Sympathomimetics

Question 1

Epinephrine receptors activated

Answer 1

Potent alpha, also activated beta 1,2

Question 2

Epinephrine clinical uses

Answer 2

Anaphylaxis, severe asthma, bronchospasm, CPR, hemodynamic instability, support myocardial contractility and vascular resistance, increase inotropy

Question 3

Epinephrine cardiovascular effects

Answer 3

Alpha-1 = arteriolar vasoconstriction and pulmonary artery vasoconstriction, predominantly located in cutaneous, splanchnic, and renal vascular beds
Alpha-2 = vasoconstriction
Beta-1 = chronotropic, inotropic, increased cardiac output
Beta-2 = vasodilation, predominantly located in skeletal muscle

Question 4

Alpha/Beta receptor balance and epinephrine

Answer 4

Alpha-1 and Beta-2 receptor balance in vasculature of an organ determines epinephrine’s overall effect on blood flow to that organ

Question 5

Overall systemic of epinephrine

Answer 5

Preferential distribution of cardiac output to skeletal muscle and increased systemic vascular resistance - renal blood flow substantially decreased

Question 6

Low v High dose epinephrine

Answer 6

Beta-2 more sensitive at low doses, effects on alpha-1 predominate at high doses

Question 7

Epinephrine blood pressure effect

Answer 7

High density of alpha receptors in venous vasculature = increased venous return, blood pressure increased by increased cardiac index and systemic vascular resistance

Question 8

Epinephrine coronary blood flow

Answer 8

Increased, even at doses that do not increase SVR

Question 9

Epinephrine airway smooth muscle

Answer 9

Bronchial SM relaxed, effect not observed in presence of beta-blockade

Question 10

Epinephrine metabolic effect

Answer 10

Most significant effect on metabolism of all catecholamines, increases glycogenolysis, and adipose tissue lipolysis

Question 11

Epinephrine electrolyte effects

Answer 11

Beta-2 stimulation activates the Na/K pump leading to movement of K into cells

Question 12

Epinephrine coagulation effects

Answer 12

Accelerates coagulation by inducing platelet aggregation and increases factor 5 activity

Question 13

Norepinephrine receptors stimulated

Answer 13

Beta-1 (equal to epinephrine) and Alpha-1, lacks Beta-2 agonist effects

Question 14

Norepinephrine cardiovascular effects

Answer 14

Beta-1 = positive chronotrope, inotrope, and dromotrope

Question 15

Norepinephrine SVR effects

Answer 15

Alpha-1 = intense arterial and venous vasoconstriction in all vascular beds besides coronary arteries

Question 16

Epinephrine v Norepinephrine on SVR

Answer 16

Norepinephrine causes greater increase in SVR, DBP, MAP, SBP

Question 17

Epinephrine v Norepinephrine on coronary circulation

Answer 17

Both dilate coronary arteries

Question 18

Dopamine receptors activated

Answer 18

Dependent upon dose administered, however, there is a large variation in patient response to the various doses of dopamine

Question 19

Low dose dopamine (0.5-3 mcg/kg/min)

Answer 19

D-1 and D-1 primarily stimulated = vasodilation, decreased arterial BP, increased renal and splanchnic vascular blood flow

Question 20

Intermediate dose dopamine (3-10 mcg/kg/min)

Answer 20

Beta-1 (primarily) stimulated = positive chronotrope and inotrope effects
Alpha receptors (secondary) in vasculature, also induces Norepinephrine release from vascular sympathetic neurons

Question 21

High dose dopamine (>10 mcg/kg/min)

Answer 21

Alpha-1 predominantly stimulated, acts like pure alpha agonist - reflex bradycardia may develop

Question 22

Dopamine clinical uses

Answer 22

Increase cardiac output in patients with decreased contractility, low systemic blood pressure, and low urine output

Question 23

Dopamine pulmonary effects

Answer 23

Increases pulmonary vascular resistance - not preferred inotrope agent in patients with pulmonary HTN or right ventricular dysfunction

Question 24

Isoproterenol receptor activated

Answer 24

Beta-1 and Beta-2 MOST POTENT activator of sympathomimetics, lacks alpha stimulating effects, causes NO vasoconstriction

Question 25

Isoproterenol cardiovascular effects

Answer 25

Potent chronotrope, inotrope, and dromotrope

Question 26

Isoproterenol cardiac output effects

Answer 26

Increases in cardiac output may be attenuated by impaired left ventricular filling due to tachycardia, as well as decreased preload from venodilation

Question 27

Dobutamine recetors activated

Answer 27

Beta-1 = potent
Beta-2 = weaker
Alpha-1 = agonist activity increases with higher doses

Question 28

Dobutamine composition

Answer 28

Comprised of two stereoisomers that exert differing effects on the Alpha and Beta receptors

Question 29

Dobutamine enantiomers

Answer 29

(-) enantiomer = potent alpha-1 agonist, weak beta-1 and beta-2 agonist
(+) enantiomer = competitive alpha-1 antagonist, potent beta-1 and beta-2 agonist

Question 30

Dobutamine primary effect

Answer 30

Positive inotrope - increases intracellular cAMP - increased Ca release from SR - increased contractility

Question 31

Dobutamine downside

Answer 31

May be ineffective in patients who require increased SVR rather than augmentation of cardiac output to increase systemic blood pressure because it lacks vasoconstrictor activity

Question 32

Ephedrine receptors activated

Answer 32

Stimulated alpha and beta receptor by stimulating release of endogenous norepinephrine

Question 33

Ephedrine use

Answer 33

5-10 mg IV commonly used to increase systemic blood pressure, heart rate, and cardiac output

Question 34

Phenylephrine receptors activated

Answer 34

Alpha-1 = pure alpha agonist

Very small ability to cause release of endogenous norepinephrine

Question 35

50-200 mcg IV bolus or 20-100 mcg/kg/min phenylephrine

Answer 35

Commonly used to treat sympathectomy from neuraxial anesthesia or from inhalation or IV general anesthetics