CV Effects of Autonomic Agonists Flashcards

1
Q

End organ receptor for PS system

A

muscarinic

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2
Q

Ganglia receptor for PS system

A

nictonic

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3
Q

Ganglia receptor for sympathetic system

A

nicotinic

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4
Q

End organ receptor for sympathetic system

A

alpha and beta adrenergic

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5
Q

Action of muscarinic receptors in heart

A
  1. reduce SA node automaticity
  2. reduce atrial inotropy
  3. increase AV refractoriness
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6
Q

Action of muscarinic receptors in vessels

A

increase arterial vasodilation

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7
Q

What is the role of ACh as a clinical therapy?

A

none –> broken down rapidly by AChE –> used agonist is an inhibitor of ACh esterase

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8
Q

MOA Edrophonium

A

AChE inhibitor –> 30 second action= IV administration

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9
Q

Side effect of edrophonium

A

abdominal cramping

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10
Q

What are the clinical uses of edrophonium

A

increase AV node refractoriness to evaluate atrial activity in situations of ventricular tachycardia but use has been replaced mostly be adenosine which does same thing w/o GI side effects

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11
Q

Where is the receptor found and what does it do? alpha1

A

vascular smooth muscle constrictor

GU smooth muscle constrictor

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12
Q

Where is the receptor found and what does it do? alpha2

A

vascular smooth muscle constrictor

platelet aggregation

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13
Q

Where is the receptor found and what does it do? beta1

A

heart - myocardial inotrope

kidney - JG cell renin secretagogue

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14
Q

Where is the receptor found and what does it do? beta2

A

vascular smooth muscle dilator

bronchial dilator

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15
Q

Where is the receptor found and what does it do? beta3

A

adipose tissue - lipolysis

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16
Q

What kind of agonist is it? epinephrine

A

alpha, beta1, beta2

17
Q

What kind of agonist is it? norepinephrine

A

alpha, beta1, (and a teence of beta2)

18
Q

What kind of agonist is it? dopamine

A

alpha, beta1, (and a teence of beta2), delta1, delta2

19
Q

Effects of epinephrine

A

alpha: skin/gi/renal vasoconstriction
beta1: cardiac intropy and chronotropy
beta2: skeletal/cardiac vasodilation

systemic:

  1. increased HR b/c beta1 overcomes baroreceptor mediated slowing
  2. increased CO (redirected away from skin,gi, kidney)
  3. +/- SVR: alpha/beta2 cancel each other out
20
Q

Effects of norephinephrine

A

alpha: skin, GI, renal vasoconstriction
beta1: cardiac inotropy/chronotropy

systemic:

  1. increase SVR b/c alpha is unopposed –> increase SAP
  2. reduce HR due to baroreceptor reflex –> beta1 opposed by strong alpha without support from b2
21
Q

Does norepi change CO?

A

no –> beta 1 is opposed by a strong alpha action on SVR/vagal discharge

22
Q

Low dose effect of dopamine

A

isolated d1 action produces renal vasodilation AKA Renal Dose Dopamine

23
Q

Mid dose effect of dopamine

A

beta1 combines with delta1 action to increase CO w/o changing SVR

24
Q

High dose effect of dopamine

A

alpha action overcomes d1 action and looks generally like norepi

25
What is the unique feature of dopamine's clinical usefulness?
dopamine is an effective pressor which in low/intermediate doses does not reduce renal blood flow
26
What kind of agonist is it? phenylephrine
alpha (and a teence of beta1 and beta2) --> synthetic
27
What kind of agonist is it? dobutamine
beta1 > beta2 >alpha
28
What kind of agonist is it? isoproterenol
beta1, beta2 (and a teence of alpha)
29
Effects of phenylephrine
alpha: skin, GI, renal vasoconstriction systemic: 1. increase SVR --> SAP 2. reduce HR b/c activation of baroreceptor reflex causes vagal discharge 3. reduce CO --> uncompensated increase in LV afterload due to SVR w/o beta-mediated inotropy
30
Effects of isoproterenol
beta1: cardiac inotropy/chronotropy beta2: skeletal/cardiac vasodilation systemic: 1. reduce SVR --> reduce SAP 2. increase HR b/c of beta1 chronotropy+ baroreceptor reflex against low SAP 3. increase CO b/c increase in LV contractility and reduced SVR
31
Effects of dobutamine
beta1: inotropy w/modest chronotropy systemic 1. increase myocardial strength w/ modest effect on everything else --> good for circulatory support in severe CHF
32
Why does dobutamine have little alpha activity?
it is produced as a racemic mixture: + enantiomer is an antagonist and - enantiomer is an agonist --> cancel each other out
33
Which of the sympathetic agonists would be best in tx of: septic shock
phenylephrine or norepinephrine * goal is to increase SVR which means you need an agent with a lot of alpha activity that is unopposed // further increasing HR or CO won't do a whole lot without dealing with the underlying issue of SVR
34
Which of the sympathetic agonists would be best in tx of: cardiogenic shock
dobutamine need to increase CO by activating beta1 // can't have alpha mediated vasoconstriction