Hypertensive Emergencies

Dr. Rulli Rosandi,

Bagian Peny.Dalam RSU Langsa
 Curriculum Vitae
Nama : Dr. Rulli Rosandi, SpPD

Tempat/Tanggal Lahir : Banda Aceh, 12 September 1977

Jabatan : Sebagai Staf Bagian Ilmu Penyakit Dalam RSU Langsa 2010-sekarang

Riwayat Jabatan :

Sebagai Dokter PTT di RSU Langsa 2001-2003

Sebagai Dokter di Puskesmas Langsa Kota 2003-2004

Riwayat Pendidikan :

Lulus Dokter Umum : FK – Univ.Brawijaya Malang ,2001

Lulus Spesialis Penyakit Dalam : FK Univ.Brawijaya Malang ,2009

Tulisan :
Association of anti dsDNA, proteinuria, and Mex-SLEDAI in patients with
Lupus Nephritis ( Indonesian Journal of Hypertension, May 2011)
 Mortality risk in relation to sex and B.P.
Systolic blood pressure
mmHg Standard risk
woman
87–97 men
98–127
128-137
138-147
148-157
158-177
178-197
> 198
Diastolic blood pressure
woman
48-68 men
69-83
83-88
88-93
93-98
98-108
108-118
> 118
0 100 200 300 400 500 600 700
800 Mortality ratio in %
Definitions
 Hypertensive Emergency: A relatively
high blood pressure with evidence of
target organ damage.

 Hypertensive Urgency: Elevated BP with

imminent risk of target organ damage
Definitions
 Acute Hypertensive Episode: SBP >180
or DBP >110 and no target organ damage

 Transient Hypertension: Hypertension

that occurs in association with
• Pain • Anxiety
• Withdrawal syndromes • Cessation of
• Some toxic substances medications
ED Evaluation
 History
• History of HTN • Compliance
• Blood pressure trends • Past medical history
• Prescribed medications • Family history
• OTC medications • Illicit drug use
 Review of systems directed at:
• CNS (HA, hemiparesis) • Renal (hematuria)
• Cardiac (CP, dyspnea)
ED Evaluation
 Physical Exam
• Appropriate sized cuff
• Measure arms and legs
• Brachial difference <20mm Hg
• Focus on areas of potential target-organ
damage
-CNS -Heart -Retina
-Pulmonary -Pulses -Renal
Cotton wool spot (soft exudates)
Cotton wool spots
Hard exudates
Retinal Hemorrhage
Disk Edema
Diagnostic Studies
 CBC-hemolytic anemia
 Glucose-hypoglycemia
 Electrolytes-hyperkalemia
 BUN/Cr-azotemia, ARF
 Urine-proteinuria, RBC cast
 CXR-Pulmonary edema, aortic dissection
 ECG-ischemia, infarction pattern
 Head CT-hemorrhage, infarction
What precipitates an emergency?
1. Non-compliance with medications in a
chronic hypertensive patient
2. Those with secondary hypertension
(e.g. pheochromocytoma, reno-vascular
hypertension, Cushing’s)
3. Hypertension during pregnancy is a
major risk factor for women
General Management Goals
 Reduce BP so autoregulation can be re-
established
 Typically, this is a ~25% reduction in
MAP
 Or, reduce MAP to 110-115
 Avoid
• Lowering the BP too much or too fast.
• Treating non-emergent hypertension
General Management Goals
 Exceptions: aortic dissection and
eclampsia

 In aortic dissection and eclampsia, BP

should be lowered to normal levels

 Search for secondary causes

Categories of Hypertensive
Emergencies
 Hypertensive encephalopathy

 Stroke syndromes
• Embolic
• Hemorrhagic
• Subarachnoid hemorrhage
Categories of Hypertensive
Emergencies
 Cardiovascular
• Acute LV failure (“Flash” pulmonary edema)
• Acute coronary syndrome
• Aortic dissection
 Pregnancy related hypertension
• Pre-eclampsia
• Eclampsia
• HELLP syndrome
Categories
 Catecholamine excess
• Pheochromocytoma
• MAOI + tyramine
• Cocaine/amphetamines/OTCs
• Clonidine withdrawal
 Other
• Renal failure
• Epistaxis
• Childhood hypertension
Hypertensive Encephalopathy
 Symptoms:
• Mental status change – somnolence,
confusion, lethargy, stupor, coma, seizure
• Focal neurologic deficit
• Headache – alone not sufficient to diagnose a
hypertensive encephalopathy
• Nausea and vomiting
 Signs:
• Papilledema, cotton wool exudates
Diagnostics
 Hypertensive encephalopathy is a
diagnosis of exclusion – thus, exclude
the other possibilities!
 Only definitive criteria is a favorable
response to BP reduction. However
clinical improvement may lag behind BP
improvement by hours to days
Pathophysiology
 A loss of cerebral autoregulation.
 Autoregulation is best studied in the
brain but present in heart and kidneys
as well
 Represents the body’s attempt to
maintain constant FLOW of blood to
perfuse the cells
Autoregulation
 In the uninjured, normotensive brain,
autoregulation is effective over MAP
ranging from about 50 – 150

 In the chronic hypertensive, this range

is increased (e.g. 80 – 180)
Autoregulation
Pathophysiology
 Loss of autoregulation leads to:
• Cerebral hyper-perfusion
• Vascular permeability
• Cerebral edema
• Vasospasm
• Ischemia
• Punctuate hemorrhages
Therapy
 Untreated, hypertensive encephalopathy
leads to coma and death
 Goal is to reduce MAP by 20-25% in the
first hour
 This will get MAP back into range where
autoregulation is re-instituted
Therapy
 Nitroprusside
• 1st line, 0.3 – 10 mcg/kg/minute
 Labetalol
 Enalaprilat
 Fenoldopam
Stroke Syndromes
Thrombo-Embolic CVA
 Represent 85% of all strokes
 BP elevations are generally mild-
moderate and represent a physiologic
response to maintain cerebral perfusion
pressure to the penumbra, which has
lost its ability to autoregulate
Embolic CVA - Dilemma
 Inappropriate lowering of the BP may
convert the potentially salvageable
ischemic penumbra to true infarction.
 However, persistent BP >185/110 is a
contraindication to thrombolytic
therapy (it significantly increases risk
of intra-cranial bleeding)
Embolic CVA –When to Rx HTN
 For thrombolytic candidates, 1-2 doses
of labetalol (5mg) or nitroglycerin paste
may be used in attempt to get BP
<185/110
 If thrombolytics are given, then the BP
MUST be aggressively kept below
185/110!
Embolic CVA – When to Rx HTN
 According to National Institutes of
Neurologic Disorders and Stroke:
• SBP <220, no treatment
• DBP <120, no treatment
 Tintinalli suggests not treating DBP <140
 Others use MAP <130
Embolic CVA – When to RX
 If complicated by:
• Aortic dissection
• Hypertensive encephalopathy
• AMI
• Renal failure
Embolic CVA –How to Rx HTN
 Goal is to reduce MAP 10-20% in
uncomplicated embolic CVA with
markedly elevated pressures
 Labetalol: 5mg doses
 Nitroglycerin paste
Why not treat everybody?
 Danger of being too aggressive in acute
CVA is well documented.
 Many studies show a worsening of
neurologic outcome when the above
guidelines are not followed.
Hemorrhagic CVA
 Unlike embolic CVA, BP elevations in
hemorrhagic CVA are profound
 However, this again represents a
physiologic response to increased
intracranial pressure (and free blood
irritating the autonomic nervous
system)
 Typically is transient
Hemorrhagic CVA – When to Rx
 Evidence to support anti-hypertensive
therapy in acute intracranial
hemorrhage is lacking
 However, modest reductions of ~20%
MAP have not been show to adversely
affect outcome
Hemorrhagic CVA - Rx
 Labetalol is agent of choice
 ACE inhibitor can be used but not as
well studied.
 Vasodilators such as nitroprusside and
nitroglycerin are contraindicated
because they may raise the ICP
Subarachnoid Hemorrhage
 A special subset of hemorrhagic CVA.
 Evidence suggests that there may be
less vasospasm and less re-bleeding if
SBP <160 or MAP <110
 Agents:
• Oral nimodipine 60mg q 4hr x 21 days
• IV nicardipine 2mg bolus, then 4-15mg/hr
Acute Left Ventricle Failure
Pathophysiology
 Abrupt, severe increase in afterload
leads to systolic and diastolic
dysfunction.
 Vicious cycle ensues:
• Heart failure causes poor coronary perfusion, LV
ischemia and worsening failure
• CHF leads to hypoxia and worsens LV ischemia
• Renal hypoperfusion leads to renin release and
this increases afterload
Signs and Symptoms
 Abrupt and severe dyspnea, tachypnea,
and diaphoresis
 Rales, wheezes, distant breath sounds,
frothy sputum, and gallop rhythm
Goals of therapy
 1. Reduce preload and afterload!
 2. Minimize coronary ischemia by
increasing supply (blood to coronary
arteries) and decrease demand (wall
tension, tachycardia)
 3. Oxygenate, ventilate, clear pulmonary
edema.
Therapy
 Nitroglycerin
• Arterial (especially coronaries) and veno-dilator,
reducing preload and afterload
 Lasix
• Initially a vasodilator, then diuretic
 Morphine
• Vasodilator and sympatholytic
 ACE inhibitor
• Interrupts the renin-angiotensin-aldosterone axis
Acute Coronary Syndrome
 Elevated BP significantly increases LV
wall tension
 Wall tension is one of main determinants
of myocardial oxygen demand.
ACS therapy goals
 Goal is to decrease wall tension by
decreasing preload and afterload.
 Typical agents do this well:
Nitroglycerin, beta-blockers, morphine
 Avoid hydralazine and minoxidil, as they
increase myocardial oxygen demand.
Treatment of Hypertensive Urgencies
 Goal: Gradual reduction of blood pressure
over 24 hours
 Treatment:
• Restart prescribed anti-hypertensive medications
for the non-compliant patient
• Clonidine • Sublingual nitroglycerine
• Captopril • Nifedipine (don’t use)
• Losartan
 Follow up within 24 hours
Treatment of Hypertensive Episode
 Treat cause of hypertensive episode
(i.e. pain, anxiety)
 Refer to a primary care physician and
start anti-hypertensive medications only
upon advice of referring physician
Why not treat all elevated BP in the
ED?
 Association of overly aggressive BP
reduction in setting of stroke with
worse neurologic outcome widely shown
 What about the person incidentally
found to have elevated BP?
From Journal of Emergency Medicine,
2000, pp 339-45.
 “Stroke Precipitated by Moderate Blood
Pressure Reduction”
 6 cases total; All presented to an ED.
2 with completely resolved TIAs and 4
with no neurological complaints at all.
 All suffered CVAs and had permanent
dysfunction or death.
Starting anti-HTN therapy in the ED
 May mislead the patient to believe that
they are cured
 May interfere with office assessment
of the true nature of the HTN
 Best treatment in the ED is likely
education regarding the chronic nature
of hypertension and need for follow up!
SIMPLE APPROACH TO HYPERTENSIVE CRISIS

BP > 220/120 mmHg

Neurological sign Headache

(encephalopathy or stroke) No neurological signs
Retinopathy grade 3-4 No target organ damage
Severe chest pain
(Ischemia or dissecting
URGENCY
aneurism)
Pulmonary edema
Eclampsia Identify the cause
Cathecolamine excess In panic attacks or anxiety use
Acute renal failure analgesic, anxiolytics
Otherwise use oral
antihypertensive agents
EMERGENCY recheck in 6-24 hours

Intravenous therapy
Principles of Therapy for
Hypertensive Emergencies
 Patients must be hospitalized for monitoring
 Dire consequences of lowering BP too quickly
 Treated with parenteral
 Lower MAP {1/3(SBP-DBP)+DBP} by no more
than 25% within minute to 1 hours or diastolic
110 mmHg, then 160/100 mmHg within 2-6
hours (JNC VII). Exception for ischemic stroke
 IV infusion is prefer than bolus
 Avoid the urge to turn to sublingual nifedipine

Hypertension,Brian C. Poole and Anitha Vijayan in Nephrology and

Subspeciality Consult,Lippincott Williams and Wilkins,2004
Intravenous Agents for Hypertensive Emergencies
Agent Onset Duration Advantage Disadvatage
Nitroprusside Immediate < 3 min Potent, Cyanide,
titratable thiocyanate
Nitroglycerine 2-5 min 3-5 min Coronary Tolerance,
perfusion variable efficacy

Fenoldopan < 5 min 5-10 min Renal perfusion Increase IOP

Hydralazine 10-20 min 3-9 hrs Eclampsia Tachycardia,

headache
Nicardipine 5-15 min 1-4 hrs CNS protection Avoid in CHF or
cardiac
ischemia
Enalaprilat 15-30 min 6 hrs CHF, acute LV Avoid in MI
failure
Diltiazem 5-10 min 2-4 hrs CNS protection, Bradycardia,hy
coronary & potension
renal perfusion
Emergency Preferred Drugs Drugs to Avoid

CVA Diltiazem Diazoxide,hydralazine (increase

Labetalol ICP)
Nitroprusside
Nicardipine
Hypertensive Encephalopathy Diltiazem Diazoxide,hydralazine (increase
Nitroprusside ICP)
Labetalol
Nicardipine
Congestive Heart Failure Nitroprusside Labetalol and Esmolol
Nitroglycerine (decreased HR)
Enalaprilate
Loop Diuretics
Myocardial infarct,Ungina Nitroglycerine Diazoxide,hydralazine (increase
Nicardipine HR,O2 demand
Nitroprusside
Diltiazem
Aortic Dissection Nitroprusside Diazoxide,hydralazine,
Labetalol nicardipine
Esmolol

Hypertensive emergencies,Roy Colven,in Emergency Medical Therapy,2000. WB saunders Company

Summary – Neurologic emergencies
 Hypertensive  Nitroprusside, goal
encephalopathy ~25 reduction
 Embolic CVA  Only if >220/120
or>185/110 for t-PA
 Hemorrhagic CVA  Labetalol for ~10-
20% reduction
 SAH  Nimodipine 60 mg
Q4hrs x 21 days
Summary – Cardiovascular emergency
 Aortic dissection  Nitroprusside +
Esmolol or Labetalol
– SBP ~100
 Acute LV failure  NTG, Lasix, MS04
for symptoms and
~10-15% reduction
 Acute coronary  NTG, MS04, beta-
syndrome blocker to symptom
improvement
Summary – Other emergencies

 Eclampsia and HELLP  Goal DBP ~90;

magnesium,
hydralazine,
labetalol, delivery!

 Catecholamine  Phentolamine +/-

excess beta blocker for
~25% reduction over
several hours
Thank You….