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EMERGENCY

Hypertensive Emergency in Adults

Moderate EvidenceUpdated: 2024-12-21

On This Page

Red Flags

  • End-organ damage (stroke, MI, aortic dissection)
  • Hypertensive encephalopathy (headache, confusion, seizures)
  • Acute heart failure / Pulmonary oedema
  • Acute kidney injury
  • Papilloedema
  • Microangiopathic haemolytic anaemia
Overview

Hypertensive Emergency in Adults

Clinical Overview

Summary

Hypertensive emergency is severe hypertension (usually SBP greater than 180 and/or DBP greater than 120 mmHg) with evidence of acute end-organ damage. In contrast, hypertensive urgency is markedly elevated BP without evidence of end-organ damage. Management differs significantly: emergencies require IV antihypertensives with controlled gradual reduction; urgencies can be managed with oral agents. The key is not the BP number but the presence of target organ damage.

Key Facts

  • Definition: Severe HTN + Target organ damage (brain, heart, kidney, eye, aorta)
  • BP threshold: Usually SBP greater than 180 / DBP greater than 120, but damage is key
  • Reduction goal: 25% in first hour; then to 160/100 over 2-6 hours
  • Avoid rapid correction: Risk of stroke, MI, renal failure
  • Exceptions: Aortic dissection (rapid reduction to SBP less than 120)
  • IV agents: Labetalol, GTN, SNP, Nicardipine

Clinical Pearls

The BP number alone does not define emergency — look for END-ORGAN DAMAGE

Rapid reduction is dangerous — except in aortic dissection

Always examine fundoscopy — papilloedema indicates hypertensive emergency

Why This Matters Clinically

Distinguishing hypertensive emergency from urgency is crucial. Over-aggressive treatment of urgencies causes harm (stroke, MI). True emergencies require careful, controlled reduction with IV agents in a monitored setting.


Epidemiology

Incidence

  • Hypertensive crisis: 1-2% of hypertensives
  • True emergency: 25% of crises
  • ED presentations: Common, often urgency rather than emergency

Demographics

  • Age: Increases with age; peak 40-60 years
  • Sex: Male predominance
  • Ethnicity: Higher in Black populations

Risk Factors

FactorMechanism
Non-complianceMost common — sudden medication cessation
Inadequately treated HTNChronic poorly controlled BP
Renal diseaseVolume and RAAS activation
Pregnancy (pre-eclampsia)Endothelial dysfunction
DrugsCocaine, amphetamines, MAOIs
PheochromocytomaCatecholamine surge
Withdrawal syndromesClonidine, alcohol

Target Organs at Risk

OrganManifestation
BrainEncephalopathy, ICH, Ischaemic stroke
HeartACS, Pulmonary oedema, LVH
KidneyAKI, Proteinuria
EyePapilloedema, Retinal haemorrhages
AortaDissection

Pathophysiology

Mechanism of End-Organ Damage

1. Failure of Autoregulation

  • Cerebral and renal blood flow normally autoregulated
  • Severe HTN exceeds autoregulatory capacity
  • Hyperperfusion → Endothelial damage → Oedema

2. Endothelial Injury

  • Mechanical shear stress damages endothelium
  • Fibrinoid necrosis of arterioles
  • Platelet activation, microthrombi
  • Microangiopathic haemolytic anaemia

3. RAAS Activation

  • Ischaemia triggers renin release
  • Further vasoconstriction
  • Vicious cycle of pressure-induced injury

Hypertensive Encephalopathy

  • Loss of cerebral autoregulation
  • Cerebral oedema (reversible if treated)
  • Features: Headache, confusion, seizures, visual changes, coma

Retinal Changes (Keith-Wagener Classification)

GradeFindings
IArteriolar narrowing
IIAV nipping
IIIFlame haemorrhages, cotton-wool spots
IVPapilloedema (defines malignant HTN)

Emergency Management

Hypertensive Emergency — Management

Step 1: Confirm End-Organ Damage

  • Neurological: Headache, confusion, focal signs, seizures → CT Head
  • Cardiac: Chest pain, dyspnoea → ECG, Troponin, CXR
  • Renal: Oliguria, rising creatinine
  • Eyes: Papilloedema, haemorrhages → Fundoscopy
  • Aorta: Tearing chest/back pain → CT Aortogram

Step 2: Controlled BP Reduction

GoalTimeframe
Reduce MAP by 25%First 1 hour
To 160/100 mmHg2-6 hours
To normal24-48 hours

IV Antihypertensives:

DrugDoseIndication
Labetalol20mg IV bolus, then 1-2 mg/min infusionMost situations
GTN5-200 mcg/minPulmonary oedema, ACS
Sodium Nitroprusside0.25-10 mcg/kg/minRapid control (cyanide toxicity risk)
Nicardipine5-15 mg/hrAlternative
Hydralazine5-10 mg IVPregnancy (pre-eclampsia)
Esmolol500 mcg/kg bolus, 50-200 mcg/kg/minAortic dissection

Special Situations:

ConditionTargetPreferred Agent
Aortic dissectionSBP less than 120 within 20 minsBeta-blocker (Esmolol) + Vasodilator
Pre-eclampsia/EclampsiaSBP less than 160, DBP less than 105Labetalol, Hydralazine, MgSO4 for seizures
Ischaemic strokeUsually do NOT lower aggressivelyPermissive HTN unless greater than 220/120
Haemorrhagic strokeTarget SBP 140IV antihypertensives
PhaeochromocytomaAlpha-blockade firstPhentolamine, then beta-blocker

[!WARNING] In ischaemic stroke, avoid aggressive BP reduction — may worsen cerebral ischaemia. Follow stroke guidelines.


Clinical Assessment

History

  • Symptoms of end-organ damage:
    • Headache, visual changes, confusion (encephalopathy)
    • Chest pain, dyspnoea (cardiac)
    • Back pain (aortic dissection)
    • Reduced urine output (renal)
  • Medication history: Recent non-compliance, cessation
  • Drug use: Cocaine, amphetamines
  • Pregnancy: Pre-eclampsia

Physical Examination

Vital Signs:

  • BP: Measure in both arms (dissection if difference greater than 20 mmHg)
  • Usually SBP greater than 180, DBP greater than 120

End-Organ Assessment:

SystemExamination
NeuroGCS, Focal signs, Papilloedema
CardioS3/S4, Murmurs, JVP, Pulmonary crackles
RenalUrine output, Oedema
EyesFundoscopy (papilloedema Grade IV = emergency)
PeripheralPulses (dissection may occlude)

Investigations

Bedside

TestPurpose
ECGLVH, Ischaemia, Strain pattern
Urine dipstickProteinuria, haematuria
Finger-prick glucoseDM, secondary cause

Laboratory

TestFindings
U and EsAKI, Hypokalaemia (if secondary)
FBCMAHA (schistocytes)
LFTsHELLP syndrome if pregnant
TroponinACS
Blood filmFragmented RBCs (MAHA)

Imaging

TestIndication
CT HeadEncephalopathy, stroke, ICH
CT AortogramSuspected dissection
CXRPulmonary oedema, cardiomegaly
EchoLV function, dissection

Consider Secondary Causes

TestSuspected Cause
Renal USSRenal artery stenosis
Plasma metanephrinesPhaeochromocytoma
Renin/AldosteroneConn's syndrome

Definitions

Hypertensive Crisis Spectrum

TermDefinition
Hypertensive UrgencySevere HTN (greater than 180/120) WITHOUT end-organ damage
Hypertensive EmergencySevere HTN WITH end-organ damage
Malignant HypertensionHTN with papilloedema (Grade IV retinopathy)
Accelerated HypertensionHTN with Grade III retinopathy (haemorrhages, exudates)

Common Hypertensive Emergencies

Presentation
Hypertensive encephalopathy
Acute aortic dissection
Acute pulmonary oedema
ACS (STEMI/NSTEMI)
Eclampsia/Pre-eclampsia
Acute kidney injury
Haemorrhagic stroke
MAHA

Treatment Approach

Emergency vs Urgency

FeatureEmergencyUrgency
End-organ damagePresentAbsent
SettingICU/HDUED observation
RouteIVOral
SpeedGradual (25% in 1 hr)Hours to days

IV Options

Labetalol:

  • Alpha and beta blocker
  • 20mg IV bolus, repeat every 10 mins (max 300mg)
  • Infusion 1-2 mg/min
  • Avoid in asthma, heart block

GTN:

  • Vasodilator (veins more than arteries)
  • 5-200 mcg/min
  • Good for ACS, pulmonary oedema

Sodium Nitroprusside:

  • Potent arterial and venous dilator
  • Rapid onset (seconds)
  • Cyanide toxicity with prolonged use

Post-Acute Management

  • Investigate for secondary causes
  • Optimise oral antihypertensive regimen
  • Lifestyle modification
  • Close BP follow-up

Complications

Organ-Specific

OrganComplication
BrainIschaemic or haemorrhagic stroke, PRES
HeartMI, Pulmonary oedema, LV failure
KidneyAKI, CKD progression
EyePermanent visual loss
AortaDissection rupture

Treatment-Related

ComplicationCause
StrokeRapid BP reduction
MIRapid BP reduction
AKIHypoperfusion if BP dropped too fast
Cyanide toxicityProlonged SNP use

Prognosis

Mortality

  • Untreated malignant HTN: 80% 1-year mortality (historically)
  • With treatment: 5-year survival greater than 80%
  • Aortic dissection: High mortality if BP not controlled

Long-Term

  • Increased CV risk
  • CKD progression common
  • Need for lifelong antihypertensive therapy

Evidence & Guidelines

Key Guidelines

  1. ESC/ESH Guidelines for Hypertension (2018) — European standard
  2. NICE NG136: Hypertension (2019) — nice.org.uk/guidance/ng136
  3. ACC/AHA Hypertension Guideline (2017)

Key Evidence

Gradual BP Reduction

  • Consensus based on case series showing harm from rapid reduction
  • Target: 25% in first hour, then gradual

INTERACT2 (2013) — Haemorrhagic Stroke

  • Intensive BP lowering (SBP 140) safe and may improve outcomes PMID: 23713578

Evidence Levels

InterventionLevel
IV antihypertensives for emergencyConsensus
Gradual reduction (25% in 1 hr)Consensus
Rapid reduction in aortic dissection1b
Avoid rapid reduction in ischaemic stroke1a

Information for Patients

What is a Hypertensive Emergency?

A hypertensive emergency is very high blood pressure that is causing damage to your organs — such as your brain, heart, kidneys, or eyes. This is different from just having high blood pressure, which usually causes no symptoms.

What Are the Warning Signs?

  • Severe headache
  • Blurred vision or seeing spots
  • Chest pain or difficulty breathing
  • Confusion or difficulty speaking
  • Weakness or numbness

What Happens in Hospital?

  • You will be closely monitored in a high-dependency area
  • Blood pressure lowering medicines given through a drip
  • Blood pressure is reduced slowly and carefully
  • Tests to check for organ damage

After Treatment

  • You will need to take blood pressure medicines regularly
  • Tests to check for any underlying cause
  • Regular check-ups with your GP or specialist

How Can I Prevent This?

  • Take your blood pressure medicines every day
  • Never stop your medicines suddenly
  • Check your blood pressure regularly
  • Reduce salt, eat healthily, exercise
  • Avoid recreational drugs (cocaine, amphetamines)

References

Primary Guidelines

  1. Williams B, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018;39(33):3021-3104. PMID: 30165516
  2. NICE. Hypertension in adults: diagnosis and management (NG136). 2019. nice.org.uk/guidance/ng136

Key Studies

  1. Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage (INTERACT2). N Engl J Med. 2013;368(25):2355-65. PMID: 23713578

Last updated: 2024-12-21

At a Glance

EvidenceModerate
Last Updated2024-12-21
Emergency Protocol

Red Flags

  • End-organ damage (stroke, MI, aortic dissection)
  • Hypertensive encephalopathy (headache, confusion, seizures)
  • Acute heart failure / Pulmonary oedema
  • Acute kidney injury
  • Papilloedema
  • Microangiopathic haemolytic anaemia

Clinical Pearls

  • The BP number alone does not define emergency — look for END-ORGAN DAMAGE
  • Rapid reduction is dangerous — except in aortic dissection
  • Always examine fundoscopy — papilloedema indicates hypertensive emergency
  • In ischaemic stroke, avoid aggressive BP reduction — may worsen cerebral ischaemia. Follow stroke guidelines.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines