Hypertensive Crisis

Yuan Zhiming
Department of Emergency Medicine
The General Hospital
Tianjin Medical University
 Contents
● Introduction
● Epidemiology

● Etiology

● Pathogenesis

● Diagnosis

● Treatment

● Prognosis
 Introduction

 Classification of hypertension
 Hypertensive crisis
 Hypertensive urgency
 Hypertensive emergency
1. Classification of hypertension

systolic BP or diastolic BP
（ mmHg ）
（ mmHg ）
Stage 1 140 ~ 159 90 ~ 99
Stage 2 160 ~ 179 100 ~ 109
stage 3 ≥180 ≥110
Stage 3 hypertension has also been called severe
hypertension or accelerated hypertension
2. Hypertensive crisis
Hypertensive crisis refers to elevated blood
pressure coupled with progressive or
impending organ damage due to high blood
pressure, usually characterized by a rise in
DBP to greater than 120 to 130 mmHg.
Hypertensive crisis comprises a spectrum of
conditions, including hypertensive urgency
and hypertensive emergency.
3. Hypertensive urgency

defined as an elevation of SBP

(>220mmHg) and/or DBP (>125mmHg)
without evidence of acute end-organ
damage.
4. Hypertensive emergency

defined as a sudden increase in systolic

and/or diastolic BP associated with end-
organ damage of the CNS, the heart, or the
kidneys.
The clinical differentiation between
hypertensive emergency and
hypertensive urgency depends on the
presence of target organ damage,
rather than the level of BP
Organ damage associated with hypertensive
emergency may include:
Changes in mental status such as
confusion or coma (encephalopathy)
Bleeding into the brain (stroke)
Heart failure
Chest pain (angina)
Fluid in the lungs (pulmonary edema)
Heart attack
Aneurysm (Bulging blood vessel)
Eclampsia (occurs during pregnancy)
What is an aneurysm?

An aneurysm is a dilation (ballooning) of

part of the blood vessel. It usually causes no
symptoms unless it ruptures. A ruptured
aneurysm is often fatal.
 Hypertensive Urgencies

Upper levels of stage 3 hypertension

Papilledema
Headache
Shortness of breath
Pedal edema
 Hypertensive Emergencies

Hypertensive encephalopathy
Acute aortic dissection
Acute pulmonary edema with respiratory failure
Acute myocardial infarction/unstable angina
Eclampsia
Acute renal failure
Microangiopathic hemolytic anemia
What is aortic dissection?

An aortic dissection begins with a tear in the

inner layer of the aortic wall.When a tear
occurs in the innermost layer of the aortic
wall, blood is then channeled into the wall of
the aorta, separating the layers of tissues. It is
a life-threatening emergency.
(A) Normal blood flow. (B) Dissection occurs when the
inner lining of the aorta tears and the blood flow
‘dissects’ between the layers of the aortic wall.
 Epidemiology
 Sixty million US inhabitants suffer from
hypertension. The vast majority of these
patients have essential hypertension.

 Fewer than 1% of these patients will

develop one or multiple episodes of
hypertensive crises.
 Preeclampsia is a pregnancy-related
hypertension. It occurs in 7% of all
pregnancies. of them, 70% are null-
gravidas and 30% are multi-gravidas. In
molar pregnancies, preeclampsia has been
described in up to 70% of cases.
The most prevalent associated complications
o Cerebral infarction 24.5%
o Encephalopathy 16.3%
o Intracerebral or subarachnoid
hemorrhage 4.5%
o Acute congestive heart failure
with pulmonary edema 36.8%
o Acute myocardial infarction or
unstable angina 12%
o Aortic dissection 2%
o Eclampsia 4.5%
 Etiology

Hypertensive crisis may occur in patients

with no history of the condition or can be
precipitated by noncompliance with
medical therapy or diet, or both; or by
inadequate treatment.
Common causes include
1. ARF
2. Acute CNS events
3. Drug-induced hypertension
4. Ingestion of tyramine-containing foods
or beverages during treatment with a
monoamine oxidase inhibitor (MAOI)
5. Pregnancy-induced epilepsia
6. Pheochromocytoma
 Pathogenesis

The exact mechanism of hypertensive crisis

is not known. The majority of patients have
known hypertension before the crisis, and the
sudden rise in BP is often related to the
underlying disease process as described
above.
 The pathophysiology
humoral vasoconstrictors release

systemic vascular resistance increases

vicious severe elevations of BP

cycle
deposition of platelets
endothelial injury,
and fibrin, a breakdown
fibrinoid necrosis
of the normal
of the arterioles
autoregulatory function

ischemia
 Diagnosis
1. Diagnosis
 Manifestations
Hypertensive crisis can be manifested by any
of the following symptoms, depending on the
end-organ involved
•CNS compromise, identified by
headache, blurred vision
•Change in mental status or coma
• Cardiovascular compromise, identified
by the chest pain of an acute coronary
syndrome or aortic dissection
• ARF, identified by a sudden absence of
urine output
• Catecholamine excess
 Physical Examination & Tests
Certain tests will be given to monitor blood
pressure and assess organ damage, including:
• Regular monitoring of blood pressure
• Eye exam(funduscopic examination) to
look for hemorrhages, exudates, and/or
papilledema
• Blood and urine testing
• Electrocardiogram
 The level of BP
There is no predetermined criterion for the
level of BP necessary to induce a
hypertensive emegency (although in 1984,
the JNC on Hypertension defined severe
hypertersion as a DBP greater than
115mmHg)
The diagnosis is based on altered end-
organ function and the rate of the rise in
BP, not the level of BP
2. Initial Evaluation of the Patient
With Hypertensive Crises

(1)The key to successful management of

patients with severely elevated BP is to
differentiate hypertensive emergencies
from hypertensive urgencies
(2)This is accomplished by a targeted
medical history and physical examination
supported by appropriate laboratory
evaluation

 Inquiry should include the use of

antihypertensive medications,
monoamine oxidase inhibitors and
recreational drugs
 The BP in all limbs should be measured
by the physician

 In obese patients, appropriately sized

cuffs should be used

 Funduscopic examination is mandatory

in all cases to detect the presence of
papilledema
 A complete blood cell count, electrolytes,
BUN, creatinine, and urinalysis should be
obtained in all patients presenting with
hypertensive crises

 A peripheral blood smear should be

obtained to detect the presence of a
microangiopathic hemolytic anemia
 a chest radiograph, ECG, and head CT
are useful in patients with evidence of
shortness of breath, chest pain, or
neurologic changes, respectively

 An echocardiogram should be obtained to

assess left ventricular function and
evidence of ventricular hypertrophy
In many instances, these tests are
performed simultaneously with the
initiation of antihypertensive therapy
 Treatment
Principle
Pharmacologic Management
Treatment in Special Situations
1. Principle

Hypertensive emergencies

 Necessitate admission of the patient

to the ICU
Require immediate control of the BP to
terminate ongoing end-organ damage, but
not to return BP to normal levels.
 The goal of therapy is to decrease the
pressure by no more than 25% within
minutes to 1-2 h and then toward a level
of 160/100 mmHg within 2-6 h; or the
MAP is lowered by 20%-25%.

Excessive reductions in pressure may

precipitate coronary, cerebral, or renal
ischemia
 During the first 24 h of treatment it is
recommended that MAP be decreased by
no more than 20%. Once the BP is
stabilized, oral antihypertensive therapy
is initiated to achieve BP values of less
than 140/90 mmHg.
 Intravenous Medications
(1) Vasodilators: such as Sodium
Nitroprusside, nitroglycerin
hydralazine, and diazoxide.
(2) Short-acting β-blockers:
labetalol ,esmolol
(3) angiotensin-converting enzyme
inhibitor(ACEI): enalaprilat
(4) Diuretic: furosemide
Hypertensive urgencies

 not necessitate admission to ICU

 BP is lowered gradually over a period of
24 to 48 h
 Usually treated with rapid-acting oral
antihypertensive agents
Oral drugs can be prescribed Such as

(1) ACEI: Captopril

(2) β-blockers: labetalol.
(3) Clonidine guanabenz, prazosin, and
minoxidil.
(4) Loop diuretic: is generally prescribed
in addition to the antihypertensive
agents.
2. Pharmacologic Management

Drugs commonly used to treat hypertension:

• Angiotensin-converting enzyme (ACE)

inhibitors
• Angiotensin receptor blockers (ARBs)
• Diuretics
• Beta-blockers
• Calcium channel blockers
• Agents that can be administered IV that
are rapid acting, are easily titratable, and
have a short half-life are recommended
• The immediate goal of IV therapy is to
reduce the diastolic BP by 10 to 15%, or to
about 110 mmHg. In patients with acute
aortic dissection, this goal should be achieved
within 5 to 10 min. In the other patients, this
end point should be achieved within 30 to 60
min. Once the end points of therapy have
been reached, the patient can be started on a
regimen of oral maintenance therapy.
• In patients who have suffered a major
cerebrovascular event, the BP should not
be lowered, except in exceptional
circumstances.
 

Triage Evaluation: Algorithm

 
Group I-High BP Group II-Urgency GroupIII-Emergency

BP >180/110 >180/110 Usually >220/140

Symptoms Headache, anxiety; Severe headache, shortness Shortness of breath, chest pain,
often asymptomatic of breath nocturia, dysarthria, weakness,
altered consciousness

Examination No target organ damage, Clinical cardiovascular Encephalopathy, pulmonary

no clinical cardiovascular disease present/stable edema, renal insufficiency,
disease cerebrovascular accident,
cardiac ischemia

Therapy Observe 1-3 hrs; Observe 3-6 hours; Baseline laboratory tests;
initiate/resume medication; lower BP with short acting intravenous line; monitor BP;
increase dosage of inadequate oral agent; adjust current may initiate parenteral therapy
agent therapy in emergency room

Plan Arrange follow-up <72 hours; Arrange follow-up Immediate admission to ICU;
if no prior evaluation, schedule evaluation <24 hours treat to initial goal BP;
appointment additional diagnostic studies
 Oral agents for treatment of hypertensive crisis
Agent Dose Onset/Duration Precautions
of Action
Captopril 25 mg PO repeat as needed; 15-30 min/6-8 hr Hypotension, renal
SL, 25 mg SL 10-20 min/2-6 hr failure in bilateral renal
artery stenosis
Clonidine 0.1-0.2mg PO, repeat 30-60 min/8-16 hr Hypotension,
hourly as required to total drowsiness, dry mouth
dose of 0.6 mg
Labetalol 200-400mg PO, repeat 1-2 hr/2-12 hr Bronchoconstriction,
every 2-3 hr heart block, orthostatic
hypotension
Prazosin 1-2 mg PO, repeat hourly as 1-2 hr/8-12hr Syncope (first dose),
needed palpitations,
tachycardia, orthostatic
hypotension
Min=minutes; hr=hour(s); PO=by mouth; SL=sublingual
Parenteral drugs for treatment of hypertensive emergency

Agent Dose Onset/Duration of Precautions

Action

Parenteral Vasodilators

Sodium 0.25-10 µg/kg/min as IV Immediate/2-3 min Nausea, vomiting; with

infusion after infusion prolonged use may cause
nitroprus-
thiocyanate intoxication,
side methemoglobinemia,
acidosis, cyanide
poisoning; bags, bottles,
and delivery sets must be
light resistant

Nitroglyc- 5-100µg as IV infusion 2-5 min/5-10 min Headache, tachycardia,

vomiting, flushing,
erin
methemoglobinemia;
requires special delivery
system due to drug binding
to PVC tubing
Nitroglycerin 5-100µg as IV infusion* 2-5 min/5-10 min Headache, tachycardia,
vomiting, flushing,
methemoglobinemia;
requires special delivery
system due to drug binding
to PVC tubing

Nicardipine 5-15 mg/hr IV infusion 1-5 min/15-30 min, but Tachycardia, nausea,
may exceed 12 hr after vomiting, headache,
prolonged infusion increased intracranial
pressure; hypotension may
be protracted after
prolonged infusions

Diazoxide 50-150 mg as IV bolus, 2-5 min/3-12 hr Hypotension, tachycardia,

repeated or 15-30 aggravation of angina
mg/min by IV infusion pectoris, nausea and
vomiting, hyperglycemia
with repeated injections
Fenolda- 0.1-0.3 µg/kg/min IV <5 min/30 min Headache, tachycardia,
pam infusion flushing, local phlebitis,
mesylate dizziness

Hydrala- 5-20 mg as IV bolus or 10 min IV/>1hr (IV) Tachycardia, headache,

zine 10-40 mg IM; repeat 20-30 min IM/4-6 hr vomiting, aggravation
every 4-6 hr (IM) of angina pectoris,
sodium & water
retention and increased
intracranial pressure

Enalapr- 0.625-1.25 mg every 6 Within 30 min/12-24 hr Renal failure in

ilat hr IV patients with
bilateral renal artery
stenosis, hypotension
Parenteral Adrenergic Inhibitors

Labetalol 20-40 mg as IV bolus 5-10 min/2-6 hr Bronchoconstriction,

every 10 min; up to 2 heart block, orthostatic
mg/min as IV infusion hypotension,
bradycardia

Esmolol 500µg/kg bolus injection 1-5 min/15-30 min First-degree heart

IV or 50-100µg/kg/min by block, congestive heart
infusion. May repeat bolus failure, asthma
after 5min or increase
infusion rate to 300 µg/kg/
min

Phentolam- 5-10 mg as IV bolus 1-2 min/10-30 min Tachycardia,

ine orthostatic hypotension

hr=hour(s); min=minute; IV=intravenous; IM=intramuscular; PVC=polyvinyl chloride

3.Treatment in Special Situations

Acute Aortic Dissection

 Hypertension After a
Cerebrovascular Accident
Preeclampsia
 Hypertensive Crises in End-Stage
Renal Disease
Acute Aortic Dissection
• This condition requires a reduction of the
shear force affecting the aorta
• The agent of choice for treatment of aortic
dissection is nitroprusside, almost always
in conjunction with a beta-adrenergic
blocking agent such as esmolol
• Agents that cause a reflex increase in
cardiac output should be avoided
Hypertension After a Cerebrovascular Accident

• Most experts advise against lowering blood

pressure in acute stroke patients without
hypertensive encephalopathy or other
cardiovascular emergencies that require the
immediate lowering of blood pressure
• Centrally acting agents should also be
avoided because of their potential to
interfere with mental status.
Preeclampsia

• Magnesium sulfate is considered the

standard of therapy as a prophylaxis for
seizure activity
• Hydralazine has been used traditionally in
the treatment of eclampsia
• Once the patient is admitted to an ICU,
labetalol or nicardipine is preferred
Hypertensive Crises in End-Stage Renal Disease

• Calcium channel blockers have been

used for these patients with some success

• Patients may require emergent

ultrafiltration in order to control the BP
 Prognosis

● Hypertensive crisis that is not managed

over the long term is associated with a
25% mortality 1 yr after the event, and
50% mortality 5 yr after the event.
● The most common causes of death are
uremia, AMI, HF, cerebrovascular
accident.
 Questions
 Explanation of terms:
Hypertensive crisis; hypertensive
urgency; hypertensive emergency
 The principles of treatment of
hypertensive crisis