GC088 Sudden Severe Chest Pain
Sudden severe chest pain is an acute, intense thoracic pain of rapid onset that requires urgent evaluation to exclude life-threatening causes such as acute coronary syndrome, aortic dissection, pulmonary embolism, tension pneumothorax, or esophageal rupture.
Sudden Severe Chest Pain: Acute Myocardial Infarction & Aortic Dissection
This lecture (GC 088) by Professor Kai-Hang Yiu is one of the highest-yield cardiology lectures for the HKUMed summative exam. It covers two life-threatening causes of sudden severe chest pain — ST-Elevation Myocardial Infarction (STEMI) and Aortic Dissection — and demands you to rapidly differentiate between them because their treatments are diametrically opposed (anticoagulation/thrombolysis kills in dissection; delayed reperfusion kills in STEMI). [1]
How this fits into exams: The examiners love testing the clinical approach to acute chest pain — differential diagnosis, ECG interpretation, biomarker kinetics, reperfusion strategies, contraindications to thrombolysis, Stanford classification, and complications of AMI. Past papers have repeatedly tested these themes. [2][3]
Structure of this lecture:
- STEMI — Pathophysiology → Clinical features → Diagnosis (Classification, ECG, Biomarkers, Imaging) → Treatment (Reperfusion + Adjunctive) → Complications → Post-MI management
- Aortic Dissection — Pathology → Classification → Clinical features → Investigations → Management
PART 1: ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
Acute myocardial infarction is defined as myocardial cell death due to prolonged myocardial ischaemia. [1]
The key event is atherosclerotic plaque rupture (or erosion) → exposes thrombogenic subendothelial collagen and lipid core → platelet adhesion and activation → thrombus formation → total coronary artery occlusion → downstream myocardial ischaemia → if sustained > 20–30 minutes → irreversible myocyte necrosis. [1]
Why does this matter clinically?
- 90% of patients with a transmural infarct have total occlusion of the relevant artery within 4 hours of pain, usually secondary to plaque fissure. [1]
- Real-world mortality is ~40% in the first 4 weeks; half of deaths occur within 2 hours, mostly due to ventricular fibrillation (VF). [1]
- This is why defibrillators and CCU admission are critical — most early deaths are arrhythmic, not pump failure.
ACS Spectrum — Old vs New Terminology
ACS is an important manifestation of atherothrombosis. The lecture explicitly shows the spectrum [1]:
| Old Term | New Term | Pathology |
|---|---|---|
| Stable angina | Stable angina | Fixed stenosis, no plaque rupture |
| Unstable angina (UA) | UA/NSTEMI | Plaque rupture, non-occlusive thrombus |
| Non-Q-wave MI | UA/NSTEMI | Partial occlusion or transient total occlusion |
| Q-wave MI | STEMI | Total occlusion, transmural necrosis |
The timing from plaque rupture to full Q-wave MI is minutes to hours for STEMI, and days to weeks for UA/NSTEMI progression. The treatment differs: STEMI needs immediate reperfusion; UA/NSTEMI needs antithrombotic therapy ± early invasive strategy.
Evolving phase (first 6 hours, up to 12 hours): [1]
- Potential for recovery of heart muscle if: (a) improve blood supply → revascularisation, (b) decrease oxygen demand → ↓ heart rate + BP
- Infarcted muscles are acidotic, with loss of Ca²⁺ and influx of K⁺ → arrhythmia
Convalescence phase: [1]
- Infarcted muscles will NOT recover
- Treatment can improve mortality/morbidity by: (a) avoiding remodelling of infarct (thinning of infarct wall + dilation of infarct zone) → aneurysm, VSD rupture, HF; (b) improving collateral circulation
Why this matters: The evolving phase is your window for reperfusion therapy. After this window, focus shifts to preventing adverse remodelling (using ACEI, beta-blockers, aldosterone antagonists). The K⁺ efflux from ischaemic cells explains why VF is so common early — the heterogeneous K⁺ gradients create re-entry circuits.
Predisposing factors for AMI: [1]
- Unusual heavy exercise
- Emotional stress
- Progression from unstable angina
- Surgical procedures
- Infection e.g. pneumonia
- Circadian periodicity — peak incidence between 0600–1200
Why 6 AM to noon? Morning catecholamine surge → ↑ heart rate, ↑ BP, ↑ platelet aggregability, ↑ coronary artery tone. This is also why beta-blockers are protective — they blunt the morning sympathetic surge.
Nature of chest pain in AMI: [1]
- Severe, maybe intolerable
- Prolonged, usually > 30 minutes
- Nature: constricting, crushing, compressing, heavy weight
- Radiation: left arm (ulnar aspect)
- Other symptoms: SOB, weakness, dizziness, palpitation, nausea, vomiting (Bezold-Jarisch reflex)
The Bezold-Jarisch reflex is a vagal reflex triggered by ischaemic stimulation of cardiac C-fibres (especially in inferior MI) → causes bradycardia, hypotension, nausea, and vomiting. This is why inferior MI patients often present with vomiting and sinus bradycardia — don't mistake it for a GI problem! [1]
What differentiates MI pain from stable angina pain?
| Feature | Stable Angina | AMI |
|---|---|---|
| Duration | 2–10 minutes | > 30 minutes |
| Trigger | Exertion, emotion, cold | Often spontaneous (can be at rest) |
| Relief | Rest, sublingual GTN | NOT relieved by rest or GTN |
| Severity | Mild to moderate | Severe, intolerable |
| Associated features | ± SOB | Sweating, nausea, angor animi (feeling of impending death) |
Atypical presentations (exam trap): ~25% of MI patients have NO chest pain, especially diabetics (autonomic neuropathy masks pain) and the elderly. They may present with acute dyspnoea, syncope, or confusion. [4]
Differential diagnosis: [1]
- Acute pericarditis — aggravated by respiratory movement, sharp, knife-like; radiates to the trapezius ridge (characteristic site of pericardial pain)
- Pulmonary embolism — haemoptysis
- Aortic dissection — radiation to back, ripping or tearing sensation
| Condition | Pain Character | Radiation | Key Discriminator |
|---|---|---|---|
| AMI | Crushing, constricting | Left arm (ulnar), jaw, neck | > 30 min, not relieved by rest/GTN |
| Aortic dissection | Tearing, ripping, maximal at onset | Interscapular back, abdomen | Pulse deficit, BP asymmetry |
| Acute pericarditis | Sharp, pleuritic | Trapezius ridge | Worse lying down, better sitting forward |
| Pulmonary embolism | Pleuritic, sudden | — | Haemoptysis, DVT signs, tachycardia |
| Pneumothorax | Sharp, unilateral, sudden | — | Hyperresonance, absent breath sounds |
Exam Trap: Trapezius Ridge
Pericardial pain radiating to the trapezius ridge is almost pathognomonic for pericarditis. This is a favourite exam discriminator because most students will say "shoulder" generically. The phrenic nerve (C3-5) innervates the pericardium and refers pain specifically to the trapezius ridge and shoulder tip. [1][5]
PART 2: DIAGNOSIS OF AMI
This is a favourite exam topic. The lecture covers all 5 types. [1]
| Type | Mechanism | Key Detail |
|---|---|---|
| Type 1 | Spontaneous MI due to atherosclerotic plaque rupture/erosion → intraluminal thrombus | The classic "heart attack." Requires evidence of ischaemia + rise/fall in cardiac biomarkers |
| Type 2 | MI due to oxygen supply/demand mismatch NOT caused by acute plaque rupture | Examples: severe anaemia, tachyarrhythmia, hypotension, coronary spasm, coronary embolism |
| Type 3 | Cardiac death with symptoms suggestive of MI and presumably new ECG changes or VF, but death occurs before biomarkers can be obtained | "Sudden cardiac death" scenario |
| Type 4A | MI related to PCI | Troponin rise > 5× 99th percentile URL after PCI |
| Type 4B | MI related to stent thrombosis | Confirmed by angiography or autopsy |
| Type 5 | MI related to CABG | Troponin rise > 10× 99th percentile URL after CABG |
Criteria for AMI Type 1 & 2 (ESC): Detection of rise and/or fall of cardiac troponin with at least one value above the 99th percentile URL, together with at least one of: [1]
- Symptoms of myocardial ischaemia
- New ischaemic ECG changes
- Development of pathological Q waves
- Imaging evidence of new loss of viable myocardium or new RWMA
- Identification of coronary thrombus (angiography/autopsy)
Type 1 vs Type 2 MI — Common Exam Discriminator
Type 1 = plaque event (atherothrombosis). Type 2 = secondary to a supply-demand mismatch (e.g., patient with stable CAD develops sepsis → tachycardia → myocardial ischaemia). The treatment is entirely different: Type 1 gets antithrombotic + revascularisation; Type 2 gets treatment of the underlying condition (e.g., treat sepsis, correct anaemia).
Biomarkers: [1]
- ↑ 2× CPK (creatinine phosphokinase) — MB isoenzyme; CPK-MM = skeletal muscle (may be confusing if given IM injection)
- SGOT — raised also in liver disease, pulmonary congestion, skeletal muscle injury
- LDH — LDH1 = cardiac, RBC; LDH4,5 = liver, skeletal muscle
- Troponin T or I (PREFERABLE):
- Not normally present in blood
- More sensitive and specific than CK-MB/CK
- Long lasting → diagnosis of MI with delayed presentation (but NOT good for reinfarction)
- "Stick" test available
- Myoglobin — first marker to increase in MI, but unspecific and eliminated quickly
Biomarker kinetics — exam favourite:
| Biomarker | Onset | Peak | Duration | Notes |
|---|---|---|---|---|
| Myoglobin | 1–2h | 6–8h | 24h | First to rise, but non-specific (also skeletal muscle) |
| CK-MB | 3–4h | 18–24h | 48–72h | Useful for detecting reinfarction (short half-life) |
| Troponin (T/I) | 3–4h | 12–24h | 7–14 days | Gold standard. High sensitivity troponin detects earlier |
| LDH | 12–24h | 48–72h | 7–10 days | Historical; rarely used now |
Why troponin is preferred: It has both higher sensitivity and specificity for myocardial injury than CK-MB. However, because troponin remains elevated for up to 14 days, it cannot distinguish reinfarction from the initial event — for that, CK-MB (which returns to baseline faster) is better. [1]
High-sensitivity troponin (hs-cTn): Current practice uses hs-cTn with serial measurements. A rise and/or fall pattern is essential to distinguish acute MI from chronic troponin elevation (e.g., renal failure, heart failure). [6]
Exam Trap: Troponin Elevation ≠ AMI
Troponin elevation indicates myocardial injury, NOT necessarily MI. Causes of troponin elevation without MI include: heart failure, myocarditis, PE, sepsis, renal failure, cardiac contusion, tachyarrhythmia, and cardiac procedures. You need clinical context + rise/fall pattern + ischaemic symptoms/ECG changes to diagnose MI. [1][6]
ST-segment elevation with pathological Q-wave formation. Sometimes T-wave inversion may be found but it is a non-specific feature. [1] ST-segment elevation indicates full-thickness cardiac muscle injury; pathological Q-wave indicates muscle necrosis; T-wave inversion indicates muscle ischaemia. [1]
ECG evolution of STEMI:
| Stage | ECG Finding | Pathological Significance | Timing |
|---|---|---|---|
| Hyperacute | Tall, peaked T waves | Early transmural ischaemia | Minutes |
| Acute | ST elevation | Full-thickness injury (current of injury) | Hours |
| Evolving | Pathological Q waves appear, ST starts to normalise | Transmural necrosis | Hours–days |
| Old/Chronic | Q waves persist, T-wave inversion may resolve | Completed infarct (scar) | Days–months |
Localisation of MI by ECG leads:
| Territory | Leads | Artery |
|---|---|---|
| Anterior | V1–V4 | LAD |
| Lateral | I, aVL, V5–V6 | LCx |
| Inferior | II, III, aVF | RCA (or LCx) |
| RV infarct | V3R, V4R (right-sided leads) | Proximal RCA |
| Posterior | Reciprocal ST depression V1–V3, tall R wave V1 | RCA or LCx |
R-side chest leads → RV infarction [1]
Why RV infarction matters: RV infarction complicates ~30% of inferior MIs. These patients are preload-dependent — giving them nitrates or diuretics drops their BP catastrophically. Treatment = IV fluids. Always do right-sided leads (V4R) in inferior STEMI! [1]
ECG Pitfalls in Diagnosis of MI: [1]
- LBBB can mask STEMI (use Sgarbossa criteria)
- Paced rhythms
- LVH with strain pattern
- Early repolarisation
- Pericarditis (diffuse ST elevation with PR depression)
- Takotsubo cardiomyopathy
High Yield: aVR ST Elevation
ST elevation in aVR is a critical finding suggesting either left main coronary artery occlusion or severe multi-vessel/proximal LAD disease (often with diffuse ST depression elsewhere). This was specifically highlighted in the ACS interactive tutorial. [7] Don't miss it — it portends a very high mortality.
Cardiac Imaging: [1]
- Echocardiogram:
- Abnormal wall motions (regional wall motion abnormalities — RWMA)
- Ventricular function → use of ACEI
- Complications: VSD, pericardial effusion, ventricular thrombus, RV infarct
- Angiogram + PTCA (percutaneous transluminal coronary angioplasty)
- Nuclear imaging (radionuclide perfusion scan)
Prior MI criteria on ECG (ESC):* [1]
- Pathological Q waves with or without symptoms, in the absence of non-ischaemic causes
- Q wave ≥ 0.03s duration and ≥ 1mm deep in 2 contiguous leads
- Any Q wave in V2–V3 ≥ 0.02s or QS complex in V2 and V3
PART 3: TREATMENT OF STEMI
Management of AMI: [1]
- General measures: Bed rest, O₂, Morphine; CCU care ± resuscitation
- Early presentation ( < 12h) → Opening of infarct-related artery:
- Fibrinolytic therapy
- Primary PTCA (PCI)
- Other measures: Anti-platelet agents, Beta-blockers, ACEI/ARB
- Complications management and rehabilitation
The occlusive coronary thrombus has three components requiring targeted treatment: [1]
- Fibrin → Plasminogen activators (tPA, rPA, TNK-tPA, SK)
- Platelets → Antiplatelet therapy (Aspirin + Clopidogrel/Prasugrel/Ticagrelor, or GP IIb/IIIa inhibitors)
- Thrombin → Antithrombin therapy (Heparin, LMWH, Fondaparinux, Bivalirudin)
Indication: [1]
- AMI — Pain + ST elevation in ≥ 2 contiguous chest leads
- Time of onset of pain < 12 hours
- Absence of contraindications — bleeding tendency, cardiogenic shock, recent head injury/stroke
Documentation of successful fibrinolysis: [1]
- Clinical: Decrease in pain
- ECG Criteria: Early resolution of ST elevation at 90 min; preservation of R wave
- Biochemical: Early peaking of CPK (normal peak 22–24h; successful thrombolysis 11–12h)
- Imaging: Radionuclide imaging, angiography
Why does CPK peak earlier with successful thrombolysis? When the artery reopens, the restoration of blood flow "washes out" intracellular enzymes from the necrotic zone into the circulation more rapidly → you see an earlier, sharper CPK peak. This is called a washout phenomenon and is actually a reassuring sign. [1]
Types of thrombolytic therapy: [1]
- Non-specific: Streptokinase (1.5 million units in 1 hour)
- Activates plasminogen to plasmin in the WHOLE circulation → systemic fibrinolysis
- Plasmin is a potent lytic agent for fibrin
- Tissue-type plasminogen activator (tPA)
- Inactive in absence of fibrin; activated in presence of fibrin → clot-specific
- More rapid lysis, lower bleeding complications
- Administered with heparin (10mg IV bolus, 50mg first hour, then 40mg over 2–3h: total 100mg)
- tPA derivatives: TNK-tPA, Lanoteplase, Reteplase
Why is tPA better than streptokinase? tPA is fibrin-specific — it activates plasminogen preferentially at the clot surface, so there's less systemic plasminogen activation and lower risk of bleeding. Streptokinase activates plasminogen everywhere (non-specific), causing systemic fibrinolysis. However, SK is much cheaper and doesn't require co-administration with heparin. [1]
Absolute contraindications: [1]
- Any prior intracranial haemorrhage (ICH)
- Known structural cerebrovascular lesion (e.g., AVM)
- Known malignant intracranial neoplasm
- Ischaemic stroke within 3 months (EXCEPT acute ischaemic stroke within 3 hours)
- Suspected aortic dissection
- Active bleeding or bleeding diathesis (excluding menses)
- Significant closed head or facial trauma within 3 months
Relative contraindications: [1]
- Chronic severe, poorly controlled hypertension
- Severe uncontrolled hypertension on presentation (SBP > 180 or DBP > 110)
- Prior ischaemic stroke > 3 months
- Traumatic or prolonged ( > 10 min) CPR or major surgery ( < 3 weeks)
- Recent (2–4 weeks) internal bleeding
- Non-compressible vascular punctures
- Prior SK/anistreplase exposure ( > 5 days ago) or allergic reaction
- Pregnancy
- Active peptic ulcer
- Current anticoagulant use (higher INR = higher bleeding risk)
High Yield: Suspected Aortic Dissection = Absolute Contraindication to Thrombolysis
Suspected aortic dissection is an ABSOLUTE contraindication to fibrinolytic therapy. [1] This is the #1 reason you must differentiate aortic dissection from STEMI before giving thrombolytics. If you lyse a dissection patient, you will worsen the haemorrhage and likely kill them. Key discriminators: tearing pain maximal at onset, radiating to back, pulse deficits, BP asymmetry.
Limitations: [1]
- Only 50% of patients receiving fibrinolysis achieve optimal myocardial perfusion
- 1/3 reocclude by 3 months
- Delayed presentation and undiagnostic ECGs
- Fibrinolytic therapy reduced in-hospital mortality by 50% vs placebo (in trials 6–8%; real world 20%)
Actions to address these: Thrombin inhibition, platelet inhibition, + PTCA; treatment in ambulance and A&E; education [1]
Primary PCI (direct angioplasty) is preferred over fibrinolysis when: [1]
- PCI can be performed within 120 minutes of first medical contact
- PCI achieves TIMI-3 flow in > 90% (vs ~50% with fibrinolysis)
- Lower risk of ICH
The critical timing concept: As the PCI-related delay (door-to-balloon minus door-to-needle time) increases, the advantage of PCI over fibrinolysis diminishes. If PCI delay exceeds 120 minutes from first medical contact, fibrinolysis should be given (especially if symptom onset < 3h). [1]
Emergency CABG is indicated for: [1]
- Failed PCI with ongoing ischaemia
- Left main or severe 3-vessel disease found at angiography
- Mechanical complications (VSD, papillary muscle rupture)
Aspirin: [1]
- ↓ Acute mortality (especially in conjunction with thrombolysis)
- ↓ Reinfarction in long-term follow-up
- Dose: 160–320 mg/day
Clopidogrel / Prasugrel / Ticagrelor — P2Y12 inhibitors for dual antiplatelet therapy (DAPT) [1]
Heparin: [1]
- SC heparin (5000u Q8H) for DVT prophylaxis — APTT not changed (or LMWH)
- IV heparin (APTT ratio 1.5–2) for preventing embolisation, mural thrombosis
- Adjunct to fibrinolytic therapy (tPA) or patients without lytic therapy
Warfarin: [1]
- For established venous thrombosis or embolisation
- Echocardiographic evidence of LV thrombus
Calcium antagonist (Diltiazem): [1]
- In non-Q-wave infarct, reduces reinfarction and improves survival in patients WITHOUT heart failure
Nitrates: [1]
- IV nitrate may reduce infarct size if mean BP > 80 mmHg
- Oral nitrate: neutral effect
Beta-blockers: [1]
- ↓ Mortality by 15% within 12h of infarct (IV)
- ↓ Long-term mortality by 25% (oral)
- Risk of hypotension and cardiogenic shock (IV) — be cautious
- Use beta-blockers WITHOUT intrinsic sympathomimetic activity: Metoprolol, Timolol
Beta-blocker: Should be given to all patients with LV dysfunction [1] ACEI: Indicated for all patients with LVEF < 40%, DM, HT, renal dysfunction [1] ARB: Indicated for patients intolerant to ACEI [1] Aldosterone receptor antagonist (e.g., eplerenone, spironolactone): [1]
- Patients on ACEI/BB with LVEF < 40% AND HF, without significant renal dysfunction or hyperkalaemia
A. Risk stratification: [1]
- Residual ischaemia → exercise test, angiogram
- Electrical instability → 24h ECG for VT or frequent ventricular arrhythmia
B. Secondary prevention: [1]
- Risk factor modulation: exercise, smoking cessation, lipid lowering (aggressive statin therapy reduces mortality; ezetimibe; PCSK9 inhibitor)
- Beta-blocker (oral), Aspirin, ACEI/ARB
- Cardiac rehabilitation and prevention: risk factor control, work, exercise, sex, alcohol, travel
ESC 2020 Lipid targets for NSTE-ACS (applies to all ACS): [1]
- LDL-C reduction ≥ 50% from baseline AND LDL-C < 1.4 mmol/L
- If not achieved with max statin → add ezetimibe
- If still not achieved → add PCSK9 inhibitor
AMI Complications: [1]
- Heart failure
- Arrhythmias (VF, VT, heart block — especially inferior MI)
- VSD (anterior MI) — new pansystolic murmur, haemodynamic deterioration
- Mitral regurgitation from papillary muscle dysfunction (inferior MI)
- Pericarditis (early: Day 1–3 from transmural necrosis; late: Dressler syndrome at 2–10 weeks, autoimmune)
| Complication | Associated Territory | Mechanism |
|---|---|---|
| VF/VT | Any, most common early | Re-entry due to heterogeneous K⁺ gradients |
| Complete heart block | Inferior MI | RCA supplies AV node |
| VSD | Anterior MI (LAD) | Septal necrosis and rupture |
| Papillary muscle rupture/dysfunction | Inferior MI (RCA) | Posteromedial papillary muscle has single blood supply (RCA) |
| LV aneurysm | Anterior MI | Thinning and bulging of necrotic wall |
| LV thrombus | Anterior MI (akinetic apex) | Stasis over akinetic segment → thrombus formation → embolism |
| Dressler syndrome | Any | Autoimmune pericarditis, 2–10 weeks post-MI |
Why is VSD more common in anterior MI but MR more common in inferior MI?
The interventricular septum is supplied by the LAD → anterior MI → septal necrosis → VSD. The posteromedial papillary muscle has a single blood supply (from the PDA, usually off the RCA), so inferior MI → papillary muscle ischaemia/rupture → acute MR. The anterolateral papillary muscle has dual supply (LAD + LCx) and is therefore relatively protected. [1]
PART 4: AORTIC DISSECTION
Pathology: Medial collagen and elastin degeneration [1] Blood violates aortic intimal and adventitial layers → False lumen is created → Dissection may extend proximally, distally, or in both directions [1]
First principles: The aortic wall has three layers — intima, media, adventitia. In aortic dissection, the intima tears and blood enters the media, separating the intima from the adventitia. This creates a false lumen that can propagate anterograde (down towards the abdomen) or retrograde (back up towards the heart). The false lumen can compress the true lumen, occlude branch vessels, and/or rupture externally. [1][8]
Causes: [1]
- Coexisting hypertension (80%) — this is the single most important risk factor
- Genetic diseases: Marfan syndrome, Familial aortic aneurysm/dissection, Ehlers-Danlos, Loeys-Dietz
- Bicuspid aortic valve
- Trauma
Additional risk factors from supporting sources: [8][9]
- Cocaine use (sudden severe hypertension)
- Pregnancy (3rd trimester, hormonal-mediated connective tissue changes)
- Vasculitis (e.g., Takayasu arteritis)
- Iatrogenic (cardiac surgery, catheterisation)
Classification: [1]
- Type A: ascending aorta involved (regardless of where the tear originates — can extend into descending)
- Type B: all dissections NOT involving the ascending aorta
| Classification | Stanford A | Stanford B |
|---|---|---|
| DeBakey equivalent | I (ascending + descending) and II (ascending only) | III (descending only) |
| Frequency | ~60–70% | ~30–40% |
| Mortality (untreated) | 1–2% per hour in first 48h | Lower, but still significant |
| Management | Emergency surgery | Medical (BP control) unless complicated |
Why Type A is an emergency: The ascending aorta is in close proximity to the coronary ostia, aortic valve, pericardium, and brachiocephalic vessels. Retrograde dissection can cause:
Symptoms: [1]
- Chronic: can be asymptomatic
- Acute: severe pain (MAXIMUM AT ONSET)
- "Tearing" quality
- Anterior chest (ascending aorta — Type A)
- Interscapular, abdomen (descending aorta — Type B)
- Complications: Syncope, CVA, ischaemic limbs, paraplegia, acute AR → CHF
Signs: [1]
- BP — high or low (tamponade)
- Pulse deficits
- Complications: AR, CVA
Key discriminator from AMI: In aortic dissection, pain is maximal at onset (sudden, explosive), whereas in AMI, pain typically builds up over minutes. This is a classic exam discriminator. [1][5]
Complications by mechanism:
| Complication | Mechanism |
|---|---|
| Acute AR | Dissection disrupts aortic valve commissures |
| MI | False lumen occludes coronary ostia (usually RCA → inferior STEMI) |
| Stroke / LOC | Carotid artery involvement |
| Paraplegia | Artery of Adamkiewicz (great anterior radiculomedullary artery) compromised |
| Mesenteric ischaemia | SMA/IMA compromised |
| AKI | Renal artery involvement |
| Limb ischaemia | Subclavian/iliac/femoral artery involvement |
| Cardiac tamponade | Retrograde dissection into pericardium → haemopericardium |
| Haemothorax | Rupture into pleural space |
Abnormal CXR in > 80% of cases [1]
- Widened mediastinum (> 6 cm at level of carina on PA film; > 8 cm on AP film) [10]
- Pleural effusion (especially left-sided — beware: suggests leaking/rupture)
- Irregular aortic contour
CT Aortogram (preferred investigation): [1]
- Newer helical CT scans have almost 100% specificity and sensitivity
- Ability to identify thrombosed false lumens
- Less invasive
- Shows intimal flap separating true and false lumens
TEE (Transoesophageal echocardiogram): [1]
- Combining TTE and TEE: sensitivities and specificities > 95%
- Very rapid (~10 minutes each exam)
- Can be done at bedside with minimal risk
- Limited visualisation of distal aorta
- False-positive results are possible
MRI: [1]
- Sensitivity and specificity of almost 100%
- Identifies intimal flaps, great vessel anatomy, type A & B, degree of AI
- Time consuming ( > 30 min) → unsuitable for unstable patients
- Patient needs to be disconnected from monitoring devices, IV pumps
- Useful for serial follow-up of chronic dissections
Practical hierarchy: CT aortogram is the go-to investigation for acute aortic dissection because it is fast, widely available, and has near-100% sensitivity/specificity. TEE is used when the patient is too unstable to leave the ward or when immediate bedside assessment is needed (e.g., intraoperatively). MRI is reserved for stable patients and chronic follow-up. [1][11]
1. Haemodynamic stabilisation: [1]
- Control BP — SBP 100–120 mmHg
- e.g., Nitroprusside — may ↑ dp/dt, so pretreat with beta-blocker
- Labetalol (combined α + β blocker — reduces both BP and dp/dt)
- Tamponade → surgical drainage
2. Definitive treatment: resection and graft [1]
- Acute Type A dissection → Emergency surgery
- Type B surgery indicated if: involves distal organs, rupture, retrograde dissection, Marfan syndrome
- Newer treatment: Stent grafts (TEVAR — thoracic endovascular aortic repair for Type B)
Why beta-blockers FIRST before nitroprusside? Nitroprusside is a pure arteriolar vasodilator that reduces afterload. But by reducing afterload, it causes reflex tachycardia and increases the rate of aortic pressure rise (dp/dt), which can propagate the dissection. Beta-blockers reduce both heart rate and dp/dt, so they must be given FIRST to blunt this reflex before adding nitroprusside. [1][12]
Why is the target SBP 100–120? Lower BP reduces the shear stress on the aortic wall, minimising the force driving dissection propagation. But you must maintain adequate end-organ perfusion (cerebral, renal, coronary). [1]
Critical Distinction: AMI vs Aortic Dissection Management
AMI: Anticoagulate, give antiplatelets, reperfuse (PCI or thrombolysis) Aortic Dissection: AVOID anticoagulation/thrombolysis (kills the patient), REDUCE BP and dp/dt, surgery for Type A
If a patient has aortic dissection that extends into a coronary ostium causing STEMI, the treatment is emergency surgery — NOT thrombolysis! [1]
The lecture slide shows the NSTEMI management algorithm. Key principles: [1]
- Antiplatelet (Aspirin + P2Y12 inhibitor)
- Anticoagulant (LMWH or fondaparinux)
- Anti-ischaemic (beta-blocker, nitrate)
- Early invasive strategy (coronary angiography ± PCI within 24–72h) for high-risk patients
- Risk stratification using GRACE score
Clinical Approach: Putting It All Together
| Feature to Assess | Why It Matters |
|---|---|
| SOCRATES (Site, Onset, Character, Radiation, Associated features, Timing, Exacerbating/Relieving, Severity) | Structured approach ensures no feature is missed |
| Onset: sudden/maximal at onset vs progressive | Sudden maximal → dissection, PE, PTX; Progressive → ACS |
| Character: crushing vs tearing vs pleuritic | Crushing = ACS; Tearing = dissection; Pleuritic = PE/pericarditis |
| Radiation: arm/jaw vs back vs trapezius ridge | Arm/jaw = ACS; Back = dissection; Trapezius = pericarditis |
| Duration: > 30 min | Distinguishes MI from stable angina |
| Relief by GTN/rest? | Angina yes; MI no |
| Risk factors | HTN, DM, smoking, hyperlipidaemia, FHx, cocaine use, connective tissue disease |
| Associated symptoms | Nausea/vomiting (Bezold-Jarisch), dyspnoea, syncope, haemoptysis (PE), limb weakness (dissection) |
| Sign | Condition |
|---|---|
| Levine's sign (clenched fist on chest) | ACS |
| Sweating, pallor, hypotension | Cardiogenic shock from large MI |
| S3 gallop, basal crepitations | Heart failure complicating MI |
| New pansystolic murmur | VSD or acute MR (post-MI complication) |
| Early diastolic murmur + wide pulse pressure | Acute AR from dissection |
| Pulse deficit, BP asymmetry between arms | Aortic dissection |
| Muffled heart sounds + hypotension + JVP↑ (Beck's triad) | Cardiac tamponade from dissection |
| Friction rub | Pericarditis (early MI complication or Dressler syndrome) |
- ECG — stat, repeat serially
- Cardiac biomarkers — hs-troponin at presentation and 3–6h later
- CXR — widened mediastinum (dissection), pulmonary oedema (HF), pneumothorax
- Bloods — CBC, RFT, LFT, lipid profile, glucose, coagulation profile
- If dissection suspected → urgent CT aortogram
- Echocardiogram — RWMA, LV function, complications (VSD, MR, pericardial effusion, LV thrombus)
- Coronary angiography → if STEMI (for primary PCI) or high-risk NSTEMI
Based on GC lecture content, past paper patterns, and clinical scenarios: [1][2][3]
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"A 58-year-old smoker presents with crushing central chest pain for 2 hours, radiating to the left arm. ECG shows ST elevation in leads II, III, aVF. What is the most likely diagnosis? What artery is involved? What immediate management would you initiate?"
- Inferior STEMI; Right coronary artery; Primary PCI (if available within 120 min) or fibrinolysis; Aspirin 300mg loading, P2Y12 inhibitor, heparin, morphine, O₂ if SpO₂ < 94%, beta-blocker (if no contraindication)
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"List the absolute contraindications to fibrinolytic therapy."
- Prior ICH, known structural cerebrovascular lesion, malignant intracranial neoplasm, ischaemic stroke < 3 months, suspected aortic dissection, active bleeding/bleeding diathesis, significant closed head/facial trauma < 3 months
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"A 70-year-old hypertensive man presents with sudden-onset severe tearing chest pain radiating to the back, maximal at onset. BP is 200/110 in the right arm and 160/90 in the left arm. What is the diagnosis? What is the first-line investigation? What is the immediate management?"
- Type A aortic dissection (until proven otherwise); CT aortogram; IV labetalol to target SBP 100–120, then consider nitroprusside; emergency surgical consultation
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"Compare and contrast the clinical features of AMI and aortic dissection." (Table format — see 1.5 above)
-
"What are the complications of anterior STEMI?"
- Heart failure, VSD (septal rupture), LV aneurysm, LV thrombus → systemic embolism, arrhythmias, pericarditis
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"Explain the difference between Type 1 and Type 2 myocardial infarction."
- Type 1 = spontaneous MI due to plaque rupture/erosion; Type 2 = MI due to O₂ supply-demand mismatch without plaque event (e.g., severe anaemia, sepsis, tachyarrhythmia)
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"Why must beta-blockers be given BEFORE nitroprusside in aortic dissection?"
- Nitroprusside causes reflex tachycardia and increases dp/dt (rate of aortic pressure rise), which propagates dissection. Beta-blockers blunt this reflex.
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"A patient with inferior STEMI develops hypotension after receiving sublingual GTN. What complication should you suspect and how do you confirm it?"
- RV infarction (preload-dependent); confirm with right-sided ECG leads (V3R, V4R); treatment = IV fluids, AVOID nitrates and diuretics
High Yield Summary
STEMI:
- Plaque rupture → total coronary occlusion → transmural necrosis
- Pain > 30 min, crushing, radiates to arm/jaw, not relieved by rest/GTN
- ECG: ST elevation in ≥ 2 contiguous leads → localise territory
- Troponin is the preferred biomarker (sensitive, specific, long-lasting)
- Reperfusion: Primary PCI (preferred if < 120 min) or fibrinolysis (if PCI delayed)
- Adjunctive: DAPT (Aspirin + P2Y12), anticoagulant, beta-blocker, ACEI/ARB, statin
- Complications: HF, arrhythmias, VSD (anterior), MR (inferior), pericarditis
- Post-MI: Risk stratification, secondary prevention (ABCDE), cardiac rehabilitation
Aortic Dissection:
- Medial degeneration → intimal tear → false lumen
- Pain maximal at onset, tearing, radiates to back
- Stanford A (ascending) = emergency surgery; Stanford B = medical management
- Target SBP 100–120 with beta-blocker FIRST (reduce dp/dt), then ± nitroprusside
- CT aortogram is the investigation of choice
- Mortality ~1% per hour untreated in first 48h
- NEVER give thrombolytics to a suspected dissection patient
Critical Differentiation for Exams:
- AMI: progressive pain, crushing → anticoagulate and reperfuse
- Dissection: maximal-at-onset pain, tearing, pulse deficits → reduce BP, avoid anticoagulation, surgery for Type A
Active Recall - Sudden Severe Chest Pain
[1] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (all pages) [2] Past papers: 2023 Fourth Summative MCQ.pdf; 2024 Fourth Summative SAQ.pdf [3] Past papers: 2022 Fourth Summative SAQ.pdf [4] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p398–401) [5] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (p15) [6] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf (p1) [7] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf (p15) [8] Senior notes: Maksim Medicine Notes.pdf (p15) [9] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p905) [10] Senior notes: Block A - Introduction to CVS investigations (including ECG).pdf (p8) [11] Senior notes: Block A - Chest Pain - Department of Radiology.pdf (p1) [12] Senior notes: Block A - Clinical Pharmacology of anti-HT and anti-HF medications.pdf (p5)
GC087 Sudden Hemiplegia Dysphagia
Sudden hemiplegia with dysphagia is an acute neurological presentation, typically due to a stroke affecting the middle cerebral artery or brainstem, resulting in unilateral motor weakness and impaired swallowing.
GC089 Syncope And Irregular Heart Beat
Syncope is a transient loss of consciousness due to cerebral hypoperfusion, and irregular heartbeat (arrhythmia) refers to abnormal cardiac rhythm disturbances, which together represent a clinical presentation where cardiac dysrhythmias may cause hemodynamic compromise leading to fainting episodes.