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Kaplan Qbank USMLE



Author4 Posts
  #1

Hey Guys...Can you explain the following concept a bit more..

Alpha-1 stimulation-->Arteriolar constriction-->Increase BP-->Increased firing of carotid sinus--->Increased vagal stimulation--?Decreased HR-->Decreased contractility

Alpha-i stimulation-->Venous constriction(increased sympathetic tone)-->Increased venous return-->Increased preload

What will happen to Cardiac output if we give an Alpha-1 agonist???I think I am missing something..Please explain



  #2

when you stimulate carotid sinus impulses to Sympathetics decrease and inpulses to Parasympathetics increase
now, if we decrease Sympathetics-->decrease contractility, decrease heart rate, conduction velocity through SA and AV nodes, because beta1 are the ones that responsible for this, also alfa 1 will not be stimulated as much
at the same time, Parasympathetics increase and vaga INHIBITING stimulation to SA and AV nodes --> decrease heart rate
so...having all above at the end we get reflecive bradicardia with decreased contractility

as for veins.
remember, that veins are BLOOD STORAGE in systemic circulation, so if we constrict veins we "squize out" some extra blood in addition to what is already in circulation -->increase preload, but it doesn;t mean that HR will be the same, it mos likely to go down to keep CO constant

the whole point of reflexes is to maintain CONSTANT MAP, so if you increase TPR, CO should go down (by decr HR and SV) this way you have same MAP

  #3

Thanks a lot babaydoc...

When there is increased TPR and Increased preload,as occurs in sympathetic stimulation,CO will go down to maintain MAP..

Based on Frank-Starling law,Increased preload wpuld lead to increased cardiac output???




  #4

this is a compensatory response and will lead to dec in sympathetic activity-when sympathetic activity is decreaesd there will be no constriction of veins







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