phenylephrine and inc. systolic pressure FA wrong?

[neurotrancer]

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Hi, I'm sure this is going to show up b/c central pharm is emphasized.

In my First Aid (2004 p. 306, 2006 p. 204), they are showing the effects of phenylephrine on systolic and diastolic pressure.

If you have alpha 1 agonism, that would increase peripheral vascular resistance and hence increase the diastolic pressure curve. However, this would also cause the baroreceptor reflex in a normotensive pt. and you get reflex bradycardia. So why does the systolic pressure increase in this set of curves (bottom left corner graph on the page) with no narrowing of the pulse pressure (i.e. dec. systolic curve, inc. diastolic curve)?

Is it because the alpha 1 agonism is so strong that the baroreceptor reflex does not overcome the increase diastolic and hence the heart will then increase its contractility in order to overcome a greater afterload?

Thanks!

 

[chintu]

good point....I don't know that I have an exact accurate answer to your question but I would propose my thoughts. Systolic BP is related to SV of heart which is indirectly proportional to afterload. I think as you said phenylephrine alpha effect is really strong that it increases afterload and so heart would pump harder to push blood against this increased afterload. I am sure the baroreceptor reflex would be de-activated (increased BP) but it would not cause bradycardia strong enough to overcome this increased afterload. And of course the diastolic pressure goes up simply due to increased TPR like u said and hence the mean BP goes up. Also, if you think about the reverse of this prazosin (an alpha antag) should activate baroreceptor reflex intheory causing reflex tachycardia but then its a good drug agains hypertension so i m sure the tachycardia is masked significantly by its peripheral effects on alpha receptors.

 

[neurotrancer]

I looked this up everywhere, referring to the phys textbook on the baroR reflex, the pharmacology textbook, Pharm for Boards and Wards, and my Kaplan Lecture books, 2 of my friends who M3, and the internet. Tough q I think.

In response to Chintu...we are supposing that the baroR reflex does not overcome the phenylephrine induced increased afterload...but the predominant tone on the heart at rest is SANS. Well...if you inc. afterload, what is the intrinsic reflex, specifically, that the heart is undergoing to match it and which is overcoming a relatively weak baroR reflex? It makes sense I suppose that the heart will match the increased afterload...I assume this is what happens with chronic HTN and the heart undergoes hypertrophy and eventual failure, but these curves are depicting an immediate matching by some mechanism intrinsic to the heart.

Seems like a detailed q but not really...there's something I must be missing here and I'm worried that I might be having some gross misconception about something relatively fundamental.

 

[Idiopathic]

Yes reflex bradycardia can occur, and rise is CO is usually minimal. The main use here is to raise the SBD/DBP to improve coronary/renal perfusion and overall mean pressure.

Not a good drug to raise pressure in someone who is hypovolemic and I believe still frowned upon in pregnancy (i.e. hypotension during delivery) but I could be wrong about that.