10/26/2013

DEFINISI

HIPERTENSI

Blood pressure: is the pressure of the blood against the walls of the arteries. results fro two for!es.
"ne is !reated b# the heart as it pu ps blood into the arteries and through the !ir!ulator# s#ste . The other is the for!e of the arteries as the# resist the blood flow.

Te$anan darah
TEKANAN DARAH

S#stoli! blood pressure is a easure of blood pressure while the heart is beating Diastoli! pressure is a easure of blood pressure while the heart is rela%ed& between heartbeats.
CARDIAC OUTPUT RESISTENSI PERIFER

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HIPERTENSI
H#pertension is defined b# persistent ele'ation of arterial blood pressure (BP). The Se'enth Report of the *oint National +o ittee on the Dete!tion& E'aluation& and Treat ent of High Blood Pressure (*N+ ,) !lassifies adult BP isolated s#stoli! h#pertension: Patients with diastoli! blood pressure (DBP) 'alues -./ Hg and s#stoli! blood pressure (SBP) 'alues 012/ Hg 3 h#pertensi'e !risis (BP 415/617/ Hg) a# be !ategori8ed as either : a h#pertensi'e e ergen!# (e%tre e BP ele'ation with a!ute or progressing target organ da age) or a h#pertensi'e urgen!# (se'ere BP ele'ation without a!ute or progressing target organ in9ur#)

PRE:3;ENSI D3N EPIDE<I";"=I

Pre'alensi nasional Hipertensi Pada Pendudu$ > ur 4 15 Tahun adalah sebesar 7.&5? @1? pendudu$ 3 eri$a engala i hipertensi 0 12/6./ Hg Te$anan darah a$an ening$at dengan berta bahn#a usia (hipertensi ban#a$ ter9adi pada lansia) enurut AH" pre'alensi hipertensi di dunia @@.B? pd thn 7//B

ETI";"=I
Hipertensi pri er (./?): tida$ di$etahui pen#ebabn#a& han#a bisa di$ontrol (fa$tor geneti$) Hipertensi se$under (1/?):
disfungsi gin9al& gagal gin9al $ronis& pen#a$it th#roid& +ushing s#ndro e "bat: de$ongestan& steroid& NS3ID <a$anan: Natriu & etanol& tira in

<ultiple fa!tors a# !ontribute to the de'elop ent of pri ar# h#pertension& in!luding:
Hu oral abnor alities in'ol'ing the reninCangiotensinC aldosterone s#ste & natriureti! Hor one& or h#perinsuline iaD 3 pathologi! disturban!e in the +NS& autono i! ner'e fibers& adrenergi! re!eptors& or barore!eptorsD 3bnor alities in either the renal or tissue autoregulator# pro!esses for sodiu e%!retion& plas a 'olu e& and arteriolar !onstri!tionD 3 defi!ien!# in the lo!al s#nthesis of 'asodilating substan!es in the 'as!ular endotheliu & su!h as prosta!#!lin& brad#$inin& and nitri! o%ide& or an in!rease in produ!tion of 'aso!onstri!ting substan!es su!h as angiotensin II and endothelin ID

3 high sodiu inta$e and in!reased !ir!ulating natriureti! hor one inhibition of intra!ellular sodiu transport& resulting in in!reased 'as!ular rea!ti'it# and a rise in BPD and In!reased intra!ellular !on!entration of !al!iu & leading to altered 'as!ular s ooth us!le fun!tion and in!reased peripheral 'as!ular resistan!e.

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P3T"FISI";"=I
<alfungsi siste reninCangiotensinCaldosteron

P3T"PHESI";"=E
Renin is an en8# e se!reted into the blood fro the $idne#s sensiti'e to !hanges in blood flow and blood pressure The pri ar# sti ulus for in!reased renin se!retion is de!reased blood flow to the $idne#s& whi!h a# be !aused b# loss of sodiu and water (as a result of diarrhea& persistent 'o iting& or e%!essi'e perspiration) Renin !atal#8es the !on'ersion of angiotensinogen into angiotensin I

P3T"PHESI";"=E
3n en8# e in the seru !alled angiotensinC !on'erting en8# e (3+E) then !on'erts angiotensin I into angiotensin II 3ngiotensin II a!ts 'ia re!eptors in the adrenal glands to sti ulate the se!retion of aldosterone:
whi!h sti ulates salt and water reabsorption b# the $idne#s& and the !onstri!tion of s all arteries (arterioles)& whi!h !auses an in!rease in blood pressure.

1NC 2II3 C)assi0i*ati n

+) . press/re *)assi0i*ati n N r(a) Prehypertensi n Stage 1 hypertensi n Stage 2 hypertensi n

0 4)

. press/re
Diast )i* +P ,(( Hg-

Syst )i* +P ,(( Hg'120 120"1&! 1#0"1$! 160 r r r r

'%0 %0"%! !0"!! 100

3ngiotensin II further !onstri!ts blood 'essels through its inhibitor# a!tions on the reupta$e into ner'e ter inals of the hor one norepinephrine

The JNC VII. JAMA 2003;289:2560-72

JNC VII and ESHESC summary: target blood pressure goals

F"<P;IF3SI HIPERTENSI
"ta$: stro$e *antung: pen#a$it 9antung $oroner& gagal 9antung <ata: hipertensif retinopati =in9al : gagal gin9al ($reatinin tinggi& proteinuria) Pen#a$it 'as$ular perifer: aneuris a

Type 0 hypertensi n
Un* (p)i*ate. C (p)i*ate. Dia4etes (e))it/s Ki.ney .isease
Kap)an ,C)ini*a) Hypertensi n6 !th e.762006BP target is to lower BP below the threshold for starting therapy

+P g a) ,((Hg'1#05!0

'1&05%0 '1&05%0

Chobanian et al. JAMA 2003;289:256072 Guidelines Co ittee. J !"#e$tens 2003;21:101153

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F"<P;IF3SI
Ris$ of +: disease doubles with e'er# 7/61/ in!rease. E'en patients with preh#pertension ha'e an in!reased ris$ of +: disease. Hg

DI3=N"SIS
Silent $iller Pengu$uran te$anan darah (sesuai$an dgn $lasifi$asi te$anan darah *N+ :II)

E'aluasi hipertensi

TER3PI
Nonfar a$ologi Far a$ologi:
Tu9uan: enurun$an ortalitas dan orbiditas #ang berhubungan dengan $erusa$an hipertensi <ortalitas dan orbiditas ber$aitan dgn organ target spt: $e9adian $ardio'as$ular6serebro'as$ular& gagal 9antung& pen#a$it gin9al

Terapi nonfar a$ologi

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Terapi Far a$ologi

firstCline options: Diuretic, ACE inhibitor, A !, and CC! G"!loc#ers may be used either to treat a spe!ifi! !o pelling indi!ation or as !o bination therap# with a pri ar# antih#pertensi'e agent for patients without a !o pelling indi!ation. H1"!loc#ers, direct renin inhibitors, central H7"agonists, peripheral adrenergic antagonists, and direct arterial $asodilators are alternati$es that a# be used in sele!t patients after pri ar# agents.

Terapi far a$ologi

Indi$asi $husus
=agal 9antung: 3+EI& diureti$& beta blo!$er& 3RB Pas!a I<: beta blo!$er& 3+EI Pen#a$it is$e ia 9antung: beta blo!$er& ++B Pen#a$it gin9al $ronis: 3+EI& 3RB& diureti$ loop Pen#a$it serebro'as$ular: 3+EI dan diureti$ tia8id Aanita ha il: etil dopa& beta blo!$er& 'asodilator Pree$la sia: hidrala8in i'& etil dopa Hipertensi urgensi Hipertensi e ergensi

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3lgorit a terapi hipertensi

Ora) antihypertensi8e .r/gs9 C)ass Dr/g ,Tra.e Na(e- Us/a) . se range in (g5.ay ,Dai)y Fre:/en*yACE inhi4it rs bena&e#$il ,a#to#$il enala#$il .osino#$il lisino#$il oe3i#$il #e$indo#$il 5uina#$il $a i#$il t$andola#$il

'(otensin)* 'Ca#oten)* '-asote,)* 'Mono#$il* '/$ini0il1 2est$il)* '4ni0as,* 'A,eon* 'A,,u#$il* 'Alta,e* 'Ma0i6*

10+%0 25+100 2.5+%0 10+%0 10+%0 7.5+30 %+8 10+%0 2.5+20 1+%

'1+2* '2* '1+2* '1* '1* '1* '1+2* '1* '1* '1*

C)assi0i*ati n Ca)*i/( Antag nists

;enerati n3 First -e$a#a il :i.edi#ine 9iltia&e Se* n.
Fe) .ipine RTD Isra.ipine CR 2erapa(i) SR Ni0e.ipine ;ITS Di)tia=e( CD

Thir.

<atest

A lodi#ine <er*ani.ipine 'h"d$o#hili,* ,)ip phi)i*-

Angi tensin II antag nists ,andesa$tan 'Ata,and* e#$osa$tan '7e0etan* i$besa$tan 'A0a#$o* losa$tan 'Co&aa$* ol esa$tan '8eni,a$* tel isa$tan 'Mi,a$dis* 0alsa$tan '9io0an*

8+32 %00+800 150+300 25+100 20+%0 20+80 80+320

'1* '1+2* '1* '1+2* '1* '1* '1*

J Clin 8asi, Ca$diol 1999;2:155

DI>RETIF
Tia8id: H+T ;oop: furose id He at $aliu : a ilorid& tria teren 3ntagonis aldosteron: spironola$ton ES diureti$ tia8id& loop: hipo$ale ia& hipo agnesia& hiper$alse ia& hiperurie ia& hipergli$e ia& hiperlipide ia& dan disfungsi se$sual

3+E Inhibitor
<engha bat angiotensin I en9adi angiotensin II 3ngiotensin II adalah 'aso$onstri$tor $uat dan 9g erangsang se$resi aldosteron 3+EI e blo$ degradasi bradi$ininCC ening$at$an efe$ penurunan te$anan darah dan ES batu$ $ering

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Pen#e$at reseptor angiotensin II (3RB)

Efe$ angiotensin II: 'aso$onstri$si& pelepasan aldosteron& a$ti'asi si pati$& pelepasan hor on antidiureti$

Beta blo!$er
Ad$enose#to$ beta;1 dan beta;2 te$dist$ibusi di selu$uh tubuh 8eta ;1: te$da#at ban"a6 di <antun= dan =in<al Menai66an den"ut <antun=1 6ot$a6tilits1 #ele#asan $enin 8eta;2: te$da#at di #a$u;#a$u1 li0e$1 #an6$eas dan otot halus $te$i >e6$esi insulin dan =li6o=enolisis 8$on6odilatasi dan 0asodilatasi 8eta blo,6e$: ?a$diosele6ti. 6e,il 6e un=6inan te$<adi s#as e b$on6us dan 0aso6onst$i6si 'beta;1 blo,6e$* 8eta;2 blo,6e$: -aso6onst$i6si dan s#as e b$on6us1 hi#e$=li6e ia

3ntihipertensi alternatif

3lfa 1 blo!$er
Pra8osin& tera8osin& do%a8osin Be$er9a pada pe buluh darah perifr& engha bat a bilan $ate$ola in pd sel otot halus en#ebab$an 'asodilatasi dan enurun$an te$anan darah. <enguntung$an ut$ la$iCla$i dgn BPH (benign prostati! h#perplasia)CCC e blo$ reseptor postsinapti$ alfaC1 adrenergi$ di te pat $apsul prostat& en#ebab$an rela$sasi dan ber$urang ha batan $eluarn#a aliran urin.

3gonis alfa 7 !entral

Flonidin dan etil dopa <enurun$an te$anan darah dengan erangsang reseptor alfaC adrenergi$ di ota$CC enurun$an aliran si pateti$ dari pusat 'aso otor di ota$ ( ening$at$an a$t parasi pateti$) dan enurun$an tonus 'agalCCC enurun$an den#ut 9antung& !ardia! output& resistensi perifer total& a$t plas a renin& dan refle% baroreseptor. Flonidin ut$ hipertensi #ang resisten obat pilihan uta a pada $eha ilan

Reserpin
<e$anis e $er9a: Reserpin enurun$an te$anan darah dgn engosong$an norefinefrin dari u9ung saraf si pateti$ dan e blo$ per9alanan NE $e granul pen#i panann#a. <engosong$an $ate$ola in dari ota$ dan io$ardiu : sedasi& depresi dan ber$urangn#a !urah 9antung

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ReserpinI
<ulai $er9a dan wa$tu paruh la bat: dosis pe berian 1%6hari. Perlu 7CB inggu efe$ antihipertensi terlihat Dapat en#ebab$an retensi natriu dan air perlu $o binasi dgn diureti$ (tia8id) Ha batan a$t si pateti$ ( ening$at$an a$t parasi pateti$) terlihat ES: hidung tersu bat& se$resi asa la bung ening$at& diare& bradi$ardia

:asodilator arteri langsung

Hidrala8in& ino$sidil <e$anis e $er9a: rela$sasi langsung otot polos arteriolar tetapi td$ en#ebab$an 'asodilatasi $e pe buluh darah 'ena. Penurunn te$anan perfusi #g $uat enga$tif$an refle$s baroreseptor en#ebab$an aliran si pateti$ ening$at CC ening$at$an den#ut 9antung& !urah 9antung dan pelepasan renin CCC ta$ifila$sis& efe$ hipotensi a$an hilang dgn pe a$aian seterusn#a. Efe$ ini dpt diatasi dgn penggunaan beta blo!$er bersa aan.

Intera$si obat

Studi $asus
;.N. is a 2.C#earCold white wo an with a histor# of t#pe 7 diabetes& obesit#& h#pertension& and igraine heada!hes. The patient was diagnosed with t#pe 7 diabetes . #ears ago when she presented with ild pol#uria and pol#dipsia. ;.N. is JK2L and has alwa#s been on the large side& with her weight flu!tuating between 1BJ and 15J lb. Initial treat ent for her diabetes !onsisted of an oral sulfon#lurea with the rapid addition of etfor in. Her diabetes has been under fair !ontrol with a ost re!ent he oglobin 31! of ,.2?. H#pertension was diagnosed J #ears ago when blood pressure (BP) easured in the offi!e was noted to be !onsistentl# ele'ated in the range of 1B/6./ Hg on three o!!asions. ;.N. was initiall# treated with lisinopril& starting at 1/ g dail# and in!reasing to 7/ g dail#& #et her BP !ontrol has flu!tuated. "ne #ear ago& i!roalbu inuria was dete!ted on an annual urine s!reen& with 1&.2@ g6dl of i!roalbu in identified on a spot urine sa ple. ;.N. !o es into the offi!e toda# for her usual followCup 'isit for diabetes. Ph#si!al e%a ination re'eals an obese wo an with a BP of 1J265B Hg and a pulse of ,5 bp .

Pertan#aan
3pa pengaruh engontrol te$anan darah pada pasien D< Berapa target te$anan darah pd pasien D< "bat antihipertensi #g ana #g dire$o endasi$an ut$ pasien tsb

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*E;3SF3N ISTI;3H BERIF>T

Pheo!hro o!#to a "rtostati$ hipotensi +hushing s#ndro e 3theros$lerosis Hirsutis e <orbiditas <ortalitas Infar$ io$ard Stro$e is$e ia Intrinsi! s# patho i eti! a!ti'it#

So e of the fa!tors in'ol'ed in the !ontrol of blood pressure

<e!hanis s b# whi!h !hroni! diureti! therap# a# lead to 'arious !o pli!ations