what is the mechanism of action of clonidine
a. direct dilation of arterioles
b. selectively block alpha1 receptors
c. reduce sympathetic outflow from vasomotor centers in the brainstem
d. prevent the release of NE from peripheral postganglionic sympathetic neurons
c. reduce sympathetic outflow
which are the predominant initial effects of B1 antagonists
a. decrease HR and decrease FOC
b. decrease HR and decrease PVR
c. decrease PVR and decrease preload
d. decrease preload and decrease CO
a. decrease in HR and decrease in FOC
what is the most likely adverse effect of a drug that causes direct vasodilation of arterioles
tachycardia
list 4 groups known as preload reducers
- diuretics
- aquaretics
- aldosterone antagonists
- venodilators
what are diuretics effects on symptoms of HF and hypertrophy
decreases symptoms and decreases hypertrophy
which is an antidiuretic hormone antagonist:
a. acetazolamide
b. conivaptan
c. eplerenone
d. triamterene
b. conivaptan
name two aquaretics
conivaptan (IV)
tolvaptan (PO)
what are the effects of auqaretics?
increase urine output, increase sodium concentration, decrease HF symptom,s, and effect BP
list two aldosterone antagonists that decrease preload
spironolactone and eplerenone
what is the MOA of aldosterone antagonists
decrease Na/ K exchange in collecting duct;
decreasing sodium and water reabsorption
what should be monitored when taking spironolactone?
potassium
list the venodilators.
what is there MOA
NTG
sodium nitroprusside
increase venous capacitance
what do venodilators do to venous return to heart and O2 demand
decrease venous return
decrease O2 demand
does sodium nitroprusside effect the arterial side or venous side more in a normal heart?
in HF?
in normal heart venouse side
in HF arterial side
list 3 afterload reducing groups
ACEI/ ARB
Beta blocker
Vasodilators
what is the MOA of ACEIs and ARBs on preload side?
blocks aldosterone
what is the MOA of ACEIs and ARBs on afterload side
blocks angio II’s vasoconstriction
how does angio II have a slow pressor response
aldosterone release
how does angio II have a rapid pressor response
altered SVR
other than decrease afterload and preload what hemodynamic effect does ACEI’s and ARBs have?
decrease remodeling and decrease hypertrophy
why does BB use seem paradoxical in HF?
they can cause drop in CO initially (bad).
over long term, have decreased mortality do to
what all is decreased by BBs in HF?
decreased: HR renin apoptosis tachyarrhythmias
BBs stop tachycardia caused from what in HF
neurohumoral mechanism
when should BB’s not be used for HF
acute situation
list two vasodilators used in afterload reduction
Nesiritide
BiDil
what is in BiDil
hydralazine and ISDN
name a synthetic brain natriuretic peptide?
what is it’s MOA
Nesiritide
MOA = vasodilation by binds to GC receptor on vascular smooth muscle
what is brain naturetic peptide
a marker of HF
what does nesiritide do by binding to GC receptor?
increase cGMP leading to relaxation
also gives diuresis
what needs to be monitored with nesiritide
renal fxn and BP
where does BiDil work? arterial or venous
both
hydralazine = arterial
ISDN = venous
what is beneficial about BiDil
decreases mortality (especially in AA pts)
what is a problem with BiDil
TID
what are the inotropic agents for HF
cardiac glycosides
beta agonists
PDE inhibitors
what is digoxins effects on electrolytes
increases Na at Na/K ATPase pump, increases Ca at Na/Ca exchanger
how does digoxin increase FOC
increases intracellular Ca
how is digoxin eliminated
renally
at what crcl is digoxin contraindicated
ClCr less than 50
which should have a lower renin level of digoxin: for HF or for arrhythmia
for HF
what happens to ejection fraction with digoxin tx?
increases (more blood flow to organs)
what is a conduction problem with digoxin
slows conduction to AV node; can cause arrhythmias