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Essential

Hipertensi
&
Hipovolemic
Shock

Prevalensi Hipertensi
prevalence of hypertension (%)

70
60

SBP > 140 mm Hg


DBP > 90 mm Hg

50

64

65

70-79

80+

54
40

44

30

21

20
10

11

18-29

30-39

0
age (yrs)

40-49

50-59

60-69

Franklin, S.S., J Hypertens 1999; 17 (suppl 5): S29-S36

Prevalensi :
Berdasar kriteria Hipertensi WHO 1968 (tekanan darah >
160/95 mmHg), prevalensi hipertensi di dunia sekitar 5-18
%. Prevalensi hipertensi di Indonesia tidak jauh berbeda
yaitu sekitar 6-15 %, walaupun dilaporkan adanya
prevalensi yang rendah yaitu :
- Ungaran
1,8 %
- Lembah Balim
0,6 %
serta adanya prevalensi yang tinggi :
- Silungkang
19,4 %
- Talang
17,8 %
Prevalensi Hipertensi di Jawa Timur hampir sama yaitu :
- Sumberpucung
(1976)
10 %
- Lawang
(1987) 11 %
- Kampak
(1987) 17 %

New Criteria (WHO-ISH 1999) 140 / 90 mmHg


22 % of American adults 18 to 70 years of age have hypertension
20 % of Indonesian adults have hypertension
Hypertensive patients
who are treated
and controlled

Hypertensive patients
who are treated
but uncontrolled

16%
23%
19%

Patients who are aware


but remain untreated
and uncontrolled
Source : Joffres et al. (1997) Am. J. Hypertension 10: 1097-1102

42%

Hypertensive patients
who are unaware

Klasifikasi Hipertensi

(JNC 7 -

2003)

Category
Normal

Systolic
(mm Hg)

Diastolic
(mm Hg)

<120

dan

<80

Pre Hipertensi

120-139

atau

80-89

Hipertensi
Stage 1
Stage 2

140-159
> 160

atau
atau

90-99
>100

Hipertensi
Berdasarkan penyebabnya dapat dibedakan :

Primer (essential)
tidak ada penyebab yang spesifik yang
dapat diidentifikasi
90-95% dari kasus hipertensi

Sekunder
diketahui penyebabnya
5-10% dari kasus hipertensi
penyakit ginjal merupakan penyebab
tersering kasus hipertensi sekunder

Etiology Hypertension

Secondary Hypertension :
Renal disease :

Renal arterial disease


Renal parenchymal disease
Renal tumors
Arteritis (polyarteritis nodosa, neurofibromatosis)

Cushings syndrome
Acromegaly
Primary aldosteronism
Pheochromocytoma

Endocrine Disorders

Coarctation of the aorta


Neurologic disorders

Increased intra cranial pressure (tumor)

Drug-induced hypertension
Corticosteroids
Amphetamines
Oral contraceptives

Psychogenic disorders

Fisiologi

SV=EDV-ESV
CO=SV x HR
BP=CO x PR

PATOPHYSIOLOGY
The factors affecting cardiac output:
- sodium intake, renal function, &
mineralocorticoids
- the inotropic effects occur via extracellular
fluid volume augmentation
- an increase in heart rate and contractility
Peripheral vascular resistance is
dependent upon the sympathetic nervous system,
humoral factors, and local autoregulation
(Sharma, 2003)

Neurohormonal control of blood


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

Increased CO

Preload

and/or

Contractility
Fluid volume

Increased PR
Vasoconstriction

Fluid volume

Renal sodium
retention
Excess
sodium
intake

Sympathetic
nervous
system

Reninangiotensinaldosterone
system

Genetic
factors
(Adapted from Kaplan, 1994)

Hypertension :
The Disease Continuum
Early Paradigm

Natural History of CVD Progression


Elevated BP

Target Organ Damage

Elevated BP

Target Organ Damage

More Recent Paradigm

Vascular Dysfunction
A Proposed Future Paradigm

Endothelial
Dysfunction

Vascular
Dysfunction

Elevated BP

Target Organ
Damage

LVH
Renal
Damage

MI

Angina
Pectoris

Stroke

Komplikasi Hipertensi
Eyes
retinopathy

Kidneys
renal failure

Brain
stroke

Heart
ischaemic heart disease
left ventricular hypertrophy
heart failure

Peripheral arterial disease

Kerusakan Target Organ!!


Kerusakan yang disebabkan
oleh hipertensi tergantung :

Besarnya peningkatan
tekanan darah

Lamanya kondisi tekanan


darah yang tidak
terdiagnosis dan tidak
diobati

Effects of blood pressure on the risk


of cardiovascular disease
Average annual incidence rate per
100
10.000

CHD

90
80
70
60
50
40
30

Stroke
CHF

20
10
0

<100
120
140
180
Systolic blood pressure (mmHg)

>180

Source : Framingham study (after Gorlin)

Symptoms

Headache
Dizziness
Fatigue
Pounding of the heart
Symptoms are not specific and no more
frequent than in patients with normotension.

Symptoms of complications : heart

failure, chest pain, claudication, vision

Evaluasi Klinis Hipertensi :


Tujuan :
1. Konfirmasi hipertensi dan tingkatnya
2. Menyingkirkan & menemukan hipertensi
sekunder
3. Menentukan kerusakan organ target
4. Mencari faktor risiko kardiovaskuler dan
kondisi
klinik lain

Riwayat Klinis :
Riwayat keluarga HT, DM, dislipidemia, PJK, stroke

atau sakit ginjal


Lama & tingkat TD sebelumnya & hasil Tx. serta efek
Adanya PJK, gagal jantung, penyakit serebrovaskuler,
ginjal, perifer, DM, pirai, dislipidemia, asma
bronkhiale, & informasi obat
Faktor risiko (diet lemak, Na & alkohol, rokok,
aktifitas fisik, & BB)
Riwayat obat-obatan (kontrasepsi, NSAID, kokain &
amfetamin) dapat TD.
Faktor pribadi, psikososial dan lingkungan.

Pemeriksaan Fisik :
Pemeriksaan fisik & TD yang teliti
Tinggi, berat, & BMI (Body mass Index)
Sistem kardiovaskuler : ukuran jantung,

gagal jantung, arteri perifer (carotis,


aorta, renal)
Paru (ronkhi & bronkhospasme),
bising abdomen.
Fundus optikus & sistim syaraf
(mengetahui kerusakan serebrovaskuler).

Technique of blood pressure measurement


recommended by the British Hypertension
Society
1.
Several time, rest 5
minutes before

2.
The patient should be
relaxed and the arm must
be supported. Ensure no
tight clothing constricts
the arm

3.
The cuff must be level with
the heart. If the circumference
exceeds 33cm, a large cuff
must be used (2/3 of arm).
Place stethoscope diaphram
over brachial artery

4.
The column of mercury
must be vertical. Inflate
to occlude the pulse
(>30 mmHg). Deflate at
2-3 mm/s. measure
systolic ( first sound /
Korotkoff I ) & diastolic
(disappearence /
Korotkoff IV or V ) to
nearest 2 mmHg

(From British Hypertension Society 1985)

Recommended Technique
for Measuring Blood Pressure

Standardized technique:
Have the patient rest for 5 minutes
Use an appropriate cuff size
Use a mercury manometer or a recently
calibrated electronic device

Recommended Technique
for Measuring Blood Pressure (cont.)
Position cuff appropriately
Increase pressure rapidly
Support arm with antecubital fossa or heart
level
To exclude possibility of auscultatory gap,
increase cuff pressure rapidly to 30 mmHg
above level of diseappearance of radial
pulse
Place stethoscope over the brachial artery

Recommended Technique
for Measuring Blood Pressure (cont.)
Drop pressure by 2 mmHg / beat:
- appearance of sound (phase I Korotkoff)
= systolic pressure
- disappearance of sound (phase V
Korotkoff) = diastolic pressure
Take 2 blood pressure measurements, 1
minute apart

Diagnosis of Hypertension
Hypertension is defined as:
- BP 140/90 mm Hg
- during 1-5 visits
- with an average of 2 readings per visit

Pengukuran tekanan darah


ambulatory
Sekarang terdapat alat otomatis untuk mengukur
tekanan darah selama 24 jam atau lebih.
Indikasi
pemeriksaan
tersebut
(ABPM
=
Ambulatory Blood Pressure Monitoring) ialah
sebagai berikut :
1. Adanya variasi tekanan darah yang besar
2. Office hypertension
3. Dicurigai adanya episode hipotensi
4. Hipertensi yang resisten terhadap pengobatan

Pemeriksaan lain-lain

Laboratorium :
Urinalisis & mikroskopik urin
Serum kalium, kreatinin, gula darah puasa & 2 jam dan
profil lemak, asam urat
Pemeriksaan tambahan :
Pemeriksaan hormonal seperti pengukuran aktifitas
renin plasma, aldosteron plasma dan katekolamin
urine atas indikasi khusus (hipertensi sekunder)

EKG & Foto polos dada


Ekhokardiografi (curiga kerusakan organ target /LVH /
lainnya)
Ultrasonografi vaskuler (curiga penyakit arteri
karotis, aorta atau perifer lain)
Ultrasonografi renal (curiga penyakit ginjal)
Angiografi

Minimal BP Goal of Therapy


Recommendations (SBP/DBP mmHg)
Patient Type

JNC VI

Uncomplicated HTN

< 140/90

Hypertension with
diabetes mellitus

< 130/85
< 130/80*
< 130/85

Heart failure
Hypertension with
renal impairment

< 125/75

*National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group.

Proteinuria > 1 g/24h.


(Bakris GL, et al for the National Kidney Foundation Hypertension and Diabetes Executive
Committees Working Group. Am J Kidney Dis. 2000) (JNC VI. Arch Intern Med. 1997)

Terapi Hipertensi

Terapi Non-farmakologis
Menurunkan berat badan (5-20
mmHg/10 kg)
Latihan dan olah raga (4-9 mmHg)
Menghindari alkohol yang berlebihan
Mengurangi asupan garam (2-8 mmHg)
Stop merokok
Menurunkan asupan lemak jenuh

Lifestyle Modification
Modification

Approximate SBP
reduction (range)

Weight reduction

520 mmHg/10 kg loss

Adopt DASH eating plan

814 mmHg

Dietary sodium reduction

28 mmHg

Physical activity

49 mmHg

Moderation of alcohol
consumption

24 mmHg

Terapi Hipertensi

Terapi Farmakologis
tujuan terapi antihipertensi
Memperbaiki fungsi endothel
untuk menurunkan resistensi vaskular
sistemik
mempertahankan curah jantung
mempertahankan suplai darah ke organ
dan jaringan
Pengobatan diberikan seumur hidup
Kepatuhan yang buruk merupakan penyebab
kegagalan terapi antihipertensi yang paling
besar

Pilihan terapi
antihipertensi
Diuretik
Beta-blocker
Antagonis kalsium
ACE-inhibitor
Angiotensin II receptor antagonis
(AIIRA / ARB)
Alpha1-blocker (sentral & perifer)

Diuretics

-blockers

AT1 receptor
blockers

1-blockers

Calcium
antagonists

ACE inhibitors
Possible combinations of different classes of antihypertensive agents.
The most rational combinations are represented as thick lines.
ACE, angiotensin-converting enzyme; AT1, angiotensin II type 1.

Algorithm for Treatment of


Hypertension

Reasons of inadequate BP Control

Acceptance of inadequate control by physician

BP goals are more aggressive than in previous


years

Lack of compliance due to :

Difficulty achieving BP control with one


agent/suboptimal regimens

perceived side effects of antihypertensive


medication(s)
frequency of dosing/multiple agents to attain
control
(Adapted from JNC VI. Arch Intern Med. 1997)

Presentasi pasien hipertensi


yang terkontrol
< 140/90 mmHg
USA
27

England
6

Canada
16

France
24

< 160/95 mmHg


Finland

Spain

20.5

20

Germany
22.5

Scotland

Australia
19

India

17.5

> 65 years

USA: JNC VI. Arch Intern Med 1997


Marques-Vidal P et al. J Hum Hypertens 1997
Canada: Joffres et al. Am J Hypertens 1997
England: Colhoun et al. J Hypertens 1998
France: Chamontin et al. Am J Hypertens 1998

Adapted from G. Mancia / L. Ruilope

WHO-ISH (1999)
Klasifikasi Derajat Tekanan Darah menurut WHO-ISH
1999 yang diadaptasi dari JNC VI 1997

1
2
3
4
5
6
7

Kategori

Sistolik
(mmHg)

Diastolik
(mmHg)

Optimal
Normal
Normal Tinggi
Hipertensi derajat 1 (ringan)
Subgrup : perbatasan
Hipertensi derajat 2 (sedang)
Hipertensi derajat 3 (berat)
Hipertensi Sistolik
(Isolated Systolic Hypertension)

120
130
130 - 139
140 - 159
140 - 149
160 - 179
180
140

80
85
85 - 89
90 - 99
90 - 94
100 - 109
110
90

Hipertensi
Secondary Hypertension :

The Renin-Angiotensin System


Alternate Pathway
Local

Circulating
Liver

Renin inhibitors

Angiotensinogen
Renin

Tissue
Non Renin pathways
- t-PA
- Cathepsin G
- Tonin

Angiotensin I
ACE inhibitor

Converting enzyme
Angiotensin II

AII receptor blockers

Angiotensin
receptors

Non-ACE pathways
- Chymase
- CAGE
- Cathepsin G

Risiko Infark Miokard dan Stroke


15

5-year risk (%)

10

5
MI

Stroke

0
0

100

200

300

Systolic blood pressure (mm Hg)


Brown, M.J., Lancet 2000;355:653-4

Cumulative Incidence of CHF :


Normotensives and Stage 1 and 2
Hypertensives
20

Stage 2+ hypertension

15
CHF
Cumulative
Incidence 10
(%)

Stage 1+ hypertension

5
Normal BP

5
10
Years From Baseline Exam

15

Lenfant C, Roccella EJ. J Hypertens Suppl. 1999;17:S3-S7.


Data from Levy D et al. JAMA. 1996;275:1557-1562.

Effects of Angiotensin II at AT1 and AT2


Receptors

AT1

AT2

Blocked by ARB s
-

Vasoconstriction
Aldosterone release
Oxidative stress
Vasopressin release
SNS activation
Inhibits renin release
Renal Na+ and H2O reabsorption
Cell growth and proliferation

Siragy H. Am J Cardiol. 1999;84:3S8S.

Vasodilation
Antiproliferation
Apoptosis
Antidiuresis/antinatriuresis
Bradykinin production
NO release

Role of A II in Vascular Disease

Reprinted with permission from Dzau VJ. Hypertension. 2001;37:1047-1052.

Target Organ Damage


Heart
Left ventricular hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
Brain
Stroke or transient ischemic attack
Chronic kidney disease
Peripheral arterial disease
Retinopathy

Total Mortality and Continuous


Ambulatory Blood Pressure
Systolic Blood Pressure
events/100 pt/yrs

Diastolic Blood Pressure


5

5
4

2
1
< 140

mm Hg

mm Hg
140-159 160-179 180-199 200+

< 80

80-89

90-99

100-109

110+

Assessment of the 24-hour blood pressure load is


a good clinical method to identify high-risk patients
Khattar, R.S. et al. Circulation 1999; 100:1071-4

Benefits of Lowering BP
Average Percent Reduction
Stroke incidence

3540%

Myocardial infarction

2025%

Heart failure

50%

Goals of Therapy
(JNC-VII)
Reduce CVD and renal morbidity and mortality.
Treat to BP <140/90 mmHg or BP <130/80 mmHg
in patients with diabetes or chronic kidney
disease.
Achieve SBP goal especially in persons >50 years
of age.

Hypertension Prevalence and


Treatment :
North America and Europe
Prevalence of Hypertension
55
50

US
Canada
Italy
Sweden
England
Spain
Finland
Germany

100
90
80

45
40
%

Patients on Therapy

70

35

% 60
50

30
25

40
30

20
15

20
10

10
5

0
Country
Wolf-Maier K et al. JAMA. 2003;289:2363-2369.

Country

RULE OF HALF
Hypertensive patients
who are treated
but uncontrolled

Patients who are aware


but remain untreated
and uncontrolled

25%

12.5%
12.5%

50%

Hypertensive patients
who are unaware

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

Hypertensive patients
who are treated
and controlled

BP Control Rates
Trends in awareness, treatment, and control of high
blood pressure in adults ages 1874
National Health and Nutrition Examination Survey
Percent
II
197680

III
(Phase 1)
198891

III
(Phase 2)
199194

19992000

Awareness

51

73

68

70

Treatment

31

55

54

59

Control

10

29

27

34

Sources: Unpublished data for 19992000 computed by M. Wolz, National Heart, Lung, and Blood Institute; JNC 6.

Antihypertensive Agents Combination


DIURETIC
AT-2 RB

-BLOCKER

-BLOCKER

Ca-ANTAGONIST

ACE INHIBITOR
ESC-ESH 2003

CVD Risk Factors


Hypertension*
Cigarette smoking
Obesity* (BMI >30 kg/m2)
Physical inactivity
Dyslipidemia*
Diabetes mellitus*
Microalbuminuria or estimated GFR <60 ml/min
Age (older than 55 for men, 65 for women)
Family history of premature CVD
(men under age 55 or women under age 65)
* Components of the metabolic syndrome.

Classification and Management


of BP for adults

* Treatment determined by highest BP category.

Initial combined therapy should be used cautiously in those at risk for orthostatic
hypotension.

Compelling Indications
for
Individual Drug Classes
Compelling Indication Initial Therapy Options Clinical Trial Basis
Heart failure

THIAZ, BB, ACEI, ARB,


ALDO ANT

ACC/AHA Heart Failure


Guideline, MERIT-HF,
COPERNICUS, CIBIS,
SOLVD, AIRE, TRACE,
ValHEFT, RALES

Postmyocardial
infarction

BB, ACEI, ALDO ANT

ACC/AHA Post-MI
Guideline, BHAT,
SAVE, Capricorn,
EPHESUS

High CAD risk

THIAZ, BB, ACE, CCB

ALLHAT, HOPE,
ANBP2, LIFE,
CONVINCE

Compelling Indications for


Individual Drug Classes

Hipovolemic Shock

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