HIPERTENSI

Konsep Dasar :
-Tekanan Darah terjadi akibat kontraksi otot jantung yang
menghadapi tahanan pembuluh darah tepi, jadi

Tekanan darah adalah : Cardiac Output (CO) X Taha

nan Vaskular Sistemik (TVS)
Mean arterial pressure (MAP) : DBP + (SBP DBP) / 3
Basic concept : Hypertension
Evaluasi penderita Hipertensi
- evaluasi penderita hipertensi ada tiga sasaran utama :

1. Menilai gaya hidup dan mengidentifikasi faktor risiko kardio

vaskular lain atau penyakit comorbid yang dapat mempengaru
hi strategi pengobatan &prognosis penderita
2. Mencoba mengidentifikasi apa penyebab dari Hipertensi

Identifiable causes of hypertension

3. Mengidentifikasi adakah target organ yang rusak atau Stroke?
Evaluasi penderita Hipertensi :
Anamnesa :
adakah risiko penyakit jantung iskemik : diabetes, hiperkolesterol
dan riwayat sakit jantung dalam keluarga
riwayat minum obat obatan
soscial historys : merokok, alkohol, level of stress at work, exercise

Pemeriksaan fisik :
pengukuran tekanan darah yang adekuat (perbandingan lengan/tungkai
kiri-kanan)
evaluasi fisik lengkap termasuk : funduskopi, tiroid, auskultasi karotis-
femoral, pemeriksaan neurologis dan body mass index

Laboratorium :
test darah : darah rutin, fungsi ginjal, profil lipid, gula darah, asam urat
EKG dan Ekokardiografi
 Causes of High Blood Pressure

Essential hypertension

Secondary hypertension
Sleep apnea
Drug-induced
Chronic kidney disease
Primary aldosteronism
Chronic steroid therapy or Cushings syndrome
Pheochomocytoma
Coarctation of the aorta
Thyroid or parathyroid disease
 Drug-Induced HTN

Amphetamines
Antidepressants
Corticosteroids
Calcineurin inhibitors
Decongestants
Ergot alkaloids
Erythropoietin stimulating agents
Estrogen-containing oral contraceptives
NSAIDS
 Risks

High blood pressure increases risk of:

Heart failure
Myocardial ischemia and infarction
Stroke
Aneurysms and dissection
Kidney disease
Retinopathy
Peripheral vascular disease
Patofisiologi (I) :
- 3 penyebab utama dari hipertensi (esensial) :

1.Predisposisi poligenetis
- secara genetis terbukti seseorang peka terhadap konsumsi garam,abnor
malitas transportasi natrium-kalsium , respon sistem saraf pusat terha
dap stimulasi psikososial, presor dan trofik neurohormonal (Angioten
sin II, katekolamin, tromboksan, fungsi barostat renal) serta gangguan
metabolisme (glukosa-lipid-resitensi insulin)

2.Faktor lingkungan
- 2 faktor lingkungan terhadap predisposisi genetis : konsumsi garam /nu
trisi kalori tinggi dan psikososial
- psikososial : kebiasaan hidup, pekerjaan, stres mental dan status sosial

3.Adaptasi struktural jantung dan pembuluh darah

-tekanan darah tinggi : memberi stimulasi fisika mekanik sehingga jantung
dan pembuluh darah akan adaptasi secara struktural ...Hipertrofi eksen
trik bila tension (wall stress) akibat preload(volume)besar...Hipertrofi kon
sentrik bila tension yang dialami afterload(resistensi) yang tinggi
 Patofisiologi (II)
TD (MAP) : CO X TVS

SV HR Blood Circuit Arteriolar

Viscosity length radius

Sympathetic Vagal tone

system

Neural Humoral Local

Diastolic Inotropic Aortic smooth muscle
receptor
filling state pressure

Right atrial Sympathetic nervous system,vagal - adrenergic - Nor-epi - ionix flux

Pressure tone, Ca2+, contractile protein - adrenergic - Angitensin II Na, K, Ca
-Dopaminergic - Vasopressin - metabolites
-Cholinergic - Serotonin - autoregula
etc etc tion...etc
Venous compliance Central venous volume
Sympatic system Na : diet & Renal loss
Patofisiologi (III)
Patofisiologi (IV)
Pathogenesis of Hypertension
Excess Reduced Endothelium
Genetic
sodium nephron Stress Obesity derived
alteration
intake number factors

Renal Decreased Sympathetic Renin- Cell

Hyper-
sodium filtration nervous angiotensin membrane
insulinemia
retention surface overactivity excess alteration

Increased
Venous
fluid
constriction
volume

Increased Functional Structural

contractability constriction hypertrophy
Increased
preload

BLOOD PRESSURE = CARDIAC OUTPUT x PERIPHERAL RESISTANCE

Hypertension = Increased Cardiac Output and/or Increased Peripheral Resistance

autoregulation

Kaplan. Clinical Hypertension. 2006

 Renin Angiotensin System
Nitric oxide (NO) Angiotensinogen
t-PA
Renin Cathepsin G
Bradykinin AI CAGE Tonin
ACE Cathepsin G
Chymase
Degradation A II
products
ACEI site of action

ARB site of AT1 receptor AT2 receptor

action
Hypertrophy/proliferation Antiproliferation
Vasoconstriction NO Release
Aldosterone release Differentiation
Antidiuretic hormone release Vasodilation
Symphatetic discharge
de Gasparo M, et al. Hypertension. Pathophysiology, Diagnosis, and Management. 2nd ed. Dzau VJ. J Hypertens.
1989;7:933-936.
 JNC VII: Klasifikasi tekanan darah

Klasifikasi tekanan Sistolik (mm Diastolik (mm

darah Hg) Hg)

Normal <120 <80

Prehipertensi 120-139 80-89

Hipertensi
140-159 90-99
tingkat 1
Hipertensi
160 100
Tingkat 2

The JNC VII. JAMA 2003;289:2560-72

 Pengobatan Hipertensi

Non farmakolgis life modification

Farmakologis
Manfaat (benefit) penurunan Tekanan Darah
- pengobatan dengan antihipertensi dapat mengurangi :

kejadian Stroke 35 40 %
kejadian infark miokard 20 25%
kejadian gagal jantung > 50%

Goal therapy of Hypertension :

Non compelling factor : < 140/90 mmhg
Compelling factor (+) (Diabetes, Renal disease ) : < 130/80mmhg
Non- Farmakologis life modification
 Rekomendasi JNC VII pola hidup untuk kontrol TD*
Modifikasi Rekomendasi Efek penurunan
tekanan darah
Penurunan berat Jaga berat badan normal 5-20 mmHg/10 kg
badan (BB) (BMI=18.5-24.9) penurunan BB
Diet DASH Diet kaya buah & sayur, rendah lemak 8-14 mmHg
(termasuk produk susu rendah lemak)
Batasi asupan <2.4 gram natrium/hari 2-8 mmHg
garam (1/4 sendok teh= 600 g Na)
(1,2 gr anak 4-8 tahun;
1,5 gr >8 tahun) **
Aktifitas fisik Latihan aerobik rutin minimal 30 4-9 mmHg
menit, 3x/minggu
Batasi alkohol <2 drinks/day (Laki) and <1 drink/day 2-4 mmHg
(perempuan)
1 drink= 150 ml wine, 45 ml wiski
DASH= Dietary Approaches to Stop Hypertension Study * Chobanian AV et al. JAMA. 2003;289:2560-2572
+ Krebs. Pediatrics. 2003;112:424430 ** Panel of Dietary Intakes for Electrolytes and Water 2004
Dasar dasar farmakologis pemilihan Obat Anti Hipertensi (OAH)

Metoda rasionil menurunkan tekanan darah meliputi :

menurunkan curah jantung
menurunkan resistensi perifer
memperbaiki komplians arteri
mempertahankan perfusi organ

Perlu diingat :
OAH yang efek utama menurunkan curah jantung berarti menurunkan
tekanan sistolik sehingga tidak selalu disertai penurunan tekanan dias
tolik bermakna
OAH yang utama mengurangi resistensi perifer(vasodilator) berarti me
nurunkan tekanan diastolik akan menurunkan tekanan sistolik
Hipertensi menetap/kronik (masalah resistensi perifer), hati hati pema
kaian OAH yang menurunkan curah jantung tanpa disertai penurunan
resistensi perifer(vasodilatasi)dapat menimbulkan hipoperfusi jaringan
 Efek Hemodinamik obat obat Antihipertensi

1. Menurunkan resistensi perifer, curah jantung dipertahankan, memper

baiki komplians arteri/perfusi organ :
- penghambat kalsium, penghambat ACE, ARB

2 .Menurunkan resistensi perifer, mempertahankan curah jantung dan per

fusi, komplians arteri tidak diketahui : penyekat alfa

3. Menurunkan resistensi perifer, mempertahankan curah jantung dan per

fusi, memperburuk komplians arteri
- vasodilator, penyekat beta dan alfa

4. Menurunkan resistensi perifer, curah jantung dan perfusi: diuretik

Farmakologis :obat dan dosis (I)
Farmakologis : obat dan dosis (II)
Penanganan Hipertensi
Antihypertension Drugs for Compelling Factors (+)
 Krisis Hipertensi
definisi : tekanan darah >180/120 mmhg dengan atau ancaman kerusakan
target organ (misalnya : iskemia jantung, edema paru, stroke, gagal ginjal)
klasifikasi : Emergensi dan Urgensi
Emergensi : terbukti adanya kerusakan target organ
Urgensi : tidak terbukti adanya kerusakan target organ
diagnosis : identifikasi kerusakan target organ dan hipertensi sekunder

penanganan :
Emergensi :
- rawat ICU, obat antihipertensi IV
- MAP diturunkan 10% jam pertama, selanjutnya 15-20% 2-3jam berikutnya
Urgensi :
- rawat jalan atau observasi sehari di RS, obat antihipertensi oral
- MAP diturunkan 25% pada 24 jam pertama
Parenteral Drugs Used for Treatment of Hypertensive Emergencies
Pharmacologic treatment should be initiated using one or
more agents from 4 medication classes ACE inhibitors,
ARBs, CCBs or thiazide-type diuretics.
These agents should be titrated to the target dose (see
table below). In black hypertensive patients, initial
therapy should include a CCB or thiazide-type diuretic.
Patients with CKD should be started on an ACE inhibitor
or ARB. If patients do not reach goal BP, add another drug
from the 4 recommended drug classes, but do not
combine an ACE inhibitor with an ARB. Note that beta-
blockers are not among the initial recommended drug
classes.
LIST OF DRUGS AND THE TARGET DOSES USED IN CLINICAL TRIALS
 Classification of Recommendations

Based on critical review of high quality randomized controlled trials

Classification of recommendations:
(A) Strong Recommendation: high certainty based on evidence that the net
benefit is substantial
(B) Moderate Recommendation: moderate certainty based on evidence that
the net benefit is moderate to substantial
(C) Weak Recommendation: at least moderate certainty based on evidence
that there is a small net benefit
(D) Recommendation against: at least modest certainty based on evidence
that there is no net benefit or that risks/harms outweigh benefits
(E) Expert Opinion: Net benefit is unclear because there is insufficient
evidence but this is what the committee recommends. Further research is
necessary.
 Summary of Recommendations
General Population 60 yrs
Initiate Tx at BP 150/90 mmHg (Grade A)
Target BP < 150/90 mmHg (Grade A)
Corollary: if BP achieved is lower than target and well tolerated, no
adjustments needed to Tx (Grade E)

General Population < 60 yrs

Initiate Tx at BP 140/90 mmHg
Target BP < 140/90 mmHg
Diastolic goal: (30-59 years Grade A; 18-29 years Grade E)
Systolic goal: (Grade E)

Population 18 yrs with CKD or DM

Initiate Tx at BP 140/90 (Grade E)
Target BP < 140/90 (Grade E)
 Summary of Recommendations

General nonblack population DM

Initial Tx should include thiazide-type diuretic, CCB, ACEI, or
ARB (Grade B)

General black population DM

Initial Tx should include a thiazide-type duretic or CCB
(General black population Grade B; black population
w/DMGrade C)

Entire population 18 yrs with CKD

Initial or add-on Tx should include an ACEI or ARB (Grade B)
 Summary of Recommendations

If BP goal not reached within 1 mo of Tx, increase

dose of initial drug or add a second agent
If goal still not reached with two agents titrated
up, third agent from the recommended list (i.e.
Thiazidetype diuretic, CCB, ACEI/ARB)may be added
Following third agent, if goal still not reached,
refer to a specialist.
Can add antihypertensive agents from other
classes
Do not use ACEI and ARB together
HYPERTENSION GUIDELINE MANAGEMENT ALGORITHM