CV Effects of Autonomic Agonists Flashcards
End organ receptor for PS system
muscarinic
Ganglia receptor for PS system
nictonic
Ganglia receptor for sympathetic system
nicotinic
End organ receptor for sympathetic system
alpha and beta adrenergic
Action of muscarinic receptors in heart
- reduce SA node automaticity
- reduce atrial inotropy
- increase AV refractoriness
Action of muscarinic receptors in vessels
increase arterial vasodilation
What is the role of ACh as a clinical therapy?
none –> broken down rapidly by AChE –> used agonist is an inhibitor of ACh esterase
MOA Edrophonium
AChE inhibitor –> 30 second action= IV administration
Side effect of edrophonium
abdominal cramping
What are the clinical uses of edrophonium
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
Where is the receptor found and what does it do? alpha1
vascular smooth muscle constrictor
GU smooth muscle constrictor
Where is the receptor found and what does it do? alpha2
vascular smooth muscle constrictor
platelet aggregation
Where is the receptor found and what does it do? beta1
heart - myocardial inotrope
kidney - JG cell renin secretagogue
Where is the receptor found and what does it do? beta2
vascular smooth muscle dilator
bronchial dilator
Where is the receptor found and what does it do? beta3
adipose tissue - lipolysis
What kind of agonist is it? epinephrine
alpha, beta1, beta2
What kind of agonist is it? norepinephrine
alpha, beta1, (and a teence of beta2)
What kind of agonist is it? dopamine
alpha, beta1, (and a teence of beta2), delta1, delta2
Effects of epinephrine
alpha: skin/gi/renal vasoconstriction
beta1: cardiac intropy and chronotropy
beta2: skeletal/cardiac vasodilation
systemic:
- increased HR b/c beta1 overcomes baroreceptor mediated slowing
- increased CO (redirected away from skin,gi, kidney)
- +/- SVR: alpha/beta2 cancel each other out
Effects of norephinephrine
alpha: skin, GI, renal vasoconstriction
beta1: cardiac inotropy/chronotropy
systemic:
- increase SVR b/c alpha is unopposed –> increase SAP
- reduce HR due to baroreceptor reflex –> beta1 opposed by strong alpha without support from b2
Does norepi change CO?
no –> beta 1 is opposed by a strong alpha action on SVR/vagal discharge
Low dose effect of dopamine
isolated d1 action produces renal vasodilation AKA Renal Dose Dopamine
Mid dose effect of dopamine
beta1 combines with delta1 action to increase CO w/o changing SVR
High dose effect of dopamine
alpha action overcomes d1 action and looks generally like norepi
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
What kind of agonist is it? phenylephrine
alpha (and a teence of beta1 and beta2) –> synthetic
What kind of agonist is it? dobutamine
beta1 > beta2 >alpha
What kind of agonist is it? isoproterenol
beta1, beta2 (and a teence of alpha)
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
Effects of isoproterenol
beta1: cardiac inotropy/chronotropy
beta2: skeletal/cardiac vasodilation
systemic:
- reduce SVR –> reduce SAP
- increase HR b/c of beta1 chronotropy+ baroreceptor reflex against low SAP
- increase CO b/c increase in LV contractility and reduced SVR
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
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
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
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
