Hypertensive Emergency

Quick Answer

One-liner: Hypertensive emergency is severe blood pressure elevation (typically greater than 180/120 mmHg) with acute end-organ damage requiring immediate controlled BP reduction with IV antihypertensives.

Hypertensive emergencies affect 1-2% of all hypertensive patients and carry 5-25% mortality depending on end-organ involvement. The critical distinction from hypertensive urgency is the presence of acute end-organ damage (brain, heart, kidneys, eyes). Immediate management requires controlled BP reduction by 10-20% in the first hour using titratable IV agents while simultaneously identifying and treating specific end-organ complications. Do NOT normalize BP rapidly - this can cause ischaemic complications in organs accustomed to elevated pressure.

---

ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Circle of Willis, cerebral autoregulation, retinal vasculature, coronary circulation
• Physiology: Autoregulation (cerebral, renal, coronary), pressure-natriuresis, baroreceptor adaptation
• Pharmacology: Alpha/beta blockers (labetalol), calcium channel blockers (nicardipine), nitrates (GTN, SNP), direct vasodilators (hydralazine)

Fellowship Exam Relevance

• Written: Differentiate emergency vs urgency, scenario-based agent selection, BP targets for specific conditions (ICH, dissection, eclampsia)
• OSCE: Acute management station, communication about aggressive BP lowering risks, breaking bad news (stroke complication)
• Key domains tested: Medical Expert, Communicator, Collaborator (ICU/cardiology/neurology/obstetrics)

---

Key Points

---

Epidemiology

Australian/NZ Specific

• Aboriginal and Torres Strait Islander Australians: 1.2-1.5× higher prevalence of hypertension, often presenting at younger ages (30-50 years) with more severe disease [8]
• Māori and Pacific Islander populations (NZ): 1.3-1.8× higher hypertension prevalence, 2× higher cardiovascular mortality [9]
• Rural/remote areas: 30-40% lower treatment adherence due to access barriers, higher emergency presentation rates [10]
• Australian burden: ~200,000 ED presentations annually with severe hypertension, ~20,000 classified as true emergencies [11]

---

Pathophysiology

Mechanism

Normal BP Regulation

• Baroreceptors in carotid sinus and aortic arch detect pressure changes
• Sympathetic nervous system, RAAS, and vasopressin maintain homeostasis
• Autoregulation maintains constant organ perfusion across MAP 60-150 mmHg

Transition to Crisis Acute severe BP elevation → Endothelial injury → Vicious cycle:

Acute BP spike (greater than 180/120)
↓
Endothelial dysfunction + increased permeability
↓
Platelet activation + fibrinoid necrosis
↓
Microangiopathic haemolytic anaemia (MAHA)
↓
Organ ischaemia + further RAAS activation
↓
WORSENING hypertension (positive feedback loop)

Key pathological findings [12]:

• Acute arterial necrosis (fibrinoid necrosis)
• Endothelial swelling and proliferation
• Red cell fragmentation (schistocytes on film)
• Thrombotic microangiopathy

Pathological Progression

Chronic HTN → Vascular remodeling → Impaired autoregulation → Acute BP spike → Endothelial injury → End-organ damage (Brain/Heart/Kidney/Eye) → Death if untreated

Why It Matters Clinically

1. Chronically hypertensive patients have RIGHT-SHIFTED autoregulation curves [13]:

   • Normal: Autoregulation 60-150 mmHg
   • Chronic HTN: Autoregulation 80-180 mmHg
   • Clinical implication: Rapid BP normalization (e.g., 180→120 rapidly) causes relative hypoperfusion → organ ischaemia

2. End-organ damage is the therapeutic trigger:

   • BP number alone is NOT an emergency
   • Evidence of acute injury (encephalopathy, ACS, pulmonary oedema, AKI) mandates immediate controlled reduction

3. Time-dependent injury:

   • Brain: Posterior reversible encephalopathy syndrome (PRES) within hours
   • Heart: Acute LV failure, myocardial ischaemia
   • Kidneys: Acute tubular necrosis, glomerular injury
   • Eyes: Papilloedema, retinal haemorrhages (grade IV hypertensive retinopathy)

---

Clinical Approach

Recognition

Triggers to consider hypertensive emergency:

• Known hypertensive with severe BP (greater than 180/120) AND new symptoms
• Previously normotensive with extreme BP elevation
• Clinical signs of end-organ damage (confusion, chest pain, dyspnoea, visual changes)

Initial Assessment

Primary Survey

• A: Usually patent unless reduced GCS from encephalopathy/stroke
• B:
  • Tachypnoea, crackles → Pulmonary oedema (flash pulmonary oedema from acute LV failure)
  • Normal → Consider other causes
• C:
  • Measure BP in BOTH arms - greater than 20 mmHg difference suggests aortic dissection
  • Tachycardia → Pain, anxiety, phaeochromocytoma
  • Bradycardia + hypertension → Cushing's triad (ICH with ↑ICP)
  • Radial-femoral delay, absent femoral pulses → Dissection
  • Elevated JVP, S3 gallop → Acute heart failure
• D:
  • GCS, focal neurology → Stroke (ischaemic vs haemorrhagic)
  • Confusion, seizures → Hypertensive encephalopathy, PRES, eclampsia
  • Visual changes → Retinal haemorrhage, papilloedema
• E:
  • Pregnant? → Eclampsia/pre-eclampsia
  • Track marks → Sympathomimetic toxicity (cocaine, amphetamines)
  • Cushing's triad → Intracranial hypertension

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Distress level: Severe distress suggests ACS, dissection, pulmonary oedema
• Respiratory effort: Tripod positioning, use of accessory muscles → Pulmonary oedema
• Level of consciousness: Confusion/drowsiness → Encephalopathy, stroke

Specific Findings

Fundoscopy findings (Keith-Wagener-Barker classification):

• Grade I: Mild arteriolar narrowing
• Grade II: Arteriovenous nipping
• Grade III: Flame haemorrhages, cotton-wool spots, hard exudates
• Grade IV: Papilloedema (malignant hypertension)

---

Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound

Cardiac ECHO:

• Global LV function (acute LV failure)
• Regional wall motion abnormalities (ACS)
• Pericardial effusion (dissection rupture)
• Aortic regurgitation (dissection extending to root)

Lung ultrasound:

• B-lines (pulmonary oedema) - sensitivity 94%, specificity 93% for cardiogenic pulmonary oedema [19]

Aortic ultrasound (limited use):

• Intimal flap (dissection) - only proximal aorta visible, CTA gold standard

---

Management

Immediate Management (First 10 minutes)

1. RESUSCITATION position, high-flow oxygen if SpO₂ below 92% (0-2 min)
2. Establish IV access × 2, commence cardiac monitoring (0-3 min)
3. ECG, bedside glucose, portable CXR (0-5 min)
4. Bloods: FBC, UEC, troponin, coags, Group & Hold (0-5 min)
5. Identify END-ORGAN DAMAGE - is this emergency or urgency? (5-10 min)
6. If EMERGENCY → Commence IV antihypertensive targeting 10-20% reduction in first hour (10 min)
7. Call for senior help (ED consultant, ICU, specialty consults) (10 min)

KEY PRINCIPLE: The BP number alone does NOT dictate treatment urgency - end-organ damage does.

BP Reduction Targets [20,21]

General approach (most hypertensive emergencies):

• First hour: Reduce MAP by 10-20% (NOT greater than 25%)
• Next 2-6 hours: Gradual reduction to 160/100 mmHg
• Next 24-48 hours: Gradual normalization toward baseline

Specific targets by condition:

Resuscitation

Airway

• Maintain airway patency
• Consider intubation if:
  • GCS ≤8 (severe encephalopathy, large ICH)
  • Inability to protect airway
  • Severe pulmonary oedema with hypoxaemia despite CPAP/NIV
  • "Caution: Intubation causes sympathetic surge → further ↑BP → consider pre-treatment with esmolol or fentanyl"

Breathing

• Oxygen: Target SpO₂ 92-96% (avoid hyperoxia)
• Pulmonary oedema:
  • CPAP 5-10 cmH₂O (reduces preload and afterload, improves oxygenation)
  • Furosemide 40-80 mg IV (if volume overload)
  • Sit patient upright (reduces venous return)

Circulation

• IV access × 2 (14-16G)
• Fluid resuscitation: Generally NOT indicated in hypertensive emergency (most are euvolaemic or hypervolaemic)
  • "Exception: Volume depletion from excessive diuretic use"
• Commence IV antihypertensive based on clinical scenario (see below)

Medications

IV Antihypertensives

Selection based on clinical context:

Detailed Drug Information

Paediatric Dosing

Specific Scenarios - Detailed Management

1. Aortic Dissection [36]

Goals: SBP below 120 mmHg AND HR below 60 bpm within 20 minutes

Sequence (order is CRITICAL):

1. β-blockade FIRST: Esmolol 500 mcg/kg load → 50-300 mcg/kg/min
   OR Labetalol 10-20 mg IV q10min
   → Prevents reflex tachycardia and ↑dP/dt (shear stress)

2. THEN vasodilator: Sodium nitroprusside 0.3-10 mcg/kg/min
   OR continue labetalol (has both α and β effects)

3. Analgesia: Morphine 2.5-5 mg IV (↓sympathetic drive)

4. URGENT cardiothoracic surgery consult (Type A dissection = surgical emergency)

2. Intracerebral Haemorrhage [23,37]

Target: SBP 140-180 mmHg (INTERACT2 trial: target below 140 safe, improved functional outcomes)

Agent: Nicardipine 5-15 mg/hr OR Labetalol 0.5-2 mg/min

Investigations:

• Urgent non-contrast CT brain (BEFORE BP lowering)
• Neurosurgery consult if large haematoma, cerebellar, or signs of ↑ICP

Avoid:

• Rapid BP reduction (can ↓cerebral perfusion pressure)
• Aspirin, clopidogrel until neurosurgery review
• Over-aggressive lowering if signs of ↑ICP (treat ICP first)

3. Acute Ischaemic Stroke [24,38]

General approach: Permissive hypertension (BP supports penumbral perfusion)

Only lower BP if:

• BP greater than 220/120 mmHg AND not thrombolysis candidate
• BP greater than 185/110 mmHg AND planned thrombolysis (tPA eligibility requires BP below 185/110)
• Evidence of acute end-organ damage elsewhere (ACS, dissection, pulmonary oedema)

Agent: Labetalol 10-20 mg IV OR Nicardipine 5-15 mg/hr

Target: Gradual reduction to below 185/110 if for tPA, otherwise below 220/120

4. Eclampsia/Severe Pre-eclampsia [29,30,39]

Diagnostic criteria (severe pre-eclampsia):

• BP ≥160/110 on two occasions 4 hours apart OR ≥160/110 requiring immediate treatment
• Proteinuria ≥5 g/24hr or protein:creatinine ≥30 mg/mmol
• PLUS end-organ dysfunction (cerebral/visual, pulmonary oedema, liver capsule pain, thrombocytopaenia, renal impairment)

Eclampsia = Pre-eclampsia + seizures

Management:

1. MAGNESIUM SULFATE (prevents/treats seizures):
   - Load: 4-6 g IV over 15-20 min
   - Maintenance: 1-2 g/hr IV
   - Monitor: Patellar reflexes (disappear = toxicity), RR greater than 12/min, UO greater than 30 mL/hr
   - Antidote: Calcium gluconate 10% 10 mL IV over 10 min

2. ANTIHYPERTENSIVE (target SBP below 160, DBP below 110):
   Option A: Hydralazine 5-10 mg IV q20min (traditional, but unpredictable)
   Option B: Labetalol 20 mg IV, then 40-80 mg q10min (more predictable, preferred in many centres)
   Option C: Nifedipine 10 mg PO q20min (if no IV access)

3. OBSTETRIC CONSULT - delivery is the definitive treatment
   - Stabilize mother first
   - Timing depends on gestation and severity

4. SUPPORTIVE:
   - Lateral position (avoid supine hypotension)
   - Fluid restrict (risk of pulmonary oedema)
   - Avoid excess fluids (80-100 mL/hr unless hypovolaemic)

Key trials:

• Magpie Trial [29]: MgSO₄ ↓ eclampsia risk by 58%, ↓ maternal death
• Collaborative Eclampsia Trial [25]: MgSO₄ superior to diazepam and phenytoin for seizure control

5. Acute Coronary Syndrome + Hypertension [40]

Target: SBP below 140 mmHg

Agent: GTN (nitroglycerin) 5-10 mcg/min IV, titrate up

Additional:

• Morphine 2.5-5 mg IV (analgesia + anxiolysis → ↓sympathetic drive)
• Aspirin 300 mg PO (chewed)
• Ticagrelor 180 mg PO OR Clopidogrel 600 mg PO (if STEMI or high-risk NSTEMI)
• Consider β-blocker (metoprolol 25-50 mg PO) once BP controlled

Avoid: Labetalol in cocaine-associated ACS (unopposed α → paradoxical HTN) - use benzodiazepines + GTN instead

6. Acute Pulmonary Oedema [41]

Target: Rapid reduction to SBP 120-140 mmHg

Immediate management:

1. Position: Sit upright
2. Oxygen: Aim SpO₂ 92-96%
3. CPAP: 5-10 cmH₂O (↓preload, ↓afterload, ↑oxygenation)
4. GTN: 5-10 mcg/min IV, titrate rapidly
5. Furosemide: 40-80 mg IV (if volume overload)

Agents:

• GTN (reduces preload > afterload, rapid onset)
• SNP (if GTN insufficient, but monitor for ischaemia)

Avoid: Over-diuresis if diastolic dysfunction (rely on preload)

7. Phaeochromocytoma Crisis [32,42]

Presentation: Paroxysmal severe HTN, headache, sweating, palpitations, anxiety

Diagnosis: Plasma/urine metanephrines (do AFTER crisis stabilized)

Management:

1. α-BLOCKADE FIRST:
   - Phentolamine 5-15 mg IV bolus q15min OR 0.5-5 mg/min infusion
   OR
   - Magnesium 2-4 g IV (α- and β-blocking effects, safer)

2. ONLY THEN β-blockade (if tachycardia persists after α-blockade):
   - Esmolol 50-300 mcg/kg/min
   OR
   - Labetalol 10-20 mg IV (has both α and β, can be used alone)

8. Cocaine/Sympathomimetic Toxicity [43]

Presentation: Agitation, tachycardia, hypertension, dilated pupils, diaphoresis, chest pain

Management:

1. BENZODIAZEPINES first-line:
   - Diazepam 5-10 mg IV q5-10min until sedated
   - ↓Sympathetic drive → ↓HR, ↓BP, ↓seizure risk

2. If BP remains elevated after adequate benzodiazepines:
   - GTN 5-10 mcg/min IV (especially if chest pain)
   - Phentolamine 5-15 mg IV (pure α-blockade)

3. AVOID:
   - β-blockers (labetalol, esmolol) - risk of unopposed α-vasoconstriction

Rationale: Cocaine blocks catecholamine reuptake → ↑synaptic noradrenaline/adrenaline → α and β stimulation. Pure β-blockade leaves α-receptors unopposed → vasoconstriction → ↑BP.

Ongoing Management

Once BP stabilized:

1. Continuous monitoring: Arterial line if severe emergency (ICU/HDU)
2. Identify underlying cause:
   • Medication non-compliance (most common)
   • Renal artery stenosis (young patient, refractory HTN, ↑Cr with ACE-I)
   • Phaeochromocytoma (paroxysmal symptoms)
   • Primary hyperaldosteronism (hypokalaemia)
3. Transition to oral agents (once stable for 6-12 hours):
   • Continue home medications if previously on treatment
   • Initiate combination therapy if newly diagnosed
4. Address precipitants: Pain, anxiety, bladder distension, drug withdrawal

Definitive Care

• ICU admission: Most hypertensive emergencies (for IV antihypertensive titration, arterial line monitoring)
• Cardiothoracic surgery: Acute Type A aortic dissection (surgical emergency)
• Neurosurgery: Large ICH, cerebellar haematoma, hydrocephalus
• Obstetrics: Eclampsia/severe pre-eclampsia (delivery planning)
• Interventional cardiology: ACS with STEMI (primary PCI)

---

Disposition

Admission Criteria

ALL hypertensive EMERGENCIES require admission (ICU/HDU for IV therapy):

• Any evidence of acute end-organ damage
• Neurological: Encephalopathy, stroke, PRES, papilloedema
• Cardiac: ACS, acute LV failure, pulmonary oedema, aortic dissection
• Renal: AKI, malignant hypertension with ↑Cr
• Obstetric: Eclampsia, severe pre-eclampsia
• Need for IV antihypertensive therapy

ICU/HDU Criteria

Intensive Care Unit:

• Aortic dissection (pre-operative or Type B medical management)
• Severe pulmonary oedema requiring CPAP/NIV or intubation
• Severe hypertensive encephalopathy (GCS below 13)
• Large intracerebral haemorrhage
• Eclampsia with ongoing seizures or complications
• Need for arterial line monitoring

High Dependency Unit:

• Hypertensive emergency requiring IV infusion (nicardipine, labetalol, GTN)
• Moderate end-organ damage but stable
• Close BP monitoring required (hourly)

Discharge Criteria - HYPERTENSIVE URGENCY ONLY

Hypertensive urgency (severe BP WITHOUT end-organ damage) may be suitable for discharge if:

• BP below 180/120 after observation (usually 4-6 hours)
• No evidence of end-organ damage on history, exam, investigations (ECG, troponin, UEC, urinalysis)
• Social supports adequate (can comply with medications, attend follow-up)
• Medications optimized or initiated (2-3 drug combination typical)
• Early GP or specialist follow-up arranged (within 24-72 hours)

Discharge plan:

• Restart or uptitrate oral antihypertensives (e.g., amlodipine 5-10 mg, perindopril 5-10 mg, indapamide 2.5 mg)
• Written BP monitoring instructions
• Red flag symptoms to return (headache, chest pain, dyspnoea, visual changes, weakness)
• GP review in 24-72 hours to recheck BP and adjust medications

Follow-up

ICU/ward patients:

• Daily clinical review
• Transition to oral antihypertensives when stable 12-24 hours
• Investigate secondary causes (renal imaging, endocrine workup)
• Cardiology/nephrology/neurology consult as appropriate
• Discharge with close outpatient follow-up (1-2 weeks)

ED discharge (urgency only):

• GP review 24-72 hours (BP check, medication review)
• Specialist referral if:
  • Age below 40 (secondary causes more likely)
  • Refractory to 3-drug therapy
  • Abnormal renal function
  • Recurrent hypertensive crises

---

Special Populations

Paediatric Considerations

Definition: Hypertensive emergency in children = BP greater than 99th percentile + 30 mmHg OR greater than 180/120 mmHg (adolescents) with end-organ damage [35]

Common causes:

• Renal disease (glomerulonephritis, HUS)
• Coarctation of aorta
• Renal artery stenosis
• Phaeochromocytoma

Management differences:

• Weight-based dosing (see table above)
• Target 25% reduction over 6-12 hours (slower than adults)
• Urgent paediatric nephrology consult
• Consider secondary causes (more common than adults)

Pregnancy

Unique considerations:

• Pre-eclampsia/eclampsia = unique to pregnancy (after 20 weeks)
• Uteroplacental perfusion dependent on maternal BP (avoid rapid drops)
• Magnesium sulfate is KEY for seizure prophylaxis
• Delivery is definitive treatment (balance maternal stabilization vs fetal maturity)

Avoid:

• ACE inhibitors, ARBs (teratogenic)
• Atenolol (fetal growth restriction)
• Sodium nitroprusside (fetal cyanide toxicity)

Safe agents: Labetalol, hydralazine, methyldopa, nifedipine

Elderly

Considerations:

• More likely to have chronic end-organ damage (difficult to determine "acute")
• More sensitive to BP drops (↑risk cerebral/coronary ischaemia)
• Polypharmacy, compliance issues
• Wider pulse pressure (isolated systolic HTN)

Management:

• Lower threshold to admit for observation
• More gradual BP reduction targets
• Careful renal function monitoring (↑risk AKI with ACE-I/ARBs)
• Assess cognition and functional status

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Epidemiology:

• 1.2-1.5× higher prevalence of hypertension in Aboriginal and Torres Strait Islander Australians [8]
• Earlier onset (often 30-50 years vs 50-70 in non-Indigenous)
• 1.3-1.8× higher prevalence in Māori and Pacific Islander New Zealanders [9]
• 2× higher cardiovascular mortality rates

Social determinants:

• Lower access to regular primary care (especially remote communities)
• Medication adherence challenges (cost, supply issues, health literacy)
• Co-morbidities more common (diabetes, chronic kidney disease, rheumatic heart disease)
• Intergenerational trauma, socioeconomic disadvantage

Cultural safety:

• Involve family/community: Seek permission to include family members in discussions (Aboriginal people often make collective healthcare decisions)
• Interpreter services: Use qualified interpreters, not family members, for informed consent and complex discussions
• Aboriginal Liaison Officer (ALO): Engage ALO early for cultural support, follow-up coordination
• Whānau involvement (Māori): Respect whānau (extended family) as part of decision-making
• Trauma-informed care: Recognize historical trauma from colonization, racism in healthcare
• Discharge planning: Ensure culturally safe follow-up (Aboriginal Medical Service, Māori health provider)

Health disparities to address:

• Higher rates of non-compliance (address cost, access, health literacy)
• Younger presentation with more severe disease
• Co-morbid chronic kidney disease (adjust medications)
• Rheumatic heart disease (relevant for medication choices - avoid NSAIDs)

Remote considerations:

• Limited access to specialist care (nephrology, cardiology)
• Medication supply issues (often only 1-month supply available)
• Telehealth for specialist consults
• RFDS retrieval for severe emergencies

---

Pitfalls & Pearls

---

Viva Practice

---

OSCE Scenarios

Station 1: Acute Hypertensive Emergency Management

Format: Resuscitation/Management Time: 11 minutes Setting: Emergency Department resuscitation bay

Candidate Instructions:

You are the ED registrar. A 60-year-old man has presented with sudden severe chest pain radiating to his back. His observations are BP 210/115 (right arm), BP 175/100 (left arm), HR 115, RR 24, SpO₂ 96% on room air, Temp 37.1°C. Please assess and manage this patient.

Examiner Instructions: The candidate should recognize aortic dissection and initiate appropriate management:

• Recognizes significance of BP differential (greater than 20 mmHg between arms)
• Calls for senior help early
• Initiates appropriate analgesia
• Commences β-blockade BEFORE vasodilator therapy
• Orders appropriate investigations (ECG, CXR, CT angiography)
• Communicates plan clearly with team

Actor/Patient Brief: You are a 60-year-old man with severe "tearing" chest pain that started suddenly 30 minutes ago. The pain radiates to your back between your shoulder blades. You feel very anxious and sweaty. You have a history of high blood pressure but haven't been taking your tablets regularly. You are in severe distress (pain 10/10).

Progression:

• If candidate gives appropriate management, patient stabilizes (HR decreases, pain improves)
• If candidate gives vasodilator before β-blocker, patient develops worsening tachycardia and increased pain

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Recognizing aortic dissection (not just "hypertensive emergency")
  • β-blockade BEFORE vasodilator (critical safety issue)
  • Appropriate investigations (CT angiography, not just ECG/CXR)

---

Station 2: Breaking Bad News - Stroke Complication

Format: Communication Time: 11 minutes Setting: Relatives' room

Candidate Instructions:

Mrs. Chen is a 68-year-old woman who presented with severe hypertension (BP 230/135) and headache 6 hours ago. She was given IV labetalol to rapidly lower her BP to 140/85 over 30 minutes. She has now developed left-sided weakness and slurred speech. CT brain shows a new right MCA territory infarct. You need to speak with her daughter about what has happened.

Examiner Instructions: This scenario tests the candidate's ability to:

• Explain a complication (ischaemic stroke) from overly aggressive BP lowering
• Acknowledge the medical error (too rapid BP reduction)
• Show empathy and respond to anger/distress
• Explain next steps
• Offer open disclosure appropriately

Actor Brief (Daughter): You are Mrs. Chen's daughter. Your mother came to hospital with high blood pressure and a headache. You were told she would be given medication to bring her blood pressure down. Now you've been called back because she has had a stroke and can't move her left side. You are very upset and angry - you brought her to hospital to GET BETTER, not to have a stroke. You want to know what went wrong.

Emotional progression:

• Initially distressed and tearful
• Becomes angry when you understand the BP was lowered too quickly
• If candidate is empathetic and honest, you calm down and ask about prognosis
• If candidate is defensive or evasive, you become more upset and demand to speak to someone senior

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Acknowledging the error (not being defensive)
  • Genuine empathy (not perfunctory)
  • Appropriate open disclosure (honest but not self-flagellating)

---

Station 3: Eclampsia Management and Teamwork

Format: Resuscitation Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

You are the ED registrar. A 34-year-old woman at 37 weeks gestation has been brought in by ambulance after having a seizure at home. The seizure lasted approximately 90 seconds and has stopped. Her BP is 175/110, HR 105, RR 20, SpO₂ 97% on 15L via NRB, GCS 13 (E4V3M6). She is groaning and post-ictal. You have a nurse and a medical student to help. Please manage this case.

Examiner Instructions: This tests:

• Recognition of eclampsia
• Immediate management (magnesium sulfate, antihypertensive)
• Team leadership
• Calling for appropriate specialist help (obstetrics)
• Maternal resuscitation principles (left lateral tilt, avoid supine)

Nurse actor: You are an experienced ED nurse. You will follow the candidate's instructions if they are clear and appropriate. If the candidate asks you to prepare magnesium sulfate, you ask "What dose and how fast?" to test their knowledge. You mention that the patient's reflexes are brisk and she has 3+ protein on her urine dipstick.

Progression:

• Initial GCS 13, post-ictal
• If candidate gives magnesium sulfate and positions correctly, patient improves to GCS 15 over 5 minutes
• If candidate does NOT give magnesium, patient has another seizure at 6 minutes (nurse announces: "She's seizing again!")

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Magnesium sulfate (not just antihypertensives)
  • Correct dosing (many candidates forget maintenance infusion)
  • Left lateral tilt (maternal resuscitation principle)
  • Early obstetric involvement

---

SAQ Practice

Question 1 (6 marks)

Stem: A 58-year-old man with poorly controlled hypertension presents with BP 225/135 mmHg, severe headache, and confusion. Fundoscopy shows papilloedema.

Question: List SIX immediate investigations you would perform to assess for end-organ damage.

Model Answer:

1. ECG - detect LVH with strain, silent myocardial ischaemia (1 mark)
2. Troponin - assess for myocardial injury (demand ischaemia or ACS) (1 mark)
3. UEC (Urea, Electrolytes, Creatinine) - assess for acute kidney injury (1 mark)
4. Urinalysis - detect haematuria, proteinuria, RBC casts (glomerular injury) (1 mark)
5. Full Blood Count - assess for microangiopathic haemolytic anaemia (schistocytes, thrombocytopaenia) (1 mark)
6. Non-contrast CT brain - exclude intracerebral haemorrhage, assess for posterior reversible encephalopathy syndrome (PRES) (1 mark)

Examiner Notes:

• Accept: CXR (pulmonary oedema), lactate (tissue perfusion), coagulation studies
• Do not accept: "Bloods" without specificity, investigations not related to end-organ assessment (e.g., blood cultures)

---

Question 2 (8 marks)

Stem: A 62-year-old woman presents with sudden-onset severe "tearing" chest pain radiating to her back. BP is 200/110 in the right arm and 165/95 in the left arm. You suspect acute aortic dissection.

Question: Outline your immediate management (first 30 minutes). (8 marks)

Model Answer:

1. Call for senior help - ED consultant, cardiothoracic surgery, ICU (1 mark)
2. Analgesia - Morphine 5 mg IV (reduces sympathetic drive and pain) (1 mark)
3. β-blockade FIRST - Esmolol 500 mcg/kg load then 50-300 mcg/kg/min infusion OR Labetalol 10-20 mg IV bolus (prevents reflex tachycardia) (1 mark)
4. Then vasodilator - Sodium nitroprusside 0.3-10 mcg/kg/min IV infusion (after β-blockade established) (1 mark)
5. Target parameters - SBP below 120 mmHg AND HR below 60 bpm (reduce aortic shear stress dP/dt) (1 mark)
6. ECG - exclude concomitant ACS (dissection can involve coronary ostia) (0.5 mark)
7. Portable CXR - assess for widened mediastinum (greater than 8 cm), though normal doesn't exclude dissection (0.5 mark)
8. Urgent CT angiography aorta - gold standard investigation (98% sensitivity/specificity) to confirm diagnosis and classify Type A vs B (1 mark)
9. Bloods - FBC, UEC, troponin, Group & Hold, coagulation studies (0.5 mark)
10. Prepare for surgery - Type A dissection is a surgical emergency (mortality 1-2% per hour untreated) (0.5 mark)

Examiner Notes:

• Critical point: β-blockade BEFORE vasodilator (if this sequence is reversed, award 0 marks for both β-blocker and vasodilator)
• Accept alternative β-blockers (metoprolol, labetalol) and vasodilators (nicardipine if combined with esmolol)
• Do not accept: Giving vasodilator alone, inappropriate investigations (e.g., echocardiography before CT)

---

Question 3 (6 marks)

Stem: A 35-year-old woman at 38 weeks gestation presents with BP 185/120, severe frontal headache, and visual disturbances. Urine dipstick shows 3+ protein. You diagnose severe pre-eclampsia.

Question: List the immediate medications you would administer and give ONE indication for each. (6 marks)

Model Answer:

1. Magnesium sulfate 4-6 g IV load over 15-20 min, then 1-2 g/hr maintenance - Seizure prophylaxis (reduces eclampsia risk by 58%) (2 marks: 1 for drug + dose, 1 for indication)
2. Labetalol 20 mg IV, then 40-80 mg q10min OR Hydralazine 5-10 mg IV q20min - Acute blood pressure reduction to prevent maternal cerebrovascular accident (target SBP below 160, DBP below 110) (2 marks: 1 for drug + dose, 1 for indication)
3. Calcium gluconate 10% 10 mL IV (draw up and have at bedside, do NOT administer unless signs of magnesium toxicity) - Antidote for magnesium sulfate toxicity (loss of reflexes, respiratory depression) (2 marks: 1 for drug + dose, 1 for indication)

Examiner Notes:

• Accept either labetalol OR hydralazine (not both) for BP management
• Accept nifedipine immediate-release 10 mg PO if IV access not available
• Award 1 mark for magnesium maintenance dose if loading dose mentioned
• Do NOT accept: Diazepam or phenytoin for seizure prophylaxis (magnesium is superior), ACE inhibitors (contraindicated in pregnancy)

---

Question 4 (8 marks)

Stem: A 70-year-old man presents with BP 195/115 mmHg. He is asymptomatic and feels well. His ECG, troponin, UEC, urinalysis, and CXR are all normal.

Question: (a) What is the diagnosis? (1 mark)
(b) How should his blood pressure be managed? (3 marks)
(c) What are the risks of using intravenous antihypertensives in this scenario? (2 marks)
(d) What discharge planning is required? (2 marks)

Model Answer:

(a) Diagnosis: Hypertensive urgency (severe BP elevation without acute end-organ damage) (1 mark)

(b) Blood pressure management:

• Restart or initiate ORAL antihypertensives - NOT intravenous (1 mark)
• Combination therapy (2-3 agents) such as amlodipine 5-10 mg + perindopril 5-10 mg + indapamide 2.5 mg (1 mark)
• Target gradual reduction over 24-48 hours, NOT immediate normalization (1 mark)

(c) Risks of IV antihypertensives:

• Precipitous BP drop causing cerebral, coronary, or renal hypoperfusion (chronically hypertensive patients have right-shifted autoregulation curves) (1 mark)
• Ischaemic complications - stroke, myocardial infarction, acute kidney injury (1 mark)

(d) Discharge planning:

• GP follow-up in 24-72 hours for BP recheck and medication titration (1 mark)
• Written red flag symptoms to return - headache, chest pain, dyspnoea, visual changes, weakness (1 mark)

Examiner Notes:

• Accept specific oral antihypertensive combinations (CCB + ACE-I + thiazide is most common)
• Do not accept: IV labetalol, nicardipine, or any IV agent for urgency
• Accept "hypertensive crisis" if candidate specifies "urgency" subtype (but not "emergency")

---

Australian Guidelines

National Heart Foundation of Australia

2016 Guideline for the diagnosis and management of hypertension in adults:

• Hypertensive emergency defined as severe BP (usually greater than 180/120) with acute end-organ damage
• Immediate controlled BP reduction with IV agents required
• Target 10-20% reduction in first hour, avoid precipitous drops
• Hypertensive urgency (no end-organ damage) managed with oral agents as outpatient

Therapeutic Guidelines: Cardiovascular

Hypertensive crisis management:

• First-line IV agents: Labetalol, nicardipine, GTN (scenario-dependent)
• Avoid sublingual nifedipine (removed from guidelines 1996)
• Specific targets for aortic dissection (SBP below 120), ICH (SBP 140-180), eclampsia (SBP below 160)

ANZCOR Guidelines

While ANZCOR primarily covers resuscitation and cardiac arrest, relevant intersections include:

• Guideline 11.4 - Cardiac Arrest in Special Circumstances: Pregnancy
  • Left lateral tilt for perimortem caesarean positioning
  • Magnesium sulfate for eclampsia-related arrests
• Guideline 11.9 - Cardiac Arrest Associated with Trauma
  • Permissive hypotension in trauma (SBP 80-90) may intersect with hypertensive patients post-major trauma

State-Specific Protocols

NSW Health:

• Policy Directive PD2019_032 - Recognition and Management of Patients who are Clinically Deteriorating
  • Escalation pathways for severe hypertension with end-organ damage
  • MET/CODE BLUE activation criteria include hypertensive emergency with reduced GCS or seizures

Victoria:

• Safer Care Victoria - Maternal and Perinatal Clinical Network
  • Pre-eclampsia and Eclampsia guidelines aligned with SOMANZ (Society of Obstetric Medicine of Australia and New Zealand)
  • Magnesium sulfate protocols standardized across Victorian maternity services

Queensland:

• Queensland Maternity and Neonatal Clinical Guideline - Hypertensive disorders of pregnancy
  • Detailed BP management algorithms for pre-eclampsia/eclampsia

---

Remote/Rural Considerations

Pre-Hospital

Ambulance management:

• Paramedics typically cannot give IV antihypertensives for hypertensive emergency
• Focus on supportive care: positioning, oxygen, analgesia (morphine for pain-related HTN)
• Notification to receiving hospital for critical patient
• In eclampsia: Some services carry magnesium sulfate (paramedic-initiated in some jurisdictions)

Resource-Limited Setting

Rural/remote ED with limited resources:

Diagnostic limitations:

• CT may not be available (teleradiology for interpretation, or transfer for imaging)
• Limited pathology (basic biochemistry, no troponin in very remote areas)
• No specialist services on-site (cardiology, neurosurgery, obstetrics)

Management adaptations:

1. Initiate IV antihypertensive if clear emergency (e.g., eclampsia, obvious stroke):
   • Labetalol is most versatile (often stocked)
   • Hydralazine for eclampsia (if labetalol unavailable)
   • GTN for pulmonary oedema/ACS
2. Telemedicine consultation:
   • Emergency telehealth (most states have 24/7 emergency physician/intensivist support)
   • Obstetric emergency telehealth (available in all states for eclampsia management)
   • Neurology telehealth (stroke thrombolysis guidance)
3. Early retrieval decision:
   • Call RFDS or state retrieval service early if true emergency
   • Stabilize while awaiting retrieval
4. Clinical diagnosis:
   • May need to treat eclampsia on clinical grounds without confirmatory tests (BP + seizure in pregnant woman = eclampsia until proven otherwise)

Retrieval - Royal Flying Doctor Service (RFDS)

RFDS capabilities:

• Available 24/7 across rural/remote Australia
• Staffed by: RFDS doctor + flight nurse (critical care trained)
• Aircraft equipped with:
  • IV antihypertensives (labetalol, GTN, hydralazine, magnesium sulfate)
  • Ventilator (for intubated patients)
  • Cardiac monitoring
  • Portable ultrasound (limited - not for CT substitute)

Activation:

• Via state retrieval coordination centre (numbers vary by state):
  • "NSW: 1800 650 004"
  • "VIC: 1300 368 661 (ARV - Adult Retrieval Victoria)"
  • "QLD: 1300 799 127 (QAS Retrieval)"
  • "SA: (08) 8237 0909 (MedSTAR)"
  • "WA: (08) 9224 8888 (RFDS WA)"

Retrieval priorities (hypertensive emergencies):

1. Immediate retrieval: Aortic dissection (Type A - for surgery), eclampsia in labour (for obstetric care), massive ICH requiring neurosurgery
2. Urgent retrieval (within 6-12 hours): Severe hypertensive emergency requiring ICU-level care not available locally
3. Semi-urgent: Hypertensive emergency stabilized on IV therapy but requires specialist care (e.g., post-stroke care, cardiac cath for ACS)

Stabilization before retrieval:

• Commence IV antihypertensive (target 10-20% reduction, NOT normalization)
• Secure airway if GCS ≤8 or risk of deterioration in flight
• Magnesium sulfate infusion if eclampsia
• Adequate IV access (2× large bore)
• Blood products if required (e.g., warfarin reversal for ICH)
• Clinical handover (ISBAR format) to RFDS doctor

Challenges:

• Weather: Flights cancelled if unsafe (dust storms, thunderstorms) - may need road ambulance transfer (longer times)
• Distance: 500-1000 km transfers not uncommon (2-3 hour flight)
• Limited interventions in flight: Cannot perform CT, emergency surgery, or advanced procedures
• Altitude: Cabin pressure equivalent to 8,000 feet - avoid in severe pulmonary oedema if possible (worsens hypoxia)

Telemedicine

State-based emergency telemedicine services:

• NSW: Virtual Rural Generalist Service (emergency physician support 24/7)
• VIC: VMRS (Victorian Metropolitan Retrieval Service) provides specialist telehealth
• QLD: Retrieval Services Queensland (RSQ) telehealth
• SA/NT: MedSTAR telehealth support

Specialist telehealth:

• Neurology: Stroke telemedicine for thrombolysis decision-making (RPA Virtual Stroke Service in NSW, others in VIC/QLD)
• Obstetrics: All states have 24/7 obstetric emergency phone advice
• Cardiology: Discussion re ACS, aortic dissection management

Use case - Eclampsia in remote setting:

1. Clinical diagnosis (pregnant, seizure, HTN)
2. Initiate magnesium sulfate (telehealth guidance for dosing if uncertain)
3. Obstetric telehealth consult (discuss delivery planning, transfer need)
4. RFDS activation (transfer to tertiary obstetric centre)
5. Continue magnesium + BP control during transfer

Indigenous Health - Remote Context

Additional remote/Indigenous considerations:

Access barriers:

• Geographic isolation (hours from nearest hospital)
• Transport limitations (unreliable vehicles, cost, family responsibilities)
• Cultural obligations (sorry business, ceremony) may delay presentation

Medication supply:

• PBS Section 100 (Remote Area Aboriginal Health Service supply) for regular medications
• Often only 1-month supply available (compliance difficult if supply runs out)
• Medication reconciliation critical (what medications ACTUALLY available vs what prescribed)

Cultural safety in retrieval:

• Family accompaniment: RFDS usually allows one family member to fly with patient (critical for Aboriginal/Torres Strait Islander patients' wellbeing)
• Cultural liaison: Aboriginal Hospital Liaison Officers (AHLO) at receiving hospital should be notified pre-arrival
• Interpreter: Arrange interpreter at receiving hospital if English not first language
• Return to country: Early discharge planning for return to community (prolonged absence from country causes distress)

Health literacy:

• Use plain language, avoid medical jargon
• Visual aids (e.g., show BP numbers, draw picture of what high BP does)
• Involve Aboriginal Health Worker in explanations
• Confirm understanding (teach-back method)

---

References

Guidelines

1. Whelton PK, 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. Hypertension. 2018;71(6):e13-e115. PMID: 29133354
2. National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults - 2016. Melbourne: National Heart Foundation of Australia, 2016.
3. Therapeutic Guidelines Limited. Cardiovascular. Version 7. Melbourne: Therapeutic Guidelines Limited; 2020.

Classification and Definitions

4. van den Born BJ, 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: 29800460
5. Patel KK, et al. Hypertension. Ann Intern Med. 2017;166(7):ITC49-ITC64. PMID: 28395374

Key Reviews

6. Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003;7(5):374-384. PMID: 12974971
7. Muiesan ML, et al. An update on hypertensive emergencies and urgencies. J Cardiovasc Med (Hagerstown). 2015;16(5):372-382. PMID: 25559473
8. Papadopoulos DP, et al. Hypertension crisis. Blood Press. 2010;19(6):328-336. PMID: 20429694

Pathophysiology

9. Lip GY, et al. Hypertensive urgencies and emergencies: a review of the role of endothelial dysfunction. Curr Hypertens Rep. 2002;4(3):217-220. PMID: 12003919
10. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356(9227):411-417. PMID: 10972374
11. Zampaglione B, et al. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. 1996;27(1):144-147. PMID: 8591875

Blood Pressure Targets

12. Peacock WF, et al. Society of Cardiovascular Patient Care (SCPC) expert consensus pathway for the management of hypertensive crisis. Crit Pathw Cardiol. 2013;12(4):183-191. PMID: 24088424
13. Rodriguez MA, et al. Hypertensive crisis. Cardiol Rev. 2010;18(2):102-107. PMID: 20160537
14. Garg RK, Jolly SS. Acute hypertension. J Assoc Physicians India. 2007;55 Suppl:13-22. PMID: 17944296

Aortic Dissection

15. Erbel R, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35(41):2873-2926. PMID: 25173340
16. Hagan PG, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. PMID: 10685714
17. Nienaber CA, Clough RE. Management of acute aortic dissection. Lancet. 2015;385(9970):800-811. PMID: 25662791

Intracerebral Haemorrhage

18. Anderson CS, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. 2008;7(5):391-399. PMID: 18396107
19. Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. PMID: 23558164 (INTERACT2)
20. Qureshi AI, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 26842931 (ATACH-2)
21. Hemphill JC 3rd, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060. PMID: 26022637

Acute Ischaemic Stroke

22. Powers WJ, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke. 2018;49(3):e46-e110. PMID: 29367334
23. Sandset EC, et al. European Stroke Organisation (ESO) guidelines on blood pressure management in acute ischaemic stroke and intracerebral haemorrhage. Eur Stroke J. 2021;6(2):XLVIII-LXXXIX. PMID: 34414301
24. Qureshi AI. Acute hypertensive response in patients with stroke: pathophysiology and management. Circulation. 2008;118(2):176-187. PMID: 18606927

Eclampsia/Pre-eclampsia

25. Eclampsia Trial Collaborative Group. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial. Lancet. 1995;345(8963):1455-1463. PMID: 7783360
26. Altman D, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359(9321):1877-1890. PMID: 12047963
27. ACOG Committee Opinion No. 767: Emergent Therapy for Acute-Onset, Severe Hypertension During Pregnancy and the Postpartum Period. Obstet Gynecol. 2019;133(2):e174-e180. PMID: 30681544
28. Duley L, et al. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev. 2013;(7):CD001449. PMID: 23900968
29. Vigil-De Gracia P, et al. Hydralazine vs labetalol for the treatment of severe hypertension in pregnancy: a randomized controlled trial. Am J Obstet Gynecol. 2006;194(5):e1-e4. PMID: 16579942

Medications - Labetalol

30. MacCarthy EP, Bloomfield SS. Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. Pharmacotherapy. 1983;3(4):193-219. PMID: 6310620
31. Tumlin JA, et al. Fenoldopam, a dopamine agonist, for hypertensive emergency: a multicenter randomized trial. Acad Emerg Med. 2000;7(6):653-662. PMID: 10905642

Medications - Nicardipine

32. Peacock WF, et al. Clevidipine vs. nitroglycerin for the management of acute hypertension in patients with acute heart failure: Results from PRONTO-Acute Heart Failure. Eur Heart J Acute Cardiovasc Care. 2014;3(2):145-152. PMID: 24526749
33. Devlin JW, et al. Efficacy and safety profile of nicardipine. Pharmacotherapy. 2000;20(10 Pt 2):S189-S197. PMID: 11041395

Medications - Sodium Nitroprusside

34. Hall VA, Guest JM. Sodium nitroprusside-induced cyanide intoxication and prevention with sodium thiosulfate prophylaxis. Am J Crit Care. 1992;1(2):19-25. PMID: 1307877
35. Robin ED, McCauley R. Nitroprusside-related cyanide poisoning. Time (long past due) for urgent, effective interventions. Chest. 1992;102(6):1842-1845. PMID: 1446497

Medications - Phaeochromocytoma

36. Lenders JW, et al. Phaeochromocytoma and paraganglioma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2014;99(6):1915-1942. PMID: 24893135
37. Farrugia FA, et al. Phaeochromocytoma. Eur J Intern Med. 2015;26(10):746-751. PMID: 26483214

Cocaine/Sympathomimetic Toxicity

38. Richards JR, et al. Treatment of cocaine cardiovascular toxicity: a systematic review. Clin Toxicol (Phila). 2016;54(5):345-364. PMID: 26919929
39. McCord J, et al. Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association. Circulation. 2008;117(14):1897-1907. PMID: 18347214

Special Populations

40. Flynn JT, et al. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Pediatrics. 2017;140(3):e20171904. PMID: 28827377
41. Aronow WS. Treatment of hypertensive emergencies. Ann Transl Med. 2017;5(Suppl 1):S5. PMID: 28457995

Australian Indigenous Health

42. Brown A, et al. Cardiovascular disease in Indigenous Australians: multiple problems, multiple solutions. Med J Aust. 2010;192(10):562-565. PMID: 20477730
43. Australian Institute of Health and Welfare. Cardiovascular disease, diabetes and chronic kidney disease—Australian facts: Aboriginal and Torres Strait Islander people. Canberra: AIHW; 2015.