HIPERTENSI

=
TEKANAN DARAH
TINGGI
Dr.B Rudy Utantio, Sp.JP
SMF Jantung RSUD Sidoarjo
10/08/16

PERUBAHAN POLA MAKAN

Kadar

lemak tinggi, protein tinggi, garam tinggi

dan kandungan serat pangan (dietery fiber)
yang rendah menyebabkan penyakit
degeneratif yang meningkat :

- penyakit jantung

- diabetes mellitus

- kanker

- osteoporosis

- hipertensi
10/08/16

PREVALENSI HIPERTENSI

Di Dunia : 5-18%
Di Indonesia :
Hasil SKRT (1995) 83/1000 anggota RT:
* Perempuan > pria
* Di luar Jawa & Bali prevalensinya >
Ungaran : 1.8%
Silungkang : 19.4 %
Lembah Balim : 0,6 %
10/08/16

HIPERTENSI ~ TEKANAN DARAH TINGGI

Masih merupakan masalah kesehatan
Silent Killer
Pembunuh terselubung !!!!
* Tidak ada keluhan
* Tidak memberikan gejala
- stroke
- penyakit jantung
koroner
- gagal ginjal, dll
10/08/16

Fenomena gunung es

The Cardiovascular Continuum of Events

ACS

Secondary
prevention

Coronary
Thrombosis

Stroke

Myocardial
Ischemia

CAD
Atherosclerosis
Primary
prevention

Risk Factors
( Dyslipidemia,
Dyslipidemia BP, DM,
Insulin Resistance, Platelets,
10/08/16
Fibrinogen, etc)

Arrhythmia and
Loss of Muscle
Remodeling

Ventricular
Dilatation
Congestive
Heart Failure
End-stage
Heart Disease
Adapted from
5
Dzau et al. Am Heart J. 1991;121:1244-1263

Hukum 50% kelompok penderita

hipertensi
Tahu punya HTN
Sudah minum obat
Tidak kontrol

Tahu punya HTN

Tidak minum obat
Tidak kontrol

25%

12.5%
12.5%

Tidak tahu
Tidak terdiagnosa

50%

Tahu punya HTN

Tetap minum obat
Kontrol teratur

10/08/16
Source : Joffres et
al. (1997) Am. J. Hypertension 10: 1097-1102

APAKAH TEKANAN DARAH ?

Tekanan dari jantung memompa darah

mengalir ke seluruh pembuluh darah (+ oksigen )
mempertahankan kehidupan
Ada 2 komponen : jantung & pembuluh darah
Jantung : Pompa bekerja non stop
Pembuluh darah : Saluran untuk aliran darah
Mengukur tekanan darah mengukur kekuatan
darah pada saat menekan dinding pemb. darah
10/08/16

A Muscular Pump

10/08/16

Dr.RIVA ROCCI
Menemukan
Sphygmomanometer
[alat pengukur
tekanan darah]
sejak ditemukannya
SPHYGMOMANOMETER
diagnosa hipertensi
dapat ditentukan secara
klinis
Dr. GOLDBLATT
Meneliti
hormon Renin
10/08/16

1890S Renin was identified fro

Extracts of rabbit renal cortex
STOCKHOLM

Robert Tigerstedt
9

SPIGMOMANOMETER
TENSI METER

10/08/16

Tekanan darah sistolik :

* Nilai atas
* Tekanan pada saat
jantung memompa
Tekanan darah diastolik :
* Nilai bawah
* Tekanan pada saat
jantung istirahat

10

TERMINOLOGI
1. Hipertensi Esensial
= HT. Primer
= HT. Idiopatik
Kausa ?
95%
2. Hipertensi Sekunder
+ 5%
Kausa
3. Penyakit Jantung Hipertensi
= Hypertensive Heart Disease ( HHD )
HT + Hipertrofi Ventrikel Kiri ( L.V.H )
10/08/16

11

4. Hypertensive Heart Failure = H.H.F

HT + Decompensatio cordis
5. Hipertensi Labil
Tekanan darah kadang-kadang
6. Krisis Hipertensi : peningkatan TD mendadak (180/120)
* HT. Gawat : kerusakan organ target yang progresif
* HT Darurat : tidak disertai kerusakan organ target
7. White Coat Hypertension
= Stress Hypertension
= Office Hypertension
= Responsive Hypertension
8. Hipertensi Sistolik
TDS 140 mmHg
9. Hipertensi Diastolik
TDD 9010/08/16
mmHg

12

WHITE COATHYPERTENSION
= Stress Hypertension
= Office Hypertension
= Responsive Hypertension
20 %
- TD di Klinik
- Pemeriksaan TD di rumah
- Pemeriksaan TD 24 jam
(ABPM = Ambulatory BP Monitoring)
= ~ Pre Hipertensi !!
( T = 120/80 139/89)
10/08/16

13

MENGAPA T.D TINGGI ??

PATOFISIOLOGI HIPERTENSI
MEKANISME HIPERTENSI
Tidak dapat dijelaskan dengan satu penyebab spesifik
HT Essensial :
Akibat Interaksi Dinamis :
- faktor genetik
- faktor lingkungan
- faktor lain
RUMUS TD = C.O X TAHANAN PERIFER
10/08/16

14

CARDIAC OUTPUT = CO
= Curah Jantung
= Darah yang dipompa oleh jantung
= HR x SV
TD = HR x SV x Periferal resistance

TAHANAN PERIFER
* Ditentukan oleh diameter pembuluh darah
arteri
10/08/16

15

FAKTOR LAIN :
Retensi sodium
Turunnya filtrasi ginjal
Me saraf simpatis
Me aktifitas RAA
Perubahan membran sel
Hiperinsulinemia
Disfungsi endotel

10/08/16

16

obes
ity

PATHOPHYSIOLOGY

(reduced
nephron number)

10/08/16

17

Peningkatan asupan sodium

Volume cairan meningkat (retensi
cairan )

preload meningkat

stroke volume meningkat

Hipertensi

10/08/16

18

Penurunan filtrasi ginjal

Retensi sodium di ginjal

Volume cairan meningkat

Preload meningkat

Stroke volume meningkat

Hipertensi

10/08/16

19

SYMPATHETIC SYSTEM BLOOD

PRESSURE REGULATION

10/08/16

20

Peningkatan Aktivitas Sistem

Renin Angiotensin Aldosteron
(RAA)

10/08/16

21

RAAS

10/08/16

22

Renin-Angiotensin Cascade
Angiotensinogen
Non-renin
(e.g. tPA)

Renin
Bradykinin

Angiotensin I
Non-ACE
(e.g. chymase)

ACE

Angiotensin II
AT1
10/08/16

AT2

ATn

Inactive
peptides
23

Peran Ang II sebagai penyebab

terjadinya HTN
Angiotensin II receptor-mediated effects that increase blood pressure
Angiotensin II

AT1-receptors

Direct vasoconstriction.
Peripheral sympathetic
activity.
CNS sympathetic
activity.
Adrenaline and
noradrenalin release

Vasoconstriction

10/08/16

Sodium reabsorption.
Aldosterone release.

Smooth muscle cell

proliferation

Renal blood flow

Blood volume

Blood pressure

Cardiac and vascular

remodelling

24

Increased RA Activity

Renin : role factor for the most

pathogenensis of HTN via
RAAS

Essential (Primary) HTN :

- High renin HTN
: 20 %
- Low renin HTN
: 30 %
- Moderate renin HTN : 50 %
10/08/16

25

Vascular sequelae of high renin

essential HTN
(Organ target of HTN)

Stroke
Heart attack
Renal damage
Retinopathy
Encephalopathy
Epistaxis
10/08/16

26

Essential Hypertension
The renin-angiotensin-aldosterone system

Liver
Kidney
Angiotensinogen

Renin
Bradykinin
ACE inhibitors

Angiotensin I
ACE inhibitors

ACE
Inactive kinins

Angiotensin II

Angiotensin II
Receptor blockers

Angiotensin II
Receptor blockers
Retention of salt
and water

10/08/16

AT1 receptor
(vasoconstriction)

Blood pressure increases

27

Vascular membrane cell alteration

Membrane ion transport abnormalities

Decreased Ca2 + - ATPase activity

Decreased activity of the Na + / K + ATPase leading to increased intracellular
Na + concentration

Intracellular milleu changes

Growth (hypertrophy) and contraction
of peripheral arteries
10/08/16

28

Endothelial Dysfunction

Reduced renal nitric oxide (NO)

synthesis (NO = primary endogen
vasodilator)
Hypertension

10/08/16

29

Obesity

Increased body mass index (BMI)

Increased total blood volume
Increased stroke volume
Increased cardiac output
Hypertension
Hyperinsulinemia-associated Obesity
HTN
10/08/16

30

DEFINISI HIPERTENSI
T.D.

Sistolik 140 mmHg dan atau

T.D. Diastolik 90 mmHg
Perubahan tekanan darah :
TDD : Selalu sama sepanjang waktu
TDS : - Sering berubah-ubah

10/08/16

31

PEMBAGIAN HIPERTENSI
( ETIOLOGI )
I.
II.

HT. Essensial / Primer ( 95 % )

HT. Sekunder ( 5 % )

10/08/16

32

HIPERTENSI ESSENTIAL

Hipertensi Primer
95 % dari semua HT
Etiologi tidak diketahui
Merupakan :
Complex Disease
Multifaceted Disease
Meliputi :
- Disfungsi sistim saraf simpatis
- Gangguan transport sodium
- Hiperaktivitas sistim RAA
- Defisiensi Renal Vasodilator Subtances
- Kelebihan hormon Mineralokortikoid
- Sodium Sensitivity
- Obesitas10/08/16

33

KAUSA HT SEKUNDER
Renal
* Polycystic Kidneys
* Renovascular Disease
B. Coarctatio Aortae
C. Endrocrine :
* Pheochromocytoma
* Cushings Syndrome
D. Pregnancy Induced HT (Pre/Eclampsia)
E. Drugs / Substances
A.

10/08/16

34

Classification of BP
JNC VI (1997)

JNC VII (2003)

Category

SBP

DBP

Category

SBP

DBP

Optimal

<120

<80

Normal

<120

<80

Normal

<130

<85

Prehypertension 120-139

130-139

85-89

High-normal
Hypertension

80-89

Treat >130/80 : DM, CRD

Hypertension

Stage 1

140-159

90-99

Stage 1

140-159

90-99

Stage 2

160-179

100-109

Stage 2

160

100

Stage 3

180

110

10/08/16

35

Blood Pressure Classification

( JNC VII 2003)
BP Classification SBP-mmHg
Normal
< 120 and < 80
Prehypertension 120-139 or
Stage 1 Hypertension 140-159
Stage 2 Hypertension 160 or

DBP-mmHg

80-89
or
90-99
100

Other classification from WHO-ISH 1999, BSH, ESC

Why JNC VII classification ??? stage I & II ???
10/08/16

36

PROSEDUR DIAGNOSIS
I.
II.
III.
IV.

Anamnesis
Pemeriksaan Fisik dan Evaluasi Klinik
Pemeriksaan Laboraturium
Pemeriksaan Lanjutan

10/08/16

37

I. ANAMNESIS

Tanpa keluhan
Sakit kepala bagian belakang
Berdebar, dada berat
Sukar konsentrasi
Sulit tidur
Riwayat penyakit dahulu
- HT + obat ?
- Kehamilan ? DM ?
- Penyakit ginjal
Faktor resiko HT
- Merokok
- Makanan asin
- Stress
10/08/16
- Obat Kontrasepsi

38

II. Pemeriksaan Fisik dan Evaluasi Klinik

SPHYGMOMANOMETER

TIDAK

APAKAH TD 140/90

YA

HT
10/08/16

39

PENGUKURAN TEKANAN
DARAH DI PRAKTEK
ATAU DI KLINIK
1.Sebelum pengukuran penderita istirahat
beberapa menit diruangan yang tenang
2. Ukuran manset, lebar 12 13 cm, panjang 35
cm (dewasa)
3. Diperiksa pada fosa kubiti dengan cuff setinggi
jantung (RAI IV)
4. TD diukur pada keadaan duduk atau terlentang
10/08/16

40

PENGUKURAN TEKANAN DARAH

5. Tekanan darah dinaikkan sampai 30 mmHg

di atas tekanan sistolik (palpasi), kemudian
diturunkan 2 mmHg / detik dan dimonitor
dengan stetoskop di atas a. brakhialis
6. Tekanan sistolik ialah tekanan pada saat
terdengar suara Korotkoff I, sedangkan
tekanan diastolik pada saat Korotkoff V
menghilang. Bila suara tetap terdengar,
dipakai patokan Korotkoff IV (muffling sound)

10/08/16

41

PENGUKURAN TEKANAN DARAH

7. Pada pengukuran pertama kali

dianjurkan pemeriksaan pada kedua
lengan, terutama bila terdapat
penyakit pembuluh darah perifer
8. Perlu pengukuran pada posisi
duduk / terlentang dan berdiri untuk
mengetahui ada tidaknya hipotensi
postural terutama pada orang tua,
diabetes mellitus dan keadaan lain
(pemberian penyekat alfa)
10/08/16

42

III. PEMERIKSAAN LABORATURIUM

1. FOTO THORAX
menilai bentuk dan ukuran jantung
2. Elektrokardiografi ( EKG )
menilai :
* Hipertrofi V.ki ( LVH)
* Abnormalitas Atrium ki
* Iskemia / infark miokard
3. Laboratorium
* DL / UL
* BUN / Kreatinin Serum
* Asam urat
* Gula Darah
* Profil Lipid
10/08/16
* Elektrolit
: NA, K

43

IV. PEMERIKSAAN LANJUTAN

OVERALL GUIDES FOR EVALUATION

DIAGNOSTIC PROCEDURE

Diagnosis

Initial

Additional

Chronic Kidney Disease

(CKD)

Urinalysis, BUN or Creatinine,

sonografy

Plasma Renin Assay ( PRA) ,

renal biopsy, IVP

Renovascular Disease

Bruit, PRA and renography

before and one hour after 50 mg
captopril

Arteriogram, renal vein resins

Coarctatio

Blood pressure in legs

Aortogram

Primary Aldosteronism

Plasma Pottasium; plasma

aldosterone; renin ratio

Urinary pottasium, plasma

aldosterone after saline infusion

Cushings syndrome

AM plasma cortisol after 1 mg

dexamethasone at bed time

Urinary cortisol after variable

doses of dexamethasone

Pheochromocytoma

Untuk Mencari penyebab

hipertensi
10/08/16
( HT sekunder )

Urinary metanephirine and

catechols; plasma catechols,
basal and after 0,3 mg clonidine

44

MANIFESTASI ORGAN TARGET

1. Cardiac
* CAD ( Coronary Artery Dis )
* LVH ( Left Ventr. Hypertrophy )
* Left Ventr. Dysfunction
* Cardiac Failure
2. Cerebrovascular
* Transient Ischaemic Attack (TIA)
* Stroke
3. Peripheral Vascular
* Intermitten Claudication
* Aneurysm
* Epistaxis
4. Renal
* S. Creatinin 1,5 mg/dl
* Proteinuria : 1+
5. Retinopathy10/08/16
:
* Papilledema / Exudates / Hemorhages

45

This left ventricle is very thickened (slightly over 2 cm in

thickness), but the rest of the heart is not greatly enlarged.
This is typical for hypertensive heart disease. The
hypertension creates a greater pressure load on the heart to
induce the hypertrophy.
10/08/16

46

The left ventricle is markedly thickened in this patient

with severe hypertension that was untreated for many
years. The myocardial fibers have undergone
hypertrophy.
10/08/16

47

Funduskopi
Untuk mencari adanya Retinopati HT.
( Keith Wagner I-IV )

10/08/16

48

10/08/16

49

10/08/16

50

TUJUAN PENGOBATAN HTN :

1.
2.

Menurunkan TD
Mencegah / melindungi organ otak,
jantung, mata dan ginjal / mengurangi
kerusakan organ target tsb.

10/08/16

51

Menurunkan komplikasi & mortalitas

Menurunkan tekanan darah

10/08/16

52

PENATALAKSANAAN
HIPERTENSI
INDIVIDUALIZED TREATMENT
Jika modifikasi gaya hidup tidak
menurunkan tekanan darah yang
diinginkan, terapi farmakologis
harus diberikan !
10/08/16

53

PENGELOLAAN HIPERTENSI
I.
II.

Non Farmakologik
Farmakologik = Obat

Terapi Non Farmakologik = Lifestyle Modifications

S
Stop Merokok
E
Exercise Teratur
H
Hindari stress ---- Kelola stress
A
Awasi minum alkohol / konsumsi garam
T
Turunkan berat badan
O.A. H : - Efek samping obat
- Kwalitas hidup
- Biaya
10/08/16

54

10/08/16

55

10/08/16

56

KAPLAN ( 1996 )
Pengobatan hipertensi adalah keseimbangan
antara :
Manfaat yang akan diterima
Resiko yang terjadi akibat ESO
Harga pengobatan yang harus dibayar

10/08/16

57

Guidelines for Initiation of AntiHypertensive Treatment

(Compendium of ESC Guidelines
07)
Thiazide diuretics
Beta-Blockers ( BB )
ACE inhibitor ( ACEI )
Calcium antagonists ( CCB )
Angiotensin II Receptor Blockers ( ARB )

Choice of antihypertensive drugs

ESC Guidelines10/08/16
Desk Reference 2007

58

Terapi Farmakologi
Medications
Diuretics- Thiazides (HCTZ), Loop (Furosemide), Potassiumsparing (Spironolactone)
Beta-Blockers- Atenolol, Nadolol, Propranolol, Bisoprolol, etc
ACE Inhibitors- Benezapril, Captopril, Cilizapril, etc
Ca+ Channel Blockers- Nifedipine, Verapamil, Diltiazem,
Amlodipin, etc
ARBs- Losartan, Valsartan, Candesartan, etc
10/08/16

59

Diuretik
Thiazide
Cara

kerja : meningkatkan ekskresi sodium &

cairan tubuh
Efek samping : hipokalemia, hiperurisemia
dan intoleransi glukosa
Kurang efektif pada disfungsi renal yang berat
Potassium

sparing diuretics

Aldosterone
10/08/16

antagonists : spironolakton
60

ACE (angiotensin converting

enzyme) Inhibitors

Cara kerja

Efek samping

Batuk
Rash
Angioneurotic edema
Taste disturbance
Hiperkalemia terutama pada gangguan fungsi renal

Sangat bermanfaat pada

Menghambat kerja enzim yang merubah angiotensin I ke angiotensin II

( vasoconstrictor)
Meningkatkan vasodilatasi
Menurunkan sekresi aldosterone

HT dengan CHF (Congestive Heart Failure), DM, CKD (Chr Kidney Dis)

Kontraindikasi

Pregnancy (kehamilan)
Bilateral renal artery stenosis
10/08/16

61

Angiotensin II Receptor Blockers

( ARB )
Cara

kerja

Menghambat

reseptor AT1, sehingga tahanan

perifer menurun

Efek

kerja sangat mirip dengan ACE

inhibitors tetapi tidak menyebabkan batuk

10/08/16

62

Beta Blockers
Menurunkan

TD dengan menurunkan cardiac

output dan menghambat sympathetically
mediated renin release dari ginjal
Kontraindikasi relatif
Asthma/COPD
Decompensated

CHF
Raynauds phenomenon
Peripheral vascular disease
Depression
Efek

samping

Kelelahan
Tangan

dan kaki terasa dingin

Impoten and disfungsi seksual
Dapat mengelabui terjadinya efek hipoglikemia pada
DM
10/08/16

63

Algorithm for Treatment of Hypertension

Lifestyle Modifications

Not at Goal Blood Pressure (<140/90 mmHg)

(<130/85 mmHg for those with diabetes or chronic kidney disease)

Stage 2 Hypertension
Initial Drug Choices

(SBP
>160 or DBP >100 mmHg)
Without Compelling
With Compelling
Indications
2-drug combination
for most (usuallyIndications
Stage 2 Hypertension
(SBP >160 or DBP >100diuretic
mmHg)
thiazide-type
and
Drug(s) for the compelling
Stage 1 Hypertension
Stage 2 Hypertension
2-drug combination for most
indications
(usually
thiazide-type
diuretic
and
ACEI, or
ARB, or BB, or CCB)
ACEI, or ARB, or BB, or CCB)

(SBP 140159 or DBP 9099

mmHg)
Thiazide-type diuretics for most.
May consider ACEI, ARB, BB, CCB,
or combination.

(SBP >160 or DBP >100 mmHg)

2-drug combination for most
(usually thiazide-type diuretic and
ACEI, or ARB, or BB, or CCB)

Other antihypertensive drugs

(diuretics, ACEI, ARB, BB, CCB)
as needed.

Not at Goal
Blood Pressure

10/08/16

Optimize dosages or add additional drugs

until goal blood pressure is achieved.
Consider consultation with hypertension
specialist.

64

JNC VI NEW BP
GOALS
<140/<90 and lower if
tolerated
<130/<85 in diabetics
(types 1 & 2 )
<130/<85 in cardiac
failure
<130/<85 in renal failure
<125/<75 in renal failure
with proteinuria > 1.0
gm/24 hr
10/08/16

WHO ISH NEW BP

GOALS
<140/90 In Elderly
< 130/85 in young,
middle-aged
<130/85 in diabetic

65

Adverse Effects of Commonly Used

Antihypertensive Agents
Diuretics

BBs

Muscle cramps
Impotence
Gout
Glucose Intolerance

Depression
Sleep disorders
Exercise Intolerance

Hypokalemia
Hyperuricemia
Hypomagnesemia
Hypercalcemia

Dysiplidemia
Glucose Intolerance
Impotence

10/08/16

CCBs
Edema
Flushing
Headache
Dizziness
GI disorders

ACEIs

ARBs

Cough
Hyperkalemia
Rash
Angioedema
Hyperkalemia ( rare )
Angioedema

Changes in heart
rate

66

ACE Inhibitor Side Effects

Cough

(15% of patients. Is reversible)

Taste disturbance (reversible)
Angiodema
First-dose hypotension
Hyperkalaemia ( esp. in patients with type
II diabetes and renal dysfunction)

10/08/16

67

HIPERTENSI SEKUNDER

10/08/16

68

Secondary HTN who to

evaluate?

Accounts

for <5% of all cases of elevated BP

Recent or sudden onset
Young people with no family history
Patients resistant to treatment
Uncontrolled

HTN on adequate doses of three

medicines one of which is a diuretic

Patients

who have

Physical

findings (abdominal bruits)

Biochemical abnormalities (unprovoked hypokalemia)
10/08/16

69

Most common causes of secondary

HTN
Renovascular

HTN
Catecholamine excess states
Mineralocorticoid excess states

10/08/16

70

Renal Angiogram

10/08/16

71

Renovascular HTN
Stenosis

of a renal artery increases renin

production from the ischemic kidney which
causes increased production of angiotensin II
(vasoconstrictor) and increased production of
aldosterone
Fibromuscular
Women

thickening of the arterial wall

younger than 40

Atherosclerotic
Older

Listen

plaque

people with risk factors for atherosclerosis

for an abdominal bruit

10/08/16

72

Endocrine Abnormalities
Hypokalemia

(low potassium) in the

absence of diuretic therapy may indicate a
state of mineralocorticoid excess
Excess aldosterone production (Conns)
Excess glucocorticoid production
(Cushings)
Hyperthyroidism
10/08/16

73

Cushings Syndrome
Hypercortisolism
Aetiologies
Iatrogenic

excess corticosteroid administration

ACTH hypersecretion by the pituitary
Bilateral adrenal hyperplasia
Signs/symptoms

hypertension, central obesity,

abdominal striae, buffalo hump, moon facies,
hirsuitism, easy bruising, hyperglycemia,
hypokalemia
Evaluation elevated free urinary cortisol, lowdose dexamethasone suppression test
Treatment resection +/- irradiation
10/08/16

74

Primary Hyperaldosteronism
Due

to excess aldosterone production

(Conns)
Usually due to an adrenal adenoma
Features include hypertension, hypokalemia
(tetany), polyuria, elevated urinary potassium,
elevated plasma/urine aldosterone, low
plasma renin
Treatment
Adrenalectomy

for Conns
Spironolactone for bilateral hyperplasia
10/08/16

75

Pheochromocytoma
Catecholamine

secreting neoplasms of the

adrenal glands (medulla) or extra-adrenal
chromaffin tissue
Headache, diaphoresis and tachycardia
Severe HTN with the induction of anesthesia
The diagnosis depends on the demonstration
of increased excretion of catecholamines or
their major metabolites in the urine
10/08/16

76

PROGNOSIS HIPERTENSI
Tergantung :
1. Stratifikasi Risiko Kardiovaskuler :
* Rendah
* Sedang
* Tinggi
* Sangat tinggi
2. Kerusakan organ target
3. Kondisi klinik yang berhubungan
4. Respon ke pengobatan
5. Kepatuhan penderita
10/08/16

77

Follow-up

For patients with BP stabilised by management, follow

up should normally be three monthly (interval should not
exceed 6 months), at which the following should be
assessed by a trained nurse:

*
*
*
*

Measurement of BP and weight

Reinforcement of non-pharmacological advice
General health and drug side-effects
Test urine for proteinuria (annually)

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Referral
A patient should be referred
to specialist when:
BP remains uncontrolled
after three concurrent
medications
Uncontrolled BP and signs
and symptoms of endorgan damage
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Hospitalization
Hospitalization should be considered if:
Very high BP
Severe headache
Chest pain
Neurologic symptoms
Altered mental status
Acutely worsening renal failure
S & S of hypertensive emergency
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Conclusion
Use

24 hour ambulatory BP monitors to

properly evaluate HTN
Treat very aggressively
Treat other cardiovascular risk factors
Watch for secondary causes of HTN

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TIGA PEDOMAN UNTUK

PENDERITA TEKANAN
DARAH TINGGI
1.

2.

3.

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Periksakan tekanan darah

secara teratur
Minum obat seperti yang
dianjurkan dokter
Patuhi dengan baik segala
nasehat dokter
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Thats all folks!

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Neurohormonal control of blood

Blood pressure = Cardiacpressure
output (CO) x Peripheral resistance (PR)
Hypertension =

Increased CO

Preload

and/or

Increased PR
Vasoconstriction

Contractility

Fluid volume

Renal sodium
retention
Excess
sodium
intake

Sympathetic
nervous
system

Reninangiotensinaldosterone
system

Genetic
factors
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(Adapted from Kaplan, 1994)

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Complications
Complications as a result of HTN include:
Stroke
Dementia
Myocardial Infarction
Congestive Heart Failure
Retinal Vasculopathy
Aortic Dissection
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Renal Disease
or Failure

90

Logical Combinations

Diuretic
-blocker

Diuretic
blocker

CCB

ACE inhibitor

CCB
-

*
-

*
-

ACE
inhibitor

-blocker

* Verapamil + beta-blocker = absolute contra-indication

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blocker

91