HYPERTENSION

Emergencies & Urgencies

Dr. Harun Hudari SpPD
DIVISION OF TROPICAL INFECTIOUS DISEASES
DEPARTMENT OF INTERNAL MEDICINE
SCHOOL OF MEDICINE, SRIWIJAYA UNIVERSITY
MOH. HOESIN HOSPITAL
PALEMBANG

Content

Introduction
Definitions
Prevalence/morbidity/mortality
Etiology & pathophysiology
Diagnosis
Causes
Differential diagnoses
Workup
Management
Treatment
Pharmacology IV Anti-hypertensives
References

Introduction

Hypertension(HPT) very common Western soc.

50 mil. US affected (world - approx. 1 billion people)
Despite awareness + treatment still 30% adults unaware
40% known with HTN - not on treatment
60% on treatment BP not controlled to <140/90 mm Hg

New data shown incr. lifetime risk of HPT

- incr. risk of CVS complications with normal
BP levels

Classification OF HYPERTENSION
Joint National Committee (JNC 7) introduced a
new classification system for HTN 2004

Normal SBP<120 and DBP<80

Prehypertension SBP 120-139 or DBP 80-89
Stage I hypertension SBP 140-159 or DBP 90-99
Stage II hypertension SBP >160 or DBP >100
Stage II HPT further divided into:
Hypertensive urgency
Hypertensive emergency

Other Terminology
Severely elevated BP (JNC VII)
Defined as BP > 180/120

accelerated HPT
term used to describe individuals with chronic
hypertension with associated group 3 KeithWagener-Baker retinopathy

malignant HPT
describe those individuals with group 4 KWB
retinopathy changes + papilledema

Definitions
HPT emergency(crisis): Is characterized by a
severe elevation in BP, complicated by evidence of
impending or progressive target/end organ
dysfunction
VS
HPT urgency: is a severe elevation in BP without
progressive target organ dysfunction
NB these definitions do not specify absolute BP
levels

Definitions
Emergencies

Symptomatic
Acute End-Organ Damage
Diastolic B.P. usually >130 mmHg

Urgencies
Asymptomatic
NO Acute End-Organ Damage
Diastolic B.P. usually >110 mmHg; Systolic
B.P. usually >180 mmHg

Conditions constituting evidence

of EOD

Hypertensive encephalopathy
Intracerebral heamorrhage
Stroke
Head trauma
Ischemic heart disease (most common)
AMI
Acute LVF with P/oedema
Unstable angina

Aortic dissection
Eclampsia
Life threatening arterial bleed

Prevalence/ morbidity/
mortality
Prevalence:
- With progress in anti-hypertensive Rx decrease in the lifetime
incidence of HPT emergencies from 7% to 1%
- Hypertensive crisis more common among elderly and black patients
- Studies HPT related problems amount for 25% of all pt visits to
medical section of ED. 33% of these - HTN emergencies.
Morbidity/mortality
- Dependent on the extent of EOD on presentation and the degree to
which BP is controlled subsequently.
- 1year survival rate has increased from 20% to more than 90% with
appropriate treatment.
- 10-year survival rate approaches 70% with approp treatment
- 1-year and 5-year mortality rate - following untreated HPT
emergency are 70 to 90% and 100% respectively

Etiology
Most common
- rapid unexplained rise in BP in pt with chronic essential HPT
- most have history of poor treatment/compliance or an abrupt discont
of their meds

Other causes
Renal parenchymal disease (80% of sec.causes)
Systemic disorders with renal involvement (SLE)
Renovascular disease (Atheroscleroses/fibromuscular dysplasia)
Endocrine ( phaeochromocytoma/cushing syndrome)
Drugs (cocaine/amphetam/clonidine withdrawal/diet pills)
CNS (trauma or spinal cord disorders Guillain-Barre
Coarctation of the aorta
Preeclampsia/Eclampsia
Postop. HPT

Pathophysiology
Not well understood
Failure of normal autoregulation + abrupt rise in SVR
Increase in SVR due to release of humoral vasoconstrictors
from the stressed vessel wall.
Endothelium plays a central role in BP homeostasis via
substances as Nitric oxide and prostacyclin
Increased pressure starts a cycle of
- endothelial damage
- local activation of clotting cascade
- fibrinoid necrosis of small vessels
- release of more vasoconstrictors
Process leads to progressive increase in resistance and further
endothelial dysfunction

Pathophysiology
Single organ inv. in approximately 83%
Two organ inv found in 14%
Multiorgan involvement found in 3% of pts
Most common clinical presentations
- cerebral infarction(24%)
- pulmonary oedema (22%)
- HPT encephalopathy(16%)
- Cong. HF (12%)
Less common presentations IC hemorrhage, aortic
dissection and eclampsia

Case example - HPT

Encephalopathy
52yr male presents to ED
worsening headache and confusion, numbness and weakness
involving right side of body, blurry vision over past 12 hrs
PMx: HPT, bilateral artery stenosis, cocaine abuse,
hyperlipidemia.
Exam:

BP 213/134
confused, papilledema on fundoscopy
Mild motor weakness (4/5) right arm
Lab studies rased creatinine
ECG LVH
CT Brain diffuse bilateral white matter changes HPT
encephalopathy

Case example HPT

Encephalopathy
Mx
admitted ICU
started on IV Nitroprusside
BP decreased to 190/100 mmHg over first 3hrs

Outcome:
Neurology symptoms resolved within 5hrs
he was switched to his usual oral regimen on
3rd day in hospital
discharged day 5 controlled BP

Hypertensive encephalopathy
Clinical manifestation of cerebral edema
and microhemorrhages seen with
dysfunction of cerebral autoregulation
Defined as an acute organic brain
syndrome or delirium in the setting of
severe hypertension

HTN Encephalopathy
Symptoms

Severe headache
Nausea and vomiting
Visual disturbances
Confusion
focal or generalized
weakness

Signs
Disorientation
Focal neurologic
defects
Focal or generalized
seizures
nystagmus

HPT Encephalopathy
Not adequately treated cerebral
heamorrhage, coma and death.
BUT with proper treatment completely
reversible
Clinical diagnoses (exclusion)

Hypertensive Retinopathy
Fundoscopy used to be considered a
definitive tool in diagnosing HTN
encephalopathy
NOW still usefull in recognizing acute
EOD as in HTN encephalopathy, but the
absence of retinal exudates, hemorrhages,
or papilledema does not exclude the
diagnoses.
Fundoscopy findings

HPT Retinopathy Fundoscopy

Keith-Wagener classification
Stage I arteriolar sclerosis with thickening, irregularity
and tortuosity
Stage II AV dipping or compression
Stage III Flame shaped haemorrhages and cotton
wool spots
Stage IV Papilledema

presence of stage III and IV lesions implies

failure of the CNS vascular autoregulation and
makes the Dx of Malignant HPT definitive

HPT Retinopathy

AV crossing changes

HPT retinopathy

HPT retinopathy

PanOptic ophtalmoscope

Diagnosis

History
1) focus on presence of Sx of end-organ dysfunction(eod)
2) any identifiable etiology

Hypertension Hx

Medication

smoking, alcohol
illicit drugs (cocaine, stimulants)

Family history

Steroid use
Estrogens
Sympathomimetics
MAO inhibitors

Social history

last known normal BP

prior diagnoses + Rx
dietary and social factors

early HPT in family members

cardiovascular and cerebrovascular disease
Diabetes
Pheochromocytoma

Pregnant?

Diagnoses

History (cont)
Symptom spesific Hx suggesting EOD
CVS Hx
previous MI/angina/arrhythmias
chest pain/SOB/Sx of CF/claudication/flank or
back pain

Neurologic Hx
prior strokes, neuro dysfunction
visual changes, blurriness, loss of visual fields, severe headaches,
nausea and vomiting, change in mental status

Renal Hx
Underlying renal disease (RF)
Acute onset changes in renal frequency (anuria/oliguria)

Endocrine Hx
diabetes, thyroid dysfunction, Cushings syndrome

Begin Treatment!

This isEmergency
a Hypertensive
Begin to look for other causes of symptoms

Diagnoses
Examination
1)
Confirm elevated BP

Proper position, appropriate cuff size

Supine and standing and both arms

2)

Asses EOD present

Fundoscopy

Chronic HPT will have findings

Acute changes
new retinal bleeds
Superficial/flame shaped
Deep/punctuate
exudates
hard/cotton wool spots
papilledema
Neck
Enlarged thryoid, carotid bruit, jugular venous distention
CVS
Enlarged heart, S3, asymmetric pulses, arrhythmias
Pulmonary
Signs of LV dysfunction ( crackles, rhonchi)
Renal
Renal bruit, abdominal masses
Neurologic
Level of consciousness, evidence of stroke, any focal signs

Workup

Lab studies
Electrolytes, urea and creatinine
FBC and smear
Urinalysis dipstix + microscopy
Optional - tox screen
- BHCG
- Endocrine testing

Imaging studies
CXR (chest pain or SOB)
Head CT/MRI brain (abn neurology)
Chest CT/TEE/Aortic angio (Aortic dissection)

Other Tests
- ECG

Management

ED considerations

Many HPT pts only small number will require emergent treatment

Primary goal of EP?

The pts syptoms of EOD and require immediate iv parenteral therapy.

VS
The pt with acutely elev BP(SBP>200 or DBP>120) without EOD
symptoms, who require initiation of medical therapy and close follow
up as outpatient /inpatient

Management
The EP must be capable of:
- Appropriately evaluating pts with an elevated BP
- Correctly classify the HPT
- Determine the aggressiveness and timing of
therapeutic interventions
- Making disposition decisions

Remember - treat the patient and not the number

Treatment
Prehospital care
- Address the manifestations of a HPT
emergency eg.chest pain or HF
- Reduction of BP not indicated in
prehospital setting
- Rapid lowering of BP can critically
decrease end-organ perfusion

Treatment

ED Care - general principles

1.
2.

Consider context of elevated BP (pain, anxiety)

Screen for EOD (Hx/workup)
- Pts without evidence of EOD d/c + f/up
Misconception - never d/c patient from ED with elevated BP ?
- oral nifedipine NOT indicated and may be dangerous!
- Pts with EOD require ICU admission and rapid but gradual lowering of BP -

using IV meds.
BP should not be lowered to normal levels

3.
-

Rapid reduction in BP below the autoregulatory range results in reduction in organ blood
flow risk of ischemia and infarction
General rule the MAP should be lowered by no more than 20% - 1 st hour

remains stable - BP lowered to 160/110 in next 2-6hrs

NB Exceptions
-

BP goals best achieved by a continuous infusion of a short-acting, titratable,

parenteral anti-HPT agent, along with
constant intensive patient monitoring

Treatment

Medication options

1. Oral antihypertensives

Chronic hypertensive
Hypertensive urgency

2. IV antihypertensives

Hypertensive emergency

Principles of Therapy
Lower B.P. over hours
Initial goal B.P. 160s/90s

Too rapid lowering may cause dire

consequences (CVA, MI)
May take several days to get to reasonable
levels
Avoid medications that cannot be controlled
(sublingual nifedipine)

Pharmacology IV anti-HPT
1. Vasodilators

Sodium nitroprusside
Nitroglycerin
Nicardipine
Fenoldapam
Hydralazine
Enalapril

2. Adrenergic inhibitors

Labetalol
Esmolol
Phentolamine

IDEAL IV ANTI-HYPERTENSIVE
Lower the BP without compromising blood
flow to critical organs
Vasodilators generally considered 1st ,
because they preserve organ blood flow in
the face of reduced perfusion and also
tend to increase CO.

Profile of an ideal IV
antihypertensive

Preserves GFR and renal blood flow

Few or no drug reactions
Little or no potential for exacerbation of co-morbid conditions
Rapid onset and offset of action
Minimal hypotension overshoot
Minimal need for continuous BP monitoring and frequent
dose titration
No acute tolerance
Ease of use and convenience
Safe and no toxic metabolites
Multiple formulations for short and long term use
Minimal symphathetic activation

Hypertensive Emergencies: Treatment

For most patients the greatest risk of treating
a hypertensive emergency is
the risk of
accompanying hypotension.
Treat with short acting, easily
I.V. drug.

titratable,

Parenteral Drugs for Treatment of

Hypertensive Emergencies
Drug

Dosage

Onset

Duration

Adverse
Effects

Indic.(I)
Contrain.(C)

Vasodilators
Nitroprusside

0.3-10
mcg/kg/min
IV infusion

1-2 min.

1-2 min.

N/V,mus.
twitch.,
cyanide,
thiocyan. tox.
intracran.
pressure

I: CHF, aortic
dissect.,
catechol.
C: hepatic,
renal insuff.

Nitroglycerin (IV)

5-100
mcg/kg/min

2-5 min.

3-5 min.

HA,
dizziness,
vomit.,
methemglo.
tolerance

I: coronary
dis., CHF
C: CVA
intracran.
pressure

Parenteral Drugs for Treatment of

Hypertensive Emergencies
Diazoxide

(Hyperstat
IV)

1-3 mg/kg
2-4 min
(up to 150
mg) IV bolus,
q5-15 min;
repeat q4-24
hr as needed

3-12 hr

Nausea,
hypotension,
flushing,
tachycardia,
hyperglycemia,
aggravation of
angina, fluid
retention

C: Syndromes
of coronary
insufficiency,
(unless used
with betablocking agent),
cerebrovascular
accident,
hypersensitivity to
sulfonamides

Parenteral Drugs for Treatment of

Hypertensive Emergencies
Fenoldopam
mesylate
(Corlopam)

0.1-1.7
micrograms/kg/min
IV infusion

Hydralazine
HCl
(Apresoline)

10-20 mg IV or IM
10-20 3-8 hr Tachycardia,
flushing,
bolus, repeat q4-6 hr as min
headache,
needed (maximum dose,
40 mg)

5-15
min

1-4 hr Headache,

dizziness,
flushing,
increased
intraocular
pressure,
hypokalemia,
dose-related
tachycardia

vomiting,
aggravation of
angina

I: Severe
hyperten-sion
with renal
insuffi-ciency
C: Glaucoma

I: CHF
C: Coronary
insufficiency,
aortic
dissection,
cerebrovascular accident
(may increase
intracranial
pressure)

Parenteral Drugs for Treatment

of Hypertensive Emergencies
Enalaprilat

(Vasotec I.V.)

1.25-5 mg q6 15
hr IV
min

6 hr Precipitous drop in
blood pressure in highrenin states, variable
response

I: CHF
C: Use with
caution in
patients with
severe renal
insufficiency
(not receiving
dialysis)

Nicardipine
HCl (Cardene)

5-15 mg/hr IV 5-20

infusion
min

1-2
hr

Tachycardia, headache, C: Greater than

flushing, local phlebitis first-degree
heart block,
CHF

Parenteral Drugs for Treatment

of Hypertensive Emergencies
Adrenergic Inhibitors
Phentolamine
(Regitine)
-blocker

5-20 mg IV, repeat

as necessary

1-2
min

10-30
min

Tachycardia,
nausea,
flushing,
abdominal
pain,
aggravation
of angina

I: Catecholamine
excess
C: Syndromes of
coronary
insufficiency

Esmolol HCl 200-500

1-2
(Brevibloc)
micrograms/kg/min min
over 1-4 min, then
50-300
micrograms/kg/min
IV infusion

10-20
min

Hypotension,
nausea,
bradycardia or
heart block,
dizziness

I: Syndromes of
coronary
insufficiency
C: Greater than
first-degree heart
block, CHF

Parenteral Drugs for Treatment

of Hypertensive Emergencies
Labetalol
HCl
(Normodyne,
Trandate)
- blocker

20-80 mg
IV bolus,
repeat as
needed
(maximum
dose, 300
mg); or 2
mg/min IV
infusion

2-10 min

2-4 hr

Hypotension,
nausea,
itching,
scalp
tingling,
dizziness

I: Syndromes of
coronary
insufficiency,
catecholamine
excess
C: > firstdegree
heart
block,
CHF,
bronchial
asthma

Sodium Nitroprusside
(Hypoten L)

MoA:

Direct smooth muscle dilator (art + ven)

Nitric oxide compound
Potent preload and afterload reducer
Causes cerebral vasodilation

Ultra short acting

Immediate onset - DoA : 10min
Dose:
0.1-0.5mcg/kg/min IV infusion
titrate to desired effect
rates>10mcg/kg/min cyanide toxicity

Adverse affects/Precautions:

Cyanide and thiocyanate toxicity (pts with liver/renal dysfunction)

Max dose, max 10min
Can cause precipitous drop in BP (hypotensive effects unpredictable)
Ideally Art.line with continuous BP monitoring
Causes significant reflex tachycardia ( incr Oxygen demand)
(angina/aortic dissection/cerebral oedema)
Nausea and vomiting
Increased ICP

Drug of choice:

Perioperative HPT
Cocaine toxicity
Aortic dissection(combination)

Neurologic syndromes

Nitroglycerin
(Nitrocine / Isoket / Tridal)

MoA:

Potent vasodilator (nitric oxide compound)

Primary affects the venous system, decrease preload (CO + BP)
Decreases coronary vasospasm

Dose: cont infusion

start 5mcg/min, incr by 5mcg/min
every 3-5min to 20mcg/min
If NO Response
increase by 10mcg/min every 3-5min,up
200mcg/min
Onset : 2-5min/DoA : 5-10min

Adverse effects/precautions:

Contra ind:

Constant monitoring is essential

Tolerance from uninterrupted use (12hr withdrawal)
Headache, tachycardia, flushing

Concurrent use with PDE-5 inhibitors - causes significant hypotension

Head trauma/cerebral haemorrhage
Severe anaemia

Drug of choice:

Acute HF
ACS

Nicardipine
(Nimodipine Nimotop)

Ca channel blocker selective arterial vasodilator

Onset: 1-5min
DoA: 15-30min
Dose: start 5mg/hr IV infusion, titrate every
15min to max 15mg/hr.
Advantages:
Cause cerebral and coronary vasodilatation

Precautions: can worsen/cause HF and

liver failure
can exacerbate renal insuff.
Ideal for CNS emergencies
Not available SA

Fenoldapam
(Carlopam)

New (not available SA)

MoA:

Peripheral dopamine agonist (high vs low doses)

causes selective neuro vasodilatation
mesenteric vasodilatation
increases renal blood flow and sodium excretion

Onset <5min, but more gentle, lasts for 30min (titratable, predictable and stable)
Standard BP monitoring is sufficient, no toxic metabolites
Dosing:

Precautions:

Start at 0.1-0.3mcg/kg/min IV infusion

May be increased in increments of 0.05-0.1mcg/kg/min every 15min, until target BP reached
Max infusion rate 1.6mcg/kg/min

Pts with glaucoma or intraocular hypertension

Dose related tachycardia can occur angina
Close BP monitoring
Close K monitoring
Caution with raised ICP

Drug of choice

Renal insuffiency
Strokes ( combination with nicardipine)

Hydralazine
(Apresoline)

MoA:

Dose:

used too much

boluses takes 20min to work
not titratable

Adverse effects/Precautions

5-20mg IV bolus or 10-40mg IM repeat every 4-6hrs

old school

Decreases systemic resistance by direct vasodilation of arterioles

tachycardia, flushing, headache

sodium and water retention
increased ICP
adjust dose in severe renal dysfunction
response may be delayed and unpredictable

Still drug of choice in pregnancy(Eclampsia), but B-blocker/Labetalol and Fenoldapam

are also safe options
Only available PO, Dihydralazine discontinued

Enalaprilat

The active component of Enalapril (hydrolyzed in liver and kidney)

MoA:
ACE inhibitor

Dose:
0.625-2.5mg every 6hr IV
Not titratable

Onset within 30 min + long half life

Adverse effects/Precautions
Contra-indicated volume depletion, renal vascular disease
Prolonged life

Expensive, not available SA

Labetalol
(Trandate)

MoA:

selective alpha blocker will reduce vascular smooth m. resistance

non-selective Beta blocker decrease cardiac inotropy and miocard O2 consumption, will prevent reflex
tachycardia

Dose:

Bolus: effect in 5-10min,max effect at 20min. (DoA: 2-6hrs)

1st dose 20mg then every 10-20min
2nd dose 40mg, 3rd dose 80mg.

Cont. infusion: 0.5 2mg/min titrate to response,max 300mg total dose

Difficult to titrate due to very wide dose range

Advantages:

smooth onset
Transition to oral Rx easy (dose equivalent)
Improve cerebral bloodflow stroke pt
No need for ICU/Arterial line

Adverse effects/precautions
Relative CI Heart failure, heart block, Asthma (bronchoconstriction)
Vomiting, scalp tingling
Impaired hepatic function
Elderly patients
Contraindicated in HPT secondary to Cocaine use/Phaeochromocytoma
(B-blocker effect outway the alpha effect, thus unapposed alpha constriction)
Drug of choice:
Aortic dissection
Hypertensive emergencies

Esmolol
(Brevibloc)

MoA:

Dose: (titratable)

Sinus bradycardia
Heart block
Cardiogenic shock
Bronchial asthma
Uncompensated CF
pregnancy

Drug of choice:

Hypotension common
nausea
Asthma
1st degree AV block
heart failure

Contraindications

bolus: 250-500mcg/kg IV over 1-3min

infusion: 50-100mcg/kg/min
may repeat bolus after 5min or increase
infusion rate to 300mcg/kg/min

Onset 1-2min / short acting

Adverse effect/Precautions

highly selective beta blocker

Aortic dissection ( with nitrate)

Not availalble anymore

Phentolamine
(Regitine)

MoA:

Dose:

renal impairment
Concurrent use with PDE-5 inhibitors
coronary or cerebral arteriosclerosis

Drug of choice

tachycardia
flushing/headache
MI
cerebrovascular spasm

Contra-indications

load 5-20mg IV every 5min or

infusion 0.2-0.5mg/min

Onset 1-2min
Adverse effect/precautions

alpha adrenergic receptor blocker

Cocaine associated HPT crisis

Pheochromocytoma HPT crisis

Not available in SA anymore

Neurological emergencies
Hypertensive encephalopathy
reduce MAP by 25% or diastole to 100mmHg
over 8 hrs
If neurology worsens, suspend Rx
Drug of choice:
Sodium nitroprusside
Labetalol

Neurological emergencies
Acute Ischemic stroke

often loss of cerebral autoregulation

ischemic region more prone to hypoperfusion
thus BP reduction not recommended
unless SBP>220 or DBP>120
UNLESS planning fibrinolysis SBP<185
and DBP< 110
Drug of choice:
Labetalol
Nicardipine
Sodium Nitroprusside

Neurological emergencies
Acutes ICH/SAH
Treatment based on clinical/radiographic
evidence of raised ICP
Raised ICP MAP<130 (1st 24hrs)
No raised ICP MAP<110
Drug of choice:
Sodium Nitroprusside
Labetalol
Nicardipine

Cardiovascular emergencies
ACS
treat if SBP>160 and/or DBP>100
Reduce MAP by 20 -30% of baseline
nitrates should be given till symptoms
subside or until DBP<100
Drug of choice:
Nitroglycerine
Labetalol
Nicardipine

CVS emergencies
Acute HF (pulmonary edema)
treat with vasodilator (additional to diuretics)
Sodium Nitroprusside in conjunction with
morphine, oxygen and loop diuretic
Enalaprilat also an option

CVS emergencies
Aortic dissection
anti-hypertensive Rx is aimed at reducing the
shear stress on aortic wall (BP and Pulse)
immediate lowering of BP lifesaving
maintain SBP<110, unless signs of end
organ hypoperfusion
preferred Rx is combination of Morphine,
B-blocker and vasodilator
Nitroprusside + Labetalol

Other disorders
Cocaine toxicity/pheochromocytoma
Hpt and tachycardia rarely require spesific Rx
Alpha adrenergic blockers preferred
B blockers can be added, but only after
alpha blockade.
Drug of choice
Phentolamine
Labetalol
Diazepam

Other disorders
Pre-eclampsia/Eclampsia
Goal SBP<160 and DBP<110 in pre-andintrapartum periods.
Platelets < 100 000, BP should be
maintained < 150/100
IV Magnesium to prevent seizures
Drug of choice:
Methyldopa
Hydralazine

Other disorders
Perioperative hypertension
target BP to within 20% of baseline, except if
potential for life threatening arterial bleeding
typically related to catecholamine surge postop.
Drug of choice:
B-blocker
Labetalol

Local
Tygerberg
F1(medical outpatients)
Nitroglycerine

Cardiology ICU
Nitroglycerine

Renal unit
Labetalol

Obstetrics
Labetalol
Hydralazine

Local
Grootte Schuur (C15)
Nitroglycerine (Tridal)

Victoria
Nitroglycerine (Tridal/Nitrocine)
Labetalol
Can get Sodium nitroprusside

Summary
HPT crisis - serious condition - associated with
EOD, if left untreated
High mortality - untreated
Main causes non-compliance and poorly
controlled chronic hypertension.
Urgency vs emergency
Treatment should be tailored to the individuals
condition
HPT urgency initial goal max 25% drop in MAP in
first 3 hours
Precipitous drop just as bad good continuous
monitoring essential

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1.
2.
3.
4.
5.
6.
7.
8.
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