Hypertensive Emergency in Adults
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.
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
| Factor | Mechanism |
|---|---|
| Non-compliance | Most common — sudden medication cessation |
| Inadequately treated HTN | Chronic poorly controlled BP |
| Renal disease | Volume and RAAS activation |
| Pregnancy (pre-eclampsia) | Endothelial dysfunction |
| Drugs | Cocaine, amphetamines, MAOIs |
| Pheochromocytoma | Catecholamine surge |
| Withdrawal syndromes | Clonidine, alcohol |
Target Organs at Risk
| Organ | Manifestation |
|---|---|
| Brain | Encephalopathy, ICH, Ischaemic stroke |
| Heart | ACS, Pulmonary oedema, LVH |
| Kidney | AKI, Proteinuria |
| Eye | Papilloedema, Retinal haemorrhages |
| Aorta | Dissection |
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)
| Grade | Findings |
|---|---|
| I | Arteriolar narrowing |
| II | AV nipping |
| III | Flame haemorrhages, cotton-wool spots |
| IV | Papilloedema (defines malignant HTN) |
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
| Goal | Timeframe |
|---|---|
| Reduce MAP by 25% | First 1 hour |
| To 160/100 mmHg | 2-6 hours |
| To normal | 24-48 hours |
IV Antihypertensives:
| Drug | Dose | Indication |
|---|---|---|
| Labetalol | 20mg IV bolus, then 1-2 mg/min infusion | Most situations |
| GTN | 5-200 mcg/min | Pulmonary oedema, ACS |
| Sodium Nitroprusside | 0.25-10 mcg/kg/min | Rapid control (cyanide toxicity risk) |
| Nicardipine | 5-15 mg/hr | Alternative |
| Hydralazine | 5-10 mg IV | Pregnancy (pre-eclampsia) |
| Esmolol | 500 mcg/kg bolus, 50-200 mcg/kg/min | Aortic dissection |
Special Situations:
| Condition | Target | Preferred Agent |
|---|---|---|
| Aortic dissection | SBP less than 120 within 20 mins | Beta-blocker (Esmolol) + Vasodilator |
| Pre-eclampsia/Eclampsia | SBP less than 160, DBP less than 105 | Labetalol, Hydralazine, MgSO4 for seizures |
| Ischaemic stroke | Usually do NOT lower aggressively | Permissive HTN unless greater than 220/120 |
| Haemorrhagic stroke | Target SBP 140 | IV antihypertensives |
| Phaeochromocytoma | Alpha-blockade first | Phentolamine, then beta-blocker |
[!WARNING] In ischaemic stroke, avoid aggressive BP reduction — may worsen cerebral ischaemia. Follow stroke guidelines.
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:
| System | Examination |
|---|---|
| Neuro | GCS, Focal signs, Papilloedema |
| Cardio | S3/S4, Murmurs, JVP, Pulmonary crackles |
| Renal | Urine output, Oedema |
| Eyes | Fundoscopy (papilloedema Grade IV = emergency) |
| Peripheral | Pulses (dissection may occlude) |
Bedside
| Test | Purpose |
|---|---|
| ECG | LVH, Ischaemia, Strain pattern |
| Urine dipstick | Proteinuria, haematuria |
| Finger-prick glucose | DM, secondary cause |
Laboratory
| Test | Findings |
|---|---|
| U and Es | AKI, Hypokalaemia (if secondary) |
| FBC | MAHA (schistocytes) |
| LFTs | HELLP syndrome if pregnant |
| Troponin | ACS |
| Blood film | Fragmented RBCs (MAHA) |
Imaging
| Test | Indication |
|---|---|
| CT Head | Encephalopathy, stroke, ICH |
| CT Aortogram | Suspected dissection |
| CXR | Pulmonary oedema, cardiomegaly |
| Echo | LV function, dissection |
Consider Secondary Causes
| Test | Suspected Cause |
|---|---|
| Renal USS | Renal artery stenosis |
| Plasma metanephrines | Phaeochromocytoma |
| Renin/Aldosterone | Conn's syndrome |
Hypertensive Crisis Spectrum
| Term | Definition |
|---|---|
| Hypertensive Urgency | Severe HTN (greater than 180/120) WITHOUT end-organ damage |
| Hypertensive Emergency | Severe HTN WITH end-organ damage |
| Malignant Hypertension | HTN with papilloedema (Grade IV retinopathy) |
| Accelerated Hypertension | HTN 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 |
Emergency vs Urgency
| Feature | Emergency | Urgency |
|---|---|---|
| End-organ damage | Present | Absent |
| Setting | ICU/HDU | ED observation |
| Route | IV | Oral |
| Speed | Gradual (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
Organ-Specific
| Organ | Complication |
|---|---|
| Brain | Ischaemic or haemorrhagic stroke, PRES |
| Heart | MI, Pulmonary oedema, LV failure |
| Kidney | AKI, CKD progression |
| Eye | Permanent visual loss |
| Aorta | Dissection rupture |
Treatment-Related
| Complication | Cause |
|---|---|
| Stroke | Rapid BP reduction |
| MI | Rapid BP reduction |
| AKI | Hypoperfusion if BP dropped too fast |
| Cyanide toxicity | Prolonged SNP use |
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
Key Guidelines
- ESC/ESH Guidelines for Hypertension (2018) — European standard
- NICE NG136: Hypertension (2019) — nice.org.uk/guidance/ng136
- 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
| Intervention | Level |
|---|---|
| IV antihypertensives for emergency | Consensus |
| Gradual reduction (25% in 1 hr) | Consensus |
| Rapid reduction in aortic dissection | 1b |
| Avoid rapid reduction in ischaemic stroke | 1a |
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)
Primary Guidelines
- Williams B, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018;39(33):3021-3104. PMID: 30165516
- NICE. Hypertension in adults: diagnosis and management (NG136). 2019. nice.org.uk/guidance/ng136
Key Studies
- 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