Hypertensive Crisis: Diagnosis and Management

dr. Dedy Kristofer Simangunsong

Dokter PTT Puskesmas Mananga, Sumba Tengah, NTT

Systemic hypertension (HTN) is a common medical condition affecting over 1 billion people
worldwide, and more than 65 million Americans.1 Overall the prevalence of hypertension
appears tobe around 3045% of the general population, with a steep increase with ageing. 2
Two thirds of patients are unaware that they have hypertension. While it is well known that
poorly controlled hypertension is a major risk factor for cardiovascular and cerebrovascular
mortality, acute severe elevation in the blood pressure can also cause acute end organ
damage.3
It is estimated that 1% to 2% of the HTN population will present with an acute and
severe elevation in BP termed hypertensive crisis.1 Given the high prevalence of
hypertension in our society, hypertensive crisis are commonly encountered in everyday
clinical practice. Prompt recognition, evaluation and treatment are of paramount importance
in preventing permanent end organ damage.3 One-year and 5-year mortality following
untreated hypertensive emergency are 70% to 90% and 100%, respectively. With adequate
blood pressure control, these mortality rates decrease to 25% and 50%, respectively.4 This
article reviews the approach to appropriately diagnosing and managing hypertensive crisis.

Definition
JNC 7 classifies blood pressure into different categories. Table 1 provides a classification of
BP for adults 18 years and older. The classification is based on the average of two or more
properly measured, seated, BP readings on each of two or more office visits.5
Table 1. Classification of blood pressure for adults5
Category
Normal
Prehypertension
Stage 1 Hypertension
Stage 2 Hypertension

Systolic (mmHg)
<120
120139
140159
160

and
or
or
or

Diastolic (mmHg)
<80
8089
9099
100

A hypertensive crisis is often described as a SBP 180 mmHg or a DBP 120 mmHg,
with or without end-organ damage.1 Hypertensive crises are traditionally subdivided in
hypertensive emergencies and urgencies.6
Hypertensive emergencies are dened as large elevations in SBP or DBP (>180 mmHg or
>120 mmHg, respectively) associated with impending or progressive OD, such as major
neurological changes, hypertensive encephalopathy, cerebral infarction, intracranial

haemorrhage, acute LV failure, acute pulmonary oedema, aortic dissection, renal failure, or
eclampsia.1,3,4,7 Hypertensive urgency is defined as those situations associated with severe
elevations in BP without progressive target organ dysfunction.3,4,7
Notably, these definitions do not specify absolute blood pressure levels as
hypertensive urgency or emergency may occur with a modest increase in blood pressure in
previously normotensive persons (eg, during pregnancy or with acute cocaine intoxication). 4
Although the absolute BP elevation is not a criterion for diagnosis, a hypertensive emergency
is most consistently seen with a DBP 120 mm Hg, and accounts for 25% to 30% of all
hypertensive crisis. Organ injury is most common with a DBP 130 mmHg unless the patient
is a child or pregnant.1
Table 2. Differences between hypertensive emergencies and urgencies8
Variable
Symptoms
Acute BP increase
Acute target organ damage
BP reduction rate
Evaluation for secondary hypertension
BP= blood pressure.

Emergencies
Yes
Yes
Yes
Minutes to hours
Yes

Urgencies
No or minimal
Yes
No
Hours to days
Yes

Epidemiology
Hypertensive crisis affects 500,000 Americans or approximately 1% of hypertensive adults.
Nearly 3.2% of patients presenting to the emergency room have a hypertensive crisis; with
the decrease in incidence of HTN as a result of the advent of medications, the incidence has
reduced substantially. Even so, the 5-year survival rate among all patients who present with a
hypertensive crisis is 74%.1
Hypertensive emergencies occur in up to 2% of hypertensive patients, with a
progressive decrease in mortality rate over the past 4 decades.8
Zampaglione et al evaluated the prevalence of hypertensive crisis in an emergency
department during 12 months, and the frequency of end-organ damage during the rst 24
hours after presentation. They found that 76% of the hypertensive crises were hypertensive
urgencies and 24% were hypertensive emergencies. Hypertensive crises were more prevalent
among patients with renal disease, including renal artery stenosis and chronic kidney
disease.1
More recent data have examined the prevalence of hospitalization for a hypertensive
emergency from 2000 to 2007 in the United States, and showed a high and increasing
incidence (from 50000 to 60000 per year) with a progressive decline in mortality (from 3 to
2.5%) since 20052007.8
Severe HTN is seen more frequently in noncompliant individuals, black men, persons
of lower socioeconomic status, and the elderly. Patients with hypertensive emergencies were

older (59.6 14.8 vs. 49.9 18.6 years, P < 0.001) and had greater DBP (129.1 12 vs.
126.6 14.4 mmHg, P < 0.05) than those with hypertensive urgencies.1
Pinna et al evaluated 333,407 patients admitted to the EDs over the one-year period,
1,546 had hypertensive crises (4.6/1,000, 95% CI 4.44.9), and 23% of them had unknown
hypertension. Hypertensive emergencies (n=391, 25.3% of hypertensive crises) were acute
pulmonary edema (30.9%), stroke (22.0%,), myocardial infarction (17.9%), acute aortic
dissection (7.9%), acute renal failure (5.9%) and hypertensive encephalopathy (4.9%).
Compared to women of similar age, men had higher likelihood of having hypertensive
emergencies than urgencies (OR=1.34, 95% CI 1.061.70).9

Etiology
Acute and severe BP elevation can occur as a complication of essential or secondary HTN, or
it can happen idiopathically. (rodriguez, vaidya) The most common cause for a hypertensive
crisis is chronic HTN with an acute exacerbation. One of the most common precipitants is
medication noncompliance.1
Table 3. Causes of hypertensive emergencies6
Essential hypertension
Renal parenchymal diseases
Renovascular diseases
Endocrine diseases
Drugs

Autonomic hyperactivity
Central nervous system disorders
Pregnancy

Poorly controlled blood pressure, antihypertensive drugs

withdrawal
Acute glomerulonephritis, vasculitis, haemolytic uraemic
syndrome, thrombotic thrombocytopenic purpura
Pheocromocytoma, Cushings syndrome, renin secreting tumors,
mineralcorticoid hypertension (rare)
Cocaine, sympathomimetics, erythropoietin, cyclosporine,
interactions with monoamine-oxidase inhibitors (tyramine),
amphetamines
Guillame-Barr syndrome, acute intermittent porphyria
Head injury, cerebral infarction/ haemorrhage, brain tumors
Eclampsia/ severe pre-eclampsia

Pathophysiology
The pathophysiology of the hypertensive crises is complex and incompletely understood. 4,6
An initial abrupt rise in vascular resistance seems to be a necessary first step. 6 hypertensive
emergencies are group of diseases that are related to acute hypertension caused by
catecholamines, the simpathetic nervous system, the vascular endothelium and acute stess. In
hypertensive urgency the stess has low intensity and the organ can endure this stress without
being damaged.10
The renin-angiotensin system plays a central role in the homeostasis of BP. A rise in
plasma renin activity (PRA) stimulates the production of angiotensin II, a vasoconstrictor that
results in increased vascular resistance and BP. In severe HTN there is amplication of the

renin-angiotensin system; a rise in levels of renin and angiotensin II leading to high

aldosterone secretion, resulting in damage to the endothelium of blood vessels, as evidenced
by brin thrombi in the vessels.1,4 It is proposed that high BP leads to high vascular reactivity
and critical levels of vasoactive agents such as norepinephrine, angiotensin II, and
vasopressin leading to natriuresis, which brings about hypovolemia, triggering even more
elevation of the vasoconstrictive agents.1,6 This leads to arteriolar broid necrosis which
precipitates endothelial damage followed by platelet deposition and release of thromboxane
which can result in a microangiopathic hemolytic anemia. 1 It further results in myointimal
proliferation/damage with an endpoint of ischemia. Ischemia releases further vasoconstrictive
agents as mentioned above, which propagates the cycle.1,4,6 Ultimately there is elevation of
asymmetric dimethylarginine, an endogenous nitric oxide synthase inhibitor. Asymmetric
dimethylarginine may play an important role in the pathogenesis of preeclampsia.1

Figure 1. Pathophysiology of Hypertension emergency4

Diagnosis
Distinguishing between hypertensive emergency and urgency is a crucial step in appropriate
management of these conditions as management differs between them. The history and
physical examination are extremely important in determining the severity of an acute
hypertensive crisis syndrome and guiding further management. Laboratory data and other

diagnostic tests such as electrocardiogram and chest radiograph can provide important
information regarding possible end-organ damage.4
History
A complete history including any previous diagnosis of hypertension/ cardiovascular
disorders/ endocrine disorders and surgeries should be performed. 8 Patients hypertensive
history, current medication regimen, last dose of antihypertensive medication taken and
medication compliance disease duration, previous BP control, the presence of previous endorgan damage should be obtained.3,4,8 It should be kept in mind that the rate of increase in BP
may be even more important than the absolute level of BP at presentation. Alcohol
consumption, some food ingestion or the use of drugs (such as corticosteroids and
mineralocorticoids, oestrogens, NSAID, cyclosporine, carbamazepine, metoclopramide and
angiogenesis inhibitors) should be investigated.8 Patients should be asked specifically
whether they abruptly stopped taking blockers or central sympatholytic agents as abrupt
cessation of these medications may lead to rebound hypertension.4
In addition, patients should be asked about symptoms suggestive of end-organ
compromise, including chest pain (myocardial ischemia/infarction, aortic dissection),
shortness of breath (acute pulmonary edema secondary to left ventricular failure), back pain
(aortic dissection), and neurologic symptoms such as headache and blurry vision. Neurologic
symptoms may be due to intracerebral or subarachnoid hemorrhage or hypertensive
encephalopathy. Hypertensive encephalopathy is an acute organic brain syndrome or delirium
related to cerebral edema believed to result from loss of cerebral vascular autoregulatory
function in the setting of severely elevated blood pressure. It is characterized by headache,
nausea, and vomiting initially, followed by altered mental status and/or seizure if
hypertension is not treated.4
Salkic et al evaluated that the most common symptoms in subjects with hypertensive
crisis were headache (74.11%), chest pain and shortness of breath (62.35%), vertigo
(49.41%), and nausea and vomiting (41.17%). The most common symptoms of hypertensive
urgency were headache (78.87%) and chest pain (56.34%), while the most common
symptoms of hypertensive emergency were chest pain (92.86%) and short- ness of breath
(71.43%).11
On the other study, the most widespread signs and symptoms at presentation for
hypertensive urgency are headache (22%), epistaxis (17%), faintness (10%), psychomotor
agitation (10%), chest pain (9%), and dyspnea (9%). In contrast, most patients with
hypertensive emergencies complain of chest pain (27%), dyspnea (22%), and neurologic
decits (21%). Associated end-organ damage includes cerebral infarction (24.5%), acute
pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart
failure (12.0%). Less often patients present with intracranial hemorrhage, acute aortic
dissection, acute MI, acute kidney injury, and eclampsia.1

Figure 2. Common sign and symptoms of hypertensive crisis on initial presentation1

Physical Examination
BP should be measured on both arms, and if a large difference between the two arms is
detected, BP should also be measured at lower limbs, with the diagnostic hypothesis of aortic
dissection. The use of a beat-to-beat device for noninvasive BP measurements has been
proposed for a more accurate BP monitoring.8
Head and neck examination must include a complete fundoscopic examination. 4 The
funduscopic examination may be particularly helpful in identifying exudates, haemorrhages
and/or papilledema; the presence of grade 34 Keith Wegener retinopathy is associated with
the presence of microvascular dysfunction and renal damage.8
All patients should undergo auscultation of the carotid arteries, heart and renal
arteries. Murmurs should suggest further investigation (carotid ultrasound, echocardiography,
renal vascular ultrasound, depending on the location of the murmur). Pulse palpation and
cardiac auscultation may reveal arrhythmias.1 An irregular pulse should raise the suspicion of
atrial brillation, including silent atrial brillation. 2 An elevated jugular venous pressure,
third heart sound, gallop, and/or pulmonary rales are evidence of heart failure. A
prominent/displaced apical impulse or a harsh intrascapular murmur is suggestive of a
coarctation of the aorta.1
A careful neurologic examination should always be completed. The presence of focal
neurologic signs indicate ischemic or hemorrhagic stroke. Delirium or a flapping tremor is
suggestive of hypertensive encephalopathy. Hypertensive encephalopathy is a diagnosis of
exclusion; other causes that must be ruled out include stroke, subarachnoid hemorrhage, and
mass lesions.4
Single-organ involvement is observed in approximately 83% of patients presenting
with hypertensive emergencies. Two-organ involvement is found in 14% of patients, and
multiorgan involvement (> 3 organ systems) is found in approximately 3% of patients.1
Laboratory Work Up

Baseline investigations include a complete blood count with peripheral smear for the
presence of schistocytes, which may suggest microangiopathic hemolytic anemia. 4 Glucose,
creatinine, electrolytes and blood urea nitrogen should be performed.8 Hypokalemia or
hypomagnesemia would predispose to arrhythmias, renal and hepatic function tests. 1
Hypokalemic metabolic alkalosis may be seen as a result of intravascular volume depletion
and secondary hyperaldosteronism.4 When a secondary form of hypertension is suspected, a
sample for plasma renin activity, aldosterone and catecholamines should be drawn, before
giving appropriate therapy. Urinalysis should be performed, searching for proteinuria and
haematuria.8
Electrocardiogram should be done to assess for left ventricular hypertrophy,
arrhythmias, acute ischemia or infarction. Cardiac biomarkers should also be checked if ACS
is suspected.3
Other Diagnostic Tests
A chest radiograph should be obtained to evaluate for pulmonary vascular congestion as well
as a widened mediastinum, which suggests aortic dissection. 4 An echocardiogram can detect
other important information inpatients with both hypertensive emergencies and urgencies; left
ventricular hypertrophy and cardiac dysfunction can be detected. 8 If aortic dissection is
suspected (based on history of chest pain, unequal pulses and/or a widened mediastinum on
chest X ray), imaging of the aorta (CT angiogram/ magnetic resonance imaging/
transesophageal echocardiogram) should be performed immediately.3
Patients presenting with altered mental status or focal neurological deficits should get
a Computed Tomography (CT) or MRI of the brain to assess for hemorrhage or infarct.1,3
Table 4. Predictive value, availability, and costeffectiveness of some markers of organ
damage2
Marker
Electrocardiography
Echocardiography, plus Doppler
Estimated glomerular filtration rate
Microalbuminuria
Carotid intimamedia thickness and plaque
Arterial stiffness (pulse wave velocity)
Anklebrachial index
Fundoscopy
Additional measurements
Coronary calcium score
Endothelial dysfunction
Cerebral lacunae/white matter lesions
Cardiac magnetic resonance
Scores are from + to ++++.

Management/ Treatment

Cardiovascular
Predictive Value
+++
++++
+++
+++
+++
+++
+++
+++

Availability
++++
+++
++++
++++
+++
++
+++
++++

Costeffectiveness
++++
+++
++++
++++
+++
+++
+++
+++

++
++
++
++

+
+
+
+

+
+
+
++

An important issue in the management of patients with hypertensive urgency or emergency is

how quickly and to what degree to lower the blood pressure. Management should be tailored
to the individual patient based not only on absolute blood pressure number, but also on the
presence or absence of end-organ damage.4
Hypertensive Urgency
Hypertensive urgency can be managed with an oral medical regimen and gradual BP control
over 12 to 24 to 48 hours; patients should not have their BP rapidly lowered to their normal
baseline. The goal is to reduce the BP to 160/100 mm Hg over hours to days with low doses
of short-acting oral antihypertensive medications.1 Mean arterial pressure should be reduced
by no more than 25% within the first 24 hours. Avoiding excessive reduction is especially
important in patients who are at highest risk for hypotensive complications, such as the
elderly, patients with severe peripheral vascular disease, and those with known severe
atherosclerotic cardiovascular and intracranial disease.4
Hospital admission is not indicated and a short-term visit by the general practitioner
or a Center for Hypertension outpatient clinic is strongly suggested. 8 These include oral
labetalol (- and - adrenergic blocker) or clonidine (central -2 agonist). Captopril has also
been suggested as a rst-line agent in the treatment of hypertensive urgency, but it needs to be
used with caution.1 The use of a combination of antihypertensive drugs may increase the
likelihood of effective BP reduction and therefore can be considered for the initial approach.
On the contrary, the sublingual administration of nifedipine is not recommended, as it induces
an unpredictable, and often too rapid and large, decrease in BP reduction.8
Hypertensive emergency
The treatment goal should aim at reducing BP according to the presentation type. 1 Because of
autoregulation, a too rapid reduction in BP can lead to worsening tissue perfusion with
ischemia and possible infarction.12 Hypertensive emergency is a clinical diagnosis and the
clinical state of the patient is more important than the absolute value of the BP.7
Hypertensive emergencies require immediate admission to an intensive care unit for
prompt BP control with a parenteral, titratable antihypertensive agent while continuously
monitoring BP, neurologic status, and urine output. BP should be efciently reduced within
minutes to an hour, and not immediately to normal levels.1,4,6,7,12
Blood pressure management in this setting requires the use of parenteral drugs, as
precise and rapid control of blood pressure is critical. 7,12 The ideal rate of blood pressure
lowering is unclear, but reducing the mean arterial pressure by 10% during the first hour and
an additional 15% within the next 2 to 3 hours has been recommended 4, with a goal reduction
to normal within 24 to 48 hours.1
Treatment of hypertensive emergency is tailored to each individual case based on the
extent of end-organ damage as well as other comorbid conditions.4 The rapid-acting
antihypertensives preferred in hypertensive emergencies are labetalol, esmolol, fenoldopam,
clevidipine, nitroprusside, and nicardipine. In addition, some patients, particularly those with

normal kidney function, may have some element of volume depletion because of the
preceding pressure natriuresis that occurred in the setting of very high BP. Thus, in the
absence of clinical signs of volume overload, some volume expansion with intravenous saline
solution will help to suppress renin secretion and to prevent signicant hypotension once the
vasodilating medications begin to act.1
In patients with aortic dissection, however, a rapid reduction of SBP <120 mmHg and
mean arterial pressure <80 mm Hg should be achieved within 5 to 10 minutes, initially with
-blockers, to decrease the pressure impulse.1
Table 5. Drug of Choice in Treatment of Specific Types of Hypertensive Emergencies4
Type of Emergency
Neurologic
Hypertensive encephalopathy
Subarachnoid hemorrhage
CVA
Renal
Acute kidney injury
Cardiac
Aortic dissection
Pulmonary edema
Cardiac ischemia
Adrenergic crisis
Pheochromocytoma
Cocaine
Eclampsia

Drug of Choice

Second-line Drugs

Nitroprusside
Nimodipine
Labetalol

Labetalol or nicardipine
Labetalol or nicardipine
Nitroprusside, enalaprilat

Nicardipine

Fenoldopam

-Blocker + nitroprusside
Nitroglycerin
Nitroglycerin -blocker

Labetalol, trimethaphan
Nitroprusside ACE inhibitor
Nitroprusside, labetalol

Nitroprusside + -blocker

Phentolamine

Methyldopa
Magnesium sulfate

Hydralazine

Prognosis
There are few data regarding the outcomes of a hypertensive crisis. In a study of 315 patients
with malignant HTN, 40% were alive after 33 months. The most common causes of death
were renal failure (39.7%), stroke (23.8%), MI (11.1%), and heart failure (10.3%).1
Furthermore, studies of patients presenting to the emergency room with a
hypertensive crisis have demonstrated that most do not receive the appropriate evaluation,
medical regimen, and discharge instructions proposed by the current guidelines. Two studies
of patients presenting to the emergency room with a hypertensive crisis found that serum
chemistry was only obtained in 70% to 73% of patients, electrocardiogram in 53% to 70% of
patients, chest x-ray in 24% to 46% of patients, and urinalysis in 43% to 44% of patients.
Two-thirds of the total number of patients evaluated did not have a funduscopic examination
in the emergency room, and only 19% discharged had modication of their antihypertensive
regimen. Overall, only 6% obtained the tests recommended by the guidelines, and 10% had
no tests performed.1

Conclusion

Hypertensive urgency and emergency are associated with significant morbidity and mortality.
Prompt recognition and early treatment is crucial in preventing or halting progressive target
organ damage. Frequent monitoring that is typically only feasible in the intensive care unit is
necessary to achieve appropriate therapeutic endpoints. Treatment must be tailored to each
patient, based on the presence of specific target organ damage and underlying comorbidities.

References

1. Rodriguez MA, Kumar SK, Caro MD. Hypertensive Crisis. Cardiology in Review
[Internet]. 2010. [cited 2016 March 11]; 18: 102107. Available from:
2. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, et al. 2013
ESH/ESC Guidelines for the management of arterial hypertension. European Heart
Journal [Internet]. 2013. [cited 2016 March 11]; 34: 21592219. Available from:
3. Mallidi J, Penumetsa S, Lotfi A. Management of Hypertensive Emergencies.
[Internet]. 2013. [cited 2016 March 11]. Available from:
4. Vaidya CK, Ouellette JR. Hypertensive Urgency and Emergency. Turner White
Communication [Internet]. 2007. [cited 2016 March 11]; Available from:
5. US. Department of Health and Human Services. The Seventh Report of the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure. 2004. [Internet]. [cited 2016 March 11]; Available from:
6. Migneco A, Ojetti V, Lorenzo AD, Silveri NG, Savi L. Hypertensive Crises:
Diagnosis and Management in The Emergency Room. European Review for Medical
and Pharmacological Sciences [Internet]. 2004. [cited 2016 March 11]; 8: 143-152.
Available from:
7. Pollack CV, Rees CJ. Hypertensive Emergencies: Acute Care Evaluation and
Management. Emergency Medicine Cardiac Research and Education Group
[Internet]. 2008. [cited 2016 March 11]; Available from:
8. Muiesana ML, Salvettia M, Amadorob V, di Sommab S, Perlinic S, Semplicini A, et
al. An Update on Hypertensive Emergencies and Urgencies. Federazione Italiana di
Cardiologia [Internet]. 2014. [cited 2016 March 11]; 16:000000. Available from:
9. Pinna G, Pascale C, Fornengo P, Arras S, Piras C, Panzarasa P, et al. Hospital
Admissions for Hypertensive Crisis in the Emergency Departments: A Large
Multicenter Italian Study. [Internet]. 2014. [cited 2016 March 25]. Available from:
10. Lagi A, Cencetti S. Hypertensive Emergencies: A New Clinical Approach. Clinical
Hypertension. [Internet]. 2015. [cited 2016 March 25]; 21: 20. Available from:
11. Salkic S, Batic-Mujanovic O, Ljuca F, Brkic S. Clinical Presentation of Hypertensive
Crises in Emergency Medical Services. Mater Sociomed. [Internet]. 2014. [cited 2016
March 25]; 26(1): 12-16. Available from:
12. van den Born BJH, Beutler JJ, Gaillard CAJM, de Gooijer A, van den Meiracker AH,
Kroon AA. Dutch Guideline for The Management of Hypertensive Crisis 2010
Revision. The Journal of Medicine. [Internet]. 2011. [cited 2016 March 25]. Available
from:

Table 6. Parenteral agents used for hypertensive emergencies7

Drug
Sodium
Nitroprusside

Dose
0.25-10g/kg/min
Avg. Effective dose 3 g/kg/min

Onset
1-2 min

Duration
3-4 minutes
after
infusion
stopped

Nitroglycerin

5g/kg/min to max 100g/kg/min

2-5 min

Fenoldopam

0.1g/kg/min to max 1.6g/kg/min

Titrate in 0.05-0.1g/kg/min
increments

10 min, max
effect in 30
min

5-10
Dilates coronary vessel
minutes
1 hour after - Increases renal blood flow
- Used without invasive BP
stopping
monitoring

Nicardipine

5 mg/hr can be increased by 2.5

mg/hr to max 15 mg/hr

Within 10
min

2-6 hours
after
stopping

Enalaprilat

1.25 mg IVP at 4-6 hr intervals,

max 5 mg in hours

15 min 4
hr to peak
effect

12-24 hours

Hydralazine

10-20 mg IV

10-20 min

1-4 hours

Increses urerine blood flow

Esmolol

Load 250-500 g/kg over 1-3 min.

Can infuse at 50-100 g/kg/min.
Titrate every 5 min with repeat
bolus and increased drip by 50
g /kg/min to max 300 g/kg/min
20mg IV over 2 min, additional
boluses every 10 min with
escalating doses of 4 mg, 80 mg to
max, cumulative dose of 300 mg.

6-20 min
after bolus.
Max effect 5
min

6-20 min
after bolus.
Max effect 5
min

Ultra-short acting

2-5 min
after bolus
with peak in
5-15 min

2-4 hours
after
stopping
infusion or

Labetalol

Advantage
Large amount of experience with
use

- Dilates coronary vessels

- Used without invasive BP
monitoring

Side Effect
- Nausea, vomiting, muscle twitching,
diaphoresis
- Inactivated by light
- Usually requares invasive intra-arterial
blood pressure monitoring
- Use cautiously in ACS as can cause
coronary steal
- Ineffective arterial vasodilator
- HA, hypotension, tachycardia
- Reflex tachycardia
- HA, dizziness, flushing, nausea
- Worsening angina
- A-fib
- Tachyphylaxis after 48 hrs
- Contraindicated in glaucoma
- HA, flushing, dizziness, hypotension,
digital dysesthesias
- Abrupt withdrawal
- Metabolized in liver, use with caution in
cirrhotic
- BP response variable, unpredictible, and
not dose-related
- May not peak for 4 hours
- Contraindicated in pragnancy
- Flushing, HA, nausea
- Sig. reflex tachycardia
- Has precipitated MI
- Use cautiosly in CKD, CAD, CVD
- Bradycardia, hypotension, seizure
- Bronchospasm, acute pulmonary edema
- Can precipitate chest pain
- Requires central access
- Use with caution in CKD

- Decreases reflex tachycardia from - Profound orthostatis

- Contraindicated in decompesated CHF,
other agents
- Doesnt affect cerebral blood flow
heart block, asthma, pheochromocytoma
- Doesnt decrease CO
- Can cause profound hypotension

Common Uses
Has been used in all
syndromes of
hypertensive
emergencies

Not use for most HE

Especially useful in HE
syndromes complicated
by renal insufficiency or
failure
Has been used
extensively in post-op
hypertension, especially
post CT surgery
Not generally useful for
HE syndrome
Used only for
eclampsia/ preeclampsia
Often used in
combination with
vasodilators to reduce
reflex tachycardia
Often used in
combinationwith
vasodilator to reduce
reflex tachycardia

Can start infusion with 1-2 min

Clevidipine

2-16 g/kg/min

last bolus

1-5 min

- Doesnt affect renal function

T 1 min, - Ultra-short acting with rapid onset,

effect last 5offset of effect
10 min after - Little to no reflex tachycardia
- Metabolism independent of renal
stopping
and hepatic function
- Arterial line not required
- No special delivery system needed,
used with periheral IV access
- Specially studied in ED

- Dizziness, nausea, vomiting, parashesia,

scalp tingling, bronkospasm.
Just resently approved, scant broad ED
experince.

associated with those

agents
Studied in post
operative hypertension,
post cardiac surgery, and
ED treatment of HE.
Potentially useful for all
types of HE.

HE = hypertensive emergency, ED= emergency department, CKD= chronic kidney disease, HA= headache, CAD= coronary artery disease, ICP= intracranial pressure, ACS, acute coronary
syndrome, CO= cardiac output