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CURRICULUM VITAE

• Nama : DR. Ria Bandiara,Dr.SpPD-KGH,FINASIM


• Riwayat Pekerjaan
1. Sekretaris Koordinator Bidang Pendidikan Profesi Dokter
Departemen Ilmu Penyakit Dalam FKUP/RS Dr Hasan Sadikin
Bandung (2004 – 2010)
2. Ketua Program Studi Pendidikan Dokter Spesialis Ilmu Penyakit
Dalam, Departemen Ilmu Penyakit Dalam FKUP/RS Dr Hasan
Sadikin Bandung (2010 – sekarang)
3. Ketua Indonesian Renal Registry (2011 – 2014.

• 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

• The 2014 JNC guidelines for BP management recommended a less


aggressive treatment approach for older hypertensive patients
than that proposed in the JNC7 guidelines

• Could increase the number of patients found to be in a


hypertensive crisis in the ED

• Hypertensive emergencies represent up to one-fourth of all ED


visits
Trends in the incidence of hypertensive emergency in US Emergency Departments,
2006–2013

Janke TA. J Am Heart Assoc. 2016;5:e004511 doi: 10.1161/JAHA.116.004511


✓ Hypertensive emergency

✓ Hypertensive urgency
Hypertensive Urgency:

• Systolic BP >180 mmHg or diastolic BP >120 mmHg


• No evidence of end-organ damage (clinical or laboratory)
• Symptoms : headache, shortness of breath and epistaxis
• Typically either noncompliant with prescribed medication
or have been lost to follow up
• Need intensification of their anti hypertensive drug
therapy
• BP reduction over several hours to days
• Optimal treatment in this population is close outpatient
follow-up
• Usually treated with oral anti hypertensives
1. Mansoor GA, Frishman WH. Heart Dis. 2002;4:358-371.
2. Varon J, Marik PE. Chest. 2000;118:214-227.
Hypertensive Emergency:
– Systolic BP >180 mmHg or diastolic BP >120 mmHg

– Evidence of end-organ damage (on-going)


• Retina
• Heart
• Brain
• kidney

– Hypertensive emergencies are associated with significant short-term


and long-term morbidity and mortality : 5-year mortality approaches
100%

– Need effective and rapid acting medication administered iv to lower


the elevated BP safely, protect target organ function, ameliorate
symptoms, reduce complications and improve clinical outcomes
1. Mansoor GA, Frishman WH. Heart Dis. 2002;4:358-371.
2. Varon J, Marik PE. Chest. 2000;118:214-227.
End-Organ Damage Characterizes
Hypertensive Emergencies

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

• Antihypertensive therapy failing to provide adequate


blood pressure control
• Failure to adhere to prescribed antihypertensive
regimens
• Lack of a primary care physician
• Illicit drug use

Varon J, Marik PE. Critical Care. 2003;7:374-384.


Current State of Hypertensive
Emergency Management
• Accelerated hypertension is among the most misunderstood
and mismanaged of acute medical problems seen in clinical
practice
• Delays in initiating therapy can cause severe complications in
target end organs
• Overzealous therapy resulting in a too-rapid reduction in
blood pressure is equally damaging
• Many clinicians fail to consider the pathophysiologic principles
involved in managing hypertensive emergencies

1. Varon J, Marik PE. Chest. 2000;118:214-227.


2. Epstein M. Clin Cornerstone. 1999;2:41-54.
Pathophysiologic Principles at
Work in the Hypertensive Milieu
Main potential mechanisms and target organ involvement in
the diagnosis of hypertensive emergency.

HIPERTENSIVE
EMERGENCY

Shantsila A. American Journal of Hypertension 2017;30(6):543-59


Pathophysiology of the Hypertensive 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

SVR = systemic vascular resistance.

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

Patients with cerebral ischemia


Increasing risk of lose their ability to autoregulate
hypertensive Ischemia
encephalopathy Normotensive

Chronic hypertensive
Increasing risk
of ischemia

0 50 100 150 200 250


MAP (mm Hg)

Adapted with permission from Varon J, Marik PE. Chest. 2000;118:214-227.


Approach to Patients
 History

▪ Duration and severity of pre-existing hypertension


▪ Presence of previous OD (renal & cerebrovascular disease)
▪ Anti hypertensive drug therapy : drug names, doses,
sudden discontinuations
▪ Degree of BP control
▪ Intake of over-the-counter preparations such as
sympathomimetic agents, and use of illicit drugs such as
cocaine should be ascertained promptly
▪ Family history of sudden death, premature cardiac disease,
endocrine disorders, hiperthyroidism

Adebayo, Emerg Med Clin N Am 2015;33:539-51


 History

▪ The most vital part of the history is assessment of signs


and symptoms associated with the patient’s chief
complaint ( eg. Chest pain, shortness of breath, urine
output, weakness or altered consciousness) and targeted
evaluation of end organs

▪ The presence of symptoms alone does not confirm a


hypertensive emergency, but it suggests that an organ
might be affected, requiring further assessment

Adebayo, Emerg Med Clin N Am 2015;33:539-51


 Examination : detect any OD
▪ Neurological examination : level of consciousness, signs of
meningeal irritation, visual fields, focal signs such as drift
of the outstreched arms
▪ Funduscopic exam : the presence of new haemorrhages,
exudates or papilloedema

▪ Cardiovascular exam : heart failure (raised jugular venous


pressure, third heart sound or gallops)
▪ Pulmonary exam : rales, hypoxia, tachipnea
▪ Abdominal bruit

Adebayo, Emerg Med Clin N Am 2015;33:539-51


 Diagnostic Testing

▪ Laboratory analysis based on which organ system could be


damaged : complete blood count, BUN, creatinine,
electrolytes, urinalysis
▪ ECG
▪ Chest radiograph
▪ Computed Tomography

Adebayo, Emerg Med Clin N Am 2015;33:539-51


 Challenge : no formal guidelines

 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

 All patients should be managed in the ICU


How Low Should You Go?

• Simple answer
– 25% reduction in MAP within 1st hour
– Target ~ 160/100 mm Hg by 2-6 hours

Marik and Varon. Critical Care 2003, 7:374-84.


How Low Should You Go?
• Better answer
– It really depends on clinical condition
• Less aggressive with ischemic stroke
• More aggressive with hemorrhagic stroke,
acute HF and aortic dissection

 Most ischemic complications develop with


reductions greater than 20 - 30 % (over 24 to
48 hours)
 Blindness, paralysis, coma, death, MI
The ideal properties of IV agents
for Hypertensive emergencies

• Ability to regulate and control blood pressure reduction

•Minimal risk of hypotension

• Rapid and predictable reduction of BP

• Minimal side effects/few adverse effects

SHORT ACTING, FAST ONSET OF ACTION, VASODILATOR, TITRATABLE,


TYPE OF ORGAN DAMAGE
Parenteral Drugs for the Treatment of Hypertensive Emergenies

Drug Dose Onset of action Duration of action

Sodium 0.25–10 g/kg/ min as IV Immediate 1–2 min


nitroprusside infusion
Nicardipine HCl 5–15 mg/h IV 5–10 min 15–30 min, may
exceed 4h
Fenoldopam 0.1–0.3  g/kg/ min IV 5 min 30 min
infusion
Nitroglycerin 5–100  g/min as IV 2–5 min 5–10 min
infusion
Enalaprilat 1.25–5 mg every 6 h IV 15–30 min 6–12 h
Hydralazine HCl 10–20 mg IV 10–20 min IV 1–4 h IV
10–40 mg IM 20–30 min IM 4–6 h IM
Labetolol HCl 20–80 mg IV bolus every 10 5–10 min 3–6 h
min
0.5–2.0 mg/min IV infusion
Phentolamine 5–15 mg IV bolus 1–2 min 10–30 min

Chobanian AV et al. JNC 7-Complete Version. Hypertension. 2003;42:1206 –1252


NICARDIPINE I.V

• Used safely in hypertensive encephalopathy, cerebral vascular


accidents and post/peri-operative
• Acts as dihydropyridine calcium channel blockers.
• Dose-dependent :
Predictable onset of action
Rapidly reduced BP.
No rebound on withdrawn
• Adverse effect : tachycardia, hypotension and headache.
• Contraindication to patient with elevated ICP at the acute stage of
cerebral stroke. 1) Nicardipine product information
2) Nathan Saphiro, Hypertensive Emergencies, 2002
3) George A. Mansoor et.al., Heart Disease : A Journal of Cardiovasbular medicine ., 2003
NITROGLYCERIN I.V

• Strong vasodilator ( arterial- and veno-dilator ) with


rapid onset and duration of action.
• Adverse effect : headache, tachycardia, nausea,
vomiting
• Caution in coronary artery disease and low SBP
• Used as an adjunct to other anti-hypertensives
• Use for acute coronary syndromes and acute
pulmonary edema

1. Nathan Saphiro, Hypertensive Emergencies, 2002


2. George A. Mansoor et.al., Heart Disease : A Journal of Cardiovasbular medicine ., 2003
DILTIAZEM I.V

• Useful for hypertensive emergency and urgency.


• Acts as Non-dihydropyridine calcium channel blockers.
• Dose-dependent :
Predictable onset of action
Rapidly reduced BP.
No rebound on withdrawl
• Adverse effect : bradycardia, hypotension, headache,
flushing.
• Has anti ischemic and anti arrhythmic effect (class-IV)
CLONIDIN IV

• Reduce peripheral sympathetic tone by central


stimulation of 2- receptor.

• Unpredictable onset of action.

• Adverse effect : sedation, dry mouth, constipation


and a tendency to a overshoot or rebound
hypertension on withdrawn.

W.H. Frishman, et al., Cardiovascular Pharmacotherapy, 1996


Usual Adult Dose for Hypertensive Emergency
0.2 mg orally once. Additional doses of 0.1 mg may be given as
needed and tolerated every hour to control patient's blood
pressure. The maximum recommended total daily dose in any
case of emergent hypertension is 0.8 mg.
Eleven severely hypertensive patients: severe left ventricular
failure, hypertensive encephalopathy, cerebral haemorrhage,
dissecting aortic aneurysm, renal failure, and severe epistaxis.
0-15 mg or 0-3 mg clonidine was given every 40 minutes. Doses of
clonidine required for control ranged from 0-15 mg (one ampoule)
to 0.9 mg (mean 0.56 mg).
It is concluded that clonidine is effective and safe in the treatment
of hypertensive emergencies.
NIFEDIPINE

1. 16 pasien diamati : meninggal 2, stroke 4, infark miokard 9,


dan aorta diseksi 1
2. Bioavailibilitas oral atau bukal buruk
3. 1985 FDA melarang penggunaannya untuk hipertensi
emergensi
4. 1996 FDA boleh digunakan dengan pengawasan ketat
apabila tidak ada obat lain

Grossman E et.al, JAMA, 1996 Oct 3-30; 276(16):1328-31. Review


SPECIFIC EMERGENCIES
ACUTE AORTIC DISSECTION
80% die within 2 weeks
• Rapid and immediate reduction of BP within 5 to 10 min is
needed
• BP should be decreased rapidly to <120 mgHg
• Therapy aim: reduce shear stress on the aortic wall by
decreasing both BP and heart rate
• Single agent option : Esmolol
• The loading dose is 500–1,000 mcg/kg/min administered
over 1 min followed by a 50 mcg/kg/min infusion rate.
The maximum infusion rate is 200 mcg.
• If the BP remains elevated after beta blockade, a vasodilator
such as iv nitroglycerin or nitroprusside may be administered

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


ACUTE LV FAILURE and PULMONARY EDEMA
80% die within 2 weeks
• The drugs of choice are iv nitroglycerin, clevidipine, or
nitroprusside with loop diuretic

• Beta blockers are contraindicated

• The BP in patients with hypertensive emergencies should be


lowered within minutes to 1 h about 20% to 25% and then
gradually to 160/100 mmHg within the next 2 to 6 h, and
then cautiously to normal over the next 24 to 48 h

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


ACUTE LV FAILURE and PULMONARY EDEMA
80% die within 2 weeks
• The initial infusion rate of IV nitroglycerin is 5 mcg/min. The
max infusion rate is 20 mcg/min.

• The initial infusion rate of intravenous sodium nitroprusside is


0.3 to 0.5 mcg/kg/min. The maximum infusion rate is 10
mcg/kg/min.

• The initial infusion rate of iv clevidipine is 1–2 mg/h. The


maximum infusion rate is 32 mg/h.

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


Acute myocardial infarction or unstable
angina pectoris and severe hypertension
• should be treated with intravenous esmolol
• IV nitroglycerin may also be administered if needed
• The target BP is <140/90 mmHg in patients with AMI or
unstable angina pectoris who are hemodynamically stable
• BP < 130/80 mmHg at hospital discharge should be
considered
• Caution should be used in lowering the BP in these patients to
avoid lowering the diastolic BP < 60 mmHg as this may
decrease coronary perfusion and aggravate myocardial
ischemia

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


Acute kidney injury
• The drugs of choice are clevidipine, fenoldopam,
and nicardipine

• The initial infusion rate of intravenous fenoldopam is 0.1 to


0.3 mcg/kg/min. The maximum infusion rate is 1.6
mcg/kg/min.

• The initial infusion rate of intravenous nicardipine is 5 mg/h.


The maximum infusion rate is 30 mg/h

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


Eclampsia or Pre-eclampsia
• The drugs of choice are hydralazine, labetalol, and nicardipine
• ACE-I, ARB, direct renin inhibitors, and sodium nitroprusside
are contraindicated in treating these patients.
• The maximum initial dose of iv hydralazine administered by
slow intravenous infusion is 20 mg. This dose may be
repeated every 4–6 h if needed.
• The initial dose of intravenous labetalol is 0.3 to 1.0 mg/kg
with a maximum initial dose of 20 mg followed by an
intravenous infusion of 0.4 to 1.0 mg/kg/h up to 3 mg/kg/h.
The total cumulative dose is 300 mg. This dose can be
repeated every 4 to 6 h if needed.

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


Stroke. 2015;46:000-000. DOI: 10.1161/STR.0000000000000069

Efficacy of Early Intensive BP-Lowering Treatment


The ED algorithm for early diagnosis and emergent interventionof ICH

Dastur CK, Yu W. Stroke and Vascular Neurology 2017;00:e000047. doi:10.1136/svn-2016-000047


Acute ischemic stroke
• The 2013 AHA/ASA acute ischemic stroke guidelines state that
it is unknown what the blood pressure target level should be
for patients with acute ischemic stroke or which
antihypertensive drug should be recommended

• These guidelines currently recommend not reducing the


blood pressure during the initial 24 h of acute ischemic stroke
unless the BP is above 220/120 mmHg or there is a specific
medical disorder that would benefit from blood pressure
reduction.

Aronow WS. Ann Transl Med 2017;5(Suppl 1):S5


Potential Approaches to
Arterial Hypertension in
Acute Ischemic Stroke
Patients Who Are
Candidates for Acute
Reperfusion Therapy
GUIDELINE FOR HYPERTENSIVE EMERGENCY TREATMENT

CARDIOVASCULAR PHARMACOTHERAPY HANDBOOK (Version Date: 01/14/2015)


GUIDELINE FOR HYPERTENSIVE EMERGENCY TREATMENT

CARDIOVASCULAR PHARMACOTHERAPY HANDBOOK (Version Date: 01/14/2015)


1. Emergency SUMMARY

- Progressive or impending target organ damage

- Require immediate BP reduction with parenteral agent

2. Treatment

- Require close BP monitoring. Should not cause

hypotension

- Different BP goal in acute ischemic stroke

- Drug regimen without clear outcome studies