A 62-year-old man with long-standing uncontrolled hypertension presents to
the emergency department with severe headache, confusion, chest discomfort, and
shortness of breath. Blood pressure is 230/140 mm Hg. Examination reveals
papilledema and bilateral pulmonary crackles. Serum creatinine is elevated. ECG
shows left ventricular hypertrophy. Diagnosis?
Diagnosis is Hypertensive Emergency.
This patient has severe hypertension with clear acute
hypertension-mediated organ damage, including severe hypertensive
retinopathy with papilledema and neurologic dysfunction consistent with probable
hypertensive encephalopathy.
His dyspnea and bilateral pulmonary crackles strongly suggest acute
hypertensive pulmonary edema or acute heart failure.
The elevated creatinine indicates renal dysfunction, but a
single elevated value cannot establish acute kidney injury without comparison
with baseline renal function.
ECG evidence of left ventricular hypertrophy represents chronic
hypertension-mediated organ damage, not acute organ injury.
The combination of extreme hypertension, papilledema, neurologic
dysfunction, and renal dysfunction is also consistent with the malignant
hypertension phenotype.
1. Definition
Hypertensive emergency is severe blood pressure elevation
associated with new or worsening acute target-organ damage,
requiring immediate evaluation and controlled blood pressure reduction.
Severe hypertension is commonly defined as:
1. SBP
>180 mm Hg
2. DBP
>120 mm Hg
However:
Acute target-organ damage, rather than the absolute blood pressure
value alone, defines hypertensive emergency.
Hypertensive emergencies may occur at lower blood pressures when the rise is
abrupt, particularly in:
1. Pregnancy-related
hypertension
2. Acute
glomerulonephritis
3. Catecholamine
excess states
4. Previously
normotensive individuals
2. Hypertensive Emergency
Hypertensive emergency generally requires:
1. Immediate
assessment
2. Admission
to an intensive care or closely monitored setting
3. Usually
intravenous, rapidly titratable antihypertensive therapy
4. Frequent
or continuous blood pressure monitoring
5. Treatment
directed at the specific acute organ injury
The affected organ determines the preferred drug, speed of blood
pressure reduction, and blood pressure target.
3. Pathophysiology
1. Severe
blood pressure elevation exceeds normal vascular autoregulatory
capacity
2. Endothelial
injury and microvascular dysfunction develop
3. Vasoconstriction,
increased vascular permeability, and tissue ischemia occur
4. Severe
microvascular injury may produce fibrinoid necrosis
5. Cerebral
autoregulatory failure may produce vasogenic cerebral edema
6. Progressive
cerebral, cardiac, renal, retinal, or vascular injury develops
Potential consequences include:
1. Hypertensive
encephalopathy
2. Cerebral
edema
3. Myocardial
ischemia
4. Acute
heart failure and pulmonary edema
5. Acute
deterioration in renal function
6. Hypertensive
retinopathy
7. Thrombotic
microangiopathy
Hypertensive encephalopathy may be associated with posterior
reversible encephalopathy syndrome (PRES).
4. Acute Target-Organ Damage
4.1 Neurologic
1. Hypertensive
encephalopathy
2. Ischemic
stroke
3. Intracerebral
hemorrhage
4. Seizures
5. Altered
mental status
6. Visual
disturbance
7. PRES
4.2 Cardiac
1. Acute
coronary syndrome
2. Acute
heart failure
3. Acute
cardiogenic pulmonary edema
4. Myocardial
ischemia
4.3 Vascular
1. Acute
aortic syndrome, including aortic dissection
4.4 Renal
1. Acute
deterioration in renal function
2. Acute
kidney injury when confirmed by a rise from baseline or other accepted
diagnostic criteria
3. Hematuria
4. Proteinuria
5. Severe
hypertension may produce thrombotic microangiopathy
6. Microangiopathic
hemolytic anemia and thrombocytopenia may occur
4.5 Ophthalmologic
1. Retinal
hemorrhages
2. Cotton-wool
spots
3. Papilledema
Papilledema indicates severe hypertensive retinal injury but is not
required for the diagnosis of hypertensive emergency.
5. Malignant Hypertension
Malignant hypertension is a hypertensive emergency
characterized by severe blood pressure elevation with acute hypertensive microvascular
injury, classically involving the retina, kidneys, and brain.
Findings may include:
1. Retinal
hemorrhages
2. Cotton-wool
spots
3. Papilledema
4. Acute
deterioration in renal function
5. Thrombotic
microangiopathy
6. Hypertensive
encephalopathy
7. Acute
heart failure
This patient's papilledema, neurologic dysfunction, and renal
dysfunction strongly support this phenotype.
6. Clinical Features
Presentation depends on the affected organ.
Common features include:
1. Severe
headache
2. Confusion
or altered mental status
3. Chest
pain or discomfort
4. Dyspnea
5. Visual
disturbance
6. Focal
neurologic deficits
7. Seizures
8. Oliguria
9. Pulmonary
crackles when acute pulmonary edema is present
7. Severe Hypertension Without Acute Target-Organ Damage
Severe blood pressure elevation may occur without new or worsening
acute target-organ damage.
These patients do not have a hypertensive emergency.
The older term hypertensive urgency is increasingly replaced
by terms such as severe hypertension or asymptomatic
markedly elevated blood pressure, depending on the guideline and
clinical setting.
Patients may have nonspecific symptoms such as:
1. Mild
headache
2. Anxiety
3. Epistaxis
The defining feature is:
No new or worsening acute target-organ damage
Rapid intravenous blood pressure reduction is generally not
indicated.
8. Diagnostic Evaluation
8.1 Initial Assessment
1. Confirm
blood pressure using an appropriate cuff and correct measurement technique
2. Repeat
measurement when clinically appropriate
3. Assess
immediately for acute target-organ damage
4. Perform
a focused neurologic examination
5. Assess
for acute heart failure and myocardial ischemia
6. Assess
renal function and urine output
7. Perform
funduscopic examination when feasible
8. Evaluate
for acute aortic syndrome when clinically suspected
In a patient with an obvious hypertensive emergency, treatment should not
be delayed merely to obtain repeated resting blood pressure measurements.
8.2 Laboratory Evaluation
Testing should be guided by the suspected organ injury and commonly
includes:
1. CBC
2. Serum
electrolytes
3. Serum
creatinine and eGFR
4. Urinalysis
5. Cardiac
troponin when myocardial ischemia is suspected
6. Peripheral
blood smear, LDH, haptoglobin, and platelet count when thrombotic
microangiopathy or microangiopathic hemolysis is suspected
8.3 Cardiac and Imaging Evaluation
Depending on the presentation:
1. ECG
2. Chest
X-ray
3. Bedside
echocardiography or lung ultrasound when acute cardiac dysfunction or
pulmonary edema is suspected
4. CT
brain for acute neurologic symptoms or altered mental status when
intracranial pathology must be excluded
5. CT
angiography when acute aortic syndrome is suspected
6. Additional
imaging according to the affected organ
9. Management of Hypertensive Emergency
9.1 Initial Management
1. Admit
to an intensive care or closely monitored setting
2. Establish
frequent or continuous blood pressure monitoring
3. Use
a rapidly titratable intravenous antihypertensive agent in
most hypertensive emergencies
4. Identify
and treat the specific acute target-organ injury
5. Avoid
uncontrolled or excessive blood pressure reduction
9.2 Common Intravenous Antihypertensive Agents
Choice depends on the affected organ and clinical situation.
1. Nicardipine
2. Clevidipine
3. Labetalol
4. Esmolol
5. Nitroglycerin
6. Sodium
nitroprusside in selected circumstances
Nicardipine and clevidipine are useful titratable arterial
vasodilators.
Labetalol is useful in many hypertensive emergencies but
should generally be avoided in active acute decompensated heart failure
or cardiogenic pulmonary edema.
Nitroglycerin is particularly useful when severe
hypertension is accompanied by acute coronary ischemia or hypertensive
cardiogenic pulmonary edema.
Nitroprusside is used selectively because of risks
including cyanide and thiocyanate toxicity, particularly with
prolonged administration or significant renal or hepatic dysfunction.
10. Blood Pressure Reduction Strategy
10.1 Core Principle
Blood pressure reduction in hypertensive emergency should be organ-specific.
The affected target organ determines:
1. The
speed of blood pressure reduction
2. The
magnitude of blood pressure reduction
3. The
preferred antihypertensive agent
4. The
appropriate blood pressure target
Excessively rapid or uncontrolled reduction may cause:
1. Cerebral
ischemia
2. Myocardial
ischemia
3. Renal
ischemia
Immediate normalization of blood pressure is usually inappropriate unless a
specific condition requires very rapid reduction.
10.2 General Target Without a Compelling Condition
For hypertensive emergency without a condition requiring a different
blood pressure target:
1. Reduce
SBP by no more than approximately 25% during the first hour
2. If
clinically stable, reduce blood pressure to approximately <160/100
to 110 mm Hg over the next 2 to 6 hours
3. Continue
gradual reduction toward normal blood pressure over the following 24 to
48 hours
This general strategy does not apply universally.
Acute aortic syndrome, ischemic stroke, intracerebral hemorrhage, acute
coronary syndrome, pulmonary edema, pregnancy-related hypertensive emergencies,
and other specific conditions require individualized targets and
treatment strategies.
11. Important Exceptions
11.1 Acute Aortic Syndrome
Rapid anti-impulse therapy is required.
1. Target
SBP <120 mm Hg, or the lowest blood pressure that maintains
adequate end-organ perfusion
2. Target
heart rate approximately 60 to 80/min
3. Begin
an intravenous beta blocker, such as esmolol or labetalol,
unless contraindicated
4. Add
an intravenous vasodilator if additional blood pressure reduction is required
A vasodilator should generally not precede beta blockade,
because reflex tachycardia can increase aortic wall stress.
11.2 Acute Ischemic Stroke
Blood pressure management depends on reperfusion therapy and associated
clinical conditions.
Patients receiving intravenous thrombolysis:
1. Lower
blood pressure to <185/110 mm Hg before intravenous thrombolysis
2. During
the first 24 hours after thrombolysis, maintain SBP approximately 140
to 180 mm Hg and DBP ≤105 mm Hg
3. Do
not target SBP <140 mm Hg, because intensive reduction
below this level does not improve functional outcomes
Patients undergoing endovascular thrombectomy:
1. A
preprocedural blood pressure of <185/110 mm Hg is a
reasonable target based on major thrombectomy trials
2. After
successful recanalization, intensive lowering of SBP to <140 mm Hg
is not recommended and may be harmful
Patients not receiving reperfusion therapy:
1. If
BP is <220/120 mm Hg and there is no other condition
requiring urgent BP reduction, active blood pressure lowering during the first 48
to 72 hours does not improve death or dependency
2. If
BP is ≥220/120 mm Hg, individualized blood pressure reduction
is generally recommended
3. An
initial blood pressure reduction of approximately 15% is
generally appropriate while balancing cerebral and systemic organ perfusion
4. Other
emergencies such as acute aortic syndrome or acute heart failure may require
more urgent blood pressure reduction despite the ischemic stroke
Avoid excessive lowering that could compromise cerebral perfusion.
11.3 Intracerebral Hemorrhage
For patients with mild to moderate spontaneous intracerebral
hemorrhage presenting with SBP 150 to 220 mm Hg:
1. Target
SBP approximately 140 mm Hg
2. Maintain
SBP approximately 130 to 150 mm Hg
3. Avoid
lowering SBP to <130 mm Hg, which may be harmful
4. Aim
for smooth, sustained blood pressure control with minimal variability
5. Begin
treatment promptly when appropriate
Blood pressure targets should be individualized in patients with:
1. Large
or severe intracerebral hemorrhage
2. Elevated
intracranial pressure
3. Compromised
cerebral perfusion
4. Need
for surgical intervention
11.4 Acute Cardiogenic Pulmonary Edema
1. Rapid
but controlled blood pressure reduction is appropriate
2. Intravenous
nitroglycerin is particularly useful in hypertensive pulmonary edema
3. Provide
oxygen when hypoxemic
4. Use
noninvasive positive-pressure ventilation when clinically
indicated
5. Use
loop diuretics when clinically significant congestion or volume
overload is present
6. Avoid
initiating beta blockers during active acute decompensated heart failure or
pulmonary edema
In this patient, dyspnea and bilateral crackles make acute
hypertensive pulmonary edema highly likely, although imaging or
bedside ultrasonography can further support the diagnosis.
12. Severe Hypertension Without Acute Organ Damage
In patients with severe blood pressure elevation but no new or
worsening acute target-organ injury:
1. Do
not routinely use intravenous antihypertensive therapy
2. Avoid
rapid or large blood pressure reductions
3. Confirm
accurate blood pressure measurement
4. Address
reversible contributors such as pain, anxiety, missed medication, or
withdrawal states
5. Reinstitute
or appropriately intensify chronic oral antihypertensive therapy
6. Arrange
timely outpatient reassessment and follow-up
For hospitalized patients with asymptomatic severe hypertension, routine
intermittent intravenous treatment or aggressive acute oral blood pressure
lowering may cause harm and should generally be avoided.
13. Prognosis and Follow-Up
1. Hypertensive
emergency is associated with substantial short-term and long-term
cardiovascular risk
2. Prognosis
depends on the type and severity of acute organ injury
3. After
stabilization, evaluate for contributing factors and secondary
hypertension when appropriate
4. Establish
durable long-term blood pressure control
5. Address
medication adherence and cardiovascular risk factors
6. Arrange
close follow-up after discharge
14. Key Clinical Insight
Severe hypertension + new or worsening acute target-organ damage =
hypertensive emergency.
Severe hypertension without acute target-organ damage does not
require rapid intravenous blood pressure reduction.
In this patient:
BP 230/140 mm Hg + confusion + papilledema + probable acute
hypertensive pulmonary edema = hypertensive emergency with acute multisystem
involvement.
The elevated creatinine indicates renal dysfunction and may
represent acute kidney injury if increased from baseline, while
ECG-detected LVH reflects chronic hypertension-mediated cardiac damage.
References
1. Jones
DW, Ferdinand KC, Taler SJ, et al. 2025
AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the
Prevention, Detection, Evaluation and Management of High Blood Pressure in
Adults: A Report of the American College of Cardiology/American Heart
Association Joint Committee on Clinical Practice Guidelines. Circulation.
2025;152(11):e114-e218. doi:10.1161/CIR.0000000000001356.
2. Prabhakaran
S, Gonzalez NR, Zachrison KS, et al. 2026 Guideline for the Early
Management of Patients With Acute Ischemic Stroke: A Guideline From the
American Heart Association/American Stroke Association. Stroke.
2026;57:e316-e436. doi:10.1161/STR.0000000000000513.
3. Greenberg
SM, Ziai WC, Cordonnier C, et al. 2022 Guideline for the Management of
Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the
American Heart Association/American Stroke Association. Stroke.
2022;53:e282-e361. doi:10.1161/STR.0000000000000407.
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