Preview of “Unit 5 CVD”

8/3/2019 Preview of Unit 5 CVD

1/29

U

nit5

D

rugsoftheCardiovascular

S

ystem


2/29

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)


3/29

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


4/29

Arry

thmias

Abnorm

alpacema

keractivity

:acelltakes

overthepacingoftheheartataratethatis

differen

tfromwha

titoughtto

be.

Ectop

icpacemake

rs:cellsgen

eratingimpu

lse

outsid

eoftheSA

node

Thefirstcelltoreachthresholdwillbeginto

pace

theheart.


5/29

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


6/29

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.


7/29

Qu

inidine

Asod

iumc

hannelblocker,notwidely

used.

Thereisa

nantimusc

ariniceffec

t.

Blocksopen&activesodiumc

hannels

.

Itwillstopanarrythmia.

Effect

iveorally

Problem:potentialforgenerating

arryth

miasduetolengtheningofthe

action

potential.


8/29

Lid

ocaine

Alsoso

diumc

han

nelblocker

;usedfor

ventriculararrythm

ias(esp.v

-fib)

Effectiv

ewithless

tendencyfor

cardiotoxicity

Usedin

travenously;firstpassmetabolis

m


9/29

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


10/29

Cla

ss2:Betaadre

nergic

anta

gonists

Slowth

eheartdownandsup

presses

arrythm

ias

Decrea

secatecho

lamineinduced

automa

ticity


11/29

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.


12/29

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


13/29

Hype

rtension

CVD

#1

killerintheUS

Essentia

lhypertension:noidentifiablecause

that

youcan

treat.Treatmentaimed

asymptoms.

Symptomsareunnoticeable.

Riskfac

tors:weight,

sex,

familyhistory,gene

tics


14/29

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


15/29

Dama

getoth

eCardiovascula

r

System

Hypertro

phyoftheh

eart.

Theheartisstretche

dandleadsto

remodeling

cardiomyopathies

Thebiggertheheart,

themorewalltensionthehe

art

hasto

generatetopu

shbloodagainstthepressure

Vascula

rdamage

Elevat

epressurecan

damagetheb

loodvessels


16/29

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


17/29

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


18/29

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


19/29

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)


20/29

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


21/29

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


22/29

Angiotension2receptorblocker

Same

actionasACEinhibit

or

Noco

ugh


23/29

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


24/29

Diuretics

Oftenfirstlinetherapy

Ifoned

rugonlyis

beingused,itisusua

lly

adiuretic

MOA:r

educeshypervolemia

Alsoappearstore

laxbloodve

ssels


25/29

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


26/29

Antianemic/H

emopoieticDrugs

Drugsthatreplace

missingfa

ctorsfor

bloodformation

Iron,vitaminB

12,

folicacid

Therap

euticuses:treatanem

ias


27/29

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


28/29

AntilipemicAge

nts

Fibroic

AcidDerivatives

Niacin

Bilesequestrant

Statins


29/29

Statins

MOA:inhibitenzymeforcholesterol

synthesis

Cang

reatlyreduc

eLDLcholesterol(30-40

%)

Advers

eeffect:

Mayn

egativelyaffecttheliver

Musc

lepain,weakness

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