Hypertensive emergency

(Redirected from Malignant hypertension)

High blood pressure without symptoms is NOT hypertensive emergency (see asymptomatic hypertension)


  • Definition: end-organ damage due to hypertension
    • Blood pressure is generally >180/120 (usually > 220/130), 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]



Clinical Features

End-Organ Dysfunction[3]

Differential Diagnosis




Consider any of the following based on the patient's clinical presentation[4]

  • CBC with peripheral smear- assess for microangiopathic hemolytic anemia
  • Chem 8 - assess renal failure and possible secondary causes
  • 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 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 (now called reversible posterior leukoencephalopathy). Most patients will show changes on MRI, although this is not necessarily indicated in the emergency department.


  • 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


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

  • Goal: Lower mean arterial or systolic pressure by no more than 10-20% in the first hour[5]
    • Then lower by an additional 5-15% over the next 23 hours for no more than 25% in the first 24 hours
    • Exception is aortic dissection which requires rapid reduction to systolic BP to 100-120 mmHg
  • Be careful of lowering BP in patients with CVA

By Drug

Drug Dose Mechanism Pros Cons Notes

0.3-0.5 mcg/kg/min IV initial infusion

Increase by 0.5 mcg/kg/min up to 2mcg/kg/min

Arterial > venodilator

1. Very effective

2. Immediate onset/offset

1. Cyanide Toxicity

2. Coronary steal?

3. Increased HR

1. Avoid in liver/renal failure

2. Avoid with increased ICP

3. Avoid in pregnancy

Nitroglycerin Start 5-100 mcg/min Veno>arteriodilation

1. Rapid on/offset

2. Increases coronary flow

Causes tachycardia

Drug of choice in patients with cardiac ischemia,

LV dysfunction, or pulmonary edema


20-80mg IV bolus q10 min OR

0.5-2 mg/min IV infusion or

200mg to 400mg PO BID


1. No change in HR, cerebral flow 2. Rapid onset

Avoid in COPD, CHF and heart block

1. Consider in ACS 2. Consider in ischemic CVA


Load 250-500 mcg/kg over 2min

Infuse 50 mcg/kg/min over 4min

- if ineffective repeat load, increase infusion rate by  50mcg/kg/min up to 300mcg/kg/min

Beta selective Rapid on/offset

Avoid in COPD, CHF


Consider in ACS


Start 5mg/h

If ineffective after 15min increased in 2.5mg/hr interval up to 15mg/hr

Decreases PVR

Good for intracranial pathology Slower onset/offset Avoid in CHF, ACS

5-15mg IV bolus q5-15min OR

0.2-0.5mg/min IV infusion

α-blocker Used for catecholamine-induced hypertension
Enalaprilat Bolus 1.25mg over 5min q6hr, titrate at 30min intervals to max of 5mg q6hr Decreases HR, SV, systemic arterial pressure Does not impair cerebral flow Variable response

1. Used in patients at risk for cerebral hypotension, CHF

2. Avoid in pregnancy


0.1 - 0.3 mg PO q12 scheduled; For hypertensive emergency, 0.2 mg x1, then 0.1 mg q1 hr PRN, max 0.6 mg total

α-2 agonist, BP effects within 30-60 min after PO dose Reduced CNS sympathetic flow, decreasing SVR, HR, BP; no renal blood flow changes; tolerance/tachyphylaxis develop quickly


10 - 20 mg slow IV/IM bolus q4-6 hr PRN, max 40 mg/dose

Peripheral vasodilator, with fall in BP beginning within 30 min, lasting 2-4 hrs Decrease in DBP > SBP; has increased HR, stroke volume and cardiac outpt; preferential vasodilation > venodilation

By Disease

Aortic Dissection

  • Rapidly reduce sys BP to 100-120; HR 60-80 within 20min
  • Adequate analgesia will decrease sympathetic drive and assist with BP and HR control
  • Avoid volume depletion
  • Prevent reflex tachycardia
    • Labetalol alone
    • Nitroprusside or nicardipine AFTER metoprolol or esmolol

Pulmonary Edema

  • Reduce BP by 20-30%
  • Promote diuresis AFTER vasodilation


  • No more than 20-30% reduction for SBP >160
  • Consider NTG, beta-blocker

Cocaine/Amphetamine Toxicitiy

  • Benzos
  • Mixed α + B blockade
    • Phentolamine OR nitroprusside AND β-blocker

Renal Failure

  • Reduce BP by no more than 20%
  • Avoid nitroprusside (renal metabolism)
  • Labetalol or nicardipine


  • Goal BP <160/110
  • Labetalol or nicardipine
  • Magnesium

Hypertensive emergency



  • Phentolamine OR (nitroprusside AND β-blocker)


  • Admit
    • Patients receiving titratable antihypertensive therapies will likely require admission to critical care unit

See Also

External Links


  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. Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.
  3. Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.
  4. 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.
  5. 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
  6. Acute Stroke Practice Guidelines for Inpatient Management of Ischemic Stroke and Transient Ischemic Attack (TIA) https://www.heart.org/idc/groups/heart-public/@wcm/@private/@hcm/documents/downloadable/ucm_309996.pdf