kuliah hipertensi upn. sabtu 15 nov 2014

7/23/2019 Kuliah Hipertensi UPN. Sabtu 15 Nov 2014

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Departemen JantungFK-UPN “Veteran”

JAKARTA . 2014

Prof.Dr.dr. ZainalMusthafa

MSi. FS. SPjP. FIHA.FAsCC

HIPERTEN

SI



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



Mechanisms Responsible for Blood

Pressure Variability



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

EP

ACE2

Cathepsin

Tonin

chymase

Aldosterone



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+



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



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



-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



al :Ensefalopathy,

Stroke emboli / infark, Strokeperdarahan,

Cidera kepala,Tumor,

Penyakit antun! / S"# /

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

Penin!katan katekolamin,

Peri operatif,



Resistensi meningkat A" #!lmonalis

$agal %ant!ng &anan

&ematian mendadak

IPERTENSI

PULMONAL



Proses Seluler

PA

'is(!ngsi Endothel

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

#rostasiklin

Thrombo+an A. Endotheli!m / 0



KLASIFIKASI PA

0" Idiopatik

." 1amilial

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

#%B

3ipertensi #ortal

#engar!h obat 4 To+in 5ain6lain



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



KLASIFIKASI PA -------3

" 3#A akibat thrombo emboli Emboli p!lmonal

Emboli non thrombos ,t!mor<parasit<benda

asing-" 5ain /lain



PATOGENESIS PA

:!lti(aktorial< a"l" )

vaso kontraksi

remodelling obstr!ksi pbdr

in(lamasi dan thrombosis



DETEKSI PA

E&$

1oto Thora+ Ekhokardiography

Angiography

$A$$>A sesak tanpa kelainan yang lain

cepat lelah

lemah

angina

syncope distensi abdomen



KLASIFIKASI KLINIS

Test (!ngsi par!

A$'

CT Angiography



PENETUAN TYPE

5AB" 'ARA3 4 I:>*5*$I

>S$ AB'*:E

TREA':I55 TES A$I*$RA#3?

BI*#S?



Dx PA

Dite!""!#

m #A# @ .9 mm3g saat tes

## ≤ 15 mmg

P!R " #



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



INTER$ENSI

BA5*

TRAS#5ATASI



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



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

Causes of secondary hypertension in the elderly



%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



*perten'%+n%n Pregnan,*

B$!!% PRE&&#RE

Classi&'ation



Classi&'ation

• %estational hypertension

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

• Pree'lampsia superimposed

upon 'hroni' hypertension

% t ti l H t i



%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



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



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



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



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.



.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



%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



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



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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