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HYPERTENSIVE CRISES

Faris Mahmud

Provisionally Registered Pharmacist

DEFINITION
Hypertensive crisis is defined as a severe
elevation in blood pressure (BP>180/110 mmHg)
If these conditions are not treated promptly, a
high rate of morbidity and mortality will ensue
These conditions are divided into two general
categories:

Hypertensive

urgencies
Hypertensive emergencies

CLASSIFICATION OF
HYPERTENSIVE CRISES

Hypertensive urgency
Severely

elevated BP above 180/110 mmHg without


evidence of end organ damage
Not immediately life threatening
Reduction of BP to a safe level may be done more slowly
(over 24 to 48 hours)

Hypertensive emergency
Severely

elevated BP with evidence of end organ damage


Usually occur when BP>180/110 mmHg, but may occur
at even lower level
Immediately life threatening
BP needs to be lowered to a safe level within minutes to
hours

Hypertensive Emergency
Severely elevated blood pressure
(BP >180/110 mmHg)
Overt symptoms of end organ
damage present:
CNS (encephalopathy,

Hypertensive Urgency
Severely elevated blood pressure
(BP>180/110 mmHg)
No evidence of end-organ damage

intracranial/subarachnoid
hemorrhage, stroke)
Heart (left ventricular failure,
pulmonary edema, MI, aortic
dissection)
Renal failure/insufficiency
Eyes (ocular hemorrhage,
funduscopic changes, blurred
vision, loss of sight)
Requires immediate pressure
reduction

May be treated over several


hours (or even days)

Requires IV therapy

May use oral or IV therapy

COMMON CAUSES OF
HYPERTENSIVE CRISES

Renal parenchymal
disease
Chronic

Primary

pyelonephritis

glomerulonephritis
Tubulointerstitial
nephritis

Systemic disorders with


renal involvement
Systemic

lupus
erythematosus
Systemic sclerosis
Vasculitides

Atherosclerotic

Renovascular

disease
Fibromuscular disease
Polyarteritis nodosa

Endocrine

Phaeochromocytoma
Conn

syndrome
Cushing syndrome

Recreational drugs
Coarctation of aorta

Pre-eclampsia/eclampsia

HYPERTENSIVE URGENCY

GOAL OF THERAPY
Initial goal is BP reduction of up to 25% over
several hours (generally, 24-48 hours)
If the patient is then stable, BP can be further
reduced toward 160/100 mmHg

Precipitous

drop in BP may lead to end-organ


ischemia or infarction

If patients tolerate this reduction well, additional


gradual reductions toward target BP values can
be attempted

APPROACH OF TREATMENT

If the patient is already on maintenance therapy,


hypertensive urgencies are best managed by
optimizing the therapy, by
adding

a new antihypertensive
increasing the dose(s) of the present medication(s)
restart the medications (if the therapy was defaulted
or interrupted)

If acute BP reduction is necessary, short-acting


oral antihypertensive may also be administered
followed

by careful observation for several hours to


assure a gradual reduction in BP

ORAL SHORT-ACTING ANTI-HTN FOR


HYPERTENSIVE URGENCIES
Drug

Dose

Onset of
action (hr)

Duration (hr)

Frequency
(prn)

Maximum
daily dose

Captopril

25 mg

0.5

1-2 hrs

450 mg

Nifedipine

10-20mg

0.5

3-5

1-2 hrs

120-180 mg

Labetalol

200-400 mg

2.0

4 hrs

2400 mg

Adapted from CPG for Management of Hypertension 3rd ed. 2008

Available at HKB:
T. Capropril 25 mg
T. Nifedipine 10 mg
T. Labetalol 100 mg

USE OF NIFEDIPINE IN
HYPERTENSIVE URGENCIES
Oral nifedipine was commonly used as a rapid-acting
therapy in the acute management of hypertension
However, its use has been associated with lifethreatening adverse events such as ischemia, MI, and
stroke (Psaty BM et al. 1995; Schwartz M et al. 1990; Fami MJ et al. 1998)

Prompt

absorption of rapidly acting CCB is followed by a


precipitous decrease in BP due to peripheral vasodilation
This reduces coronary perfusion, induces a reflex tachycardia,
and increases myocardial oxygen consumption (Grossman E et al. 1996)
Decreased cerebral blood flow has also been reported with
sublingual nifedipine (Gemici K et al. 2003)

Elderly patients with underlying coronary or


cerebrovascular disease, volume depletion, or concurrent
use of other anti-HTN drugs are at increased risk for
significant adverse events (Summers K et al. 2009)

USE OF CAPTOPRIL IN
HYPERTENSIVE URGENCIES

Oral captopril is as effective as nifedipine in acutely


reducing BP in both urgent and emergent conditions
(Misra A et al. 1993; Kosuoglu B et al. 1991)

Captopril has been reported to increase cerebral blood


flow to a greater extent in patients with BP >180/120
mmHg compared to nifedipine (Gemici K et al. 2003)
First-dose hypotension is a common limiting factor with
captopril use (Summers K et al. 2009)

Most

likely to occur in patients with high renin levels such


as those who are volume depleted or those receiving diuretics
Under these circumstances, initial doses should not exceed
12.5 mg, with repeat doses an hour or more later if necessary

Caution: captopril can induce severe renal failure in


patients with bilateral renal artery stenosis

USE OF LABETALOL IN
HYPERTENSIVE URGENCIES

Use of labetalol have been shown to be effective to


lower BP in acute settings (Gonzalez ER et al. 1991; Zell-Kanter
M, Leikin JB 1991; Atkin S et al 1992)

Labetalol can cause profound orthostatic


hypotension
Patients

should remain in the supine position and


should be checked for orthostasis before ambulation.

Labetalol should be avoided in patients with


asthma, bradycardia, or advanced heart block.

HYPERTENSIVE
EMERGENCY

GOAL OF THERAPY

Immediate reduction of BP is required


to

limit progression of target organ damage


to prevent development of new target organ damage

Initial goal is BP reduction of up to 25% within minutes to


hours
If the patient is then stable, BP can be reduced toward
160/100 mm Hg within the next 2 to 6 hours

Precipitous

drop in BP may lead to end-organ ischemia or infarction

If patients tolerate this reduction well, additional gradual


reductions toward goal BP values can be attempted after 24 to
48 hours
The exception to this goal is for patients with an acute
ischemic stroke

maintaining

time

an elevated BP is needed for a much longer period of

APPROACH TO TREATMENT

Antihypertensive drug therapy has been shown


to improve mortality and morbidity in patients
presenting with hypertensive emergencies (Vadera R.
2011)

Optimal pharmacotherapy depends on the


specific organ at risk

Drugs

Dose

Onset of

Duration

Remarks

action
Sodium
nitroprusside

0.25-10 mcg/kg/min

seconds

1-5 min

Caution in
renal failure

Labetalol

IV bolus 50 mg (over at
least 1 min) may
repeat at 5 min
interval
IVI 2 mg/min
(max 200 mg)

<5 min

3-6 hr

Caution in
renal failure

Nitrates

5-100 mcg/min

2-5 min

3-5 min

Prefered in ACS
& APO

Hydralazine

IV 5-10 mg may repeat


after 20-30 min
IVI 200-300 mcg/min
initially, maintenance
50-150 mcg/min

IV: 10-20 min


IVI: 20-30
min

3-8 hr

Caution in ACS,
CVA and
dissecting
aneurysm

Nicardipine

IV 10-30 mcg/kg over 1


min
IVI 2-10 mcg/kg/min

5-10 min

1-4 hr

Caution in AHF
and ACS

Adapted from CPG for Management of Hypertension 3rd ed. 2008

Esmolol

IV 250-500 mcg/kg over 3-10 min


10-30 min Used in
1-2 min
Only Inj Hydralazine
and Inj Labetalol are currently available at perioperative
HKB
IVI 50-200 mcg/kg/min
situations

NEUROLOGIC EMERGENCIES
Hypertensive encephalopathy
Hypertensive encephalopathy was used to describe the
encephalopathic findings associated with the malignant
hypertensive phase
Results from hydrostatic exudation of fluid into the brain
due loss of blood-brain barrier integrity
The clinical symptoms are usually reversible with prompt
initiation of therapy
The treatment target is to reduce the MAP 25% over 8
hours (Pancioli AM. 2007)
Labetalol, nicardipine, esmolol are the preferred
medications (Pancioli AM. 2007)
Nitroprusside and hydralazine should be avoided (Pancioli AM.
2007)

NEUROLOGIC EMERGENCIES
Acute ischemic stroke
Brain vascular occlusion results in depletion of
oxygen and ATP to the neurons
UNLESS the patient is receiving IV fibrinolysis,
ntihypertensive medications should be withheld
unless the BP is >220/120 mmHg (Castillo J et al. 2004)
An

elevated BP (up to 220/120 mmHg) is desirable to aid


cerebral perfusion

If

the patient is receiving IV fibrinolysis - then, the goal


BP is < 185/110 mmHg to minimize risk for hemorrhage
(Adams HP et al. 2007; Khaja AM, Grotta JC. 2007)

Preferred medications are labetalol and


nicardipine (Adams HP et al. 2007)

NEUROLOGIC EMERGENCIES
Intracerebral hemorrhage / hemorrhagic
stroke
Bleeding that occurs directly into the brain
parenchyma
The usual mechanism is thought to be leakage
from small intracerebral arteries damaged by
chronic hypertension
The treatment is based on evidence of increased
intracranial pressure (ICP) (Anderson CS et al. 2008)
For the 1st 24 hours after onset:

With increased ICP, maintain the MAP < 130 mmHg or


SBP < 180 mmHg
Without increased ICP, maintain the MAP < 110 mmHg or
SBP < 160 mmHg

NEUROLOGIC EMERGENCIES
Intracerebral hemorrhage / hemorrhagic
stroke
Preferred medications are labetalol, nicardipine,
and esmolol (Anderson CS et al. 2008)
Avoid nitroprusside and hydralazine (Anderson CS et al.
2008)

NEUROLOGIC EMERGENCIES
Subarachnoid hemorrhage (SAH)
Extravasation of blood into the subarachnoid
space
~80% of non-traumatic SAH are due to a
ruptured berry aneurysm related to
hemodynamic stress on the arterial walls
Preferred medications are labetalol, nicardipine,
and esmolol (Anderson CS et al. 2008)
Avoid nitroprusside and hydralazine (Anderson CS et al.
2008)

CARDIOVASCULAR EMERGENCIES
Aortic Dissection
Separation of the layers within the aortic wall
Occurs when blood pushes into the intima-media
space through a tear in the intimal layer
Can be rapidly fatal, even with immediate
medical attention
Treatment goal is to maintain maintain the SBP
at < 110 mm Hg, unless signs of end-organ
hypoperfusion are present (Cheung AT, Hobson RW. 2008)

CARDIOVASCULAR EMERGENCIES
Aortic Dissection
Preferred treatment includes a combination of
narcotic analgesic (morphine), B-blockers
(labetalol, esmolol), and vasodilators
(nicardipine, nitroprusside) (Cheung AT, Hobson RW. 2008)
Non-DHP

CCB (verapamil, diltiazem) are an


alternative to beta blockers

AVOID B-blockers if there is aortic valvular


regurgitation or cardiac tamponade (Cheung AT, Hobson
RW. 2008)

CARDIOVASCULAR EMERGENCIES
Acute Coronary Syndrome & Heart Failure
Treatment is indicated if the BP rises >160/100
mm Hg (Diercks EB, Ohman EM. 2008)
Reduce

the BP by 25% of baseline

For ACS, B-blockers and nitrates are the


preferred drugs (Diercks EB, Ohman EM. 2008)
Thrombolytics

are contraindicated if the BP is


>185/100 mm Hg

In LVF with APO, nitroprusside or nicardipine,


plus nitrates and a loop diuretic (frusemide) are
recommended

PREECLAMPSIA/ECLAMPSIA

Treatment is indicated when BP >160/110 mm


Hg in the antepartum and intrapartum periods
(Barton JR. 2008)

If

the platelet count is less than 100,000 cells mm3,


target BP < 150/100 mm Hg

The preferred medications are hydralazine,


labetalol, and nifedipine (Barton JR. 2008)
Should also be treated with IV magnesium
sulfate to avoid seizures
Avoid nitroprusside, ACE inhibitors, esmolol (Barton

JR. 2008)

CONCLUSION
Hypertensive urgencies and emergencies both are characterized
by the presence of very elevated BP, typically greater than
180/120 mm Hg
Hypertensive urgencies are ideally managed by adjusting
maintenance therapy, by adding a new antihypertensive, and/or
by increasing the dose of a present medication
Hypertensive urgency requires BP reductions with oral
antihypertensive agents to stage 1 values over a period of hours
to days
Hypertensive emergencies are situations that require immediate
BP reduction to limit new or progressing target-organ damage
Hypertensive emergencies require parenteral therapy, at least
initially, with one of the specific agents listed
In most of the hypertensive emergencies, IV labetalol are
preferred unless contraindicated

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