Cardiovascular Drugs- Sympathomimetics Flashcards
endogenous catecholamines
- epinephrine
- norepinephrine
- dopamine
synthetic catecholamines
- isoproterenol
- dobutamine
synthetic noncatecholamines
- ephedrine
- amphetamine
- phenylephrine
selective alpha2-adrenergic agonists
- clonidine
- dexmedetomidine
selective beta2-adrenergic agonists
- albuterol
- terbutaline
- ritodrine
sympathetic nervous system activation causes
- cardiac stimulation (increased HR and BP, contractility, susceptibility to ectopy)
- bronchdilation
- vasoconstriction (decreased flow to skin, GI tract, renal)
- vasodilation (improved blood flow to skeletal muscle)
- CNS stimulation- increased cognition (except alpha 2)
- increased blood sugar (lipolysis & glycogenolysis)
- increased rate of coagulation
lipolysis is
breakdown of lipids
glycogenolsysi is
splitting up of glycogen in the liver, yielding glucose
used to increase __ or increase __ after sympathetic blockade caused by regional anesthesia
contractility
vasular tone
used to __ or __ BP (to prevent tissue ischemia) during the time required to correct for hypovolemia or excessive inhaled anesthesia
increase or maintain
used to __ of asthmatic
relax bronchoconstriction
used to manage __
anaphylaxis
used to prolong __
regional anesthesia
direct
bind to receptors and activate them directly (catecholamines and phenylephrine)
indirect causes the release of
norepinephrine from postganglionic sympathetic nerve endings (amphetamine)
indirect blocks
the reuptake of norepinephrine to make more in circulation (cocaine, tricyclic antidepressants)
indirect agent might not be effective if patient has
denervation injury, or depletion of NT
tachyphylaxis
the greater the concentration of the sympathomimetic, the lower the number of receptors in tissues or decreased response
catecholamines are inactivated by enzymes
- monoamine oxidase (MAO)
- Catechol-O-methyltransferase (COMT)
catecholamines termination of effect influenced more by
uptake back into postganglion sympathetic nerve endings
catecholamines are filtrated by
the lungs of norepinephrine and dopamine
noncatecholamines are inactivated by
MAO only- slower
epinephrine stimulates
both alpha and beta
most potent alpha stimulator
epinephrine
epinephrine stimulation
alpha1=alpha2; beta1=beta2
epinephrine is given
IV or subq (causes vasoconstriction which slows absorption)
epinephrine __ soluble
poorly lipid; lack of cerebral effects
epinephrine uses
- decrease absorption and prolong duration of local anesthetics
- treatment of anaphylactic reactions
- treatment of cardiac arrest
- increase myocardial contractility
low dose epinephrine dose
0.01-0.03 mcg/kg/min
low dose epinephrine beta 1
increases HR, BP, CO, inotropy
low dose epinephrine beta 2
decrease in DBP due to decrease in SVR (vasodilation in skeletal muscle vessels)
moderate dose epinephrine dose
0.03-0.15 mcg/kg/min
moderate dose epinephrine beta 1
- increase in SBP, HR, CO, inotropy (increase in venous return)
- increase in susceptibility to arrhythmias
- mixed with alpha
large dose epinephrine dose
> 0.15 mcg/kg/min
large dose of epinephrine stimulates
beta and alpha-1 but alpha predominates
large dose epinephrine beta and alpha 1
vasoconstriction of the skin, mucosa, and hepatorenal vessels (decreased renal blood flow), SVT common
epinephrine respiratory effects
smooth muscle relaxed in the bronchi (beta 2)
if beta antagonist is present with epinephrine the respiratory effects is
the alpha1 effect causes bronchoconstriction
epinephrine metabolic effect
most significant effect of all catecholamines
epinephrine __ blood glucose
increase
metabolic effect of epinephrine of beta 2
increase glycogenolysis and lipolysis
metabolic effect of epinephrine of alpha 2
inhibits release of insulin (hyperglycemia)
epinephrine effects on electrolytes
beta 2- stress induced hypokalemia (activation of the sodium-potassium pump on RBCs)
epinephrine causes __ K
initial increased
it follows glucose out of hepatic cells
epinephrine ocular effects
alpha 1- contraction of the radial muscles of the iris causes pupil dilation; contraction of the orbital muscles causing bulging of the eyes (exophthalmus)
epinephrine GI/GU effects
relaxation of GI smooth muscle
epinephrine GI/GU beta effects
relaxation of the detrusor muscle of the bladder
epinephrine GI/GU alpha1 effects
contracts the sphincter muscles
norepinephrine is
a naturally occurring catecholamines released from postganglionic sympathetic nerve endings
norepinephrine is a potent __ agonist with __ agonist effect, but little __ effect
alpha
beta1
beta2
norepinephrine stimulation
alpha1=alpha2; beta1»beta2
norepinephrine clinical use
vasoconstrictor to increase SVR and raise BP
infiltration of norepinephrine into subq tissue can
cause necrosis due to vasoconstriction
can treat infiltration for norepinephrine with
phentolamine
norepinephrine alpha 1 CV effects
- vasoconstriction of both arterial and venous vessels of all vascular beds
- increased SVR, MAP, increased venous return
- decreased HR
norepinephrine beta 1 CV effects
overshadowed by the alpha 1 effects causing a decrease in CO, decreased tissue perfusion, decreased kidney blood flow
norepinephrine respiratory effects
no beta 2
norepinephrine metabolic effects
hyperglycemia unlikely
norepinephrine dose
0.02-0.4 mcg/kg/min
low dose norepinephrine stimulation
beta 1 selective; increase HR, inotropy
high dose norepinephrine stimulation
alpha 1, alpha 2, beta 1; increase SVR, BP, but decreased HR (baroreceptor reflex)
norepinephrine bolus
dilute; 4-16 mcgs (intermittent boluses- less bradycardia than phenylephrine)
dopamine
endogenous NT in the nervous system (central and peripheral)
dopamine stimulation
D1=D2»beta»alpha