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Discussion Starter · #1 ·
hi can someone pls highlight me on why is it that we use dopamine for treatment of shock.

dopamine causes renal vasculature smooth muscle relaxation (vasodilation) which increases RBF n GFR n also increase in Na secretion. won't that cause an exacerbation of the shock?

say the ptt has hypovolemic shock, wont increasing renal perfusion cause more loss of fluid. DA also causes dilation of the coronary vessels, so the cardiac muscle is getting good supply of O2, n perhaps with the low TPR, this will allow the heart to increase in rate. this in turn increases blood flow n eventually get the BP to increase stabilizing the ptt. but this will all take a while wont it? so y before any of this, should we administer DA for treatment of shock? or is there a specific type of shock for the administration of DA?:eek:

im so confused!!!!:confused::confused:
 

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hi can someone pls highlight me on why is it that we use dopamine for treatment of shock.

:dopamine causes renal vasculature smooth muscle relaxation (vasodilation) which increases RBF n GFR n also increase in Na secretion. won't that cause an exacerbation of the shock?

say the ptt has hypovolemic shock, wont increasing renal perfusion cause more loss of fluid. DA also causes dilation of the coronary vessels, so the cardiac muscle is getting good supply of O2, n perhaps with the low TPR, this will allow the heart to increase in rate. this in turn increases blood flow n eventually get the BP to increase stabilizing the ptt. but this will all take a while wont it? so y before any of this, should we administer DA for treatment of shock? or is there a specific type of shock for the administration of DA?:eek:

im so confused!!!!:confused::confused:
hi,
the effect of dopamine is dose mediated, as you increase the amount , 1st D1 than BETA1 than ALPHA1,.and the dose given in shock is high so it activate a1 receptor mostly,and as you must be knowing :) which cause vaso constriction, urinary rentention.
hope it help.
:happy
 
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it is a beta -1 agonist for the heart in cardiogenic shock

dopamine is given in cardiogenic shock when the heart is failing... dopamine is a Beta 1 agonist... it acts as positive inotropic and chronotropic agent and thus gives revitality to the failing heart!!! it is given in cardiogenic shock preferably!!! not hypovolemic or neurogenic shock!!!
 

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In fact dobutamine the synthetic analog of dopamine is watz clinically preferred over dopamine for cardiogenic shock...

another fact that i m just mentioning for the sake of revision is that ketamine is the anesthetic of choice in pts going into cardiogenic shock because it is the only cardiostimulator anesthetic, rest are all cardiodepressive!!!
 

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No wonder..............

ketamine is dear a dissociative anaesthesia..............primary site of action is in the CORTEX and SUBCORTICAL AREA...............
heart rate,cardiac output and BP would be elevated due to sympathetic stimulation.....................................
Thats why it is dangerous for hypertensives and in ischaemic heart disease but GOOD for Hypovolemic patient......................:happy::))
 

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hard work always have more weightage than good luck my dear................

GOOD LUCK FAVORS THOSE WHO WILLING TO DO HARD WORK MY DEAR....................................:happy:
 

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Discussion Starter · #8 ·
thank u for all the replies.:)

yes i understand now...i think... although if i may, i wanna correct kabutar11 a little. the dopamine is given to a dose till it affects beta-1 not alpha-1. because alpha-1 will cause reflex bradycardia with increased TPR.

but yes u are ryte, that's how it works, D-1 receptors, then with increasing dose beta-1, then to alpha-1. the only thing is that i was wondering if u start off with a smaller dose, wont it cause loss of fluids from the kidneys? but with all the explanation, this is what i'm taking home:

Dobutamine is given for cardiogenic shock ptts (after an acute MI perhaps), and the dose given will hit the D-1 receptors first to increase coronary supply but soon after, the dobutamine dose aims for beta-1 receptors increasing HR, thus improving TPR.

did i get it right?:eek:
 

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thank u for all the replies.:)

yes i understand now...i think... although if i may, i wanna correct kabutar11 a little. the dopamine is given to a dose till it affects beta-1 not alpha-1. because alpha-1 will cause reflex bradycardia with increased TPR.

but yes u are ryte, that's how it works, D-1 receptors, then with increasing dose beta-1, then to alpha-1. the only thing is that i was wondering if u start off with a smaller dose, wont it cause loss of fluids from the kidneys? but with all the explanation, this is what i'm taking home:

Dobutamine is given for cardiogenic shock ptts (after an acute MI perhaps), and the dose given will hit the D-1 receptors first to increase coronary supply but soon after, the dobutamine dose aims for beta-1 receptors increasing HR, thus improving TPR.

did i get it right?:eek:
I think that sounds exactly right... I love how these kinds of questions and this forum in general help clarify the little doubts in even the big three areas - Cardio, Respiratory and Renal...
 

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thank u for all the replies.:)

yes i understand now...i think... although if i may, i wanna correct kabutar11 a little. the dopamine is given to a dose till it affects beta-1 not alpha-1. because alpha-1 will cause reflex bradycardia with increased TPR.

but yes u are ryte, that's how it works, D-1 receptors, then with increasing dose beta-1, then to alpha-1. the only thing is that i was wondering if u start off with a smaller dose, wont it cause loss of fluids from the kidneys? but with all the explanation, this is what i'm taking home:

Dobutamine is given for cardiogenic shock ptts (after an acute MI perhaps), and the dose given will hit the D-1 receptors first to increase coronary supply but soon after, the dobutamine dose aims for beta-1 receptors increasing HR, thus improving TPR.

did i get it right?:eek:
Yes you are right :), I mentioned the alpha to clarify the point you mentioned as your main objection for its use :mad:
 

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thank u for all the replies.:)

yes i understand now...i think... although if i may, i wanna correct kabutar11 a little. the dopamine is given to a dose till it affects beta-1 not alpha-1. because alpha-1 will cause reflex bradycardia with increased TPR.

but yes u are ryte, that's how it works, D-1 receptors, then with increasing dose beta-1, then to alpha-1. the only thing is that i was wondering if u start off with a smaller dose, wont it cause loss of fluids from the kidneys? but with all the explanation, this is what i'm taking home:

Dobutamine is given for cardiogenic shock ptts (after an acute MI perhaps), and the dose given will hit the D-1 receptors first to increase coronary supply but soon after, the dobutamine dose aims for beta-1 receptors increasing HR, thus improving TPR.

did i get it right?:eek:
the reason we give dopamine even though it may seem it will increase GFR is because renal medulla has lowest o2 tension and is thus most affected in case of shock, if shock is severe enough (which it is most of the time) ATN and ARF will occur, and this can kill a patient. hence better to keep renal perfusion even though patient is hypovolemic.
 
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