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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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-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,&'%a -
,&'%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,&'%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
4pseudo*asculo(enesis5 or 4*ascular mimicry5 (left). In preeclampsia, cytotrophoblasts fail to adopt an invasive
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