dobutamine and isoprotenerol: arterial systolic P

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DrPettans

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B1 receptor activation increases Heart Rate and Contractility, which increases Cardiac output. It also increases systolic arterial pressure (how is this systolic pressure increased?).

B2 receptor activation causes vasodilation, which decreases systemic vascular resistance, which decreases Arterial dyastolic pressure. (any effect on systolic arterial pressure?)

Dobutamine acts on B1 receptors > B2 receptors. (bigger effect on B1).
So, it increases HR, contractility and systolic arterial pressure (again, how?), and has a mild vasodilatory effect which may decrease arterial dyastolic pressure: pulse pressure is increased.

Isoprotenerol acts on B1 receptors = B2 receptors. (same intensity of effect on both).
So, it increases HR, contractility, and keeps arterial systolic pressure relatively unchanged (same thing: why?). It also has vasodilatory effects that decrease systemic vascular resistance and this decreases dyastolic arterial pressure and decreases mean arterial pressure. Pulse pressure is also increased.

Hope you can help guys, thank you!
 
Systolic blood pressure is a function of Stroke volume (HR x SV = CO), that's simple physiology. Anything that increases these two (eg B1 stimulation or Dobutamine) will increase CO hence increasing systolic bp.
This is just like diastolic bp is a function or TPR/SVR. If you decrease TPR/SVR (B2 activation), diastolic bp decreases.

Not sure about your point regarding isoproterenol. Would like to know the answer to it myself.

If you look at the graph given in first aid about isoproterenol, it does show an initial little bit of increase in systolic bp (that goes with the physiology I mentioned above). But then there's definitely something else coming into play that's maintaining the systolic bp, rather bringing it a little down. I can't figure out what that thing is. If someone can please.
 
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When your contractility increases your stroke volume increases. This means that the volume ejected into your aorta increases. With a realtively stable compliance of the aorta, this means your systolic pressure will increase.

In my experience, Dobutamine tends to be pressure neutral because of the vasodilatory effects and in many cases will cause a rapid drop in bp.
 
Thank you both, i see contractility is responsible for systolic pressure :increased stroke volume means increased pressure against aorta (thank you for that), and CO= SVxHR.

Still don't get why isoproterenol keeps a relatively constant systolic blood pressure. I was thinking about it and this is the only explanation I can find, but I might be wrong:

Maybe as isoproterenol produces vasodilation due to its beta 2 effect, this vasodilation decreases venous return, and this means less stroke volume, hence less systolic pressure, counteracting the beta 1 effect.

what do you think?
 
Not sure about that, because MAP is decreased. If you have FA just go to the graphic where it explains it in the pharma section. The graphic is somewhat like the one I post here, where Isoproterenol is represented by drug "X" on the left. There's also another line between those two in FA that is paralell to the lower one, meaning MAP is decreased as well as dyastolic P.
 

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B1 increases SP. B2 decreases DP.
How? B1 excites the muscles to pump more and harder; it most likely a intracellular or Ca++ mechanism.
B2 opens vasculature.
Combine the two effects: we get actions = heart pump more + peripheral vasculature open.
 
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