Primary Hypertension

HIPERTENSI ESENSIAL
(HIPERTENSI PRIMER)
OUTLINE

 PENDAHULUAN
 EPIDEMIOLOGI
 DEFINISI
 PATOGENESIS
 PATOFISIOLOGI HIPERTENSI - KERUSAKAN
ORGAN TARGET
PENDAHULUAN

Masalah hipertensi :

 Meningkatnya prevalensi Hipertensi

 Pasien Hipertensi : terapi (-) ; target (-)
 Komplikasi Hipertensi (HTN)
keberhasilan penanganan HTN tergantung
edukasi pasien & komunikasi thd kepatuhan
minum obat
OUTLINE

 PENDAHULUAN
 EPIDEMIOLOGI
 DEFINISI
 PATOGENESIS
 PATOFISIOLOGI HIPERTENSI - KERUSAKAN
ORGAN TARGET
 EPIDEMIOLOGI

 Peningkatan populasi usia lanjut  peningkatan Hipertensi

 >50% populasi usia >65 tahun (HTN sistolik dan/atau
diastolik)

 Pengendalian hipertensi tidak menunjukkan laju yang

meningkat kurva mendatar

 Pengendalian hipertensi hanya mencapai 34% dari seluruh

pasien hipertensi
Epidemiologi…

 Data hipertensi yang lengkap dari negara maju (15-

25% populasi dewasa)

 Indonesia? (6-15%)
 The National Health and Nutrition Examination
Survey (NHANES) tahun 1999-2000 :
- Insiden hipertensi pada orang dewasa : 29-31 % (
58 – 65 juta orang penderita Hipertensi di Amerika)
- Terjadi peningkatan 15 juta dari data NHANES
tahun 1988-1991
Kesenjangan antara jumlah penderita HTN dan kontrol
tekanan darah

80 73
68 70 Patient
70 Awareness
55 59
60 54
51 Treatment
Adults, %

50

40
31 34
29 27
30 Control

20
10
10

0
NHANES II NHANES III NHANES III 1999–2000*
1976–1980 1988–1991 1991–1994

*Computed by M. Wolz (unpublished data cited by Chobanian et al.)

Adapted from Chobanian AV, et al. JAMA. 2003;289:2560-2572.

8
OUTLINE

 PENDAHULUAN
 EPIDEMIOLOGI
 DEFINISI
 PATOGENESIS
 PATOFISIOLOGI HIPERTENSI - KERUSAKAN
ORGAN TARGET
DEFINISI

 Tekanan darah : refleksi kardiovaskular

 Tekanan darah sistolik : nilai curah jantung

dpt berubah dalam waktu singkat (aktifitas fisik ringan, emosi)

Tekanan darah diastolik : refleksi resistensi perifer

sukar dipengaruhi faktor emosi, aktifitas fisik ringan

 HIPERTENSI : kondisi abnormal hemodinamik

( fungsi pengaturan / kontrol )
batasan hipertensi dipakai kriteria tek. drh sistolik dan/atau
tek.drh diastolik
 DEFINISI
 Tekanan nadi (pulse pressure/PP) = TD sistolik – TD
diastolik

 Tekanan arteri rata-rata (mean arterial pressure/MAP) =

(TD sistolik + 2xTD diastolik)/3

11 | Presentation Title | Presenter Name | Date

Definisi…

HIPERTENSI

• ESSENSIAL (PRIMER ) : 90-95%

• SECONDARY : 5-10%
Definisi…

 HIPERTENSI ESENSIAL (HIPERTENSI PRIMER) :

hipertensi yang tidak diketahui penyebabnya

 HIPERTENSI SEKUNDER :
hipertensi yang diketahui penyebabnya (hipertensi
karena sebab-sebab yang diketahui)
Definisi…
SECONDARY HYPERTENSION
HIPERTENSI SEKUNDER
AND
(SECONDARY HYPERTENSION)
IDENTIFIABLE CAUSE OF HYPERTENSIO
/

HIPERTENSI KARENA SEBAB-

SEBAB YG DIKETAHUI
N
(IDENTIFIABLE CAUSE OF
HYPERTENSION)
Hipertensi Sekunder
 Sleep apnea
 Drug-induced or related causes
 Chronic kidney disease
 Primary aldosteronism
 Renovascular disease
 Chronic steroid therapy and Cushing’s syndrome
 Pheochromocytoma
 Coarctation of the aorta
 Thyroid or parathyroid disease

JNC 7 Express. JAMA. 2003 Sep 10; 290(10):1314

KLASIFIKASI HIPERTENSI

 Klasifikasi Hipertensi pada orang dewasa :

JNC 7 (The Seventh Report of The Joint National
Committee on Prevention Detection, Evaluation, and
Treatment of High Blood Pressure)

WHO (World Health Organization) ; ISH (International

Society of Hypertension); ESH (European Society of
Hypertension); BSH (British Hypertension Society); CHEP
(Canadian Hypertension Education Program)
 KLASIFIKASI HIPERTENSI JNC 7 – 2003
Dewasa usia > 18 tahun

Blood Pressure (mm Hg) Category

Systolic Diastolic

<120 and <80 Normal

120-139 or 80-89 Prehypertension

140-159 or 90-99 Stage 1 hypertension

≥160 or ≥100 Stage 2 hypertension

Isolated hypertension : usia >55 tahun  TDS ≥ 140 dan

TDD < 90 mmHg
Chobanian AV, et al. Hypertension 2003;42:1206-52
OUTLINE

 PENDAHULUAN
 EPIDEMIOLOGI
 DEFINISI
 PATOGENESIS
 PATOFISIOLOGI HIPERTENSI - KERUSAKAN
ORGAN TARGET
 HIPERTENSI :
The Disease Continuum

Early Paradigm

Natural History of CVD Progression

Elevated BP Target Organ Damage
More Recent Paradigm

Vascular Dysfunction Elevated BP Target Organ Damage

A Proposed Future Paradigm

Endothelial Vascular Elevated BP Target Organ

Dysfunction Dysfunction Damage Angina
? LVH Pectoris
Renal MI Stroke
Damage
 Patogenesis Hipertensi

MULTIFAKTORIAL

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25 | Presentation Title | Presenter Name | Date
 Arterial stiffness

Pulse picks up speed as it moves distally;

then wave reflected back at peak PVR
Proximal Aorta: Compliant (accepts SV with low SBP)
Femoral
Brach. stiffer
Radial

Energy distending
arterial tree in systole
returned in diastole
due to proximal aorta
elasticity
Endothelial dysfunction

27 | Presentation Title | Presenter Name | Date

Endothelial dysfunction

28 | Presentation Title | Presenter Name | Date

 PATOGENESIS

Hipertensi primer :

Penyakit multifaktorial yg timbul terutama karena interaksi

faktor2 risiko tertentu yaitu :

faktor risiko : diet dan asupan garam, stres, ras,

obesitas, merokok, genetis

sistim saraf simpatis : tonus simpatis dan variasi

diurnal

keseimbangan antara modulator vasodilatasi dan

vasokonstriksi pembuluh darah : endotel,
remodeling endotel, otot polos dan interstitium

pengaruh sistim otokrin setempat  sistem RAA

FAKTOR2 YANG BERPENGARUH PADA PENGENDALIAN TE
asupan Na jumlah stress perubahan obesitas faktor2 yg
berlebih nefron genetis berasal dari
Endotel

retensi permukaan Aktifitas Renin perubahan hiper-

Na ginjal filtrasi Berlebih Angiotensin membran sel insulinemia
Saraf simpatiis release

volumekonstriksi vena
cairan
konstriksi hipertrofi
Preload kontraktilitas
fungsional struktural

TEKANAN DARAH CURAH JANTUNG TAHANAN PERIFER

Hipertensi
= Peningkatan CJ
X Peningkatan TP
= dan/atau
autoregulation
Kaplan
 RENIN – ANGIOTENSIN – ALDOSTERON
SISTEM (RAAS)

RENIN

 Renin merupakan suatu substrat yg mengubah

angiotensinogen menjadi angiotensin I

 Sel juxtaglomerulus ginjal merupakan tempat pembentukan

primer sintesis renin, juga tempat penyimpanan dan
penglepasan renin

 Renin aktif disekresi atas respons 3 mekanisme regulasi :

1) mekanisme intra renal (reseptor vaskular, makula densa)
2) mekanisme simpatoadrenergik, 3)mekanisme humoral
ANGIOTENSINOGEN

 Adalah suatu protein yang dibentuk dari reaksi pemecahan

proteolitik angiotensins

 Pembentukan sistemik dan tisu angiotensinogen adalah

suatu kompleks multifaktorial melalui variasi molekul2

 Tekanan arteri tergantung konsentrasi sistemik dan tisu

angiotensinogen
ANGIOTENSIN CONVERTING ENZYME (ACE)

 Angiotensin Converting Enzyme (ACE) juga dikenal

sebagai kinanase II

 ACE merubah angiotensin I menjadi angiotensin II

(vasokonstriktor) dan inaktivasi bradikinin (vasodilatasi)

 ACE ditemukan pada sel endotel, terutama di paru, retina,

dan otak
ANGIOTENSIN II

 Menstimulasi produksi aldosteron

 Menstimulasi sekresi ADH dari kelenjar pituitary
 Merupakan vasokonstriktor sangat potent
 Menstimulasi rasa haus
 Menstimulasi penglepasan katekolamin melalui medula
adrenal

ANGIOTENSIN III

 Menstimulasi produksi aldosteron tanpa vasokonstriksi

INTERAKSI RAAS - HIPERTENSI

Renin-Angiotensin Sistem (RAS) atau Renin-Angiotensin-

Aldosteron Sistem (RAAS) adalah sistem hormon yang
mengatur tekanan darah jangka panjang dan volume
ekstraselular tubuh
AKTIVASI RAAS
Sistem diaktivasi jika terjadi volume darah berkurang atau
tekanan darah turun , misalnya kondisi perdarahan

 Jika perfusi juxtaglomerular aparatus ginjal menurun, maka

sel juxtaglomerus melepaskan enzim Renin

 Renin memecah suatu peptida inaktif yg disebut

Angiotensinogen, yang akan berubah menjadi Angiotensin
I

 Angiotensin I kemudian diubah menjadi Angiotensin II oleh

Angiotensin-converting enzyme (ACE), yang banyak
dijumpai di kapiler paru

 Angiotensin II adalah produk bioaktif utama renin-

angiotensin sistem. Angiotensin II berfungsi sebagai
hormon endokrin, otokrin/parakrin dan intrakrin.
 Peranan ANGIOTENSIN II – HIPERTENSI

 Angiotensin II merupakan vasokonstriktor poten 

konstriksi pembuluh darah  tekanan perifer meningkat 
tekanan darah

 Angiotensin II juga meningkatkan sekresi aldosteron 

reabsorbsi Na+
ALDOSTERON

 Suatu mineralokortikoid yg diproduksi di sel zona

glomerulosa dari korteks adrenal

 Meningkatkan reabsorbsi Na+ pada tubulus kolekting

kortikal dan sekresi K dan H
 Renin-Angiotensin-Aldosterone Sistem

 Asupan tinggi Na+  mensupresi sistem

 Penurunan tiba-tiba Na+ akan mengaktivasi RAS 
stimulasi aldosteron  retensi Na+ di ginjal

 Restriksi Na+ yang lama  meningkatkan sensitifitas

adrenal terhadap angiotensin (aldosteron)  sensitifitas
pembuluh darah menurun
 RAS and SNS both control of SBP

RAS = renin-angiotensin system; SNS = sympathetic nervous system;

HTN = hypertension; CHF = congestive heart failure; ESRD = end-stage renal
disease; CAD = coronary artery disease; LVH = left ventricular hypertrophy

Brooks DP, Ruffolo RR. J Hypertens 1999;17(Suppl 2):S27-S32

OUTLINE
 PENDAHULUAN
 EPIDEMIOLOGI
 DEFINISI
 PATOGENESIS
 PATOFISIOLOGI HIPERTENSI - KERUSAKAN ORGAN
TARGET
 HIPERTENSI DAN
KERUSAKAN ORGAN TARGET

Atherosclerosis* Stroke
Vasoconstriction
Vascular hypertrophy Hypertension
LV hypertrophy
HTN Fibrosis
DEATH
Remodeling Heart failure
Apoptosis MI
GFR
Proteinuria
Aldosterone release
Renal failure
Glomerular sclerosis
*preclinical data
LV = left ventricular; MI = myocardial infarction; GFR = glomerular filtration rate
Adapted from Willenheimer R et al Eur Heart J 1999;20(14):997-1008; Dahlöf B J Hum Hypertens 1995;9(suppl 5):S37-S44;
Daugherty A et al J Clin Invest 2000;105(11):1605-1612; Fyhrquist F et al J Hum Hypertens 1995;9(suppl 5):S19-S24;
Booz GW, Baker KM Heart Fail Rev 1998;3:125-130; Beers MH, Berkow R, eds. The Merck Manual. 17th ed.
Whitehouse Station, NJ: Merck Research Laboratories, 1999:1682-1704; Anderson S Exp Nephrol 1996;4(suppl 1):34-40;
Fogo AB Am J Kidney Dis 2000;35(2):179-188.
 Komplikasi Hipertensi

Eyes Brain Kerusakan Target Organ!!

retinopathy stroke

Kerusakan yang disebabkan

Heart oleh hipertensi tergantung :
ischemic heart disease
Kidneys
renal failure
left ventricular hypertrophy • Besarnya peningkatan
heart failure tekanan darah
• Lamanya kondisi tekanan
darah yang tidak
terdiagnosis dan tidak
Peripheral arterial disease
diobati
 HIPERTENSI – PENYAKIT KARDIOVASKULAR
Endothelial Dysfunction

Oxidative Stress & Inflammation

CV
Disease

Ross. N Engl J Med. 1999;340:115-126.

Ross. N Engl J Med. 1999;340:115-126.

KESIMPULAN

 Prevalensi hipertensi makin meningkat (15-25%), namun

pengendalian hipertensi hanya mencapai 34%

 Hipertensi esensial merupakan penyakit multifaktorial yang timbul

karena interaksi : faktor risiko, sistim saraf simpatis, keseimbangan
antara modulator vasodilatasi dan vasokonstriksi, pengaruh sistem
renin-angiotensin-aldosteron

 Disfungsi endotel dan vaskular menyebabkan hipertensi, yg

selanjutnya menyebabkan kerusakan target organ : jantung, otak,
penyakit ginjal kronis, penyakit arteri perifer, retinopati

 Pengobatan hipertensi di masa yg akan datang akan mengarah

pada pencegahan disfungsi endotel dan vaskular
 Blood pressure measurement

dr. Agus Sudomo, Sp.S(K)

Bagian Neurologi
FK-UNS/ RSUD Dr Moewardi
Surakarta
Pentingnya akurasi pengukuran TD
 Ketidakakuratan pengukuran TD dapat menimbulkan
masalah  perbedaan 5 mmHg membawa akibat yang
besar

 Overestimasi orang dengan prehipertensi  hipertensi

 Underestimasi orang dengan hipertensi  normotensi/
klasifikasi HTN yang berbeda

Perlu diketahui faktor-faktor yang mempengaruhi

akurasi pengukuran TD
 Only an observer who is aware of the
factors that lead to false readings should
measure blood pressure !!!!
Critical issues
 Choice of the blood pressure measuring device
 Posture of the subject and arm during the measurement
 Selection of correct cuff size
 Standardization of the measurement protocol
1.Consider patient factors:
No caffeine in the preceding hour.
No smoking or nicotine in the preceding 15-30
minutes.
No use of substances containing adrenergic
stimulants such as phenylephrine or
pseudoephedrine (may be present in nasal
decongestants or ophthalmic drops).
Bowel and bladder comfortable.
Quiet, warm environment.
No tight fitting clothing on arm or forearm.
No acute anxiety, stress, or pain.
2. The patient/client should be calmly seated for at
least 5 minutes, with his or her back well
supported and arm supported at the level of the
heart. His or her feet should touch the floor and
legs should not be crossed.
3. Explain the procedure to the patient/client and
instruct him/her not to talk prior to and during the
procedure.
4. Choose the appropriate cuff size. If the cuff is too
small → BP high; too big → BP low.
5. Palpate the brachial artery. Position the cuff at the
level of the heart by centering the bladder over
the brachial artery. Wrap the cuff snugly around
the arm so that the edge of the cuff is 3 cm/1-1½”
(2 finger widths) above the antecubital fossa
(crease of the elbow). The patient/client’s arm
should be relaxed and therefore must be
supported either on a hard surface such as a
table or by the person carrying out the procedure.

6. Ensure the sphygmomanometer is at eye level.

7. Determine the level of maximal inflation to exclude the
possibility of an auscultatory gap:
 Palpate the radial pulse.
 Quickly inflate the cuff until the radial pulse is no longer
palpable. Note this pressure on the sphygmomanometer
and add an additional 30 mmHg. This is the maximal
inflation level.
 Rapidly deflate the cuff.
 Wait 30-60 seconds before reinflating the cuff.

8. Place the diaphragm of the stethoscope gently over the

brachial artery. The ear tips should be directed down and
forward.
9. Rapidly and steadily inflate the cuff to the maximal
inflation level (30 mmHg above the point where the radial
pulse disappeared).

10.Release the air in the cuff so that the pressure falls at a

steady rate of 2 mmHg per beat

11.Do not reinflate the cuff once the air is being released to
recheck either the systolic or diastolic pressure. Wait 30 -
60 seconds then repeat the procedure from step 10.

12.Note the systolic pressure at the onset of two (2)

consecutive beats and diastolic pressure at the point
which sounds disappear. Read the pressure to the closest
2 mmHg mark on the manometer.
13. Listen for at least 10-20 mmHg below the last
sound to ensure that sound has completely
disappeared, and then deflate the cuff rapidly.

15. If sound continues until 0 mmHg, record when

the sound muffles (Phase IV) to indicate diastolic
pressure.

16. If sounds are difficult to hear, reposition the arm

and relocate the brachial artery by palpation.
Repeat steps 9-14.
16. Record systolic/diastolic pressure as well as
patient/client’s position, cuff size, arm used for
measurement. Note any auscultatory gap, or
irregular pulse. If sounds are heard close to zero,
record both Phases IV and V.

17. Repeat the procedure on the opposite arm.

18. Repeat the procedure in 1-2 minutes on the arm

that had the highest reading.
 American Heart Association Guidelines for In-Clinic Blood
Pressure Measurement
Recommendation
Patient should be seated
comfortably, with back
supported, legs uncrossed, and
upper arm bared.
Patient’s arm should be
supported at heart level.
Cuff bladder should encircle 80
percent or more of the patient’s
arm circumference.
Comments
Diastolic pressure is higher in the seated position,
whereas systolic pressure is higher in the supine
position.An unsupported back may increase
diastolic pressure; crossing the legs may
increase systolic pressure.
If the upper arm is below the level of the right
atrium, the readings will be too high; if the upper
arm is above heart level, the readings will be too
low.If the arm is unsupported and held up by the
patient, pressure will be higher.
An undersized cuff increases errors in
measurement.
 Recommendation Comments
Mercury column should be deflated Deflation rates greater than 2 mm per
at 2 to3 mm per second. second can cause the systolic pressure to
appear lower and the diastolic pressure to
appear higher.

The first and last audible sounds

should be recorded as systolic and
diastolic pressure, respectively.
Measurements should be given to
the nearest 2 mm Hg.

Neither the patient nor the person Talking during the procedure may cause
taking the measurement should talk deviations in the measurement.
during the procedure.

Information from Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, et al.; Subcommittee of Professional and Public Education
of the American Heart Association Council on High Blood Pressure Research. Recommendations for blood pressure measurement in
humans and experimental animals. Part 1: blood pressure measurement in humans. Hypertension 2005;45:142–61.
Recommended Cuff Sizes for Accurate Measurement of
Blood Pressure

Patient Recommended cuff size

Adults (by arm circumference)
22 to 26 cm 12 x 22 cm (small adult)
27 to 34 cm 16 x 30 cm (adult)
35 to 44 cm 16 x 36 cm (large adult)
45 to 52 cm 16 x 42 cm (adult thigh)
Children (by age)*
Newborns and premature infants 4 x 8 cm
Infants 6 x 12 cm
Older children 9 x 18 cm

*—A standard adult cuff, large adult cuff, and thigh cuff should be
available for use in measuring a child’s leg blood pressure and for
children with larger arms
Criteria of measurement in different methods
Systolic BP Diastolic BP
mmHg mmHg
Clinic BP 140 90

Home BP 135 85

Ambulatory BP
24 hour 130 80
Day 135 85
Night 120 70
Japan Society of Hypertension 2009
 Ambulatory Blood Pressure Monitoring - ABPM

1. 24 hour B.P monitoring (every 15 minutes)

2. Today - 24 hour B.P. control is essential
3. Identifies dippers and non-dippers
4. Excludes white coat hypertension

69
Stage 2 hypertensive dipper
Hypertensive Non-Dipper
TERIMA KASIH