kuliah hipertensi upn. sabtu 15 nov 2014
TRANSCRIPT
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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,&'%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
endothelial phenotype. Instead1 in*asion of the spiral arteries is shallo31 and they remain small caliber1 resistance*essels 6right). :aynard S<<Ann!" Rev" :ed" .G" 9D)0/G
-7PERTEN&I!N
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%eficient
*ascular
remodelin(
Vascular
dysfunction
#teroplacental
insufficiency
Ele*ated
subpressor
An( II
Acti*ation
of decidual
RA&
Proteinuria
s.$T/ s En"
Vascular
maladaptation
Placental hypo8ia
idney
C!rrent *pinion in ephrology and 3ypertension .< 0).02/..
.i(ure 9 : %ecidual RA& acti*ation and the placental release of antian(io(enic factors may
e8plain the manifestations of human preeclampsia
Assessin( CV% ris+: the effect of hi(h blood pressure
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D
*ther risk (actorsH anddisease history
Normal
&BP /2;</2=
or %BP >;<>9
-i(h Normal
&BP /?;</?=
or %BP >@<>=
"rade /
&BP /9;</@=
or %BP =;<==
"rade 2
&BP /;</=
or %BP /;;</;=
"rade ?
&BP />;
or %BP //;
o other risk (actors Average risk Average risk 5oF added risk:oderate added
risk
3igh added
risk
0/. risk (actors 5oF added risk 5oF added risk:oderate added
risk
:oderate added
risk
ery high
added risk
@2 risk (actors<
metabolic syndrome<
target organ damage or
diabetes
:oderate added
risk
3igh added
risk
3igh added
risk
3igh added
risk
ery high
added risk
Associated clinical
conditions
3igh added
risk
ery high added
risk
ery high added
risk
ery high added
risk
ery high
added risk
C- &ardio/as&#lar disease; S% systoli& lood !ress#re; -% diastoli& lood !ress#re#idelines Co33ittee. J Hy!ertens 200";21:1011–105"; J Hy!ertens 2007;21:1105–11'7
Appro+imate absol!te risk in patients over years o( age
Blood #ress!re ,mm3g-
0/09 09/. ./2 2
7 7/9 9/G @G
Cardiovasc!lar event rate in 0 years
Risk o( cardiovasc!lar death in 0 years ,SC*RE-
* Includes smoking, abdominal obesity and age
The B-& recommendations for combinin(
blood pressure lo3erin( dru(s
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D @@ years
aaaaaaaaaa
@@ years or blac+
patients at any a(e
&tep /
&tep 2
&tep ?
&tep 9 Add: further diuretic therapy or alpha)bloc+er or beta)bloc+er Consider see+in( specialist ad*ice
A: ACE inhibitor or ARB1 if ACE inhibitor intolerant C:
Calcium)channel bloc+er %: %iuretic 6thiaideF
A
A C or %
or
GC %
National Collaborating Centre for Chronic Conditions. Hypertension: management inadults in primary care: partial update.London: Royal College of Physicians, 2006
blood pressure)lo3erin( dru(s
G
B3S< British 3ypertension Society; ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker
2;; update
A CG A %G
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8uestions9
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8
?
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