HYPERTENSIVE

EMERGENCY
ROHMAN AZZAM, SPd., SKep., MKep, SpKMB., (Ns)
Introduction:
 Hypertension is sustained elevation of
the resting arterial pressure
 In 1998 AHA: > 63 million American
have hypertention (BP >140/90 mmHg)
 Mortality is greater than other health
problem
Introduction:

 A hypertensive emergency is a
condition in which elevated blood
pressure results in target organ
damage.
 The systems primarily involved
include the central nervous system,
the cardiovascular system, and the
renal system.
Introduction:
 Sekitar 1% ps dg hipertensi esensial berkembang
menjadi hipertensi malignant, tetapi kenapa terjadi
demikian belum diketahui dg jelas.
 Karakteristik lesi vaskuler berupa nekrosis fibrinoid dari
arteriol dan srteri-arteri kecil, yg menyebabkan
manifestasi klinik kerusakan organ.
 RBC mengalami kerusakan sebagai akibat melewati
pembuluh darah yang terobstruksi oleh defosit fibrin,
sehingga dpt terjadi anemia hemolitik.

http://emedicine.medscape.com/article/166129-overview
 Another pathologic process is the dilatation of cerebral arteries
following a breakthrough of the normal autoregulation of
cerebral blood flow. Under normal conditions, cerebral blood
flow is kept constant by cerebral vasoconstriction in response to
increases in blood pressure.
 In patients without hypertension, flow is kept constant over a
mean pressure of 60-120 mm Hg. In patients with hypertension,
flow is constant over a mean pressure of 110-180 mm Hg
because of arteriolar thickening.
 When blood pressure is raised above the upper limit of
autoregulation, arterioles dilate. This results in hyperperfusion
and cerebral edema, which cause the clinical manifestations of
hypertensive encephalopathy.

http://emedicine.medscape.com/article/166129-overview
Hypertensive emergencies

 Include:
 Malignant hypertension
 Accelerated hypertension
 Both, similar outcomes and therapies.
 In order to diagnose malignant
hypertension: papilledema (must be
present).

Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiol Rev. 2010
Malignant hypertension

Papilledema. Note the swelling of the optic disc, with blurred margins.

http://emedicine.medscape.com/article/166129-overview
Accelerated hypertension and
hypertensive urgency
 Accelerated hypertension is defined as a recent
significant increase over baseline blood pressure that is
associated with target organ damage. This is usually
seen as vascular damage on funduscopic examination,
such as flame-shaped hemorrhages or soft exudates, but
without papilledema.
 Hypertensive urgency must be distinguished from
hypertensive emergency. Urgency is defined as severely
elevated blood pressure (ie, systolic >220 mm Hg or
diastolic >120 mm Hg) with no evidence of target organ
damage.

http://emedicine.medscape.com/article/166129-overview
Accelerated hypertension and
hypertensive urgency
 Hypertensive emergencies require immediate
therapy to decrease blood pressure within
minutes to hours
 In contrast, no evidence suggests a benefit
from rapidly reducing blood pressure in patients
with hypertensive urgency. In fact, such
aggressive therapy may harm the patient,
resulting in cardiac, renal, or cerebral
hypoperfusion.

http://emedicine.medscape.com/article/166129-overview
 Classification BP for Adulth 18/> Year Old

Category Systolic pressure Diastolic pressure Follow-up

(mm Hg) (mm Hg)
Optimal <120 <80

Normal <130 <85 Recheck in 2 yr

High-normal 130-139 85-89 Recheck in 1 yr

Hypertension:

Stage I 140-159 90-99 Confirm within 2 mo

Stage II 160-179 100-109 Evaluation or refer to

source of care within 1 mo
Stage III ≥180 ≥110 Evaluation or refer to
source of care within 1
week or immediate

National Institutes of Health

Hypertension
 Primary: unkown etiology
 Secondary, contibuting factors:
 Increase in secretion cathecolamine
 Increase in of renin by kidneys
 Increase serum sodium and blood volume
 Increase in plasma & extracellular fluid volume
 Reduction in kidney perfusion pressure
 Impairment of control mechanism in kidneys
 Alteration adrenal cortical hormon secretion
 Causes of Secondary Hypertension

Renal disease Endocrine disorder Congenital disorder Pregnancy-induced Drug-induced

disorder disorder
Acute glomurulonephritis Cushing syndrome Adrenal hyperplasia Pregnancy-induced Cyclosporine
Chronic pyelonephritis Hyperparathyroidism Coarctation of the aorta hypertension (PIH) Oral contraceptives
Hydronephritis Pheochromocytoma Preeclampsia Steroid
Renal tumors Primary aldosteronsim Eclampsia
Renovascular
hypertension
Hypertensive crisis

 Terjadi pd 1% populasi hipertensi

 Dapat terjadi nekrosis vaskuler jika:
 Tekanan diastolik >120 mmHg
 MAP ≥150 mmHg
 Jika tdk diobati, berakibat fatal (75%, dlm 1 th)
 Hypertensive crisis 1 th: mortalitas 30%
 Hypertensive crisis 5 th: mortalitas 50%
 Mean Arterial Pressure (MAP)

Sistolic BP + 2(Diatolic BP): 3 70-105 mmHg

Contoh : Seorang memilki TD 200/100 mmHg

Maka MAP-nya adalah: 200 + (2x100)/3
200 + 200/3
400/3 = 133 mmHg
Hypertensive crisis
 Dpt berkembang hypertensi encepalopati, sbg
akibat dilatasi pemb darah serebral karena tdk
mampu lagi melakukan autoregulasi.
 Aliran drh yg meningkat, dan tekanan yg
berlebihan mendorong cairan ke jaringan
perivaskuler, menimbulkan edema serebral.
 Tekanan yg ekstrim dpt menyebabkan
kerusakan arteriola: nekrosis fibrinoid di dinding
pembuluh intima dan media
 Organ lain yang juga rentan: mata dan ginjal
(kebutaan dan renal failure)
Complication of Hypertension
 Nephrosclerosis
 Coronary artery disease,
 Angina
 Myocard infark
 Heart failure
 Stroke
 Peripheral vascular disease
Assessment

 Primary survey
 Secondary survey
History & Risk Factors

 Psychologic stress
 Diet high in sodium
 Cigarete smoking
 Familial: genetic factor
 Environment factor
Clinical Presentation

Early indicator:
 Seringkali tanpa gejala
 Discomfort
 Faigue
 Dizziness
 Headache
Assessment
Late indicator:
 Throbbing suboccipital  Signs of heart failure:
headache  Dyspnea on exertion
 Irritability  Orthopnea
 Confusion  Paroxysmal nocturnal
 Somnolence dyspnea
 Stupor  Angina

 Visual loss  Renal symptom:

 Focal deficits  Hematuria
 Coma  Nocturia
 Azotemia
Pemeriksaan Fisik
 Pengukuran BP:
 Diukur setelah 5 mnt istirahat
 Dilakukan 2 kali/> dalam waktu 2 menit
 Dihitung reta-rata perbedaannya
 Jika bedanya > 5 mmHg:
 Ukur kembali
 Kalibrasi manometer/pakai alat automatic
 Tanyakan kapan terakhir merokok, mengkonsumsi
produk nikotin, caffein, adrenergic stimulant, krn dpt
meningkatkan BP
Cardiac Assessment

 Evaluasi left ventricular hypertrophy (LVH)

 LVH dpt di palpasi dg telapak tangan pd area
mitral (5th ICS pd MCL)
 S4/gallop dg bell stetoscop
 Jika terdapat cardiac failure atau LVH, apical
impuls akan terasa dekat di ALL
 Semua nadi perifer perlu dipalpasi di kedua sisi
 Pada coarctation aorta nadi femoral dikedua
sisi lemah, sedangkan di radial dan brachial
normal
(ICS: intercostal space; MCL: mid clavicular line; ALL: anterior axillary line)
Eye Assessment

 Funduscopy: hemoragik, exudate

 Kemampuan membaca, mengenali
objek/orang
Neurologic Assessment

 Dpt memperlihatkan defisit neurologi

akibat iskemik/infark serebral
dimanifestasikan dg:
 Babinski refleks (+)
 Hemiparesis
 Hemiplegi
 Confusion
 Perubahan kognitif
Diagnostic Tests
 Tes yang definitif utk hipertensi: ukur BP
 Jika diketahui hipertensi, beberapa tes lain perlu
dilakukan utk mendiagnosis kerusakan pd organ lain atau
utk mendiagnosis kondisi yg menyebabkan hipertensi
sekunder
 Meliputi, al:
 ECG

 Echocardiography

 Chest x-ray

 Urinalysis/urine culture

 Blood studies
Collaborative Management
Treatment of hypertensive  Medikasi:
crisis Nitroprusside


 Turunka segera dg cepat  Labetalol hydrochloride

 Tujuan:  Esmolol

 Nicardipine
 menurunkan MAP tdk
 Enalaprilat
lebih dari 25% dlm 2
jam  Hydralazine

 Nitroglyserin
 lalu, turunkan hingga
mencapai 160/100  Phentolamine

dlm 2-6 jam  Nifedipine

 Oral: captropil,
clonidine, labetalol
 Ubah gaya hidup
 Surgical teratment

(MAP: mean arterial pressure)

Nitroprusside
 Sering dipakai krn efek vasodilatasinya yg cepat
 Dosis awal 10-25 μg q5min, ditingkatkan 5-10 μg q5min
 Sampai pengobatan via oral efektif, pertahankan dosis
nitroprusside 0.25-10 μg/kg/min
 Obat ini mempunyai waktu kerja yang pendek, dan BP akan
naik kembali segera jika drip dihentikan
 Monitoring BP penting utk mencegah hipotensi
 Ketika antihipertensi oral telah dapat menurunkan BP, maka
nitropruside weaning perlu dilakukan utk mencegah hipotensi
 Nitroprusside dimetabolisme menjadi thiocynate yg dpt
menyebabkan: mual, kelelahan, tinitus, penglihatan kabur, dan
delirium
 Kadar thiocynate serum perlu di cek setelah 48 jam
penggunaan dan selanjutnya scr teratur di cek ulang
 Kadar thiocynate yg aman: <10 mg/dl
(q5min: tiap 5 menit)
Labetalol hydrochloride
 Merupakan fast-acting α and β-blocker, dpt juga
digunakan utk hypertensive crisis
 Diberikan iv, perlahan, dimulai 20-80 mg, dpt diulang
q10min atau diberikan melalui continuous infusion 2
mg/min
 Pertahankan ps dlm posisi supine selama injeksi dan 1
jam setelahnya
 Cek BP q5min sebanyak 6 x dan kemudian q30min
 Monitor adanya bronchospasm atau hipotensi ortostatik
Esmolol

 Merupakan fast-acting β-blocker, dg

onset of action 1-2 mnt dan durasi 10-20
mnt
 Dosis awal 250-500 μg/kg/mnt utk 1 mnt,
kemudian 50-100 μg/kg/mnt utk 4 mnt
 Waspadai hipotensi
 Dpt menyebabkan bronchospasm,
hindari pada ps asthma
Nicardipine

 Merupakan potent calsium chanel

blocker
 Diberikan 5-15 mg/jam
 Onset of action: 5-10 mnt; duration: 1-4
jam
 Dpt menyebabkan takikardia, headache,
flushing
Enalaprilat

 Merupakan ACE inhibitor

 Dosis 1.25-5 mg iv bolus, diberikan dlm waktu
>5 mnt
 Dapat diulangi q6h
 Efek puncak dosis iv pertama akan tampak
pada 4 jam, tetapi pd dosis berikutnya efek
puncak terjadi 1 jam sesudah pemberian.
 Hati-hati pd ps dg renal failure
 Hindari pada acute myocard infark

(ACE: adrenergic converting enzyme; q6h: tiap 6 jam)

Hydralazine

 Merupakan potent vasodilator

 Diberikan 10-20 mg iv bolus atau 10-40 mg im
 Onset of action: 10-30 min, duration: 2-6 h
 Efek samping: takikardia, headache, vomiting,
angina.
Nitroglyserin

 Merupakan vasodilator koroner dan perifer

 50 mg dlm vial ditambahkan ke dalam 250 ml
D5W
 Diberikan via infus 5 μg/mnt
 Onset of action-nya cepat, monitor BP
 Ditingkatkan 5-10 μg, q3-5 min
 Efek samping yg sering muncul nyeri kepala,
beri analgetik
Phentolamine

 Merupakan α-adrenergic blocking agent

 Obat ini menurunkan afterload
 Dosis 5-15 mg iv
 Onset of action: 1-2 min
 Hati-hati pd ps coronary artery disease
Nifedipine

 JANGAN gunakan obat ini utk

hypertensive emergency

(Swearingen & Keen, 2001, p 333)

Mengubah Gaya Hidup

 Mempertahankan BB normal
 Kurangi intake alkohol: <1 oz/day
 Modifikasi intake sodium: 2-3 g
 Berhenti merokok
 Regular aerobic exercise: 30 mnt, 3-
5x/minggu, target HR maksimal 60-80%
 Pertahankan intake potasium, calsium
dan magnesium adekuat
Surgical Treatment

 No surgical intervention for primary

hypertension
 Surgical for secondary hypertension:
 Coarctation aorta: remove narrowed area
of vessel with insertion Teflon aortic graft
 Renal artery stenosis: grafting or renal
artery angioplasty
 Pheochromocytoma: surgical removal of
tumor
Nursing Diagnosis

 Altered tissue perfusion:

cardiopulmonary, cerebral, renal
 Pain: headache
 Sensory/perceptual alteration
Nursing Interventions
Perubahan perfusi jaringan: kardiopulmonal, serebral, dan
renal bd interupsi aliran darah akibat vasokonstriksi yg
terjadi krn terganggunya mekanisme normal pengontrolan
BP; interupsi aliran vena akibat vasodilatasi atau edema
jaringan yang terjadi karena hilangnya autoregulasi

 Tujuan:
Dalam 24 jam perfusi membaik
 Kriteria hasil:
 BP: 110-160/70-110 mm Hg (dbn)

 MAP: 70-105 mm Hg

 Kekuatan otot bilateral sama dan normal

 Orientasi thd org, tempat, waktu

 Output urine: ≥ 0.5 ml/kg/jam

 BB stabil

 Dlm 24 jam tek sistolik <140 mm Hg, diatolik <90 mm Hg,

dg MAP: 75-105 mm Hg
Perubahan perfusi jaringan: kardiopulmonal, serebral, dan
renal bd interupsi aliran darah akibat vasokonstriksi yg
terjadi krn terganggunya mekanisme normal pengontrolan
BP; interupsi aliran vena akibat vasodilatasi atau edema
jaringan yang terjadi karena hilangnya autoregulasi

 Intervensi:
 Monitor BP & MAP q1-5 min selama mendapat medikasi;
q15 min jika telah stabil. Waspadai penurunan/peningkatan
mendadak
 Bersama dokter, diskusikan utk menentukan rentang ideal
kontrol BP dan dosis maksimal nitroprusside. Panduan yg
biasanya digunakan:
 Sistolic BP <140-160 mm Hg
 MAP < 140 mm Hg
 Diastolic BP <90 mm Hg
 Jika terjadi hipotensi, kurangi/hentikan nitroprusside
infusion sampai tekanan naik kembali
 Perubahan perfusi jaringan: kardiopulmonal, serebral, dan
renal bd interupsi aliran darah akibat vasokonstriksi yg
terjadi krn terganggunya mekanisme normal pengontrolan
BP; interupsi aliran vena akibat vasodilatasi atau edema
jaringan yang terjadi karena hilangnya autoregulasi

 Intervensi:
 Kaji defisit neurologi: cek status neurologi/jam. Jika tlh stabil
cek q4h
 Monitor perubahan hasil pemeriksan funduscopi. Konsulkan
jika ada perubahan: perdarahan
 Kaji penurunan perfusi renal:
 Monitor I&O, BB/hari
 Konsul jika output urine <0.5 ml/kg/jam utk 2 jam berturut2
atau jika penambahan BB ≥ 1 kg
 Waspadai azotemia (peningkatan BUN), penurunan creatinin
clearance, peningkatan creatinin serum

(Nilai lab optimal: BUN ≤20 mg/dl; creatinin clearance ≥9.5 ml/mnt; creatinin serum ≤1.5 mg/dl)
Nyeri kepala bd edema serebri akibat
peningkatan tekanan perfusi

 Tujuan:
Dalam 24 jam ps memperlihatkan peningkatan
kenyamanan
 Kriteria hasil:
 Keluhan nyeri berkurang/(-)

 Relaks; meringis (-)

 Skala nyeri: 0 (dg skala 0-10)

Nyeri kepala bd edema serebri akibat
peningkatan tekanan perfusi

 Intervensi:
 Monitor headache scr sering
 Beri obat nyeri sesuai program. Kaji efektivitasnya
 Ajarkan teknik relaksasi, guided imagery,
progresive muscle relaxation, music therapy
 Pertahankan lingkungan tenang, kurangi
distraktor/stimulasi yang berlebihan, batasi
pengunjung
Gg sensori-persepsi bd penurnan tajam
penglihatan akibat cedera retina yang terjadi
karena peningkatan tekanan perfusi

 Tujuan:
Dalam 24-48 jam diagnosis ini ps persepsi sensori
membaik
 Kriteria hasil:
 Dpt mengenali objek/orang/membaca

 Memperlihatkan pergerakan yg terkoordinasi

 Intervensi:
 Kaji tajam penglihatan, koordinasi gerakan

 Lakukan pemeriksaan funduskopi/8 jam

 Jika tajam penglihatan menurun, bantu ADL

 Yakinkan gg visual biasanya membaik bila BP turun

Terimakasih
WASSALAM