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Prof.Dr.dr.

Zainal
Musthafa
MSi. FS. SPjP. FIHA.
FAsCC

HIPERTEN
SI
Departemen Jantung
FK-UPN Veteran
JAKARTA . 2014

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 interval 2 menit

Mechanisms Responsible for Blood


Pressure Variability

Cathepsin
Tonin

chymase

Aldosterone

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AD-0445-07-BM06.ppt

EP
ACE2

Rationale for dual RAS blockade with an ACE


inhibitor and ARB
Bradykinin/NO

Angiotensin I
ACE-independent
ANG II formation
by Chymase, etc.

ACE
Inhibitor
Inactive fragments
Vasodilation
Tissue protection

Angiotensin II

Angiotensin II escape
Bradykinin?

ARB

AT1 RECEPTOR
Vasoconstriction
Sodium retention
SNS activation
Inflammation
Growth-promoting effects
Aldosterone
Apoptosis

NO?
AT2 RECEPTOR
Vasodilation
Natriuresis
Tissue regeneration
Inhibition of inappropriate cell growth
Differentiation
Anti-inflammation
Apoptosis

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


AT = angiotensin; SNS = sympathetic nervous system
Hanon S, et al. J Renin Angiotensin Aldosterone Syst 2000;1:147150; Chen R, et al. Hypertension
2003;42:542547; Hurairah H, et al. Int J Clin Pract 2004;58:173183; Steckelings UM, et al. Peptides
2005;26:14011409

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Hypertension Treatments
Rules of Halves

Hypertension

50 % not diagnosed

50 % Diagnosis

50 % not treated

50 % Treated

50 %
7 million pts poorly controlled
Hypertension in practice 2nd, Beevers & MacGregor

50 % well treated
(12.5 % of all
hypertensives)

al :
Ensefalopathy,
Stroke emboli / infark, Stroke
perdarahan,
Cidera kepala,
Tumor,
Penyakit jantung / SKA /
Deseksi Aorta,
Edema paru,
Penyakit Ginjal,
Peningkatan katekolamin,
Peri operatif,

HIPERTENSI
PULMONAL
Resistensi meningkat A. Pulmonalis
Gagal Jantung Kanan
Kematian mendadak

Proses Seluler
HPA

Disfungsi Endothel
Keseimbangan bioaktif al :
Nitrous Oxide (NO)
Prostasiklin
Thromboxan A2
Endothelium 1

KLASIFIKASI HPA
1. Idiopatik
2. Familial
3. Berhubungan dengan

Penyakit Jaringan
PJB
Hipertensi Portal
Pengaruh obat / Toxin
Lain-lain

KLASIFIKASI HPA -------2

4. HPA akibat penyakit Jantung Kiri

Gangguan fungsi Atrium / ventrikel kiri


Gangguan katup jantung kiri

5. HPA akibat penyakit Paru / Hipoksia

PPOM
Penyakit paru intrestitial
Gangguan tidur
Hipoventilasi alveoli
Ketinggian
Kelainan pertumbuhan

KLASIFIKASI HPA -------3

6. HPA akibat thrombo emboli

Emboli pulmonal
Emboli non thrombos (tumor,parasit,benda
asing)

7. Lain lain

PATOGENESIS HPA
Multifaktorial, a.l. :
vaso kontraksi
remodelling
obstruksi pbdr
inflamasi dan thrombosis

DETEKSI HPA
GANGGUAN
sesak tanpa kelainan yang lain
cepat lelah
lemah
angina
syncope
distensi abdomen

EKG
Foto Thorax
Ekhokardiography
Angiography

KLASIFIKASI KLINIS
Test fungsi paru
AGD
CT
Angiography

PENETUAN TYPE
LAB. DARAH / IMUNOLOGI
USG ABDOMEN
TREADMILL TES
AGIOGRAPHY
BIOPSY

Dx HPA
Ditegakkan

m PAP > 25 mmHg saat tes


PWP 15 mmHg
PWR > 3

TATALAKSANA
UMUM
batasi aktifitas
hindari ketinggian
cegah inflasi
cegah anemia / Hb
obat-obatan /

Obat
ANTI KOAGULAN
DIURETIK
OKSIGENASI
INOTROPIK
CCB / VASODILATASI
VASO DILATASI
DLL

INTERVENSI
BALON
TRANSPLANTASI

Isolated Systolic
Hypertension (ISH)
Tekanan sistolik > 140 mmHg dan
tekanan diastolik < 90 mmHg 1)
Framingham study: 57.4% pria dan
65.1% wanita menderita ISH 2)
18% populasi usia > 65 tahun termasuk
ISH borderline (sistolik 140-159 mmHg,
diastolik > 90 mmHg) 2)
1). 1999 WHO - International Society of Hypertension Guidelines for the Management of Hypertension
2). Kaplan N.M., Isolated Systolic Hypertension in Difficult Hypertension: P
ractical Management and Decision Making, Martin Dunitz Ltd, 1995

I ni ti al A ssessm ent a nd M an agem ent

elderly

Causes of secondary hypertension in the elderly


Drugs

Corticosteroid
Estrogen replacement
Non-steroidal anti-inflammatory
Alcohol
Ergotamine
Antihistamine/sympathomimetic decongestants
Liguorice

Renal

Renal artery stenosis


Pyelonephritis
Glomerulonephritis
Obstructive neuropathy
Analgesic nephropathy
Polycystic kidney disease
Connective tissue disease

Endocrine

Conn's syndrome
Cushing's syndrome
Pheochromocytoma
Acromegaly
Hyperparathyroidism

Neurological Spinal cord disease


Raised intracranial pressure
Other

Coarction of the aorta


Psedohypertension

Hypertension
in Pregnancy

BLOOD PRESSURE

Classification

Gestational hypertension
Preeclampsia-eclampsia
Chronic hypertension
Preeclampsia superimposed
upon chronic hypertension

Gestational Hypertension
Elevated BP first detected
after 20 weeks of gestation
without proteinuria
= transient hypertension

BP N

Proteinuria
()

Gestational
Hypertension
BP

20th week
of pregnancy

BP N

Proteinuria 12 weeks
()
postpartum

Preeclampsia
The syndrome of new onset of
hypertension & proteinuria after
20 weeks of gestation in a
previously normotensive woman
Preeclampsia Eclampsia

BP N

Proteinuria
()

BP

20th week
of pregnancy

BP N/

Proteinuria 12 weeks
(+)
postpartum

Chronic Hypertension
SBP > 140 mmHg and / or DBP > 90
mmHg that antedates pregnancy, is
present before the 20th week of
pregnancy, and persists longer than
12 weeks postpartum
Chronic Hypertension
BP

BP

Proteinur 20th week Proteinur


ia
ia
of pregnancy
()
()

BP

delivery

BP

12 weeks
postpartum

Superimposed Preeclampsia
Worsening HT w/ new onset
proteinuria in a woman w/
chronic HT
Superimposed preeclampsia upon
Underlying HT
BP
Proteinuria
()

BP

20th week Proteinuria


(+)
of pregnancy

BP
12 weeks Proteinuria
postpartum ( - )/(+)

Pathomechanism
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.

Endothelial cell dysfunction


appears to be the central
pathomechanism in the
pathogenesis of

FIGURE 1. Abnormal placentation in preeclampsia


In normal placental development, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries,
transforming them from small-caliber resistance vessels to high-caliber capacitance vessels capable of providing
placental perfusion adequate to sustain the growing fetus. During the process of vascular invasion, the
cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as
pseudovasculogenesis or vascular mimicry (left). In preeclampsia, cytotrophoblasts fail to adopt an invasive
endothelial phenotype. Instead, invasion of the spiral arteries is shallow, and they remain small caliber, resistance
vessels (right).
Maynard S,,Annu. Rev. Med. 2008. 59:6178

HYPERTENSION

Uteroplacental
insufficiency

Vascular
dysfunction

Kidney

Proteinuria

Deficient
vascular
remodeling

Activation
of decidual
RAS

sFLT1
s EnG

Placental hypoxia

Elevated
subpressor
Ang II
Vascular
maladaptation

Figure 4 : Decidual RAS activation and the placental release of antiangiogenic factors may
explain the manifestations of human preeclampsia
Current Opinion in Nephrology and Hypertension 2007, 16:213220

Assessing CVD risk: the effect of high blood pressure


Blood Pressure (mmHg)
Other risk factors* and
disease history

Normal
SBP 120129
or DBP 8084

High Normal
SBP 130139
or DBP 8589

Grade 1
SBP 140159
or DBP 9099

Grade 2
SBP 160179
or DBP 100109

Grade 3
SBP >180
or DBP >110

No other risk factors

Average risk

Average risk

Low added risk

Moderate added
risk

High added
risk

12 risk factors

Low added risk

Low added risk

Moderate added
risk

Moderate added
risk

Very high
added risk

>3 risk factors,


metabolic syndrome,
target organ damage or
diabetes

Moderate added
risk

High added
risk

High added
risk

High added
risk

Very high
added risk

Associated clinical
conditions

High added
risk

Very high added


risk

Very high added


risk

Very high added


risk

Very high
added risk

Approximate absolute risk in patients over 60 years of age


1015%

1520%

2030%

30%

Cardiovascular event rate in 10 years

<4%

45%

58%

>8%

Risk of cardiovascular death in 10 years (SCORE)

*90
Includes smoking, abdominal obesity and age
CVD = cardiovascular disease; SBP = systolic blood pressure; DBP = diastolic blood pressure
Guidelines Committee. J Hypertens 2003;21:10111053; J Hypertens 2007;21:11051187

The BHS recommendations for combining


blood pressure-lowering drugs
55 years or black
patients at any age

< 55 years
aaaaaaaaaa
Step 1

Step 2

Step 3

Step 4

C or D
A

or

Add: further diuretic therapy or alpha-blocker or beta-blocker


Consider seeking specialist advice

A: ACE inhibitor or ARB, if ACE inhibitor intolerant C:


Calcium-channel blocker
D: Diuretic (thiazide)
BHS, British Hypertension Society; ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker

2006 update

National Collaborating Centre for Chronic Conditions. Hypertension: management in


adults in primary care: partial update. London: Royal College of Physicians, 2006

Questions?

TERIMA KASIH

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