the increased contractility and therefore increased cardiac output that the body doesn't have to compensate as much, dropping the PVR?

It's easiest to understand dobutamine when you compare it to dopamine.

Dobutamine is a beta1 and beta2 agonist. So along with the positive inotropy/chronotropy/dromotropy that you get with the beta 1, you also stimulate beta2 receptors which cause vasodilation (hence the decreased SVR) This is a great property for patients who need a decrease in their afterload (CHF), but can be problematic if they are hypovolemic. Dobutamine, on the other hand, has alpha properties as well. So you will see vasoconstriction and an increase in SVR. Good luck. Hope that helps :wink2:

Dobutamine, on the other hand, has alpha properties as well. So you will see vasoconstriction and an increase in SVR. Good luck. Hope that helps

I am pretty sure you meant DOPAMINE, it has alpha 1 agonism at higher doses.

Another consideration is an anaphylactoid reaction to the components of dobutamine. There are case reports of these kinds reactions to the components of dobutamine. Sulfites if I remember correctly.

I've never heard of dobutamine dropping blood pressure (?). I usually choose it over milrinone for this reason. If your BP is sufficient or high, milrinone is great, though slower to react to titration.

Can anyone help me in the terminology of PVR vs. SVR? I assume the people mentioning PVR meant "peripheral vascular resistance," yes? PVR as I have studied it and have referred to it is actually "pulmonary vascular resistance," which dobutamine can affect, but has a marginal role in BP, CO, or SVR. SVR is systemic vascular resistance (= 80*(MAP - CVP)/CO). Dobutamine--in my experience--usually decreases SVR by increasing CO, not decreasing BP. Maybe it's just my population--open hearts in ICU. I'd love to hear more CRNAs respond with experience in the OR.

I've had some pts react to dobutamine with profound HYPERtension (usually also with tachycardia), but only rarely. I've usually only seen significant effects on BP and HR when dosing greater than 10 mcg/kg/min.

Thanks for a conversation on something other than anesthesia school!

I know this is the CRNA forum but I wanted to make sure I got a sound answer on my question. Why can there be a drop in BP with dobutamine gtts? I know that it increases cardiac output, but [i']physiologically[/i], what causes a BP drop?

Dobutamine has mainly B1 agonist and inotropic effects. It also has minor alpha(vasoconstriction) and B2(vasodilation) effects.

Usually you will see no BP difference b/c the increased cardiac output will offset the effects of the vasodilation by B2 stimulation.

Everyone act differently w/ this drug.

Sometimes the increased cardiac output w/ the alpha effect has more effect than the vasodilation, thus u will see an increased BP. The greater the dosage, the more alpha effect you will see even though this effect may be minor compared to dopamine.

Then sometimes the vasodilation is more profound than the increased cardiac output, in which u will see decreased blood pressure.

So which way will the pt go? Mostly depends on comorbidity. And in some is just a coin flip.

In general Dobutamine can cause tachyarrythmias. In many patients it can trigger afib c RVR. That said, rapid heart rate = decreased filling time = decreased stroke volume and decreased bp and output.

I hope this helps.

Pretty much the right info is given here. Dobutamine has historically been considered a strong B1-selective agonist. Now however, that opinion has changed slightly. (Goodman and Gilman's The Pharmacological Basis of Therepeutics is cited for a good bit of this info.) Dobutamine is a racemic mixture, which means that there is a mixture of (+) and (-) stereoisomers, or two mirror image molecules in mixture. The (-) isomer is a potent A1 agonist, and can cause quite a large increase in SVR via A1-mediated vasoconstriction. The (+) isomer, however is a strong A1 antagonist, and counteracts the effects of the (-) isomer. Both isomers are strong B receptor agonists, slightly preferential to B1.. The activity of the (+) isomer is about 1000% more potent at the B receptor than the (-) isomer is at the A1 receptor. So, the balance of A1 vs B stimulation is off, in favor of B stimulation.

Although B1 is preferred by dobutamine, the stimulation of B2 receptors does exist. B2 agonism will cause vasodilation at the skeletal muscle, forcing blood to engorge muscle in preparation for increased activity expected with increased sympathetic response. This pooling of blood will decrease the preload slightly, and in some patients will be enough to notice a change in the SVR/ABP. The A1 stimulation in some patients is not enough to counteract this decrease in preload. There will also be a reflex withdrawal of intrinsic sympathetic tone when cardiac output is increased. The result of these items will cause the ABP and SVR to drop, profoundly in some patients, with use of dobutamine.

Further, dobutamine is preferential in increasing inotropy, or contractility, over chronotropy, or heart rate. This is thought to be the effect of stimulation of the A1 receptors in the cardiac muscle. At equal inotropic dosages of dobutamine and isoproterenol (a B agonist useful at increasing heart rate), dobutamine produces less of a rate increase than isoproterenol at the sinoatrial node. The increase in atrioventricular and intraventricular conduction is the same. So, if you are looking for rate increase, isoproterenol is a better choice.

Dobutamine does not stimulate the dopaminergic receptors, and will not increase renal blood flow any more than proportional increases associated with increases in cardiac output. Tolerance to dobutamine will result from the downregulation of B receptors, causing the clinician to increase infusion rates. As a result, the earliest signs of dobutamine toxicity are seen - tachycardia and arrhythmias. In this case, it would be prudent to change to a phosophodiesterase III inhibitor, such as milrinone.

Milrinone should not be confused with dobutamine. They are different in chemical structure, action, or effect. Milrinone causes the inhibition of phosphodiesterase III, which is an enzyme that breaks down cyclic adenosine monophosphase, or cAMP. cAMP causes an increase in myocardial contractile force, as well as arterial and veno-dilation. The combined effect of these three actions improves cardiac output via an increase in SV and a decrease in SVR. The increased inotropic effects are greater than those seen with dobutamine and the decrease in SVR is greater than seen with nitroprusside. Milrinone is a better drug choice, in my opinion, for the patient with severe heart failure than dobutamine.

This turned out to be a very in depth response to a simple question, and I apologize for that.

Maybe I don't understand your question, but there can be a lot of reasons for a BP drop. I assume you are talking about ICU and not a surgical situation.

In surgery, you need to be aware of blood loss, inadequate fluid replacement, position changes, vagal nerve stimulation, depth of anesthesia and many other reasons. In anesthesia we identify the cause and treat it appropriately. Giving medications is usually the last thing I do, but I know you are in a different setting.

I think the OP is asking about the physiological mechanisms of precipitous blood pressure drops due to dobutamine.