JUNE 2023 | VOLUME 25 | ISSUE 6

Emergency Medicine Practice Evidence-Based Education • Practical Application

CLINICAL CHALLENGES:
• What defines hypertensive
emergency?
• What are the most common and
dangerous end-organ dysfunctions
to watch for?
• How do the different society
guidelines define and treat
hypertensive emergencies?

Authors
Ari B. Davis, DO
Department of Emergency Medicine, Einstein
Medical Center, Philadelphia, PA

Kyle Hughes, MD
Department of Emergency Medicine, Einstein
Medical Center, Philadelphia, PA

Jonathan Pun, MD
Department of Emergency Medicine, Einstein
Medical Center, Philadelphia, PA

Scott Goldstein, DO, FACEP,

FAEMS, EMT-PHP
Director, Division of EMS/Disaster Medicine,
Einstein Healthcare Network, Philadelphia, PA
Peer Reviewers
Aman Pandey, MD
Assistant Professor, Emergency Medicine,
University of Florida Health Jacksonville,
Jacksonville, FL
Christopher R. Tainter, MD, RDMS,
FACEP, FCCM
Clinical Professor, Department of
Anesthesiology, Division of Critical Care,
University of California San Diego, San Diego,
CA
Prior to beginning this activity, see “CME
Information” on page 2.
Hypertensive Emergencies:
Guidelines and Best-Practice
Recommendations
n Abstract
Due to a variety of demographic and public health factors, the
number of emergency department visits related to hypertensive
emergencies has increased dramatically in recent decades,
making it imperative that clinicians clearly understand the
current treatment guidelines and definitions for the spectrum
of hypertensive disease. This issue reviews current evidence on
identifying and managing hypertensive emergencies and the
differences between expert opinions on diagnosing and managing
these emergencies. Clear protocols differentiating patients with
hypertension from patients with hypertensive emergencies are
needed to appropriately manage this patient population.

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This issue is eligible for CME credit. See page 2. EBMEDICINE.NET

 CME Information
Date of Original Release: June 1, 2023. Date of most recent review: May 10, 2023. Termination date: June 1, 2026.
Accreditation: EB Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide
continuing medical education for physicians.
Credit Designation: EB Medicine designates this enduring material for a maximum of 4 AMA PRA Category 1 CreditsTM. Physi-
cians should claim only the credit commensurate with the extent of their participation in the activity.
Specialty CME: Included as part of the 4 credits, this CME activity is eligible for 2 Pharmacology CME credits, subject to your state and institu-
tional approval. For more information, contact Customer Service at 678-366-7933.
ACEP Accreditation: Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Cat-
egory I credit per annual subscription.
AAFP Accreditation: The AAFP has reviewed Emergency Medicine Practice, and deemed it acceptable for AAFP credit. Term of approval is from
07/01/2022 to 06/30/2023. Physicians should claim only the credit commensurate with the extent of their participation in the activity. This session,
Hypertensive Emergencies: Guidelines and Best-Practice Recommendations, is approved for 4.0 enduring material AAFP Prescribed credits.
AOA Accreditation: Emergency Medicine Practice is eligible for 4 Category 2-A or 2-B credit hours per issue by the American Osteopathic Association.
Needs Assessment: The need for this educational activity was determined by a practice gap analysis; a survey of medical staff, including the
editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation responses from
prior educational activities for emergency physicians.
Target Audience: This enduring material is designed for emergency medicine physicians, physician assistants, nurse practitioners, and residents.
Goals: Upon completion of this activity, you should be able to: (1) identify areas in practice that require modification to be consistent with current
evidence in order to improve competence and performance; (2) develop strategies to accurately diagnose and treat both common and critical ED
presentations; and (3) demonstrate informed medical decision-making based on the strongest clinical evidence.
CME Objectives: Upon completion of this activity, you should be able to: (1) define hypertensive emergency, including its clinical presentations,
diagnostic criteria, and potential complications; (2) explain the epidemiology and pathophysiology of hypertensive emergency, including risk
factors and underlying mechanisms; (3) discuss the current evidence-based approaches to the management of hypertensive emergency; and (4)
describe the different multidisciplinary society guidelines and how to use them.
Discussion of Investigational Information: As part of the activity, faculty may be presenting investigational information about pharmaceutical
products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as
continuing medical education and is not intended to promote off-label use of any pharmaceutical product.
Disclosure: It is the policy of EB Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME activities.
All individuals in a position to control content have disclosed all financial relationships with ACCME-defined ineligible companies. EB Medicine
has assessed all relationships with ineligible companies disclosed, identified those financial relationships deemed relevant, and appropriately
mitigated all relevant financial relationships based on each individual’s role(s). Please find disclosure information for this activity below:
Planners Faculty
• Daniel J. Egan, MD (Course Director): Nothing to Disclose • Ari B. Davis, DO (Author): Nothing to Disclose
• Andy Jagoda, MD (Editor-in-Chief): • Kyle Hughes, MD (Author): Nothing to Disclose
l Pfizer (Consultant/Advisor) • Jonathan Pun, MD (Author): Nothing to Disclose
l Janssen (Consultant/Advisor) • Scott Goldstein, DO (Author): Nothing to Disclose
l Abbott Laboratories (Consultant/Advisor) • Aman Pandey, MD (Peer Reviewer): Nothing to Disclose
• Kaushal Shah, MD (Associate Editor-in-Chief): Nothing to Disclose • Christopher R. Tainter, MD (Peer Reviewer): Nothing to Disclose
• Aimee Mishler, PharmD (Pharmacology Editor): Nothing to Disclose
• Joseph D. Toscano, MD (Research Editor): Nothing to Disclose
• Dorothy Whisenhunt, MS (Content Editor): Nothing to Disclose
• Cheryl Belton, PhD (Content Editor): Nothing to Disclose
Commercial Support: This issue of Emergency Medicine Practice did not receive any commercial support.
Earning CME Credit: Go online to https://www.ebmedicine.net/CME and click on the title of the test you wish to take. When completed, a CME
certificate will be emailed to you.
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 Case Presentations
A 62-year-old man presents via EMS with swelling of his legs that makes it hard for him to walk...
• EMS states he wasn’t able to walk because of his lower extremity swelling. Vital signs en route are:
temperature, 37°C; heart rate, 90 beats/min; blood pressure, 193/118 mm Hg; respiratory rate, 20
breaths/min; and oxygen saturation, 94% on room air.
• The patient reports his medication was across the room, and he wasn’t able to reach it due to his inabil-
ity to walk from his leg swelling. He states he has a history of congestive heart failure with a left ventric-
CASE 1

ular ejection fraction of 25%. He pulls out from his jacket a copy of his latest echocardiogram report.
• On physical examination, you notice he has bilateral lower extremity pitting edema and that he is
becoming increasingly more tachypneic. On pulmonary examination, you hear fine crackles bilaterally
and diffusely. You notice his oxygen saturation is dropping on the monitor, despite just having put him
on 2 L of oxygen via nasal cannula. As you continue to talk to him, his oxygen requirements increase to
non-rebreather mask.
• You wonder what type of hypertensive emergency this is, and what treatment must be implemented
immediately?

A 76-year-old man presents to the ED with his family, who are concerned he might have dementia…
• The family informs you that he is normally a sweet old man, but recently he has been having episodes
of confusion and agitation. Yesterday, the police found him walking along the highway in his bathrobe.
• His family tells you he has a history of diabetes and hypertension. They don’t know if he has been
CASE 2

taking his medications regularly or what his medications are.

• His temperature is 37°C; blood pressure, 236/113 mm Hg; heart rate, 62 beats/min; respiratory rate, 14
breaths/min; and oxygen saturation, 96% on room air. His blood glucose level is 185 mg/dL.
• On examination, he is alert and oriented to name only. He complains of a “headache all over,” seeing
strange flashing lights, and is annoyed by your continued questioning. As you continue, he no longer
participates in the physical examination and begins to have jerking movements.
• Which medication(s) should you use to treat him?

A 59-year-old woman presents to the ED after being seen at her primary care physician’s office…
• Her doctor was concerned because her blood pressure was 206/120 mm Hg. Her blood pressure
normally runs high, but they had never seen it this high.
CASE 3

• The patient states that she feels fine. She denies any vision changes, headache, chest pain, or shortness
of breath. Her past medical history is relevant for hypertension and pre-diabetes. She states that she
did not take her blood pressure medications this morning, since her primary care doctor‘s office told
her to not eat or drink anything prior to getting her laboratory work today.
• You wonder whether anything needs to be done in the ED about her blood pressure…

n Introduction Several definitions have been used to classify

Hypertensive emergency is a clinical syndrome of
significantly elevated blood pressure (BP) associated
with rapidly progressive end-organ damage. While
survival from hypertensive emergency has improved
considerably in recent years, it is still associated with
significant morbidity and mortality, as case-controlled
studies have reported an all-cause mortality of 10% at
5 years, with 20% of patients requiring kidney trans-
plantation.1 To identify patients who need intensive
treatment and to avoid harm in those who do not,
a thorough history, physical examination, and clini-
cal assessment are required. Unfortunately, unclear
terminology for describing these patients clinically is
often a source of confusion and can present a barrier
to appropriate recognition and management.
severe hypertension and hypertensive emergencies.
The terms hypertensive urgency, hypertensive crisis,
and malignant hypertension are historically defined as
severely elevated BP without evidence of end-organ
damage. With some variability from study to study,
severe hypertension is usually defined as systolic
BP (SBP) ≥180 mm Hg or a diastolic BP (DBP) ≥110
mm Hg. The key distinction of severe hypertension
from a hypertensive emergency is the lack of rapidly
evolving end-organ damage in severe hypertension.
Differentiating this collection of terms is the first step
in the safe management of hypertensive patients. For
this review, a BP of ≥180/110 mm Hg and a mean
arterial pressure (MAP) of ≥135 mm Hg will be used
to define severe hypertension. The designation of

JUNE 2023 • www.ebmedicine.net 3 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.

severe hypertension may be helpful to alert clinicians
to assess for the presence of end-organ damage, but
it will not constitute a hypertensive emergency. This
issue of Emergency Medicine Practice will discuss the
best available evidence for identification and man-
agement of hypertensive emergencies.
n Critical Appraisal of the Literature
A literature review was conducted in the Cochrane
Database of Systematic Reviews, the Cochrane Central
Register of Controlled Trials, and PubMed for articles
published between 2000 and 2023 using the terms
hypertensive crisis, hypertensive emergency, malignant
hypertension, and hypertensive emergencies. Specific
hypertensive emergency terms acute ischemic stroke,
aortic dissection, and acute heart failure were also
searched. 5180 articles were screened, and of those,
122 articles were included for discussion and evaluation.
Of the articles included, there were few well-
designed randomized controlled trials (RCTs) evalu-
ating optimal BP management during hypertensive
emergencies. Among all hypertensive emergencies,
the strongest evidence to guide optimal BP manage-
ment is from patients with intracranial hemorrhage
(ICH). The American Heart Association (AHA)/Ameri-
can Stroke Association (ASA)2 and European Stroke
Organisation (ESO)3 guidelines reference the ATACH4
and INTERACT trials5,6 as high-quality randomized
trials that give clinicians strong evidence for a specific
BP target, making treatment recommendations similar
across multiple guidelines.
Other hypertensive emergencies, such as in acute
coronary syndromes (ACS), have no well-designed
clinical trials to direct optimal BP management, and
therefore recommendations can differ widely between
guidelines. For example, the AHA/American College
of Cardiology (ACC) non-ST-elevation myocardial
infarction (NSTEMI) guidelines recommend intrave-
nous (IV) nitroglycerin for patients who are hyperten-
sive, with a B level of evidence,7 while the European
Society of Cardiology (ESC) guidelines specifically
state that there is no indication for nitrate treatment
in patients with an NSTEMI, beyond symptomatic
treatment.8 Similarly, the AHA/ACC published guide-
lines for hypertension management in ACS with a
recommended target BP <140/90 mm Hg (class of
recommendation 2a, level of evidence C),9 while ESC
guidelines mention no specific target for BP manage-
ment, stating that nitrates, angiotensin-converting en-
zyme (ACE) inhibitors, angiotensin II receptor block-
ers (ARBs), and beta blockers can be used during the
acute phase of BP management.10
With limited well-designed prospective studies
and conflicting recommendations between guide-
lines, the ESC and AHA/ACC both published broad
guidelines on how to manage all hypertensive emer-
gencies. Table 1 lists the ESC-recommended MAP or
SBP reductions for each hypertensive emergency.12
The AHA/ACC simplify hypertensive emergency
management to reducing BP by a maximum of 25%
in the first hour and then to 160/100-110 mm Hg over
the next 2 to 6 hours for all hypertensive emergencies
except aortic dissections, pre-eclampsia/eclampsia,
and pheochromocytoma crisis.11
Guidance on which antihypertensive agent to use
for managing hypertensive emergencies is even more
sparse than BP targets, with no blinded prospective

Table 1. Hypertensive Emergencies Requiring Immediate Blood Pressure Lowering12

Clinical Presentation Timeline and Target BP First-line Treatments Alternative Treatments
Malignant hypertension with or without throm- Several hours; Labetalol, nicardipine Nitroprusside, urapidil
botic microangiopathy or acute renal failure MAP −20% to −25%
Hypertensive encephalopathy Immediate; MAP −20% to −25% Labetalol, nicardipine Nitroprusside
Acute ischemic stroke and SBP >220 mm Hg or 1 hour; MAP −15% Labetalol, nicardipine Nitroprusside
DBP >120 mm Hg
Acute ischemic stroke with indication for 1 hour; MAP −15% Labetalol, nicardipine Nitroprusside
thrombolytic therapy and SBP >185 mm Hg or
DBP >110 mm Hg
Acute hemorrhagic stroke and SBP >180 mm Hg Immediate; SBP 130-180 mm Hg Labetalol, nicardipine Urapidil

Acute coronary event Immediate; SBP <140 mm Hg Nitroglycerine, labetalol Urapidil

Acute cardiogenic pulmonary edema
Acute aortic disease
Eclampsia and severe pre-eclampsia/HELLP
Immediate, SBP <140 mm Hg
Immediate; SBP <120 mm Hg and
heart rate <60 beats/min
Immediate; SBP <160 mm Hg and
DBP <105 mm Hg
Nitroprusside or nitroglycerine Urapidil (with loop diuretic)
+ loop diuretic
Esmolol + nitroprusside or Labetalol or metoprolol
nitroglycerine or nicardipine
Labetalol or nicardipine + Not applicable
magnesium sulfate

Abbreviations: BP, blood pressure; DBP, diastolic blood pressure; HELLP, hemolysis, elevated liver enzymes and low platelets; MAP, mean arterial
pressure; SBP, systolic blood pressure.
Bert-Jan van den Born, Gregory Y H Lip. ESC Council on Hypertension position document on the management of hypertensive emergencies. European
Heart Journal – Cardiovascular Pharmacotherapy. Volume 5, Issue 1. By permission of European Society of Cardiology.

JUNE 2023 • www.ebmedicine.net 4 ©2023 EB MEDICINE

trials comparing one antihypertensive agent to an-
other. There are some prospective and retrospective
studies comparing labetalol to nicardipine for manag-
ing acute ischemic strokes and ICH; however, none
found a difference in patient-centered outcomes.13-17
Although there are no strong data to recommend
a class of antihypertensive for each hypertensive
emergency, some guidelines do make specific rec-
ommendations (eg, beta blockers for acute aortic
dissection) based on retrospective studies and expert
opinion.18,19 The American College of Obstetricians
and Gynecologists (ACOG) acknowledge there is no
single agent that is superior to another in manag-
ing severe hypertension in pregnancy.20 More well-
designed trials comparing antihypertensive agents for
each specific hypertensive emergency are needed.
n Etiology And Pathophysiology
Hypertensive emergencies are more likely in per-
sons aged >60 years, and those who are Black,
male, underinsured or uninsured, and those who live
in lower-socioeconomic areas.21 While the precise
pathophysiology of hypertensive emergency re-
mains unclear, dysfunctional autoregulation appears
Figure 1. Pathophysiology of Hypertensive Emergencies
Eric Adua. Decoding the mechanism of hypertension through multiomics profiling. Journal of Human Hypertension. Volume 37, Issue 4. Pages 253-264.
2023. Available at: https://www.nature.com/articles/s41371-022-00769-8/figures/1 Used, without changes, according to Creative Commons Attribution
4.0 International Licence
JUNE 2023 • www.ebmedicine.net
to play a significant role. In persons with normal BP
regulation, there is an appropriate balance between
normal vital organ perfusion, hypoperfusion, and
hyperperfusion. The balance between cardiac out-
put and peripheral vascular resistance depends on
a complex set of integrated actions between the
cardiovascular, neural, renal, and endocrine sys-
tems that is not fully understood. (See Figure 1.) A
multisystem approach to BP regulation allows the
body to respond to internal and external demands
such as hypervolemia or hypovolemia, thirst, infec-
tion, trauma, and rapid changes in position.22,23 The
sympathetic nervous system also plays a major role,
particularly during times of physical stress, by in-
creasing cardiac output and arterial vasoconstriction.
Endothelial function is also important in modulating
BP regulation. The endothelium of the vascular wall
acts as a regulator of BP by secreting vasodilators and
vasoconstrictors in response to various stimuli.22,23
While the underlying mechanisms of primary hy-
pertension and hypertensive emergency are not fully
understood, there seems to be several overlapping
causes. The initial event appears to be an abrupt rise
in BP from a known or unknown stimulus followed by
compensatory mechanisms arising from the vascular
5 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
endothelium. Initially, the endothelium releases the
vasodilator, nitric oxide, to compensate for the in-
crease in intravascular pressure. The arterioles sense a
rise in BP and, in turn, arterial smooth muscle relaxes,
causing vasodilation to reduce the rise in BP. A vicious
cycle occurs, with prolonged arterial smooth muscle
relaxation leading to prolonged endothelial dysfunc-
tion and an inability to release additional nitric oxide,
resulting in a further increase in BP. 24
Inflammation is also a major factor in endothelial
dysfunction. The mechanical shear forces on the vas-
cular wall result in endothelial damage and dysfunc-
tion. Endothelial dysfunction results in the expres-
sion of inflammatory markers such as endothelin-1,
endothelial adhesion molecules, and cytokines. The
inflammatory component of hypertension is be-
lieved to promote coagulation, platelet aggregation,
endothelial layer permeability, and vasoconstriction.
Thus, there appears to be a complex interaction of
the renin-angiotensin-aldosterone system, sympa-
thetic nervous system, and endothelial dysfunction,
regardless of the initial stimulus. There is also evi-
dence that angiotensin II activates the expression of
genes for proinflammatory cytokines and activation
of transcription factor NF-kB, causing a direct toxic
effect to the vessel wall. An increased level of von
Willebrand factor, von Willebrand factor prepeptide,
plasmin-antiplasmin complexes, and reduced levels
of ADAMTS (a disintegrin and metalloproteinase with
thrombospondin motifs)13 are seen in patients with
hypertensive emergency, suggesting that thrombotic
microangiopathy may also play a role.23,25
It is the rate of change of BP that increases the
likelihood of end-organ damage, as the degree of BP
elevation does not always correlate with the severity
of end-organ damage.26 Individuals with long-stand-
ing hypertension may have adaptive autoregulatory
changes that protect organs from sudden increases
in BP. In previously normotensive patients who have
acute hypertension (eg, pregnant women with pre-
eclampsia), hypertensive emergency can occur at
lower MAPs. Alternatively, patients with chronic hy-
pertension may have extremely elevated BP without
hypertensive emergency.
n Differential Diagnosis
As the term implies, hypertensive emergency carries
a significant mortality rate, and clinical manifesta-
tions are considered life-threatening. A differential
diagnosis for hypertensive emergencies can be found
in Table 2, page 7. Primary causes of hypertensive
emergency refers to cases where no underlying cause
for the sudden increase in BP can be identified. In
these cases, the increase in BP is due to a combina-
tion of genetic, environmental, and lifestyle factors,
including obesity, lack of exercise, and a diet high in
sodium. In patients presenting to the ED with primary
JUNE 2023 • www.ebmedicine.net
hypertensive emergencies, a secondary cause can be
found in 20% to 40%.27 Secondary causes of hyper-
tensive emergency refers to cases where the sudden
increase in BP is a result of an underlying medical con-
dition. It is important to differentiate between primary
and secondary causes of hypertensive emergency,
because the management of each condition differs. In
cases of primary hypertensive emergency, the goal of
treatment is to lower the BP gradually to avoid further
end-organ damage. In cases of secondary hyperten-
sive emergency, the underlying condition must be
identified and treated, which can help control the BP.
n Prehospital Care
Prehospital providers can be critical to early iden-
tification of hypertensive emergencies. In the
prehospital setting, hypertensive emergencies are
typically not treated directly in the field. This is consis-
tent with ESO3 and European Academy of Neurology
(EAN) guidelines.28 The AHA and ASA do not make
any recommendations regarding this topic.11
Nitroglycerin is often given for chest pain sus-
pected to be cardiac in nature and occasionally due
to acute heart failure, consistent with the 2017 ACC/
AHA guidelines.11 Of note, pain relief following ad-
ministration of nitroglycerin is not diagnostically help-
ful to differentiate ACS.29 Important questions to ask
prior to administration of nitroglycerin include wheth-
er the patient has used nitrates or phosphodiesterase
inhibitors (eg, sildenafil or tadalafil), since concomitant
administration can result in precipitous hypotension.
A full set of vital signs should always be obtained
by emergency medical services, if possible, and re-
ported on arrival to the ED. IV access should also be
obtained in the prehospital setting to expedite medi-
cation administration in the hospital, whether to con-
trol BP or to administer time-sensitive medications for
underlying etiologies. In patients with symptoms of
an acute ischemic stroke (which may be seen with se-
vere hypertension), the patient’s last-known-well time
is also helpful to guide care, as it has been shown
that decreased time from ischemic stroke onset to
administration of thrombolytics improves outcomes.
Reducing BP for thrombolytic candidacy prehospital
may improve door-to-needle time; however, no trials
have established this. The INTERACT4 trial is cur-
rently recruiting patients to study this question.
n Emergency Department Evaluation
History
A hypertensive emergency can be identified based
on the patient’s past and present history and results
of the physical examination, laboratory analysis,
and imaging. There is no specific BP threshold that
defines hypertensive emergency; however, guidelines
recommend that patients with BP readings ≥180/110
6 ©2023 EB MEDICINE
Table 2. Differential Diagnosis of Hypertensive Emergencies
System Differential Diagnosis Clinical Findings and Features Workup
Brain Hypertensive encephalopathy Headache, nausea, vomiting, confusion, seizures, Diagnosis of exclusion, MRI brain to
Posterior reversible encephalopathy coma evaluate for edema
syndrome
Reversible posterior
leukoencephalopathy syndrome
Acute ischemic stroke Focal neurological deficits Diagnosis of exclusion, MRI brain to
evaluate for ischemia
Subarachnoid hemorrhage Thunderclap headache, meningismus CT/CTA/MRI brain, lumbar puncture
Intracranial hemorrhage Stroke-like symptoms, Cushing triad (bradycardia, CT brain
respiratory depression/irregularity, widened pulse
pressure), fixed dilated pupil
Hypertensive retinopathy Visual acuity changes Fundoscopy
Arteries Aortic dissection Acute heart failure, acute coronary syndromes, CTA chest, abdominal/thoracic
cardiac tamponade, ischemic limb, stroke, ultrasound, angiography
mesenteric ischemia, renal failure
Pre-eclampsia/eclampsia/HELLP Severe headache, visual disturbances, altered Urinalysis, serum creatinine, platelet
mental status, seizure count, liver function tests
Hypertensive retinopathy Vision changes, often asymptomatic Fundoscopy
Thrombotic thrombocytopenic purpura Fever, anemia, thrombocytopenia, altered mental CBC, CMP, PT, PTT, fibrinogen,
status, renal failure LDH
Hemolytic-uremic syndrome Renal failure, anemia, thrombocytopenia
Disseminated intravascular coagulation Coagulopathy, thrombosis
Polyarteritis nodosa Cutaneous lesions, fatigue, weight CRP, ESR, CTA, angiography
loss, fever, arthralgia
Takayasu arteritis Aortic regurgitation, claudication, bruits CTA/MRI chest, angiography,
ESR/CRP
Kidney Acute renal failure Oliguria, confusion, pericarditis Urinalysis, BMP, renal ultrasound
Scleroderma renal crisis Oliguria, anemia
Acute glomerulonephritis Recent upper respiratory infection or skin infection Urinalysis, BMP, C3/C4, CBC
Renal artery stenosis Young-onset hypertension, abdominal bruit Duplex renal ultrasound, CTA/MRA
Heart Myocardial infarction Chest pain, shortness of breath Electrocardiogram, troponin
Congestive heart failure Shortness of breath, lower extremity edema, Chest x-ray, +/- brain natriuretic
jugular vein distension, S3/S4 peptide, electrocardiogram
Substance/ Tyramine reaction Monoamine oxidase inhibitor use, tyramine-rich Medication reconciliation
medication diet, sympathomimetic syndrome (diaphoresis,
induced mydriasis, tachycardia, hyperthermia)
Abrupt withdrawal of clonidine, Reflex tachycardia, headache
ACE inhibitors, or beta blockers
Serotonin syndrome Altered mental status, hyperthermia, tachycardia,
clonus, hyperreflexia
Sympathomimetic exposure Diaphoresis, mydriasis, tachycardia, hyperthermia +/- urine drug screen
Withdrawal (alcohol, benzodiazepines) Autonomic hyperactivity, seizures, delirium tremens Diagnosis of exclusion
Endocrine Cushing syndrome Hyperpigmentation, hirsutism, amenorrhea 24-hour urinary free cortisol or
dexamethasone suppression test
Pheochromocytoma Episodic hypertension, tachycardia, flushed skin Plasma/urine metanephrines, CT
adrenal
Hyperthyroidism Exophthalmos, goiter, hyperreflexia TSH, free T3/T4
Other Burns Blisters, eschar, electrical injury Clinical diagnosis
Pain Tachycardia

Abbreviations: ACE, angiotensin-converting enzyme; BMP, basic metabolic panel; CBC, complete blood cell count; CMP, comprehensive metabolic panel;
CRP, C-reactive protein; CT, computed tomography; CTA, CT angiography; ESR, erythrocyte sedimentation rate; HELLP, hemolysis, elevated liver
enzymes, and low platelets; LDH, lactate dehydrogenase; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; PT, prothrombin;
PTT, partial thromboplastin time; TSH, thyroid-stimulating hormone.

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mm Hg be evaluated promptly because they are
at increased risk for adverse cardiovascular out-
comes.11,30 It is important to remember that during
the clinical evaluation, regardless of the BP measure-
ment, the emphasis remains on determining whether
end-organ damage is present or imminent.
A thorough evaluation must include the
patient’s prior hypertensive history, including current
antihypertensive medications as well as compliance.
Any recent medication changes must also be noted.
Special attention must be paid to a patient’s history
of over-the-counter medications such as cough
and cold medications (particularly those containing
pseudoephedrine or phenylephrine), as well as
substances such as cocaine, methamphetamines, or
other sympathomimetics. A complete medication
history should be conducted to identify other
medications that are not used for treatment of
hypertension that may lead to a presentation of
hypertension (eg, monoamine oxidase [MAO]
inhibitors, serotonergic medications).
When asking about past medical history, it is
important to inquire about any pre-existing organ
dysfunction to distinguish it from an acute process.
Data from a 2021 meta-analysis demonstrate that
the risk for hypertensive emergency is higher in
patients with a history of comorbid cardiovascular
conditions, such as chronic kidney disease (odds
ratio [OR], 2.9), coronary artery disease (OR,
1.65), or stroke (OR, 1.77).31 In a large multicenter
study of patients hospitalized with acute severe
hypertension, the presence of either chronic kidney
disease or acute kidney injury was associated with
worse outcomes, including increased length of
hospitalization. Even after accounting for baseline
renal dysfunction, the presence of acute kidney injury
or an acute deterioration in kidney function during
hospitalization was associated with morbidity and
predicted mortality.32 Women should be asked about
pregnancy and postpartum status as well as previous
peripartum diseases such as gestational diabetes,
hypertension, and pre-eclampsia or eclampsia.
A social history should include a rough estimate
of sodium intake, general diet intake (eg, tyramine-
rich foods) as well as the consumption of alcohol or
other gamma-aminobutyric acid (GABA)-agonists,
including their abrupt cessation, all of which can
increase the likelihood of hypertensive emergencies.
Physical Examination
The physical examination should include serial BP
measurements with an appropriate-sized cuff on both
arms while the patient is in a resting position. Patients
should be seated comfortably, with back supported,
legs uncrossed, and all clothing covering the cuff
removed. The patient’s arm should be supported at
heart level, as measurements above and below this
level may give misleading readings. The cuff blad-
JUNE 2023 • www.ebmedicine.net
der should encircle 80% or more of the patient’s arm.
An undersized cuff will typically overestimate the BP
and an oversized cuff will underestimate the BP. Initial
pressure measurement in the ED is often transiently
elevated. Simply allowing the patient to rest quietly
and repeating the test will often lead to a more ac-
curate reading.33
MAP is often the preferred measurement of BP
for several reasons: (1) automated oscillometric BP
cuffs measure MAP directly, effectively making it more
accurate than systolic or diastolic readings, which are
calculated based on the MAP reading; (2) systemic
autoregulation adapts to changes in MAP, and the risk
for hypertensive emergency therefore appears to be
more closely related to MAP rather than SBP;34,35 and
(3) titration of antihypertensive medications is usually
based on a single variable, and by using MAP, there
is a less variability compared to systolic or diastolic
readings. Unfortunately, most of the society recom-
mendations described do not use MAP.
The comprehensiveness of each part of the physi-
cal examination should be dictated by the patient’s
chief complaint. There are key findings the clinician
should be aware of, as they may indicate underlying
end-organ damage. Table 3 lists the most common
presenting symptoms of hypertensive emergency and
the most common sequelae of end-organ damage.
Lung and heart auscultation should be performed for
signs of congestive heart failure or pulmonary edema
(third heart sound, elevated jugular venous pres-
sure, and crackles on lung examination). A new-onset
cardiac murmur may signify papillary muscle rupture
during an acute myocardial infarction or type A aortic
dissection. Evaluation of the abdomen should include
assessment for a bruit/mass that can suggest renal
artery stenosis and aortic aneurysm.
The neurologic examination should note mental
status changes such as delirium and depressed
level of consciousness, which are found in patients
with hypertensive encephalopathy. Lateralizing
signs, however, are uncommon in hypertensive
Table 3. Common Symptoms and Sequelae
of Hypertensive Emergencies11,36
Most common presenting symptoms of hypertensive emergency:
• Shortness of breath (29%)
• Chest pain (26%)
• Headache (23%)
• Altered mental status (20%)
• Focal neurologic deficit (11%)
Most common sequelae of hypertension-induced end-organ
damage:
• Pulmonary edema/heart failure (32%)
• Ischemic stroke (29%)
• Acute coronary syndromes (18%)
• Hemorrhagic stroke (11%)
• Acute aortic syndrome (aortic dissection) (2%)
• Hypertensive encephalopathy (2%)
8 ©2023 EB MEDICINE
 encephalopathy not complicated by ischemic brain Figure 2. Malignant Hypertension on
injury and suggest a vascular event. Fundoscopic Imaging
Traditionally, patients with suspected hypertensive
emergency warrant fundoscopic examination, since the
presence of grade III or IV hypertensive retinopathy is a
sign of microvascular dysfunction and impaired cere-
bral autoregulation, and can be the only sign of end-
organ damage.23,37 Retinopathy grade III or IV is pres-
ent when bilateral cotton wool spots, flame-shaped
hemorrhages, and/or papilledema are found by means
of retinal examination. An image of these findings can
be seen in Figure 2. There are currently no guidelines
or significant evidence to suggest whether all patients
being evaluated for hypertensive emergency require
fundoscopic examination. Therefore, the decision to
perform fundoscopy is ultimately provider-dependent.
Recently, the BARKH-based algorithm was
proposed by the Department of Medicine Emergen-
cies and Hypertension Unit, in Padova, Italy for quick
identification of hypertensive emergencies and their
associated acute organ damage. Figure 3 outlines
Image shows flame-shaped hemorrhages, cotton wool spots, and
the BARKH algorithm. The acronym stands for Brain, papilledema consistent with grade III/IV retinopathy.
Arteries, Retina, Kidney, and Heart, and offers a sim- Reprinted with permission of https://EyeRounds.org, the University of
plified, streamlined approach to assessing the patho- Iowa. https://eyerounds.org/atlas/photos/malignant-HTN.jpg
logical changes associated with hypertensive emer-
gency. Although the list is not exhaustive, it offers
emergency clinicians a quick bedside tool to help aid n Diagnostic Studies
decision-making. For more detailed treatment recom- Patients who present with a BP ≥180/110 mm Hg-
mendations, see the “Treatment” section, beginning without signs or symptoms of a possible underlying
on page 11. hypertensive emergency should not be subjected to
routine diagnostic studies in the
10 G. P. ROSSI ET AL. emergency department (ED) on
Figure 3. The BARKH Algorithm the basis of their hypertension
alone. It is well-documented that
Grade III arterial HT evaluating for end-organ dam-
age in asymptomatic patients
Evidence of BARKH
does not change ED manage-
(HT-Mediated Organ Damage) ment, nor does it improve
outcomes. It does, however,
increase the likelihood for un-
necessary hospitalizations.38,39
Brain Arteries Re�na Kidney Heart Patients who present with
(Stroke (Acute aor�c (Grade III-IV (Acute renal (Acute Heart asymptomatic hypertension are
or syndromes Keith-Wagener- insufficiency failure,
hypertensive or Barker or pulmonary
at no increased risk for major
encephalopathy) (Pre)eclampsia re�nopathy) thrombo�c edema) adverse cardiovascular events,
or HELLP) microangiopathy) acutely. Any subsequent major
adverse cardiovascular event in
patients who are discharged with
asymptomatic hypertension is
Hypertensive Emergency likely secondary to other risk fac-
tors such as age, sex, diabetes,
Rapid BP reduc�on with i.v. drugs chosen according to BARKH atrial fibrillation or prior cardio-
vascular disease, or consequenc-
igure 2. Simplified brain, arteries, retina, kidney and/or heart (BARKH)-based algorithm for a quick identification of the es hyperten-
of chronic hypertension that
ve emergenciesAbbreviation:
(HEs) and the associated
BARKH, acute organ
brain, arteries, retina,damage. If BARKH
kidney, heart; involvement
BP, blood pressure; is detected,
HELLP, the reduction would
hemolysis, of BP values
not immediately benefit
hould be undertaken withliver
elevated i.v. enzymes,
treatment;andin low
any platelets;
other case,
HT, an oral treatment is recommended. BP: blood pressure; HT: hyperten-
hypertension.
on; HELLP: haemolysis elevated
Management liver enzymes
of hypertensive low platelets.
emergencies: a practical approach. Gian Paolo Rossi, Giacomo Rossitto,
from aggressive antihyperten-
Chiarastella Maifredini, et al. Blood Pressure. 2021. Volume 30, Issue 4. Reprinted by permission of sive therapy or further inpatient
Taylor & Francis Ltd, http://www.tandfonline.com evaluation.38,40
etermining prognosis. Accordingly, to save the Pathophysiological considerations and implication
atient’s life, an immediate
JUNE decrease of BP values to
2023 • www.ebmedicine.net for management9 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
mit the extension of organ damage, is mandatory
The speed and severity of BP elevation are the main
12]. Consensus exists (Class of Recommendation I,
 If a patient does present with symptoms sug-
gestive of an underlying hypertensive emergency,
diagnostic studies should focus on areas that may
reveal end-organ damage.
Basic Laboratory Analysis
The laboratory workup for patients suspected of
having hypertensive emergency may include testing
to assess renal function, electrolyte balance, and
red blood cell parameters. Suspicion may come
from reports of fatigue, generalized weakness,
excessive fluid loss from vomiting/diarrhea, and
dehydration, or other elements obtained from
the history and physical examination. If there is
suspicion for renal injury, testing may include a
basic chemistry panel (including creatinine) and
urinalysis with microscopy to assess for significant
changes in glomerular filtration rate, proteinuria,
red blood cells, and cellular casts that may indicate
renal parenchymal disease. A complete blood cell
count can be helpful to assess for the presence
of anemia and thrombocytopenia, which can be
indicative of a microangiopathic hemolytic process.
A lactate dehydrogenase level and haptoglobin
level can also be obtained to help determine the
degree of hemolysis.
For patients presenting with altered mental status
or neurologic deficits, a point-of-care glucose level
should be obtained to exclude acute hypoglyce-
mia. If there is concern for myocardial injury, cardiac
troponin-I (cTnI), a cardiac-specific protein with a very
high sensitivity and specificity for myocardial injury,
should be obtained. Patients with elevated cTnI have
a higher risk for mortality, independent of other clini-
cally relevant variables, including baseline character-
istics and comorbidities.41 Additional studies may be
Figure 4. Left Ventricular Hypertrophy
Left: Image shows thickening of the myocardium of the left ventricle.
Right: Electrocardiogram (ECG) shows evidence of left ventricular hypertrophy with increased R-wave amplitude
in the left-sided ECG leads (I, aVL, V4-6) and increased S-wave depth in the right-sided leads (III, aVR, V1-3).
Additionally, there are discordant T-wave inversions in leads V5 and V6 that are consistent with left heart strain. diagnosis (T2-weighted
JUNE 2023 • www.ebmedicine.net
indicated on a case-by-case basis, although routine
pregnancy testing is generally relevant in the appro-
priate population.
Electrocardiogram
If there is concern for myocardial ischemia or
dysrhythmia (eg, chest pain, palpitations, shortness
of breath), an electrocardiogram (ECG) should be
obtained, although ECG is not particularly sensitive in
detecting left ventricular hypertrophy, and its sensitiv-
ity varies according to body habitus. The presence
of left ventricular hypertrophy is associated with
long-standing hypertension, increased incidence of
cardiovascular disease, and early death.42 In addi-
tion to left ventricular hypertrophy, the presence of
a left heart strain pattern on ECG has been shown
to identify patients with greater left ventricle mass, a
higher prevalence of echocardiographic left ventricu-
lar hypertrophy that is more likely to be concentric,
and lower myocardial contractility and higher estimat-
ed myocardial oxygen demand.43 The classic strain
pattern is typically described as ST depression with a
down-sloping convex ST segment and discordant T-
wave inversions in the lateral precordial leads. Figure
4 shows the characteristic ECG findings seen in left
ventricular hypertrophy with strain pattern.
Imaging Studies
Imaging studies should be tailored to clinical con-
cerns. A chest radiograph may be useful to evaluate
for interstitial pulmonary edema or cardiomegaly, or it
may show a widened mediastinum in the setting of a
thoracic aortic dissection. A point-of-care ultrasound
by an experienced clinician may help identify aortic
dissection, evidence of left ventricular hypertrophy, di-
minished ejection fraction, pulmonary edema, or other
causes of elevated blood
pressure, such as bladder
outlet obstruction.
CT imaging of the
head is useful when
assessing for acute
intracranial hemorrhage
(ICH), and is often indi-
cated if there is concern
for cerebrovascular
ischemia or hypertensive
encephalopathy. See
Figure 5, page 11, for
common locations of
ICH seen on CT imaging.
CT imaging can suggest
hypertensive encepha-
lopathy in certain clini-
cal contexts; however,
an MRI of the brain is
needed to confirm the
10 ©2023 EB MEDICINE
FLAIR MRI).44 While CT may not be as sen- Figure Access
5. Common Locations of Intracranial
sitive as MRI in identifying regions of brain
Open
Hemorrhage Secondary to Hypertension
edema, it is usually more readily available,
takes less time to perform, and is essential and
for ruling out other intracranial lesions. mass
When conducted within 6 hours of Ha
symptom onset, noncontrast head CT
remains the gold standard for diagnosing
using
subarachnoid hemorrhage (SAH), with a toma
negative predictive value of 99.9%.46 CT area,
sensitivity for intracranial blood decreases to A
substantially over time, particularly in the
subarachnoid space. To confirm the di-
mult
agnosis, a lumbar puncture is required. of h
If a CT is nondiagnostic for exclusion of slice)
ICH, xanthochromia or red blood cells tion,
in the cerebrospinal fluid from a lumbar
puncture are highly suggestive of SAH. CT
to be
angiography of the brain is often used to MR
look for intracranial aneurysms that often ence
cause SAH.47 matio
Figure 6 shows the classic findings with
posterior reversible encephalopathy syn-
requ
drome (PRES) seen on MRI. Papilledema, of de
a surrogate marker for cerebral edema, is be
can also be evaluated using ultrasound to ation
measure the optic nerve sheath diameter.
Figure
Reproduced1 from
Typical locations
Stroke and of hypertensive
Vascular Neurology. Cyrus K. Dastur, ICH
WenguiareYu.putamen
Volume 2, caver
Optic nerve sheath diameter >5 mm
has been shown to be 95% sensitive for (A), thalamus (B), subcortical white matter (C), pons (D) Ltd.
Issue 1. Pages 21-29. Copyright 2017, with permission from BMJ Publishing Group and CT
papilledema and is therefore a feasible tool cerebellum (E). Thalamic and subcortical haemorrhages often vascu
to assess for increased intracranial pres- extend into ventricles (B and C). CAA, drug abuse or vascular sign’.
sure.45 (See Figure 7, page 12.) Figure 6.
anomaly High
often Signal-Intensity
causes lobar haemorrhage Vasogenic
Posterior (F).
reversible ICH,Edema
encephalopathy on
syndrome Liman et al.
ciated
Magnetic Resonance
intracerebral haemorrhage; Imaging of the amyloid
CAA, cerebral Brain angiopathy.
risk
n Treatment HTN
Acute Decompensated Heart Failure newe
Treatment of hypertensive acute
Lobar ICH is commonly the result of cerebral amyloid
angiopathy (CAA).14 Amyloid deposition in small-sized to the ‘
decompensated heart failure (ADHF)
should focus both on lowering the pa- medium-sized cortical perforators may lead to the haem
tient’s SBP as well as improving respiratory rupture of these vessels, resulting in asymptomatic micro- signifi
distress. Three interventions that are often requi
employed to manage hypertensive ADHF
haemorrhages or symptomatic lobar haemorrhages.14
Non-lobar ICH is most often the result of long-standing ation
are noninvasive positive-pressure ventila-
tion (NIPPV), diuretics, and vasodilators. All high blood pressure resulting in lipohyalinosis of small Re
of these interventions have varying degrees perforating arteries of the basal ganglia, thalamus, pons ation
of evidence in improving patient outcomes. exam
and cerebellum, leading to deep haemorrhages, often
Because this review is focused on BP man- vascu
agement during hypertensive emergencies, with extension into the ventricles.12 15 The most common
NIPPV for ADHF will not be discussed. locations of hypertensive ICH are the putamen, thal-
amus, subcortical white matter, pons and cerebellum
Diuretics
(figure 1). EMER
There is conflicting evidence about the ICH
utility of early IV diuretic use in ADHF. One Secondary ICH is associated with a number of con-
study showed early administration of IV genital
High and acquired
signal-intensity
shine through on DWI ADC values.conditions
vasogenic edema
and elevated such as
on magnetic resonance
(b) Cytotoxic edema, characterized vascular
signal elevation,malfor-
FIGURE 4. Diffusivity in PRES. (a) Vasogenic edema, characterized by increased signal in T2, normal signal or variable T2
imaging
by T2
of the brain,
DWI hypersignal
given
diuretics reduces in-hospital mortality in consistentADC
mations,
and corresponding withreduction
posterior
tumours,
reversible
(circle). encephalopathy
coagulation
Vasogenic syndrome.
edema is virtually always
disorders,
co-present (arrows).
use of or m
Thomas G. Liman, Eberhard Siebert, Matthias Endres. Posterior reversible
ADHF. A post hoc analysis of a large multi- PROGNOSIS their
anticoagulants
encephalopathy
AND OUTCOME and
syndrome. thrombolytic
Current Opinion inof 0.2 agents,
Neurology.
(95% Volume
CI, cerebral vascu-the
32,
0.15-04)[33 Issue
].
&&
1. Pages
However, 25-
given
center prospective registry enrolling ADHF Even though PRES has gained
35. By permission increased
of Wolters attention
Kluwer Health Inc.heterogeneity of studies with differences in outcome
https://journals.lww.com/co-neurology/ 3 16 17 (EMS
patients in the ED (REALITY-AHF registry) data litis,
since drug
its first abuse
description more than and cerebral
two decades ago, venous
variables (e.g. thrombosis.
Abstract/2019/02000/Posterior_reversible_encephalopathy_syndrome.6.aspx
in-hospital death, functional outcome
on outcome from prospective studies are
still lacking.
with modified Rankin scale, Glasgow outcome scale),
study populations and case numbers, results have to toma
In most cases, PRES has a good short-term and be interpreted with caution. Furthermore, mortality
long-term prognosis if treated fast and adequately and morbidity in PRES are also dependent on the sever
JUNE 2023 • www.ebmedicine.net 11 clinical symptoms are revers-
© 2023underlying
EB MEDICINE. ALL RIGHTS RESERVED.
EARLY DIAGNOSIS
and MRI findings and disease, that is women with PRES in
ible after several hours or days [31]. However, cerebral eclampsia have a better prognosis than patient with Sta
hemorrhage or ischemia and irreversible neurologi- chemotherapy-associated PRES in incurable
ICH should be suspected in any patient with severe
cal deficits or death occur. Studies reported complete cancer patients. (ABC
resolution of edema and clinical recovery in 70-90% In all available studies, death occurred in 8-17%
 demonstrated that patients who received any dosage mon, with close monitoring of urine output. If little or
of IV furosemide within 60 minutes of arrival had a no diuretic response is seen, the diuretic dose can be
3-fold lower in-hospital mortality than those who re- doubled.
ceived IV furosemide later during their stay. However,
it should be noted there were significant baseline dif- Vasodilators
ferences between the early treatment and non-early Multiple large systematic reviews and RCTs have
treatment groups. The early groups were (1) more demonstrated that vasodilators are safe and effective
likely to present via ambulance; (2) presented with in lowering SBP in ADHF, but fail to show any consis-
more acute symptom onset; (3) had higher BPs and tent improvement in short- or long-term survival.53-56
heart rates; and (4) had significantly more patients This may be due to different phenotypes observed in
with symptoms suggestive of being volume over- patients with ADHF. Some patients’ symptoms may
loaded (peripheral edema, pulmonary edema, rales, be secondary to an acute increase in left ventricular
jugular vein distension, and orthopnea). There was afterload, leading to rapid fluid redistribution into the
also no standardized dosage of IV furosemide ob- lungs, while others may experience a gradual increase
served. Each of these confounders, alone, could lead of cardiac filling pressures related to pre-existing
to earlier recognition and treatment.48 Two other post structural heart disease. ESC guidelines state that
hoc analyses from different multicenter prospective patients of the former phenotype may benefit from
registries enrolling ADHF patients in the ED showed nitrates or nitroprusside to decrease afterload,51 while
no in-hospital mortality difference between early AHA guidelines state that the role of nitroglycerin and
versus late loop diuretic administration; however, nitroprusside is uncertain and recommend their use
one study was limited by similar baseline differences only as an adjuvant, to decrease preload, for relief of
between early and non-early treatment groups (eg, dyspnea in hypertensive patients.52
pulmonary edema, elevated jugular vein distension, Administering a high-dose nitroglycerin IV bolus 1.2 a 8 mL
and dyspnea),49 and the other did not report the tim- (600 mcg to 4 mg administered over several minutes), (preparación
: 2 amp de
ing or quantity of diuretics given.50 The 2021 ESC51 followed by a nitroglycerin infusion (started at 50-
25 mg/100
and 2022 AHA guidelines52 recommend using loop 100 mcg/min and titrated down based on symptom mL)
diuretics for those with signs of volume overload, as improvement and SBP) has been shown to be safe57,58
they provide the most rapid and effective diuresis for and may help reduce intensive care unit (ICU) admis-
patients with ADHF. The general recommendation sions.59 A systematic review found, with a moderate
LETTERSof
TOan IV EDITOR
THE dose 1 to 2 times the patient’s equivalent quality of evidence, that high-dose nitrates may lower
maintenance dose of their oral loop diuretic is com- rates of mechanical ventilation, improve BP, shorten
length of stay, and lower
Figure 7. Optic Nerve Sheath Evaluation Using Ocular Ultrasound rates of ICU admission;
however, the authors not-
ed that these conclusions
are limited due to the
heterogeneity and varying
quality of studies in-
cluded.58 A well-designed
RCT is needed to clarify
the utility of high-dose
nitroglycerin for patients
with acute increases in
volume overload.
Clevidipine has also
shown to be effective in
quickly reducing SBP in
patients with hypertensive
ADHF, possibly making it
an alternative if nitrates
are contraindicated,
FIGURE. A, Essential structures of the eye visualized with ocular point-of-care ultrasound. Ocular point-of-care ultrasound (POCUS)
Ocular point-of-care ultrasound (POCUS) can be performed using a high-frequency linear array transducer
although nicardipine may
can be used to visualize the dimensions of critical ocular structures (A) at the bedside. This representative image (B) shows an ocular
through a closed eyelid on a supine patient. View A: Diagram of the structures visualized using POCUS. View be a more available and
POCUS image taken at the bedside using a 7.5-mHz linear probe through a closed eyelid on a supine patient. The diameter of the
B: The
optic nerve diameter
should of the optic
be measured nerve3 is
at a point mmmeasured
posterior3 to
mm theposterior to the retina.
retina. Increased heightIncreased height
of the optic disc of
andthe diametercost-effective
optic disc
expanded of option.60,61
and expanded diameter of the optic nerve sheath (>5 mm) are indicative of papilledema,
the optic nerve are indicative of papilledema, which may be indicative of elevated intracranial pressure. a sign of elevated Patients may develop
intracranial pressure.
tolerance to nitroglycerin,
Reprinted from Mayo Clinic Proceedings. Volume 95, Issue 9. Gregory W. Heinicke, Justin M. Chen, Emily J.
Cox, et al. A case of elevated intracranial pressure diagnosed with point-of-care ocular ultrasound. Pages 2046-
requiring higher doses or
A 5.8 mm2048.
cutoff for ONSD
Copyright 2020, aswith
a diag- thisfrom
permission case, by the patient’s photo-
Elsevier. transition
Data Previously Presented at: 2019 Society of to a different
nostic criteria for IIH previously phobia). Additionally, use of POCUS General Internal Medicine Annual Meeting,
Washington, DC, May 8 e May 11, 2019. Con-
yielded a sensitivity of 90% and can facilitate compliance with the ference proceedings available at: Abstracts from
JUNE
specificity of 2023
84%7•; www.ebmedicine.net
however, this reduced imaging recommendations 12 ©2023 EB MEDICINE
the 2019 Annual Meeting of the Society of Gen-
criterion may need to be refined as from the Choose Wisely Campaign, eral Internal Medicine. J Gen Intern Med.
elevated ONSD and optic disc height while also soothing some concerns 2019;34(Suppl 2): 99-867 (Abstract ID
vasodilator.62 Authors of a small retrospective study
comparing nicardipine to nitroglycerin for ADHF in the
ICU found a significant number of patients who were
given nitroglycerin required nicardipine for BP control,
and they theorized that this may reflect patients devel-
oping a tolerance to nitroglycerin.63
Urapidil, which is not available in the United States
but is available in Europe, is a sympatholytic vasodila-
tor that might improve short-term cardiac function
when given in the ED, although further studies are
necessary to determine its efficacy.64
Other Treatments
Additional treatments used historically for ADHF
include morphine and nesiritide. Morphine should not
be used in the management of patients with ADHF, as
multiple studies have shown that patients who receive
morphine have an increased mortality risk, estimated
to be 5-fold higher than those who do not receive
morphine.65,66 Nesiritide should also not be used to
manage ADHF. The ASCEND-HF trial, a large double-
blinded RCT, demonstrated that nesiritide provided
no clinical benefit and was significantly more likely to
cause hypotension.67
Blood Pressure Targets
There are no RCTs or large studies to demonstrate
a specific target SBP that is best for patients with
hypertensive ADHF. The ESC and AHA guidelines do
not mention any specific target for SBP.51,52 A post
hoc analysis of the REALITY-AHF study reported that
patients in the ED whose SBP was reduced by >25%
may have had a higher mortality rate; however, this
study did not report any baseline characteristics of
the BP groups that could explain the difference in
mortality and had several limitations to consider.68
Therefore, it is reasonable to target lowering SBP by
10% to 25% for patients with hypertension and ADHF.
Acute Ischemic Stroke
Once noncontrast CT excludes ICH as a cause
for a patient’s stroke-like symptoms, treatment
should be guided by whether the patient will re-
ceive a thrombolytic medication or a mechanical
thrombectomy. The decision to perform one or
both of these interventions should be made by an
interventionalist or neurologist. For patients receiving
thrombolytics or mechanical thrombectomy, AHA/
ASA and ESO guidelines both recommend lowering
BP to <185/110 mm Hg prior to the intervention and
maintaining BP <180/105 mm Hg for 24 hours post
intervention.2,3 Only one RCT has assessed outcomes
in patients managed at different BP ranges prior to
thrombolysis. The ENCHANTED trial randomized
patients to SBP 130 to 140 mm Hg or SBP <180
mm Hg prior to receiving IV alteplase. The authors
found a statistically significant reduction in ICH in
the intensive BP control group; however, post hoc
JUNE 2023 • www.ebmedicine.net
analysis found a statistically significant increase in
90-day mortality.6,69 For patients receiving mechani-
cal thrombectomy, there are no RCTs that assess
optimal BP management prior to intervention. AHA/
ASA and ESO recommendations to lower BP to
<185/110 mm Hg prior to intervention stem primarily
from inclusion criteria of prior clinical trials in which
patients received thrombolytic medications, and then
additional prospective data demonstrated a statisti-
cally significant increased mortality and functional
disability in those with elevated BP before and after
receiving thrombolytic medications or mechanical
thrombectomy.70-74 ESO guidelines do not mention
any specific antihypertensive medication to use; the
AHA/ASA recommend using nicardipine, clevidipine,
or labetalol, though there are no data or recommen-
dations regarding one medication over another.75,76
For patients who are not receiving antithrombotic
agents or a mechanical thrombectomy, there is no
strong evidence to identify an optimal BP in the
first few hours after onset of symptoms. If patients
are hypertensive >220/120 mm Hg, both AHA/ASA
and ESO guidelines state that lowering BP no more
than 15% is reasonable and likely to be safe, with
no evidence to suggest that doing so improves or
worsens outcomes.2,3 Recommendations to treat
excessive hypertension are supported by data from
multiple large retrospective and prospective studies
demonstrating a U-curve pattern in the relationship
between admission SBP and mortality.77-79 That being
said, one should be extremely careful when lowering
SBP, as reducing admission SBP >15% is significantly
associated with worse outcomes, especially for those
aged >70 years.80 Additional RCTs evaluating BP
management within the first few hours of symptom
onset are needed to clarify whether there is any ben-
efit or harm to reducing BP in patients not receiving
antithrombotic agents or mechanical thrombectomy.
Acute Coronary Syndromes
ACS includes STEMI, NSTEMI, and unstable angina.
Although unstable angina is considered its own entity
within ACS, new high-sensitivity troponin testing has
made the diagnosis of unstable angina quite rare, and
its management will not be discussed here.
Blood Pressure Targets
During the acute stage of ACS (ie, within the first
24 hours, or prior to definitive treatment with
thrombolysis or percutaneous coronary intervention),
there are no good data to suggest an optimal BP
target. ESC guidelines specify a normotensive target
for NSTEMI patients, while AHA guidelines do not
comment on any target BP. There are, however, corre-
lations between admission BP and patient outcomes.
It is well documented that an SBP <100 mm Hg on
admission is a strong predictor of increased mortality
within 6 months, reflected in clinical decision-making
13 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
tools such as GRACE and TIMI.81-83 Multiple large
prospective studies have shown lower in-hospital
mortality rates and reduced major adverse cardio-
vascular events in patients who are hypertensive on
presentation.83-85 Acute hypertension in patients with
ACS may signify good cardiac function in response
to significant stress, and is associated with improved
outcomes. AHA and ESC STEMI management guide-
lines state that SBP >180 mm Hg and DBP >110
mm Hg are relative contraindications to fibrinolytic
therapy, but caution that BP frequently fluctuates in
the early stages of ACS, and management should be
focused first on pain control and clinical stabilization.9
Beta Blockers
The AHA and ESC guidelines recommend admin-
istering beta blockers with high beta-1 affinity (eg,
metoprolol) to hypertensive patients with STEMI.10,88
(Class I, level of evidence A, for oral administration;
class IIA, level of evidence B for IV administration.)
Multiple RCTs have demonstrated that beta block-
ers can reduce recurrent myocardial infarctions
and ventricular fibrillation, and decrease infarction
size.86,87 However, patients with SBP <120 mm Hg,
age >70 years, or a heart rate >110 beats/min who
were given IV beta blockers were found to have a
statistically significant higher risk for developing
cardiogenic shock. AHA guidelines cite these findings
as contraindications to giving beta blockers to STEMI
patients in the first 24 hours, while ESC guidelines
cite only ADHF, hemodynamic instability, or high-
degree atrioventricular block as contraindications.88
A recent Cochrane review that included these studies
stated that beta blockers probably reduce the long-
term risk for all-cause and cardiovascular mortality.89
Although AHA/ESC guidelines state that beta block-
ers can be used to treat hypertension in patients
with ACS, it is recommended to lower the BP slowly
and avoid DBP <60 mm Hg, to maintain coronary
perfusion. Well-designed RCTs directed at BP control
prior to definitive treatment in patients with ACS are
needed to clarify the relationship between BP and
patient outcomes.89
Nitrates
Both the AHA and ESC guidelines state that the
use of IV nitrates for patients with STEMI who are
hypertensive may be useful in the acute phase;
however, neither cite evidence for this or a specific
BP target.10,88 Both the AHA and ESC guidelines
recommend IV nitrates for hypertensive patients
with NSTEMI. For the use of nitrates in ACS, both
guidelines reference studies conducted more than
20 years ago.7,8 A recent systematic review evaluated
these studies and found a mortality benefit at day 2
from nitrate therapy within 24 hours.90 No mortality
benefit was found at day 10 or >30 days. The authors
concluded that nitrates should be routinely given to
JUNE 2023 • www.ebmedicine.net
patients with ACS. Although a mortality benefit was
seen in this systematic review, there are no RCTs with-
in the last 20 years to clarify whether nitrate therapy
improves mortality.
Intracerebral Hemorrhage
Blood Pressure Targets
Relative to other hypertensive emergencies, ICH has
the most data to support recommendations for a
specific BP target. There is debate about how much
BP should be lowered to optimize outcomes.91 Both
the AHA/ASA and ESO guidelines recommend im-
mediately lowering SBP to <140 mm Hg when ICH
is recognized, and maintaining SBP between 130
and 150 mm Hg, but not <130 mm Hg, to prevent
hematoma expansion.3,92 The largest RCTs to assess
mortality and degree of disability for patients with
ICH are the INTERACT-2 and ATACH-2 trials, where
patients’ SBPs were lowered to either <140 mm Hg or
<180 mm Hg.5,93 The AHA/ASA guideline specifically
states their recommendations are based on these 2
trials and the subsequent post hoc analyses of these
trials. A pooled analysis of both studies found that for
every 10-mm Hg reduction from 170 mm Hg, there
was a trend toward lower mortality rates, smaller
hematoma expansion, and better functional recovery,
with a statistically significant reduced rate of neurolog-
ical deterioration in patients with an SBP maintained
between 120 and 130 mm Hg.94 A post hoc analysis
of ATACH-2 showed statistically significant higher
rates of neurologic deterioration and cardiac-related
adverse events in patients maintained between 100
and 140 mm Hg, which is in contrast to what a post
hoc analysis of ATACH-2 trial alone found.4,74
Lowering SBP when ≥180 mm Hg clearly im-
proves patient outcomes, potentially reaching a peak
benefit when lowered <140 mm Hg; however, other
variables such as SBP variability and relative SBP
reduction are important to be cognizant of when con-
sidering BP goals. The pooled analysis of ATACH-2
and INTERACT-2 showed statistically significant
improved functional recovery when SBP was reduced
40 to 59 mm Hg below the baseline SBP; however,
reduction ≥60 mm Hg worsened outcomes.94 The
analysis also found a greater variability in SBP had
a statistically significant greater number of adverse
events and neurologic deterioration, and a post hoc
analysis of INTERACT-2 identified variability in SBP as
one of the strongest predictors of worse outcomes in
the first few hours of treatment.95
Clinicians should be cognizant of iatrogenic
hypotension, as a large prospective study found it to
be the highest risk factor for mortality, with its great-
est risk in the first 6 hours.96 One might hypothesize
that invasive (ie, arterial line) measurement of SBP
reduces SBP variability, making it superior to nonin-
vasive devices; however, there are no data to support
this hypothesis.
14 ©2023 EB MEDICINE
Antihypertensive Medications
The AHA/ASA and ESO do not mention a specific anti-
hypertensive to use, and recommend using medication
that has a fast time of onset and short half-life, to pre-
vent excessive BP lowering and allow for easy titration,
reducing the potential for variability.3,92 One retrospec-
tive study did not show a difference in hospital mor-
tality or functional recovery, and there are conflicting
results from studies comparing time to BP goal, time at
BP goal, and variability of BP between nicardipine and
labetalol.13-17 Therefore, either nicardipine or labetalol
are reasonable first-line medications.
To summarize, both nicardipine and labetalol ef-
fectively and safely reduce SBP in patients with ICH,
with no clear evidence to suggest one works better
than the other. A small pilot study demonstrated the
efficacy of clevidipine to reduce SBP in patients with
ICH,97 while another retrospective study found no dif-
ference in time to SBP goal, length of stay, mortality,
or disposition between nicardipine and clevidipine.98
When choosing an antihypertensive agent, clinicians
should consider practicability, variability, pharmaco-
logical profile, and potential side effects of the agent.
Subarachnoid Hemorrhage
There are little to no data to guide treatment in
patients with non–aneurysmal SAH. When caring
for patients with an aneurysmal SAH, the focus is
primarily on prevention of rebleeding within the first
12 hours, as this has been shown to worsen patient
outcomes.47,99,100 Elevated BP is a known risk factor
for rebleeding; however, there are no good data
to support the benefit of lowering BP in the acute
phase of SAH.101 A 2021 Cochrane review found a
single RCT from the 1980s evaluating the effect of
BP reduction, ultimately finding no significant benefit
to lowering BP.102 AHA/ASA guidelines recommend
lowering SBP to <160 mm Hg; ESO guidelines
recommend lowering SBP <180 mm Hg; and the
Neurocritical Care Society guidelines recommend
treating only extreme hypertension (MAP >110 mm
Hg).47,99,100 No specific antihypertensive agent is
mentioned in any of these guidelines.
Aortic Dissection
To date, there have been no RCTs evaluating specific
BP targets during the acute management of aortic
dissection, although there are several retrospective
evaluations.103 There are also no randomized studies
that have evaluated the efficacy of different medical
treatments for aortic dissections. The 2022 ACC/AHA
guidelines recommend reducing the patient’s heart
rate to 60 to 80 beats/min and then lowering SBP to
<120 mm Hg, citing one small retrospective study
and expert opinion.104 It also recommends using an IV
beta blocker before lowering the patient’s BP to pre-
vent any possible reflex tachycardia.19 There are no
data to suggest a specific beta blocker or vasodilator
JUNE 2023 • www.ebmedicine.net
is more efficacious than another.11,18,30 It is reason-
able to use a fast-acting, easily titratable beta blocker
(such as esmolol) as a first-line agent to immediately
control the patient’s heart rate. The ESC guidelines
also recommend using an IV beta blocker to simul-
taneously lower a patient’s heart rate and SBP. ESC
guidelines cite a SBP goal of <120 mm Hg, with no
specific heart rate.18 If a patient has a contraindication
to beta blockers, nondihydropyridine calcium chan-
nel blockers (such as diltiazem or verapamil) could
be an alternative for heart rate control. Vasodilators
recommended by the ACC/AHA guideline include
nicardipine, clevidipine, and nitroprusside.19
Hypertensive Encephalopathy
Hypertensive encephalopathy is most commonly seen
with BP > 220/120 mm Hg.105 There are no RCTs to
suggest a specific goal in BP reduction or which anti-
hypertensive agent to use.44,105 The International So-
ciety of Hypertension guidelines recommend immedi-
ately reducing MAP by 20% to 25% using nicardipine
or labetalol as first-line agents.30 PRES is a form of
encephalopathy diagnosed on CT or MRI and can be
seen in hypertensive encephalopathy; however, one
should be careful not to attribute the presence of
PRES to the patient’s hypertension. PRES can be pres-
ent in normotensive and even hypotensive patients.
Retrospective studies have also shown no difference
in BP in those diagnosed with PRES compared to con-
trols.44,106 Additional steps should be taken to identify
other causes of the patient’s PRES, such as immuno-
suppressive/cytotoxic drugs, a flare of the patient’s
autoimmune disorder, or renal failure.44,105
Severe Pre-Eclampsia and Eclampsia
Blood Pressure Targets
This review will discuss only the management of
hypertension in patients with pre-eclampsia with
severe features and eclampsia. BP targets differ
widely among guidelines. ESC guidelines recom-
mend hospital admission when patients have a single
BP reading ≥170/110 mm Hg; however, they do not
specify the timing of when the high BP reading should
be confirmed, nor do they specify which weeks of
gestation this applies to.107 ACOG is more specific in
their guidelines, recommending hospital admission
for women after 20 weeks’ gestation who have pre-
eclampsia with severe features. ACOG defines this as
SBP >160 mm Hg or DBP >110 mm Hg, confirmed by
a repeat BP 15 minutes later; or 2 BP readings ≥140/90
mm Hg (and ≤160/110 mm Hg) 4 hours apart, with
thrombocytopenia, impaired liver function, renal
insufficiency, pulmonary edema, new-onset headache
unresponsive to medication, or visual disturbances.20
ACOG recommends treating hypertensive patients
quickly, as they are at an increased risk for cerebro-
vascular accidents, and patients with BP <140/90 mm
Hg have lower rates of pre-eclampsia, eclampsia,
15 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
and preterm delivery.20 Whether strict BP control to
<140/90 mm Hg reduces cardiac- and neurovascular-
associated morbidity and mortality remains unclear.
Antihypertensive Medications
For pregnant patients, ACOG guidelines specifi-
cally recommend IV labetalol, IV hydralazine, or oral
immediate-release nifedipine as first-line therapies to
manage acute severe hypertension (SBP ≥160 mm Hg
or DBP ≥110 mm Hg that is persistent for 15 minutes
or more).20 See Table 4 for dosage and timing recom-
mendations. One Cochrane review found no evidence
that one medication is more effective or provides im-
proved outcomes for the fetus and mother; however, a
meta-analysis of 21 trials comparing hydralazine to oth-
er antihypertensive medications found that hydralazine
was associated with more adverse outcomes, which
included maternal hypotension, placental abruption,
adverse effects on fetal heart rate, caesarean delivery,
maternal oliguria, stillbirth, and low Apgar score at 1
minute. The authors concluded that the results warrant
advising against using hydralazine as first-line treat-
ment; however, they were not robust enough to guide
clinical practice.109,110 Efficacy and risk of side effects
from these antihypertensive medications should be
further evaluated with larger head-to-head RCTs. There
is evidence that IV nicardipine can adequately treat
hypertension in antepartum and postpartum patients
and should be considered for treatment-resistant hy-
pertension after using hydralazine, labetalol, or imme-
diate-release nifedipine.111-113 Whether nicardipine
can be considered a first-line agent requires additional
studies, but its use as a continuous infusion may limit
its practicality.
For pregnant patients with pre-eclampsia with
severe features or those with eclampsia, the ACOG
guidelines recommend magnesium sulfate at a
loading dose of 4 to 6 g IV over 20 to 30 minutes,

Table 4. Selected Medications Commonly Used in Hypertensive Emergencies108

Drug Name Dosage Max Dose Onset of Duration Adverse Mechanism of Action
Action of Action Effects
Clevidipine Initial: 1-2 mg/hr IV 32 mg/hr 2-4 min 5-15 min Hypotension, Nondihydropyridine calcium
Titrate: 2 mg/hr q90 sec reflex channel blocker
Max: 32 mg/hr tachycardia

Enalaprilat 1.25 mg-5 mg IV q6 hr 5 mg/24 hrs 15 min 12-24 hr Hypotension, Angiotensin-converting

hyperkalemia, enzyme inhibitor
cough

Esmolol Loading dose: 0.5-1mg/kg IV over No max dose, 1-2 min 10-30 min Hypotension, Selective beta-1 receptor
1 min but titrated to bradycardia antagonist
Maintenance: 50-300 mcg/kg/min IV effect
Titrate: 5-50 mcg/kg/min q5min

Hydralazine 10-20 mg IV every 6 hr 40 mg/24 hr 5-20 min 12-24 hr Hypotension, Direct-acting smooth
tachycardia, muscle relaxant
headache
Labetalol 20 mg IV; may repeat q10 min 300 mg/24h 2-5 min 2-18 hr Hypotension, Non-selective beta receptor
Max cumulative dose: 300 mg/24hr bradycardia antagonist and alpha
receptor antagonist
Magnesium 4-6g IV over 15-30 min No max dose, Immediate 30 min to Hypotension, Smooth muscle relaxant
sulfate Maintenance: 1-3 g/hr but titrated to 2 hr flushing, (vasodilator), calcium
effect weakness, channel blocker, anti-
respiratory arrhythmic
depression

Nicardipine Initial: 5 mg/hr IV 15 mg/hr Immediate 5-15 min Hypotension, Nondihydropyridine calcium
Titrate: 2.5 mg/hr every 5-15 min reflex channel blocker
Max: 15 mg/hr tachycardia
Nitroglycerin 5 mcg/min IV 200 mcg/min Immediate 3-5 min Hypotension, Vasodilator
Titrate: 5 mcg/min q3-5 min up to headache,
20 mcg/min; can increase by flushing
10-20 mcg/min every 3-5 min up to
200 mcg/min
Sodium Initial: 0.25-0.5 mcg/kg/min IV 2 mcg/kg/min Immediate 1-10 min Hypotension, Vasodilator, releases nitric
nitroprusside Titrate: 0.5 mcg/kg/min q5-10 min for more than cyanide toxic- oxide
Max: 2 mcg/kg/min 10 min ity, thiocyanate
toxicity, avoid
if possible

Abbreviations: IV, intravenous; q, every.

JUNE 2023 • www.ebmedicine.net 16 ©2023 EB MEDICINE

followed by a maintenance dose of 1 to 2 g/hr as a
seizure prophylaxis or treatment.20 The efficacy of
magnesium has been well-demonstrated by mul-
tiple large RCTs, and it can more than halve the risk
of developing eclampsia.114,115 ACOG guidelines
acknowledge that a therapeutic range of 4.8 to 9.6
mg/dL to prevent eclampsia is questionable.20,116
When administering magnesium sulfate, the patient’s
deep tendon reflexes and respiratory status should be
reassessed frequently, in addition to urine output, as
it may cause respiratory depression and is excreted
almost exclusively in the urine.20
A checklist ACOG developed specifically for
hypertensive emergency treatment is available here:
https://www.acog.org/-/media/project/acog/acogorg/
files/forms/districts/smi-hypertension-bundle-
emergency-checklist.pdf
Acute Renal Failure
There is no consensus as to what degree of acute kid-
ney injury constitutes acute renal failure, nor whether
there is benefit to rapid BP management. The Inter-
national Society of Hypertension guidelines recom-
mend using either nicardipine or labetalol as first-line
therapy for acute renal failure associated with severe
hypertension, while ACC/AHA guidelines recommend
using nicardipine, clevidipine, or fenoldopam.11,30
The ACC/AHA guidelines directly contradict the
Kidney Disease Improving Global Outcomes (KDIGO)
guidelines, which state that there is no utility for
fenoldopam to manage acute kidney injury, as it has
not shown efficacy in improving outcomes.117 There
are no RCTs to suggest one medication is preferable
over another, nor a specific BP target. Reducing SBP
or MAP by a maximum of 25% might be a reasonable
option, if hypertensive emergency is the suspected
cause of the acute renal failure.11,30
Oral Versus Intravenous Antihypertensives
As previously stated, there is no utility in emergently
treating a patient’s hypertension if the clinician does
not believe the BP is directly related to the patient’s
symptoms. Many patients will likely have evidence of
underlying end-organ damage (such as proteinuria)
on diagnostic evaluation, especially if their chronic
hypertension is poorly controlled. IV antihyperten-
sives should be given only if the clinician believes the
patient’s symptoms and end-organ damage is second-
ary to an acute rise in the patient’s BP and needs to be
rapidly corrected. For example, if a patient presents
hypertensive and short of breath, but is found on
diagnostic workup to have pneumonia with no signs of
end-organ damage that could explain their shortness
of breath, the patient’s high BP should not be treated
with IV antihypertensives. Optimal treatment of severe
hypertension in this population is close outpatient fol-
low-up, with a gradual move toward oral antihyperten-
sive medications.11 No validated studies have shown
JUNE 2023 • www.ebmedicine.net
that acutely reducing BP in ED patients who present
with severe hypertension has any benefits in short-term
risk reduction. In its 2013 clinical policy, the American
College of Emergency Physicians (ACEP) discouraged
initiation of BP medication in the ED for asymptomatic
patients with hypertension. However, clinicians can
consider initiating BP medications for those who are
at high risk, such as patients who are Black, elderly,
uninsured, or likely to be lost to follow-up.118
There are no studies comparing oral to IV medi-
cation in the management of hypertensive emer-
gencies. Therefore, if the clinician decides to treat a
patient’s hypertensive emergency to improve their
symptoms and prevent further end-organ damage, it
is recommended to use fast-acting, easily titratable,
and reliable IV antihypertensives.
n Controversies and Cutting Edge
Arterial Monitoring
Due to advancements in ED capabilities, the use of
invasive BP monitoring (ie, arterial lines) has increased
in recent years. Invasive BP monitoring allows for
more accurate, real-time BP measurements, which
subsequently allows for more rapid therapeutic ad-
justment, and presumably higher-quality care. How-
ever, there is currently substantial variation in practice
as to who receives arterial lines.119 Unfortunately,
there are no good data to help guide this decision,
and there is no consensus as to what the standard of
care should be. Current indications for an arterial line
might include labile BPs, concern for inadequate or
inaccurate automated oscillometric BP cuff readings,
or clinical deterioration despite noninvasive manage-
ment. Realistically, an arterial line is probably unnec-
essary in most cases of hypertensive emergency for a
few reasons: (1) the pain of arterial line insertion can
exacerbate hypertension, (2) there is no prospective
evidence to show this procedure is beneficial or nec-
essary, and (3) current BP targets are mostly arbitrary
and poorly defined with the exception of ICH and
acute ischemic stroke. Until more conclusive evidence
exists, this will remain a topic of debate.
Beta Blockers in Cocaine-Induced Hypertension
The use of beta blockers in patients with cocaine-
induced severe hypertension is controversial. Medi-
cal folklore has taught that there is a theoretical risk
for unopposed alpha adrenergic stimulation when
using beta blockade in conjunction with cocaine use,
leading to unopposed vasoconstriction. This belief
is founded on a small number of studies and case
reports that have not been replicated and were based
mostly on adverse patient-reported events, with few
statistically relevant data.120-122 To date, the only
statement that can be made is that unopposed alpha
stimulation after beta blockade in cocaine toxicity is
inconsistent, unpredictable, and a rare phenomenon
17 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
that can be addressed with the use of vasodilating
medications titrated to counteract vasoconstriction.
n Disposition
All patients diagnosed with hypertensive emergency
require hospital admission. The ACC/AHA Task Force
recommends admitting adults with hypertensive emer-
gencies to an ICU for continuous monitoring of BP
and for parenteral administration of antihypertensive
agents. An intermediate care unit may also be consid-
ered, depending on hospital resources.
Patients presenting to the ED who do not meet
criteria for hypertensive emergency can be safely dis-
charged with close outpatient follow-up for repeat BP
monitoring and consideration of hypertensive medi-
cation management. Additionally, initiation of oral an-
tihypertensive medications in the ED does not appear
to be necessary. In 2 recent studies, one involving
2839 patients seen in an ED5 and another involving
58,535 outpatients38 who presented with significantly
elevated BP levels but no end-organ damage, were
either observed for a few hours after treatment with
oral antihypertensive agents and follow-up versus
follow-up without initiation of oral antihypertensive
treatment. These studies demonstrated very low rates
of morbidity/mortality, and no significant difference
in prognosis for those treated acutely, compared with
those who were discharged with rapid follow-up.
n Summary
Hypertensive emergency is associated with substantial
morbidity and in-hospital mortality, thus requiring im-
mediate treatment. Patients with severely elevated BP
(≥180/110 mm Hg or MAP ≥135 mm Hg) should be
rapidly assessed for evidence of hypertensive emer-
gency to prevent further end-organ damage. Assess-
ment should focus on a thorough history and physical
examination, with additional testing, as needed, based
on clinical features present on evaluation. Hypertensive
emergencies should be managed with careful titration
of antihypertensives, guided by the type of end-organ
damage, and frequently reassessed. Patients with no
evidence of hypertensive emergency do not need
BP management and can be discharged with primary
care follow-up. There is limited strength to the recom-
mendations and guidance on treatment, as the major-
ity of data are retrospective in nature. Many subjects
discussed within this issue lack quality prospective
blinded control trials.
n Time- and Cost-Effective Strategies
• Patients with no evidence of hypertensive emer-
gency do not need BP management and can be
discharged with primary care follow-up.
Risk Management Caveat: Make sure the patient
has adequate access to primary care prior to con-
sidering discharge. Patients with severe hyperten-
sion often need medication adjuncts or adjust-
ments, and lack of follow-up can lead to repeat
visits and detrimental long-term effects.
• Epistaxis, proteinuria, chronic renal failure, and
headaches do not qualify as signs of target end-
organ damage.
Risk Management Caveat: While these findings
in themselves are not signs of end-organ dam-
age, they can be ominous signs of other etiolo-
gies and should be addressed accordingly.
• Troponin-I elevation is not associated with in-
creased mortality in hypertensive emergency and
does not need to be routinely obtained if there is
no concern for ACS.
Risk Management Caveat: Atypical presenta-
tions of ACS as seen in elderly, female, and
diabetic populations should be considered. Other
diagnostics such as ECG and bedside ultrasound,
in addition to cardiac risk factors, should be con-
sidered when considering the diagnosis of ACS.
Troponin-I elevation due to decreased kidney
function, demand ischemia, or chronic heart fail-
ure should also be considered.

Class of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II
• Always acceptable, safe • Safe, acceptable Class III Indeterminate
• Definitely useful • Probably useful • May be acceptable • Continuing area of research
• Proven in both efficacy and effectiveness • Possibly useful • No recommendations until further
Level of Evidence: • Considered optional or alternative research
Level of Evidence: • Generally higher levels of evidence treatments
• One or more large prospective studies • Nonrandomized or retrospective stud- Level of Evidence:
are present (with rare exceptions) ies: historic, cohort, or case control Level of Evidence: • Evidence not available
• High-quality meta-analyses studies • Generally lower or intermediate levels • Higher studies in progress
• Study results consistently positive and • Less robust randomized controlled trials of evidence • Results inconsistent, contradictory
compelling • Results consistently positive • Case series, animal studies, • Results not compelling
consensus panels
• Occasionally positive results

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2023 EB Medicine. www.ebmedicine.net. No part of this publication may be reproduced in any format without written consent of EB Medicine.

JUNE 2023 • www.ebmedicine.net 18 ©2023 EB MEDICINE

 Clinical Pathway for Managing Hypertensive Emergencies
in the Emergency Department

Severe hypertension (MAP ≥135 mm Hg or

SBP ≥180 mm Hg, or DBP ≥110 mm Hg)

Is there evidence of end-organ damage? • No indication for blood pressure

(See Figure 3, BARKH algorithm for NO reduction
list of end-organ damage) • Consider discharge with primary
care follow-up
YES

Is there a potential secondary cause Treat the underlying cause

YES (eg, alcohol withdrawal,
of the hypertension?
uncontrolled pain)
NO

• This is a hypertensive emergency

• Treat the underlying condition

Heart Kidney Arteries Brain/Retina

Acute coronary Aortic dissection: Hypertensive

Acute renal failure:
syndromes: • Esmolol for a goal HR encephalopathy/
• Reduce MAP by a
• IV/SL/topical nitroglycerin <60 beats/min and SBP retinopathy:
maximum of 25% in the
or IV metoprolol (if no risk <120 mm Hg (consider • Reduce MAP by 20%-25%
first hour (Class II)
factors present: age >70, addition of nicardipine if using IV nicardipine or
• Appropriate first-line
HR >110 beats/min, SBP unable to reach BP goal) labetalol as first-line agent
agents include nicardipine,
<120 mm Hg) to achieve (Class II) (Class II)
clevidipine, or labetalol
no more than 25% MAP Severe pre-eclampsia, Intracerebral hemorrhage:
(Class II)
reduction within 1st hour eclampsia, or HELLP: • Lower BP to SBP
(Class II) • Magnesium sulfate at a <140 mm Hg using IV
Acute heart failure: loading dose of 4-6 g IV nicardipine or labetalol
• NIPPV over 20-30 min, followed (Class I)
• Short-term high-dose by a maintenance infusion Acute ischemic stroke:
nitroglycerin titrated down of 1-2 g/hr (Class I) • If receiving thrombolytics
after symptoms relief • BP should be decreased or mechanical
(Class II) to <160/110 mm Hg thrombectomy, lower to
• BP reduction no greater with IV labetalol (or IV goal BP <185/110 mm Hg
than 25% within 1st hour hydralazine if unable to prior to intervention and
(Class II) tolerate labetalol) (Class maintain a BP <180/105
• IV diuretics (2-3 × PO II) mm Hg (Class II)
dose) (Class II) • If no intervention and
BP is ≥220/120 mm Hg,
consider lowering BP by
no more than 15%
(Class II)

Abbreviations: BP, blood pressure; DBP, diastolic blood pressure; HELLP, hemolysis, elevated liver enzymes, low platelets; HR, heart rate; IV, intravenous;
MAP, mean arterial pressure; NIPPV, noninvasive positive-pressure ventilation; PO, orally; SBP, systolic blood pressure; SL, sublingual.
For Class of Evidence definitions, see page 18.

JUNE 2023 • www.ebmedicine.net 19 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.

 Risk Management Pitfalls for Hypertensive Emergencies
in the Emergency Department
1. “The labs and imaging I ordered should have
been enough to tell if there was end-organ
damage.” Physical examination findings should
guide the clinician’s decision to obtain advanced
imaging and laboratory analysis. There are nu-
merous presenting complaints for patients with
severe hypertension, and historical features can
be subtle. The more time spent asking the appro-
priate questions, such as medication compliance,
as well as subtle examination findings as simple
as a murmur can help confirm the diagnosis.
2. “The patient‘s BP was really high; I thought
it must have been hypertensive emergency.”
Severe hypertension is a frequent presenting
complaint and referral to the ED. Unfortunately,
overdiagnosis of hypertensive emergency among
patients with severe hypertension is common and
often inaccurate. This can lead to inappropriate
admissions as well as harm to patients who do
not have end-organ damage and are started on
parenteral antihypertensive medication.
3. “The patient should be normotensive.”
Treating hypertensive emergency too
aggressively is just as dangerous as failure to
treat. It is important to remember each patient’s
autoregulatory mechanisms adapt over time
and are unique to the individual, thus a normal
BP may lead to hypoperfusion in a patient with
chronically elevated blood pressure. Try to avoid
treating a numerical value.
4. “We had difficulty getting IV access, so we
started with oral medications.” Using oral,
intramuscular, or intranasal medications to treat
hypertensive emergency is inadvisable, as they
are not easily titratable. Treatment should consist
of short-acting, titratable parenteral medications
to avoid treatment errors, dose stacking, and
poor patient outcomes.
5. “We needed a second agent to control the
BP.” There is often more than one compounding
variable contributing to the patient’s
hypertension. Failing to treat pain, agitation,
substance withdrawal, or urinary retention
as causes of hypertension will often lead to
treatment failure.
JUNE 2023 • www.ebmedicine.net
6. “At first I treated the systolic pressure,
but then I realized the diastolic pressure
was way too high.” Not using MAP can
cause inconsistencies in treatment and lead to
treatment errors. Automated oscillometric BP
cuffs measure the MAP directly. This also allows
for dosing of antihypertensive medications to
be titrated against a single variable. Attempting
to titrate antihypertensive infusions with systolic
and diastolic BPs simultaneously can lead to
overshooting your target pressure.
7. “Metoprolol is a beta blocker just like
labetalol.” While metoprolol is a beta blocker,
its beta-1 receptor selectivity acts almost
exclusively as a rate control agent, and it has
little vasodilatory effect, unlike labetalol, which is
a nonselective beta blocker that also has alpha
antagonist effects. Metoprolol has very little role
in the treatment of hypertensive emergency.
8. “She was having a hypertensive emergency;
fluids will only make it worse.” Not considering
volume depletion as a cause of hypertension
(intravascularly volume-depleted due to renin-
angiotensin system activation and sodium
excretion) is a frequent mistake. Using bedside
ultrasound in conjunction with other examination
features and diagnostics (eg, urine output, skin
turgor) to evaluate intravascular volume status
can help to mitigate this issue.
9. “The BP was better after an hour, so I gave
him oral medications.” Trying to transition from
an antihypertensive infusion to an oral agent
can be dangerous. Treatment of hypertensive
emergency should be a gradual and frequently
monitored process over the course of days.
10. “Why didn’t my middle-aged White female
patient respond like my chronic hypertensive
elderly Black male patient?” Not considering
age, sex, race, and concomitant conditions when
deciding on a treatment approach can cause
unexpected results. There is substantial evidence
that ethnicity, sex, and age all play a large role in
an individual’s response to different medications.
Consider these factors when choosing an agent
and make dosing adjustments accordingly.
20 ©2023 EB MEDICINE
 Case Conclusions
For the 62-year-old man who presented by EMS with swelling of his legs and worsening shortness of
breath…
CASE 1

Based on the patient‘s history of congestive heart failure and physical examination, you believed that he
was having acute “flash” pulmonary edema. Point-of-care ultrasound showed bilateral B-lines, and chest
x-ray showed cardiomegaly with pulmonary congestion. He was immediately started on CPAP and given
a high-dose nitroglycerin infusion, with relief of symptoms. The patient was given furosemide IV and was
admitted for further management of his flash pulmonary edema.

For the 76-year-old man with history of diabetes and hypertension who presented with altered
mental status and then started seizing...
CASE 2

He was given IV lorazepam for his seizure, and you ordered a stat CT head, which appeared to be normal.
You performed a bedside ocular ultrasound, which showed evidence of papilledema, raising concern for
cerebral edema. An MRI was obtained, which showed posterior cerebral edema, confirming the diagnosis,
He was treated for PRES with a nicardipine infusion.

For the 59-year-old woman with elevated BP who presented to the ED from her primary care
physician’s office…
You obtained extensive past medical, social, and family history, and found no increased risk factors for
CASE 3

hypertensive emergency. Her review of systems and physical examination, including visual acuity, was
unremarkable. Based on your clinical evaluation, you had very low concern for end-organ damage. Given
her lack of5 significant risk factors and your low level of concern for poor follow-up, you discussed strict
Recommendations
return precautions with
To Apply theinpatient and advised her to follow up with her primary care doctor in the next few
Practice
days for a repeat evaluation.

5 Recommendations
To Apply in Practice
5 Things
5 That Will Change
Recommendations
Your Practice
To Apply in Practice
1. Consider using the MAP instead of only the
SBP or DBP when assessing BP.
2. Any patient diagnosed with hypertensive
emergency needs to be started on short-
acting IV antihypertensive medication that
allows for titration.
3. The use of oral antihypertensive medications
in the ED to decrease a patient’s BP is a prac-
tice that may be unnecessary.
4. Patients who do not meet the criteria for
hypertensive emergency may be discharged
with outpatient follow-up. Evaluating for
end-organ damage in asymptomatic patients
does not change ED management or improve
outcomes.38,39
5. The degree of BP elevation does not always
correlate with the severity of end-organ dam-
age, and may indicate a better prognosis for
the patient, such as in ACS.83-85
n References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, random­
ized, and blinded trial should carry more weight than
a case report.
To help the reader judge the strength of each
reference, pertinent information about the study will
be included in bold type following the ref­erence,
where available. In addition, the most informative
references cited in this paper, as determined by the
authors, will be noted by an asterisk (*) next to the
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1000 patients) DOI: 10.1056/NEJMoa1603460
94. Moullaali TJ, Wang X, Martin RH, et al. Blood pressure control
and clinical outcomes in acute intracerebral haemorrhage:
a preplanned pooled analysis of individual participant data.
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95. Manning L, Hirakawa Y, Arima H, et al. Blood pressure variability
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prospective study; 432 patients)
97. Allison TA, Bowman S, Gulbis B, et al. Comparison of
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in patients with stroke. J Intensive Care Med. 2019;34(11-
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98. Graffagnino C, Bergese S, Love J, et al. Clevidipine rapidly and
safely reduces blood pressure in acute intracerebral hemor-
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99. Steiner T, Juvela S, Unterberg A, et al. European Stroke
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100. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Criti-
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ence. Neurocrit Care. 2011;15(2):211-240. (Guideline)
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(Cochrane review; 3 studies)
103. Mussa FF, Horton JD, Moridzadeh R, et al. Acute aortic dis-
section and intramural hematoma: a systematic review. JAMA.
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104. Kumar KU, Zhao Q, Bai X, et al. Controlled heart rate and blood
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106. Rabinstein AA, Mandrekar J, Merrell R, et al. Blood pressure
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107. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al. 2018
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sive emergencies. UpToDate. Accessed May 10, 2023. https://
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25 © 2023 EB MEDICINE. ALL RIGHTS RESERVED.
1. When administering nitroglycerin, which of the
following medications would cause concern if
it had been taken earlier that day?
a. Amlodipine
b. Lisinopril
c. Tamsulosin
d. Sildenafil
2. A 70-year-old man with a history of diabetes
and coronary artery disease presents from his
primary care provider for high blood pressure
(BP). On examination, he is noted to have a
BP of 180/110 mm Hg. Which of the following
symptoms would be least likely to contribute
to a diagnosis of hypertensive emergency?
a. Vision changes
b. Chest pain
c. Headache
d. Oliguria
3. A 56-year-old man with no previous seizure
history presents after sustaining a tonic-clonic
seizure. He is post ictal but protecting his air-
way. His past medical history is significant for
a new diagnosis of colon cancer for which he
just started immunotherapy. His BP is 200/115
mm Hg. Which diagnostic study confirms pos-
terior reversible encephalopathy syndrome?
a. Ocular ultrasound
b. Fundoscopy
c. Magnetic resonance imaging (MRI)
d. Electroencephalogram
4. A 58-year-old man with no past medical history
presents to the ED with poison ivy rash. His
BP is 185/110 mm Hg. Review of systems
is negative, and his workup is negative for
evidence of end-organ damage. Which of the
following is the most appropriate disposition?
a. Obtain a head CT
b. Admit to the progressive care unit on a
nicardipine infusion
c. Initiate 2 antihypertensives and admit to the
general medical floor
d. Discharge home with close primary care
follow-up
5. Which of the following medications has
been shown to be significantly more likely
to cause hypotension in patients with acute
decompensated heart failure?
a. Clevidipine
b. Nitroglycerine
c. Nesiritide
d. Nicardipine
JUNE 2023 • www.ebmedicine.net
6. A 47-year-old man presents with a severe,
sudden, and unrelenting headache for 3 hours.
He denies a previous history of headaches. His
BP is 210/110 mm Hg. What is the best next
step to diagnose the patient’s condition?
a. Lumbar puncture
b. Noncontrast head CT
c. Cerebral angiography
d. Brain MRI
7. A patient presents with an acute ischemic
stroke and qualifies for thrombolysis. Prior
to administering thrombolytics, which of the
following should be done?
a. Maintain BP >200 mm Hg
b. Initiate a heparin infusion
c. Reduce BP to <185/110 mm Hg and maintain
BP <180/105 mm Hg
d. Perform mechanical thrombectomy
8. A patient with acute ischemic stroke and
BP of 226/125 mm Hg is not a candidate
for antithrombotic agents or mechanical
thrombectomy. What do the AHA/ASA and
ESO guidelines say is a reasonable BP recom-
mendation?
a. Reduce the BP by no more than 15%
b. Reduce the SBP to <140 mm Hg
c. Reduce the SBP to <130 mm Hg
d. There is no reason to reduce the BP if he is
not receiving any intervention
9. A patient presents with hypertensive
emergency and acute coronary syndrome.
Which of the following may be a risk factor for
increased development of cardiogenic shock
when administering IV beta blockers?
a. Heart rate <110 beats/min
b. Age <70 years
c. SBP >120 mm Hg
d. Acute pulmonary edema
10. A 25-year-old woman is 35 weeks‘ pregnant
and presents with a BP of 175/99 mm Hg
and pre-eclampsia with severe symptoms.
According to the American College of
Obstetricians and Gynecologists guidelines,
which of the following medications should be
initiated immediately?
a. Oral captopril
b. Oral metoprolol
c. IV labetalol
d. IV esmolol
26 ©2023 EB MEDICINE
The Emergency Medicine Practice Editorial Board
EDITOR-IN-CHIEF
Andy Jagoda, MD, FACEP
Professor and Chair Emeritus,
Department of Emergency
Medicine; Director, Center for
Emergency Medicine Education
and Research, Icahn School of
Medicine at Mount Sinai, New
York, NY
ASSOCIATE EDITOR-IN-CHIEF
Kaushal Shah, MD, FACEP
Assistant Dean of Academic
Advising, Vice Chair of
Education, Professor of
Clinical Emergency Medicine,
Department of Emergency
Medicine, Weill Cornell School of
Medicine, New York, NY
EDITORIAL BOARD
Saadia Akhtar, MD, FACEP
Associate Professor, Department
of Emergency Medicine,
Associate Dean for Graduate
Medical Education, Program
Director, Emergency Medicine
Residency, Mount Sinai Beth
Israel, New York, NY
William J. Brady, MD
Professor of Emergency
Medicine and Medicine;
Medical Director, Emergency
Management, UVA Medical
Center; Operational Medical
Director, Albemarle County Fire
Rescue, Charlottesville, VA
Calvin A. Brown III, MD
Director of Physician
Compliance, Credentialing
and Urgent Care Services,
Department of Emergency
Medicine, Brigham and Women's
Hospital, Boston, MA
Peter DeBlieux, MD
Professor of Clinical Medicine,
Louisiana State University School
of Medicine; Chief Experience
Officer, University Medical
Center, New Orleans, LA
Deborah Diercks, MD, MS,
FACEP, FACC
Professor and Chair, Department
of Emergency Medicine,
University of Texas Southwestern
Medical Center, Dallas, TX
JUNE 2023 • www.ebmedicine.net
Daniel J. Egan, MD
Harvard Affiliated Emergency
Medicine Residency,
Massachusetts General Hospital/
Brigham and Women's Hospital,
Boston, MA
Marie-Carmelle Elie, MD
Professor and Chair, Department
of Emergency Medicine
University of Alabama at
Birmingham, Birmingham, AL
Nicholas Genes, MD, PhD
Clinical Assistant Professor,
Ronald O. Perelman Department
of Emergency Medicine, NYU
Grossman School of Medicine,
New York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine,
Carolinas Medical Center,
University of North Carolina
School of Medicine,
Chapel Hill, NC
Steven A. Godwin, MD, FACEP
Professor and Chair, Department
of Emergency Medicine,
Assistant Dean, Simulation
Education, University of
Florida COM-Jacksonville,
Jacksonville, FL
Joseph Habboushe, MD MBA
Assistant Professor of Clinical
Emergency Medicine,
Department of Emergency
Medicine, Weill Cornell School
of Medicine, New York, NY; Co-
founder and CEO, MDCalc
Eric Legome, MD
Chair, Emergency Medicine,
Mount Sinai West & Mount Sinai
St. Luke's; Vice Chair, Academic
Affairs for Emergency Medicine,
Mount Sinai Health System, Icahn
School of Medicine at Mount
Sinai, New York, NY
Keith A. Marill, MD, MS
Associate Professor, Department
of Emergency Medicine, Harvard
Medical School, Massachusetts
General Hospital, Boston, MA
Angela M. Mills, MD, FACEP
Professor and Chair, Department
of Emergency Medicine,
Columbia University Vagelos
College of Physicians &
Surgeons, New York, NY
27
Charles V. Pollack Jr., MA, MD,
FACEP, FAAEM, FAHA, FACC,
FESC
Clinician-Scientist, Department
of Emergency Medicine,
University of Mississippi School
of Medicine, Jackson MS
Ali S. Raja, MD, MBA, MPH
Executive Vice Chair, Emergency
Medicine, Massachusetts General
Hospital; Professor of Emergency
Medicine and Radiology, Harvard
Medical School, Boston, MA
Robert L. Rogers, MD, FACEP,
FAAEM, FACP
Assistant Professor of Emergency
Medicine, The University of
Maryland School of Medicine,
Baltimore, MD
Alfred Sacchetti, MD, FACEP
Assistant Clinical Professor,
Department of Emergency
Medicine, Thomas Jefferson
University, Philadelphia, PA
Robert Schiller, MD
Chair, Department of Family
Medicine, Beth Israel Medical
Center; Senior Faculty, Family
Medicine and Community
Health, Icahn School of Medicine
at Mount Sinai, New York, NY
Scott Silvers, MD, FACEP
Associate Professor of
Emergency Medicine, Chair of
Facilities and Planning, Mayo
Clinic, Jacksonville, FL
Corey M. Slovis, MD, FACP,
FACEP
Professor and Chair Emeritus,
Department of Emergency
Medicine, Vanderbilt University
Medical Center, Nashville, TN
Stephen H. Thomas, MD, MPH
Department of Emergency
Medicine, Beth Israel Deaconess
Medical Center and Harvard
Medical School, Boston, MA
Ron M. Walls, MD
Professor and COO, Department
of Emergency Medicine, Brigham
and Women's Hospital, Harvard
Medical School, Boston, MA
© 2023 EB MEDICINE. ALL RIGHTS RESERVED.
CRITICAL CARE EDITORS
William A. Knight IV, MD,
FACEP, FNCS
Associate Professor of
Emergency Medicine and
Neurosurgery, Medical Director,
EM Advanced Practice Provider
Program; Associate Medical
Director, Neuroscience ICU,
University of Cincinnati,
Cincinnati, OH
Scott D. Weingart, MD, FCCM
Editor-in-Chief, emCrit.org
PHARMACOLOGY EDITOR
Aimee Mishler, PharmD, BCPS
Emergency Medicine Pharmacist,
St. Luke's Health System,
Boise, ID
RESEARCH EDITOR
Joseph D. Toscano, MD
Chief, Department of Emergency
Medicine, San Ramon Regional
Medical Center, San Ramon, CA
INTERNATIONAL EDITORS
Peter Cameron, MD
Academic Director, The Alfred
Emergency and Trauma Centre,
Monash University, Melbourne,
Australia
Andrea Duca, MD
Attending Emergency Physician,
Ospedale Papa Giovanni XXIII,
Bergamo, Italy
Suzanne Y.G. Peeters, MD
Attending Emergency Physician,
Flevo Teaching Hospital, Almere,
The Netherlands
Edgardo Menendez, MD,
FIFEM
Professor in Medicine and
Emergency Medicine; Director of
EM, Churruca Hospital of Buenos
Aires University, Buenos Aires,
Argentina
Dhanadol Rojanasarntikul, MD
Attending Physician, Emergency
Medicine, King Chulalongkorn
Memorial Hospital; Faculty
of Medicine, Chulalongkorn
University, Thailand
Edin Zelihic, MD
Head, Department of Emergency
Medicine, Leopoldina Hospital,
Schweinfurt, Germany
 Points & Pearls
QUICK READ
JUNE 2023 | VOLUME 25 | ISSUE 6
Points
• Hypertensive urgency, hypertensive crisis, and
malignant hypertension are terms that have his-
torically been used to describe severely elevated
blood pressure (BP) with no evidence of end-
organ damage.
• Hypertensive emergency is a clinical syndrome of
significantly elevated BP that is associated with
end-organ damage.
• Hypertensive emergencies are more likely
among patients aged >60 years, male, Black,
underinsured or uninsured, and/or living in lower
socioeconomic areas.21 These factors should be
considered in disposition.
• The patient history should include any pre-exist-
ing end-organ dysfunction, so it can be differenti-
ated from an acute process.
• The mnemonic, BARKH (brain, arteries, retina,
kidney, heart), summarizes the most likely loca-
tions of end-organ damage. (See Figure 4.)
• Choose fast-acting, easily titratable, and reliable
IV antihypertensive drugs. (See Table 1.)
Acute Decompensated Heart Failure
• The 3 primary interventions: noninvasive positive-
pressure ventilation, diuretics, and vasodilators.
Acute Ischemic Stroke
• When noncontrast CT excludes intracerebral
hemorrhage (ICH) as a cause, BP manage-
ment will depend on the treatment plan chosen
(thrombolytics or mechanical thrombectomy).
Acute Coronary Syndromes
• There are no definitive data on BP targets, but
there is evidence that patients with ACS who
present with elevated BP have better out-
comes.83-85 Management should focus on pain
control and clinical stabilization.9
Intracerebral Hemorrhage
• ICH has the most evidence regarding BP targets
and timelines, but guidelines disagree on recom-
mendations.
• In ICH, iatrogenic hypotension presents the high-
est risk for mortality.96
Subarachnoid Hemorrhage
• There are few to no data on BP targets for SAH,
and guidelines disagree, with no specific antihy-
pertensive drug recommendations.47,99-102
JUNE 2023 • www.ebmedicine.net
Hypertensive Emergencies:
Guidelines and Best-Practice
Recommendations
Pearls
• Severe hypertension is usually defined: systolic
BP (SBP ≥180 mm Hg, diastolic BP (DBP) ≥110
mm Hg, or mean arterial pressure (MAP) ≥135.
• The degree of BP elevation does not always
correlate with severity of end-organ damage;
it is the rate of change of BP that increases the
damage.26
• In patients presenting to the ED with primary
hypertensive emergencies, a secondary cause
can be found in 20%-40% of cases.27 It is im-
portant to investigate the causes, as manage-
ment will differ.
• The comprehensiveness of the physical ex-
amination is dictated by the chief complaint,
as this may indicate underlying end-organ
damage. See Table 3 for the most common
symptoms and etiologies.
• Diagnostic studies will be directed by clinical
findings. See Table 2 for an extensive differen-
tial diagnosis summary, by system, including
recommended workups.
• Patients who do not meet criteria for hyperten-
sive emergency can be safely discharged with
close outpatient follow-up for monitoring and
medication management.
Aortic Dissection
• 2022 ACC/AHA guidelines recommend reducing
heart rate to 60-80 beats/min and then lowering
SBP to <120 mm Hg,19,104 with a beta blocker, be-
fore lowering BP to prevent reflex tachycardia.19
Hypertensive Encephalopathy
• Most commonly seen with BP >220/120 mm Hg
• Posterior reversible encephalopathy syndrome
(PRES), if seen, may not be attributable to BP.44,106
Severe Pre-Eclampsia and Eclampsia
• ACOG recommends hospital admission for pa-
tients >20 weeks‘ gestation who have pre-eclamp-
sia with severe features.20
Acute Renal Failure
• If hypertensive emergency is the suspected cause,
reducing SBP or MAP 25% is a reasonable op-
tion.11,30
28 ©2023 EB MEDICINE