PENANGANAN HIPERTENSI EMERGENSI

Dr. Librantoro, SpJP, FIHA

PENYAKIT KARDIO VASKULAR

HIPERTENSI

Prevalensi : 1 milyar Mortalitas : + 7.1 juta MONICA-JAKARTA 1993-2000 : 16.9 % 17.9 %

 Peningkatan TD sistolik sebesar 20 mm Hg atau 10 mm Hg TD diastolic) 2 X mortalitas kardiovaskular.

High normal blood pressure (BP) meningkatkan risiko terjadinya hipertensi sebesar 5 X.

MANAJEMEN HIPERTENSI

Perubahan pola hidup

Terapi Farmakologi HIPERTENSI Penurunan berat badan PENYAKIT KARDIO VASKULAR

Poirrier et al. 2006 Tiap Kg Menurunkan TD Sistolik 1-2 mmHg & Diastolik 1-4 mmHg

HYPERTENSION(JNC-7class.)
SBP-mmHg
NORMAL PREHYPERTENSION STAGE 1 STAGE 2

DBP-mmHg
AND<80

<120

120-139
140-159 >=160

or 80-89
or 90-99 >=100

Excess sodium intake

Reduced nephron nunber

Stress

Genetic Alteration

Obesity

Endothelium derived factor

Renal sodium retention

Decreased filtration surface

Sympathetic Nervous overactivity

Renin angiotensin excess

Cell membrane alteration

Hyperinsulinemia

Fluid volume

Venous Constriction

Preload

Contractility

Functional Constriction

Structural Hypertrophy

BLOOD PRESSURE = CARDIAC OUTPUT Hypertension = Increased CO

X and/or

PERIPHERAL RESISTANCE Increased PVR

Autoregulation

Beberapa Faktor yang terlibat dalam kontrol tekanan darah

(Kaplan, 2002)

Sympathetic Nervous System Regulation of Blood Pressure

CNS Adrenal Gland Adrenergic Catecholamin Tone es Arteries Resistance

Baroreceptor Reflexes Vein s Capacitance

Afterload
Preload Cardiac Output Volume/Pressure Renin/Angiotensin

Heart

Kidney

Blood Pressure

Renin Substrate

Renin-Angiotensin-Aldosterone Regulation of Blood Pressure

Renin Angiotensi nI Angiotensin II

Aldosteron e
Vasoconstriction

Kidney
Sodium & Water Reabsorption

Adrenal Cortex

Blood Pressure

MANAJEMEN HIPERTENSI
PERUBAHAN GAYA HIDUP

DEFINISI
Krisis Hipertensi Adalah peningkatan tekanan darah yang sangat tinggi (>180/120 mmHg) dan dapat diklasifikasikan sebagai hipertensi emergensi dan hipertensi urgensi. Hipertensi emergensi Merupakan suatu keadaan yang jarang dijumpai, yang memerlukan penurunan tekanan darah sesegera mungkin untuk membatasi atau menghindari kerusakan organ target lebih lanjut.

Hipertensi urgensi Keadaan dimana tidak terdapat tanda-tanda kerusakan organ target dan memerlukan penurunan tekanan darah secara bertahap dengan terapi oral dalam 24-48 jam.

Keadaan-keadaan yang dapat timbul pada hipertensi emergensi :

Hipertensi ensefalopati Kejadian intrakranial akut Diseksi aorta akut Sindroma koroner akut (angina tidak stabil/infark miokard akut) Gagal jantung akut Eklamsia

Manifestasi Klinis Krisis Hipertensi

Neurologis : Sakit kepala, kejang, penurunan kesadaran Mata : retinal bleeding , edema papil Jantung : Nyeri dada, edema paru Ginjal : Azotemia,proteinuria, oligouria Kebidanan : Preeclampsia

Hypertensive Emergencies
Stroke Encephalopathy

Aortic Dissection

Decompensated Heart Failure

Acute Coronary Syndrome Acute Renal Failure

Eclampsia

Severe Hypertension
BP > 180/120 mm Hg Progressive Target Organ Damage?
Yes HT Emergency No

1st Episode HT Urgency

Oral Rx in ED Clinic : 24h

Frequent Episodes Uncontrolled HT

Parenteral Rx Admit to ICU

Refill Rx Clinic in 72h

PENANGANAN HIPERTENSI EMERGENSI Di ruang ICU/ICCU Bed rest Menggunakan antihipertensi intra vena Menurunkan tekanan arteri rata-rata (mean arterial pressure/MAP) tidak lebih dari 25 % dalam beberapa menit sampai 2 jam Menurunkan tekanan darah sampai + 160/100 mm Hg dalam 2-6 jam

Ideal Pharmacologic Agents for Hypertensive Crises

- Fast acting, stable - Rapidly reversible - Titratable without significant effect - Parenteral administration

JNC 7, 2003

JNC 7 Recommendation for Hypertensive Emergency

Drugs
Sodium nitroprusside Nitroglycerin Labetolol HCl Fenoldopan HCl Nicardipine HCl

Dosage
0.25-10 ugr/kg/min 5-500 ug/min 20-80 mg every 10-15 min or 0.5-2 mg/min 0.1-0.3 ug/kg/min 5-15 mg/h

Onset
Immediate 1-3 minutes 5-10 minutes <5 minutes 5-10 minutes

Duration
1-2 minutes after infusion stopped 5-10 minutes 3-6 minutes 30=60 minutes 15-90 minutes

Esmolol HCl

250-500 ug/kg/min IV bolus, 1-2 minutes then 50-100 ug/kg/min by infusion; may repeat bolus after 5 minutes or increase infusion to 300 ug/min

10-30 minutes

JNC 7, 2003

CHEST 2007 Recommendation for Hypertensive Emergency

Acute Pulmonary edema / Systolic dysfunction
Acute Pulmonary edema/ Diastolic dysfunction Acute Ischemia Coroner

Nicardipine, fenoldopam, or nitropruside combined with nitrogliceryn and loop diuretic

Esmolol, metoprolol, labetalol, verapamil, combined with low dose of nitrogliceryn and loop diuretics Labetalol or esmolol combined with diuretics

Hypertensive encephalopaty
Acute Aorta Dissection Preeclampsia, eclampsia Acute Renal failure / microangiopathic anemia Sympathetic crises/ cocaine oveerdose Acute postoperative hypertension Acute ischemic stroke/ intracerebral bleeding

Nicardipine, labetalol, fenoldopam

Labetalol or combined Nicardipine and esmolol or combine nitropruside with esmolol or IV metoprolol Labetalol or nicardipine Nicardipine or fenoldopam Verapamil, diltiazem, or nicardipine combined with benzodiazepin Esmolol, Nicardipine, Labetalol Nicardipine, labetalol, fenoldopam
CHEST, 2007

AHA / ASA 2007 Recommendation for Hypertensive Emergency

Drug
Labetalol Nicardipine Esmolol Enalapril Hydralazine Nipride NTG

I.V. Bolus Dose

5 20 mg every 15 NA 250 ug/kg IVP loading dose 1,25-5 mg IVP every 6 h 5 20 mg IVP every 30 NA NA

Continous Infus Rate

2 mg/min (max 300mg/d) 5-15 mg/h 25-300 ug/kg/m NA 1,5-5 ug/kg/m 0,1-10 ug/kg/m 20-400 ug/m

AHA/ASA Guideline, 2007 update. Stroke. 2007;38: 2001-2023.)

Sodium Nitroprusside
Sodium nitroprusside is the treatment of choice for hypertensive encephalopathy. Both an arterial and venous dilator. IV administration and lowers BP within one or two minutes. Short half-life: 2 minutes. Initial dose: 0.5ug/kg/min. Disadvantages: increased coronary steal. Therefore, sodium nitroprusside is not the drug of choice in hypertensive emergencies that manifest as AMI or CHF Adverse effects: hypotension. Contraindicated in pregnancy : cross the placenta..

Nicardipine
Nicardipine is a second generation dihydropyridine derivative Calcium Channel Blocker with high vascular selectivity and strong cerebral and coronary vasodilatory activity Onset of actions : 1 to 5 min, Duration of actions of 4 to 6 h

CHEST, 2007

Nitroglycerin
Dilator of coronary arteries promotes redistribution of blood flow to all areas of the myocardium. Drug of choice for hypertensive emergencies associated with myocardial ischemia or CHF. Half-life: four minutes. Disadvantages: hypotension and reflex tachycardia.

Hydralazine
It is not recommended in hypertensive emergencies involving the CNS because it increases CBF and intracranial pressure. It is unsuitable for CV-related hypertensive emergencies because of reflex tachycardia and increased myocardial oxygen consumption. It is routinely used for eclampsia because it had no apparent effect on the fetal circulation.

Nifedipine
Nifedipine is a calcium antagonist that produces a coronary and peripheral vasodilation. 10 to 30 minutes onset of action. Adverse effects: neurologic sequelae, fetal distress, MI, and decreased renal perfusion.

The biggest mistake in treating hypertensive emergencies is over-correction of BP.

Catatan :
- Nifedipin sublingual tidak digunakan lagi sebagai terapi hipertensi emergensi/urgensi, karena penurunan tekanan darah yang tiba-tiba dapat menimbulkan iskemia pada ginjal, otak dan pembuluh darah koroner.

PENANGANAN HIPERTENSI URGENSI Ruang perawatan biasa Bed rest Diet rendah garam Terapi antihipertensi oral Penurunan tekanan darah bertahap 24-48 jam

OBAT-OBAT YANG DIGUNAKAN PADA PENANGANAN HIPERTENSI URGENSI

Nama Obat Kaptopril Nitrogliserin Nikardipin Isradipin Labetalol Klonidin Furosemid Golongan Penghambat EKA Vasodilator Antagonis kalsium Antagonis kalsium Penyekat dan Agonis Diuretik Dosis 25- 50 mg 1,25-2,5 mg 30 mg 1,25-5 mg 200-1200 mg 0,1-0,4 mg 40-80 mg

ALGORITMA PENANGANAN HIPERTENSI

OBAT-OBAT ANTI HIPERTENSI ORAL

Contraindications of oral (SL) antihypertensive agents

Disadvantages: unpredictable dose-reponse effects, longer onset, longer half-life.

Nifedipine

Labetalol
Both a selective alpha-1 antagonist and nonselective betaantagonist MAP and peripheral vascular resistance are reduced more than the heart rate. Does not reduce CBF Drug of choice when there is an excess of catecholamine, such as pheochromocytoma or clonidine withdrawal. Labetalol is frequently used as a second-line therapy in cases of hypertensive encephalopathy. Half-life: 2-3 hrs. Disadvantages: large volume of distribution, unpredictable dose-reponse, slow onset of action, long half-life. Induce bronchospasm and worsen CHF.