Ihd, Pericardial Diseases, Cardiomyopthy & Chf

8/20/2019 Ihd, Pericardial Diseases, Cardiomyopthy & Chf

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ISCHEMIC HEART DISEASE

ATHEROSCLEROSIS

MAJOR RISK FACTORS OF ATHEROSCLEROSIS

•Cigarette smoking• Hypertension (BP > 140/9o(mm/hg) or (on Antihypertensive medication)

• o! H" cho#estero#• "ia$etes me##it%s• &ami#y history o' CH"• Age (en > 4 years* +omen > years)• i'e sty#e risk 'actors• ,$esity (B1 > -0 kg/m.)• Physica# inactivity• Atherogenic diet•

EMERGING RISK FACTORS.

• ipoprotein (a)• Homocystine• Prothrom$otic 'actors (&i$rinogen)• Pro in'#ammatory 'actors( CP)• mpaired 'asting g#%cose• 2%$c#inica# atherogenesis

RISK FACTOR AND RELATIVE RISK OF FUTURE CARDIOVASCULAR ADVERSE EVENTS

ipoprotein (a)

Homocystine

3

5ota# Cho#estero#

"3Cho#estero#

sCA31

2er%m amy#oid3A

Apo#ipoprotein3B

5C6H" ratio

hs3CP

hs3CP75C6H"

080 1 4

hsCP? high reactivity C3reactive protein*

siCA3#? so#%$#e interce##%#ar adhesion mo#ec%#e31*H"C? high density #ipoprotein cho#estero#





DIETRY MANAGEMENT

BENEFICIAL CARDIOVASCULAR EFFECTS OF SELECTED DIETRY COMPONENTS• ,mega - 'atty acids • DD5rig#ycerides? DP#ate#et Aggregation• High &i$re "iet • D5C? D" cho#estero#• 2tero# esters • D5C D" cho#estero#• 2oya protein • D5rig#ycerides D " cho#estero#• ;itamin : • D" o@idative s%scepti$i#ity• ;itamin C • ecyc#es ;itamin A• &o#ic acid/;itamin B • DHomocystiene #eve#s• oderate a#coho# cons%mption • H" Cho#estero# DB#ood Coag%#ation

OMEGA-3 FATTY ACIDS

Protects &rom H"/CA"ed%ction in orta#ity &rom CA"/2C"

HYPOLIPIDEMIC EFFECT ANTI-THROMBOTIC EFFECT ANTI-ARRHYTHMOGENIC

EFFECT

• D5C #eve#s• " #eve#s• H" #eve#s

• Anti3p#ate#et• Anti3in'#ammatory e''ect

• 2ta$i#isation o' mem$rane phospho#ipids

THERAPEUTIC LIFE STYLE CHANGES

NCEP – ATP-III (Nat!"a# C$!#%t%'!# E)*at!" P'!+'a,,% – A)#t T'%at,%"t Pa"%#

NUTRIENT RECOMMENDED INTAKE

• 2at%rated &at • EF o' 5ota# Ca#ories(5C)• Po#y%nsat%rated &at • =pto 10F o' 5C• Car$ohydrate • =pto 0F o' 5C• &i$re • 03-0 gm/day• Proteins • =pto 1F o' 5C• Cho#estero# • 00mg/day• 5ota# ca#ories • Ba#ance :nergy ntake G :@pendit%re• 2a#t • g/day

OMEGA – 3 PUFA

arine 2o%rces:icosapentaenoic acid(:PA)"ocosahe@aenoic acid("HA)



ANGINA

TYPESSTABLE UNSTABLE PRIN/METAL0VARIANT

• Chest Pain or armdiscom'ort on e''ort thatis6

e#ieved in 10min/rest/nitro3g#ycerine8

$y e@ertion8• o in cardiac markers• :C sho!s 25

depression8

• Angina pain !hen t occ%rs at rest #asting

>10 min8 t is more severe? 'reI%ent

G pro#onged8• o e#evation in cardiac

markers• :C sho!s 25

depression8

• Angina pain that occ%rs atrest? not re#ated toe@ercise8

• ,cc%rs d%e to ;asospasm• :C sho!s 25 e#evation8• o e#evation in cardiac

markers

MYOCARDIAL INFARCTION DEFINATION

MI RELATED TO ISCHEMIA DUE TO PRIMARY CORONARY EVENT

• "etection o' rise and/or 'a## o' cardiac $iomarkers (pre'era$#y troponin) !ith at #east one va#%e a$ovethe 99th percenti#e o' the %pper re'erence #imit (=) together !ith evidence o' myocardia# ischemia!ith at #east one o' the 'o##o!ing6

2ymptoms o' ischemia8 :C changes indicative o' ne! ischemia (ne! 2535 changes or ne! #e't $%nd#e $ranch $#ock JBBBK) "eve#opment o' patho#ogica# L !aves in the :C8 3 maging evidence o' ne! #oss o' via$#e myocardi%m or ne! regiona# !a## motion a$norma#ity8

MI RELATED SUDDEN CARDIAC DEATH

• 2%dden? %ne@pected cardiac death? invo#ving cardiac arrest? o'ten !ith symptoms s%ggestive o' myocardia# ischemia? and

• accompanied $y pres%ma$#y ne! 25 e#evation? or ne! BBB? and• evidence o' 'resh throm$%s $y coronary angiography and/or at a%topsy? $%t death occ%rring $e'ore

$#ood samp#es co%#d $e o$tained? or at a time $e'ore the appearance o' cardiac $iomarkers in theB#ood8

MI ASSOCIATED 1ITH PCI

• By convention? increases o' $iomarkers greater than M- @ 99th percenti#e =M have $een designated as de'ining MPC3re#ated myocardia# in'arction

MI ASSOCIATED 1ITH CABG

• By convention? increases o' $iomarkers greater than M@ 99th percenti#e =M 7• ne! patho#ogica# L !aves or ne! BBB? or angiographica##y doc%mented ne! gra't or

native coronary artery occ#%sion? or • imaging evidence o' ne! #oss o' via$#e myocardi%m have $een

"esignated as de'ining CAB3re#ated myocardia# in'arction8

CRITERIA FOR PRIOR MYOCARDIAL INFARCTION

• Any one o' the 'o##o!ing criteria meets the diagnosis 'or prior myocardia# in'arction8 "eve#opment o' ne! patho#ogica# L !aves !ith or !itho%t symptoms maging evidence o' a region o' #oss o' via$#e myocardi%m that is thinned and 'ai#s to contract? in the

a$sence o' a? non3ischemic ca%se8 Patho#ogica# 'indings o' a hea#ed or hea#ing myocardia# in'arction8



ECG

STABLE - ST

DEPRESSIO

N

UNSTABLE -

STDEPRESSIO

N

PRINZMETA

L - ST

ELEVATION

MI

STEMI - ST

ELEVATION

NSTEMI - ST

DEPRESSIO

N

HYPERACUTE 'T'

WAVES

TERMINALQRS

CHANGES

STELEVATION

T WAVEINVERSION

PATHOLOGI

CAL Q WAVE

ECG CHANGES

ECG CHANGES OF MI IN ORDER

THE SITE OF INVOLVEMENT OF ARTERIES AND THE CORRESPONDING SITES OF

MYOCARDIAL LESIONS

e't ant8 "escending artery (4030F)Anterior !a## o' #e't ventric#e near ape@Ant8 portion o' ventric%#ar sept%mApe@ Circ%m'erentia##yCA (-0340F)n'8 post? !a## o' #e't ventric#ePost portion o' ventric%#ar septaen'8 post? right ventric%#ar 'ree !a## in some cases

e't circ%m'#e@ (130F)atera# !a## o' #e't ventric#e e@cept at ape@



COMMON UNCOMMON RARE (NEVER

ENCOUNTERED

• e't anterior descending(A") artery (4030F)

• ight coronary artery (-0340F)

• e't circ%m'#e@ coronaryartery (130F)

• e't main coronary artery• 2econdary $ranches e8g8? "iagona# $ranches o'

A" artery argina# $ranches

• Penetratingintramyocardia# $ranches

o' coronary arteries

ANTERIOR1ALL MYOCARDIAL INFARCTION SUBDIVIDED INTO

TVPE OF M.I LEADS INVOLVED

:@tensive anterior !a## 8 2tandard #ead ead A; andA## precordia# #eads (;13;)

An anterosepta# !a## 8 eads ; to ;4An antero#atera# !a## 88 2tandard #ead ? #ead A; and

eads ;4 to ;Apica# !a## 88 ;3;

n'erior !a## 88 2tandard #eads and ead A;&

n'eroposterior !a## 88 2tandard #ead ? ead A;&;1 ;

n'ero#atera# !a## 882tandard #ead ? ead A;&; ;

DIAGNOSIS

CARDIAC MARKERSEN/YME SEEN AT PEAKS AT RETURNS TO

NORMAL

Creatinin phosphokinase 34 hrs 4 hrs 43E hrs8

actate dehydrogenase 4 hrs 4 3 days A'ter 10 days

yog#o$in 3- hrs 3 E31 hrs5roponin 3 !ithin 43 hrs 4 hrs E310 days5roponin 3 5 !ithin 4 3 hrs 4 hrs E310 days

THALLIUM SCANNING2

• 5ha##i%m301 is %sed is inNected ; !hi#e pt8 s e@ercising on trade mi##8I"t%''%tat!"2

• orma# yocardia# 5iss%e63 hot spot8• schemic yocardia# 5iss%e63hot spot d%ring rest G co#d on e@ertion8• n'racted yocardia# 5iss%e63co#d spot on $oth rest G e@ertion8

OO,5:OO 5ha##i%m scan di''erentiate orma#? schemic G n'racted tiss%e8



HYBERNATION 4. STUNNED MYOCARDIUM

AC=5: C,,A ,CC=2,

2CH:C ;:5C=A "2&=C5,

:A :P:&=2,

P:225:5 ;:5C=A "2&=C5,

":A:" 2P,5A:,=2 :C,;: ,&;:5C=A &=C5,

CH,C 2:;:: C,,A 25:,22

CH,C :"=C5, B,," &,+ G2CH:A

:5AB,C A"AP5A5,

CH,C C,5AC5: "2&=C5,

:;A2C=A2A5,

P,;:" C,5AC5: &=C5,

STUNNED MYOCARDIUM HYBERNATING MYOCARDIUM

TREATMENT OF MI & ANGINA

PRIN/METAL ANGINA

2%$#ing%a# itro3g#ycerine Ac%te :pisodeong Acting itrates Prevent ec%rrencesCCBQs Prevention o' Coronary Artery 2pasmR3B#ockers ;aria$#e esponse

MYOCARDIAL INFARCTION

ST-ELEVATION MI (STEMI

mmediate anagement +ith ,Aorphine ,@ygen itrates Aspirin

2tart AdN%vant 5reatmentS3$#ocker itro3g#ycerine(;)

Heparin(;)

eper'%sion 5herapy(1hrs)5hrom$o#ysis (streptokinase):ar#y Primary PCA'ter 1hrs throm$o#ysis is o' no %se8



MANAGEMENT OF NSTEMI0 UNSTABLE ANGINA

mmediate treatment !ith ,A G Bed est3 ,PH:

,3 ,T: 3 5A5:2

A3 A2P

Antischemic 5herapy6 5A5:2? R B,C<: Antithrom$otic 5hreapy6 A2P7C,P",:

Anticoag%#ant 5herapy6 H:PA (=&H/+H)

o! isk High isk

Patient is Candidate 'or :ar#y Conservative 5reatment Patient is Candidate 'or :ar#y nvasive 5reatment

CONSERVATIVE TREATMENT INVASIVE TREATMENT

Contin%e Antischemic 5herapyContin%e Antithrom$otic 5hreapyContin%e Anticoag%#ant 5herapy+atch'%# !aiting:C G Cardiac markers monitoring

evasc%#arisation !ithPCCAB 5H,B,22 C,5A"CA5:"

ST ELEVATED M.I.

• 5hrom$o#ysis?• PC?• Bypass 2%rgery

NON ST ELEVATED M.I.

• PC?• Bypass s%rgery

THROMBOLYSIS CONTRAINDICATED

THROMBOLYTICS

D')+ 6• 2treptokinase %sed most#y high $ene'it #o! risk (C $#eed)• r5PA A#tep#ase tenectep#ase retep#ase

I"*at!"2

• Ac%te 25:

• Chest pain e ne! 25: and BBBC0I2-

Assess c#inica# risk



• Prior /C haemorrhage• 2tr%ct%ra# cere$ra# vasc%#ar #esion• a#ignant /C neop#asm• schemic 2troke !ithin -months• 2%spected aortic dissection•

B#eeding diathesis• &acia# tra%maT,"+2

dea##y e in -0 min%tes - ho%rsB%t i' de#ayed ti## 1 ho%r i' PC is not avai#a$#eCan $e ti## 4 ho%r on#y i' PC is not avai#a$#eC!,#*at!" !5 St'%t!6"a%2

• H Hypotension• I /C haemorrhage• F &ever• I Anaphy#a@is

Arrhythmias

OO,5:OO !ith hypotension s%ggest carcinogenic shock and in these cases the reper'%sion therapy isAngiop#asty / $ypass not throm$o#ytics8 RV INFARCT TREATMENT

Best moda#ity o' t/t in in'erior 88

eper'%sion therapy5hrom$o#ytic orPC

Best moda#ity o' t/t in in'erior 88comp#icated $y ight ventric%#ar

; '#%ids

COMPLICATIONS OF MI

• Arrhythmias ;&(common ca%se o' re#ated deaths)

• nterventric%#ar septa# r%pt%re8• &ree !a## r%pt%re3Haemopercardi%m• Papi##ary %sc#e %pt%re

CARDIOMYOPATHY

SYMPTOMATIC CARDIOMYOPATHY

DILATED

CARDIOMYOPATHY

RESTRICTIVE

CARDIOMYOPATHY

HYPERTROPHIC

CARDIOMYOPATHY

2ysto#ic "ys'%nction "iasto#ic "ys'%nction "iasto#ic "ys'%nctionEJECTION FRACTION7389 EJECTION FRACTION:389 EJECTION FRACTION:389



HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

PATHPHYSIOLOGY

• 2epta# Hypertrophy Asymmetrica# septa# hypertrophy8

• "ynamic ; ,%t'#o! ,$str%ction t is re#ated to narro!ing o' the s%$ aortic area as a conseI%ence o' opposition o' anterior mitra#

va#ve #ea'#et against hypertrophied sept%m in mid systo#e (225,C A5:, ,5, 2A)

CLINICAL SPECTRUM OF HOCM

ASYMPTOMATIC PATIENT

SUDDEN DEATH&irst c#inica# mani'estation o' disease (common#y in yo%ng ad%#ts a'ter sport)SYMPTOMATIC

SYMPTOMS SIGNS

• "yspnoea• Angina• &atig%e• syncope

• "o%$#e or trip#e pericardia# imp%#se• Brisk carotid %pstroke• 24• 2ysto#ic m%rm%r

Harsh? diamond shaped Best heard at #o!er #t sterna $order

as !e## as ape@ $%t no radiation toneck

FACTORS AFFECTING INTENSITY OF MURMUR

CONDITION 1HICH ; OBSTRUCTION &

INTENSITY OF MURMUR

CONDITION 1HICH OBSTRUCTION &

INTENSITY OF MURMUR

• &AC5, 2 ,CA"AC,5AC55

:@ercise 2ympathomimetic amines "igita#is

• &AC5, +HCH D2:2 ;:5C=A;,=:

;a#sa#va manoe%vre 2%dden standing itrog#ycerine Amy# nitrate 5achycardia

• D A,5C P:":C: G A&5:,A"

• &AC5, 5HA5 D ,CA"AC,5AC55

R3$#ockers CCBQs

• &AC5, +HCH ;:5C=A;,=:

Passive #eg raising :@pansion o' $#ood vo#%me 2%pine position

• A,5C P:":C: G A&5:,A" Phny#ephrine Hand grip 2I%atting

MANAGEMENT OF HOCM

• Avoidance o' stren%o%s physica# activity• S3$#ockers

DH DBP D2ti''ness o' ; D&ata# arrhythmias

• CCBQs (;erapami# "i#tiaUem) D2ti''ness o' ;



D:#evated "iasto#ic Press%re• Amiadarone• 2%rgica# yomectomy

DRUGS C0I IN HOCM

DRUGS THAT ;SES MYOCARDIAL CONTRACTILITY

• 2ympathomimetic amines• "igita#is• R3$#ockers

DRUGS THAT SES VENTRICULAR VOLUME

• itrates• "i%retics

PERICARDIAL DISEASES

CARDIAC TAMPONADE

INTRODUCTION

• t is a condition characterised $y presence o' '#%id in pericardia# space !hich #eads to sedintrapericardia# press%re8

CAUSES2

• 5ra%maCLINICAL FEATURE2

SYMPTOMS2

• BeckQs 5riad8 V;P "ecreased BP %''#ed Heart 2o%nds

SIGNS2

• V;P ses Prominent T3decent8 A$sent 3 !ave8

• P%#ses Parado@%s• <%ss%ma#Qs sign3most#y a$sent $%t can a#so $e present !hen pericardi%m starts organising8

INVESTIGATION2

• :C63 e#ectrica# A#ternance8•

" echo63 2ho!s pericardia# e''%sion ; siUe8

CONSTRICTIVE PERICARDITIS

INTRODUCTION2

• t is a CH,C c#inica# condition characteriUed $y organisation o' pericardi%m #eading to D pericardia# space8

CAUSES2

• 5ra%ma• Cardiac operation• ediastina# irradiation• P%r%#ent in'ection• eop#astic diseases• he%matoid arthritis (not ac%te rhe%matic 'ever)



• 2:C0F2

• &atig%e• Hypotension• e'#e@ 5achycardia8

O0E2-

• V;P3sed Prominent T decent3a$sent Prominent present8

• <%ss%ma#Qs sign 7ve• P%#ses parado@%s ve• 5apping ape@ $road $ent sign• W sI%are root sign• :I%a#isation o' diasto#ic press%re

INVESTIGATION2

ECG2

• o! vo#tage comp#e@es<D ECHO2

• 5hickened pericardi%m• Pericardia# ca#ci'ication• ;3siUe norma#

CHARACTERISTIC TAMPONADE CONSTRICTIVE

PERICARDITIS

RESTRICTIVE

CARDIOMYOPAT

HY

RVMI .

C#"*a#

P%#s%s parado@%s N%g%#ar veins

Prominent y descentProminent @ descent<%ssma%#Qs sign5hird heart so%ndPericardia# knock

Common

A$sent PresentA$sent (are)A$sentA$sent

=s%a##y a$sent

=s%a##y present=s%a##y presentPresentA$sent ,'ten present

are

arePresentPresentareA$sent

are

arearePresentay $e presentA$sent

E#%*t'!*a'!+'a,

#o! :C v o # t a g e:#ectrica# a#ternans

ay $e present ay $e present

ay $e presentA$sent

ay $e presentA$sent

A$sent A$sent

E*$!*a'!+'a$=

5hickened pericardi%mPericardia# ca#ci'icationPericardia# e''%sion; siUeyocardia# thicknessight atria# co##apse and ;"Cncreased ear#y 'i##ing?↑ mitra# '#o! ve#ocity:@aggerated respiratory variationin '#o! ve#ocity

A$sentA$sentPresent=s%a##y sma##

orma#PresentA$sent

Present

Present,'ten presentA$sent=s%a##y norma#

orma#A$sentPresent

Present

A$sent A$sent A$sent=s%a##y norma#=s%a##y increasedA$sentPresent

A$sent

A$sentA$sentA$sent:n#arged

orma#A$sentay $e present

A$sent

CT0MRI 5hickened/ca#ci'ic pericardi%m3

A$sent Present A$sent A$sent

Ca'a* *at$%t%'>at!"

:I%a#iUation o' diasto#ic proced%res

=s%a##y present =s%a##y present =s%a##y a$sent A$sent or present

Cardiac $iopsy he#p'%# o o 2ometimes o

2I%are oot 2ign 7ve 777ve 7ve 3ve



OO,5:OOA Positive <%ss%ma#Qs 2ign s are n Cardiac 5amponade8 ts Presence 2%ggests 5hat An ,rganiUing ProcessG :picedia# Constriction Are Present n Addiction 5o :''%sion8

CONGESTIVE HEART FAILUREINTRODUCTION

• t is characteriUed $y o' cardiac p%mp dys'%nction #eading to decrease in stroke vo#%me? cardiac o%tp%t? $#ood press%re and per'%sion8

PATHOPHYSIOLOGY2

Heart &ai#%re

↓sed rena# per'%sion ed%ced Cardiac ,%tp%t

ncreased enin 2ympathetic nervo%s activation

ncreased Angiotensin ncreased periphera# resistance

ncreased a#dosterone ;asoconstriction hydrostatic press%re

ncreased 2odi%m and !ater retention

FEATURES OF LEFT HEART FAILURE & RIGHT HEART FAILURE

LEFT HEART FAILURE RIGHT HEART FAILURE

t heart 'ai#%re is de'ined as a c#inica# syndrome!here the dominant 'eat%re is '#%id congestion in the#%ngs (p%#monary) rather than in the systemiccirc%#ation85he p%#monary capi##ary !edge press%re is typica##y

e#evated (PC+P)Predominant symptoms are re#ated to passive

t heart 'ai#%re is de'ined as a c#inica# syndrome!here the dominant 'eat%re is '#%id congestion in thesystemic circ%#ation5he p%#monary capi##ary !edge press%re is norma#( norma# PC+P) %n#ess rt8 Heart 'ai#%re is ca%sed

secondary to #e't sided heart 'ai#%re (ed PC+P) (PC+P is not e#evated in iso#ated H&)



congestion o' #%ngs p%#monary edema"yspnoea,rthopneaP"Co%gh !ith pink 'rothy sp%t%ma#es/Crack#es

Periphera# edemaAscitesCongestive hepatomeg#yCongestive sp#eenomega#y+t8 ain

oct%ria

aised V;PPositive HepatoN%g%#ar e'#e@8

THE FRAMINGHAM HEART STUDY CRITERIA

MAJOR CRITERIA MINOR CRITERIA

P"

eck vein distensiona#esCardiomega#yAc%te p%#monary edema2- ga##op veno%s press%re ( >1 cm)Circ%#ation time>sHepatoN%g%a#r re'#e@ positive

Ank#e edema

ight co%ghHepatomrga#yP#e%ra# e''%sion;ita# capacity red%ced $y one third 'rom predicted5achycardia (>10)

MAJOR OR MINOR CRITERIA

+eight #oss o' more than 48kg over days in responce to treatmentDEFINITE TREATMENT

maNor criteria or one maNor G minor criteria8

INVESTIGATIONS

SIGNS OF PULMONARY VENOUS HYPERTENSION

(n order o' appearance !ith increasing p%#monary veno%s press%re)• ;asc%#ar edistri$%tion

=pper #o$e veno%s distension• nterstitia# edema

<er#ey B #ines Perihi#ar haUe Bronchia# c%''ing

• A#veo#ar edema Airspace opacities Perihi#ar $at !ing distri$%tion C#ears rapid#y !ith di%retics

• P#e%ra# e''%sionsBRAIN NATRIURETIC PEPTIDE IN THE DIAGNOSIS OF HEART FAILURE

• 5he natri%retic peptide system impacts sa#t and !ater hand#ing and press%re reg%#ation and ?mayin'#%ence myocardia# str%ct%re and '%nction8

• Brain natri%retic peptide is a hormone that is re#eased 'rom myocardia# ce##s in the atria and in somecases the ventric#es in response to vo#%me e@pansion8

• 5he re#ease o' $oth AP and BP is increased in heart 'ai#%re as ventric%#ar ce##s are recr%ited tosecrete $oth AP and BP in response to high ventric%#ar 'i##ing press%res8

• 5he p#asma concentrations o' $oth hormones are increased in patients !ith asymptomatic andsymptomatic #e't ventric%#ar dys'%nction? permitting their %se in diagnosis8



HYPONATREMIA

"%e to sed A"H"%e to sed AP? BP G CP8;% BNP? '!-BNP

MANAGEMENT OF HEART FAILURE

• ,nce 5he C#inica# "iagnosis ,' Heart &ai#%re s Con'irmed Assess &or &#%id etention8 t s mportant5o 5reat 5he Patients &#%id etention Be'ore 2tarting An AC: nhi$itor8

• Beta B#ockers 2ho%#d Be 2tarted ,nce 5he &#%id etention Has Been 5reated8

DRUGS USED2

AIM OF DRUG THERAPY IN CHF

e#ie' o' congestive and #o! o%tp%t symptoms and Arrest and reversa# o' disease progressionrestoration o' cardiac per'ormance and pro#ongation o' s%rviva#

INOTROPIC DRUGS ACE INHIBITORS

• "igo@in Captopri#• "o$%tamine :na#apri#• "opamine isinopri#• Amrinone amipri#• i#irinone 5rando#apri#

DIURETICS AT-II ANTAGONISTS

• &%rosemides osartan• 5hiaUides Candesartan• B%metanide r$esartan• Hydroch#orthiaUide osartan• eto#aUone

VASODILATOR @ BLOCKERS

• AC: inhi$itor Bisopro#o#• A531 antagonist Carvedi#o#• Hydra#aUine etopro#o#• itrate



@ BLOCKER

• etopro#o#• Bisopro#o#• Carvedi#o#

OO,5:OO

AC:Qs ed%ces 5he orta#ity By 0F

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Ihd, Pericardial Diseases, Cardiomyopthy & Chf

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