Dobutamine / medium-dose Epi tracing

[Evil_Abed]

---

Members don't see this ad.

Quick question regarding the cardiovascular tracing for dobutamine/medium-dose epinephrine. According to the Kaplan stuff, there's no increase in MAP with these drugs, so the MAP tracing stays flat, with the only things changing being the heart rate and pulse pressure (B1 effect). Their reasoning is that the a1 and B2 effects on SVR and MAP cancel each other out, so you're left with B1 effects predominating.

However, wouldn't the B1 effect of increased HR, increased SV, and thus, increased cardiac output cause an increase in MAP? My reasoning is that MAP = (CO x SVR) - CVP and since dobutamine/medium-dose epinephrine increases cardiac output, there should be an increase in MAP.

Is that reasoning correct or am I missing something here? Thanks in advance.

 

[evilbooyaa]

While I don't remember every little bit about this topic, would it not be reasonable to say that the drop in SVR offsets the increase in CO?

Here is something I pulled from google:

"The overall cardiovascular response to low-to-moderate circulating concentrations of epinephrine is increased cardiac output and a redistribution of the cardiac output to muscular and hepatic circulations with only a small change in mean arterial pressure. Although cardiac output is increased, arterial pressure does not change much because the systemic vascular resistance falls due to β2-adrenoceptor activation. At high plasma concentrations, epinephrine increases arterial pressure because of binding to α-adrenoceptors on blood vessels, which offsets the β2-adrenoceptor mediated vasodilation."

Source: http://www.cvphysiology.com/Blood Pressure/BP018.htm

 

[Evil_Abed]

Yea, I understand that part. From what I understand, at medium doses, epinephrine has B1, B2, and a1 effects --> the a1 and B2 effects on SVR and MAP cancel out, leaving the B1 effects to be predominant. So, the tracing looks just like the tracing for dobutamine (which is more activity on B1 than B2 receptors). So, there shouldn't be much B2-mediated vasodilation to offset the B1-mediated increase in CO. At least, that's how I'm thinking about it.

 

[aldolase]

I am also confused on this. I was thinking a1 and b2 cancel out each other and b1 effect alone would increase HR, CO and thus MAP. Also, in kaplan it was mentioned that reflex bradycardia would only lower HR but not MAP. Now, I know that the point of reflex is to lower the BP not just the heart rate.

 

[tantacles]

I am also confused on this. I was thinking a1 and b2 cancel out each other and b1 effect alone would increase HR, CO and thus MAP. Also, in kaplan it was mentioned that reflex bradycardia would only lower HR but not MAP. Now, I know that the point of reflex is to lower the BP not just the heart rate.

Typically, they don't cancel each other out. At low concentrations, the Beta effects predominate. At higher concentrations, the alpha effects predominate.

Thus, my understanding is that at low concentrations, you'll see vasodilation in the systemic arteries as well as a modest increase in heart rate (both reflex from the dilation and direct agonism of epi on B1 receptors).

At high doses, you'll see vasoconstriction from the A1 action (these receptors are "harder" to activate and require a higher dose of epinephrine), but you don't see reflex bradycardia because the B1 receptors are still stimulated heavily by the epinephrine. You should see an increase in MAP here.

Our classes never dealt with medium doses; only low and high.

With regard to tracings as compared to dobutamine, I have no idea.

 

[yehhhboiii]

Typically, they don't cancel each other out. At low concentrations, the Beta effects predominate. At higher concentrations, the alpha effects predominate.

Thus, my understanding is that at low concentrations, you'll see vasodilation in the systemic arteries as well as a modest increase in heart rate (both reflex from the dilation and direct agonism of epi on B1 receptors).

At high doses, you'll see vasoconstriction from the A1 action (these receptors are "harder" to activate and require a higher dose of epinephrine), but you don't see reflex bradycardia because the B1 receptors are still stimulated heavily by the epinephrine. You should see an increase in MAP here.

Our classes never dealt with medium doses; only low and high.

With regard to tracings as compared to dobutamine, I have no idea.

the concentration effect is due to the fact that epi has greater affinity for beta receptors but there are more alpha receptors overall so once you're basically using up all the beta receptors, you start seeing more alpha effect

 

[Instatewaiter]

With regard to tracings as compared to dobutamine, I have no idea.

If anything dobutamine lowers MAP.

It has B1 activity and B2 activity and thus is an inodilator. It causes essentially the equivalent amount of decrease in SVR as an increase in cardiac output. So, MAP is usually unchanged occasionally you see a good deal of hypotension.

 

[tantacles]

the concentration effect is due to the fact that epi has greater affinity for beta receptors but there are more alpha receptors overall so once you're basically using up all the beta receptors, you start seeing more alpha effect

Agreed 100%. I often remember things in more simplistic terms, and it's nice to see the real thing written out.