HIPERTENSI

OLEH :
Dr. Dra. Nurhaedar Jafar, Apt, M.Kes

PROGRAM STUDI ILMU GIZI

FAKULTAS KESEHATAN MASYARAKAT
UNIVERSITAS HASANUDDIN
MAKASSAR
2010

DAFTAR ISI

Hal

HALAMAN JUDUL
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SURAT KETERANGAN
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ii
DAFTAR ISI
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iii
A. Latar

Belakang
1

B. Pengertian

Hipertensi

....
1
C.. .Klasifikasi

Hipertensi

2
D.. .Patofisiologi

Hipertensi

8
E....Pengobatan

Hipertensi
10

DAFTAR PUSTAKA

Hipertensi
A. Pengertian
Hipertensi atau penyakit darah tinggi sebenarnya adalah suatu
gangguan pada pembuluh darah yang mengakibatkan suplai oksigen dan
nutrisi yang dibawa oleh darah terhambat sampai ke jaringan tubuh yang
membutuhkan. Hipertensi sering kali disebut sebagai pembunuh gelap
(Silent Killer), karena termasuk penyakit yang mematikan tanpa disertai
dengan gejala-gejalanya lebih dahulu sebagai peringatan bagi korbannya
(Lanny Sustrani, dkk, 2004).
Hipertensi adalah suatu keadaan dimana tekanan darah meningkat
melebihi batas normal. Batas tekanan darah normal bervariasi sesuai dengan
usia. Berbagai faktor dapat memicu terjadinya hipertensi, walaupun
sebagian besar (90%) penyebab hipertensi tidak diketahui (hipertensi

essential). Penyebab tekanan darah meningkat adalah peningkatan kecepatan

denyut jantung, peningkatan resistensi (tahanan) dari pembuluh darah dari
tepi dan peningkatan volume aliran darah (Kurniawan, 2002).
Penyakit hipertensi merupakan penyakit kelainan jantung yang
ditandai oleh meningkatnya tekanan darah dalam tubuh. Seseorang yang
terjangkit penyakit ini biasanya berpotensi mengalami penyakit-penyakit
lain seperti stroke, dan penyakit jantung (Rusdi dan Nurlaela, 2009).
Dari definisi-definisi diatas dapat diperoleh kesimpulan bahwa
hipertensi adalah suatu keadaan di mana tekanan darah menjadi naik
karena gangguan pada pembuluh darah yang mengakibatkan suplai
oksigen dan nutrisi yang dibawa oleh darah terhambat sampai ke jaringan
tubuh yang membutuhkannya.
B. Klasifikasi
Beberapa klasifikasi hipertensi:
a. Klasifikasi Menurut Joint National Commite 7
Komite eksekutif dari National High Blood Pressure Education
Program

merupakan

sebuah

organisasi

yang

terdiri

dari

46

professionalm sukarelawan, dan agen federal. Mereka mencanangkan

klasifikasi JNC (Joint Committe on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure) pada tabel 1, yang dikaji oleh
33 ahli hipertensi nasional Amerika Serikat (Sani, 2008).
Tabel 1
Klasifikasi Menurut JNC (Joint National Committe on Prevention,
Detection, Evaluatin, and Treatment of High Blood Pressure)
Kategori
Tekanan Darah
menurut JNC 7
Normal

Kategori
Tekanan Darah
menurut JNC 6
Optimal

Tekanan
dan/
Darah Sistol atau
(mmHg)
< 120
dan

Tekanan
Darah Diastol
(mmHg)
< 80

Pra-Hipertensi
Hipertensi:
Tahap 1
Tahap 2
-

Nornal
Normal-Tinggi
Hipertensi:
Tahap 1
Tahap 2
Tahap 3

120-139
< 130
130-139

atau
dan
atau

80-89
< 85
85-89

140-159
160
160-179
180

atau
atau
atau
atau

90-99
100
100-109
110

(Sumber: Sani, 2008)

Data terbaru menunjukkan bahwa nilai tekanan darah yang
sebelumnya

dipertimbangkan

normal

ternyata

menyebabkan

peningkatan resiko komplikasi kardiovaskuler. Data ini mendorong

pembuatan klasifikasi baru yang disebut pra hipertensi (Sani, 2008).
b. Klasifikasi Menurut WHO (World Health Organization)
WHO dan International Society of Hypertension Working Group
(ISHWG) telah mengelompokkan hipertensi dalam klasifikasi optimal,
normal, normal-tinggi, hipertensi ringan, hipertensi sedang, dan
hipertensi berat (Sani, 2008).
Kategori
Optimal
Normal
Normal-Tinggi

Tabel 2
Klasifikasi Hipertensi Menurut WHO
Tekanan Darah Tekanan Darah
Sistol (mmHg)
Diatol (mmHg)
< 120
< 130
130-139
140-159
140-149
160-179
180
140

Tingkat 1 (Hipertensi Ringan)

Sub-group: perbatasan
Tingkat 2 (Hipertensi Sedang)
Tingkat 3 (Hipertensi Berat)
Hipertensi sistol terisolasi
(Isolated
systolic
hypertension)
Sub-group: perbatasan
140-149
(Sumber: Sani, 2008)
c. Klasifikasi Menurut Chinese Hypertension Society

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

Menurut Chinese Hypertension Society (CHS) pembacaan tekanan

darah <120/80 mmHg termasuk normal dan kisaran 120/80 hingga
139/89 mmHg termasuk normal tinggi (Shimamoto, 2006).

Tabel 3
Klasifikasi Hipertensi Menurut CHS
Tekanan Darah Sistol
(mmHg)
< 120
120-129
130-139
Tekanan Darah Tinggi
140-159
160-179
180
140

Tekanan Darah Diastol

(mmHg)
< 80
80-84
85-89
90-99
100-109
110
90

CHS-2005
Normal
Normal-Tinggi
Tingkat 1
Tingkat 2
Tingkat 3
Hypertensi Sistol
Terisolasi

(Sumber: Shimamoto, 2006)

d. Klasifikasi menurut European Society of Hypertension (ESH)
Klasifikasi yang dibuat oleh ESH adalah:
1. Jika tekanan darah sistol dan distol pasien berada pada kategori
yang berbeda, maka resiko kardiovaskuler, keputusan pengobatan,
dan perkiraan afektivitas pengobatan difokuskan pada kategori
dengan nilai lebih.
2. Hipertensi sistol terisolasi harus dikategorikan berdasarkan pada
hipertensi sistol-distol (tingkat 1, 2 dan 3). Namun tekanan diastol
yang rendah (60-70 mmHg) harus dipertimbangkan sebagai resiko
tambahan.
3. Nilai batas untuk tekanan darah tinggi dan kebutuhan untuk
memulai pengobatan adalah fleksibel tergantung pada resiko
kardiovaskuler total.

Tabel 4
Klasifikasi menurut ESH
Kategori
Tekanan
Tekanan
Darah Sistol
Darah Diastol
(mmHg)
(mmHg)
Optimal
< 120
dan
< 80
Normal
120-129
dan/atau 80-84
Normal-Tinggi
130-139
dan/atau 85-89
Hipertensi tahap 1
140-159
dan/atau 90-99
Hipertensi tahap 2
160-179
dan/atau 100-109
Hipertensi tahap 3
180
dan/atau 110
Hipertensi
sistol 140
Dan
< 90
terisolasi
(Sumber: Mancia G, 2007)
e. Klasifikasi menurut International Society on Hypertension in Blcks
(ISHIB) (Douglas JG, 2003)
Klasifikasi yang dibuat oleh ISHIB adalah:
1) Jika tekanan darah sistol dan diastole pasien termasuk ke dalam dua
kategori yang berbeda, maka klasifikasi yang dipilih adalah
berdasarkan kategori yang lebih tinggi.
2) Diagnosa hipertensi pada dasarnya adalah rata-rata dari dua kali
atau lebih pengukuran yang diambil pada setiap kunjunga.
3) Hipertensi sistol terisolasi dikelompokkan pada hipertensi tingkat 1
sampai 3 berdasarkan tekanan darah sistol ( 140 mmHg) dan
diastole ( < 90 mmHg).
4) Peningkatan tekanan darah yang melebihi target bersifat kritis
karena setiap peningkatan tekanan darah menyebabkan resiko
kejadian kardiovaskuler.

Tabel 5

Klasifikasi Hipertensi Menurut ISHIB

Tekanan
Tekanan
Darah Sistol
Darah Diastol
(mmHg)
(mmHg)
Optimal
< 120
dan
< 80
Normal
< 130
dan/atau
< 85
Normal-Tinggi
130-139
dan/atau
85-89
Hipertensi Tahap 1 140-159
dan/atau
90-99
Hipertensi Tahap 2 160-179
dan/atau
100-109
Hipertensi Tahap 3 180
dan/atau
110
Hipertensi Sistol 140
dan
< 90
terisolasi
(Sumber: Douglas JG, 2003)
f. Klasifikasi berdasarkan hasil konsesus Perhimpunan Hipertensi
Kategori

Indonesia (Sani, 2008).

Pada pertemuan ilmiah Nasional pertama perhimpunan hipertensi
Indonesia 13-14 Januari 2007 di Jakarta, telah diluncurkan suatu
konsensus mengenai pedoman penanganan hipertensi di Indonesia
yang ditujukan bagi mereka yang melayani masyarakat umum:
1) Pedoman yang disepakati para pakar berdasarkan prosedur standar
dan ditujukan untuk meningkatkan hasil penanggulangan ini
kebanyakan diambil dari pedoman Negara maju dan Negara
tetangga, dikarenakan data penelitian hipertensi di Indonesia yang
berskala Nasional dan meliputi jumlah penderita yang banyak
masih jarang.
2) Tingkatan hipertensi ditentukan berdasarkan ukuran tekanan darah
sistolik dan diastolik dengan merujuk hasil JNC dan WHO.
3) Penentuan stratifikasi resiko hipertensi dilakukan berdasarkan
tingginya tekanan darah, adanya faktor resiko lain, kerusakan
organ target dan penyakit penyerta tertentu.
Tabel 6

Klasifikasi Hipertensi Menurut Perhimpunan Hipertensi Indonesia

Kategori

Tekanan Darah
Sistol (mmHg)
Normal
<120
Prehipertensi
120-139
Hipertensi Tahap 1 140-159
Hipertensi Tahap 2 160-179
Hipertensi
Sistol 140
terisolasi
(Sumber: Sani, 2008)

dan/atau
Dan
Atau
Atau
Atau
Dan

Tekanan Darah
Diastol (mmHg)
<80
80-89
90-99
100
<90

Klasifikasi hipertensi menurut bentuknya ada dua yaitu hipertensi

sistolik dan hipertensi diastolik (Smith, Tom, 1986:7). Pertama yaitu
hipertensi sistolik adalah jantung berdenyut terlalu kuat sehingga dapat
meningkatkan angka sistolik. Tekanan sistolik berkaitan dengan tingginya
tekanan pada arteri bila jantung berkontraksi (denyut jantung). Ini adalah
tekanan maksimum dalam arteri pada suatu saat dan tercermin pada hasil
pembacaan tekanan darah sebagai tekanan atas yang nilainya lebih besar.
Kedua yaitu hipertensi diastolik terjadi apabila pembuluh darah
kecil menyempit secara tidak normal, sehingga memperbesar tahanan
terhadap aliran darah yang melaluinya dan meningkatkan tekanan
diastoliknya. Tekanan darah diastolik berkaitan dengan tekanan dalam
arteri bila jantung berada dalam keadaan relaksasi diantara dua denyutan.
Sedangkan menurut Arjatmo T dan Hendra U (2001) faktor yang
mempengaruhi prevalensi hipertensi antara lain ras, umur, obesitas, asupan
garam yang tinggi, adanya riwayat hipertensi dalam keluarga.

Klasifikasi hipertensi menurut sebabnya dibagi menjadi dua yaitu

sekunder dan primer. Hipertensi sekunder merupakan jenis yang penyebab
spesifiknya dapat diketahui (Lanny Ssustrani, dkk, 2004).
Klasifikasi hipertensi menurut gejala dibedakan menjadi dua yaitu
hipertensi Benigna dan hipertensi Maligna. Hipertensi Benigna adalah
keadaan hipertensi yang tidak menimbulkan gejala-gejala, biasanya
ditemukan pada saat penderita dicek up. Hipertensi Maligna adalah
keadaan hipertensi yang membahayakan biasanya disertai dengan keadaan
kegawatan yang merupakan akibat komplikasi organ-organ seperti otak,
jantung dan ginjal (Mahalul Azam,2005).
C. Patofisiologi
Aktivitas kedua

adalah menstimulasi sekresi

aldosteron

dari

korteks adrenal. Aldosteron merupakan hormon steroid yang memiliki

peranan

penting

pada

ginjal. Untuk mengatur volume

cairan

ekstraseluler, aldosteron akan mengurangi ekskresi NaCl (garam)

dengan cara mereabsorpsinya dari tubulus ginjal. Naiknya konsentrasi
NaCl akan diencerkan kembali dengan cara meningkatkan volume cairan
ekstraseluler yang pada gilirannya akan meningkatkan volume dan tekanan
darah (Anggraini, 2008).

Renin

Angiotensin I

Angiotensin I Converting Enzyme (ACE)

Angiotensin II

Sekresi hormone ADH rasa haus

Stimulasi sekresi aldosteron dari

korteks adrenal

Urin sedikit pekat & osmolaritas

Ekskresi NaCl (garam) dengan
mereabsorpsinya di tubulus ginjal
Mengentalkan
Konsentrasi NaCl
di pembuluh darah

Menarik cairan intraseluler ekstraseluler

Volume darah

Diencerkan dengan volume

ekstraseluler

Tekanan darah

Volume darah

Tekanan darah

Gambar 1. Patofisiologi hipertensi.

(Sumber: Rusdi & Nurlaela Isnawati, 2009)
Tekanan yang dibutuhkan untuk mengalirkan darah melalui sistem
sirkulasi dilakukan oleh aksi memompa dari jantung (cardiac output/CO)
dan dukungan dari arteri (peripheral resistance/PR). Fungsi kerja masingmasing penentu tekanan darah ini dipengaruhi oleh interaksi dari berbagai
faktor yang kompleks. Hipertensi sesungguhnya merupakan abnormalitas
dari faktor-faktor tersebut, yang ditandai dengan peningkatan curah
jantung dan / atau ketahanan periferal. Selengkapnya dapat dilihat pada
bagan.

Gambar 3: Beberapa faktor yang mempengaruhi tekanan darah

(Sumber: Kaplan, 1998 dalam Sugiharto, 2007)
D. Pengobatan hipertensi
Kelas obat utama yang digunakan untuk mengendalikan tekanan darah
adalah :
1. Diuretik
Diuretik menurunkan tekanan darah dengan menyebabkan diuresis.
Pengurangan volume plasma dan Stroke Volume (SV) berhubungan
dengan dieresis dalam penurunan curah jantung (Cardiac Output, CO)
dan tekanan darah pada akhirnya. Penurunan curah jantung yang utama
menyebabkan resitensi perifer. Pada terapi diuretik pada hipertensi
kronik volume cairan ekstraseluler dan volume plasma hampir kembali
kondisi pretreatment.
a. Thiazide

Thiazide adalah golongan yang dipilih untuk menangani hipertensi,

golongan lainnya efektif juga untuk menurunkan tekanan darah.
Penderita dengan fungsi ginjal yang kurang baik Laju Filtrasi
Glomerolus (LFG) diatas 30 mL/menit, thiazide merupakan agen
diuretik yang paling efektif untuk menurunkan tekanan darah.
Dengan menurunnya fungsi ginjal, natrium dan cairan akan
terakumulasi maka diuretik jerat Henle perlu digunakan untuk
mengatasi efek dari peningkatan volume dan natrium tersebut. Hal
ini akan mempengaruhi tekanan darah arteri. Thiazide menurunkan
tekanan darah dengan cara memobilisasi natrium dan air dari
dinding arteriolar yang berperan dalam penurunan resistensi
vascular perifer.
b. Diuretik Hemat Kalium
Diuretik Hemat Kalium adalah anti hipertensi yang lemah jika
digunakan tunggal. Efek hipotensi akan terjadi apabila diuretik
dikombinasikan dengan diuretik hemat kalium thiazide atau jerat
Henle. Diuretik hemat kalium dapat mengatasi kekurangan kalium
dan natrium yang disebabkan oleh diuretik lainnya.
c. Antagonis Aldosteron
Antagonis Aldosteron merupakan diuretik hemat kalium juga tetapi
lebih berpotensi sebagai antihipertensi dengan onset aksi yang
lama (hingga 6 minggu dengan spironolakton).
2. Beta Blocker
Mekanisme hipotensi beta bloker tidak diketahui tetapi dapat
melibatkan menurunnya curah jantung melalui kronotropik negatif dan
efek inotropik jantung dan inhibisi pelepasan renin dan ginjal.

a. Atenolol, betaxolol, bisoprolol, dan metoprolol merupakan

kardioselektif pada dosis rendah dan mengikat baik reseptor 1
daripada reseptor 2. Hasilnya agen tersebut kurang merangsang
bronkhospasmus dan vasokontruksi serta lebih aman dari non
selektif bloker pada penderita asma, penyakit obstruksi
pulmonari kronis (COPD), diabetes dan penyakit arterial perifer.
Kardioselektivitas merupakan fenomena dosis ketergantungan dan
efek akan hilang jika dosis tinggi.
b. Acebutolol, carteolol, penbutolol, dan pindolol memiliki aktivitas
intrinsik simpatomimetik (ISA) atau sebagian aktivitas agonis
reseptor .
3. Inhibitor Enzim Pengubah Angiotensin (ACE-inhibitor)
ACE membantu produksi angiotensin II (berperan penting dalam
regulasi tekanan darah arteri). ACE didistribusikan pada beberapa
jaringan dan ada pada beberapa tipe sel yang berbeda tetapi pada
prinsipnya merupakan sel endothelial. Kemudian, tempat utama
produksi angiotensin II adalah pembuluh darah bukan ginjal. Pada
kenyataannya, inhibitor ACE menurunkan tekanan darah pada
penderita dengan aktivitas renin plasma normal, bradikinin, dan
produksi jaringan ACE yang penting dalam hipertensi.
4. Penghambat Reseptor Angiotensin II (ARB)
Angiotensin II digenerasikan oleh jalur renin-angiotensin
(termasuk ACE) dan jalur alternatif yang digunakan untuk enzim lain
seperti chymases. Inhibitor ACE hanya menutup jalur reninangiotensin, ARB menahan langsung reseptor angiotensin tipe I,

reseptor yang memperentarai efek angiotensin II. Tidak seperti

inhibitor ACE, ARB tidak mencegah pemecahan bradikinin.
5. Antagonis Kalsium
CCB menyebabkan relaksasi jantung dan otot polos dengan
menghambat saluran kalsium yang sensitif terhadap tegangan sehingga
mengurangi masuknya kalsium ekstra selluler ke dalam sel. Relaksasai
otot polos vasjular menyebabkan vasodilatasi dan berhubungan dengan
reduksi tekanan darah. Antagonis kanal kalsium dihidropiridini dapat
menyebbakan aktibasi refleks simpatetik dan semua golongan ini
(kecuali amilodipin) memberikan efek inotropik negative.
Verapamil menurunkan denyut jantung, memperlambat konduksi
nodus AV, dan menghasilkan efek inotropik negative yang dapat
memicu gagal jantung pada penderita lemah jantung yang parah.
Diltiazem menurunkan konduksi AV dan denyut jantung dalam level
yang lebih rendah daripada verapamil.
6. Alpha blocker
Prasozin, Terasozin dan Doxazosin merupakan penghambat
reseptor 1 yang menginhibisi katekolamin pada sel otot polos vascular
perifer yang memberikan efek vasodilatasi. Kelompok ini tidak
mengubah aktivitas reseptor 2 sehingga tidak menimbulkan efek
takikardia.
7. VASO-dilator langsung
Hedralazine dan Minokxidil menyebabkan relaksasi langsung otot
polos arteriol. Aktivitasi refleks baroreseptor dapat meningkatkan
aliran simpatetik dari pusat fasomotor, meningkatnya denyut jantung,
curah jantung, dan pelepasan renin. Oleh karena itu efek hipotensi dari

vasodilator langsung berkurang pada penderita yang juga mendapatkan

pengobatan inhibitor simpatetik dan diuretik.
8. Inhibitor Simpatetik Postganglion
Guanethidin dan guanadrel mengosongkan norepinefrin dari
terminal simpatetik postganglionik dan inhibisi pelepasan norepinefrin
terhadap respon stimulasi saraf simpatetik. Hal ini mengurangi curah
jantung dan resistensi vaskular perifer .
9. Agen-agen obat yang beraksi secara sentral
10. VASO-dilator langsung

Pengobatan hipertensi masyarakat dengan menggunakan :

a. Bayam
Bayam merupakan sumber magnesium yang sangat baik. Tidak
hanya melindungi Anda dari penyakit jantung, tetapi juga dapat
mengurangi tekanan darah. Selain itu, kandungan folat dalam
bayam dapat melindungi tubuh dari homosistein yang membuat
bahan kimia berbahaya. Penelitian telah menunjukkan bahwa
tingkat tinggi asam amino (homosistein) dapat menyebabkan
serangan jantung dan stroke.
b. Biji bunga matahari.
Kandungan magnesiumnya sangat tinggi dan biji bunga matahari
mengandung pitosterol, yang dapat mengurangi kadar kolesterol
dalam tubuh. Kolesterol tinggi merupakan pemicu tekanan darah
tinggi, karena dapat menyebabkan penyumbatan pembuluh darah.
Tapi, pastikan mengonsumsi kuaci segar yang tidak diberi garam.
c. Kacang-kacangan
Kacang-kacangan, seperti kacang tanah, almond, kacang merah
mengandung magnesium dan potasium. Potasium dikenal cukup
efektif menurunkan tekanan darah tinggi.
d. Pisang
Buah ini tidak hanya menawarkan rasa lezat tetapi juga membuat
tekanan darah lebih sehat. Pisang mengandung kalium dan serat
tinggi yang bermanfaat mencegah penyakit jantung. Penelitian juga
menunjukkan bahwa satu pisang sehari cukup untuk membantu
mencegah tekanan darah tinggi.
e. Kedelai
Banyak sekali keuntungan mengonsumsi kacang kedelai bagi
kesehatan. Salah satunya adalah menurunkan kolesterol jahat dan

tekanan darah tinggi. Kandungan isoflavonnya memang sangat

bermanfaat bagi kesehatan.
f. Kentang
Nutrisi dari kentang sering hilang karena cara memasaknya yang
tidak sehat. Padahal kandungan mineral, serat dan potasium pada
kentang sangat tinggi yang sangat baik untuk menstabilkan tekanan
darah.
g. Cokelat pekat (dark chocolate)
Karena kandungan flavonoid dalam cokelat dapat membantu
menurunkan tekanan darah dengan merangsang produksi nitrat
oksida. Nitrat oksida membuat sinyal otot-otot sekitar pembuluh
darah untuk lebih relaks, dan menyebabkan aliran darah
meningkat.
h. Avokad
Asam oleat dalam avokad, dapat membantu mengurangi kolesterol.
Selain itu, kandungan kalium dan asam folat, sangat penting untuk
kesehatan jantung

DAFTAR PUSTAKA

Page 1

PART I
INTRODUCTION
A. Background
Hypertension is a chronic disease that is often called the silent
killer because patients generally do not know that they suffer
hypertension before their blood pressure checked. In addition, patients
hypertension is generally not a sign or symptom experienced before they
happen
complications (Chobanian et al., 2004).
Patients with hypertension in the United States is estimated at about 77.9
million
or 1 of 3 population in 2010. The prevalence of hypertension in 2030
expected to rise as much as 7.2% of the estimated year 2010. Data
2007-2010 showed that as many as 81.5% of patients with hypertension
realized
that that they had hypertension, 74.9% received treatment with
52.5% of patients with controlled blood pressure (systolic blood pressure
<140
mmHg and diastolic <90 mmHg) and 47.5% of patients whose blood
pressure is not
controlled. The percentage of men who suffer from hypertension is
higher than

women up to the age of 45 years from the age of 45-64 years and the
same percentage,
then from 64 years and above, the percentage of women who suffer
hypertension is higher than men (Go et al., 2014).
Hypertension is one of the biggest risk factors cause
morbidity and mortality in cardiovascular disease (Kearney et al., 2005).
From 1999 to 2009, mortality due to hypertension increased
Page 2

2
17.1% (Go et al., 2014) with the number of deaths due to complications
hypertension reached 9.4 million per year (WHO, 2013).
Hypertension can lead to myocardial infarction, stroke, failed
kidneys, and death if not detected early and treated appropriately
(James et al., 2014). Approximately 69% of heart attack patients, 77% of
stroke patients, and
74% of patients with congestive heart failure (CHF) with hypertension
with pressure
Blood> 140/90 mmHg (Go et al., 2014). Hypertension causes of death in
45% of patients with heart disease and 51% of deaths in patients with
stroke
in 2008 (WHO, 2013). In addition, hypertension is also costing the
not least with the direct and indirect costs are spent on
in 2010 amounted to $ 46.4 billion (Go et al., 2014).
The prevalence of hypertension in Indonesia at 26.5% in 2013, but
diagnosed by health personnel and / or a history of taking medication
only
of 9.5%. This indicates that the majority of cases of hypertension in
undiagnosed and affordable public health services (Ministry of Health
RI, 2013
b
). Indonesian health data profiles in 2011 states that
hypertension is one of the 10 diseases with inpatient cases
Most in the hospital in 2010, with the proportion of 42.38% of cases of
men and
57.62% of women and 4.8% of patients died (MoH RI, 2012).
Hypertension and other cardiovascular diseases in hospitals in
Special Region of Yogyakarta is the highest cause of death (Health
DIY, 2013). Basic medical research results in 2013 put in Yogyakarta
as third in the number of cases of hypertension in Indonesia based
diagnosis

Page 3

3
and / or a history of taking the medication. This increase compared from
basic medical research results in 2007, which occupies Yogyakarta
tenth in the number of cases of hypertension based on the diagnosis and /
or
history taking medication (MoH RI, 2013
b
).
Along with the increase in cases of hypertension and complications that
can
happen if hypertension is not handled properly, then the use of drugs
rational in hypertensive patients is one important element in the
achievement of the quality of health and medical care for patients
according to the standard
which is expected. Irrational use of medicines can cause
the incidence of unwanted drug reactions, exacerbating the disease, up to
death. In addition, the cost becomes very high (WHO, 2004).
The above considerations, encourage researchers to conduct
study of rationality use of antihypertensive drugs in patients
hypertension. The study was conducted in patients hospitalized in the
Hospital PKU
Muhammadiyah Yogyakarta with the consideration that the increase
the number of cases of hypertension in 2013 compared with 2012. In
In 2013, hypertension is one of the 10 leading causes of hospitalization
The Hospital of PKU Muhammadiyah Yogyakarta and ranks
The third cause of hospitalization in non-communicable diseases. This is
different from
in 2012, where hypertension is not included in the 10 leading causes of
hospitalization
the largest inpatient at the hospital. Another consideration that the
Hospital
PKU Muhammadiyah is a private hospital type B (Associate) in
Yogyakarta.
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4
B. Problem Formulation
1. How do the characteristics of hypertensive patients hospitalized in the
Hospital PKU

Muhammadiyah Yogyakarta period January to December 2013 based on

age,
gender, history of hypertension, the diagnosis of other diseases and
complications,
as well as blood pressure levels?
2. What is the pattern of use of drugs in hypertensive patients
hospitalized at Home
Pain PKU Muhammadiyah Yogyakarta January-December 2013?
3. How rationality use of antihypertensive drugs that include precision
indication, drug, patients, and dosage in hypertensive patients
hospitalized at Home
Pain PKU Muhammadiyah Yogyakarta January-December 2013
based on the standard primary therapy JNC 7?
C. Objective
1. Knowing the characteristics of hypertensive patients hospitalized in
the Hospital PKU
Muhammadiyah Yogyakarta period January to December 2013 based on
age,
gender, history of hypertension, the diagnosis of other diseases and
complications,
and blood pressure levels.
2. Knowing the patterns of drug use in hypertensive patients hospitalized
at Home
Pain PKU Muhammadiyah Yogyakarta period from January to
December, 2013.
3. Knowing rationality which includes the use of antihypertensive drugs
accuracy indication, drug, patients, and dosage in hypertensive patients
hospitalized in
PKU Muhammadiyah Hospital in Yogyakarta period from January to
December
2013 based on the standard primary therapy JNC 7.
Page 5

5
D. Benefits Research
1. As a source of information about the use of antihypertensive drugs in
patients
hypertension.
2. As an input to improve the quality of medical care homes
ill.
3. Adding knowledge and experience for researchers.

E. Review of Literature
1. Definition and Classification of Hypertension
Hypertension was defined by increased arterial blood pressure
persistent. Increased systolic blood pressure is generally> 140 mmHg or
diastolic blood pressure> 90 mmHg (MOH, 2006) except when the blood
pressure
210 mmHg systolic or diastolic blood pressure 120 mmHg (Setiawati
and
Bustani, 1995).
Classification of blood pressure by Chobanian et al. (2004) for patients
adults (age 18 years) based on the average of two measurements of
blood pressure or
more on two or more clinical visits can be seen in Table I.
Table I. Classification of Hypertension (Chobanian et al., 2004)
Classification of blood pressure
Systolic blood pressure
(MmHg)
Diastolic blood pressure
(MmHg)
Normal
Prehypertension
Hypertension level 1
Hypertension level 2
<120
120-139
140-159
160
and <80
or 80-89
or 90-99
or 100
Patients who suffer from hypertension, most likely also be able to
hypertensive crisis. Hypertensive crisis is a clinical disorder
Page 6

6
characterized by very high blood pressure is systolic pressure> 180
mmHg or diastolic pressure> 120 mmHg, which might cause
or signs of organ damage has occurred. Hypertensive crisis include
hypertension

hypertensive emergency and urgency. Hypertensive emergencies ie blood

pressure
extreme increases with acute progressive organ damage, so that the
pressure
Blood should be taken down immediately (within minutes and hours) to
prevent
further organ damage. Hypertensive urgency is high blood pressure
in the absence of progressive organ damage that lowered blood pressure
within a few hours to a day at the level of blood pressure values I (MOH
RI, 2006).
2. Etiology of Hypertension
Hypertension based etiology is divided into two, namely hypertension
primary or essential and secondary hypertension.
a. Primary Hypertension
Approximately 95% of patients with hypertension is essential
hypertension
(Primary). The cause of essential hypertension is still unknown, but
factors
Genetic and environmental believed to play a role in causing
essential hypertension (Weber et al., 2014). Genetic factors may cause
increase in the activity of the renin-angiotensin-aldosterone system and
the nervous system
sympathetic and salt sensitivity on blood pressure. In addition to genetic
factors,
environmental factors that affect, among others, the consumption of salt,
obesity and unhealthy lifestyle (Weber et al., 2014) and consumption
Page 7

7
alcohol and smoking (Mansjoer et al., 1999).
Decrease in sodium excretion in normal arterial pressure state
is an early event in essential hypertension. Decreased excretion
sodium can lead to increased fluid volume, cardiac output, and
peripheral vasoconstriction that increases blood pressure. Environmental
factors
can modify gene expression in an increase in pressure. Stress, obesity,
smoking, physical inactivity, and the consumption of large amounts of
salt
considered as an exogenous factor in hypertension (Robbins et al., 2007).
b. Secondary hypertension

Secondary Hypertension affects approximately 5% of patients with

hypertension (Weber
et al., 2014). Secondary hypertension is caused by the presence of
comorbid disease
or the use of certain drugs that can increase blood pressure.
Certain medications, either directly or indirectly, may cause
hypertension or aggravate hypertension. Discontinuation of the drug use
or treat comorbid conditions accompanying the first stage
in the treatment of secondary hypertension (MOH, 2006). Some causes
Secondary hypertension can be seen in Table II.
Table II. The cause of hypertension that can be identified (MOH,
2006)
Disease
Drug
Chronic kidney disease
Primary hyperaldosteronism
Renovascular disease
Cushing syndrome
Phaeochromocytoma
Koarktasi aorta
Thyroid or parathyroid disease
Corticosteroids, ACTH
Estrogens (birth control pills usually grading
high estrogen)
NSAIDs, COX-2 inhibitors
Phenylpropanolamine and analog
Cyclosporine and takromilus
Erythropoietin
Sibutramin
Antidepressants (especially venlafaxine)
Page 8

8
3. Clinical Symptoms of Hypertension
Most people with hypertension do not feel the symptoms of the
disease. There is
mistake of thinking that often occurs in the community that people with
hypertension always feel the symptoms of the disease. In reality it is
mostly
hypertensive patients do not feel any symptoms of the
disease. Hypertension sometimes

cause symptoms such as headache, shortness of breath, dizziness, chest

pain,
palpitations, and epistaxis. These symptoms are dangerous if ignored, but
not a yardstick severity of hypertension (WHO, 2013).
4. Pathophysiology of Hypertension
Blood pressure is a complex trait that is determined by
interaction of various factors such as genetic and environmental factors
two variables that affect hemodynamic cardiac output and resistance
total peripheral (Robbins et al., 2007). Cardiac output is a factor that
determine the value of systolic blood pressure and total peripheral
resistance determines
diastolic blood pressure values. The increase in blood pressure may
occur as a result of
increase in cardiac output and / or an increase in total peripheral
resistance (Saseen and
MacLaughlin, 2008).
The kidneys have a role in controlling blood pressure through
the renin-angiotensin-aldosterone system. Mechanisms of blood pressure
regulation by
kidney can be seen in Figure 1.
Page 9

9
Figure 1. Mechanism of regulation of blood pressure by the kidneys
(Saseen and MacLaughlin, 2008)
Renin produced by cells of renal justaglomerulus change
angiotensinogen to angiotensin-1, then converted to angiotensin-1
angiotensin-2 by angiotensin converting enzyme (ACE). Angiotensin-2
can
binds to angiotensin-2 receptor type 1 (AT1) or angiotensin receptor-2
type 2 (AT2). AT1 receptor stimulation can increase blood pressure
through
pressor effects and blood volume (Saseen and MacLaughlin, 2008).
Pressor effect of angiotensin-2 include vasoconstriction, stimulation of
the release
catecholamines from the adrenal medulla, and increase the activity of the
nervous system
sympathetic (Saseen and MacLaughlin, 2008). In addition, angiotensin-2
stimulates
synthetic aldosterone from the adrenal cortex which causes sodium and
water retention.

Retention of sodium and water have resulted in an increase in blood

volume, the increase
total peripheral resistance, and ultimately increase in blood pressure
(Saseen and
MacLaughlin, 2008; Saseen, 2009).
Page 10

10
Blood pressure is also regulated by adrenergic nervous system which can
cause contraction and relaxation of the blood vessels. Stimulation
-2 receptors in the sympathetic nervous system causes a decrease in
neural
sympathetic that can lower blood pressure. -1 receptor stimulation on
causing peripheral vasoconstriction which can increase the pressure
blood. -1 receptor stimulation on cardiac causes an increase in heart
rate
and contractility, whereas stimulation of -2 receptors in arteries and
veins
causes vasodilation (Saseen and MacLaughlin, 2008; Saseen,
2009).
5. Complications of Hypertension
High blood pressure in the long term will damage the endothelial
arteries and accelerate atherosclerosis. Complications of hypertension
including
damage to organs such as the heart, eyes, kidneys, brain, and blood
vessels
large. Hypertension is a major risk factor for cerebrovascular disease
(Stroke, transient ischemic attack), coronary artery disease (myocardial
infarction,
angina), renal failure, dementia, and atrial fibrillation. When patients
with hypertension
have risk factors for cardiovascular disease, then there is an increase in
mortality and morbidity due to cardiovascular disorders. Patients with
hypertension have an increased risk for coronary disease meaningful,
stroke, peripheral artery disease, and heart failure (Dosh, 2001).
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11
6. Treatment of Hypertension
The main goal of therapy is to reduce mortality and hypertension
morbidity associated with hypertension and associated with damage

target organ (such as cardiovascular, heart failure, and kidney

disease). Target
blood pressure is <140/90 mmHg for uncomplicated hypertension and
<130/80 mm Hg for patients with diabetes mellitus and chronic renal
failure (Chobanian
et al., 2004). Treatment of hypertension include:
a. Non-pharmacological therapy
People with prehypertension and hypertension should do
lifestyle modifications such as weight loss if overweight
by keeping the body in the range of body mass index (BMI) is 18.5 to
24.9;
adopt a diet Dietary Approaches to Stop Hypertension (DASH)
rich in fruits, vegetables, and low fat dairy products; decrease
salt consumption is not more than 100 mEq / L; physical activity
regularly such as walking 30 minutes / day; and limiting consumption
alcohol is not more than 2 times / day in men and 1 times / day in women
(Chobanian et al., 2004). In addition, patients are also advised to
stop smoking (Weber et al., 2014). Lifestyle modification
can lower blood pressure, increase the efficacy of antihypertensive drugs,
and
reduce the risk of cardiovascular complications (Chobanian et al.,
2004).
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12
b. Pharmacologic Therapy
The selection of drugs for treatment of hypertension depends on
blood pressure levels and the presence of disease
complications. Medicines
antihypertensives such as diuretics, beta-blockers (BB), angiotensin
converting
enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs),
and calcium
channel blocker (CCB) is the primary agent that can reduce
morbidity and mortality. Antihypertensive medications such as -1
blockers, -2
central agonists, and vasodilators are used alternative sufferers
after getting the drug of first choice (Chobanian et al., 2004).
Type of drug that is often used in the treatment of hypertension:
i. Angiotensin converting enzyme inhibitors (ACEI)
Angiotensin converting enzyme inhibitors (ACEI) inhibit

directly angiotensin converting enzyme (ACE) and blocking

conversion of angiotensin-1 to angiotensin-2. This action reduces
angiotensin-2 that can cause vasoconstriction and secretion
aldosterone. The existence of another pathway that produces
angiotensin-2
ACEI result does not preclude the full production
angiotensin-2 so ACEI not cause effects on metabolism.
Bradykinin accumulates in some patients due to inhibition of ACE
prevent damage and inactivation of bradykinin. Bradykinin can
resulting in vasodilation by releasing nitrous oxide, but
bradykinin also can cause coughing. Examples of drugs
ACEI group is captopril, enalapril, and lisinopril (Saseen, 2009).
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13
Angiotensin converting enzyme inhibitors (ACEI) should be avoided
in patients with renal artery stenosis as likely to cause
acute renal failure. In addition, the ACEI is also contraindicated in
patients
angioedema and pregnant women (Barranger et al., 2006; BPOM RI,
2008;
WHO, 2009). ACEI side effects are most often dry cough,
rash, and headache. Hyperkalemia may occur in patients with disease
kidney or diabetes (Barranger et al., 2006).
ii. Angiotensin receptor blockers (ARBs)
Angiotensin-2 produced by the two pathways involving enzymes
namely the RAAS (renin-angiotensin-aldosterone system) involving
ACE
and alternative pathways using kimase enzyme (Carter et al., 2003).
Angiotensin converting enzyme inhibitors (ACEI) only inhibit the effects
angiotensin generated through RAAS, whereas ARBs inhibit
angiotensin-2 from all pathways. Angiotensin receptor blockers (ARBs)
directly inhibit angiotensin-2 receptor type 1 (AT1) which
mediate the effects of angiotensin-2 vasoconstriction, aldosterone
release,
sympathetic nerve activation, release of antidiuretic hormone, and
constriction
efferent arterioles of the glomerulus. Angiotensin receptor
blockers (ARBs) are not
block angiotensin-2 receptor type 2 (AT2). This causes the effect
that benefit from stimulation of AT2 such as vasodilation, improvement

network, and the inhibition of cell growth remains intact with

use of ARBs (MOH, 2006). Example ARB is valsartan,
Candesartan, irbesartan, and losartan (Chobanian et al., 2004).
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14
The use of ARBs is usually well tolerated, because
does not cause coughing and rarely cause angioedema (Weber
et al., 2014). Angiotensin receptor blockers (ARBs) should be used in
caution in patients with liver and kidney damage as well as
contraindicated in pregnancy. Side effects include dizziness ARB,
fatigue, diarrhea, pain, and infection (Barranger et al., 2006).
iii. Diuretics
Diuretics lower blood pressure, especially with
emptying deposits of sodium in the body. Diuretics decrease
blood pressure by reducing blood volume and cardiac output, but
after 6-8 weeks then return to normal cardiac output while
vascular resistance decreased. Sodium expected role in
vascular resistance by increasing the stiffness of the blood vessels and
nerve reactivation. This is probably associated with increased
sodium-calcium exchange which resulted in an increase in calcium
intracellular (Benowitz, 2009).
Four subclass diuretic used to treat
hypertension are thiazides, loop, potassium retaining agent, and
antagonists
aldosterone. Especially thiazide diuretics class is the first line
in hypertensive patients. Potassium retaining diuretics have a weak effect
when used alone but gives an additive effect when combined
with a thiazide or loop group. Aldosterone antagonists have effect
more potent with a slow onset of action (MOH, 2006).
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15
Examples of thiazide diuretics are hydrochlorothiazide, chlorthalidone,
and indapamid.
Ie loop diuretics bumetanide, torsemid, and furosemide. Retaining
diuretics
potassium is amiloride and triamterene. Aldosterone antagonists are
eplerenone and spironolactone (Chobanian et al., 2004).
Diuretics especially thiazide diuretics are contraindicated in
hypersensitivity to thiazides or sulfonylureas, anuria, pregnancy,

hyponatremia, symptomatic hyperuricemia, gout, hypokalemia

persistent, hypercalcemia, Addison's disease, severe hepatic impairment,
and
severe renal impairment (creatinine clearance <30 ml / min), while
ie loop diuretics furosemide is contraindicated in
hypersensitivity to loop diuretics or sulfonylureas, gout, anuria, and
patients with hepatic coma due to cirrhosis (NFKDOQI, 2004; Lacy et
al., 2006;
BPOM RI, 2008; WHO, 2009). Potassium retaining diuretics may
cause hyperkalemia, especially in patients with kidney disease
Chronic or diabetes and in patients using ACEI, ARB,
NSAIDs, or potassium supplements. Aldosterone antagonists can cause
hyperkalemia (MOH, 2006).
v. Beta blockers (beta blockers)
Beta receptor consists of a receptor beta-1 and beta-2 receptors.
Beta-1 receptors are found in the heart and kidney function in
regulate heart rate, renin release, and cardiac contractility.
Beta-2 receptors are found in the lungs, liver, pancreas, and smooth
muscle
arterial function in regulating bronchodilation and vasodilation. Insulator
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16
beta lowers blood pressure by reducing cardiac output and
reduce the release of renin from the kidney (Barranger et al., 2006;
Weber
et al., 2014).
Beta blockers that binds to beta-1 receptors are
because it does not inhibit the cardioselective beta-2 receptor and not
stimulate bronchoconstriction. The drugs included in the baffle
beta-1 such as metoprolol, betaksolol, atenolol, asebutolol, and
bisoprolol
safer in patients with asthma, chronic obstructive lung, and
vascular disease. At high doses, selective beta blockers loss
kardioselektifitasnya (Barranger et al., 2006). Some beta blockers
have intrinsic sympathomimetic activity (ISA). Asebutolol,
karteolol, penbutolol, and pindolol are beta blockers ISA working
as a partial agonist at the beta receptor (MOH, 2006). Beta blockers
ISA can stimulate beta receptor but with a weaker action
of the actual beta agonists. When given to patients with a pulse
weak heart, then the ISA beta-blockers may increase the rate

heart. The opposite occurs in patients at rest

or do an activity that can cause tachycardia, where the
these patients ISA beta-blockers may reduce heart rate
because of the dominance of the nature of beta blockers (Saseen, 2009).
Beta blockers should
avoided in
patients with
BB hypersensitivity, hypotension, pregnancy, bradycardia, AV block
degree 2 and 3, pulmonary edema, cardiogenic shock, and heart failure
Page 17

17
decompensation except the use of carvedilol, metoprolol extended
release, and bisoprolol (NFKDOQI, 2004; Barranger et al., 2006; Lacy
et al., 2006). The most common side effects of beta blockers is
fatigue, drowsiness, dizziness, bronchospasm, nausea, and vomiting
(Barranger et al., 2006).
v. Calcium channel blockers (CCB)
Calcium channel blockers (CCB) lowers blood pressure
by inhibiting the flow of calcium ions through the channel L on smooth
muscle cells
artery. There are two types namely dihydropyridine CCB such as
amlodipine and
nifedipine who worked dilate the arteries, as well as such
nondihidropiridin
dilitiazem and verapamil are working dilate the arteries to the effect that
weaker than dihydropyridine, but has the effect of reducing the rate
and cardiac contractility. The first generation CCB such as verapamil and
dilitiazem can accelerate the progression of congestive heart failure in
patients with cardiac dysfunction. The use of first-generation CCB
should be avoided except for the therapy in patients with angina,
hypertension, or
arrhythmia (Barranger et al., 2006; Weber et al., 2014). Dilitiazem and
verapamil should be avoided in patients with AV block grade 2 and 3,
kongesif heart failure due sitolik dysfunction, hypotension, bradycardia,
and
arterial fibrillation (NFKDOQI, 2004; Barranger et al., 2006; BPOM RI,
2008; WHO, 2009). Nifedipine short action should be avoided in patients
hypertension or hypertensive emergencies because it causes blood
pressure
diastolic irregular and tachycardia (Barranger et al., 2006).

Page 18

18
The main side effect of CCB that cause peripheral edema
which is common in high doses. These side effects can be reduced
by combining together with ACEI or ARB CCB. Calcium
channel blocker (CCB) shows the effect of the dihydropyridine
beneficial in patients with cardiovascular disease and stroke.
Calcium
channel
blockers
(CCB)
nondihidropiridin
not
recommended in patients with heart failure, but it is preferable to
patients with a rapid heart rate and to control the rate
heart in atrial fibrillation patients who can not tolerate
beta blockers. Calcium channel blockers (CCB) nondihidropiridin also
can reduce proteinuria. Calcium channel blockers (CCB) has
blood pressure lowering effects when combined with the large
ACEI or ARB (Weber et al., 2014).
vi. Alpha-1 blockers
Alpha-1 blockers work on peripheral blood vessels and
inhibit catecholamine decision on smooth muscle cells, causing
vasodilatation and lower blood pressure (ALLHAT, 2003) without
causing a decrease in cardiac output and tachycardia (Cross, 2006).
Examples of alpha-1 blockers are prazosin, doxazosin, and terazosin
(Chobanian et al., 2004).
Alpha-1 blockers should be avoided in patients with disease
because it can increase the risk of cardiovascular death (Barranger
et al., 2006). Unwelcome side effects of alpha-1 blockers are
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19
The first dose phenomenon characterized by temporary dizziness or
fainting, palpitations, and syncope 1-3 hours after the first
dose. Hypotension
orthostatic dizziness and can continue with continuous administration.
Its use should be careful in elderly patients. Alpha blockers
pass through the blood-brain barrier and may cause adverse effects in

central nervous system such as loss of energy, fatigue, and depression

(MOH,
2006).
vii. Central alpha-2 agonist
Clonidine and methyldopa lowering blood pressure, especially
by stimulating alpha-2 adrenergic receptors in the brain. This excitation
reduce the flow of the sympathetic vasomotor center in the brain, cardiac
output,
and peripheral resistance (Barranger et al., 2006). The use of alpha-2
agonists
Chronic central cause sodium and water retention, especially in
use of methyldopa. Clonidine low doses can be used to
without the addition of a diuretic to treat hypertension. Methyldopa
should
supplied with diuretics to prevent the onset of the antihypertensive effect
which occur with long-term use, except in pregnancy
(MOH, 2006).
Termination of the use of alpha-2 agonists central suddenly
can cause rebound hypertension. This effect is thought to be caused
by increasing the release of norepinephrine. Methyldopa may cause
hepatitis or hemolytic anemia, but these effects are rare. Methyldopa
should be stopped immediately if there is an increase in serum
transaminase or
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20
persistent liver alkaline phosphatase (Oparil et al., 2003).
viii. Direct arterial vasodilator
Antihypertensive effect of hydralazine and Minoxidil caused
by direct relaxation of arteriolar smooth muscle but did not cause
vasodilation to veins. Both drugs also cause
strong decrease in perfusion pressure activates baroreceptor reflex.
Baroreceptor activation causes increased sympathetic flow,
thereby increasing the heart rate, cardiac output, and release
renin (MOH, 2006). Direct arterial vasodilator may cause
fluid retention and tachycardia, so its use should be combined
with diuretics and beta blockers or other drugs (clonidine, dilitiazem,
or verapamil) that can reduce heart rate (Barranger et al.,
2006).
Hydralazine is contraindicated in patients with disease
coronary artery and mitral valvular heart disease rhemautic. Minoxidil

contraindicated in patients with pheochromocytoma, acute

myocardial infarction, and dissecting aortic aneurysm. Side effects of
hydralazine is the occurrence of lupus-like syndrome (doses> 300 mg /
day),
dermatitis, fever, and peripheral neuropathy. Minoxidil can cause
hirsutism (Barranger et al., 2006).
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21
Oral antihypertensive drugs commonly used by Chobanian et al.
(2004) are listed in Table III.
Table III. Oral antihypertensive drugs (Chobanian et al., 2004)
Drug classes
antihypertensive
These types of drugs
Blend usual dose
(Mg / day)
Frequency
common daily
ACEI
Benazepril
10-40
1
Captopril
25-100
2
Enalapril
5-40
1-2
Fosinopril
10-40
1
Lisinopril
10-40
1
Moeksipril
7.5 to 30
1
Perindopril
4-8
1

Quinapril
10-80
1
Ramipril
2.5-20
1
Trandopril
1-4
1
ARB
Candesartan
8-32
1
Eprosartan
400-800
1-2
Irbesartan
150-300
1
Losartan
25-100
1-2
Olmesartan
20-40
1
Telmisartan
20-80
1
Valsartan
80-320
1-2
Thiazide diuretics
Klorotiazid
125-500
1-2
Chlorthalidone
12.5 to 25
1
Hydrochlorothiazide
12.5 to 50
1

Politiazid
2-4
1
Indapamid
1.25 to 2.5
1
Metolazon
0.5-5
1
Loop diuretics
Bumetanide
0.5-2
2
Furosemide
20-80
2
Torsemid
2,5-10
1
Potassium retaining diuretics
Amiloride
5-10
1-2
Triamterene
50-100
1-2
Receptor antagonists
aldosterone
Eplerenone
50-100
1
Sprinolokton
25-50
1
BB
Atenolol
25-100
1
Betaksolol
5-20
1

Bisoprolol
2,5-10
1
Metoprolol
50-100
1-2
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22
Table III. Continued ...
Drug classes
antihypertensive
These types of drugs
Blend usual dose
(Mg / day)
Frequency
common daily
BB
Metoprolol extended
release
50-100
1
Nadolol
40-120
1
Propranolol
40-160
2
Propranolol longacting
60-180
1
Timolol
20-40
2
BB with intrinsic
symphatomimetic activity
Asebutolol
200-800
2
Penbutolol

10-40
1
Pindolol
10-40
2
The combination of alpha blockers
and beta
Carvedilol
12.5 to 50
2
Labetalol
200-800
2
Dihydropyridine CCB
Amlodipine
2,5-10
1
Felodipine
2.5-20
1
Isradipine
2,5-10
2
Nicardipine sustained
release
60-120
2
Long-acting nifedipine
30-60
1
Nisoldipine
10-40
1
CCB nondihidropiridin
Dilitiazem extended
release
180-420, 120-540
1
Verapamil immediate
release
80-320

2
Verapamil long acting
120-480
1-2
Verapamil
120-360
1
Alpha-1 blockers
Doxazosin
1-16
1
Prazosin
2-20
2-3
Terazosin
1-20
1-2
Alpha-2 agonists and drug action
other central
Clonidine
0.1 to 0.8
2
Clonidine patch
0.1-0.3
1 times / week
Methyldopa
250-1000
2
Reserpine
0.1-0.25
1
Guanfasin
0.5-2
1
Vasodilatator artery
Hydralazine
25-100
2
Minoxidil
2.5 to 80
1-2

Ket. ACEI: angiotensin converting enzyme, ARB: angiotensin receptor

blocker, CCB:
calcium channel blockers, BB: beta blockers
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23
Hypertension treatment algorithm can be seen in Figure 2.
Figure 2. Algorithm hypertension therapy (Chobanian et al., 2004)
The Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)
states antihypertensive drugs in most patients with hypertension should
Modifications style
life
Blood pressure is not on target
(<140/90 mmHg) (<130/80 mmHg
for diabetes or kidney disease
Chronic)
Drug choice
Without disease complications
Hypertension level I
(SBP 140-159 mmHg
or DBP 90-99
mmHg)
Most diuretics
thiazides, can
considered
ACEI, ARB, BB, CCB
or combination
Hypertension level II
(SBP 160 mmHg or
DBP 100 mmHg)
Most of the
a combination of two drugs
(Usually a diuretic
thiazide and ACEI or
ARB or BB or
CCB)
Medicines for
disease complications (see
Table IV)
Other antihypertensive drugs

(Diuretics, ACEI, ARB,

BB, CCB) in accordance
needs
Blood pressure is not on target
With disease complications
Optimize dose or give
additional drugs to the target
Blood pressure is reached.
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24
is a thiazide diuretic. This recommendation is mainly for patients with no
indication
complications with hypertension grade I, but it is possible to use
Similarly other antihypertensive drugs such as beta blockers, ACEI,
ARB, CCB, or
combination. Patients with hypertension level II should begin therapy
with
combination of two antihypertensive drugs of different classes
(Chobanian et al.,
2004).
Disease in hypertensive complications include heart failure, postinfarction
infarction, high risk of coronary disease, diabetes, chronic kidney
disease, and
prevention of stroke. Management of hypertension in patients with
indications
disease complications require special consideration. Based on the JNC 7,
indications of complications requiring certain antihypertensive drugs as
The first line. Recommended drug class is the result of consideration
from a variety of clinical trials on the use of a class of drugs in
hypertension
with disease complications (Chobanian et al., 2004). Selection of
hypertension therapy
with disease complications can be seen in Table IV.
Table IV. Selection of hypertension therapy with disease
complications (Chobanian et al., 2004)
Disease complications
Recommendations drug
BB diuretics
ACEI

ARB
CCB
ALDO ANT
Heart failure

Post myocardial infarction

High risk of coronary disease

Diabetes

Chronic kidney disease

Prevention of stroke

Ket. ACEI: angiotensin converting enzyme , ARB: angiotensin receptor

blocker , CCB:
calcium channel blockers , BB: beta blockers, ALDO ANT: aldosterone
antagonist
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7. Rationality Antihypertensive Drug Use

Irrational use of drugs is one of the world's problems.
World Health Organization (WHO) estimates that there are more than
50%
improper use of drugs in the prescribing, preparation, and sales.
Approximately 50% are also not used properly by the patient (WHO,
2002).
Irrational use of drugs can cause drug reactions
undesirable, drug resistance, exacerbating the disease, and death. Besides
The costs to be very high (WHO, 2004).
Rational drug use is said when patients receive drugs
according to clinical need, according to the dosage, and duration of
administration, as well as the cost of
issued for the drug are low for patients and
community. The right medication to be effective, quality, and safety
(WHO, 1987).
Criteria for rational use of medicines known as the principle of four right
one
alert, the appropriate indications, right drug, right patient, right dose, and
alert
to the side effects of the drug (Imono, 2003).
Precise indication means the drug to be used based on the
Accurate diagnosis of the disease and that treatment with the drug
therapy
safe and effective. Means the selection of appropriate drug treatment was
based on
consideration of the safety and efficacy ratio of the best among drug
there. Right patients means no contraindications or special conditions
facilitate the emergence of side effects and drug therapy can be accepted
by
patients. Right dose mean dose, lane, when, duration of administration in
accordance with the
the condition of the patient. Wary of the side effects of drugs means to
implement
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action to control the major side effects of drugs appropriately (Imono,
2003).
F. Description Empirical

This study was conducted to determine the characteristics of patients

with hypertension,
treatment patterns, and the rationality of the use of antihypertensive
drugs include
indication accuracy, precision medicine, patient precision, and accuracy
of dose on
hypertensive patients hospitalized in the Hospital of PKU
Muhammadiyah Yogyakarta
the period of January to December, 2013.

Penderita hipertensi di Amerika Serikat diperkirakan sekitar

77.900.000
atau 1 dari 3 penduduk pada tahun 2010. Prevalensi hipertensi pada
tahun 2030
diperkirakan akan meningkat sebanyak 7,2% dari estimasi tahun
2010. data yang
2007-2010 menunjukkan bahwa sebanyak 81,5% pasien dengan
hipertensi menyadari
bahwa mereka mengalami hipertensi, 74,9% menerima pengobatan
dengan
52,5% pasien dengan tekanan darah terkontrol (tekanan darah
sistolik <140
mmHg dan diastolic <90 mmHg) dan 47,5% dari pasien yang
tekanan darah tidak
dikendalikan. Persentase pria yang menderita hipertensi lebih tinggi
dari
wanita sampai usia 45 tahun dari usia 45-64 tahun dan persentase
yang sama,
kemudian dari 64 tahun ke atas, persentase perempuan yang
menderita
hipertensi lebih tinggi dibandingkan laki-laki (Go et al., 2014).

Hipertensi merupakan salah satu faktor risiko penyebab terbesar

morbiditas dan mortalitas penyakit kardiovaskular (Kearney et al.,
2005).
Dari tahun 1999 sampai 2009, kematian akibat hipertensi
meningkat