HYPERTENSIVE CRISIS

Vidhia Umami
Division of Nephrology & Hypertension, Department of Internal
Medicine
Faculty of Medicine, University of Indonesia Dr. Cipto Mangunkusumo
Hospital
Jakarta

Case Scenarios

A 56 yo male with no significant PMH

presents to the ER with headache,found to
have BP 210/120 mmHg and papilledema.

An 82 yo male with h/o HTN,chronic renal

insufficiency
presents
for
a
routine
physical,found to have BP of 230/130 mmHg.

A 76 yo female is brought to the ER by the

family due to altered mental status.BP is
240/120 mmHg with no focal neuro findings.

Hypertension Prevalence (%) in

Indonesia
1995 s/d 2007

Estimated 1 % of hypertension patient developed hypertensive emergency

(Papadopoulos, Blood pressure 2010)

Source: SKRT, Surkesnas , Riskesdas

Note: 1995 and 2001: mercury blood pressure
2004 and 2007: digital blood pressure

EPIDEMIOLOGY

In the US: More than 60 million Americans, about 25-30% of

the population, have hypertension. Of these individuals,
70% have mild disease, 20% moderate, and 10% severe
hypertension (diastolic BP [DBP] >110 mm Hg). Approximately
1-2% develop a hypertensive emergency with end-organ
damage.

Mortality/Morbidity: Morbidity and mortality depend on the

extent of end-organ damage on presentation and the degree
to which BP is controlled subsequently. BP control may
prevent progression to end-organ impairment. I yr mortality
in untreated pts. >90%.5 yr survival of all presentations
is 74%.

Race: African Americans have a higher

hypertensive emergencies than Caucasians.

Sex: Males are at greater risk of hypertensive emergencies

than females.

Age:Most commonly in middle-aged people.Peak age:40-50yrs.

incidence

of

Epidemiology

Hypertensive crises represented more than

fourth of all medical urgencies/emergencies.

one

76% urgencies
24% emergencies

Hypertensive urgencies frequently present with:

Headache (22%)
Epistaxis (17%)
Faintness and psychomotor agitation (10%)

Types
of
end-organ
damage
associated
hypertensive emergencies include:

with

Cerebral infarction (24%)

Acute pulmonary edema (23%)
Hypertensive encephalopathy (16%)
Cerebral hemorrhage (4.5%)
Blood Pressure, 2010; 19:328-336

DEFINITION (JNC VII)

DEFINITIONS

Systolic blood pressure >180 and diastolic >120mmHg.

Patients with hypertension can be classified into categories based

upon their symptoms and the organ systems that are affected at the
time of presentation:
-HYPERTENSIVE EMERGENCY:
is severe hypertension with acute
impairment of an organ system (e.g., central nervous system [CNS],
cardiovascular, renal). In these conditions, the blood pressure (BP)
should be lowered aggressively over minutes to hours.
Presence of papilledema indicates MALIGNANT HYPERTENSION.
-HYPERTENSIVE URGENCY: the BP is a potential risk but has not yet
caused acute end-organ damage. These patients require BP control over
hours to days.
-ACCELERATED HYPERTENSION: recent significant increase over baseline
blood pressure. Examination usually showed vascular damage on
fundoscopic examination, such as flame-shaped hemorrhages or soft
exudates, but without papilledema.
HYPERTENSIVE ENCEPHALOPATHY: sudden, marked elevation of BP with
severe headache and altered mental status, reversible by reduction of
BP.

Hypertensive Crises

Hypertensive Urgency

Hypertensive Emergency

Markedly elevated BP
Markedly elevated BP
Without severe symptoms or
With acute or progressing
progressive target organ damage
target organ damage
BP should be reduced within hours BP should be reduced immediate
Oral agents
Parenteral agents

Kaplan NM ,Hypertensive Crises in : Clinical hypertension

Precipitating factors in hypertensive crisis

1.

Accelerated sudden rise in blood pressure in

patient with preexisting essential
hypertension

2.

Renovascular hypertension

3.

Glomerulonephritis-acute

4.

Eclampsia

5.

Pheochromocytoma

6.

Antihypertensive withdrawl syndromes

7.

Head injuries

8.

Renin secreting tumors

9.

Ingestion of cathecolamine precursor in

patients taking MAO inhibitors

Pathophysiology
Critical Degree of Hypertension
Local effect
Prostaglandin,
freeradical, etc
Endothelial Damage

Systemic effect
RAAS, Catechol,
Vasopressin
Pressure Natriuresis

Platelet deposition

Hypovolemia

Mitogenic & migration factors

Further increase in vasopressor
Myointimal proliferation

Further rise in BP & Vascular damage

Tissue Ischemia

Kaplans Clinical Hypertension, 2010

CLINICAL MANIFESTATION

(Zampaglione, 1996)

Main Forms Of Presentation Of

Hypertensive Emergencies in the
Emergency Department
Hypertensive Emergencies
Hypertensive
encephalopathy

Symptoms
Headache, visual
disturbance, vommiting,
altered level of
consciousness

Severe Hypertension with Neurological deficit,

stroke/cerebral
altered level of
hemorrhage
consciousness
Hypertensive left
ventricular failure

Cough,

dyspnea,
orthopnea, rapidly
progressive dyspnea

Accelerated-malignant
hypertension

Visual changes,
headache, renal failure,
(Angelats, 2010)

Main Forms Of Presentation Of

Hypertensive Emergencies in the
Emergency Department.(2)

Hypertensive Emergencies

Symptoms

Hypertension and aortic

dissection

Chest pain and/or

intense abdominal pain,
vegetatism, signs of
poor perfusion

Hypertension with acute

coronary syndrome

Chest pain

Use of drugs :
amphetamines, LSD,
cocaine, xtc

Tachycardia, sweating,
altered mood and/or
level of consciousness

Severe preeclampsia or
eclampsia

Oligouria,
microangiopathic anemia

(Angelats, 2010)

Management Principles:
Hypertensive Urgency

No need for hospital admission.

Slow and controlled reduction in BP

Treated with oral agents

Close follow-up as out patients

Marik PE.Varon J. Chest.2007;131:1949

JNC VII
Treatment Recommendations

Admit to ICU for continuous BP monitoring

and parenteral administration of appropriate
agent.
Initial goal: arterial BP by no more than
25% within min to 1 hr (aortic dissection 10
min) or DBP to 110 mmHg over 1 hr.

Then, if stable, to 160/100-110 mmHg

within next 2-6 hr.

Excessive BP reduction precipitating renal, cerebral, or

coronary ischemia should be avoided.
Gradual further reduction over next 24-48 hr
Exception: ischemic stroke.

Oral agents may

Cobanian
AV et al. Hypertension.2003;42:1206
urgency

be

used

for

HTN

MANAGEMENT

(Rodriguez, 2010)

Sublingual Drugs for

Treatment of Hypertensive
Emergencies

Captopril

25 mg SL reduced BP starting at 15 min - 120 min

success rate 83%

Nifedipine

10 mg SL reduced BP starting at 10 120 min

success rate 90%

Wu SG et al. Nephron. 1993;65:284

Haude M et el. Clin Cardiol.1991;14:463

Parenteral Drugs for Treatment of

Hypertensive Emergencies based on
JNC 7

Drugs

Dose

Onset

Duration
of Action

Sodium
nitroprusside

0.25-10 ugr/kg/min

Immediate

1-2 minutes
after infusion
stopped

Nitroglycerin

5-500 ug/min

1-3 minutes

5-10 minutes

Labetalol HCl

20-80 mg every 10-15

min or 0.5-2 mg/min

5-10 minutes

3-6 minutes

Fenoldopam HCl

0.1-0.3 ug/kg/min

<5 minutes

30-60 minutes

Nicardipine
HCl

5-15 mg/h

5-10 minutes

15-90
minutes

Esmolol HCl

250-500 ug/kg/min IV 1-2 minutes

bolus, then 50-100
ug/kg/min by
infusion; may repeat
bolus after 5 minutes
or increase infusion
to 300 ug/min

10-30 minutes

Chobanian AV et al, The JNC 7 report, JAMA 2003;389-2560-70

Overview of intravenous drugs for the treatment of

hypertensive emergencies
Drug
Esmolol

Onset of
action
1 2 min

Half
life
10 - 30
min

Dose

Contraindications and
adverse effects

0.5 I mg/kg as bolus; 50 -300 2nd

or
3rd
degree
AV
g/kg/min as continuous infusion block,
systolic
heart
failure,
COPD
(relative); bradycardia

Phentolamine 1 2 min

3 5 min

1 5 mg, repeat after 5 15 Tachyarrhythmia,

min, until goal BP is reached;
pectoris
0.5 1.0 mg/h as continuous
infusion

Ketanserin

1 2 min

30 60
min

5 mg as bolus injection, repeat Prolonged QT interval,

after 5 min (max 30 mg); 2 6 2nd
or
3rd
degree
AV
mg/h as continuous infusion
block;
bradycardia,
hypokalaemia

Labetalol

5 10
min

3 6 hr

0.25 0.5 mg/kg; 2- 4 mg/min 2nd

or
3rd
degree
AV
until
goal
BP
is
reached, block;
systolic
heart
thereafter 5 20 mg/h
failure,
COPD
(relative); bradycardia

Nicardipine

5 15
min

30 40
min

5 15 mg/h as continuous Liver failure

infusion, starting dose 5 mg/h,
increase every 15 30 min with
2.5 mg until goal BP, thereafter
decrease to 3 mg/h

Nitroglyceri 1 5 min
ne

3 5 min

200
g/min,
increase every 5 min

Nitroprussid Immediate
e

1 2 min

angina

g/min

0.3 10 g/kg/min, increase by Liver/

kidney
failure
0.5 g/kg/min every 5 min until (relative);
cyanide
The
Journal of Medicine;
goalNetherland
BP
intoxication may 2011,

vo

Parenteral Drugs for Treatment of

Hypertensive Emergencies based on CHEST 2007
Acute Pulmonary
edema / Systolic
dysfunction

Nicardipine, fenoldopam, or nitropruside

combined with nitrogliceryn and loop
diuretic

Acute Pulmonary edema/

Diastolic dysfunction

Esmolol, metoprolol, labetalol, verapamil,

combined with low dose of nitrogliceryn and
loop diuretics

Acute Ischemia Coroner

Labetalol or esmolol combined with

diuretics

Hypertensive
encephalopaty

Nicardipine, labetalol, fenoldopam

Acute Aorta Dissection

Labetalol or combined Nicardipine and

esmolol or combine nitropruside with
esmolol or IV metoprolol

Preeclampsia,
eclampsia

Labetalol or nicardipine

Acute Renal failure /

microangiopathic
anemia

Nicardipine or fenoldopam

Sympathetic crises/
cocaine oveerdose

Marik Paul
E, Varonor
Joseph,
CHEST 2007;131:194
Verapamil,
diltiazem,
nicardipine
combined with benzodiazepin

PROGNOSIS

So,.
A 56 yo male with no significant PMH presents to the
ER with headache,found to have BP 210/120mmHg
and papilledema. - MALIGNANT HYPERTENSION,
HYPERTENSIVE EMERGENCY

An 82 yo male with h/o HTN,chronic renal

insufficiency presents for a routine physical,found to
HYPERTENSION,
have BP of 230/130mmHg.- ACCELERATED
HYPERTENSIVE URGENCY
76 yo female is brought to the ER by the family due
to altered mental status.BP is 240/120 mmHg with no
focal neuro findings. HYPERTENSIVE ENCEPHALOPATY,
HYPERTENSIVE EMERGENCY

Thank You