phase 0 mediated by
fast sodium channels, cell depolarizes
phase 1 mediated by
potassium channels open, cell begins to repolarize
phase 2 mediated by
slow calcium channels open, potassium channels open
PLATEAU
phase 3 mediated by
slow sodium channels close, potassium channels stay open and potassium rushes out, cell reporalizses quickly
phase 4
resting membrane potential around -90
pressure =
flow x resistance
MAP =
CO x SVR
CO =
HR x SV
how to increase MAP
increase HR
increase SV
increase SVr
alpha 1 location and action
vasculature, vasoconstrictions
alpha 2 location and action
brain, sedation/sympathetic inhibition
beta 1 location and action
heart, ionotropy/chronotropy/dromotropy
beta 2 location and action
lung, bronchodilattion
what group constitutes a catecholamine and increases beta and alpha activity
hydroxyl substition
what do amine substitutions do
larger increases beta activity
increasing side chain distance…
increases sympathomimetic activity
increases duration of action
where is dopamine synthesized
kidney
where does dopamine bind
a1, b1, D1
low levels of dopamine bind
D1; increases renal flow
moderate levels of dopamine bind
b1, increases BP and HR
high levels of dopamine bind
a1, vasoconstriction
where does norepinephrine bind
a1 mostly
where does epi bind
non selective (a1, b1, b2)
where does phenylephrine bind, what is its action, what is a risk
a1, vasoconstriction
increases preload and BP
risk: reflex brady
where does ephedrine bind
a1, b1, b2
ephedrine causes ____ because of _____
tachyphylaxis, NE depletion
digoxin MOA
inhibits sodium potassium pump, increased intra cellular ca+
new guidelines for stage 1 htn
130-139/80-89
new guidelines for stage 2 htn
more than 140/more than 90
three MOA for anti HTN drugs
effects on autonomic NS
inhibitor of RAAS
peripheral vasodilation
dihydropyradines work where
vasculatur
non-dihyrdopyradines work where
heart
non selective beta blockers should not be used in
obstructive disease