Professional Documents
Culture Documents
Pendidikan Dokter
FK UNAIR 1979
Organisasi profesi :
• Ikatan Dokter Indonesia (IDI)
• Perhimpunan dokter Ahli Penyakit Dalam Indonesia (PAPDI)
• Perhimpunan Nefrologi Indonesia (PERNEFRI)
• International Society of Nephrology (ISN)
Penulis Utama :
• GGA di RSUD Dr. Soetomo
• Nutrisi pada CKD
• PAD pada CKD
• Hypertension Target Organ Damage: How to Prevent?
• Nutritional Management in CKD and KetoAcid Therapy
Etiology
Pathophyisiology
Definition
Management
Introduction
• Hypertension is silent killer
• Poorly controlled hypertension is major risk for
Cardio and cerebrovascular morality
Acute severe elevation in the blood pressure can
cause acute end organ damage
• 1-2% of all the hypertensive patients present in
emergency room with hypertensive emergency at least
once in their lifetime
• Prompt recognition, evaluation and treatment are very
important in preventing permanent end organ damage
• But most of the recent guidelines do not give explicit
the management of Hypertensive crisis
500
0
introduction Yr 2000 Yr 2025
28% ---------------------------------
Unaware of their
hypertension
39% ---------------------------------
Not Receiving therapy
65% ---------------------------------
Do not have their BP
controlled to levels below
140/90 mmHg
48%
Not treated (n = 2,458) Both are at equally
increased risk compared
with controlled BP
(p>0.05)
35%
BP uncontrolled
(n = 1,756)
17%
BP controlled (n = 872)
Only 24%
Hypertension
Aware of
Hypertensive
Status
• Common associations
– Previous history of hypertension
– Lack of a primary care physician
– Non adherence to antihypertensive regimen
– Elicit drug use
Thaha
Kirk J.Pak et al The Oschner J 2014
Epidemiology
Emergency cases in ER Hipertensive Crisis
Other case HT Crisis Urgency HT Emergency HT
27% 24%
73% 76%
(times nl)
High intake
• Stimulates vasoconstrictor
substance from the kidney
Normal intake
• Initiate & Perpetuate
0 50 100 150 200
PVR increased
HNPE DIC
Urgency
Increased BP
Without or minimal Target organ Damage
mostly DBP >120 mmHg Reduced BP within hours
Not determined by BP level, but rather the imminent 22
compromise vital organ function Uptodate, 2015
Complications of Hypertension:
End-Organ Damage
Hypertension
Infarct,hemorrhage ACS,ALO
,encephalopathy
Aortic Dissection
Renal Failure,
KW-Papiledema Proteinuria
Slide Source
CHD = coronary heart disease
Thaha
Hypertension Online
CHF = congestive heart failure www.hypertensiononline.org
LVH = left ventricular hypertrophy Chobanian AV, et al. JAMA. 2003;289:2560-2572.
Patient Evaluation
Additional
Physical Evaluation Special
Examination Consideration
Ophthalmoscopy
History Taking BP both arms Radiographic
ECG
Symptoms Cardiac- CT
Electrolytes
Hypertension Pulmonary MRI
Scr
Drugs Pulses TTE/TEE
Urinalysis
Abdominal Cardiac Marker
HCG
Thaha
28
Hypertension Research 34, 367-371 (March 2011)
The Patients
www. Gacguidelines.ca
Hypertensive Emergency Management
www.gacguidelines.ca
Treatment of Hypertensive Emergencies
Drug Mechanism Dose Onset of Duration Adverse Effects*
Vasodilators of Action Action of Action
Nicardipine Calcium 5-15 mg IV 5-15 min 15-30 Tachycardia, Most hypertensive
hydrochloride channel every hour min, headache, emergencies except
blocker may flushing, nausea, acute heart failure
exceed vomiting, local
4 hr phlebitis
Fenoldopam Dopamine- 0.1-0.3 µg/ >5 min 30 min Tachycardia, Most hypertensive
mesylate 1receptor kg/min IV headache, nausea, emergency; caution
agonist infusion flushing with glaucoma
Clevidipine Calcium 1-2 mg/hr 2-4 min 5-15 min Tachycardia, Most hypertensive
butyrate channel IV infusion; headache, emergencies; caution
blocker inc rease flushing, heart with severe aortic
every 5-10 failure stenosis, acute heart
min up to deterioration failure
16 mg/hr
Sodium ↑ Cyclic 0.25-10 Immedia 1-2 min Nausea, vomiting, Caution in situations
nitroprusside GMP, µg/kg/min te muscle twitching, associated with CNS
blocks IV thiocyanate and manifestations,
intracellular infusion† cyanide hepatic or renal
Ca2+ increase intoxication, failure; probably
impaired cerebral should be avoided if
autoregulation, given other agents,
coronary steal especially
syndrome fenoldopam
Treatment of Hypertensive Emergencies
Drug Mechanism Dose Onset of Duration Adverse Effects*
Vasodilators of Action Action of Action
Nitroglycerin ↑ Nitrate 5-100 µg/min 2-5 min 5-10 min Headache, Coronary ischemia,
receptors IV infusion vomiting, pulmonary edema
methemoglobine-
mia,tachyphylaxis,
tolerance with
prolonged use
Enalaprilat ACE 1.25-5 mg 15-30 6-12 hr Precipitous fall in Acute left
inhibitor every 6 hr IV min BP in high-renin ventricular
states, variable failure; avoid in
response, acute acute myocardial
renal failure infarction
Isradipine Calcium 0.15 µg/kg 1-10 1-2 hr Headache, flushing, Perioperative,
channel /min IV, incre- min peripheral edema, pregnancy
blocker ase by 0.0025 dizziness,
µg/kg /min tachycardia
every 15 min.
Maintenance
infusion 0.15
µg/kg/min
Hydralazine Opens K+ 10-20 mg IV 10-20 1-4 hr Tachycardia, Must be given with
hydrochloride channels min flushing, concomitant IV
headache, β-blockers to avoid
vomiting, precipitation of
aggravation of angina but not a
Treatment of Hypertensive Emergencies
Drug Mechanis Dose Onset of Duration Adverse Effects*
Vasodilators m Action of Action
of Action
Adrenergic Inhibitors
Discharge :
After exclusion of acute end-organ damage
Ascertain that the blood pressure is stable or improving
Patients at high risk for acute cardiovascular events
should probably be admitted
www.gacguidelines.ca
Within Few Hours
Oral furosemide (if the patient is volume overloaded) at a
dose of 20 mg (or higher if the renal function is not normal)
• Observed few hours, reduction 20-30 mmHg, longer acting afterwards, follow up
• Sublingual nifedipine is contraindicated in this setting
and should not be used.
Fast acting
Easily titratable
Rapidly reversible and safe
No single agent has these characteristics
Drugs alternatives
Primary Condition Therapy
Acute aortic dissection Labetalol or nicardipine + esmolol,
nitroprusside + esmolol
Hypertensive encephalopathy Labetalol, nicardipine, fenoldopam,
clevidipine
Acute myocardial ischemia Nitroglycerin + esmolol, fenoldopam,
labetolol
Congestive heart failure Loop diuretic, Nitrogliserin, enalaprilat
Eclampsia Hydralazine, nicardipine, labetalol
Pheochromocytoma Phentolamine, labetalol
Acute pulmonary edema Sodium nitroprusside, nicardipine,
fenoldopam, loop diuretic, nitroglycerin
Acute ischemic stroke/intracerebral bleed Nicardipine, fenoldopam, labetalol,
clevidipine
Acute renal failure/MAHA Nicardipine, fenoldopam
40
Adapted from Varon et al. 2012
Nicardipine
• Second generation DHP CCB.
• Strong cerebral and coronary vasodilation. J Emerg Med 1987:5:463-473
I, arterial intima showing gross proliferative change and ‘onion skin’ appearance; L, severely
narrowed arterial lumen; M, arterial media; T, tubular atrophy and interstitial fi brosis.
Oxford Handbook of Nephrology and Hypertension. Simon Steddon,
Neil Ashman, Alistair Chesser John Cunningham. 2nd Edition, 2014.
Rostral ventrolateral medulla (RVLM) (+)
Kidney
1 receptors
Vasoconstriction
Renal blood flow
Wall thickening of artery / arteriole
– <should
• How 160/100,
thislong-term <140/90 mmHg
goal be achieved
• Rapidity
– Moreof/ blood pressure
less quickly, lowering
quite room