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Departemen JantungFK-UPN “Veteran”

 JAKARTA . 2014

Prof.Dr.dr. ZainalMusthafa

MSi. FS. SPjP. FIHA.FAsCC

HIPERTEN

SI

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Persiapan yang benar dan waktu cukup.

Peralatan yang baik dan sesuai.

Penderita dalam keadaan tenang (istirahat 5 menit)

Tidak minum kopi atau merokok 30 menit sebelumnya

Pemeriksa yang sehat pendengarannya

Mengetahui standar pengukuran tekanan darah

Pengukuran dilakukan 2 kali dengan interal 2 menit

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Mechanisms Responsible for Blood

Pressure Variability

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!2"!#"!5 0!$3!$05 PM %&'05'0#'M0*.ppt

EP

ACE2

Cathepsin

Tonin

chymase

 Aldosterone

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6

Bradykinin/NO

Inactive fragments

Angiotensin I

Angiotensin II

AT1 RECEPTOR  AT2 RECEPTOR 

Rationale for dual RAS blockade with an ACE

inhibitor and ARB

ARB

Vasoconstrictionodi!m retention

N activationInf"ammation

#ro$t%&'romoting effectsA"dosteroneA'o'tosis

ACEIn%i(itor

Vasodi"ationNatri!resis

Tiss!e regenerationIn%i(ition of ina''ro'riate ce"" gro$t%

)ifferentiationAnti&inf"ammation

A'o'tosis

Vasodi"ationTiss!e 'rotection

ACE&inde'endentAN# II formation(y C%ymase* etc+

,Angiotensin II esca'e-

Bradykinin.

NO.

 ACE = angiotensin converting enzyme; ARB = angiotensin II receptor blocker;

 AT = angiotensin; SS = sympathetic nervo!s system

Hanon S, et al. J Renin Angiotensin Aldosterone Syst 2000;1:147–150; Cen R, et al. Hy!ertension200";42:542–547; H#raira H, et al. $nt J Clin %ra&t 2004;5':17"–1'"; Ste&(elings )*, et al. %e!tides2005;26:1401–140+

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!2"!#"!5 0!$3!$05 PM %&'05'0#'M0*.ppt +

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!2"!#"!5 0!$3!$05 PM %&'05'0#'M0*.ppt ,

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-ypertension in practice 2nd eeers / Macregor 

Hypertension Treatments

Rules of Halves

7 million pts

Hypertension

50 % Diagnosis50 % not diagnosed

50 % Treated50 % not treated

50 % well treated(12.5 % of allypertensives!

50 %poorly "ontrolled

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al :Ensefalopathy,

Stroke emboli / infark, Strokeperdarahan,

Cidera kepala,Tumor,

Penyakit antun! / S"# /

$eseksi #orta,Edema paru,Penyakit %inal,

Penin!katan katekolamin,

Peri operatif,

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 Resistensi meningkat A" #!lmonalis

 $agal %ant!ng &anan

 &ematian mendadak

IPERTENSI

PULMONAL

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Proses Seluler

PA

 'is(!ngsi Endothel

 &eseimbangan bioakti( al ) itro!s *+ide ,*-

 #rostasiklin

 Thrombo+an A.  Endotheli!m / 0

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KLASIFIKASI PA

0" Idiopatik

." 1amilial

2" Berh!b!ngan dengan #enyakit %aringan

#%B

3ipertensi #ortal

#engar!h obat 4 To+in 5ain6lain

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KLASIFIKASI PA -------2

7" 3#A akibat penyakit %ant!ng &iri $angg!an (!ngsi Atri!m 4 ventrikel kiri $angg!an kat!p 8ant!ng kiri

9" 3#A akibat penyakit #ar! 4 3ipoksia ##*:

#enyakit par! intrestitial

$angg!an tid!r 

3ipoventilasi alveoli

&etinggian

&elainan pert!mb!han

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KLASIFIKASI PA -------3

" 3#A akibat thrombo emboli Emboli p!lmonal

Emboli non thrombos ,t!mor<parasit<benda

asing-" 5ain /lain

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PATOGENESIS PA

:!lti(aktorial< a"l" )

 vaso kontraksi

 remodelling obstr!ksi pbdr 

 in(lamasi dan thrombosis

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DETEKSI PA

 E&$

 1oto Thora+ Ekhokardiography

 Angiography

$A$$>A sesak tanpa kelainan yang lain

 cepat lelah

 lemah

 angina

 syncope distensi abdomen

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KLASIFIKASI KLINIS

 Test (!ngsi par!

 A$'

 CT Angiography

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PENETUAN TYPE

 5AB" 'ARA3 4 I:>*5*$I

 >S$ AB'*:E

 TREA':I55 TES A$I*$RA#3?

 BI*#S?

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Dx PA

Dite!""!#

 m #A# @ .9 mm3g saat tes

 ## ≤ 15 mmg

 P!R " #

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TATALAKSANA

UMUM

 batasi akti(itas

 hindari ketinggian cegah in(lasi

 cegah anemia 4 3b

 obat6obatan 4

 ANTI !A"#$AN

 %I#RETI

 !&I"ENA&I

 IN!TR!PI CCB ' VA&!%I$ATA&I

 VA&! %I$ATA&I

 %$$

!bat

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INTER$ENSI

 BA5*

 TRAS#5ATASI

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Isol!te% S&stoli'

H&(erte#sio# )ISH*• Tekanan sistolik @ 07 mm3g dan

tekanan diastolik D mm3g 0-

• 1ramingham st!dy) 9"7 pria dan9"0 Fanita menderita IS3 .-

• 0G pop!lasi !sia @ 9 tah!n termas!k

IS3 borderline ,sistolik 07609D mm3g<diastolik @ D mm3g- .-

!). !,,, 1- ' nternational 4ociety o -ypertension uidelines or the Management o -ypertension

2). 6aplan 7.M. Isolated Systolic Hypertension in Difficult Hypertension: P 

  ractical Management and Decision Making  Martin &unit8 9td !,,5

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$n%t%a& A''e''ment an( )anagement elderly 

Causes of secondary hypertension in the elderly

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%ru(s   Corticosteroid

Estro(en replacement

Non)steroidal anti)inflammatory

Alcohol

Er(otamine

Antihistamine'sympathomimetic decon(estants

$i(uorice

Renal   Renal artery stenosis

Pyelonephritis

"lomerulonephritis

!bstructi*e neuropathy

Anal(esic nephropathy

Polycystic +idney disease

Connecti*e tissue disease

Endocrine   Conn,s syndrome

Cushin(,s syndrome

Pheochromocytoma

Acrome(aly

-yperparathyroidism

Neurolo(ical   &pinal cord disease

Raised intracranial pressure

!ther    Coarction of the aorta

Psedohypertension

*perten'%+n

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*perten'%+n%n Pregnan,*

B$!!% PRE&&#RE

Classi&'ation

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Classi&'ation

• %estational hypertension

• Pree'lampsia(e'lampsia• Chroni' hypertension

• Pree'lampsia superimposed

upon 'hroni' hypertension

% t ti l H t i

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%estational Hypertension

• Ele)ated *P &rst dete'tedafter + -eeks of !estation

-ithout proteinuria. transient hypertension

e'tat%+na&

*perten'%+n

20th week

of pregnancy

Pr+te%nur%a /

Pr+te%nur%a /

+P N +P

12  weeks

postpartum

+P N

P l i

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Pree'lampsia

• The syndrome of ne- onset ofhypertension proteinuria after+ -eeks of !estation in apre)iously normotensi)e -oman

Pree,&amp'%a -

,&amp'%a

20th week

of pregnancy

Pr+te%nur%a /

Pr+te%nur%a

+P N +P

12  weeks

postpartum

+P N,

Chroni' Hypertension

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Chroni' Hypertension

• S*P 0 12 mmH! and / or $*P 0 3mmH! that antedates pre!nan'y, ispresent before the +th -eek of

pre!nan'y, and persists lon!er than1+ -eeks postpartum

3r+n%, *perten'%+n

Proteinuria

4 5 6

20th week

of pregnancy

Proteinuria

4 5 6

+P +P +P +P

12  weeks

postpartum

delivery

Superimposed Pree'lampsia

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Superimposed Pree'lampsia

• 7orsenin! HT -/ ne- onsetproteinuria in a -oman -/

'hroni' HT

20th week

of pregnancy

Pr+te%nur%a

/

Pr+te%nur%a

+P +P  

uper%mp+'e( pree,&amp'%a up+nUn(er&*%ng T

12  weeks

postpartum

Pr+te%nur%a

- 6

+P  

Pathome'hanism

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Pathome'hanism

Endothelial 'ell dysfun'tionappears to be the 'entralpathome'hanism in the

patho!enesis of

Functions of the endothelium

•  Regulate vascular permeability

• Regulate vascular cell growth

• Mediate inflammatory and

immune mechanism

• Modulate lipid oxidation

  ( metabolic activity )

Endothelial dysfunction

 An imbalance between relaxing and

contracting factors between

 anti -and pro-coagulant mediators

or growth-inhibiting and growth

promoting factors.

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.I"#RE /0 Abnormal placentation in preeclampsiaIn normal placental de*elopment1 in*asi*e cytotrophoblasts of fetal ori(in in*ade the maternal spiral arteries1

transformin( them from small)caliber resistance *essels to hi(h)caliber  capacitance *essels capable of pro*idin(

placental perfusion adeuate to sustain the (ro3in( fetus0 %urin( the process of *ascular in*asion1 the

cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype1 a process referred to as

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