b-blockers and afterload -- mechanism?

[Malpractice]

how do beta-blockers decrease afterload?

---

Members don't see this ad.

 

[winkleweizen]

how do beta-blockers decrease afterload?

by decreasing renin and causing vasodilatation

 

[kstreet]

by decreasing renin and causing vasodilatation

Decreasing renin is thru Beta 1 (probably the most important aspect in treating CHF/post MI heart)

Vasodilation would be if you had a Beta 2 agonist.

Beta Blockers also decrease the oxygen requirements of the heart by decreasing contractility, because both Beta 1 and Beta 2 increase contractility.

Edit: Just to add another point

Decades ago, docs never considered using Beta blockers as a way to treat CHF or a heart at risk because it just didn't make sense. Why would you want to decrease contractility in a failing heart? Hence, why digoxin was such a popular option b/c that would make the heart pump stronger.

What docs realized more recently is that if you make life easier on the heart, by decreasing afterload and decreasing contractility (and decrease oxygen req of the heart), you improve the outcome for the patient. The best way to decrease afterload is to get rid of fluid, therefore we want to decrease renin. The best way to decrease contractility is to stop sympathetic outflow to the heart. Beta Blockers do both of these.

 

[winkleweizen]

Wait wouldnt decreasing renin lead to a decrease in vasoconstriction or (vasodilation)

 

[hyrule]

Wait wouldnt decreasing renin lead to a decrease in vasoconstriction or (vasodilation)

yup
beta agonist = constriction
blocker = dilation and decreased afterload

 

[kstreet]

Wait wouldnt decreasing renin lead to a decrease in vasoconstriction or (vasodilation)

Hm, I think it would lead to a decrease in aldosterone activity and a decrease in fluid/sodium reuptake.

 

[kstreet]

yup
beta agonist = constriction
blocker = dilation and decreased afterload

Not certain about that. Beta blockers are contraindicated in people with vasospastic disorders because they cause vasoconstriction due to decreased Beta 2 activity. Or am I totally off?

 

[winkleweizen]

Hm, I think it would lead to a decrease in aldosterone activity and a decrease in fluid/sodium reuptake.

Yeah i think its a double whammy...decrease in Aldo and a decrease in ATII which is a vasoconstrictor.

So i guess lower Aldosterone and subsequent atii inhibition would decrease afterload.


FA page 281 says b blockers affect afterload and end up with a higher EDV(which i guess would be an increased preload)

 

[kstreet]

Yeah i think its a double whammy...decrease in Aldo and a decrease in ATII which is a vasoconstrictor.

So i guess lower Aldosterone and subsequent atii inhibition would decrease afterload.


FA page 281 says b blockers affect afterload and end up with a higher EDV(which i guess would be an increased preload)

Ah Ang 2, totally on spot with that. The higher EDV is because of the decrease in contractility which would allow for more filling time.

 

[Zoom-Zoom]

Ah Ang 2, totally on spot with that. The higher EDV is because of the decrease in contractility which would allow for more filling time.

Sorta.. beta blockers increase the PQ interval (lengthen diastole, slow AV conduction, etc.) and that allows for more filling time. This will increase preload and keep ejection relatively constant via the starling law while slowing HR.

Afterload is a nonprecise term and I wouldn't dwell on this specific example for Step 1. True, B-Blockers will prevent any constriction due to ATII, but ATII's main physiologic role as a constrictor is normally only relevant to the kidneys. So the main effect on afterload is via renin/volume, but this is a slow effect and wouldn't be significant acutely.

 

[Cardiol]

It is my hypothesis that beta blockers are favourable in heart failure because they reduce afterload by slowing the rate of LV ejection, i.e. slower acceleration of contraction and flow. The aortic and arterial wall consists of viscoelastic material, with less resistance to slow than to rapid stretching. Slower stretching corresponds to a functional increase in arterial compliance. In other words, more blood/stroke volume can be ejected with less work when the rate of ejection is slow. More details can be found in:Soma et al, J Am Soc Echocardiogr 2000;13(12):1000-8

 

[velamj]

B1 receptors stimulate renin release. blocking beta 1 therefore decreases renin which subsequently decreases blood volume (decreased afterload). wild guess but r u asking this bc of Uworld 1944?