title: "Week 6: Chest Pain"
Week 6: Chest Pain
1. Systematic Approach to Chest Pain
The First 3-4 Minutes Are Key
Allow the patient to tell their narrative with open questions. This often provides the majority of diagnostic information.
Aim: don't miss the killers, stabilise physiology, and hand over a coherent plan. You don't need the perfect diagnosis in minute 5.
The ED Philosophy
"We can't always say what it is, but we can say what it's not."
The primary role in ED is to exclude life-threatening causes, not to diagnose every case of chest pain.
Cannot Miss Diagnoses
- Acute Coronary Syndrome (ACS (Acute Coronary Syndrome)) - most commonly ruled out
- Aortic Dissection
- Pulmonary Embolism (PE (Pulmonary Embolism))
- Tension Pneumothorax
- Cardiac Tamponade
- Boerhaave Syndrome (oesophageal rupture)
Chest Pain: Can't-Miss Diagnoses
Rule out the killers • Escalate early if unstable • Repeat ECG if ongoing pain
Pressure/heaviness ± diaphoresis
Dynamic ECG changes • CAD risks
Sudden severe pain • "ripping" to back
Pulse/BP differential • neuro deficit
Pleuritic pain + dyspnoea • tachycardia
Hypoxia • VTE risk factors
Severe dyspnoea • unilateral absent sounds
Hypotension • tracheal deviation late
Shock + raised JVP (may be subtle)
Muffled sounds/pulsus paradoxus
Post-vomiting chest pain • toxicity
Subcutaneous emphysema
2. Differential Diagnosis
| Category | Conditions |
|---|---|
| Cardiac | ACS (Acute Coronary Syndrome), Myocarditis, Pericarditis, Aortic dissection |
| Respiratory | PE (Pulmonary Embolism), Pneumothorax, Pneumonia, Pleuritis |
| GI | GORD, Oesophageal spasm, Boerhaave syndrome |
| MSK | Costochondritis (Tietze), Muscle strain, Rib fracture |
| Other | Anxiety/panic, Herpes zoster, Referred pain |
3. Pain History - SOCRATES
- S - Site - Where is the pain?
- O - Onset - When did it start? What were you doing?
- C - Character - What does it feel like?
- R - Radiation - Does it spread anywhere?
- A - Associated symptoms - Nausea, dyspnoea, diaphoresis?
- T - Time course - Constant? Intermittent? Duration?
- E - Exacerbating/alleviating - What makes it better or worse?
- S - Severity - Score out of 10
Classic Pain Patterns
| Diagnosis | Characteristic Pain Features |
|---|---|
| ACS (Acute Coronary Syndrome) | Central/left, crushing "elephant on chest," radiates to L arm/jaw, associated with nausea, diaphoresis, dyspnoea |
| Aortic Dissection | Sudden onset, tearing, radiates to back, worst pain of life, at rest |
| Pericarditis | Sharp, pleuritic, worse lying flat, better sitting forward, preceded by viral illness |
| PE (Pulmonary Embolism) | Pleuritic, sudden onset, associated dyspnoea, haemoptysis |
| Pneumothorax | Sudden onset pleuritic pain, dyspnoea, unilateral |
| MSK | Sharp, localized, worse with movement, reproducible on palpation |
Right arm/shoulder radiation is often MORE specific for severe cardiac pain than left arm radiation!
4. Risk Factors for ACS (Acute Coronary Syndrome)
Major Risk Factors (Coronary Artery Disease)
- Male sex
- Age >50 years
- Known coronary artery disease
- Hypertension
- Diabetes mellitus
- Dyslipidaemia
- Current smoker
- Family history of premature CAD
- Chronic kidney disease
- Alcohol/recreational drug use
- Autoimmune conditions
Clinical Examination in ACS (Acute Coronary Syndrome)
Often unremarkable! The money is in the history and risk factors. Look for:
- Haemodynamic instability
- Signs of heart failure (if severe MI (Myocardial Infarction))
- Features that support or refute differentials
5. ECG (Electrocardiogram) Interpretation in Chest Pain
Don't overcall isolated changes. In chest pain, look for a territorial pattern with reciprocal changes and compare with prior ECG (Electrocardiogram)s before calling STEMI.
Key ECG (Electrocardiogram) Patterns
| ECG (Electrocardiogram) Finding | Interpretation |
|---|---|
| ST elevation + reciprocal changes | STEMI (ST-Elevation Myocardial Infarction) - territorial distribution |
| Diffuse ST elevation, PR depression, NO reciprocal changes | Pericarditis |
| T wave inversion V1-V4 + inferior leads | Right ventricular strain (PE (Pulmonary Embolism)) |
| S1Q3T3 pattern | Classically taught for PE (Pulmonary Embolism) but not specific |
| New LBBB with ischaemic symptoms | May mask occlusion MI — apply (modified) Sgarbossa criteria + clinical picture |
S1Q3T3 is often taught for PE (Pulmonary Embolism) but is not very specific. The T wave inversion in V1-V4 + inferior leads (right heart strain pattern) is more reliable.
Pericarditis vs STEMI (ST-Elevation Myocardial Infarction) on ECG (Electrocardiogram)
| Feature | Pericarditis | STEMI (ST-Elevation Myocardial Infarction) |
|---|---|---|
| ST elevation | Diffuse, widespread | Territorial (follows coronary distribution) |
| Reciprocal changes | Absent (except aVR, V1) | Present |
| PR segment | Depressed (elevated in aVR) | Normal |
| ST morphology | Concave ("smiley face") | Often convex ("frowny face") |
STEMI Localization (12-lead)
| Leads with ST elevation | Territory | Culprit artery (most common) |
|---|---|---|
| II, III, aVF | Inferior | RCA (sometimes LCx) |
| V1-V4 | Anteroseptal/anterior | LAD |
| I, aVL, V5-V6 | Lateral | LCx or diagonal |
| V7-V9 (posterior leads) | Posterior | LCx or RCA |
ST elevation must be in contiguous leads (adjacent leads viewing the same territory)
Inferior STEMI can involve the RV: check V4R and avoid nitrates if hypotensive
Posterior MI often shows ST depression with tall R waves in V1-V3. Confirm with V7-V9 leads and treat as STEMI
STEMI Equivalents and High-Risk Patterns
de Winter T waves (upsloping ST depression with tall symmetric T waves in V2-V4) indicate proximal LAD occlusion - treat as STEMI
Wellens pattern (biphasic or deep T wave inversion in V2-V3 after pain resolves) indicates critical LAD stenosis - avoid stress testing
ST elevation in aVR with diffuse ST depression suggests left main or triple-vessel ischemia
In LBBB or paced rhythms, concordant ST elevation ≥1 mm is a high-risk occlusion MI sign (Sgarbossa)
ACS Pharmacology Essentials
Initial ACS (Acute Coronary Syndrome) management: antiplatelet therapy (aspirin) plus a P2Y12 inhibitor (clopidogrel or ticagrelor) plus anticoagulation (heparin).
STEMI (ST-Elevation Myocardial Infarction) requires reperfusion therapy: primary PCI (Percutaneous Coronary Intervention) (preferred) or fibrinolysis if PCI delayed.
Avoid nitrates in suspected RV infarction or hypotension (preload dependent) — give IV fluids instead.
ACS first-line antiplatelet: aspirin 300 mg chewed/dissolved (if no contraindication).
Q: STEMI (ST-Elevation Myocardial Infarction) with PCI (Percutaneous Coronary Intervention) within 60 min: load [], [], and a [___] inhibitor. A: aspirin; heparin; P2Y12
Q: PCI (Percutaneous Coronary Intervention) delay >60 min with thrombolysis planned: give [] + [] + anticoagulation. A: aspirin; clopidogrel
Q: Clopidogrel loading dose for thrombolysis: age under 75 = [] mg; age 75+ = [] mg. A: 300; 75
DAPT + Anticoagulation Doses (adult, local protocol)
| Medication | Loading dose | Maintenance |
|---|---|---|
| Aspirin | 300 mg chewed/dissolved | 100 mg daily |
| Ticagrelor | 180 mg | 90 mg BD |
| Clopidogrel | 600 mg for PCI; 300 mg for thrombolysis (75 mg if age 75+) | 75 mg daily |
| UFH (heparin) | 60-70 units/kg IV bolus (max 5000) | Infusion with aPTT monitoring |
UFH bolus in ACS/PCI is 60-70 units/kg IV (max 5000 units), followed by infusion with aPTT titration.
Primary PCI is preferred when it can be delivered promptly. If PCI will be delayed and there are no contraindications, fibrinolysis is appropriate, followed by transfer for angiography and possible rescue PCI if reperfusion fails.
Major contraindications to thrombolysis include prior intracranial haemorrhage, known intracranial lesion, suspected aortic dissection, and active bleeding.
Fibrinolysis reduces mortality in eligible STEMI but carries a bleeding risk (including intracranial haemorrhage), so careful selection is essential.
Q: When is supplemental oxygen indicated in ACS? A: If hypoxaemic (SpO2 <94%) or in shock; avoid routine oxygen if normoxaemic.
Persistent chest pain: consider IV opioid (fentanyl or morphine) after initial measures.
GTN spray is sublingual and may be repeated every 5 minutes if pain persists.
Contraindications to GTN: allergy, HR under 50 or over 150, SBP under 100, acute CVA, head trauma.
Opioid Analgesia in ACS: Morphine vs Fentanyl
Fentanyl and morphine are not hemodynamically equivalent. Fentanyl is much cleaner cardiovascularly, which is why NSW (and most modern ACS protocols) prefer it in patients near the hypotension cliff.
The key difference is histamine release:
| Property | Morphine | Fentanyl |
|---|---|---|
| Histamine release | Yes (non-IgE mediated) | Minimal to none |
| Peripheral effect | Vasodilation + venodilation | Largely neutral |
| BP effect | ↓↓ (dose-dependent, unpredictable) | ↔ / mild ↓ |
| Onset (IV) | 5-10 min | 1-2 min |
| Titration | Slower | Tight, incremental |
Morphine causes non-IgE-mediated histamine release → vasodilation + venodilation → ↓SVR + ↓preload → BP drops. This can tip marginal MI patients into hypotension.
Fentanyl has minimal histamine release → less peripheral vasodilation → BP effect is mostly neutral at analgesic doses. Same opioid receptor class, different peripheral chemistry.
Morphine unloads the venous system (↓preload), which can be catastrophic in:
- RV infarction (preload-dependent)
- Volume-dependent states
- Elderly patients
Fentanyl largely spares preload.
Both opioids blunt sympathetic tone (↓pain → ↓sympathetic drive), but morphine's peripheral vasodilation stacks on top of this central effect. Fentanyl's effect is mostly central analgesia.
Avoid opioids if SBP under 100 mmHg (NSW Health rule)
In MI analgesia:
- Morphine = analgesia + hemodynamic gamble
- Fentanyl = analgesia with guardrails
What is the most appropriate next step for analgesia?
What is the best next step?
6. Troponin Physiology
Structure and Function
Cardiac troponin is a complex of 3 subunits:
- Troponin I - exclusive to cardiac muscle (what we measure)
- Troponin T
- Troponin C
Function: Controls actin-myosin interaction through calcium binding. When calcium binds troponin, it moves tropomyosin away from myosin binding sites, allowing muscle contraction.
Troponin Timeline
- Detectable: 2-4 hours after MI
- Peak: 18-24 hours
- Returns to baseline: 10-14 days
Non-ACS (Acute Coronary Syndrome) Causes of Raised Troponin
- Pulmonary embolism (right heart strain)
- Myocarditis/Pericarditis
- Sepsis
- Renal failure
- Heart failure
- Tachyarrhythmias
- Cardiac contusion
- Post-cardiac surgery
- Stroke/SAH (Subarachnoid Haemorrhage)
- Burns
- Extreme exertion
A patient with chest pain, dyspnoea, and raised troponin is NOT always an ACS (Acute Coronary Syndrome)! Consider PE (Pulmonary Embolism) causing right heart strain with secondary troponin release.
7. Risk Stratification Scores
EDACS (Emergency Department Assessment of Chest pain Score)
| Criterion | Points |
|---|---|
| Age 18-45 | +2 |
| Age 46-50 | +4 |
| Age 51-55 | +6 |
| Age 56-60 | +8 |
| Age 61-65 | +10 |
| Age 66-70 | +12 |
| Age 71-75 | +14 |
| Age 76-80 | +16 |
| Age 81-85 | +18 |
| Age >85 | +20 |
| Male sex | +6 |
| Known CAD or ≥3 risk factors (if age 18-50) | +4 |
| Diaphoresis | +3 |
| Pain radiates to arm/shoulder/neck/jaw | +5 |
| Pain worsens with inspiration | -4 |
| Pain reproduced by palpation | -6 |
Low risk: Score less than 16
HEART Score (6-week MACE risk)
- H - History - Slightly (0), Moderately (1), Highly (2) suspicious
- E - ECG (Electrocardiogram) - Normal (0), Non-specific ST changes (1), Significant ST deviation (2)
- A - Age - Under 45 (0), 45-64 (1), Over 64 (2)
- R - Risk factors - None (0), 1-2 (1), >2 or known CAD (2)
- T - Troponin - Normal (0), 1-3x normal (1), >3x normal (2)
Interpretation:
- 0-3: Low risk (1.7% MACE) - consider discharge
- 4-6: Intermediate risk (12% MACE) - observation
- 7-10: High risk (65% MACE) - admission for intervention
8. PAXA Pathway (NSW)
Pathway for Acute Coronary Syndrome Assessment
Algorithm Flow
- Initial ECG (Electrocardiogram) - STEMI (ST-Elevation Myocardial Infarction)? Yes -> Cath lab. No -> Continue
- Non-ischemic cause? Yes -> Senior review, exit pathway
- Risk stratify using clinical criteria and validated scores
- Serial troponins at 0 and 2 hours
- Disposition based on risk category
High-Sensitivity Troponin Interpretation
Positive Troponin: >50 ng/L at any time
Positive Delta Troponin: Change of >15 ng/L between 0 and 2 hour samples (up OR down)
Risk Categories and Disposition
| Risk | Criteria | Disposition |
|---|---|---|
| High Risk | Positive troponin, dynamic ECG (Electrocardiogram) changes, haemodynamic instability, ongoing chest pain | Admit cardiology, consider cath lab |
| Intermediate | Not high or low risk | Admit without invasive monitoring OR discharge with early follow-up |
| Low Risk | Age under 45, atypical symptoms, no CAD, non-ischaemic ECG (Electrocardiogram), symptom-free, OR low validated risk score | Discharge with GP follow-up |
Low Clinical Risk Criteria (all must be present)
- Age under 45 years
- Symptoms atypical for angina
- No known coronary artery disease
- Non-ischaemic ECG (Electrocardiogram)
- Symptom-free at assessment
9. Bedside Investigation Summary
| Test | Purpose |
|---|---|
| ECG (Electrocardiogram) | Ischaemia, arrhythmia, pericarditis, PE (Pulmonary Embolism) strain |
| CXR (Chest X-Ray) | Pneumothorax, pneumonia, heart failure, wide mediastinum (dissection) |
| Bilateral BP (Blood Pressure) | >20 mmHg difference suggests aortic dissection |
| Troponin | Myocardial injury (serial 0h and 2h) |
| D-dimer | PE (Pulmonary Embolism) (only if low/intermediate Wells; use a validated pathway) |
| POCUS | Effusions, RV (Right Ventricle) strain, pneumothorax |
D-dimer caveats:
- Only useful if low-risk Wells score - high risk needs CTPA regardless
- Do not use D-dimer to "rule out" PE (Pulmonary Embolism) when pre-test probability is high
10. Practice Questions
What is the most likely diagnosis?
What is the most likely diagnosis?
What is the most appropriate ED (Emergency Department) disposition?
11. Atrial Fibrillation
Atrial fibrillation (AF (Atrial Fibrillation)) is the most common sustained cardiac arrhythmia. Most morbidity/mortality is from thromboembolic complications (stroke).
Classification
| Type | Definition |
|---|---|
| Paroxysmal | Self-terminating, usually within 48 hours |
| Persistent | Lasts >7 days, or requires cardioversion |
| Long-standing persistent | Continuous AF (Atrial Fibrillation) >1 year |
| Permanent | AF (Atrial Fibrillation) accepted by patient and physician |
Management Principles
- Rate vs rhythm control
- Anticoagulation (prevent stroke)
- Treat underlying cause (sepsis, thyroid, etc.)
- Lifestyle (weight loss, reduce alcohol)
Rate Control vs Rhythm Control
| Rate Control | Rhythm Control |
|---|---|
| Beta-blocker (metoprolol, atenolol) | Electrical cardioversion (higher success) |
| Non-DHP CCB (diltiazem, verapamil) | Chemical cardioversion (flecainide if no heart disease) |
| Digoxin (if above don't work) | Amiodarone if LVEF <40% or CAD |
| Target <110 bpm | Catheter ablation for refractory cases |
Rate control preferred if:
- AF (Atrial Fibrillation) >48 hours AND not anticoagulated (risk of left atrial thrombus)
- Asymptomatic
- Elderly
Rhythm control preferred if:
- Symptomatic
- Recent onset (<12 months)
- Reduced LVEF
Anticoagulation
CHA₂DS₂-VASc Score - assess stroke risk to guide anticoagulation
- Oral anticoagulation unless very low stroke risk
- DOACs preferred (apixaban, rivaroxaban, dabigatran)
- Warfarin for valvular AF (Atrial Fibrillation) (mechanical valve, rheumatic mitral stenosis)
Do NOT use antiplatelets (aspirin, clopidogrel) for stroke prevention in AF (Atrial Fibrillation) — they do not reduce stroke risk and add bleeding.
Unstable AF (Atrial Fibrillation)
Rapid AF (Atrial Fibrillation) with hypotension/hypoperfusion is a medical emergency.
- Follow ALS (Advanced Life Support) guidelines
- Consider synchronized DC cardioversion
- Look for underlying cause (ACS (Acute Coronary Syndrome), PE (Pulmonary Embolism), sepsis)
What is the appropriate management?
12. Stroke and TIA
Stroke is the #1 cause of AF (Atrial Fibrillation)-related mortality. AF (Atrial Fibrillation) increases stroke risk 5-fold due to left atrial thrombus formation.
Transient Ischaemic Attack (TIA)
A TIA is a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia without acute infarction.
TIA is a medical emergency - 10-15% of TIA patients have a stroke within 90 days, with highest risk in the first 48 hours.
FAST Recognition
- F - Face drooping (ask to smile)
- A - Arm weakness (raise both arms)
- S - Speech difficulty (slurred, confused)
- T - Time to call emergency services
Amaurosis Fugax
Amaurosis fugax = painless, transient monocular vision loss ("curtain descending over vision")
- Caused by retinal artery embolism (usually from carotid atherosclerosis or cardiac source)
- Classically lasts seconds to minutes
- A form of retinal TIA - requires urgent investigation
Amaurosis fugax is monocular (one eye) because it affects the retinal artery. Binocular visual symptoms suggest posterior circulation (vertebrobasilar) pathology.
TIA Workup
| Investigation | Purpose |
|---|---|
| CT (Computed Tomography) head | Exclude haemorrhage, identify established infarct |
| Carotid Doppler/CTA | Assess for carotid stenosis (surgical candidate?) |
| ECG (Electrocardiogram) | Identify AF (Atrial Fibrillation) as embolic source |
| Echo | Cardiac source of embolism (thrombus, PFO, valvular disease) |
| Bloods | FBC (Full Blood Count), coagulation, lipids, glucose, HbA1c |
ABCD² Score - TIA Risk Stratification
- A - Age ≥60 years (+1)
- B - Blood pressure ≥140/90 at presentation (+1)
- C - Clinical features: unilateral weakness (+2), speech disturbance without weakness (+1)
- D - Duration: ≥60 min (+2), 10-59 min (+1)
- D - Diabetes (+1)
Risk interpretation:
- Score 0-3: Low risk (~1% 2-day stroke risk)
- Score 4-5: Moderate risk (~4% 2-day stroke risk)
- Score 6-7: High risk (~8% 2-day stroke risk)
What is the most likely diagnosis?
13. Rapid Response and MET Criteria
Between-the-Flags System (NSW):
| Vital Sign | Yellow Zone (Clinical Review) | Red Zone (MET/Rapid Response) |
|---|---|---|
| Heart Rate (Heart Rate) | <50 or >120 | <40 or >140 |
| Systolic BP (Systolic Blood Pressure) | <100 or >180 | <90 or >200 |
| Respiratory Rate (Respiratory Rate) | <10 or >25 | <8 or >30 |
| Oxygen Saturation (Peripheral Oxygen Saturation) | <95% | <90% |
| Temperature | <35.5°C or >38.5°C | <35°C or >39.5°C |
| Consciousness | New confusion | Unresponsive (P or U) |
| Urine output | <0.5 mL/kg/hr for 2 hours | Nil output |
Escalation Pathways
MET Call Triggers:
- Any vital sign in the red zone
- Staff member concerned about a patient (clinical worry criterion)
- Seizure
- Cardiac arrest
Clinical Review Triggers:
- Any vital sign in the yellow zone
- Failure to respond to treatment within 30 minutes
14. Acute Pulmonary Oedema (APO)
APO = fluid in the lungs from cardiac failure
Clinical features: Acute dyspnoea, orthopnoea, pink frothy sputum, bilateral crackles, elevated JVP, peripheral oedema.
APO Management
| Priority | Intervention | Mechanism |
|---|---|---|
| Position | Sit upright, legs dependent | ↓ venous return (preload) |
| Oxygen | Target SpO₂ ≥94% | Correct hypoxia |
| GTN | Sublingual then IV infusion | Venodilation → ↓preload; arteriodilation → ↓afterload |
| Frusemide | 40-80 mg IV | Venodilation (acute) + diuresis (delayed 30-60 min) |
| NIV | CPAP 10 cmH₂O or BiPAP | ↑ alveolar recruitment, ↓ work of breathing, ↓ preload |
| Morphine | Controversial — avoid routinely | Anxiolysis but ↑ mortality in some studies |
Morphine in APO is controversial.
Evidence suggests morphine may increase mortality in APO (respiratory depression, delayed NIV). Avoid routine use — use GTN and NIV as primary therapies instead.
Which is the most appropriate first-line vasodilator?
15. Capacity Assessment and Ethics
Capacity Assessment
Four criteria for decision-making capacity:
- Understand — Can the patient understand the relevant information?
- Retain — Can they hold the information long enough to make a decision?
- Weigh — Can they weigh the risks and benefits?
- Communicate — Can they express their decision?
All four must be present for the patient to have capacity for that specific decision.
Capacity ≠ agreement with the doctor.
A patient with capacity can refuse treatment even if the doctor believes it's unwise — this is the principle of autonomy. Document the discussion thoroughly.
Not-For-Resuscitation (NFR) Orders
NFR is NOT 'do nothing' — it's a plan for appropriate care:
- Specifies which interventions are appropriate and which are not
- Must be reviewed regularly and when clinical status changes
- Should reflect the patient's values and goals of care
- Requires documentation, communication to the team, and ideally patient/family involvement
Advance Care Directives (ACD)
| Component | Description |
|---|---|
| ACD | Written document outlining patient's wishes for future care when they lose capacity |
| Enduring Guardian | Person appointed to make health decisions when patient lacks capacity |
| Person Responsible | Hierarchy: spouse → carer → close friend/relative (NSW Guardianship Act) |
Ethical Principles
| Principle | Definition | Example in Critical Care |
|---|---|---|
| Autonomy | Patient's right to make informed decisions | Refusing intubation |
| Beneficence | Acting in the patient's best interest | Recommending surgery |
| Non-maleficence | "First, do no harm" | Avoiding futile treatment |
| Justice | Fair allocation of resources | ICU bed allocation |
Week 6 Study Checklist
Click to expand or view deep dives
Sources
- CC Bible
- CSANZ ACS guidelines
- EDACS + HEART score derivation/validation studies
- NSW Health chest pain pathways (incl. accelerated troponin protocols like PAXA)