Hypertensive emergency: Difference between revisions
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''High blood pressure without symptoms is NOT hypertensive emergency (see [[asymptomatic hypertension]])'' | ==Background== | ||
*''High blood pressure without symptoms is NOT hypertensive emergency (see [[asymptomatic hypertension]])'' | |||
*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<ref>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</ref> | |||
**From 2006-2013, hypertensive emergencies occurred in approximately 2 per 1000 adult ED visits<ref name="AHA2024">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</ref> | |||
== | ===Updated Terminology (AHA 2024)=== | ||
* | ''The 2024 AHA Scientific Statement recommends retiring the terms "hypertensive urgency" and "hypertensive crisis"''<ref name="AHA2024"/> | ||
* | *'''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=== | ===Etiology=== | ||
*Idiopathic | *Idiopathic (medication nonadherence most common) | ||
*[[Sympathomimetic]] drug use | *[[Sympathomimetic]] drug use | ||
*[[Preeclampsia]] | *[[Preeclampsia]] | ||
*Acute [[glomerulonephritis]] | *Acute [[glomerulonephritis]] | ||
*[[Pheochromocytoma]] | |||
*Renal artery stenosis | |||
*MAOI interactions | |||
===Prehospital=== | ===Prehospital=== | ||
*Prehospital BP measurements should be considered reliable<ref>Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.</ref> | *Prehospital BP measurements should be considered reliable<ref>Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.</ref> | ||
*Acute lowering of BP is not typically recommended | *Acute lowering of BP is not typically recommended in the prehospital setting | ||
*Focus on ABCs (assess need for [[intubation]] or [[BiPAP|respiratory support]]) | *Focus on ABCs (assess need for [[intubation]] or [[BiPAP|respiratory support]]) | ||
*Provide care of treatable etiologies | *Provide care of treatable etiologies | ||
| Line 21: | Line 33: | ||
==Clinical Features== | ==Clinical Features== | ||
===End-Organ Dysfunction (BARKH Mnemonic)<ref name="AHA2024"/><ref>Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.</ref>=== | |||
*Acute | Use the BARKH mnemonic to systematically evaluate for target-organ damage: | ||
** | *Brain | ||
* | **[[Hypertensive encephalopathy]] (visual disturbances, [[seizure]], delirium) | ||
* | **[[Intracranial hemorrhage]] | ||
* | **Acute [[Stroke (Main)|ischemic stroke]] | ||
** | *Arteries | ||
** | **[[Aortic dissection]] | ||
** | *Retina | ||
**High-grade [[hypertensive retinopathy]] (hemorrhages, exudates, papilledema) | |||
*Kidney | |||
**[[Acute kidney injury]] (often with microscopic hematuria) | |||
**[[Microangiopathic hemolytic anemia]] (MAHA) / thrombotic microangiopathy<ref>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</ref> | |||
*Heart | |||
**Type-II [[myocardial infarction]] / unstable angina | |||
**Acute LV failure with [[pulmonary edema]] | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
| Line 35: | Line 54: | ||
==Evaluation== | ==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<ref name="AHA2024"/> | |||
===Workup=== | ===Workup=== | ||
''Consider any of the following based on the patient's clinical presentation''<ref>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.</ref> | ''Consider any of the following based on the patient's clinical presentation''<ref>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.</ref><ref name="AHA2024"/> | ||
*CBC with peripheral smear | *CBC with peripheral smear — assess for microangiopathic hemolytic anemia (schistocytes) | ||
*Chem 8 | *Chem 8 — assess renal failure and possible secondary causes | ||
*LDH, haptoglobin — if MAHA suspected | |||
*[[Troponin|Cardiac enzymes]] | *[[Troponin|Cardiac enzymes]] | ||
*[[Urinalysis]] | *[[Urinalysis]] — assess renal failure, glomerulonephritis, preeclampsia | ||
*[[ECG]] — [[LVH]], [[myocardial ischemia|ischemia]] | |||
*[[ECG]] | *[[Ultrasound]] — evaluate for aortic dissection, bladder outlet obstruction, or depressed myocardial function | ||
*[[CT head]] | *[[Fundoscopic Exam]] — evaluate for hypertensive retinopathy or papilledema | ||
**Hypertensive encephalopathy is thought to be secondary to alteration in cerebral auto-regulation leading to [[posterior reversible encephalopathy syndrome]] | *[[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=== | ===Diagnosis=== | ||
*Must have evidence of end-organ dysfunction | *Must have evidence of end-organ dysfunction | ||
**''High blood pressure without symptoms is NOT hypertensive emergency (see [[asymptomatic hypertension]])'' | **''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'' | **''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== | ==Management== | ||
*Goal: Lower | '''High blood pressure without end organ damage is NOT hypertensive emergency (see [[asymptomatic hypertension]])''' | ||
**Then lower | *Goal: Lower MAP by 20-25% in the first hour<ref name="AHA2025">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</ref><ref>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</ref> | ||
**Exception is [[aortic dissection]] which requires rapid reduction | **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]] | *Be careful of lowering BP in patients with [[CVA]] | ||
*Do NOT use IV antihypertensives for asymptomatic elevated BP, even if markedly elevated<ref name="AHA2024"/> | |||
===By Drug=== | ===By Drug=== | ||
====First-Line Agents==== | |||
{| class="wikitable" | {| class="wikitable" | ||
|- | |- | ||
| Line 67: | Line 98: | ||
| '''Notes''' | | '''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)<ref name="CLUE">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</ref> | |||
| | |||
1. Onset 5-15 min (slower than clevidipine) | |||
2. Duration ~30-60 min; can accumulate | |||
3. Reflex tachycardia possible | |||
| | | | ||
1. | 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<ref>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</ref> | |||
|- | |||
| [[Clevidipine]] | |||
| | | | ||
1 | 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. | 1. Ultra-short half-life (~1 min); truly titratable | ||
2. | 2. Organ-independent metabolism (ester hydrolysis in blood; safe in hepatic/renal failure) | ||
3. | 3. Rapid onset (~2-3 min) | ||
4. Lower risk of overshoot hypotension vs nicardipine | |||
| | | | ||
1. | 1. Lipid emulsion vehicle (monitor triglycerides if >24hr) | ||
2. | 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<ref>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</ref> | |||
3. Similar initial BP control to nicardipine; nicardipine may have more sustained control<ref>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.</ref> | |||
|- | |- | ||
| [[Labetalol]] | | [[Labetalol]] | ||
| | | | ||
20- | 20 mg IV bolus initially | ||
Then 20-80 mg IV bolus q10 min '''OR''' | |||
0.5-2 mg/min IV infusion | 0.5-2 mg/min IV infusion | ||
Max cumulative bolus dose 300 mg | |||
| Beta>α-blocker | | Beta > α-blocker | ||
| | | | ||
1. No change in HR | 1. No significant change in HR or cerebral blood flow | ||
2. Rapid onset | |||
2. Rapid onset (5-10 min) | |||
3. Safe in pregnancy | |||
| | | | ||
Avoid in COPD, CHF | 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%)<ref name="CLUE"/> | |||
| | | | ||
1. Consider in ACS | 1. Consider in ACS (when beta-blockade appropriate) | ||
2. Consider in ischemic CVA | 2. Consider in ischemic CVA | ||
3. First-line in aortic dissection (provides rate and BP control) | |||
|} | |||
====Second-Line / Specific-Use Agents==== | |||
{| class="wikitable" | |||
|- | |||
| '''Drug''' | |||
| '''Dose''' | |||
| '''Mechanism''' | |||
| '''Pros''' | |||
| '''Cons''' | |||
| '''Notes''' | |||
|- | |- | ||
| [[Esmolol]] | | [[Esmolol]] | ||
| | | | ||
Load 250-500 mcg/kg over | Load 250-500 mcg/kg over 1 min | ||
Infuse 50 mcg/kg/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 selective | | Beta-1 selective | ||
| | | | ||
1. Very rapid on/offset (half-life 9 min) | |||
2. Easily titratable | |||
| | | | ||
Consider in ACS | 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]] | | [[Phentolamine]] | ||
| | | | ||
5- | 5-15 mg IV bolus q5-15 min '''OR''' | ||
0.2-0. | 0.2-0.5 mg/min IV infusion | ||
| α-blocker | | 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. | 1. Increases renal blood flow and natriuresis | ||
2. | 2. No toxic metabolites | ||
| | | | ||
1. Reflex tachycardia | |||
2. Avoid in glaucoma (increases IOP) | |||
| | | | ||
Consider in hypertensive emergency with AKI/renal failure<ref>Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.</ref> | |||
|- | |||
| [[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]] | | [[Hydralazine]] | ||
| | | | ||
10 - 20 mg slow IV/IM | 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<ref name="AHA2024"/> | |||
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.''<ref name="AHA2024"/> | |||
===By Disease=== | ===By Disease=== | ||
====[[Aortic Dissection]]==== | ====[[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 volume depletion | ||
* | *Avoid nitroprusside without prior beta-blockade | ||
====[[Pulmonary Edema]]==== | ====[[Pulmonary Edema]]==== | ||
*Reduce BP by 20-30% | *Reduce BP by 20-30% | ||
*Nitroglycerin is drug of choice (reduces preload) | |||
*Clevidipine or nicardipine are alternatives<ref>Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.</ref> | |||
*Promote diuresis AFTER vasodilation | *Promote diuresis AFTER vasodilation | ||
*Avoid beta-blockers in acute decompensated heart failure | |||
====[[ACS]]==== | ====[[ACS]]==== | ||
*No more than 20-30% reduction for SBP >160 | *No more than 20-30% reduction for SBP >160 | ||
*Consider | *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<ref>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</ref> | |||
====[[Renal Failure]]==== | ====[[Renal Failure]]==== | ||
*Reduce BP by no more than 20% | *Reduce BP by no more than 20% | ||
*Avoid nitroprusside (renal metabolism) | *Avoid nitroprusside (cyanide metabolite accumulates in renal failure) | ||
*Labetalol | *Clevidipine (organ-independent metabolism), nicardipine, or fenoldopam (increases renal blood flow) | ||
*Labetalol is an alternative | |||
====[[Eclampsia]]/[[Pre-eclampsia]]==== | ====[[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)<ref name="INTERACT3">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</ref> | ||
* | *INTERACT3 demonstrated improved functional outcomes (OR 0.86, 95% CI 0.76-0.97) and reduced mortality with bundled care approach<ref name="INTERACT3"/> | ||
*Nicardipine, clevidipine, or labetalol | |||
*Avoid nitroprusside (increases ICP) | |||
*Care bundle also includes concurrent management of hyperglycemia, pyrexia, and anticoagulation reversal | |||
*See [[ICH#Guidelines|current ICH guidelines]] for full recommendations | |||
====[[ | ====[[CVA|Ischemic Stroke]]==== | ||
* | *[[SAH]]: See [[Subarachnoid Hemorrhage (SAH)]] | ||
* | *If thrombolytic treatment is planned: goal SBP <185 and DBP <110 before administration<ref>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</ref> | ||
* | *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<ref>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.</ref> | |||
====[[ | ====[[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<ref name="AHA2025"/> | ||
* | *Asymptomatic markedly elevated BP (formerly "urgency"): | ||
* | **Do NOT treat with IV antihypertensives in the ED<ref name="AHA2024"/> | ||
** | **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<ref name="AHA2024"/> | |||
<div style="display:none"> | |||
{{MedicationDose|drug=Nicardipine|dose=5-15 mg/hr|route=IV drip|context=1st line antihypertensive|indication=Hypertensive emergency|population=Adult|onset=5-15 min|duration=4-6 hr|notes=Preferred 1st line; titratable}} | |||
{{MedicationDose|drug=Labetalol|dose=20 mg IV bolus, double q10 min (max 300 mg) or 0.5-2 mg/min drip|route=IV|context=1st line antihypertensive|indication=Hypertensive emergency|population=Adult|onset=5-10 min|duration=3-6 hr}} | |||
{{MedicationDose|drug=Clevidipine|dose=1-2 mg/hr, titrate by doubling q90 sec|route=IV drip|context=Antihypertensive|indication=Hypertensive emergency|population=Adult|max_dose=32 mg/hr|onset=2-4 min|notes=Ultra-short acting}} | |||
{{MedicationDose|drug=Nitroglycerin|dose=5-200 mcg/min|route=IV drip|context=Antihypertensive (preload reduction)|indication=Hypertensive emergency|population=Adult|onset=1-5 min|notes=Preferred for ACS or pulmonary edema}} | |||
{{MedicationDose|drug=Nitroprusside|dose=0.25-10 mcg/kg/min|route=IV drip|context=Antihypertensive|indication=Hypertensive emergency|population=Adult|onset=immediate|notes=Cyanide toxicity risk; use only when others fail}} | |||
{{MedicationDose|drug=Esmolol|dose=500 mcg/kg bolus then 50-300 mcg/kg/min|route=IV drip|context=Antihypertensive (rate control)|indication=Hypertensive emergency|population=Adult|onset=1-2 min|duration=10-30 min|notes=Ultra-short acting beta-blocker}} | |||
{{MedicationDose|drug=Hydralazine|dose=5-20 mg IV q4-6 hr|route=IV|context=Antihypertensive|indication=Hypertensive emergency|population=Adult|onset=10-30 min|duration=2-6 hr|notes=Unpredictable; generally avoid}} | |||
{{MedicationDose|drug=Enalaprilat|dose=0.625-1.25 mg IV q6 hr|route=IV|context=ACE inhibitor|indication=Hypertensive emergency|population=Adult|onset=15-60 min|notes=Avoid in renal artery stenosis}} | |||
{{MedicationDose|drug=Fenoldopam|dose=0.1-1.6 mcg/kg/min|route=IV drip|context=Antihypertensive (renal protective)|indication=Hypertensive emergency|population=Adult|onset=5-15 min|notes=DA-1 agonist; renal protective}} | |||
{{MedicationDose|drug=Phentolamine|dose=5-15 mg IV|route=IV|context=Pheochromocytoma crisis|indication=Hypertensive emergency|population=Adult|onset=1-2 min|duration=10-30 min|notes=For catecholamine excess states}} | |||
</div> | |||
==See Also== | ==See Also== | ||
*[[Hypertension (main)]] | *[[Hypertension (main)]] | ||
| Line 270: | Line 449: | ||
*[[IV nitroglycerine alternatives]] | *[[IV nitroglycerine alternatives]] | ||
== | == Calculators == | ||
{{ | {{MAP_Calculator}} | ||
==External Links== | |||
*[http://www.emdocs.net/hypertensive-crisis-pearls-and-pitfalls-for-the-ed-physician/ emDocs - Hypertensive Emergency: Pearls and Pitfalls for the ED Physician] | |||
*[https://emcrit.org/ibcc/htn/ EMCrit IBCC - Hypertensive Emergency] | |||
*[https://www.emdocs.net/2024-aha-scientific-statement-on-management-of-elevated-blood-pressure/ emDocs - 2024 AHA Scientific Statement Review] | |||
==References== | ==References== | ||
Latest revision as of 09:24, 22 March 2026
Background
- High blood pressure without symptoms is NOT hypertensive emergency (see asymptomatic hypertension)
- 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
- Idiopathic (medication nonadherence most common)
- Sympathomimetic drug use
- Preeclampsia
- Acute glomerulonephritis
- Pheochromocytoma
- Renal artery stenosis
- MAOI interactions
Prehospital
- Prehospital BP measurements should be considered reliable[3]
- Acute lowering of BP is not typically recommended in the prehospital setting
- Focus on ABCs (assess need for intubation or respiratory support)
- Provide care of treatable etiologies
- CHF
- Respiratory failure from pulmonary edema
- Acute pain
Clinical Features
End-Organ Dysfunction (BARKH Mnemonic)[2][4]
Use the BARKH mnemonic to systematically evaluate for target-organ damage:
- Brain
- Hypertensive encephalopathy (visual disturbances, seizure, delirium)
- Intracranial hemorrhage
- Acute ischemic stroke
- Arteries
- Retina
- High-grade hypertensive retinopathy (hemorrhages, exudates, papilledema)
- Kidney
- Acute kidney injury (often with microscopic hematuria)
- Microangiopathic hemolytic anemia (MAHA) / thrombotic microangiopathy[5]
- Heart
- Type-II myocardial infarction / unstable angina
- Acute LV failure with pulmonary edema
Differential Diagnosis
Hypertension
- Hypertensive emergency
- Stroke
- Sympathetic crashing acute pulmonary edema
- Ischemic stroke
- Intracranial hemorrhage
- Preeclampsia/Eclampsia
- Autonomic dysreflexia
- Scleroderma renal crisis
- Acute glomerulonephritis
- Type- I myocardial infarction
- Volume overload
- Urinary obstruction
- Drug use or overdose (e.g stimulants, especially alcohol, cocaine, or Synthroid)
- Renal Artery Stenosis
- Nephritic and nephrotic syndrome
- Polycystic kidney disease
- Tyramine reaction
- Cushing's syndrome
- Obstructive sleep apnea
- Pheochromocytoma
- Hyperaldosteronism
- Hyperthyroidism
- Anxiety
- Pain
- Oral contraceptive use
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]
See Also
Calculators
Mean Arterial Pressure (MAP)
| Parameter | Value |
|---|---|
| Systolic BP (mmHg) | |
| Diastolic BP (mmHg) | |
| MAP | mmHg |
| 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. |
|
External Links
- emDocs - Hypertensive Emergency: Pearls and Pitfalls for the ED Physician
- EMCrit IBCC - Hypertensive Emergency
- emDocs - 2024 AHA Scientific Statement Review
References
- ↑ 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
- ↑ 2.0 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
- ↑ Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.
- ↑ Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.
- ↑ 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
- ↑ 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.
- ↑ 7.0 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
- ↑ 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
- ↑ 9.0 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
- ↑ 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
- ↑ 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
- ↑ 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.
- ↑ Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.
- ↑ Fink JT, Singh I. Treatment of hypertensive emergencies. Proc (Bayl Univ Med Cent). 2017;30(2):214-216.
- ↑ 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
- ↑ 16.0 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
- ↑ 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
- ↑ 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.
