Sympathomimetics Flashcards
Epinephrine receptors activated
Potent alpha, also activated beta 1,2
Epinephrine clinical uses
Anaphylaxis, severe asthma, bronchospasm, CPR, hemodynamic instability, support myocardial contractility and vascular resistance, increase inotropy
Epinephrine cardiovascular effects
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
Alpha/Beta receptor balance and epinephrine
Alpha-1 and Beta-2 receptor balance in vasculature of an organ determines epinephrine’s overall effect on blood flow to that organ
Overall systemic of epinephrine
Preferential distribution of cardiac output to skeletal muscle and increased systemic vascular resistance - renal blood flow substantially decreased
Low v High dose epinephrine
Beta-2 more sensitive at low doses, effects on alpha-1 predominate at high doses
Epinephrine blood pressure effect
High density of alpha receptors in venous vasculature = increased venous return, blood pressure increased by increased cardiac index and systemic vascular resistance
Epinephrine coronary blood flow
Increased, even at doses that do not increase SVR
Epinephrine airway smooth muscle
Bronchial SM relaxed, effect not observed in presence of beta-blockade
Epinephrine metabolic effect
Most significant effect on metabolism of all catecholamines, increases glycogenolysis, and adipose tissue lipolysis
Epinephrine electrolyte effects
Beta-2 stimulation activates the Na/K pump leading to movement of K into cells
Epinephrine coagulation effects
Accelerates coagulation by inducing platelet aggregation and increases factor 5 activity
Norepinephrine receptors stimulated
Beta-1 (equal to epinephrine) and Alpha-1, lacks Beta-2 agonist effects
Norepinephrine cardiovascular effects
Beta-1 = positive chronotrope, inotrope, and dromotrope
Norepinephrine SVR effects
Alpha-1 = intense arterial and venous vasoconstriction in all vascular beds besides coronary arteries
Epinephrine v Norepinephrine on SVR
Norepinephrine causes greater increase in SVR, DBP, MAP, SBP
Epinephrine v Norepinephrine on coronary circulation
Both dilate coronary arteries
Dopamine receptors activated
Dependent upon dose administered, however, there is a large variation in patient response to the various doses of dopamine
Low dose dopamine (0.5-3 mcg/kg/min)
D-1 and D-1 primarily stimulated = vasodilation, decreased arterial BP, increased renal and splanchnic vascular blood flow
Intermediate dose dopamine (3-10 mcg/kg/min)
Beta-1 (primarily) stimulated = positive chronotrope and inotrope effects Alpha receptors (secondary) in vasculature, also induces Norepinephrine release from vascular sympathetic neurons
High dose dopamine (>10 mcg/kg/min)
Alpha-1 predominantly stimulated, acts like pure alpha agonist - reflex bradycardia may develop
Dopamine clinical uses
Increase cardiac output in patients with decreased contractility, low systemic blood pressure, and low urine output
Dopamine pulmonary effects
Increases pulmonary vascular resistance - not preferred inotrope agent in patients with pulmonary HTN or right ventricular dysfunction
Isoproterenol receptor activated
Beta-1 and Beta-2 MOST POTENT activator of sympathomimetics, lacks alpha stimulating effects, causes NO vasoconstriction
Isoproterenol cardiovascular effects
Potent chronotrope, inotrope, and dromotrope
Isoproterenol cardiac output effects
Increases in cardiac output may be attenuated by impaired left ventricular filling due to tachycardia, as well as decreased preload from venodilation
Dobutamine recetors activated
Beta-1 = potent Beta-2 = weaker Alpha-1 = agonist activity increases with higher doses
Dobutamine composition
Comprised of two stereoisomers that exert differing effects on the Alpha and Beta receptors
Dobutamine enantiomers
(-) enantiomer = potent alpha-1 agonist, weak beta-1 and beta-2 agonist
(+) enantiomer = competitive alpha-1 antagonist, potent beta-1 and beta-2 agonist
Dobutamine primary effect
Positive inotrope - increases intracellular cAMP - increased Ca release from SR - increased contractility
Dobutamine downside
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
Ephedrine receptors activated
Stimulated alpha and beta receptor by stimulating release of endogenous norepinephrine
Ephedrine use
5-10 mg IV commonly used to increase systemic blood pressure, heart rate, and cardiac output
Phenylephrine receptors activated
Alpha-1 = pure alpha agonist
Very small ability to cause release of endogenous norepinephrine
50-200 mcg IV bolus or 20-100 mcg/kg/min phenylephrine
Commonly used to treat sympathectomy from neuraxial anesthesia or from inhalation or IV general anesthetics
