Kelainan Kasus(%)
Stroke penyumbatan pembuluh darah otak 24,5
Stroke perdarahan otak dan batang otak 4,5
Penurunan kesadaran karena hipertensi 16,3
Edema pulmonal akut 22,5
Gagal jantung kongestif akut 14,3
Penyakit jantung koroner akut 12,0
Pecah pembuluh darah besar (aorta) 2,0
Eklamsia (kejang akibat hipertensi) 2,0
KOMPLIKASI KRONIK HIPERTENSI PADA
ORGAN PENTING LAINNYA
• Retinopati hipertensif
• Gagal ginjal kronik
• Tuli sensorineural
• Penyumbatan pembuluh darah tepi
(PAD)
• Penyakit saraf tepi (Neuropati perifer)
Hipertensi Bisa Sembuh ?
Saat seseorang menderita hipertensi,
penyakit tersebut tidak akan sembuh total.
Mempertahankan
berat badan ideal
Mengurangi konsumsi
garam
Hindari stress dan
olahraga rata-rata 30
menit tiap hari
Mengontrol kadar
kolesterol dan gula darah
Laki-laki : Wanita = 2 : 1
Insidensi pada populasi kulit putih menurun
(Australia & New Zealand)
Insidensi pada populasi kulit hitam, Asia dan
Suku Indian meningkat
DEFINISI
Hipertensi Emergensi
• Hipertensi berat dengan TDD > 120 mm Hg
• Terdapat KOT AKUT (otak, jantung, ginjal)
• Menurunkan TD dalam menit – jam dengan
menggunakan obat antihipertensi intravena
• Perlu perawatan di ICU
DEFINISI
Hipertensi Urgensi
• Hipertensi berat dengan TDD > 120 mm Hg
• Tidak terdapat KOT AKUT
• Bisa bergejala / tanpa gejala (sakit kepala
hebat, cemas, sesak nafas)
• Menurunkan TD dalam 24 – 48 jam
menggunakan obat oral
• Tidak perlu perlu perawatan di ICU
DEFINISI
Hipertensi Maligna :
• Hipertensi Berat
• Disertai kelainan retina Keith – Wagener –
Barker stad IV :
- papil edema
- pendarahan retina
- eksudasi retina
• Biasa menggambarkan hipertensi emergensi
dengan kelainan SSP
DEFINISI
Hipertensi Akselerasi
• Hipertensi berat disertai kelainan retina
• Keith – Wagener – Barker stad III :
- perdarahan retina
- eksudasi retina
- tanpa papil edema
Nilai absolut dari kenaikan TD itu sendiri tidaklah begitu
penting, sebab kenaikan TD tiba-tiba yang sedang saja
pada orang yang sebelumnya normotensif sudah dapat
menyebabkan KOT yang kritis (contohnya: preeklamsia
atau glomerulonefritis akut) atau pada pasien dengan
penyakit penyerta seperti aorta desekans atau infark
miokard akut.
PATOFISIOLOGI
Ke tekanan darah
mendadak
KOT Akut
Patofisiologi – peran kenaikan TD
Critical Degree of Hypertension
Systemic effects
Local effects
(Renin-angiotensin,
(prostaglandins, free
catechol, vasopressin)
radical, etc
Myointimal proliferation
Tissue ischemia
Patofisiologi peran ke TD
Kenaikan mendadak TD Isemia jaringan
Stress pd
NO Nekrosis fibrinoid
Kerusakan
endotel pd
Systemic effects
Local effects
(Renin-angiotensin,
(prostaglandins, free
catechol, vasopressin)
radical, etc
Myointimal proliferation
Tissue ischemia
“Break through Vasodilatation”
Cerebral Auto-regulation in Hypertensive
Patients
Cerebral Blood
Flow
Increased risk of
encephalopathy Normotension
Increased risk of
ischemic Chronic hypertensive
60 120 180
Hipertensi :
95% tak diketahui – essensial
5% diketahui - sekunder
Tipe Kasus(%)
Infark serebral 24,5
Perdarahan intraserebral dan Subarakhnoidal 4,5
Hipertensi Ensefalopati 16,3
Edema pulmonal akut 22,5
Gagal jantung kongestif akut 14,3
Infark miokardial akut dan angina tak stabil 12,0
Aorta disekans 2,0
Eklamsia 2,0
Manifestasi klinik
3. Pemeriksaan penunjang
Severe Hypertension in Emergency
Departement
NO YES
NO YES
Sodium IV 0.25-10 mg/kg/min Within 1-2 min decreased decreased no effect decreased
nitroprusside seconds
Labetolol IV (20-to 80-mg 5-10 min 2-6 hr no effect decreased decreased no effect
bolus/10 min)
Fenoldopam IV 0.1-0.6 mg/kg/min 10-15 min 10-15 min no effect decreased increased increased
Nicardipine IV 2-10 mg/hr 5-10 min 2-4 hr no effect decreased increased no effect
Esmolol IV 80-mg bolus over 30 6-10 min 20 min no effect no effect decreased no effect
second, followed by 150
mg/kg/min infusion
Hydralazine IV bolus (10-20 mg) 10 min 2-6 hr no effect decreased Increased no effect
Table Recommended antihhypertensive agents for hypertensive crisis
Therapeutic goal First do no harm, avoid Reduction of BP, Redution of BP Reduction of Reduction of
hypoperfusion especially by Decrease shear orces by excessive
Do not exceed 20% vasodilatation myocardial reduction of BP sympathomimetic
reduction of BP Promote diuresis oxygen demand and tachycardia drive
Risk of therapy Cerebral autoregulation is Diuretics and Blocker can Nitroprusside is Unopposed blockade
disrupted in the ischemic angiotensin converting exacerbate left extremely potent can cause alpha
brain enzyme inhibitor can ventricular failure and requires storm and increase
Patients demonstrate exacerbate renal continuous intra- cocaine toxicity
marked lability of BP with dysfunction arterial BP
any agent, and monitoring
hypoperfusion of the brain
can occur
Pearls There is no clear evidence of Diuretics are slow to Blockade also Avoid volume Measure core
benefit with intensive control work reduces mortality depletion in temperature and treat
of BP in the setting of stroke Angiotensin converting associated with patients requiring hyperthermia if
enzyme inhibitor has ventricular IV dye or going present
rapid onset of action arrhythmia for general Consider the
IV nitrates dilate anesthesia possibility of
capacitance vessels at multidrug use
low doses, higher
doses dilate arterioles
and lower BP
Pengobatan Hipertensi Emergensi
BP(mmHg) Follow up
a Diuretics should be considered in patients with volume overload only. In oliguric patients, hemofiltration
may be necessary.
b Nitroprusside may be considered if no alternatives are available, but the dose and duration must be
limited to avoid toxicity.
Oral drugs for hypertensive urgencies