Post on 07-Apr-2018
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U
nit5
D
rugsoftheCardiovascular
S
ystem
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Cardiot
onicdru
gs
Drugsth
atincreasethestrength
oftheheart.
Drugsfo
rafailinghe
art.
Thehe
artbecomesw
eakerasapu
mp.
Canhappenoverma
nyyearsorrapidlyinresponseto
injury
Goalsfo
rtreatment:
increaseCO
andincreas
e
pumping
efficiencyw
hilereducingcardiacwo
rk
(increasepreloadan
ddecreaseafterload)
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Card
iacGlyc
osides(digoxin)
MOA:in
creasescon
tractilityinth
eheartmuscle
Increa
sesintracellula
rcalciumionconcentrationa
nd
increasestheforceo
fcontraction.
Increa
sesCOandre
lievesedemaifitispresent
S/E:nar
row
therapeuticwindow,
longhalflife
Developmentofarrythmias
Canin
duceAVblock
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Arry
thmias
Abnorm
alpacema
keractivity
:acelltakes
overthepacingoftheheartataratethatis
differen
tfromwha
titoughtto
be.
Ectop
icpacemake
rs:cellsgen
eratingimpu
lse
outsid
eoftheSA
node
Thefirstcelltoreachthresholdwillbeginto
pace
theheart.
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4cla
ssesofdrugsforArrythmias
Sodium
channelblockers:delaytheupward
spikew
hichthenw
illtakelonge
rtotriggerthe
action
potential.Delayphase4
tospikeof
AP
Calciumc
hannelblockers:sam
eMOAas
above
Blockingbetareceptors:slows
automaticity
Potass
iumc
hannelblockers:willcausethe
cellt
o
takelongert
ogetbackto
resting
membranepotentia
landslows
theheartrat
e.
Makes
thewholeA
Pprocessta
kelonger
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Class
1:Sodiumc
hanne
lblockers
Bindt
ochannels
intheinac
tiveand
active
state,
they
prolongth
eperiodin
which
thesechannelsdont
work.
Thesedrugswilllengthenthetimeittake
s
forthechanneltogobackto
theresting
state.
Especially
effectiveinsitesof
isch
emia.
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Qu
inidine
Asod
iumc
hannelblocker,notwidely
used.
Thereisa
nantimusc
ariniceffec
t.
Blocksopen&activesodiumc
hannels
.
Itwillstopanarrythmia.
Effect
iveorally
Problem:potentialforgenerating
arryth
miasduetolengtheningofthe
action
potential.
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Lid
ocaine
Alsoso
diumc
han
nelblocker
;usedfor
ventriculararrythm
ias(esp.v
-fib)
Effectiv
ewithless
tendencyfor
cardiotoxicity
Usedin
travenously;firstpassmetabolis
m
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Amilo
ridorane
Potass
iumc
hannelblocker&sodiumc
hann
el
blocke
r.
Alsoblockscalcium
channels&
beta-
adrene
rgicrecepto
rs.
Effectiveinorallys
uppressinga
rrythmias.
Lesslikelytoprodu
cearrythmia
s.
Hasa
verylongha
lflifeandhasatendency
togoc
rystalizeinthetissue
Pulm
onaryfibrosis
isthelimitingsideeffect
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Cla
ss2:Betaadre
nergic
anta
gonists
Slowth
eheartdownandsup
presses
arrythm
ias
Decrea
secatecho
lamineinduced
automa
ticity
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Clas
s3:
Pot
ass
ium
channe
l
blocke
r(sodalol)
Pro
longs
theac
tio
npo
ten
tiala
ndre
frac
tory
perio
d.
Ifyouleng
then
the
APittake
slonger
to
ge
t
bac
kto
theres
ting
po
ten
tialan
dlonger
un
tilthece
llscan
fireaga
in.
Pro
duc
es
thesam
earry
thmiasas
qu
inidine.
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Class
4:Calciumchannelblockers
(ver
apamil)
Worksthesame
wayasthe
sodium
chann
elsblockers,
theyhav
ea
prefer
enceforop
en/activechannels.
But
theyworksa
ttheSA&A
Vnode,
plac
eswherecalciumcurrentsaredriving
thecurrent
Effectiveforatria
larrythmia
sandcircu
s
movements
Canw
eakenthe
cardiacmu
scleover
time
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Hype
rtension
CVD
#1
killerintheUS
Essentia
lhypertension:noidentifiablecause
that
youcan
treat.Treatmentaimed
asymptoms.
Symptomsareunnoticeable.
Riskfac
tors:weight,
sex,
familyhistory,gene
tics
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T
arge
tsfor
treatm
en
t
CO:sympa
tho
lytic
s
Vascularres
istance:sympat
ho
lytics,
dir
ec
t
ac
tingvaso
dila
tors,
drugs
tha
tinterfere
withthe
RAAsystem
Fluidvo
lume:
diur
etics
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Dama
getoth
eCardiovascula
r
System
Hypertro
phyoftheh
eart.
Theheartisstretche
dandleadsto
remodeling
cardiomyopathies
Thebiggertheheart,
themorewalltensionthehe
art
hasto
generatetopu
shbloodagainstthepressure
Vascula
rdamage
Elevat
epressurecan
damagetheb
loodvessels
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Centr
allyactingsymp
atholytic
(clo
nidine)
MOA:a
lpha-2adrenergicagonistinthe
brain.Whenthosereceptors
areturned
on
itdecre
asessymp
atheticout
flow.
When
thathappen
syouseea
decreasein
vascu
larresistanc
eanddecreaseinCO.
Uses:H
TN
S/E:se
dation&depression
ReboundHTN
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Centra
llyac
ting
(guanefidine&r
eserpine)
MOA:
preven
tsthere
lease
ofnor-epi
from
n
erve
term
ina
ls
Dec
reasevascu
larres
istancean
da
decreaseo
fCO
2nd
line
drug
S/E:s
evere
hypo
tens
ion
Res
erp
inecanc
ross
the
BBB
&cancaus
e
dep
letiono
fcate
cho
lam
ines,
common
ly
causes
depress
ion
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Alph
a(1)Blockers(
prazosin)
MOA:blockalphare
ceptorsinperipheral
arteriole
s.
Thearter
iolesdilatea
ndtheBPfa
lls.
Drugs
areveryusefu
linloweringB
P
S/E:1s
tdosehypotension-->dizzin
ess(postural
hypotens
ion)
Drows
iness
Fluidr
etention
tachyc
ardia
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Be
taBlock
er(propranolol)
MOA:blocksbetaad
renergicrec
eptors,
decreas
ingcardiaco
utputandheartrate-->
decreas
ingBP
Decreaseinvascularresistancean
ddilationarter
ioles
Indicatio
ns:HTN,arrythmias
S/E:dec
reaseincon
tractilityofh
eart,reboun
d
HTN
Contrain
dications:asthma(b-2receptors)
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Calciumch
annelblockers
(verapamil)
MOA:b
locksthec
alciumc
ha
nnelsin
smooth
musclean
dcardiacmuscle.
Nota
llC
a++chan
nelblockers
arethesam
e;
same
workbetter
forarrythmia
s(verapamil),
some
arebetterfo
rthebloodvessels
(nifed
ipine)
S/E:de
creasecon
tractilityin
theheart
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ACEinhibitor
s
MOA:in
hitbitsang
iotens
inco
nvert
ing
enzyme
Decre
ases
BPinprac
tica
llyev
eryone
Indicat
ions:
HTN
Advers
ee
ffec
ts:c
ommon
drycoug
h
C/I:pre
gnancy
du
etoten
den
cy
toward
rena
lstressan
dp
oten
tia
lren
alfailure
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Angiotension2receptorblocker
Same
actionasACEinhibit
or
Noco
ugh
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CalciumC
h
annelB
lockers
MOA:c
ausevaso
dilation
Therap
euticuses:HTN,suptraventricular
tachycardia,angin
e
Note:b
etterantihypertensive
agentfor
African
Americans
(incombo
w/diuretic
s
CI:not
forpatientswithCHF
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Diuretics
Oftenfirstlinetherapy
Ifoned
rugonlyis
beingused,itisusua
lly
adiuretic
MOA:r
educeshypervolemia
Alsoappearstore
laxbloodve
ssels
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An
tihypote
nsiveA
gents
Thesed
rugsincreas
ebloodpres
sure
How?
Increa
seperipheralr
esistance(ie;alphaagonist)
Increa
seCO(
ie;betaagonist)
Increa
se(replace)flu
idvolume(ie;
wholeblood)
Therape
uticuses:ch
ronicsymptomatic
hypoten
sion,acuteh
ypotension,
replacebllod
volume
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Antianemic/H
emopoieticDrugs
Drugsthatreplace
missingfa
ctorsfor
bloodformation
Iron,vitaminB
12,
folicacid
Therap
euticuses:treatanem
ias
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Drug
sa
ffect
ing
Coagu
lation
Hemosta
tics-speed
up
bloo
dclo
tting
Usedtotreathemorr
hage
An
ticoagu
lan
ts-slow
down
bloodc
lotting,
decreas
eris
ko
fc
lotting
Workby
blockingtheformationofthrombin&fibrin,
decreasespla
telet
aggrega
tion
Therapeu
ticuses:venou
sthrom
bos
is,
pre
ven
tcoronary
thrombos
is,
anycon
dition
tha
tresu
lts
inbloo
drema
ining
in
heart
aftersy
stole
Thrombo
lytics:
drugs
tha
tdissolv
ec
lots
MOA:
causeplasmin
ogentoconve
rttoplasmin
Therapeuticuse:any
clot
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AntilipemicAge
nts
Fibroic
AcidDerivatives
Niacin
Bilesequestrant
Statins
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Statins
MOA:inhibitenzymeforcholesterol
synthesis
Cang
reatlyreduc
eLDLcholesterol(30-40
%)
Advers
eeffect:
Mayn
egativelyaffecttheliver
Musc
lepain,weakness