Hypertensive emergency

(Redirigido desde «Hypertensive encephalopathy»)

Background


  • Definition: acute target-organ damage due to severely elevated blood pressure
    • Blood pressure is generally ≥180/110-120, but presence of end-organ damage defines disease (not absolute blood pressure number)
    • 1%-6% of all ED patients will present with severe hypertension, but less than half of those will have target organ damage[1]
    • From 2006-2013, hypertensive emergencies occurred in approximately 2 per 1000 adult ED visits[2]

Updated Terminology (AHA 2024)

The 2024 AHA Scientific Statement recommends retiring the terms "hypertensive urgency" and "hypertensive crisis"[2]

  • Hypertensive emergency: SBP ≥180 or DBP ≥110-120 mmHg with new or worsening target-organ damage
  • Asymptomatic markedly elevated BP: SBP ≥180 or DBP ≥110-120 mmHg without target-organ damage (replaces "hypertensive urgency")
  • Asymptomatic elevated BP: SBP >130 or DBP >80 mmHg without target-organ damage

Etiology

Prehospital

Clinical Features

End-Organ Dysfunction (BARKH Mnemonic)[2][4]

Use the BARKH mnemonic to systematically evaluate for target-organ damage:

Differential Diagnosis

Hypertension

Evaluation

BP Measurement

  • Ensure proper cuff size and technique before initiating treatment
  • Confirm with repeat measurement in both arms; patient should be seated, back supported, feet on floor
  • For patients receiving IV antihypertensives, arterial line monitoring is preferred for accuracy[2]

Workup

Consider any of the following based on the patient's clinical presentation[6][2]

  • CBC with peripheral smear — assess for microangiopathic hemolytic anemia (schistocytes)
  • Chem 8 — assess renal failure and possible secondary causes
  • LDH, haptoglobin — if MAHA suspected
  • Cardiac enzymes
  • Urinalysis — assess renal failure, glomerulonephritis, preeclampsia
  • ECG — LVH, ischemia
  • Ultrasound — evaluate for aortic dissection, bladder outlet obstruction, or depressed myocardial function
  • Fundoscopic Exam — evaluate for hypertensive retinopathy or papilledema
  • CXR — evaluate for pulmonary edema or widened mediastinum (dissection)
  • CT head — in hypertensive encephalopathy, may not show acute hemorrhage or other acute pathology
    • Hypertensive encephalopathy is thought to be secondary to alteration in cerebral auto-regulation leading to posterior reversible encephalopathy syndrome. Most patients will show changes on MRI, although this is not necessarily indicated in the emergency department.

Diagnosis

  • Must have evidence of end-organ dysfunction
    • High blood pressure without symptoms is NOT hypertensive emergency (see asymptomatic hypertension)
    • Symptoms such as headache, epistaxis and dizziness are not evidence of acute end-organ damage and they are not indication for acute BP reduction

Management

High blood pressure without end organ damage is NOT hypertensive emergency (see asymptomatic hypertension)

  • Goal: Lower MAP by 20-25% in the first hour[7][8]
    • Then lower gradually to 160/100 mmHg over the next 2-6 hours
    • Then cautiously to normal over the next 24-48 hours
    • Exception is aortic dissection which requires rapid reduction of systolic BP to 100-120 mmHg
  • Be careful of lowering BP in patients with CVA
  • Do NOT use IV antihypertensives for asymptomatic elevated BP, even if markedly elevated[2]

By Drug

First-Line Agents

Drug Dose Mechanism Pros Cons Notes
Nicardipine

Start 5 mg/hr IV

Increase by 2.5 mg/hr q5-15min

Max 15 mg/hr

Dihydropyridine CCB; decreases PVR

1. Effective for most hypertensive emergencies

2. Good for intracranial pathology

3. Does not increase ICP

4. Achieves target BP in >90% within 30 min (CLUE trial)[9]

1. Onset 5-15 min (slower than clevidipine)

2. Duration ~30-60 min; can accumulate

3. Reflex tachycardia possible

1. Avoid in decompensated CHF, severe aortic stenosis

2. Often considered first-line for most hypertensive emergencies

3. In CLUE subgroup with EOD, 3.65× odds of reaching target vs labetalol[10]

Clevidipine

Start 1-2 mg/hr IV

Double q2 min until approaching target

Then titrate by smaller increments q5-10 min

Max 32 mg/hr

Dihydropyridine CCB; arterial vasodilator

1. Ultra-short half-life (~1 min); truly titratable

2. Organ-independent metabolism (ester hydrolysis in blood; safe in hepatic/renal failure)

3. Rapid onset (~2-3 min)

4. Lower risk of overshoot hypotension vs nicardipine

1. Lipid emulsion vehicle (monitor triglycerides if >24hr)

2. Higher cost than nicardipine

3. Risk of rebound HTN after discontinuation

1. Avoid in soy/egg allergy, severe aortic stenosis

2. Effective in stroke, perioperative HTN[11]

3. Similar initial BP control to nicardipine; nicardipine may have more sustained control[12]

Labetalol

20 mg IV bolus initially

Then 20-80 mg IV bolus q10 min OR

0.5-2 mg/min IV infusion

Max cumulative bolus dose 300 mg

Beta > α-blocker

1. No significant change in HR or cerebral blood flow

2. Rapid onset (5-10 min)

3. Safe in pregnancy

1. Avoid in COPD, decompensated CHF, 2nd/3rd degree heart block, severe bradycardia

2. Less effective at reaching target BP than nicardipine in CLUE trial (82.5% vs 91.7%)[9]

1. Consider in ACS (when beta-blockade appropriate)

2. Consider in ischemic CVA

3. First-line in aortic dissection (provides rate and BP control)

Second-Line / Specific-Use Agents

Drug Dose Mechanism Pros Cons Notes
Esmolol

Load 250-500 mcg/kg over 1 min

Infuse 50 mcg/kg/min

If ineffective, repeat load and increase infusion by 50 mcg/kg/min up to 300 mcg/kg/min

Beta-1 selective

1. Very rapid on/offset (half-life 9 min)

2. Easily titratable

1. Avoid in COPD, decompensated CHF, severe bradycardia

2. Does not significantly lower BP alone in severe HTN

1. First-line for rate control in aortic dissection

2. Consider in ACS

3. Often used WITH a vasodilator (nicardipine/clevidipine)

Nitroglycerin Start 5 mcg/min IV; titrate up to 200 mcg/min Venodilator > arteriodilator

1. Rapid onset/offset

2. Increases coronary blood flow

3. Reduces preload (ideal for pulmonary edema)

1. Reflex tachycardia

2. Headache common

3. Tachyphylaxis with prolonged use

Drug of choice in patients with cardiac ischemia, LV dysfunction, or pulmonary edema

Nitroprusside

0.3-0.5 mcg/kg/min IV initial

Max 2 mcg/kg/min (some refs up to 10)

Arterial > venodilator

1. Very effective

2. Immediate onset/offset

1. Cyanide toxicity (especially with renal/hepatic failure or prolonged use)

2. Coronary steal

3. Increased ICP

4. Requires light-protected tubing

Generally considered second- or third-line; safer alternatives preferred (nicardipine, clevidipine)

Avoid in liver/renal failure, increased ICP, pregnancy

Phentolamine

5-15 mg IV bolus q5-15 min OR

0.2-0.5 mg/min IV infusion

α-blocker Rapid onset Reflex tachycardia

Used for catecholamine-induced hypertension (pheochromocytoma, sympathomimetic toxicity)

Fenoldopam

0.1-0.3 mcg/kg/min IV

Titrate q15 min

Max 1.6 mcg/kg/min

Dopamine-1 agonist

1. Increases renal blood flow and natriuresis

2. No toxic metabolites

1. Reflex tachycardia

2. Avoid in glaucoma (increases IOP)

Consider in hypertensive emergency with AKI/renal failure[13]

Enalaprilat Bolus 1.25 mg IV over 5 min q6hr, titrate at 30 min intervals to max of 5 mg q6hr ACE inhibitor; decreases HR, SV, systemic arterial pressure Does not impair cerebral blood flow Variable and unpredictable response

1. Consider in high-renin states, CHF

2. Avoid in pregnancy

3. Limited role in ED

Hydralazine

10-20 mg slow IV/IM q4-6 hr PRN

Max 40 mg/dose

Direct arterial vasodilator; onset 10-30 min, duration 2-4 hrs Extensive safety data in pregnancy

1. Unpredictable dose-response

2. Prolonged duration; not titratable

3. Reflex tachycardia

4. Can increase ICP

Not recommended as first-line outside of pregnancy due to unpredictable response and inability to titrate[2]

Primarily used in eclampsia/preeclampsia

Note: Oral clonidine loading ("clonidine slam") is an outdated practice and is not recommended for hypertensive emergency in the ED. IV titratable agents are preferred.[2]

By Disease

Aortic Dissection

  • Target SBP 100-120 and HR <60 within 20 min
  • Beta-blockade BEFORE vasodilation to prevent reflex tachycardia
    • Esmolol (preferred for titratability) OR labetalol alone
    • Add nicardipine or clevidipine if BP remains elevated after adequate beta-blockade
  • Adequate analgesia will decrease sympathetic drive
  • Avoid volume depletion
  • Avoid nitroprusside without prior beta-blockade

Pulmonary Edema

  • Reduce BP by 20-30%
  • Nitroglycerin is drug of choice (reduces preload)
  • Clevidipine or nicardipine are alternatives[14]
  • Promote diuresis AFTER vasodilation
  • Avoid beta-blockers in acute decompensated heart failure

ACS

  • No more than 20-30% reduction for SBP >160
  • Nitroglycerin preferred (increases coronary flow)
  • Consider beta-blocker (esmolol or labetalol) if no contraindication
  • Avoid nicardipine/clevidipine as sole agents (lack antianginal properties)

Cocaine/Amphetamine Toxicity

  • Benzodiazepines first (addresses underlying sympathetic surge)
  • If refractory: nicardipine or clevidipine (pure vasodilators)
  • Phentolamine for refractory cases
  • Avoid pure beta-blockers (risk of unopposed alpha-stimulation)
  • Labetalol (mixed alpha/beta) remains debated; some guidelines permit, others advise against[15]

Renal Failure

  • Reduce BP by no more than 20%
  • Avoid nitroprusside (cyanide metabolite accumulates in renal failure)
  • Clevidipine (organ-independent metabolism), nicardipine, or fenoldopam (increases renal blood flow)
  • Labetalol is an alternative

Eclampsia/Pre-eclampsia

  • Goal BP <160/110
  • Labetalol, nicardipine, or hydralazine
  • Magnesium sulfate for seizure prophylaxis/treatment
  • Avoid ACE inhibitors/ARBs, nitroprusside (teratogenic/fetal cyanide risk)
  • Definitive treatment is delivery

Intracerebral Hemorrhage

  • Target SBP <140 mmHg, initiated within 1 hour (INTERACT3 care bundle)[16]
  • INTERACT3 demonstrated improved functional outcomes (OR 0.86, 95% CI 0.76-0.97) and reduced mortality with bundled care approach[16]
  • Nicardipine, clevidipine, or labetalol
  • Avoid nitroprusside (increases ICP)
  • Care bundle also includes concurrent management of hyperglycemia, pyrexia, and anticoagulation reversal
  • See current ICH guidelines for full recommendations

Ischemic Stroke

  • SAH: See Subarachnoid Hemorrhage (SAH)
  • If thrombolytic treatment is planned: goal SBP <185 and DBP <110 before administration[17]
  • If no thrombolytics: consider BP reduction only if SBP >220 or DBP >120
  • Nicardipine, clevidipine, or labetalol are all effective and safe
  • Clevidipine may facilitate faster door-to-thrombolytic times due to rapid onset[18]

Pheochromocytoma

  • Alpha-blockade first: Phentolamine
  • Then add beta-blocker only after adequate alpha-blockade
  • Nicardipine or clevidipine are alternatives

Disposition

  • Hypertensive emergency: Admit to ICU or monitored setting for IV antihypertensive titration and close hemodynamic monitoring[7]
  • Asymptomatic markedly elevated BP (formerly "urgency"):
    • Do NOT treat with IV antihypertensives in the ED[2]
    • Restart home medications
    • Assess for and address contributing factors (pain, anxiety, medication nonadherence, urinary retention)
    • Arrange close outpatient follow-up (24-72 hours)
    • Evidence suggests potential harm from acute IV treatment of asymptomatic elevated BP[2]


Nicardipine 5-15 mg/hr IV drip (onset 5-15 min, duration 4-6 hr) — Preferred 1st line; titratable Labetalol 20 mg IV bolus, double q10 min (max 300 mg) or 0.5-2 mg/min drip IV (onset 5-10 min, duration 3-6 hr) Clevidipine 1-2 mg/hr, titrate by doubling q90 sec IV drip (onset 2-4 min) (max 32 mg/hr) — Ultra-short acting Nitroglycerin 5-200 mcg/min IV drip (onset 1-5 min) — Preferred for ACS or pulmonary edema Nitroprusside 0.25-10 mcg/kg/min IV drip (onset immediate) — Cyanide toxicity risk; use only when others fail Esmolol 500 mcg/kg bolus then 50-300 mcg/kg/min IV drip (onset 1-2 min, duration 10-30 min) — Ultra-short acting beta-blocker Hydralazine 5-20 mg IV q4-6 hr IV (onset 10-30 min, duration 2-6 hr) — Unpredictable; generally avoid Enalaprilat 0.625-1.25 mg IV q6 hr IV (onset 15-60 min) — Avoid in renal artery stenosis Fenoldopam 0.1-1.6 mcg/kg/min IV drip (onset 5-15 min) — DA-1 agonist; renal protective Phentolamine 5-15 mg IV IV (onset 1-2 min, duration 10-30 min) — For catecholamine excess states

See Also

Calculators

Mean Arterial Pressure (MAP)

Mean Arterial Pressure (MAP)
Parameter Value
Systolic BP (mmHg)
Diastolic BP (mmHg)
MAP mmHg
Interpretation
70–105 Normal — Adequate perfusion pressure.
<65 Low — Risk of end-organ hypoperfusion. Target MAP ≥65 in septic shock (SSC 2021).
>105 Elevated — Consider antihypertensive therapy based on clinical context.
References
  • Formula: MAP = DBP + (SBP – DBP) / 3
  • Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines. Intensive Care Med. 2017;43(3):304-377. PMID 28101605.

External Links

References

  1. ↑ Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252. doi:10.1161/01.HYP.0000107251.49515.c2
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Bress AP, Anderson TS, Flack JM, et al. The management of elevated blood pressure in the acute care setting: a scientific statement from the American Heart Association. Hypertension. 2024;81(8):e94-e106. doi:10.1161/HYP.0000000000000238
  3. ↑ Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.
  4. ↑ Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.
  5. ↑ Cremer A, Amraoui F, Lip GY, et al. From malignant hypertension to hypertension-MOD: a modern definition for an old but still dangerous emergency. J Hum Hypertens. 2016;30(8):463-466. doi:10.1038/jhh.2015.82
  6. ↑ 2013 Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension. J Hypertens. 2013;31(10):1925-1938.
  7. ↑ 7.0 7.1 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. Hypertension. 2025;82(10):e212-e316. doi:10.1161/HYP.0000000000000249
  8. ↑ Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48(5):316-325. doi:10.1016/j.pcad.2006.02.004
  9. ↑ 9.0 9.1 Peacock WF, Varon J, Baumann BM, et al. CLUE: a randomized comparative effectiveness trial of IV nicardipine versus labetalol use in the emergency department. Crit Care. 2011;15(3):R157. doi:10.1186/cc10289
  10. ↑ Levy PD, Mahn JJ, Miller J, et al. Intravenous nicardipine and labetalol use in hypertensive patients with signs or symptoms suggestive of end-organ damage in the emergency department: a subgroup analysis of the CLUE trial. BMJ Open. 2013;3(3):e002338. doi:10.1136/bmjopen-2012-002338
  11. ↑ Brehaut SS, Roche AM. Emergency department and critical care use of clevidipine for treatment of hypertension in patients with acute stroke. Crit Pathw Cardiol. 2025;24(1):e0375. doi:10.1097/HPC.0000000000000375
  12. ↑ Storey C, Pouliot J. Evaluation of the efficacy and safety of nicardipine versus clevidipine for blood pressure control in hypertensive crisis. J Emerg Med. 2024;67(3):e267-e275.
  13. ↑ Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.
  14. ↑ Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.
  15. ↑ Richards JR, Garber D, Laurin EG, et al. Treatment of cocaine cardiovascular toxicity: a systematic review. Clin Toxicol (Phila). 2016;54(5):345-364. doi:10.3109/15563650.2016.1142090
  16. ↑ 16.0 16.1 Ma L, Hu X, Song L, et al. The third Intensive Care Bundle with Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT3): an international, stepped wedge cluster randomised controlled trial. Lancet. 2023;402(10395):27-40. doi:10.1016/S0140-6736(23)00806-1
  17. ↑ Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update. Stroke. 2019;50(12):e344-e418. doi:10.1161/STR.0000000000000211
  18. ↑ Brehaut SS, Roche AM. Emergency department and critical care use of clevidipine for treatment of hypertension in patients with acute stroke. Crit Pathw Cardiol. 2025;24(1):e0375.
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