1 - Vasoconstrictors Flashcards
Alpha 1
widely distributed, multiple organ systems
increase intracellular calcium = constriction (ischemia)
smooth muscle contraction
bronchoconstriction
stops insulin secretion - use glucose (hyperglycemia)
mydriasis - open up eyes
relax GI
Alpha 2
precedex, clonidine, CNS - check and balances
picks up norepi, when enough picked up, neg feedback
“agonist activity is antagonistic”
postsynaptic - sedation, decreased SNS outflow, platetl aggregation, decreased BP
Beta 1
heart
increased rate, speed of conduction, increased force
Beta 2
opposite alpha 1, smooth muscle relaxation, peripheral vasodilation improves oxygen exchange bronchodilation increased insulin secretion reduced GI mobility SNS shuts down GI, PNS starts GI
Acetylcholine
binds to cholinergic receptors (nicotinic and muscarinic)
acetycholinesterase breaks down Ach
ephedrine
direct and indirect effect
direct
indirect - sitm norepi and alpha 1 effects
Catecholamine vs sympathomimetic
- OH group on 3 and 4 position of benzyne ring makes catechol
- all sympathomimetics are derived from beta phenylethylamine
Catecholamine metabolism
rapid, via enzymes
MAO and COMT
non-catechol (structure) can be broken down by MAO but not COMT
non-natural will not be recycled
**inhibition of MAO will further increase time
sulfoconjugation reactions
genetics, changes med metabolism
SULT1A3/SULT1A4 polymorphisms effect phenylephrine
Vasoconstrictors
hemodynamic - increase afterload
reflex changes - decreased HR, decreased conduction
Vasoconstrictors - non cardiac effects
bronchodilate
glycogenolysis
CNS stim (low lipid solubility)
Vasoconstrictor contraindications
LV failure worsens
exacerbate RV failure
decreased RBF
mask hypovolemia
low dose epi
1-2 mcg/min, beta 2
decreased SVR, better overall oxygenation
intermediate dose epi
4 mcg/min, beta 1
help heart, increased HR, contractility, increased arythmia risk
high dose epi
> 10 mcg/min, alpha 1
reflex brady can occur (dt mass increase in SVR)