Escolar Documentos
Profissional Documentos
Cultura Documentos
• Riwayat Pendidikan
– 2001 Spesialis Penyakit Dalam FK UNPAD
– 2006 Konsultan Ginjal Hipertensi
– 2012 Sarjana Strata 3/Doktor FK UNPAD
Management of Hypertensive
Emergency
Ria Bandiara
Div of Nephrology & Hypertension Internal Medicine Dept
Faculty of Medicine Unpad / Hasan Sadikin Hospital
Bandung
Objectives
• To define hypertensive emergencies and identify the major risk
factors involved
• To explain key principles of pathophysiology in hypertensive
emergencies patient reinforcing the importance of gradual
downward titration of elevated blood pressure to prevent
complications
• To examine clinical approach to patients with hypertensive
emergencies
• To examine the specific management of a hypertensive emergency
in specific conditions
• Nearly 70% of all patients with a first-time MI, stroke, or
CHF have poorly controlled BP
✓ Hypertensive urgency
Hypertensive Urgency:
Brain
Hypertensive encephalopathy Retina
Stroke Hemorrhages
Exudates
Papilledema
Cardiovascular System
Unstable angina
Acute heart failure
Acute myocardial infarction
Acute aortic dissection Kidney
Dissecting aortic aneurysm Hematuria
Proteinuria
• Eclampsia/pre-eclampsia Decreasing renal function
• Peri-operative hypertension
• A Pheochromocytoma crisis
• Sympathomimetic hypertensive crisis caused by cocaine, amphetamine, MAO-I
• Abrupt cessation of clonidine or other sympatholytic drugs
Adapted from Varon J, Marik PE. Chest. 2000;118:214-227.
Major Risk Factors for Hypertensive
Emergencies
HIPERTENSIVE
EMERGENCY
Hypertensive
Emergency Vasoconstriction, often
Circulating vasoconstrictors with intravascular
hypovolemia
End organ Abrupt SVR
ischemia – Increased circulating
catecholamines
Loss of Abrupt BP – Activation of renin-
autoregulatory function angiotensin-aldosterone
system
– Altered autoregulatory
Endothelial function
damage
1. Ault NJ, et al. Am J Emerg Med. 1985;3(6 suppl):10-15. 2. Wallach R, et al. Am J Cardiol. 1980;46:559-565.
3. Varon J, et al. Chest. 2000;118:214-227. 4. Kincaid-Smith P. J Hypertens. 1991;9:893-899.
Putative vascular pathophysiology of
hypertensive emergencies
Endothelial/Vascular Smooth Muscle Interactions
• Triggers of acute changes
in vascular resistance
– Excess catecholamines
(CAT)
– Angiotensin II (ATII)
– Vasopressin (ADH)
– Aldosterone
– Thromboxane (TxA2)
– Endothelin (ET1)
– Low nitric oxide (NO) or
prostaglandin (PGI2)
• Abrupt rise in BP
– Promotes expression of
cellular adhesion
molecules (CAMs)
Vascular Smooth Muscle Contraction
Is Calcium Dependent
Ca++
Calcium influx into vascular
smooth muscle
may occur via opening of
L-type calcium channels
Ca++ plus calmodulin
Myosin kinase Release of intracellular stores
may also be a source of Ca++
Actin-myosin interaction
Contraction
Ca++
Adapted with permission from Frishman WH, et al. Curr Probl Cardiol. 1987;12:285-346.
Cerebral Autoregulation Is Central to Treatment
of Hypertensive Crises
Patients with chronic hypertension
Cerebral Blood Flow autoregulate cerebral blood flow
around higher set points
Chronic hypertensive
Increasing risk
of ischemia
Goals :
• Establish diagnosis + recognize ongoing TOD
• Prevent further TOD by reducing the BP in a controlled,
predictable, and safe way
• Supportive therapy
• Treat the patients and not the number
• Simple answer
– 25% reduction in MAP within 1st hour
– Target ~ 160/100 mm Hg by 2-6 hours
2. Treatment
hypotension