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Cardiology > B agonists > Flashcards

B agonists Flashcards

1
Q

Sympathetic vs Parasympathetic NS: anatomic location, preganglionic vs postganglion fiber length, transmitter at ganglia and transmitter at organs

A
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2
Q

Receptor types in peripheral autonomic nervous system

A
  • parasympathetic: muscarinic
  • sympathetic: a and B
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3
Q

Cardiac and vascular effect of muscarinic R activation

A

cardiac: decrease automaticity, decrease inotropy of atrium, increase refractoriness,
- vasculature: vasodilate systemic arterioles, minimal effect on systemic veins

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4
Q

Vagal reaction aka fainting: how it happens

A
  • vagal discharge leads to profound bradycardia (slow SA automaticity, slow AV conduction)
  • decrease SVR bc vasodilation
  • net effect is massive decrease in SAP accompanied by inappropriate bradycardia
  • may be provoked by fear or pain or inappropriate sensitivity of carotid sinus
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5
Q

Direct and indirect parasympathetic agonists

A
  • direct: ACh but it does not have a clinical use bc of rapid degradation by AChE
  • so indirect= AChE inhibitor–edrophonium
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6
Q

Edrophonium action and side effect

A
  • ultra short acting AChEI given IV that stimulated parasympathetic discharge
  • also causes profound abdominal cramping by stimulating contraction of GI smooth muscle
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7
Q

Edrophonium clinical uses

A
  • increasing AV node refractoriness for brief periods
  • useful in dx SV tachycardias, breaking SVTs due to AVNRT or AVRT
  • mostly superceded by adenosine which does same things but without abdominal cramps
  • longer actings = almost no clinical use (physostigmine, neostigmine) or as insecticides/terrorism (sarin gas)
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8
Q

Adrenergic R types and locations and actions

A
  • a1: vascular smooth muscle (kidney, GI, skin)= constrictor, GU smooth muscle constrictor
  • a2: vascular smooth muscle constrictor, platelet aggregation
  • B1: heart: inotrope (ventricular), chronotrope (SA and AV node)=increase metabolic rate, kidney renin secretion
  • B2: vascular smooth muscle (heart, skeletal muscle) and airway smooth muscle dilator
  • B3: adipose tissue lipolysis
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9
Q

Basic structure of adrenergic agonists

A
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10
Q

Endogenous adrenergic agonist receptor activities

A
  1. Epi: mixed a, B1, B2
  2. NE: mixed a, B1 agonist with little B2
  3. mixed a, B1 with little B2; isolated d1 activity at low doses
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11
Q

Impact of Epi

A
  1. skin, GI, renal arteriolar smooth muscle contraction
  2. B1: increase HR and inotropy
  3. B2: skeletal and cardiac VSMC vasodilate
    - net: not really SVR change, increase HR since B1>baroR slowing, increase CO, increase BP
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12
Q

NE impacts

A
  1. skin, GI renal vasoconstrict
  2. increase HR and inotropy
  3. no effect on skeletal m or cardiacl muscle dilation

Net: increase SVR (no offsetting B2 vasodilation), decrease HR due to baroR reflex (B1 overwhelmed), CO is unchanged or slighly decreased but shunted away from GI, skin, kidney, increase MAP due to increased SVR

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13
Q

Impact of dopamine

A
  • low dose: isolated d1R= renal vasodilation
  • intermediate dose: B1 action combines with d1 to increase CO with minimal effect on SVR
  • high dose: a action overwhelms d1 and effect is like NE
  • consequently, DA is effective pressor which in low to intermediate doses does not reduce renal blood flow
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14
Q

3 synthetic adrenergic agonists and their R they act on

A
  1. phenylepherine: a-selective
  2. isoproterenol: B1 and B2 with little a
  3. dobutamine: B1 with little net a activity
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15
Q

Phenylephrine effects

A
  • a selective: skin, GI, renal vasoconstriction
  • net increase SVR, decrease HR due to baroR reflex, decrease CO (uncompensated increase in LV afterload, no B activity to change contractility, CO away from skin, GI, renal); increase in MAP
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16
Q

Isoproterenol activity

A
  • B1 and B2= increase inotrophy and HR, and heart and skeletal muscle vasodilation
  • decrease SVR, increase HR (synergism with vagal response), increase CO (not importantly redistributed), possible slight decrease in MAP
17
Q

Dobutamine

A
  • little net a activity and B1 is mainly inotropic with modest chronotropic activity
  • relatively pure inotrope with modest effect on HR and peripheral circulation
  • effective for cirulatory support in severe CHF
18
Q

Clinical uses of adrenergic agonists

A
  • adjunctive rx to shock where there is an inadequate delivery of oxygen and other metabolic substrates to the tissues
  • remember the underlying definitive rx of shock is to treat the underlying cause, but adrenergic agonists can be used as adjunctive rx to offer hemodynamic support until definitive rx can take effect
19
Q

2 most effetive adrenergic agonists for distributive septic shock

A

phenylephrine and NE: need to decrease SVR!! HR is already through the rough and BP is still low

20
Q

Which B agonist is best for cardiogenic shock rx?

A

-Dobutamine: nearly pure B1 and need to increase CO in this shock

Cardiology (27 decks)

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