beta blockers 2 Flashcards
preganglionic fibers are
myelinated, rapid
post ganglionic
un-myelinated, slower
sns arise from
thoracolumbar outflow
adrenal medulla releases
epinephrine
pns arise from
craniosacral outflow
2 types pns receptors
nicotinic, muscarinic
what breaks down acetylcholine
acetylcholinesterase to choline and acetic acid
norepinephrine is broken down by what in the nerve synapse
MAO or sequestered in storage vesicles for release
norepi that diffuses away from synapse is inactivated by
COMT
beta 1 effects with agoinism
increased HR increased conduction increased contractility increased renin releast (ALL EFFECTS ON HEART)
beta 2 effects with agonism
skeletal muscle relaxation bronchodilation gluconeogenesis glycogenolysis vasodilation (some)
alpha1 actions with agonsm
works on arterial blood vessels
increases constriction
increases BP
can cause reflex bradycardia secondary to baroreceptor mediated reflex
alpha2 actions with agonism
negative feedback, when receptor is activated there is a decrease in norepi release, when blocked NE release increases
s/e alpha block
orththostatic hypertension, baroreceptor med. tachycardia
which alpha blocker causes covalent binding
phenoxybenzamine
which alpha blockers are reversible
prazosin, yohimbe, phentolamine
phenolamine
nonselective alpha blocker. tx htn emergency, hyperreflexia, pheochromo, reversible binding
effects of phentolamine
decreased bp due to vasodilation (peripheral), hr increased, co increased
phenoxybenzamine
nonselective alpha blocker
uses phenoxybenzamine
excesive vasoconstriction secondary to shock but only after volume rescucitation
effects phenoxybenzamine
vasodilation, decreased bp
what cannot happen with phenoxybenzamine
compensatory vasoconstriction, get large drops in bp
1/2 life phenoxybenzamine
24 hours
onset phenoxybenzamine
60 minutes
onset phentolamine
2 min, duration 10-15
prazosin
selective alpha 1, less liekely to cause tachycardia. dilates arteries and veins
yohimbe
selective alpha 2, increased release norepinephrine used to treat idiopathic orthostatic htn
gold standard beta blocker
propanolol
do b blockers cros bbb
yes and placenta can cause hypoglycemia, bradycardia and hypotension in fetus
what are all beta antagonists derived from
isoproterenol
partial antagonist
presece of intrinsic sympathomim activity
pure antagonist
absence of intrinsic sympatho activity
beta blockers with intrinsic activity
timolol, pindolol, acebutalol
selective beta blockers beta 1
metoprolol, esmolol, atenolol
metoprolol effects
negative inotrope and chronotrope. 10% protein binding, 1/2 time 3-4 hours
atenolol
renal excretion 1/2 time 6-7 hours
no insulin induce hypoglycemia, may be used in diabetics
esmolol
5 min onset, 10-30 min duration
1/2 life 9 minutes.
rapid ester hydrolysis
propanolol
pure antagonist, decreases hr and cardiac output,decreases peripheral vascular return, increase myocardial o2, but with decrease hr and contractility decreases myocardial o2
propanolol metabolism
hepatic, 70% on first pass, 90-95% protein bound 1/2 time 2-3 hours
nadolol
no metabolism, excreted unchanged in urine, 1/2 time 20-40 hours
pindolol
partial antagonist, minimal resting bradycardia 40-60% protein bound, 1/2 time is 3-4 hours
timolol
elimination 1/2 time 4 hours, tx glaucoma
contraindications to beta blockers
prexist av block or heart failure not caused by tachycardia, diabetics secondary to hypoglycemia masking
if give beta blocker to hypovolemic pt with compensatory tachy what happens
profound drops in bp
effects on heart represent
removal sns innervation
weak left ventricle after beta blocker may
go into heart failure
what happens with epi and beta blockers
may enhance vasodilatory effect
pvd and beta blockers
may have cold hands/feet
s/s excess myocardial depression
decreased hr, decreased co, hypotension, cardiogenic shock, bronchospasm, vent depression, seizures, prolonged intravent contraction
tx myocardial depress
atropine 7mcg/kg then beta agonist isoproterenol or pure agonist
glucadon which stimulates adenylate cyclase and intracellular cmp, pacer or HD
potassium and beta blockers
when beta blocked stops facilitation of k intracellularlly and can increase k level
s/e labetalol
orthostatic hypotension, heart block, chf
labetalol is
alpha1 selective, beta1 and beta2 nonselective
1/2 time labetalol
5-8 hours, prolonged with liver disease onset 5-10 minutes
actions labetalol
decrease bp and svr, stops reflex tachycardia, co unchanged
dose of labetalol
0.1-0.5mg/kg
