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Dr. Santoso C.
The syndrome of hypertensive emergency was first described by Volhard & Fahr in 1914 and was characterized by severe accelerated hypertension (also called malignant-accelerated hypertension), accompanied by evidence of renal disease and by signs of vascular injury to the heart, brain, retina and kidney, and by a rapidly fatal course ending in heart attack, renal failure or stroke .
DEFINITION
The 2003 Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) defi nes hypertensive crisis as a systolic BP (SBP) >179 mmHg or a diastolic BP (DBP) >109 mmHg with or without acute target organ involvement.
HYPERTENSIVE EMERGENCIES
Diagnosis : Papiledema must be present
Papiledema. Note the swelling of the optic disc, with blurred margins
HYPERTENSIVE EMERGENCIES
Develop in up to 1% of patients with essential hypertension Elevated blood pressure results in target organ damage The systems primarily involved include :
CNS CVS Renal system
Hypertensive urgency :
Severely elevated BP (systolic >180 mmHg; or diastolic >110 mm Hg) No evidence of ongoing or imminent target organ dysfunction related to the current episode of hypertension
Schematic representation of autoregulation of cerebral blood flow in normotensive and hypertensive subjects. In both groups, initial increases or decreases in mean arterial pressure are associated with maintenance of cerebral blood flow due to appropriate changes in arteriolar resistance. More marked changes in pressure are eventually associated with loss of autoregulation, leading to a reduction (with hypotension) or an elevation (with marked hypertension) in cerebral blood flow. These changes occur at higher pressures in patients with hypertension, presumably due to arteriolar thickening. Thus, aggressive antihypertensive therapy will produce cerebral ischemia at a higher mean arterial pressure in patients with underlying hypertension. Redrawn from Kaplan, NM, Lancet 1994; 344:1335.
PATHOPHYSIOLOGY
The reason is poorly understood Mechanical and humoral factors Mechanical stress and endothelial injury leading to :
Increased permeability Activation of the coagulation cascade and platelets Deposition of fibrin.
Endothelial injury and fibrinoid necrosis Release of additional vasoactive mediators Activate RAA system result in further vasoconstriction and production of proinflammatory cytokines Volume depletion due to pressure natriurresis further stimulates the release of vasoconstrictor These collective mechanisms can culminate in end organ hypoperfusion, ischemia and dysfunction
Dilatation of cerebral arteries following a breakthrough of the normal autoregulation of cerebral blood flow. This results in hyperperfusion and cerebral edema, which causes the clinical manifestations of hypertensive encephalopathy
OTHER CAUSES :
Complications of pregnancy Use of cocaine, MAOIs, oral contraceptives Withdrawal of alcohol, beta-blockers, or alpha stimulants Renal artery stenosis Pheochromocytoma Aortic coarctation Hyperaldosteronism Hyper and hypothyroidism
CLINICAL MANIFESTATIONS
Most often occurs in patients with long -standing uncontrolled hypertension. Marked elevation in BP, usually above 180/120 mmHg. Retinal hemorrhages, exudates and papilledema. Malignant nephrosclerosis, leading to acute kidney injury, hematuria and proteinuria. Neurologic symptoms due to intracerebral or subarachnoid bleeding, lacunar infarcts, or hypertensive encephalopathy.
EVALUATION
Duration and previous level of high BP Quantification of smoking and physical activity, weight gain and dietary intake Screening for symptoms of malignant hypertension, focusing on the cardiac, renal, and CNS Underlying medical disorders The patients medications and other drugs should be thoroughly reviewed The most common presentations : chest pain, dyspnea and neurologic deficit
PHYSICAL EXAM
Palpation of kidneys Auscultation of abdominal murmurs ( renovascular hypertension); Auscultation of heart sound and murmurs (aortic coarctation or aortic stenosis) Murmurs over neck arteries Motor or sensory neurological defects Abnormal cardiac rhythms, ventricular gallop Pulmonary rales Fundoscopic abnormalities in the retina Intravascular volume status Absence, reduction or asymmetry of pulses in lower extremities and ischemic skin lesions Body weight, waist circumference and body mass index.
CARDIOVASCULAR SYSTEM
Presenting symptoms :
Angina Myocardial infarction Congestive heart failure Pulmonary edema
Blood pressure must be checked in both arms to screen for aortic dissection or coarctation Volume status must be assessed
Encephalopathy (severe hypertension, headache, vomiting, visual disturbance, mental status changes, seizure, and retinopathy (papil edema) Focal signs mandate screening for cerebral hemorrhage, infarct or the presence of a mass
THE FOLLOWING CONDITIONS SHOULD ALSO BE CONSIDERED : Stroke Intracranial mass Head injury Epilepsy or postictal state Connective-tissue disease (especially lupus with cerebral vasculitis) Drug overdose or withdrawal Cocaine or amphetamine ingestion Acute anxiety Thrombotic thrombocytopenic purpura
WORKUP
Initial lab studies : CBC and electrolytes (including calcium), BUN, creatinine, glucose, coagulation profile, and urinalysis Others are as indicated : cardiac enzymes, urinary catecholamines, and TSHs, and 24hour urine collection for VMA and catecholamines.
1. RADIOLOGIC STUDIES
Chest radiograph Others are as indicated :
Head CT scanning Transesophageal Echocardiogram Renal angiography
2. Electrocardiography
Hipertensi urgensi
> 180/110 mmHg
Hipertensi emergensi
Evaluasi
Sering kali > 220/140 mmHg Dapat tidak Sakit kepala hebat, sesak Nyeri dada, sesak berat, bergejala; sakit nafas, edema gangguan status mental, kepala defisit neurologik fokal Tidak ada kerusakan Biasanya tidak ada Kerusakan organ akut organ akut kerusakan organ akut, yang mengancam jiwa tetapi mungkin terdapat (contoh : infark miokard peningkatan kreatinin akut, stroke, ensefalopati, serum gagal ginjal akut dan gagal jantung) Turunkan tekanan Turunkan tekanan darah Turunkan tekanan darah darah dalam hitungan dalam 24 hingga 72 jam segera; turunkan 15 hari hingga 25% dalam 2 jam Rawat jalan Biasanya dapat dilakukan Rawat inap, di unit rawat jalan perawatan intensif Oral, kerja panjang Oral, dengan onset Intravena cepat; kadang-kadang diperlukan intravena Dalam 3 hingga 7 Dalam 24 hingga 72 jam Intensif hari
Obat
Labetalol Klonidin
Dosis
200 400 mg po 0,1 0,2 mg po; dapat diulang tiap jam hingga max 0,6 mg 12,5 25 mg po
Kaptopril
15 60 mnt
Dapat mempresipitasi gagal ginjal akut pada stenosis arteri renalis bilateral Hindari nifedipin sub lingual atau kerja pendek karena risiko stroke, infark miokard akut dan hipotensi berat Sakit kepala, takikardia, flushing, edema perifer Sinkope (dosis pertama), takikardi, hipotensi postural
30 mg po
20 mnt
Amlodipin Prazosin
5 10 mg po 1 2 mg po
30 50 mnt 2 4 jam
Obat
Sodium nitroprusid
Dosis
0,25-2,0 g/kg/mnt iv
Nitrogliserin
Nikardipin
5 g/mnt, titrasi 5 g/mnt tiap 5 hingga 10 mnt ingga maksimum 60 g/mnt 5 mg/jam, dinaikkan 2,5 mg/jam tiap 5 mnt hingga maksimum 15 mg/jam
Fenoldopam
Labetalol
Klonidin
0,1 g/kg/mnt sbg dosis inisial, dinaikkan 0,05 hingga 0,1 g/kg/mnt hingga maksimum 1,6 g/kg/mnt Bolus inisial 20 mg, bolus iv dapat 2-5 mnt/2-4 jam diulang 20 80 mg atau infus 2 mg/mnt dengan dosis max 300 mg/24 jam 0,15-0,3 mg iv tiap 40 mnt
1-5 mnt/15-30 mnt, tapi mungkin lebih dari 12 jam setelah pemberian lama < 5 mnt/30 mnt
Sakit kepala, pening, flushing, mual, edema, takifilaksis, meningkatkan tekanan intrakranial
Spasme bronkus, hipotensi, pening, mual/muntah, hipotensi orthostatik, blokade irama jantung
Diltiazem
Verapamil Enalapril
Dosis inisial 0,25 mg/kg diberikan 3-30 mnt dalam 2 mnt, diikuti infus 5-15 g/kg/mnt atau 15-45 mg/jam (BB 50 kg) 5-10 mg iv; dapat diikuti dengan 1-5 mnt/30-60 mnt infus 3-25 mg/jam 0,625-1,250 mg iv tiap 6 jam 15-60 mnt/12-24 jam
Efek paradoksal berupa kenaikan tekanan darah dapat dijumpai pada sebagian pasien setelah dosis inisial, kondisi ini dapat dicegah dengan pemberian fentolamin iv Sedasi, mulut kering, konstipasi, rebound hipertensi Hipotensi, flushing
Hambatan irama jantung Gagal ginjal pada pasien stenosis arteri renalis bilateral, hipotensi
kombinasi
TERIMA KASIH