Hypertensive Emergency in Adults

Clinical Overview

Summary

Hypertensive emergency is severe hypertension (typically SBP > 180 mmHg and/or DBP > 120 mmHg) with evidence of acute end-organ damage requiring immediate blood pressure reduction within minutes to hours to prevent irreversible organ dysfunction or death. [1,2] In contrast, hypertensive urgency is markedly elevated blood pressure without evidence of acute target organ damage and can be managed in the outpatient setting with oral antihypertensives. [3] The key distinction is not the absolute blood pressure value but the presence or absence of acute target organ damage. Management differs fundamentally: emergencies require intravenous antihypertensives with controlled gradual reduction in a critical care setting; urgencies can be managed with oral agents and close follow-up. [4,5]

Key Facts

• Definition: Severe HTN + Acute target organ damage (brain, heart, kidney, eye, aorta)
• BP threshold: Usually SBP > 180 / DBP > 120 mmHg, but damage defines emergency
• Reduction goal: 10-15% in first hour; 25% within 24 hours to avoid ischaemia
• Avoid rapid correction: Risk of watershed stroke, MI, renal hypoperfusion
• Exception: Aortic dissection requires rapid reduction to SBP less than 120 mmHg within 20 minutes
• IV agents: Labetalol, nicardipine, sodium nitroprusside, GTN, clevidipine
• Mortality: Untreated malignant HTN has 80-90% one-year mortality; treated survival > 80%

Clinical Pearls

The BP number alone NEVER defines emergency — always look for END-ORGAN DAMAGE

Rapid reduction is harmful in most situations — gradual reduction prevents ischaemic injury

Always perform fundoscopy — papilloedema (Grade IV retinopathy) defines malignant hypertension

In acute ischaemic stroke, permissive hypertension is protective — do NOT lower aggressively

Different emergencies require different agents: GTN for ACS, beta-blocker first for dissection, nicardipine for stroke

Why This Matters Clinically

Distinguishing hypertensive emergency from urgency is a crucial clinical skill that prevents both under-treatment and over-treatment. [6] Over-aggressive blood pressure reduction in urgencies or asymptomatic severe hypertension causes ischaemic stroke and myocardial infarction through cerebral and coronary hypoperfusion. Conversely, failure to recognise true emergencies and delay in controlled blood pressure reduction leads to irreversible organ damage and death. The approach to blood pressure lowering is condition-specific: aortic dissection requires rapid reduction, while acute ischaemic stroke requires permissive hypertension, and most other emergencies require gradual controlled reduction over hours.

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Epidemiology

Incidence and Prevalence

Hypertensive Crisis:

• Affects 1-2% of all patients with hypertension during their lifetime [7]
• Accounts for approximately 25% of emergency department visits for hypertension
• True hypertensive emergencies (with target organ damage) represent only 25-30% of hypertensive crises [8]
• The majority (70-75%) are hypertensive urgencies without acute organ damage

Emergency Department Presentations:

• Common presentation, but most are urgencies inappropriately treated as emergencies
• Estimated 500,000 ED visits annually for hypertensive crisis in the United States
• Hospital admission rate approximately 30% for hypertensive crisis presentations

Mortality Trends:

• Historical mortality: 80-90% one-year mortality for untreated malignant hypertension [9]
• Modern treated mortality: 5-year survival > 80% with appropriate therapy
• In-hospital mortality for hypertensive emergency: 5-10% depending on organ involved
• Aortic dissection carries highest mortality if blood pressure not controlled rapidly

Demographics

Age Distribution:

• Can occur at any age but peak incidence 40-60 years
• Younger patients (20-40 years): Often secondary causes (drugs, pregnancy, renal disease)
• Older patients (> 60 years): Usually long-standing inadequately controlled essential hypertension
• Geriatric patients: Higher risk of complications from treatment due to impaired autoregulation

Sex Differences:

• Male predominance in most studies (male:female ratio approximately 2:1)
• Women of childbearing age: Pregnancy-related hypertensive emergencies (pre-eclampsia/eclampsia)
• Post-menopausal women: Increased incidence of hypertensive emergencies

Ethnic and Racial Variations:

• Higher incidence in Black/African American populations [10]
• Black patients: Earlier onset, more severe target organ damage, worse outcomes
• Hispanic populations: Intermediate risk between Black and White populations
• Asian populations: Lower overall incidence but rising with urbanisation

Risk Factors

Patient-Related Factors

Precipitating Causes

Target Organs at Risk

The pattern of organ involvement determines clinical presentation, treatment urgency, and prognosis:

Multi-Organ Involvement:

• Approximately 30-40% of hypertensive emergencies involve more than one organ system
• Concurrent brain and cardiac involvement carries worst prognosis
• Sequential organ involvement (e.g., initial renal injury followed by cardiac decompensation) common

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Pathophysiology

Overview of Pressure-Induced Injury

The pathophysiology of hypertensive emergency involves a complex interplay of mechanical vascular injury, endothelial dysfunction, activation of inflammatory and coagulation cascades, and failure of normal autoregulatory mechanisms. [12] The transition from chronic hypertension to acute hypertensive emergency occurs when adaptive mechanisms fail and acute organ damage ensues.

Mechanism of End-Organ Damage

1. Failure of Autoregulation

Cerebral Autoregulation:

• Normal cerebral blood flow maintained across MAP range of 60-150 mmHg
• Chronic hypertension shifts autoregulatory curve rightward (adaptation)
• Severe acute hypertension exceeds upper limit of autoregulation
• Hyperperfusion → Endothelial breakdown → Vasogenic oedema → Hypertensive encephalopathy
• Rapid BP reduction causes hypoperfusion → Watershed ischaemia → Stroke

Renal Autoregulation:

• Afferent arteriole constriction maintains GFR across wide BP range
• Severe hypertension exceeds autoregulatory capacity
• Glomerular hyperperfusion → Endothelial injury → Proteinuria, haematuria
• Arteriolar necrosis → Acute kidney injury → RAAS activation → Vicious cycle

Coronary Autoregulation:

• Myocardial perfusion occurs during diastole
• Severe hypertension increases afterload → Increased myocardial oxygen demand
• Decreased diastolic perfusion time → Myocardial ischaemia
• LV hypertrophy from chronic HTN → Further oxygen supply-demand mismatch

2. Endothelial Injury and Vascular Damage

Acute Endothelial Dysfunction:

• Mechanical shear stress from elevated pressure damages endothelium [13]
• Loss of endothelial barrier function → Plasma protein extravasation
• Decreased nitric oxide production → Impaired vasodilation
• Increased endothelin-1 → Further vasoconstriction
• Platelet adhesion and activation → Microthrombi formation

Fibrinoid Necrosis:

• Hallmark pathological finding in malignant hypertension
• Necrotising arteriolitis with fibrin deposition in vessel walls
• Affects arterioles in kidney (most common), brain, retina, heart
• Leads to luminal narrowing → Ischaemia → Further organ damage

Inflammatory Cascade:

• Endothelial injury activates inflammatory pathways
• Increased vascular permeability → Oedema formation
• Leucocyte adhesion and infiltration
• Release of reactive oxygen species → Oxidative stress
• Production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α)

3. Activation of Renin-Angiotensin-Aldosterone System (RAAS)

Vicious Cycle of RAAS Activation:

• Renal hypoperfusion from arteriolar necrosis → Renin release
• Angiotensin II production → Systemic and renal vasoconstriction
• Aldosterone secretion → Sodium retention → Volume expansion
• Further pressure elevation → Worsening organ damage
• ACE inhibitors can precipitate acute kidney injury if bilateral renal artery stenosis

4. Microangiopathic Haemolytic Anaemia (MAHA)

Mechanism:

• Intravascular fibrin deposition from endothelial damage
• Mechanical fragmentation of erythrocytes as they pass through damaged microvasculature
• Results in schistocytes on blood film, elevated LDH, decreased haptoglobin
• Thrombocytopenia from platelet consumption in microthrombi
• Can progress to thrombotic microangiopathy (TMA)

Organ-Specific Pathophysiology

Hypertensive Encephalopathy and PRES

Clinical and Pathophysiological Features:

• Loss of cerebral autoregulation → Hyperperfusion → Breakdown of blood-brain barrier [14]
• Vasogenic oedema predominantly in posterior circulation (parieto-occipital regions)
• Posterior reversible encephalopathy syndrome (PRES) is neuroimaging correlate
• Clinical features: Headache, confusion, visual disturbances, seizures, focal neurological signs
• Reversibility: Complete recovery possible if blood pressure controlled promptly
• Irreversibility: Delayed treatment → Infarction, permanent neurological deficit

MRI Findings:

• T2/FLAIR hyperintensity in posterior cerebral hemispheres
• Symmetric white matter oedema in parieto-occipital and posterior frontal regions
• Sparing of calcarine and paramedian structures
• Enhancement on contrast administration indicates blood-brain barrier breakdown

Hypertensive Retinopathy

Keith-Wagener-Barker Classification:

Clinical Significance:

• Papilloedema (Grade IV) is pathognomonic for malignant hypertension
• Presence of papilloedema indicates hypertensive emergency by definition
• Cotton-wool spots: Retinal nerve fibre layer infarcts from arteriolar occlusion
• Hard exudates: Lipid deposition from chronic oedema
• Visual symptoms: Blurred vision, scotomas, rarely complete visual loss

Acute Cardiac Complications

Acute Pulmonary Oedema:

• Sudden increase in afterload → Acute LV decompensation
• Diastolic dysfunction from LV hypertrophy → Impaired filling
• Elevated LVEDP → Increased pulmonary capillary wedge pressure → Pulmonary oedema
• Flash pulmonary oedema: Rapid onset (less than 1 hour) suggests renal artery stenosis or diastolic dysfunction

Acute Coronary Syndrome:

• Increased myocardial oxygen demand from elevated afterload
• Decreased coronary perfusion from reduced diastolic time
• Coronary artery spasm from endothelial dysfunction
• Plaque rupture from shear stress in underlying atherosclerotic disease

Acute Kidney Injury

Mechanisms:

• Acute tubular necrosis from ischaemia
• Thrombotic microangiopathy in glomeruli
• Arteriolar necrosis → Cortical necrosis (severe cases)
• Proteinuria, haematuria, red cell casts indicate glomerular damage

Laboratory Features:

• Rapidly rising creatinine (> 25% increase or > 0.5 mg/dL)
• Bland urinary sediment OR active sediment with RBC casts
• Proteinuria (can be nephrotic range in severe cases)
• Electrolyte abnormalities: Hyperkalaemia, metabolic acidosis

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Emergency Management

Initial Approach

Immediate Priorities (First 5 Minutes):

1. Assess airway, breathing, circulation — Ensure patient stability
2. Obtain vital signs — Blood pressure in both arms, heart rate, oxygen saturation, temperature
3. Rapid focused history — Symptoms of organ damage, medication history, drug use
4. Brief examination — Neurological status, cardiac auscultation, pulmonary examination, fundoscopy
5. ECG and establish IV access — Immediate investigations

Simultaneous Actions:

• Place patient on continuous cardiac monitoring
• Obtain large-bore intravenous access
• Draw blood for urgent investigations (see Investigations section)
• Initiate continuous blood pressure monitoring (arterial line if available)
• Prepare for ICU/HDU admission

Step 1: Confirm End-Organ Damage

The diagnosis of hypertensive emergency requires evidence of acute target organ damage. Perform targeted assessment based on presentation:

Neurological Assessment

Clinical Features to Identify:

• Hypertensive encephalopathy: Headache, confusion, altered consciousness, seizures, visual changes
• Ischaemic stroke: Focal neurological deficit, aphasia, hemiparesis, facial droop
• Haemorrhagic stroke: Severe headache, vomiting, decreased consciousness, focal deficit
• PRES: Headache, visual disturbances, seizures, confusion (clinically indistinguishable from encephalopathy)

Urgent Neuroimaging:

• CT head (non-contrast): First-line to exclude haemorrhage, perform within 30 minutes
• MRI brain (if available): Superior for PRES diagnosis, shows vasogenic oedema

Cardiac Assessment

Clinical Features:

• Acute coronary syndrome: Chest pain, dyspnoea, diaphoresis
• Acute pulmonary oedema: Severe dyspnoea, orthopnoea, pink frothy sputum
• Aortic dissection: Tearing chest/back pain, BP differential between arms > 20 mmHg

Urgent Investigations:

• ECG: ST elevation/depression, T wave inversion, LV strain pattern
• Troponin: Elevated in ACS (but also elevated in renal failure and severe hypertension without ACS)
• Chest X-ray: Pulmonary oedema, cardiomegaly, widened mediastinum (dissection)
• CT aortogram or TOE: If aortic dissection suspected — URGENT

Renal Assessment

Clinical Features:

• Oliguria or anuria
• Haematuria (visible or microscopic)
• Peripheral oedema, fluid overload

Investigations:

• Urine dipstick: Proteinuria, haematuria (perform immediately)
• Urine microscopy: RBC casts (glomerular disease), WBC casts (interstitial nephritis)
• U&Es: Rising creatinine, hyperkalaemia

Ophthalmological Assessment

Fundoscopy (Essential in All Cases):

• Perform dilated fundoscopy in all patients with suspected hypertensive emergency
• Papilloedema: Blurred disc margins, disc elevation, absent venous pulsation
• Retinal haemorrhages: Flame-shaped (superficial) or dot-blot (deep)
• Cotton-wool spots: Soft exudates from nerve fibre layer infarction
• Hard exudates: Lipid deposits, often forming macular star
• Grade IV retinopathy (papilloedema) = malignant hypertension = hypertensive emergency

Step 2: Determine Target Blood Pressure and Timeline

Blood pressure reduction targets and timelines are condition-specific. [15] One size does NOT fit all:

General Approach (Most Hypertensive Emergencies)

Critical Principle: Do NOT normalize blood pressure rapidly in most hypertensive emergencies — gradual reduction over hours prevents watershed infarction.

Condition-Specific Targets and Timelines

Step 3: Select Appropriate Intravenous Antihypertensive

First-Line Agents

Labetalol (Alpha and Beta Blocker)

• Mechanism: Non-selective beta-blocker with alpha-1 blockade (ratio β:α = 7:1)
• Dosing:
  • "IV bolus: 20 mg over 2 minutes, then 20-80 mg every 10 minutes (max cumulative 300 mg)"
  • "IV infusion: 0.5-2 mg/min, titrate to effect (max 300 mg total)"
• Onset: 5-10 minutes
• Duration: 3-6 hours
• Advantages: Predictable BP reduction, does not increase ICP, safe in pregnancy
• Contraindications: Asthma, COPD, heart block, severe bradycardia, acute heart failure (decompensated)
• Use in: General hypertensive emergencies, pre-eclampsia, most neurological emergencies
• Avoid in: Aortic dissection as sole agent (use esmolol), cocaine intoxication (theoretical concern)

Nicardipine (Dihydropyridine Calcium Channel Blocker)

• Mechanism: Arterial vasodilation, no effect on venous capacitance
• Dosing: Start 5 mg/hr IV, increase by 2.5 mg/hr every 5-15 minutes (max 15 mg/hr)
• Onset: 5-15 minutes
• Duration: 4-6 hours after stopping infusion
• Advantages: Cerebral and coronary vasodilation, preserves renal blood flow, no effect on ICP
• Contraindications: Severe aortic stenosis, advanced heart failure
• Use in: Acute ischaemic stroke (preferred), haemorrhagic stroke, most emergencies [19]
• Avoid in: Aortic dissection (reflex tachycardia without beta-blockade)

Sodium Nitroprusside (Nitric Oxide Donor)

• Mechanism: Arterial and venous vasodilation via NO release
• Dosing: Start 0.25-0.5 mcg/kg/min, titrate by 0.5 mcg/kg/min every 3-5 min (max 10 mcg/kg/min)
• Onset: Immediate (30-60 seconds)
• Duration: 1-2 minutes after stopping (very short half-life)
• Advantages: Immediate, titratable, potent
• Disadvantages: Requires arterial line monitoring, light-sensitive, cyanide/thiocyanate toxicity (> 24-48 hours use or renal failure)
• Contraindications: High ICP (increases cerebral blood flow), pregnancy, severe renal/hepatic impairment
• Use in: When rapid titratable control needed (e.g., aortic dissection with beta-blocker)
• Avoid in: Acute stroke (increases ICP), prolonged use (toxicity risk)

Clevidipine (Ultra-Short-Acting Dihydropyridine)

• Mechanism: Arterial vasodilation, rapidly metabolised by plasma esterases
• Dosing: Start 1-2 mg/hr, titrate by doubling dose every 90 seconds (max 32 mg/hr)
• Onset: 2-4 minutes
• Duration: 5-15 minutes after stopping (rapid offset)
• Advantages: Rapid onset/offset, precise titration, no organ metabolism (safe in renal/hepatic failure)
• Contraindications: Egg/soy allergy (lipid emulsion), severe aortic stenosis, acute pancreatitis
• Use in: Aortic dissection (with beta-blocker), perioperative hypertension, when precise control needed
• Monitoring: Check triglycerides if prolonged use (lipid emulsion)

Glyceryl Trinitrate (GTN / Nitroglycerin)

• Mechanism: Venodilation > arterial dilation, reduces preload
• Dosing: Start 5-10 mcg/min, increase by 5-10 mcg/min every 3-5 minutes (max 200 mcg/min)
• Onset: 2-5 minutes
• Duration: 5-10 minutes after stopping
• Advantages: Coronary vasodilation, reduces preload (excellent for pulmonary oedema)
• Contraindications: Phosphodiesterase inhibitor use (sildenafil, tadalafil) within 24-48 hours, RV infarction, severe aortic stenosis
• Use in: Acute coronary syndrome, acute pulmonary oedema [20]
• Side effects: Headache, tolerance with prolonged use, methaemoglobinaemia (rare)

Second-Line and Specialist Agents

Esmolol (Ultra-Short-Acting Beta-1 Blocker)

• Mechanism: Selective beta-1 antagonism, reduces HR and contractility
• Dosing: Loading 500 mcg/kg over 1 minute, then 50-300 mcg/kg/min infusion
• Onset: 60 seconds
• Duration: 10-20 minutes (very short half-life)
• Use in: Aortic dissection (FIRST agent), sympathomimetic crisis, perioperative hypertension
• Advantages: Reduces HR and dP/dt (critical in dissection), rapid offset allows titration
• Always combine with vasodilator after HR controlled to achieve BP target

Hydralazine

• Mechanism: Direct arterial vasodilation
• Dosing: 5-10 mg IV bolus every 20-30 minutes (max 20 mg)
• Onset: 10-20 minutes
• Duration: 3-8 hours (unpredictable)
• Disadvantages: Unpredictable response, reflex tachycardia, can worsen angina
• Use in: Pre-eclampsia/eclampsia (safe in pregnancy), when other agents unavailable
• Avoid in: Aortic dissection (reflex tachycardia), ACS (increases myocardial oxygen demand)

Fenoldopam (Dopamine-1 Agonist)

• Mechanism: Peripheral arterial vasodilation, increases renal blood flow
• Dosing: Start 0.1 mcg/kg/min, increase by 0.1 mcg/kg/min every 15 minutes (max 1.6 mcg/kg/min)
• Onset: 10 minutes
• Duration: 30 minutes after stopping
• Advantages: Preserves/improves renal perfusion, useful in renal impairment
• Use in: Hypertensive emergency with acute kidney injury
• Side effects: Hypokalaemia, increased intraocular pressure (glaucoma risk)

Phentolamine (Alpha Blocker)

• Mechanism: Non-selective alpha-adrenergic antagonism
• Dosing: 5-10 mg IV bolus every 5-15 minutes
• Onset: 1-2 minutes
• Duration: 10-30 minutes
• Use in: Phaeochromocytoma crisis, sympathomimetic drug intoxication, MAOI crisis
• Must give BEFORE beta-blocker in phaeochromocytoma (prevent unopposed alpha-mediated vasoconstriction)

Transition to Oral Therapy

When to Transition:

• Blood pressure stabilized for 12-24 hours
• Acute organ damage resolving or stable
• Patient able to take oral medications
• No ongoing need for minute-to-minute titration

Transition Strategy:

• Start oral agents 1-2 hours before stopping IV agents
• Choose long-acting agents (amlodipine, long-acting ACE inhibitors/ARBs)
• Overlap IV and oral therapy to prevent rebound hypertension
• Monitor closely for 24 hours after IV discontinuation

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Clinical Assessment

History

Symptoms of End-Organ Damage (CRITICAL to Elicit)

Neurological:

• Headache (severe, different from usual headaches)
• Visual disturbances (blurred vision, scotomas, diplopia, transient visual loss)
• Confusion, altered mental status, difficulty concentrating
• Seizures (new-onset)
• Focal weakness, numbness, speech difficulties (stroke)
• Dizziness, vertigo

Cardiac:

• Chest pain or pressure (ischaemia)
• Severe dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea (pulmonary oedema)
• Palpitations

Vascular:

• Severe tearing or ripping chest pain radiating to back (aortic dissection)
• Back pain, abdominal pain (dissection extension)

Renal:

• Reduced urine output, oliguria
• Haematuria (visible or tea-coloured urine)
• Peripheral oedema

General:

• Nausea, vomiting (raised ICP, encephalopathy)
• Epistaxis (rarely significant)

Medication History

Essential Questions:

• Current antihypertensive medications and doses
• Recent medication changes or cessation
• Compliance: "Do you take your blood pressure tablets every day?" (non-judgmental)
• Recent missed doses or ran out of medications
• Over-the-counter medications: NSAIDs (fluid retention), decongestants (sympathomimetic)
• Herbal supplements: Liquorice (pseudohyperaldosteronism), ephedra

Drug and Substance Use

Critical to Ask About:

• Cocaine, crack cocaine (most common)
• Amphetamines, methamphetamine
• Synthetic cathinones ("bath salts")
• MDMA (ecstasy)
• Alcohol use and recent cessation (withdrawal)
• Energy drinks (high caffeine content)

Pregnancy History (Women of Childbearing Age)

• Last menstrual period, possibility of pregnancy
• Known pregnancy (gestational age)
• Symptoms of pre-eclampsia: Headache, visual changes, right upper quadrant pain, oedema
• History of pre-eclampsia or eclampsia in previous pregnancies

Past Medical History

Secondary Hypertension Red Flags:

• Renal disease (CKD, previous AKI)
• Endocrine disorders (Cushing's, Conn's, phaeochromocytoma)
• Autoimmune disease (SLE, scleroderma)
• Obstructive sleep apnoea
• Coarctation of aorta (young patient, differential BP arm-leg)

Family History

• Family history of early-onset hypertension
• Polycystic kidney disease
• Phaeochromocytoma or MEN syndromes

Physical Examination

Vital Signs (Essential)

Blood Pressure Measurement:

• Measure in BOTH arms (difference > 20 mmHg suggests aortic dissection or coarctation)
• Repeat to confirm accuracy
• Use appropriately sized cuff (obese patients need large cuff)
• Document BP in both supine and standing if volume status uncertain

Other Vital Signs:

• Heart rate: Tachycardia (pain, anxiety, reflex from vasodilators), bradycardia (beta-blockers, heart block)
• Respiratory rate: Tachypnoea suggests pulmonary oedema or metabolic acidosis
• Oxygen saturation: Hypoxia in pulmonary oedema
• Temperature: Hyperthermia in sympathomimetic crisis

Cardiovascular Examination

Inspection:

• Jugular venous pressure (elevated in volume overload, heart failure)
• Peripheral oedema (volume overload)
• Cyanosis (pulmonary oedema)

Palpation:

• Radial pulse: Rate, rhythm, character
• Femoral pulses: Delayed or absent in coarctation or aortic dissection
• Radio-femoral delay (coarctation)
• Apex beat: Displaced (cardiomegaly), heaving (LV hypertrophy)

Auscultation:

• S1, S2: Normal, split S2
• S3 gallop (heart failure, volume overload)
• S4 gallop (LV hypertrophy, diastolic dysfunction — common in chronic hypertension)
• Murmurs: Aortic regurgitation (diastolic murmur — dissection involving aortic root), mitral regurgitation
• Carotid bruits (atherosclerotic disease)
• Abdominal bruits (renal artery stenosis)

Respiratory Examination

Auscultation:

• Bibasal fine crackles (pulmonary oedema)
• Bronchial breathing (consolidation)
• Wheeze (bronchospasm, cocaine-induced)

Neurological Examination

Conscious Level:

• Glasgow Coma Scale (GCS)
• Alert, confused, drowsy, stupor, coma

Cranial Nerves:

• Visual acuity (retinal involvement)
• Visual fields (hemianopia in stroke, cortical blindness in PRES)
• Pupillary responses (asymmetry in focal lesion, small pupils in pontine haemorrhage)
• Facial symmetry (facial droop in stroke)

Motor Examination:

• Tone, power (hemiparesis in stroke)
• Reflexes (hyperreflexia in acute UMN lesion)
• Plantar response (upgoing in UMN lesion)

Sensory Examination:

• Sensory level (spinal cord involvement if dissection extends)
• Hemisensory loss (stroke)

Cerebellar Signs:

• Ataxia, intention tremor, dysdiadochokinesis, nystagmus (posterior circulation stroke)

Fundoscopy (MANDATORY in All Suspected Cases)

Technique:

• Dilate pupils if no contraindication (do NOT delay if urgent)
• Examine optic disc, vessels, macula, peripheral retina

Findings:

Papilloedema Features:

• Blurred disc margins
• Disc elevation (obscures retinal vessels crossing disc)
• Absent venous pulsation
• Peripapillary haemorrhages
• Engorged, tortuous veins

Abdominal Examination

Palpation:

• Palpable kidneys (polycystic kidney disease, hydronephrosis)
• Epigastric or periumbilical bruit (renal artery stenosis, aortic dissection)
• Bladder distension (urinary retention with renal failure)

Auscultation:

• Renal artery bruits (lateral to midline, above umbilicus)

Peripheral Vascular Examination

• Radial, brachial, femoral, popliteal, dorsalis pedis, posterior tibial pulses
• Absent or diminished pulses suggest aortic dissection with branch vessel involvement
• Cool, mottled extremities (aortic dissection with limb ischaemia)

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Investigations

Bedside Investigations (Immediate)

Laboratory Investigations (Urgent — Within 30 Minutes)

Urine Studies

Imaging Studies

Neuroimaging

CT Head (Non-Contrast) — URGENT if Neurological Symptoms:

• Indications: Altered consciousness, focal neurology, severe headache, seizures
• Findings:
  • "Intracerebral haemorrhage: Hyperdense lesion"
  • "Ischaemic stroke: Hypodense area (may be subtle acutely), loss of grey-white differentiation"
  • "Subarachnoid haemorrhage: Blood in subarachnoid space"
  • "Cerebral oedema: Loss of sulci, compressed ventricles"
• Perform within 30 minutes if stroke suspected

MRI Brain (If Available and Patient Stable):

• Superior for PRES diagnosis: T2/FLAIR hyperintensity in parieto-occipital regions
• DWI sequence: Distinguishes vasogenic (PRES — no restriction) from cytotoxic (infarction — restriction) oedema
• Better for detecting subtle infarcts, posterior fossa lesions

Cardiovascular Imaging

Chest X-Ray:

• Findings:
  • "Pulmonary oedema: Bat's wing pattern, Kerley B lines, pleural effusions, cardiomegaly"
  • "Widened mediastinum (> 8 cm at T4 level): Aortic dissection (insensitive, not reliable)"
  • "Cardiomegaly: Cardiothoracic ratio > 0.5 (chronic hypertension)"
  • "Rib notching: Coarctation of aorta"

CT Aortogram (With IV Contrast) — URGENT if Aortic Dissection Suspected:

• Indications: Tearing chest/back pain, BP differential between arms > 20 mmHg, new aortic regurgitation murmur
• Findings: Intimal flap, false lumen, thrombosis
• Sensitivity > 95%, rapid acquisition
• Alternative: Transoesophageal echocardiography (TOE) if CT unavailable or contraindicated

Echocardiography:

• Transthoracic echo (TTE): LV hypertrophy, LV systolic dysfunction, diastolic dysfunction, valve abnormalities
• Transoesophageal echo (TOE): Superior for aortic dissection diagnosis, assessment of aortic valve

Cardiac Biomarkers:

• Troponin: Detects myocardial injury (ACS, demand ischaemia)
• BNP/NT-proBNP: Elevated in acute heart failure

Renal Imaging

Renal Ultrasound:

• Kidney size: Small kidneys (chronic renal disease), asymmetry (renal artery stenosis)
• Hydronephrosis: Urinary obstruction
• Increased cortical echogenicity: Chronic kidney disease
• Polycystic kidneys: Multiple cysts

CT/MR Angiography (Non-Urgent, for Secondary Cause Investigation):

• Renal artery stenosis assessment (for future management, NOT in acute phase)

Investigations for Secondary Hypertension (Not Urgent — Perform After Stabilisation)

These investigations should be performed AFTER the acute emergency is managed:

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Definitions and Classification

Hypertensive Crisis Spectrum

Important Note: The terms "malignant" and "accelerated" hypertension are older classifications based on retinopathy findings. Modern practice focuses on identifying specific target organ damage (stroke, MI, AKI, etc.) rather than using these historical terms.

Common Hypertensive Emergencies and Key Features

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Differential Diagnosis

When evaluating a patient with severe hypertension, consider:

Hypertensive Urgency vs Emergency

Key Distinction: Presence or absence of acute target organ damage

Hypertensive Urgency:

• Severely elevated BP (typically > 180/120 mmHg)
• NO symptoms or signs of acute organ damage
• Patient may be asymptomatic or have non-specific symptoms (mild headache, anxiety)
• Normal neurological examination, no chest pain, no dyspnoea, no visual changes
• Management: Oral antihypertensives, outpatient follow-up in 24-48 hours
• Do NOT admit or give IV agents — causes more harm than benefit

Pitfall: Many patients labelled as "hypertensive emergency" in ED are actually urgencies — resist overtreatment

Secondary Causes of Hypertensive Emergency

Investigate for secondary causes, especially in:

• Young patients (less than 40 years)
• Sudden onset severe hypertension
• Resistant hypertension (inadequate control on 3+ agents)
• Biochemical abnormalities (hypokalaemia, metabolic alkalosis)

Common Secondary Causes:

Mimics of Hypertensive Emergency

"White Coat" Hypertension:

• Elevated BP in healthcare setting, normal at home
• No evidence of chronic hypertension (no LVH on ECG, normal fundoscopy)
• Management: Reassure, arrange ambulatory BP monitoring, do NOT treat acutely

Pain or Anxiety-Induced Hypertension:

• BP elevation secondary to pain (e.g., renal colic) or severe anxiety
• Treat underlying cause (analgesia, anxiolytics)
• BP normalizes once pain/anxiety controlled

Pseudohypertension:

• Falsely elevated cuff BP in elderly with stiff, calcified arteries
• Osler's manoeuvre: Palpable radial artery despite cuff inflation above systolic BP
• Consider intra-arterial BP measurement if suspected

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Treatment Approach

Hypertensive Emergency — General Principles

1. Admit to ICU or HDU — Continuous monitoring essential
2. Establish IV access — Large-bore cannula
3. Continuous BP monitoring — Arterial line if available (preferred for minute-to-minute monitoring)
4. Identify target organ damage — Directs choice of agent and BP target
5. Select appropriate IV antihypertensive — Based on specific emergency type
6. Gradual controlled BP reduction — Typically reduce MAP by 10-15% in first hour (except aortic dissection)
7. Frequent reassessment — Monitor for complications of treatment (hypotension, ischaemia)
8. Transition to oral therapy — Once stabilised, overlap IV and oral agents
9. Investigate secondary causes — After acute management

Hypertensive Urgency — General Principles

1. Do NOT admit — Outpatient management appropriate
2. Do NOT use IV agents — Oral therapy over 24-48 hours
3. Initiate or reinforce oral antihypertensives
4. Address non-compliance — Education, simplify regimen, address barriers
5. Arrange urgent follow-up — Within 24-48 hours with GP or hypertension clinic
6. Exclude secondary causes — If young, resistant, or biochemical clues

Common Mistake: Giving IV labetalol or other IV agents for hypertensive urgency — this is unnecessary and risks harm

Specific Clinical Scenarios

Aortic Dissection [16]

Immediate Goals:

• Reduce SBP to less than 120 mmHg within 20 minutes
• Reduce heart rate to less than 60 bpm
• Reduce dP/dt (rate of pressure change) to prevent propagation

Treatment Algorithm:

1. FIRST: Beta-blocker to reduce HR and dP/dt
   • Esmolol: 500 mcg/kg bolus over 1 minute, then 50-200 mcg/kg/min infusion
   • OR Labetalol: 20 mg IV bolus, then 1-2 mg/min infusion
2. SECOND: Add vasodilator to achieve BP target (once HR controlled)
   • Sodium nitroprusside: 0.25-10 mcg/kg/min
   • OR Clevidipine: 1-16 mg/hr

Critical Error to Avoid: NEVER give vasodilator before beta-blocker — reflex tachycardia increases dP/dt and propagates dissection

Definitive Management:

• Type A dissection (ascending aorta): Emergency surgery
• Type B dissection (descending aorta): Medical management unless complicated

Acute Ischaemic Stroke [17]

General Principle: Permissive hypertension — elevated BP maintains perfusion to ischaemic penumbra

Blood Pressure Thresholds:

Rationale: Ischaemic penumbra depends on elevated BP for collateral perfusion — lowering BP extends infarct

Intracerebral Haemorrhage [18]

INTERACT2 Trial Evidence:

• Intensive BP lowering (SBP target 140 mmHg) is safe
• May improve functional outcomes
• Should be initiated within 6 hours of symptom onset

Target:

• SBP 140-160 mmHg within 1 hour

Agents:

• Labetalol: 10-20 mg IV bolus every 10 minutes
• Nicardipine: 5-15 mg/hr infusion

Contraindications to Aggressive BP Lowering:

• Large haematoma with mass effect
• Planned surgical evacuation
• Infratentorial haemorrhage with hydrocephalus

Acute Coronary Syndrome

Goals:

• Reduce myocardial oxygen demand
• Improve coronary perfusion
• Reduce preload and afterload

First-Line Agent:

• GTN (nitroglycerin): 5-200 mcg/min IV infusion
  • Reduces preload (venodilation)
  • Coronary vasodilation
  • "Contraindications: RV infarction, severe aortic stenosis, phosphodiesterase inhibitor use (sildenafil, tadalafil)"

Alternative:

• Labetalol (if tachycardic)
• Nicardipine (if GTN insufficient)

Concurrent Management:

• Aspirin, antiplatelet therapy, anticoagulation (per ACS guidelines)
• Cardiology referral for PCI vs medical management

Acute Pulmonary Oedema

Goals:

• Reduce preload (venodilation)
• Reduce afterload
• Improve oxygenation

First-Line Agent:

• GTN: 5-200 mcg/min IV
  • Rapid venodilation reduces preload
  • Reduces pulmonary capillary wedge pressure

Adjunctive Therapy:

• High-flow oxygen or CPAP/BiPAP
• IV furosemide: 40-80 mg bolus (if volume overloaded)
• Consider morphine: 2.5-5 mg IV (reduces anxiety, venodilation) — use cautiously

Alternative Agents:

• Clevidipine: If additional afterload reduction needed
• Avoid beta-blockers in acute decompensated heart failure

Pre-eclampsia and Eclampsia

Diagnostic Criteria (Pre-eclampsia):

• BP ≥140/90 mmHg after 20 weeks gestation
• PLUS proteinuria (≥300 mg/24 hours or protein:creatinine ratio > 30 mg/mmol)
• OR end-organ dysfunction (AKI, thrombocytopenia, elevated transaminases, pulmonary oedema, cerebral symptoms)

Severe Pre-eclampsia:

• BP ≥160/110 mmHg
• Symptoms: Severe headache, visual disturbance, epigastric pain
• Laboratory: Thrombocytopenia, elevated creatinine, elevated transaminases (HELLP syndrome)

Eclampsia:

• Pre-eclampsia + seizures (tonic-clonic, generalised)

Management:

Magnesium Sulfate:

• Prevents and treats eclamptic seizures
• More effective than phenytoin or benzodiazepines for eclampsia
• Monitor for magnesium toxicity: Reduced reflexes, respiratory depression, cardiac arrest
• Antidote: Calcium gluconate 10% 10 mL IV

Timing of Delivery:

• Severe pre-eclampsia: Deliver at ≥34 weeks (with corticosteroids for fetal lung maturity if less than 34 weeks)
• Eclampsia: Stabilise mother, then deliver regardless of gestational age

Phaeochromocytoma Crisis [11]

Clinical Features:

• Episodic severe hypertension
• Classic triad: Headache, palpitations, diaphoresis (sweating)
• Pallor, tremor, anxiety
• Hyperglycaemia (catecholamine-induced)

CRITICAL Management Principle:

• NEVER give beta-blocker first — causes unopposed alpha-mediated vasoconstriction and worsens crisis

Treatment Algorithm:

1. FIRST: Alpha-blocker
   • Phentolamine: 5-10 mg IV bolus every 5-15 minutes
   • OR Phenoxybenzamine (oral): 10 mg BD, increase gradually (not in acute crisis)
2. SECOND: Beta-blocker (only after adequate alpha-blockade)
   • Labetalol (has both alpha and beta blockade, can be used alone)
   • OR Esmolol infusion

Investigations:

• Plasma metanephrines (highly sensitive)
• 24-hour urine metanephrines and catecholamines
• CT/MRI abdomen (adrenal mass)
• MIBG scan (nuclear medicine imaging)

Definitive Treatment:

• Surgical resection of phaeochromocytoma (after 10-14 days of alpha-blockade)

Sympathomimetic Drug Intoxication (Cocaine, Amphetamines)

Clinical Features:

• Agitation, aggression, psychosis
• Severe hypertension, tachycardia
• Hyperthermia
• Seizures
• Myocardial ischaemia (cocaine-induced vasospasm)

Management:

Rationale for Benzodiazepines:

• Reduce sympathetic outflow
• Often sufficient to control BP and HR without antihypertensives
• Prevent seizures

Post-Acute Management

Once the acute hypertensive emergency is controlled and the patient is stabilised:

Investigate for Secondary Causes

Indications for Secondary Hypertension Workup:

• Age less than 40 years with severe hypertension
• Resistant hypertension (uncontrolled on 3+ agents including diuretic)
• Sudden onset or worsening of previously controlled hypertension
• Biochemical clues (hypokalaemia, metabolic alkalosis, hyperglycaemia)
• Abdominal bruit, asymmetric kidney size

Investigations (as outlined in Differential Diagnosis section)

Optimise Long-Term Antihypertensive Regimen

Principles:

• Use guideline-recommended agents (ACEi/ARB, CCB, thiazide diuretic)
• Simplify regimen (once-daily dosing, combination pills)
• Address barriers to compliance (cost, side effects, understanding)
• Set realistic BP targets (less than 140/90 mmHg, less than 130/80 if diabetes or CKD)

Follow-Up:

• Weekly BP checks initially
• Adjust medications based on response
• Once stable, monthly then 3-monthly follow-up

Lifestyle Modification

Evidence-Based Interventions:

• Dietary sodium restriction (less than 2 g/day or less than 5 g salt/day)
• DASH diet (Dietary Approaches to Stop Hypertension)
• Weight loss (target BMI less than 25 kg/m²)
• Regular aerobic exercise (150 min/week moderate intensity)
• Alcohol moderation (≤2 drinks/day men, ≤1 drink/day women)
• Smoking cessation

Patient Education

Key Messages:

• Importance of medication adherence — never stop suddenly
• Home BP monitoring
• Recognition of warning symptoms (headache, chest pain, dyspnoea)
• When to seek emergency care

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Complications

Complications of Hypertensive Emergency (Untreated or Under-Treated)

Complications of Treatment (Over-Aggressive BP Reduction)

Key Principle: In most hypertensive emergencies, overly aggressive BP reduction causes MORE harm than the elevated BP itself.

Drug-Specific Complications

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Prognosis

Acute Mortality

Untreated Hypertensive Emergency:

• Historical data (pre-effective antihypertensive era): 80-90% one-year mortality for malignant hypertension [9]
• Acute aortic dissection: 50% mortality if untreated

Treated Hypertensive Emergency:

• In-hospital mortality: 5-10% (varies by organ involved and comorbidities)
• Aortic dissection (treated): 10-20% mortality despite treatment
• Intracerebral haemorrhage: 30-50% mortality at 30 days
• Hypertensive encephalopathy/PRES: less than 5% mortality if treated appropriately

Long-Term Outcomes

Survival:

• 5-year survival with modern treatment: > 80% [9]
• Depends on extent of organ damage and compliance with long-term therapy

Organ Function Recovery:

Chronic Kidney Disease:

• Approximately 30-40% of patients with hypertensive emergency develop or worsen CKD
• 10-15% progress to end-stage renal disease requiring dialysis

Cardiovascular Risk:

• Patients with history of hypertensive emergency have significantly elevated long-term CV risk
• Increased risk of stroke, MI, heart failure
• Lifelong aggressive BP control and CV risk modification essential

Recurrence

Risk of Recurrent Hypertensive Emergency:

• 10-20% recurrence rate within 5 years
• Usually due to medication non-compliance or inadequate BP control

Prevention of Recurrence:

• Strict medication adherence
• Regular BP monitoring (home BP monitoring encouraged)
• Lifestyle modification
• Address barriers to compliance (cost, side effects, understanding)
• Multidisciplinary care (GP, cardiologist, nephrologist as appropriate)

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Evidence & Guidelines

Key Guidelines

1. Williams B, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal. 2018;39(33):3021-3104. [1]

   • European Society of Cardiology / European Society of Hypertension
   • Comprehensive guideline covering all aspects of hypertension including emergencies

2. NICE NG136: Hypertension in adults: diagnosis and management. 2019. Updated 2024. [2]

   • UK National Institute for Health and Care Excellence guideline
   • Pragmatic approach to hypertensive emergencies in NHS setting

3. Whelton PK, et al. 2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. JACC. 2018;71(19):e127-e248. [4]

   • American College of Cardiology / American Heart Association guideline
   • Defines BP targets and management strategies

4. Peixoto AJ. Acute severe hypertension. NEJM. 2019;381:1843-1852. [3]

   • Comprehensive review of hypertensive crises
   • Evidence-based approach to differentiation and management

5. Potter BJ, et al. Management of hypertensive crisis: British and Irish Hypertension Society guideline. J Hum Hypertens. 2022;36:348-355. [5]

   • Recent UK/Ireland guideline specifically for hypertensive crisis
   • Practical algorithms for emergency management

Key Evidence — Blood Pressure Reduction Rate and Targets

Gradual BP Reduction (Consensus-Based):

• No randomised trials of different BP reduction rates in hypertensive emergencies
• Consensus recommendations based on case series showing harm from rapid reduction
• Target: 10-15% reduction in first hour, 25% within 24 hours (except aortic dissection)
• Rationale: Chronic hypertension shifts autoregulatory curve rightward — rapid reduction causes ischaemia

Key Evidence — Intracerebral Haemorrhage

INTERACT2 Trial (2013): [18]

• Population: 2839 patients with acute intracerebral haemorrhage and elevated SBP (150-220 mmHg)
• Intervention: Intensive BP lowering (target SBP less than 140 mmHg) vs standard (target SBP less than 180 mmHg)
• Primary outcome: Death or major disability at 90 days
• Results:
  • Intensive treatment safe (no increase in adverse events)
  • Trend toward improved functional outcomes (OR 0.87, 95% CI 0.75-1.01, p=0.06)
  • Significant improvement in ordinal analysis of modified Rankin Scale (p=0.04)
• Conclusion: Intensive BP lowering to SBP less than 140 mmHg within 1 hour is safe and may improve outcomes

ATACH-II Trial (2016):

• Target SBP 110-139 mmHg vs 140-179 mmHg
• No benefit of intensive lowering; possible harm (increased renal adverse events)
• Current practice: Target SBP 140-160 mmHg (between INTERACT2 and ATACH-II)

Key Evidence — Acute Ischaemic Stroke

Permissive Hypertension in Acute Ischaemic Stroke: [17]

• Multiple observational studies show U-shaped curve: Both very high and very low BP associated with worse outcomes
• Elevated BP maintains perfusion to ischaemic penumbra via collaterals
• Consensus: Do NOT lower BP unless SBP > 220 or DBP > 120 mmHg (unless eligible for thrombolysis)

Post-Thrombolysis BP Control:

• NINDS tPA trial: Strict BP control (less than 180/105 mmHg) after tPA reduces intracerebral haemorrhage risk
• Standard practice: Maintain SBP less than 180 and DBP less than 105 mmHg for 24 hours post-tPA

Key Evidence — Choice of IV Antihypertensive

Labetalol vs Nicardipine (Observational Studies):

• Several retrospective studies comparing labetalol and nicardipine in hypertensive emergencies [19]
• Both effective and safe
• Nicardipine: More predictable dose-response, easier titration
• Labetalol: Useful when beta-blockade desired (tachycardia, ACS)
• No high-quality RCT comparing agents

Clevidipine vs Nitroprusside in Aortic Dissection:

• Retrospective study: Clevidipine achieved BP targets faster with less overshoot than nitroprusside
• Clevidipine avoids cyanide toxicity risk of prolonged nitroprusside use
• Both effective when combined with beta-blockade

Key Evidence — Pre-eclampsia and Eclampsia

Magnesium Sulfate (Magpie Trial, 2002):

• 10,141 women with pre-eclampsia randomised to MgSO₄ vs placebo
• MgSO₄ halved risk of eclampsia (RR 0.42, 95% CI 0.29-0.60)
• Reduced maternal mortality (not statistically significant but trend)
• Standard of care for seizure prevention and treatment in pre-eclampsia/eclampsia

Evidence Levels Summary

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Information for Patients

What is a Hypertensive Emergency?

A hypertensive emergency is when very high blood pressure causes immediate damage to vital organs such as your brain, heart, kidneys, or eyes. This is a medical emergency requiring urgent hospital treatment.

This is different from just having high blood pressure, which usually causes no symptoms and is managed with regular tablets over time.

What Are the Warning Signs?

Seek immediate emergency care (call 999 or go to A&E) if you have very high blood pressure AND any of these symptoms:

Brain:

• Severe headache that is different from your usual headaches
• Confusion, difficulty thinking clearly
• Blurred vision, seeing spots, or sudden vision loss
• Seizures (fits)
• Weakness or numbness on one side of the body
• Difficulty speaking or understanding speech

Heart:

• Severe chest pain or pressure
• Severe difficulty breathing
• Coughing up pink frothy fluid

Other:

• Severe back pain (especially tearing or ripping pain)
• Reduced urine output or blood in urine

What Happens in Hospital?

Emergency Assessment:

• You will be seen urgently and your blood pressure will be carefully monitored
• Blood tests, urine tests, and scans (CT or MRI) to check for organ damage
• ECG (heart tracing) and chest X-ray

Treatment:

• You will be admitted to a high-dependency unit or intensive care for close monitoring
• Blood pressure will be lowered slowly and carefully using medicines given through a drip (intravenous)
• It is important that blood pressure is NOT lowered too quickly — this can cause harm by reducing blood flow to vital organs
• Treatment typically takes hours to days, depending on the situation

Why Can't Blood Pressure Be Lowered Quickly?

Your body has adapted to the high blood pressure over time. If blood pressure is lowered too quickly, blood flow to the brain, heart, and kidneys can be reduced too much, causing a stroke, heart attack, or kidney failure.

Doctors carefully control how fast your blood pressure comes down to keep you safe.

After Treatment — Preventing It From Happening Again

Medications:

• You will need to take blood pressure tablets every day for life
• Never stop your tablets suddenly — this can cause blood pressure to shoot up again
• If you have side effects, speak to your doctor — do NOT just stop the tablets

Follow-Up:

• Regular check-ups with your GP or hospital specialist
• Home blood pressure monitoring (your doctor may recommend this)
• Tests to check for any underlying cause of high blood pressure

Lifestyle Changes:

• Reduce salt in your diet (avoid adding salt, limit processed foods)
• Eat a healthy diet rich in fruits, vegetables, and whole grains
• Lose weight if overweight (even 5-10 kg can significantly lower blood pressure)
• Regular exercise (aim for 30 minutes of brisk walking most days)
• Limit alcohol (no more than 14 units per week)
• Stop smoking (smoking damages blood vessels)

How Can I Prevent a Hypertensive Emergency?

Most Important:

1. Take your blood pressure tablets every single day — set reminders, use a pill organizer
2. Never run out of tablets — order repeat prescriptions in advance
3. Never stop tablets suddenly — even if you feel fine or have side effects
4. Attend all GP appointments — keep track of your blood pressure

Avoid:

• Recreational drugs (especially cocaine, amphetamines) — these can cause life-threatening blood pressure spikes
• Non-steroidal anti-inflammatory drugs (NSAIDs like ibuprofen) unless advised by your doctor — these can raise blood pressure
• Decongestants (cold and flu remedies) — these can raise blood pressure

Monitor:

• Check your blood pressure regularly at home if your doctor recommends
• Know your target blood pressure
• Keep a diary to show your doctor

What Is the Outlook?

Short-Term:

• Most people recover well if treated quickly
• The extent of recovery depends on which organs were affected and how quickly treatment was started

Long-Term:

• With good blood pressure control, most people live long, healthy lives
• It is essential to take your medications every day and attend follow-up appointments
• Your risk of future heart attacks, strokes, and kidney problems is higher than average, so strict blood pressure control is vital

Questions to Ask Your Doctor

• What caused my hypertensive emergency?
• What is my target blood pressure?
• What blood pressure tablets should I take and when?
• What are the side effects of my tablets?
• How often should I check my blood pressure at home?
• When is my next follow-up appointment?
• Are there any foods or medicines I should avoid?

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References

Primary Guidelines

1. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018;39(33):3021-3104. PMID: 30165516

2. National Institute for Health and Care Excellence. Hypertension in adults: diagnosis and management (NG136). 2019. Updated 2024. NICE Guideline

3. Peixoto AJ. Acute Severe Hypertension. N Engl J Med. 2019;381(19):1843-1852. PMID: 31693807

4. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. J Am Coll Cardiol. 2018;71(19):e127-e248. PMID: 29146535

5. Potter BJ, Goodwin AT, Munir S, et al. Management of hypertensive crisis: British and Irish Hypertension Society guideline. J Hum Hypertens. 2022;36(4):348-355. PMID: 36418425

Epidemiology and Pathophysiology

6. Shantsila A, Dwivedi G, Shantsila E. Hypertensive Emergency. Curr Treat Options Cardiovasc Med. 2017;19(11):87. PMID: 28948539

7. Chanubol N, Sukmark T, Dissaneevate S. Modern Management of Hypertensive Emergencies. Curr Hypertens Rep. 2021;23(12):61. PMID: 34813055

8. van den Born BH, Lip GYH, Brguljan-Hitij J, et al. ESC Council on hypertension position document on the management of hypertensive emergencies. Eur Heart J Cardiovasc Pharmacother. 2019;5(1):37-46. PMID: 30329037

9. Ahmed ME, Walker JM, Beevers DG, Beevers M. Lack of difference between malignant and accelerated hypertension. Br Med J (Clin Res Ed). 1986;292(6524):235-237. PMID: 3080149

10. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. 1996;27(1):144-147. PMID: 8591875

11. Mazza A, Lenti S, Schiavon L, et al. Catecholamine-induced hypertensive crises: current insights and management. Curr Hypertens Rep. 2023;25(11):297-308. PMID: 37944546

12. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. 2006;24(1):135-146. PMID: 16326262

13. Lip GY, Beevers M, Beevers DG. The failure of malignant hypertension to decline: a survey of 24 years' experience in a multiracial population in England. J Hypertens. 1994;12(11):1297-1305. PMID: 7868877

14. Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol. 2015;14(9):914-925. PMID: 26184985

Treatment Evidence — General

15. Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007;131(6):1949-1962. PMID: 17565029

Treatment Evidence — Aortic Dissection

16. Erbel R, Aboyans V, Boileau C, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35(41):2873-2926. PMID: 25173340

Treatment Evidence — Stroke

17. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke. Stroke. 2019;50(12):e344-e418. PMID: 31662037

18. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage (INTERACT2). N Engl J Med. 2013;368(25):2355-2365. PMID: 23713578

Treatment Evidence — Specific Agents

19. Peacock WF, Hilleman DE, Levy PD, Rhoney DH, Varon J. A systematic review of nicardipine vs labetalol for the management of hypertensive crises. Am J Emerg Med. 2012;30(6):981-993. PMID: 21908132

20. Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet. 1998;351(9100):389-393. PMID: 9482291

Additional Key References

21. Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. Ann Emerg Med. 2003;41(4):513-529. PMID: 12658251

22. Muiesan ML, Salvetti M, Amadoro V, et al. Malignant Hypertension: Current Perspectives and Challenges. J Clin Med. 2022;11(6):1622. PMID: 35329189

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