Chest Pain

Chest pain is a symptom of discomfort or distress in the thoracic region that may originate from cardiac, pulmonary, gastrointestinal, musculoskeletal, or psychogenic causes, requiring prompt evaluation to exclude life-threatening conditions.

Epidemiology

Risk Factors

These are best organised by the aetiology they predispose to, because in the exam and in clinical practice you use risk factors to shift your pre-test probability:

Modifiable	Non-Modifiable
Abdominal obesity	Family history of premature CVD (1st-degree male < 55 y or female < 65 y)
Hypertension	Male sex
Hyperlipidaemia (esp. ↑LDL, ↓HDL)	Advanced age
Cigarette smoking
Diabetes mellitus
Sedentary lifestyle / lack of exercise
Unhealthy diet

^[1]^[2]

Anatomy and Function

Understanding the anatomy of the chest is essential because the source of pain depends on which structures are involved, and the pattern of pain referral depends on their innervation.

The aetiologies of chest pain can be systematically classified by organ system. Below is a comprehensive framework that integrates the probability diagnoses and serious diagnoses from the lecture slides ^[8].

Systematic Aetiological Classification

A. Cardiovascular Causes

Aetiology	Pathophysiology	HK Relevance
Stable angina / Chronic coronary syndrome	Fixed coronary atherosclerotic stenosis → O₂ demand > supply during exertion → myocardial ischaemia → metabolite accumulation (adenosine, lactate, K⁺) → stimulation of cardiac sympathetic nerves → pain ^[1]^[2]	Very common; rising prevalence with ageing population and increasing metabolic syndrome
Acute coronary syndrome (UA/NSTEMI/STEMI)	Acute atherosclerotic plaque rupture/erosion → thrombus formation → dynamic coronary obstruction → ischaemia even at rest → if complete occlusion: transmural infarction (STEMI) ^[1]^[2]	Leading cardiovascular cause of death in HK
Aortic dissection	Tear in aortic intima → blood enters media → creates false lumen → false lumen dilates, true lumen collapses → end-organ malperfusion ^[5]	Hypertension extremely prevalent in HK elderly population; must always exclude
Pericarditis / Myopericarditis	Inflammation of pericardium → irritation of phrenic nerve endings in parietal pericardium → sharp, pleuritic pain; if effusion develops → cardiac tamponade	Viral causes common; TB pericarditis important in HK given local TB burden
Mitral valve prolapse	Myxomatous degeneration of mitral valve leaflets → prolapse into LA during systole → may cause atypical chest pain (mechanism unclear; possibly papillary muscle traction or associated autonomic dysfunction) ^[8]	Often discovered incidentally; included in Murtagh's "pitfalls"
Aortic stenosis	↑LV afterload → LV hypertrophy → ↑myocardial O₂ demand with ↓coronary perfusion reserve → subendocardial ischaemia → exertional angina even with normal coronaries	Degenerative AS increasingly common in ageing HK population
Hypertrophic cardiomyopathy (HCMP) — particularly apical HCMP	↓Vasodilatory reserve → subendocardial ischaemia → chest pain (atypical or typical angina) ^[9]. 25–30% of HCMP in Japan and HK is apical type (vs 1–2% elsewhere)	Very high yield for HK exams — disproportionately common in East Asian populations
Pulmonary hypertension	↑RV wall stress → subendocardial hypoperfusion of RV → exertional chest pain ^[6]	Consider in patients with chronic lung disease, recurrent PE, connective tissue diseases
Cardiac tamponade	Pericardial fluid accumulation → ↑intrapericardial pressure → impaired diastolic filling → ↓cardiac output → shock; pain is from pericardial stretching	TB, malignancy (lung, breast), uraemia, post-MI (Dressler syndrome)

B. Pulmonary and Pleural Causes

Aetiology	Pathophysiology	HK Relevance
Pulmonary embolism	DVT embolises to pulmonary vasculature → V/Q mismatch → hypoxia; if large → acute RV failure → haemodynamic collapse. Pleuritic pain occurs when emboli cause pulmonary infarction → parietal pleural inflammation ^[6]	Important to consider in post-operative, immobilised, malignancy patients
Pneumothorax	Air enters pleural space → loss of negative intrapleural pressure → lung collapse → sudden pleuritic pain + dyspnoea. Tension PTX: one-way valve → progressive air accumulation → mediastinal shift → obstructive shock ^[7]	Primary spontaneous: young, tall, thin males; Secondary: COPD and TB very relevant in HK
Pneumonia / Pleuritis (pleurisy)	Infection → alveolar and pleural inflammation → exudate on parietal pleura → stimulation of intercostal nerves → pleuritic chest pain ^[8]	Pneumonia is a top cause of death in HK; TB must always be considered
Pleural effusion	Pleuritic chest pain usually ↓ in intensity with ↑effusion size (because inflamed pleural surfaces are no longer in contact) ^[10]	TB pleural effusion is a classic presentation in HK
Lung cancer	Direct chest wall invasion, rib erosion, pleural involvement, nerve compression (brachial plexus in Pancoast tumour), mediastinal infiltration ^[4]	2nd commonest cancer, 1st in mortality in HK ^[4]. In HK females, > 75% are adenocarcinoma and < 40% are smokers ^[4]
Mediastinitis	Infection/inflammation of mediastinal tissues → deep, severe, poorly localised chest pain + systemic sepsis ^[8]	Rare but life-threatening; may follow oesophageal perforation (Boerhaave syndrome)

C. Gastrointestinal Causes

Aetiology	Pathophysiology
Gastro-oesophageal reflux disease (GERD)	Reflux of gastric acid into oesophagus → mucosal inflammation → visceral afferent stimulation at T1–T5 → retrosternal burning/non-cardiac chest pain ^[3]. In Asians: atypical presentation with ↑NCCP ^[3]
Oesophageal spasm (diffuse oesophageal spasm)	Simultaneous contractions of circular muscle of oesophageal body → episodic chest pain that may mimic angina ^[11]. Responds to nitrates (smooth muscle relaxant) — a diagnostic pitfall
Peptic ulcer disease	Imbalance between aggressive factors (acid, pepsin) > protective mechanisms (mucus, bicarbonate, prostaglandins, mucosal blood flow) → mucosal erosion → visceral pain ^[12]. Epigastric pain may be perceived as lower chest pain
Biliary colic	Gallstone impaction in cystic duct → gallbladder spasm → visceral pain referred to epigastrium/right upper quadrant/right chest/right shoulder (phrenic nerve pathway) ^[8]
Oesophagitis / oesophageal ulceration	Direct mucosal damage (acid, medications like bisphosphonates, infections in immunocompromised) → odynophagia and chest pain
Oesophageal perforation (Boerhaave syndrome)	Transmural tear (usually from forceful vomiting) → mediastinal contamination → mediastinitis + subcutaneous emphysema → severe chest pain + systemic sepsis

D. Musculoskeletal Causes

Aetiology	Pathophysiology
Musculoskeletal chest wall pain (including costochondritis)	Inflammation of costochondral junctions (Tietze syndrome if swelling present) or intercostal muscle strain → somatic pain via intercostal nerves → sharp, well-localised, reproducible on palpation/movement ^[8]
Rib fracture	Trauma or pathological fracture (osteoporosis, metastasis) → periosteal inflammation → localised sharp pain worsened by breathing and movement
Thoracic spine pathology	Degenerative disc disease, vertebral compression fracture, nerve root compression → radicular pain wrapping around the chest wall in a dermatomal distribution

E. Neurological / Dermatological Causes

Aetiology	Pathophysiology
Herpes zoster (shingles)	Reactivation of varicella-zoster virus in dorsal root ganglion → vesicular rash in a dermatomal distribution. Pre-eruptive phase (pain before rash appears) can perfectly mimic other causes of chest pain for 2–3 days ^[8]
Intercostal neuralgia	Compression or irritation of intercostal nerves (post-herpetic, post-thoracotomy, tumour infiltration) → burning, shooting pain along affected dermatome

F. Psychogenic Causes

Aetiology	Pathophysiology
Psychogenic: stress, anxiety, depression (accounts for ~10% of chest pain presentations) ^[8]	Autonomic hyperarousal → hyperventilation → respiratory alkalosis → coronary and peripheral vasoconstriction + muscle tension → chest tightness and paraesthesia. Also heightened visceral and somatic pain sensitivity (central sensitisation)
Panic disorder	Recurrent, unexpected panic attacks with abrupt surge of intense fear + autonomic symptoms (palpitations, chest pain, dyspnoea, diaphoresis) ^[13]. Somatic symptoms may prompt help-seeking → frequently presents to ED as "chest pain"
Somatic symptom disorder	Chest pain as one of multiple somatic symptoms with excessive thoughts/worries/behaviours related to the symptoms ^[14]. High health care utilisation, doctor-shopping, repeated negative workups ^[14]

G. Other / Rare Causes

Aetiology	Notes
Bornholm disease (epidemic pleurodynia)	Coxsackievirus B infection → inflammation of intercostal muscles/pleura → sudden, severe, paroxysmal chest/abdominal pain ("devil's grip") + fever ^[8]
Tumours of spinal cord and meninges	Can cause thoracic radicular pain ^[8]
Aortic aneurysm (without dissection)	Compression of surrounding structures (e.g., RLN compression → hoarseness by thoracic aortic aneurysm) ^[15]. Pain from stretching of aneurysm sac → indicates impending rupture ^[15]
Cocaine/amphetamine-induced chest pain	Direct coronary vasospasm + accelerated atherosclerosis + ↑myocardial O₂ demand (due to ↑HR, ↑BP from sympathomimetic effects)

Must-Know: The 'Big Six' Life-Threatening Causes of Acute Chest Pain

Never miss these six — they can kill within hours if unrecognised:

Acute Coronary Syndrome (ACS)
Aortic Dissection
Pulmonary Embolism (PE)
Tension Pneumothorax
Cardiac Tamponade
Oesophageal Rupture (Boerhaave syndrome)

These form the backbone of your "rule-out" approach in any acute chest pain presentation.

Classification

Chest pain can be classified in several clinically useful ways:

Acute Chest Pain	Stable / Chronic Chest Pain
ACS, aortic dissection, PE, tension PTX, tamponade, Boerhaave	Stable angina, GERD, musculoskeletal, malignancy, psychogenic

Cardiac (Ischaemic)	Pleuritic	Musculoskeletal	Oesophageal
Dull, constricting, squeezing	Sharp, stabbing, worse with inspiration	Sharp, localised, reproducible on palpation	Burning, retrosternal, related to swallowing/posture

Acute Chest Pain ^[1]^[2]:

Potentially severe or life-threatening	Relatively benign causes
Acute coronary syndrome (ACS)	Episode of stable angina
Acute decompensated heart failure	GERD
Aortic dissection	Small pneumothorax
Acute pulmonary embolism	Musculoskeletal pain
Tension or massive pneumothorax	Panic attack
Pneumonia
Myopericarditis ± cardiac tamponade

Stable Chest Pain ^[1]^[2]:

Potentially severe	Benign
Stable ischaemic heart disease	GERD and other oesophageal pathologies
Subacute/chronic pulmonary embolism	Musculoskeletal pain
Malignancy with pleural/chest wall involvement	Psychogenic chest pain
Pulmonary hypertension	Herpes zoster

Feature	Typical Angina (all 3 present)	Atypical Angina (2 of 3)	Non-anginal Chest Pain (≤1 of 3)
Constricting discomfort in chest/jaw/shoulder/arm	✓	±	±
Provoked by exertion or emotional stress	✓	±	±
Relieved by rest and/or GTN within 5 min	✓	±	±

Clinical Features

The clinical features are best understood when linked to the underlying pathophysiology. Below is a comprehensive system-by-system breakdown of symptoms and signs.

A. Symptoms

The OPQRST mnemonic (Onset, Provocation/Palliation, Quality, Region/Radiation, Severity, Timing) is the framework for characterising chest pain.

OPQRST	Feature	Pathophysiological Basis
Onset	ACS: typically takes minutes to develop, may occur at rest or with exertion ^[1]^[2]	Acute plaque rupture → thrombus → dynamic obstruction → ischaemia at rest
	Stable angina: builds up gradually in proportion to intensity of exertion ^[1]^[2]	Fixed stenosis → O₂ demand exceeds supply only during exertion
Provocation	Exertion, emotional stress, cold weather, heavy meals	All increase myocardial O₂ demand (↑HR, ↑BP, ↑contractility) against a fixed stenosis
Palliation	Rest (stable angina), sublingual GTN within 5 min	Rest ↓O₂ demand; GTN causes venodilation (↓preload → ↓wall stress → ↓O₂ demand) and coronary vasodilation
Quality	Typically dull, constricting, choking, 'heavy'. Described as squeezing, crushing, burning, aching or even as breathlessness ^[1]^[2]	Visceral afferent fibres from the heart produce a diffuse, poorly localised sensation (unlike somatic pain)
	Levine's sign: characteristic gesture of a clenched fist on chest when describing angina ^[1]^[2]	Reflects the constricting, diffuse nature of the pain — patients cannot point with one finger
	Patients often emphasise it is a discomfort, not a pain ^[1]^[2]
Region/Radiation	Retrosternal, radiating to left arm, shoulder, jaw, neck, epigastrium	Cardiac visceral afferents enter spinal cord at T1–T5, converging with somatic afferents from these dermatomes
Severity	Variable; ACS typically more severe and prolonged than stable angina	Degree of ischaemia correlates with severity. Complete occlusion → maximal ischaemia
Timing	Stable: < 30 min, predictable with exertion. ACS: > 20 min, at rest, crescendo pattern	Stable: ischaemia resolves with rest. ACS: persistent obstruction → prolonged ischaemia → risk of infarction

Associated symptoms in ACS:

Diaphoresis (autonomic activation → sympathetic discharge → sweating)
Nausea/vomiting (vagal stimulation, especially in inferior MI via proximity of diaphragmatic surface to vagal fibres)
Dyspnoea (LV dysfunction → ↑LV filling pressures → pulmonary congestion)
Sense of impending doom (massive sympathetic discharge)
Syncope (↓cardiac output from arrhythmia or massive MI)

Exam Tip: Anginal Equivalents

Elderly, diabetics (autonomic neuropathy), and women may present WITHOUT classic chest pain. Instead, they present with "anginal equivalents" — isolated dyspnoea, diaphoresis, nausea, fatigue, or syncope. A high index of suspicion is required.

Feature	Description	Pathophysiological Basis
Onset	Abrupt onset ^[5]	Sudden intimal tear → immediate mechanical disruption
Quality	Sharp, tearing, knife-like ^[5]	Longitudinal shearing force as blood enters the aortic media
Site	Anterior chest (Type A) / Back or abdomen (Type B) ^[5]	Type A involves ascending aorta (anterior mediastinum); Type B involves descending aorta (posterior mediastinum/abdomen)
Radiation	Radiates anywhere in thorax or abdomen ^[5]	Dissection can propagate along the entire aortic length, and pain migrates with it — "migratory pain" is classic
Maximum at onset	Sudden onset, maximum at onset ^[1]^[2]	Unlike ACS which builds up, dissection pain is maximal immediately because the mechanical disruption is instantaneous

Associated features of aortic dissection ^[5]:

Pulse deficit: weak or absent carotid, brachial, or femoral pulse — due to intimal flap obstructing branch vessel ostia or compression by expanding false lumen hematoma
Blood pressure discrepancy: > 20 mmHg difference between arms (same mechanism as pulse deficit)
Hypertension (Type A: 25–35%; Type B: 70%) — often the underlying cause and still present at presentation
Hypotension (Type A: 25%; Type B: 5%) and syncope — due to:
- Aortic regurgitation
- Cardiac tamponade (blood leaks into pericardial space)
- Acute myocardial infarction (dissection extends into coronary ostia)
- Hemothorax or hemoperitoneum (aortic rupture into pleural/peritoneal cavity)
Early diastolic decrescendo murmur with wide pulse pressure → aortic regurgitation ^[5] (dissection disrupts aortic root geometry, preventing leaflet coaptation)
Focal neurological deficits ^[5] due to:
- Paraplegia (spinal cord — artery of Adamkiewicz compromised)
- Altered level of consciousness (carotid artery involvement)
- Horner's syndrome (superior cervical ganglion compression)
- Hoarseness (left recurrent laryngeal nerve compression)

Feature	Description	Pathophysiological Basis
Quality	Sharp, stabbing, pricking, knife-like ^[1]^[2]	Somatic pain from inflamed parietal pleura via intercostal nerves — well-localised
Provocation	↑ with inspiration ^[1]^[2]	Inspiration expands the lung → inflamed parietal and visceral pleura rub against each other → pain
Site	Usually lateral, well-localised to area of pathology	Parietal pleura has precise somatotopic innervation
Radiation	Ipsilateral shoulder tip if diaphragmatic pleura involved	Phrenic nerve (C3–C5) innervates diaphragmatic pleura → pain referred to shoulder tip (same dermatome)

Specific features by cause:

Pulmonary Embolism ^[6]:

Acute onset pleuritic chest pain, dyspnoea, haemoptysis (occurs late with infarction) if small/medium PE
Collapse/syncope, crushing central chest pain, shock, sudden death if massive PE
Sinus tachycardia on ECG with right heart strain pattern (RBBB, S1Q3T3) if massive ^[6]
Why crushing central chest pain in massive PE? → Acute RV dilatation → RV ischaemia (↑wall stress, ↓coronary perfusion) → mimics ACS

Pneumothorax ^[7]:

Sudden onset unilateral pleuritic chest pain + SOB
Generally does not correlate with size (a small pneumothorax can be very painful)
Disproportionately severe in SSP (less respiratory reserve)

Pneumonia/Pleurisy:

Pleuritic pain + productive cough + fever + dyspnoea
Pain indicates involvement of parietal pleura (the lung parenchyma itself is insensate)

Feature	Description	Pathophysiological Basis
Quality	Sharp, stabbing	Somatic pain from inflamed parietal pericardium via phrenic nerve
Provocation	Worse lying flat, better sitting forward/leaning forward	Lying flat → heart falls back onto inflamed posterior pericardium → ↑contact → ↑pain. Sitting forward → heart falls away from pericardium → ↓contact
Radiation	Trapezius ridge (virtually pathognomonic)	Phrenic nerve (C3–C5) innervates parietal pericardium; trapezius ridge is in C3–C4 dermatome
Associated	Fever, preceding viral illness, friction rub on auscultation	Viral pericarditis is commonest cause; friction rub = inflamed pericardial surfaces rubbing

Feature	Description	Pathophysiological Basis
Quality	Retrosternal burning ^[1]^[2]	Acid contact with oesophageal squamous epithelium → chemical mucosal injury → visceral afferent stimulation
Provocation	Posturally aggravated: bending, stooping, lying flat ^[3]	These positions ↑gravitational reflux of gastric acid through an incompetent LES
Palliation	Antacids, PPI, sitting upright	Neutralise acid or reduce production; upright position uses gravity to ↓reflux
Associated	Heartburn, acid regurgitation, water brash (reflex salivary gland stimulation as acid enters throat) ^[3]	Refluxate irritates oesophageal and pharyngeal mucosa
Mimicry	Non-cardiac chest pain (NCCP) — can perfectly mimic angina ^[3]	Shared T1–T5 visceral afferents with heart

Diffuse oesophageal spasm ^[11]:

Episodic chest pain that may mimic angina
Sometimes associated with transient dysphagia
Usually in late middle age

Feature	Description	Pathophysiological Basis
Quality	Sharp, well-localised	Somatic pain via intercostal nerves — precisely localised
Provocation	Pain after exertion, with movement, palpation ^[1]^[2]	Mechanical stress on inflamed costochondral junctions, muscles, or periosteum
Palliation	Rest, NSAIDs, avoiding provoking movements	Reduces mechanical stress and inflammation
Duration	Often persistent (hours to days), positional	Unlike cardiac pain which is typically < 30 min
Reproducibility	Tenderness reproducible on palpation	Key distinguishing feature from cardiac pain — visceral pain is NOT reproducible on palpation

Feature	Description	Pathophysiological Basis
Quality	Variable — can be sharp, dull, pressure-like	Not linked to a single structural mechanism; involves central pain processing abnormalities, hypervigilance
Context	Stress, anxiety, depression ^[8]	Autonomic hyperarousal, hyperventilation, muscle tension
Associated	Sighing, hyperventilation, perioral/digital paraesthesia, palpitations	Hyperventilation → ↓PaCO₂ → respiratory alkalosis → ↓ionised calcium → neuromuscular excitability → paraesthesia and tetany
Duration	Often prolonged (hours), vague location
Panic disorder	Recurrent unexpected panic attacks with autonomic symptoms ^[13]	Abrupt surge of intense fear → cognitive and autonomic cascade

Exam Pearl: Features Against Cardiac Chest Pain

The following features argue AGAINST a cardiac cause:

Pain that is sharp, stabbing, or knife-like (unless pericarditis)
Pain reproducible by palpation of the chest wall
Pain lasting < 30 seconds or continuously for days
Pain that varies with position (unless pericarditis)
Pain localised to a fingertip-sized area
Pain that occurs AFTER (not during) exertion

However, remember that atypical presentations of ACS do exist — never completely exclude ACS based on character alone in a high-risk patient.

B. Signs

Physical examination findings should be linked back to the suspected pathology:

Relevant Pathophysiology Deep Dives

Key points from lecture slides ^[8]:

Key history: usual features of pain including aggravating and relieving factors (movement, exercise, rest, swallowing, breathing, eating). Note associated symptoms (fever, cough, dizziness, overexertion, syncope, recent viral illness). Family history especially cardiac disease including unexplained sudden death.
Key examination: Vital signs especially pulse (including nature) and temperature. Palpation of chest wall. Basic cardiovascular and respiratory examination.
Key investigations: No investigation usually required. Consider ECG and CXR.
Diagnostic tips:
- Most cases of chest pain in children are of unknown aetiology and probably psychogenic
- Chest pain is more common in adolescents
- Less than 5% of cases are caused by cardiac disease
- Myocardial ischaemia is rare in children but consider it in any child with exercise-induced pain, adolescents with longstanding diabetes, and children with sickle cell anaemia

High Yield Summary

Definition: Chest pain is a syndromic complaint categorised into typical cardiac, atypical, or non-cardiac based on clinical features.

Big Six Life-Threatening Causes: ACS, aortic dissection, PE, tension pneumothorax, cardiac tamponade, oesophageal rupture.

Murtagh's Framework: Probability diagnoses (musculoskeletal, psychogenic, angina); Serious (MI/UA, dissection, PE, pneumonia, PTX, pericarditis, cancer); Pitfalls (MVP, oesophageal spasm, GERD, biliary colic, PUD); Psychogenic (10%).

Angina Features: Dull/constricting/squeezing, retrosternal, provoked by exertion, relieved by rest/GTN < 5 min, Levine's sign. ACS = pain at rest, > 20 min.

Aortic Dissection: Abrupt onset, maximal at onset, tearing/knife-like, anterior (Type A) or back (Type B), migratory. Pulse deficit, BP discrepancy, AR murmur. HT is the most important RF.

PE: Pleuritic chest pain + dyspnoea ± haemoptysis (small/medium); syncope + shock + crushing chest pain (massive). S1Q3T3 on ECG.

Pneumothorax: Sudden pleuritic pain + SOB. Tension PTX = clinical diagnosis + obstructive shock → needle decompression first.

GERD/Oesophageal: Retrosternal burning, postural aggravation, mimics angina (shared T1–T5 afferents). Asian presentation atypical with ↑NCCP.

Pericarditis: Sharp, worse lying flat, better sitting forward, trapezius ridge radiation, friction rub.

Apical HCMP: 25–30% of HCMP in HK/Japan — angina from ↓vasodilatory reserve, giant T-wave inversion on ECG.

Key Exam Signs: BP discrepancy (dissection), pulsus paradoxus (tamponade), absent breath sounds + hyperresonance (PTX), reproducible tenderness (musculoskeletal), dermatomal rash (zoster).

Children: Most chest pain is benign/psychogenic; < 5% cardiac; consider ischaemia if exercise-induced, longstanding DM, or sickle cell disease.

Active Recall - Chest Pain: Definition, Epidemiology, Etiology, and Clinical Features

Differential Diagnosis of Chest Pain

The differential diagnosis of chest pain is one of the broadest in clinical medicine. The key intellectual task is not to memorise a long list, but to stratify by risk (life-threatening vs benign), categorise by system (cardiac, pulmonary, GI, MSK, neuro, psych), and then use specific discriminating features (onset, quality, radiation, provocating/palliating factors, associated symptoms, risk factors) to narrow the field. Think of it as a funnel: start wide, risk-stratify immediately, then refine.

Differential Diagnosis Stratified by Clinical Setting

This is the emergency department scenario. The priority is to rule out life-threatening causes before considering benign ones.

Potentially severe or life-threatening ^[1]^[2]:

Diagnosis	Key Discriminating Features	Why It's Dangerous
Acute coronary syndrome (ACS)	Dull compressive central chest pain at rest, radiating to jaw/neck/left arm, lasts > 20–30 min with gradual onset ^[1]; autonomic features (diaphoresis, N/V); angina equivalents in elderly/DM ^[2]	Ongoing myocardial necrosis → cardiogenic shock, fatal arrhythmia
Aortic dissection	Sudden, excruciating, tearing/ripping pain at anterior chest, radiating to interscapular region/back/abdomen; may occur with heavy isometric exercise or extreme BP elevation ^[1]; pulse deficit, BP discrepancy between arms; Hx of HTN, connective tissue disorder ^[1]	Rupture → haemorrhagic death; coronary/cerebral malperfusion
Acute pulmonary embolism	Severe pleuritic pain with sudden onset; dyspnoea ± cyanosis and collapse if massive; S/S of DVT; a/w thrombophilia ^[1]; sinus tachycardia, RV strain pattern (RBBB, S1Q3T3) ^[6]	Massive PE → obstructive shock → cardiac arrest
Tension or massive pneumothorax	Unilateral, sharp, localised pleuritic pain with sudden onset; dyspnoea; Hx of trauma or underlying lung disease ^[1]; absent breath sounds + hyperresonance + tracheal deviation	Mediastinal shift → obstructive shock
Pneumonia	Pleuritic pain + productive cough + fever + dyspnoea; consolidation signs on exam	Sepsis, respiratory failure
Myopericarditis ± cardiac tamponade	Sharp, pleuritic pain of variable duration, positional (improves sitting forward); retrosternal, radiating to shoulder/neck; insidious onset, may be a/w prodromal viral illness ^[1]; friction rub; Beck's triad if tamponade	Tamponade → obstructive shock
Acute decompensated heart failure	Dyspnoea > pain; bilateral crackles, S3, raised JVP, peripheral oedema; Hx of cardiac disease	Pulmonary oedema, cardiogenic shock

Relatively benign causes ^[1]^[2]:

Diagnosis	Key Discriminating Features
Episode of stable angina	Predictable with exertion, resolves with rest/GTN < 5 min, CCS grading ≤ III
GERD	Retrosternal burning pain a/w supine position and recent eating/drinking; may radiate to back; may be a/w dysphagia ^[1]
Small pneumothorax	Mild pleuritic pain, minimal SOB, haemodynamically stable
Musculoskeletal pain	Sharp intense pain ± local tenderness ± preceded by trauma; may vary with posture/movement ^[1]; reproducible on palpation
Panic attack	No predictable pattern of pain; ± hyperventilation features (dizziness, perioral/digital paraesthesia); Hx and features of anxiety ^[1]

Important Exam Concept

"One must be careful to attribute a chest pain to psychogenic causes merely basing on features of anxiety, as the prospect of a heart disease is a frightening experience and organic heart diseases may coexist with anxiety" ^[1]. In other words, a patient with anxiety features can still have an ACS. Always rule out life-threatening causes FIRST.

This is the outpatient or clinic scenario. The priority shifts towards identifying occult serious disease while managing common causes.

Potentially severe ^[1]^[2]:

Diagnosis	Key Discriminating Features
Stable ischaemic heart disease	Exertional chest discomfort with typical quality and duration; predictable threshold; relieved by rest/GTN
Subacute/chronic pulmonary embolism	Progressive exertional dyspnoea ± pleuritic pain; risk factors for VTE; may develop into CTEPH
Malignancy with pleural/chest wall involvement	Persistent, progressive pain; weight loss, haemoptysis, smoking Hx; may have bone pain (metastases)
Pulmonary hypertension	Exertional dyspnoea, exertional chest pain, exertional syncope; loud P2; progressive RV failure signs

Benign ^[1]^[2]:

Diagnosis	Key Discriminating Features
GERD and other oesophageal pathologies	Postural aggravation, meal-related, burning quality; response to PPI trial
Musculoskeletal pain	Reproducible tenderness, movement-related, no cardiac risk factors
Psychogenic chest pain	Inconsistent patterns; hyperventilation features; Hx of anxiety/depression
Herpes zoster	Severe, unilateral dermatomal burning pain; ± rash (may come after pain or without pain → zoster sine herpete) ^[1]

The table below is the master reference for differentiating every major cause. The key principle: each diagnosis has a signature pattern — learn the signature, and you can differentiate efficiently.

System	Diagnosis	Quality	Onset	Duration	Provocation / Palliation	Radiation	Key Associated Features
CVS	ACS	Dull, constricting, crushing	Minutes to develop	> 20–30 min	Rest does NOT relieve; GTN may partially relieve	Jaw, neck, L arm, epigastrium	Diaphoresis, N/V, SOB, syncope
	Stable angina	Dull, constricting	Gradual with exertion	< 2–10 min	↑ by 4Es (eating, exertion, emotion, environment); ↓ by rest, GTN ≤ 5 min ^[2]	Same as ACS	None or mild SOB
	Aortic dissection	Tearing, ripping, knife-like	Sudden, maximal at onset	Persistent	NOT positional; may be a/w heavy lifting / extreme HTN	Back, abdomen (migratory)	Pulse deficit, BP discrepancy, neurological deficits, new AR murmur
	Pericarditis	Sharp, pleuritic	Subacute	Hours to days	Worse lying flat; better sitting forward	Trapezius ridge	Friction rub, preceding viral illness, fever
	Aortic stenosis	Exertional angina	Gradual with exertion	Minutes	Exertion, resolves with rest	Similar to angina	Syncope, SOB (classic triad); ESM radiating to carotids
	HCMP	Atypical or typical angina	Variable	Variable	Exertion	Variable	Palpitations, syncope; giant T-wave inversion if apical type
Resp	PE	Pleuritic (small); crushing (massive)	Sudden	Variable	Inspiration (if pleuritic)	Shoulder tip (if diaphragmatic)	Dyspnoea, haemoptysis, DVT signs, tachycardia
	Pneumothorax	Sharp, pleuritic	Sudden	Persistent until resolved	Inspiration	Ipsilateral shoulder	SOB; absent breath sounds + hyperresonance
	Pneumonia / pleurisy	Sharp, pleuritic	Over hours	Days	Inspiration, coughing	None specific	Productive cough, fever, rigors, consolidation signs
	Lung cancer	Dull/aching or pleuritic	Insidious	Weeks–months	May be constant	Shoulder/arm (Pancoast)	Weight loss, haemoptysis, clubbing, LN
GI	GERD	Burning, retrosternal	After meals / lying down	Minutes–hours	Bending, stooping, lying flat; ↓ by antacids/PPI	Throat	Heartburn, acid regurgitation, water brash
	Oesophageal spasm	Constricting, crushing (mimics angina)	Spontaneous or with meals	Seconds–minutes	May respond to GTN or warm water	Back	Dysphagia; corkscrew oesophagus on barium swallow ^[16]
	Peptic ulcer	Burning, gnawing, epigastric	Meal-related	Hours	GU: ↑ after meal; DU: ↓ after meal, ↑ 2h post-prandially ^[3]	Back (if posterior ulcer)	Haematemesis, melaena; NSAID/H. pylori Hx
	Biliary colic	Intense, dull, constant (NOT colicky despite the name)	After fatty meal	> 30 min to hours	NOT ↑ by movement; NOT ↓ by squatting or bowel movement ^[3]	Right scapula, right shoulder	Nausea, diaphoresis; Murphy's sign if cholecystitis
	Pancreatitis	Epigastric, boring	Acute	Hours–days	Worse supine; better leaning forward	Straight through to back	Nausea, vomiting; alcohol/gallstone Hx
MSK	Costochondritis	Sharp, localised	Gradual or after strain	Days–weeks	Palpation, movement, deep breathing	None	Reproducible tenderness at costochondral junctions
	Rib fracture	Sharp, well-localised	Post-trauma / cough	Days–weeks	Breathing, coughing, palpation	Along rib	Cough fracture in elderly/osteoporotic
	Spinal dysfunction	Dermatomal, aching/burning	Insidious	Chronic	Spinal movement, posture	Dermatomal distribution	May be a/w back pain
Neuro	Herpes zoster	Burning, lancinating	Pre-rash: 2–3 days before vesicles	Days–weeks	Touch (allodynia)	Along dermatome	Vesicular rash on erythematous base; dermatomal
Psych	Panic disorder	Variable; often sharp, atypical	Abrupt (minutes)	Minutes–hours	Unpredictable; unexpected; not confined to known situations ^[13]	Diffuse	≥ 4 autonomic symptoms: palpitations, sweating, trembling, SOB, choking, nausea, dizziness, paraesthesia, derealisation, fear of dying ^[13]
	Somatic symptom disorder	Variable, chronic, multiple	Insidious	Months–years	Disproportionate concern	Variable	High healthcare utilisation, doctor-shopping, repeated negative workups ^[14]

Differential Diagnosis in Specific Clinical Scenarios

Feature	ACS	Aortic Dissection	PE	Tension PTX	Pericarditis/Tamponade
Onset	Gradual (minutes)	Sudden, maximal at onset	Sudden	Sudden	Subacute (hours–days)
Quality	Dull, crushing	Tearing, ripping	Pleuritic (sharp)	Pleuritic (sharp)	Sharp, pleuritic
Radiation	L arm, jaw, neck	Back, abdomen (migratory)	Shoulder tip	Ipsilateral shoulder	Trapezius ridge
Position	No change	No change	No change	No change	Better sitting forward
Respiration	No change	No change	Worse on inspiration	Worse on inspiration	Worse on inspiration
BP	May be ↑ or ↓	Discrepancy between arms	↓ if massive	↓ with tracheal deviation	Pulsus paradoxus
ECG	ST↑ / ST↓ / T changes	Often normal; may show ST↑ if coronary involved	Sinus tachy, S1Q3T3, RBBB	Low voltage (if tension)	Diffuse ST↑, PR↓
CXR	Usually non-diagnostic	Widened mediastinum	Hampton hump, Westermark sign	Absent lung markings, tracheal shift	Globular heart (if effusion)
Key Hx	CVD risk factors, prior angina	HTN, Marfan, bicuspid AV	Immobilisation, malignancy, OCP	Tall/thin, COPD, trauma	Recent viral illness

Critical Pitfall: Aortic Dissection Mimicking STEMI

Aortic dissection extending into the coronary ostia (usually the right coronary artery → inferior STEMI pattern) can present with genuine ST elevation on ECG. If you give thrombolytics without first excluding dissection, the patient bleeds out through the torn aorta. Always consider dissection in the differential of STEMI, especially when the pain is tearing, maximal at onset, or there is BP discrepancy / pulse deficit. A CT aortography or transoesophageal echo should be done urgently if clinical suspicion is high before committing to thrombolysis (but do not delay primary PCI if dissection is excluded).

These are systemic conditions that present as or exacerbate chest pain:

Depression: Can present with somatic symptoms including chest pain; also ↓pain threshold and ↑health anxiety
Anaemia (indirect): Does not cause chest pain directly, but ↓O₂-carrying capacity → unmasked angina in patients with co-existing (even subclinical) CAD. This is why anaemia is listed as a condition that may exacerbate angina ^[1]^[2]
Spinal dysfunction: Thoracic disc disease, facet joint arthropathy → dermatomal or referred chest wall pain

High Yield Summary

Framework: Use Murtagh's five-box approach — Probability diagnosis (MSK, psychogenic, angina), Serious (ACS, dissection, PE, PTX, pneumonia, pericarditis, cancer), Pitfalls (MVP, oesophageal spasm, GERD, biliary colic, PUD), Rarities (pancreatitis, Bornholm, cocaine, HCMP), Masquerades (depression, anaemia, spinal dysfunction).

Acute DDx priority: ACS > aortic dissection > PE > tension PTX > tamponade > pneumonia. ECG + troponin + CXR within 10 minutes.

Key discriminators:

Maximal at onset → dissection, PTX, PE (NOT ACS)
Tearing to back + BP discrepancy → dissection
Pleuritic + DVT signs → PE
Absent breath sounds + hyperresonance → PTX
Positional (better sitting forward) → pericarditis
Reproducible on palpation → musculoskeletal
Burning, postural, meal-related → GERD
Responds to GTN → angina OR oesophageal spasm (pitfall!)

Children: < 5% cardiac; MSK and idiopathic predominate; consider cardiac in exercise-induced pain, longstanding DM, sickle cell.

Never attribute chest pain to anxiety/psychogenic until life-threatening causes are excluded — organic disease and anxiety coexist.

Critical pitfall: Dissection can mimic STEMI (coronary ostial involvement); thrombolysis in dissection is lethal.

Active Recall - Differential Diagnosis of Chest Pain

References

^[1] Senior notes: Ryan Ho Cardiology.pdf (p54–58, "Chest Pain", "Other Causes of Chest Pain", "Clinical Approach to Chest Pain") ^[2] Senior notes: Ryan Ho Fundamentals.pdf (p199–203, "Chest Pain", "Other Causes of Chest Pain", "Clinical Approach to Chest Pain") ^[3] Senior notes: Ryan Ho GI.pdf (p53, p56–57, "Dyspepsia", "GERD") ^[5] Senior notes: felixlai.md (Acute Aortic Syndrome, Aortic Dissection — clinical manifestation, differential diagnosis) ^[6] Senior notes: Ryan Ho Haemtology.pdf (p131, "VTE spectrum and differentials"); Ryan Ho Respiratory.pdf (p133, "PE") ^[8] Lecture slides: murtagh merge.pdf (p25–26, "Chest pain in adults"; p28–29, "Chest pain in children") ^[13] Senior notes: Ryan Ho Psychiatry.pdf (p170, p178–179, "Panic Disorder") ^[14] Senior notes: Ryan Ho Psychiatry.pdf (p202–203, "Somatic Symptom Disorder") ^[16] Senior notes: Ryan Ho GI.pdf (p68, "Diffuse Oesophageal Spasm"); felixlai.md (Achalasia differential diagnosis) ^[17] Senior notes: Ryan Ho Respiratory.pdf (p20, "Psychogenic hyperventilation features")

Diagnostic Criteria for Key Aetiologies

Because "chest pain" is a symptom and not a single disease, there is no single set of diagnostic criteria for it. Instead, you apply the relevant diagnostic criteria for whichever aetiology you are trying to confirm or exclude. Below are the criteria for the most important causes you must know.

1. Acute Coronary Syndrome — Diagnostic Criteria

Type	Description	Key Feature
Type 1	Spontaneous MI due to primary coronary event (plaque erosion/rupture, fissuring, dissection)	Atherothrombotic mechanism; needs coronary angiography ± intervention
Type 2	MI secondary to ischaemia due to supply-demand imbalance (coronary spasm, anaemia, hypotension, tachyarrhythmia)	Treat the underlying cause, not necessarily PCI
Type 3	Sudden cardiac death with symptoms of ischaemia + new ischaemic ECG changes/LBBB but death before biomarkers available	Post-mortem diagnosis or clinical presumption
Type 4a	MI associated with PCI (cTn > 5× 99th URL)	Procedural complication
Type 4b	MI associated with verified stent thrombosis	Stent thrombosis on angiography or autopsy
Type 5	MI associated with CABG (cTn > 10× 99th URL)	Peri-operative complication

Why Distinguish Type 1 vs Type 2 MI?

This matters enormously for management. Type 1 MI is driven by atherothrombosis → needs dual antiplatelet therapy + anticoagulation + revascularisation. Type 2 MI is driven by supply-demand mismatch (e.g., sepsis with tachycardia causing demand ischaemia in a patient with stable CAD) → treating the precipitant (e.g., fluids, blood transfusion, rate control) is more important than invasive coronary intervention.

The ECG is the single most important initial investigation in chest pain because it divides ACS into pathways with different treatment urgency:

ECG Pattern	Diagnosis	Implication
ST elevation (+ reciprocal depression)	STEMI	Significant arterial occlusion leading to transmural MI ^[1] → urgent reperfusion (PCI or thrombolysis)
ST depression / T-wave inversion / dynamic changes	NSTEMI (if troponin +ve) or UA (if troponin –ve)	Partial occlusion / microembolisation → risk-stratify → medical Mx ± early invasive strategy
Normal / non-specific	Possible ACS — serial ECGs + troponins needed	Cannot rule out ACS on single normal ECG

STEMI ECG features (sequential) ^[1]:

ST elevation + reciprocal ST depression (usually disappears after acute phase)
Pathological Q waves (85% persist indefinitely)
Inverted T waves (usually ↓ amplitude after acute phase)

Persistent ST segment elevation after STEMI should raise suspicion for ventricular aneurysm ^[1].

Wells score for PE — clinical assessment ^[18]:

Description	Score
Clinical symptoms of DVT (leg swelling, pain with palpation)	3.0
Other diagnosis less likely than PE	3.0
Immobilisation ≥ 3 days or surgery in previous 4 weeks	1.5
Previous DVT/PE	1.5
Tachycardia (HR > 100)	1.5
Haemoptysis	1.0
Malignancy	1.0

Interpretation ^[18]:

Traditional (3-level)	Score
High	* > 6.0*
Moderate	2.0 – 6.0
Low	* < 2.0*

Simplified (2-level, recommended by NICE)	Score
PE likely	* > 4.0*
PE unlikely	≤ 4.0

Why does this work? Each item represents either a risk factor for VTE or a clinical finding that makes PE more likely relative to other diagnoses. The score is not diagnostic in itself — it determines the pathway (D-dimer first vs straight to CTPA).

There is no single validated "Wells-like" score universally adopted, but the ADD-RS (AHA/ACC 2010, updated ESC 2024) stratifies pre-test probability:

Category	Feature	Score
High-risk conditions	Marfan / connective tissue disorder, family Hx of aortic disease, known aortic valve disease, known thoracic aortic aneurysm, previous aortic manipulation/surgery	1 (if any present)
High-risk pain features	Chest/back/abdominal pain that is abrupt onset, severe intensity, or described as tearing/ripping/sharp	1 (if any present)
High-risk examination features	Pulse deficit, BP discrepancy > 20 mmHg, focal neurological deficit + pain, new aortic diastolic murmur + pain, hypotension/shock	1 (if any present)

ADD-RS 0: Low probability → D-dimer; if negative, dissection essentially ruled out
ADD-RS 1: Intermediate → urgent imaging (CT aortography or TOE)
ADD-RS ≥ 2: High probability → urgent imaging without delay

Investigation Modalities: Key Findings and Interpretations

A. First-Line Investigations (Performed in ALL Acute Chest Pain)

The ECG is the most important first-line investigation in acute chest pain. It should be performed within 10 minutes of presentation and is the gatekeeper to reperfusion therapy.

Perform 12-lead ECG as soon as possible ^[1].

Diagnosis	ECG Findings	Pathophysiological Explanation
STEMI	ST elevation + reciprocal ST depression → pathological Q waves → T-wave inversion ^[1]	Transmural ischaemia → injury current flowing from ischaemic to normal myocardium → ST vector points towards infarct zone. Pathological Q = electrical "window" through dead tissue
NSTEMI / UA	ST depression, T-wave inversion, or dynamic ST-T changes	Subendocardial ischaemia → injury current vector points away from leads → ST depression. T-wave inversion = repolarisation abnormality from ischaemic myocardium
Pericarditis	Diffuse concave-up ("saddle-shaped") ST elevation + PR depression in multiple leads, NOT in a single coronary territory	Epicardial inflammation → diffuse injury current. PR depression = atrial inflammation (atrial injury current). Key distinction from STEMI: diffuse (not territorial), concave-up (not convex), PR depression present
PE	Sinus tachycardia; massive: S1Q3T3 pattern, RBBB, right axis deviation, T-wave inversion V1–V4, AF ^[6]^[18]	Acute RV pressure overload → RV dilatation → altered cardiac axis → S1Q3T3. RV strain → T-wave inversion in right-sided leads. Tachycardia = compensatory for ↓CO
Aortic dissection	Often normal; may show ST elevation if coronary ostial involvement (typically inferior → RCA) ^[5]	Dissection extending to RCA ostium → genuine ischaemia. PITFALL: giving thrombolytics here is lethal
Stable IHD	Pathological Q waves (previous MI), LBBB, ST/T changes, LVH, arrhythmias ^[1]^[2]	Old infarct scar → permanent Q waves. LVH → repolarisation abnormality mimicking ischaemia
Pneumothorax	Low voltage, electrical alternans (if large), axis deviation away from PTX side	Air in pleural space insulates electrical signals. Mediastinal shift alters cardiac axis

ECG Localisation of STEMI

The leads showing ST elevation tell you which coronary territory is involved:

Anterior (V1–V4): LAD occlusion
Lateral (I, aVL, V5–V6): LCx occlusion
Inferior (II, III, aVF): RCA (or sometimes LCx) occlusion
Posterior (tall R in V1–V2, ST depression V1–V3): Posterior descending artery (usually RCA)
Right ventricular (ST↑ in V4R): Proximal RCA occlusion

This localisation matters because it predicts complications (e.g., inferior MI → vagal stimulation → bradycardia; anterior MI → largest territory → worst LV function).

Cardiac enzymes daily × 3 days (repeat troponin 6–12h later if 1st Tn is normal) ^[1]^[2].

Biomarker	Timing	Interpretation
High-sensitivity troponin (hs-cTnT or hs-cTnI)	Detectable from 1–3h after onset; peaks 12–24h; normalises 5–14 days	Gold standard for myocardial injury. Rise-and-fall pattern = acute injury. Persistently elevated = chronic (e.g., CKD, HF). Modern rapid rule-out protocols (0/1h or 0/2h) allow early exclusion of MI if both baseline and repeat hs-cTn are below specific thresholds with no significant delta change
CK-MB	Rises 3–6h; peaks 12–24h; normalises 2–3 days	Less specific than troponin (also ↑ in skeletal muscle injury). Mainly useful for detecting re-infarction (because it clears faster than troponin)
Myoglobin	Earliest to rise (1–2h); normalises < 24h	Very sensitive but very non-specific. Largely superseded by hs-cTn

Cardiac enzymes checked: cTnT, cTnI, CK-MB ^[5].

Why troponin and not CK-MB as the gold standard? Because troponins (cTnT and cTnI) are structural proteins unique to cardiac myocytes (not found in skeletal muscle in significant amounts), whereas CK-MB is also present in skeletal muscle (just in lower proportion). Troponin therefore has higher specificity for myocardial injury.

Important causes of troponin elevation WITHOUT ACS (Type 2 MI or non-ischaemic myocardial injury):

Myocarditis, pericarditis
Heart failure (myocyte stretch → troponin leak)
Pulmonary embolism (RV strain)
Sepsis/critical illness
Renal failure (↓clearance + chronic myocardial stress)
Takotsubo cardiomyopathy
Aortic dissection (coronary malperfusion or aortic root haematoma)

CXR: usually non-diagnostic in ACS, look for other causes (e.g., aortic dissection, PE, pneumonia, or pneumothorax) ^[1]^[2].

Diagnosis	CXR Findings	Pathophysiological Explanation
ACS	Usually normal; may show pulmonary oedema (bat-wing opacity, upper lobe diversion, Kerley B lines) if LVF	Acute LV failure → ↑LVEDP → ↑pulmonary venous pressure → pulmonary oedema
Aortic dissection	Irregular or wavy aortic outline; widening of aortic silhouette; widening of mediastinum (erect PA > 6 cm, supine AP > 8 cm); unable to see aortic knuckle and descending aorta ^[5]	False lumen expands aortic diameter → widened mediastinal shadow. Haemothorax if rupture into pleural space (usually left-sided)
Pneumothorax	Absent lung markings with visible visceral pleural line; lung collapse towards hilum. Tension: mediastinal shift to contralateral side	Air in pleural space separates visceral from parietal pleura. In tension: progressive air accumulation pushes mediastinum
Pneumonia	Lobar consolidation with air bronchograms; patchy infiltrates (bronchopneumonia); parapneumonic effusion	Alveolar filling with inflammatory exudate → opacification. Air bronchograms = patent bronchi surrounded by consolidated (airless) alveoli
PE	Often non-specific (normal in 12–22%); Hampton hump (peripheral wedge-shaped opacity); Westermark sign (focal oligaemia); enlarged pulmonary artery; blunted costophrenic angle (effusion); linear atelectasis ^[6]	Hampton hump = pulmonary infarction. Westermark = absent blood flow distal to embolus → focal lucency. Atelectasis = surfactant loss from ischaemic alveoli
Pericardial effusion	Globular "water-bottle" cardiac silhouette	Fluid surrounds heart → uniform enlargement of cardiac shadow
HF / APO	Cardiomegaly, upper lobe venous diversion, bilateral perihilar bat-wing opacities, Kerley B lines, pleural effusions (usually bilateral, R > L)	Raised pulmonary venous pressure → fluid transudation into interstitium (Kerley B lines) then alveoli (bat-wing)

Basic bloods: CBC, L/RFT, lipid profile (≤ 24h), aPTT/INR (as baseline for heparin) ^[1]^[2].

Test	What to Look For	Clinical Rationale
CBC	Anaemia (may exacerbate IHD), ↑WBC (infection, stress response), ↓PLT (bleeding risk) ^[19]	Anaemia → ↓O₂ delivery → unmasks subclinical CAD (Type 2 MI). Leucocytosis → pneumonia, sepsis, or stress response in MI
L/RFT	↑U/Cr (AKI from shock; baseline before contrast), ↑ALT/AST (shock liver), electrolytes ^[19]	Renal function essential before CT contrast. Hypokalaemia predisposes to arrhythmias in ACS
Lipid profile	LDL, HDL, TG, total cholesterol	Prognostic and guides long-term statin therapy. Must be done ≤ 24h of presentation (lipids fall after acute MI)
HbA1c / fasting glucose	Screen for DM	DM = major CAD risk factor; also predicts worse outcomes in ACS
TFT	Thyrotoxicosis, hypothyroidism	Thyrotoxicosis → high-output state → may precipitate angina; hypothyroidism → dyslipidaemia
aPTT/INR	Baseline before heparin ^[1]^[2]	Essential before initiating anticoagulation
ABG + lactate	↓PaO₂ (PE, pneumonia, PTX); lactic acidosis (shock/poor tissue perfusion); metabolic acidosis ^[19]	Lactate is the best surrogate for tissue perfusion adequacy. Type 1 respiratory failure (↓PaO₂, N/↓PaCO₂) in PE ^[6]
D-dimer	↑ in PE, DVT, aortic dissection, DIC, sepsis ^[19]	Fibrin degradation product. Sensitive but not specific → high NPV in low-risk patients ^[6]. Used in PE and aortic dissection (ADD-RS 0) rule-out pathways
Cardiac enzymes / BNP	MI (cause or consequence of shock); BNP for HF ^[19]	BNP/NT-proBNP released from stretched ventricular myocytes → quantifies volume/pressure overload

B. Cause-Specific Investigations

Investigation	Indication	Key Findings / Interpretation
Serial 12-lead ECG	Repeat at least daily × 3 days (more frequently in severe cases) ^[1]^[2]	Dynamic ST-T changes on serial ECGs strongly suggest ongoing ischaemia. New Q waves = completed infarction
Serial troponin	Repeat troponin 6–12h later if 1st Tn is normal ^[1]^[2]; modern 0/1h or 0/2h rapid rule-out with hs-cTn	Rule-in: hs-cTn above 99th URL with significant delta. Rule-out: both values very low with minimal delta
Echocardiography	Recommended by ESC 2013: evaluate (1) regional wall motion abnormalities (2) LVEF → important prognostic parameter (3) other structural cardiac conditions ^[1]^[2]	New RWMA = evidence of ischaemia/infarction. LVEF guides prognosis and determines need for ICD. Also detects mechanical complications (MR, VSD, free wall rupture, aneurysm)
Invasive coronary angiography	Gold standard for coronary anatomy; indicated in STEMI (primary PCI), high-risk NSTEMI, failed medical therapy	Direct visualisation of coronary stenosis. Allows simultaneous PCI if indicated

Choice of investigation depends on pre-test probability (PTP) of CAD ^[1]^[2].

Principle: different tests have different sensitivity and specificity → suitable for different groups. Diagnostic testing is only useful for PTP between 15% and 85% ^[1].

If PTP > 85%: assume CAD → invasive angiography
If PTP < 15%: assume no CAD → look for non-cardiac causes

Test	Useful In	Not For	Interpretation
Coronary CT angiography (CTA)	Low-intermediate PTP (15–50%); adequate breath-holding; HR ≤ 65 bpm; Agatston score < 400; younger individuals; LVH (↑ risk of FP in stress testing) ^[1]	Severe obesity; CKD (calcification + contrast nephropathy); prior CABG; prior stenting (metal artefact); asymptomatic screening ^[1]	CT calcium (Agatston) score: > 130 HU = calcium, score > 100 → significant CAD risk. BUT poor correlation with degree of luminal stenosis → zero calcium cannot rule out stenoses in symptomatic patients. CT coronary angiogram: significant stenosis = ≥ 70%. Advantage: excellent NPV (99–100%) in low-intermediate PTP ^[1]
Exercise tolerance test (ETT)	Low-intermediate PTP (15–65%); normal baseline ECG; not on anti-ischaemic drugs ^[1]	Abnormal baseline ECG (LBBB, paced rhythm, WPW, AF, LVH, digoxin); limited exercise tolerance due to non-cardiac disease ^[1]	Positive test: horizontal or downsloping ST depression ≥ 0.1 mV (1 mm) 80 ms after J point during exercise ^[1]. Also note Duke Treadmill Score for prognosis. Exercise capacity itself is a powerful prognostic marker
Stress imaging (echo, MRI, SPECT, PET)	Intermediate-high PTP (50–85%); abnormal baseline ECG (where ETT is unreliable); unable to exercise (use pharmacological stress with dobutamine or adenosine)	—	Stress echo: new RWMA during stress = inducible ischaemia. Stress MRI: perfusion defect or new RWMA. SPECT/PET: reversible perfusion defect = ischaemia; fixed defect = scar
Invasive coronary angiography	High PTP ( > 85%); high-risk features on non-invasive testing; failed medical therapy; post-ACS for definitive anatomy	Low PTP (unnecessary risk)	Gold standard for coronary anatomy. Allows FFR (fractional flow reserve) to assess functional significance of intermediate stenoses (FFR ≤ 0.80 = haemodynamically significant)

Exam Pearl: Why Not Just Do Coronary Angiography on Everyone?

Invasive coronary angiography carries procedural risks (vascular access complications ~1–2%, contrast nephropathy, coronary dissection, stroke ~0.1%, radiation). In low PTP patients, the probability of finding significant disease is so low that the risks of the procedure outweigh the benefits. Non-invasive testing acts as a gatekeeper — only those with positive non-invasive tests (or very high clinical probability) proceed to the catheter lab.

Modality of choice is highly dependent on haemodynamic stability and pre-test probability ^[6].

Situation	Approach
Haemodynamically unstable (sBP < 90 or drop ≥ 40)	Definitive testing NOT indicated → bedside LL venous duplex (for DVT) or TTE (for RV strain/clot-in-transit) → treat empirically with parenteral anticoagulation + thrombolysis ^[6]
Haemodynamically stable, PE likely (Wells > 4)	Immediate CTPA ^[6]; if CTPA unavailable → start anticoagulant while waiting
Haemodynamically stable, PE unlikely (Wells ≤ 4)	D-dimer → if negative: PE excluded → if positive: CTPA ^[6]

CT pulmonary angiography (CTPA) ^[6]:

First-line diagnostic test (Sens 91%, Spec 78%)
Contrast-enhanced spiral CT with contrast timed to highlight pulmonary arteries
Pulmonary embolus visible as filling defects within pulmonary arteries
Sensitivity decreases for very peripheral subsegmental emboli
Contraindicated in renal impairment or contrast allergy

V/Q scan ^[6]:

Indication: now limited to those contraindicated for CTPA (renal failure, contrast allergy, pregnancy)
Interpretation: normal scan essentially rules out PE; unmatched defects are diagnostic (Sens 41%, Spec 97%); matched defects may be due to underlying lung pathology
Most informative with otherwise normal lung and clear CXR

Supportive investigations ^[6]:

Venous duplex of proximal leg veins: incompressibility and filling defect (up to 50% –ve in acute PE)
Echocardiography: assessment of RV strain in acute massive PE (RV dilatation, D-shaped septum, McConnell's sign = akinesia of RV free wall with apical sparing)

Diagnosis ^[5]:

Investigation	Findings	Notes
CXR	Irregular/wavy aortic outline; widening of aortic silhouette; widening of mediastinum (erect PA > 6 cm, supine AP > 8 cm) ^[5]	Screening only; sensitivity ~60–70%. Normal CXR does NOT exclude dissection
ECG	Differentiate aortic dissection from AMI ^[5]; often normal or non-specific; may show ST elevation if coronary involvement	MUST do to identify co-existing coronary malperfusion
Echocardiogram	Look for aortic regurgitation, pericardial effusion, and presence of dissection flap ^[5]	TTE: sensitivity ~60% for ascending dissection. TOE: sensitivity ~98% — better for Type A. Can be done at bedside in unstable patients
CT angiography (CTA)	Indicated in haemodynamically stable patients. Diagnosis by identification of true and false lumens. Compressed true lumen is the key radiological finding. True lumen is usually smaller; false lumen is usually larger ^[5]	Gold standard in stable patients. Sensitivity and specificity both > 95%. Shows extent of dissection, branch vessel involvement, and complications
MR angiography	Similar accuracy to CTA; no radiation or iodinated contrast	Limited by availability and scan time — not for acute unstable patients
Cardiac enzymes (cTnT, cTnI, CK-MB)	Rule out concomitant MI ^[5]	Troponin may be elevated from coronary malperfusion or myocardial contusion

Investigation	Findings	Notes
CXR (erect PA)	Visible visceral pleural edge with absent lung markings beyond it; lung collapse towards hilum; deep sulcus sign (supine film)	Size estimation: distance from chest wall to pleural line at hilum level. BTS: > 2 cm = large PTX
CT thorax	More sensitive than CXR for small pneumothoraces; quantifies size accurately	Usually reserved for complex cases, secondary PTX, or when CXR is equivocal
Bedside ultrasound	Absent lung sliding + absent comet-tail artefacts + lung point = diagnostic	Increasingly used in ED; faster than CXR; sensitivity ~90%

Tension PTX is a clinical diagnosis — do NOT delay treatment for imaging ^[7].

Investigation	Findings
ECG	Diffuse concave-up ST elevation + PR depression (stage I); ST normalisation (stage II); T-wave inversion (stage III); normalisation (stage IV). Sinus tachycardia. Low voltage if effusion
Echocardiography	Pericardial effusion; diastolic collapse of RA/RV if tamponade
Blood tests	↑CRP, ↑ESR; troponin may be ↑ if myopericarditis
Cardiac MRI	Pericardial enhancement with gadolinium = active inflammation; quantifies effusion

Investigation	Findings
PPI trial (empirical)	Symptomatic improvement with 2-week PPI trial strongly supports GERD as cause of NCCP
Upper endoscopy (OGD)	Oesophagitis, Barrett's, ulcers; biopsy if indicated
24-hour pH monitoring / impedance	Gold standard for GERD diagnosis — quantifies acid exposure time
Oesophageal manometry	Diagnoses motility disorders: diffuse oesophageal spasm (simultaneous contractions), achalasia (absent peristalsis + failed LES relaxation)
Barium swallow	Corkscrew oesophagus (spasm); bird-beak sign (achalasia)
Abdominal USG	Gallstones, cholecystitis (thickened GB wall, pericholecystic fluid, Murphy's sign)
Serum amylase/lipase	↑↑↑ (> 3× ULN) diagnostic of acute pancreatitis

Key investigations available to the GP are ECG, cardiac enzymes, and CXR — in most instances help confirm the diagnosis ^[8]. Specialist investigations including imaging are confined to hospitals and cardiology centres ^[8].

Acute chest pain initial workup ^[1]^[2]:

Admit CCU if high-risk (ongoing chest pain, ↓BP, APO, ventricular arrhythmia)
Bed rest with continuous ECG monitoring
12-lead ECG stat and repeat at least daily × 3 days
Cardiac enzymes daily × 3 days (repeat troponin 6–12h if 1st Tn normal)
Basic bloods: CBC, L/RFT, lipid profile (≤ 24h), aPTT/INR
CXR: look for other causes
If likely ACS → initiate anti-anginal, antiplatelet, anticoagulant, statin, ACEI/ARB
Consider IV morphine if nitrates do not completely relieve pain
Reperfusion therapy if indicated

For shock evaluation ^[19]:

ECG: arrhythmia, ST changes (ischaemia, pericarditis), low-voltage (pericardial effusion), S1Q3T3/RV strain (PE)
CBC/D: anaemia with bleeding, ↑eosinophil (anaphylaxis), ↑/↓WCC (sepsis)
L/RFT: AKI, shock liver, electrolyte disturbance
ABG + lactate: lactic acidosis, ventilation assessment
Cardiac enzymes / BNP
Clotting + D-dimer: PE, DIC
CXR: pneumonia, PTX, pulmonary oedema, widened mediastinum
± Bedside USG: cardiac pathologies, PTX, effusion, DVT

High Yield Summary

ACS diagnosis: Rise-and-fall of troponin (preferably hs-cTn) above 99th URL + ≥1 of: ischaemic symptoms, new ST-T/LBBB, pathological Q, imaging RWMA, intracoronary thrombus. Type 1 (atherothrombotic) vs Type 2 (supply-demand mismatch) distinction is critical for management.

ECG is king in acute chest pain: STEMI → immediate reperfusion; diffuse ST↑ + PR↓ → pericarditis; S1Q3T3 → PE; widened mediastinum on CXR → dissection. Serial ECGs are essential — a single normal ECG does NOT exclude ACS.

PE workup: Wells score → if unlikely: D-dimer → if positive: CTPA. If likely: straight to CTPA. If unstable: bedside echo + empiric thrombolysis.

Dissection workup: CXR (widened mediastinum but sensitivity only 60–70%), ECG (to differentiate from AMI), echocardiogram (AR, effusion, flap), CT aortography (gold standard in stable patients — true vs false lumen, compressed true lumen is key finding).

Stable CAD testing: PTP-driven. Low-intermediate → CT coronary angiography (excellent NPV). Normal baseline ECG → ETT. Abnormal baseline ECG → stress imaging. High PTP → invasive angiography.

Troponin interpretation: Rise-and-fall = acute injury. Persistently elevated = chronic (CKD, HF). Many non-ACS causes exist. Modern 0/1h and 0/2h rapid rule-out protocols with hs-cTn allow early discharge of low-risk patients.

Tension PTX: Clinical diagnosis — do NOT wait for CXR. Needle decompression first.

Active Recall - Diagnostic Criteria, Algorithm and Investigations for Chest Pain

Management by Specific Aetiology

1. Acute Coronary Syndrome (ACS)

ACS is the single most important cause to manage correctly because (a) it's common, (b) it's time-sensitive, and (c) every treatment decision has strong evidence behind it.

If likely ACS, then initiate anti-anginal (nitrates, β-blocker ±), antiplatelet (aspirin, clopidogrel), anticoagulant (LMWH), early statin and ACEI/ARB ^[1]^[2].

Admit CCU if high-risk (ongoing chest pain, ↓BP, APO, ventricular arrhythmia) ^[1]^[2].

Step	Treatment	Mechanism / Rationale	Key Details
Bed rest	Continuous ECG monitoring ^[1]^[2]	Reduces myocardial O₂ demand (↓HR, ↓BP, ↓contractility); monitoring detects arrhythmias early	CCU setting with defibrillator access
Oxygen	Supplemental O₂ only if SpO₂ < 90%	Corrects hypoxaemia. Routine high-flow O₂ is NOT recommended (DETO2X-AMI trial showed no benefit and potential harm from hyperoxia-induced coronary vasoconstriction)	Target SpO₂ 94–98%
Pain relief	IV morphine if nitrates do not relieve pain completely ^[1]^[2]	Opioid agonist → analgesia + anxiolysis + venodilation (↓preload → ↓O₂ demand). Give with antiemetic (metoclopramide) as morphine causes nausea via CTZ stimulation	2.5–5 mg IV titrated; C/I: respiratory depression, hypotension
Antiplatelet 1	Aspirin (loading 300 mg then 75–100 mg daily) ^[1]^[2]	Irreversibly inhibits COX-1 → blocks thromboxane A₂ (TXA₂) synthesis → ↓platelet aggregation. TXA₂ is a potent platelet activator released from activated platelets	C/I: true aspirin allergy (not intolerance), active GI bleed
Antiplatelet 2	Clopidogrel (loading 300–600 mg then 75 mg daily) or ticagrelor (180 mg then 90 mg BD) or prasugrel (60 mg then 10 mg daily) ^[1]^[2]	P2Y₁₂ receptor antagonists → block ADP-mediated platelet activation. ADP is the second major pathway of platelet aggregation after TXA₂. DAPT = Dual AntiPlatelet Therapy = aspirin + P2Y₁₂ inhibitor	Ticagrelor preferred over clopidogrel in most ACS (PLATO trial); prasugrel for STEMI going to PCI (TRITON-TIMI 38). Clopidogrel if ticagrelor/prasugrel C/I or high bleeding risk
Anticoagulant	LMWH (enoxaparin 1 mg/kg SC BD) or UFH (bolus + infusion, target aPTT 1.5–2.5×) ^[1]^[2]	Potentiates antithrombin III → inhibits factor Xa (LMWH) or both factor Xa and thrombin (UFH). Prevents thrombus propagation on top of ruptured plaque. Fondaparinux (factor Xa inhibitor) is an alternative	LMWH preferred over UFH in NSTE-ACS (easier dosing, no monitoring). UFH preferred if PCI planned (easily reversible with protamine, can monitor with ACT)
Anti-anginal	Nitrates (sublingual GTN → IV GTN if pain persists) ^[1]^[2]	Nitric oxide donor → venodilation (↓preload → ↓wall stress → ↓O₂ demand) + coronary vasodilation. "nitro" = nitrogen, referring to the nitrate group that releases NO	C/I: hypotension (SBP < 90), recent PDE5 inhibitor use (sildenafil within 24h, tadalafil within 48h) → risk of severe hypotension
Anti-anginal	β-blocker (metoprolol, bisoprolol) ^[1]^[2]	Blocks β₁-adrenergic receptors on heart → ↓HR, ↓contractility, ↓BP → ↓myocardial O₂ demand. Also anti-arrhythmic (class II)	C/I: acute decompensated HF, cardiogenic shock, severe bradycardia, 2nd/3rd-degree AV block, severe asthma. Start early but cautiously in haemodynamically stable patients
Statin	Early high-intensity statin (atorvastatin 80 mg) ^[1]^[2]	HMG-CoA reductase inhibitor → ↓cholesterol synthesis → upregulates hepatic LDL receptors → ↓LDL. Also has pleiotropic effects: plaque stabilisation (↓inflammation, ↑endothelial function), antithrombotic	Start within 24h regardless of baseline LDL. Check lipid profile ≤ 24h (falls after acute MI)
ACEI/ARB	ACEI (ramipril, perindopril) or ARB if ACEI-intolerant ^[1]^[2]	Blocks RAAS → ↓afterload + prevents adverse ventricular remodelling (fibrosis, dilatation) post-MI. Proven mortality benefit particularly in anterior MI, LV dysfunction, HF, DM	C/I: bilateral renal artery stenosis, hyperkalaemia, pregnancy, severe hypotension. Start within 24h if stable

The ACS Drug Cocktail — Memory Aid: MONA-B-SACH

Morphine, Oxygen (if needed), Nitrates, Aspirin — Beta-blocker — Statin, ACEI, Clopidogrel (or ticagrelor), Heparin (LMWH). This covers the initial management of essentially all ACS patients. The order reflects urgency: pain relief first, then antiplatelet/anticoagulation to halt thrombus progression, then secondary prevention agents.

Reperfusion therapy if indicated (most STE-ACS, selected NSTE-ACS) ^[1]^[2].

The goal: restore blood flow through the occluded coronary artery as quickly as possible to salvage ischaemic myocardium. Every minute of delay = more myocardial death. "Time is muscle."

Modality	Indication	Details
Primary PCI (percutaneous coronary intervention)	Preferred reperfusion strategy for STEMI if available within 120 minutes of first medical contact	Catheter-based approach: coronary angiography → identify culprit lesion → balloon angioplasty + drug-eluting stent (DES) placement. Achieves TIMI-3 flow in ~90% (vs ~55% for thrombolysis). Door-to-balloon target: ≤ 90 min
Fibrinolysis	STEMI when PCI not available within 120 min	IV fibrinolytic agent (alteplase, tenecteplase, streptokinase) activates plasminogen → plasmin → dissolves fibrin clot. Must be given within 12h of symptom onset (ideally < 3h). Door-to-needle target: ≤ 30 min

Fibrinolytic agents:

Alteplase (tPA): fibrin-specific, short half-life, given as bolus + infusion. "alte" = altered form of tissue plasminogen activator
Tenecteplase (TNK-tPA): single IV bolus, weight-adjusted — most convenient in pre-hospital setting
Streptokinase: non-fibrin-specific, antigenic (cannot repeat within 6 months due to antibody formation), cheaper

Contraindications to fibrinolysis ^[1]:

Absolute	Relative
Previous haemorrhagic stroke at any time	Severe uncontrolled HTN on presentation (BP > 180/110)
Other strokes or CVA within 3 months (except acute ischaemic stroke within 4.5h)	History of chronic severe poorly controlled HTN
Known malignant intracranial neoplasm	History of prior ischaemic stroke > 3 months
Known structural cerebrovascular lesion (e.g., AVM)	Traumatic or prolonged ( > 10 min) CPR
Active bleeding or bleeding diathesis	Oral anticoagulant therapy
Suspected aortic dissection	Major surgery < 3 weeks
Significant closed head or facial trauma within 3 months	Non-compressible vascular punctures
Intracranial or intraspinal surgery within 2 months	Recent internal bleeding (within 2–4 weeks)
Severe uncontrolled HTN unresponsive to emergency therapy	Pregnancy
For streptokinase: prior treatment within previous 6 months	Active peptic ulcer

Critical Exam Point: Aortic Dissection is an ABSOLUTE Contraindication to Fibrinolysis

Suspected aortic dissection is listed as an absolute contraindication ^[1]. This is because fibrinolysis would dissolve the thrombus that may be partially sealing the false lumen, leading to catastrophic haemorrhage. This is why you MUST consider dissection in the differential of every STEMI before giving thrombolytics — especially when the pain is tearing, maximal at onset, or there is pulse deficit / BP discrepancy.

Successful fibrinolysis documented by ^[1]:

Clinical: ↓ chest pain
ECG: accelerated nodal or idioventricular rhythm, resolution of ST elevation ≥ 50% in worst ECG lead at 60–90 min after fibrinolytic
Biochemical: early peaking of CK at 11–12h (cf normal 22–24h) — this paradoxical early enzyme peak reflects washout of enzymes from reperfused infarcted tissue

Not all NSTE-ACS patients need urgent catheterisation. The timing of invasive strategy depends on risk:

Risk Category	Features	Timing of Invasive Strategy
Very high risk	Haemodynamic instability, cardiogenic shock, recurrent/ongoing chest pain despite medical Mx, life-threatening arrhythmias, mechanical complications	Immediate (within 2h)
High risk	Rise/fall in troponin, dynamic ST/T changes, GRACE score > 140	Early invasive (within 24h)
Intermediate risk	DM, eGFR < 60, LVEF < 40%, early post-infarct angina, prior PCI/CABG, GRACE 109–140	Invasive (within 72h)
Low risk	None of the above	Conservative medical management; consider non-invasive testing for ischaemia

Treatment	Rationale	Duration
DAPT (aspirin + P2Y₁₂ inhibitor)	Prevents stent thrombosis and recurrent atherothrombotic events	12 months post-ACS (then aspirin indefinitely)
High-intensity statin	LDL target < 1.4 mmol/L (or ≥ 50% reduction)	Indefinite
ACEI/ARB	Ventricular remodelling prevention, BP control	Indefinite (especially if LVEF ↓, anterior MI, HF, DM)
β-blocker	↓Sudden cardiac death, ↓reinfarction (especially if LVEF ↓)	At least 1 year; indefinite if HF
Mineralocorticoid receptor antagonist (eplerenone)	↓Mortality in post-MI with LVEF ≤ 40% and HF or DM (EPHESUS trial)	Indefinite if LVEF ≤ 40%
Lifestyle modification	Smoking cessation, exercise rehabilitation, dietary changes, weight loss, BP control, glycaemic control	Lifelong
Cardiac rehabilitation	Exercise-based rehabilitation programme — ↓cardiovascular mortality by ~25%	Start early post-discharge

2. Aortic Dissection

The core principle: reduce the shearing force on the aortic wall by lowering both blood pressure and dP/dt (the rate of rise of aortic pressure, which is proportional to the force of LV ejection). BP alone is insufficient — you must reduce the "impulse" of each heartbeat.

Drug	Class	Target	Mechanism
Labetalol (IV) ^[5]	Combined α + β blocker	HR 60–70 bpm ^[5]	β-blockade → ↓HR, ↓contractility, ↓dP/dt. α-blockade → vasodilation → ↓BP. First-line because it addresses both targets simultaneously
Sodium nitroprusside (IV) ^[5]	Vasodilator	SBP 100–120 mmHg ^[5]	Direct NO donor → arterial + venous dilation → ↓BP. Must be given WITH a β-blocker first — otherwise reflex tachycardia from vasodilation increases dP/dt and worsens dissection
Esmolol (IV)	Ultra-short-acting β₁-selective blocker	HR 60–70	Alternative to labetalol; very short half-life (9 min) allows rapid dose titration. Useful if concerned about tolerability
IV GTN	Nitrate vasodilator	Adjunct for BP	Similar role to nitroprusside but less potent; also requires β-blocker first

Why β-Blocker BEFORE Vasodilator?

The higher the BP, the more blood going into the false lumen and the more extensive the dissection ^[5]. But pure vasodilation (without β-blockade) causes reflex tachycardia → ↑dP/dt → ↑shearing force → worse dissection. Always start β-blocker first to blunt the reflex, then add vasodilator to achieve target SBP.

Type	Management	Rationale
Stanford Type A (ascending aorta involved)	Emergency surgery: replacement of ascending aorta ± aortic root ± aortic valve ± coronary reimplantation (Bentall procedure if root involved)	Ascending dissection has extremely high mortality without surgery (~1–2% per hour in the first 48h). Risk of cardiac tamponade, severe AR, coronary malperfusion
Stanford Type B (descending aorta only)	Medical management (anti-impulse therapy) unless complicated	Uncomplicated Type B has lower mortality with medical therapy than surgery
Complicated Type B	Thoracic endovascular aortic repair (TEVAR) or open surgery	Complications: malperfusion syndrome (visceral, renal, limb ischaemia), rupture, persistent pain, uncontrolled HTN, rapid aortic expansion

General measures: book CCU/ICU if haemodynamically unstable ^[6]:

Secure central venous access
Supplemental O₂
Treatment of circulatory shock: IV fluid or plasma expander
Avoid inotropes, diuretics, and vasodilators → treat as hypovolemic shock ^[6]
Opiates to relieve pain and distress ^[6]
External cardiac massage may dislodge/break up large central embolus if moribund ^[6]

Why avoid inotropes initially and treat as hypovolemic? Because in massive PE, the RV is acutely dilated and struggling. The LV is under-filled (not enough blood getting past the pulmonary vascular bed). IV fluid loading (cautious, ~500 mL bolus) increases preload to the RV → may help push blood through the obstructed pulmonary circulation. Vasodilators would drop the already low systemic BP further.

Severity	Treatment
Massive PE (haemodynamically unstable)	Thrombolysis (alteplase 10 mg IV bolus then 90 mg over 2h) + parenteral anticoagulation (UFH preferred). Surgical embolectomy or catheter-directed therapy if thrombolysis C/I or fails
Submassive PE (haemodynamically stable but RV dysfunction/elevated troponin)	Anticoagulation + close monitoring. Consider thrombolysis if clinical deterioration
Non-massive PE	Anticoagulation: LMWH bridge → DOAC (rivaroxaban or apixaban — can start without bridging) or warfarin (target INR 2–3, needs LMWH bridge until therapeutic). Duration: ≥ 3 months; longer if unprovoked or ongoing risk factors

Anticoagulation in special situations ^[6]:

Cancer patients: prefer LMWH (or DOAC) over warfarin; continue > 6 months if active cancer ^[6]
Pregnancy: LMWH throughout (warfarin crosses placenta → teratogenicity, fetal ICH) ^[6]
HIT (heparin-induced thrombocytopenia): heparin C/I → non-heparin parenteral anticoagulants (argatroban, fondaparinux) → bridge to warfarin ^[6]

Management depends on type (primary vs secondary), size, and symptoms ^[7]:

Presentation	Management	Details
Tension pneumothorax	Emergency needle decompression	Insert 14G angiocath into 5th ICS mid-axillary line (or 2nd ICS MCL). Listen for "hissing sound" → converts tension PTX into open PTX. Insert chest tube afterwards ^[7]
Asymptomatic PSP ≤ 2 cm or asymptomatic SSP ≤ 1 cm	Conservative: discharge with early CXR in 2–4 weeks ± high-flow O₂ (esp for SSP) ^[7]	High-flow O₂ rationale: nitrogen washout from blood → increases pleural-blood N₂ gradient → accelerates reabsorption of pleural air (normally ~1.25% per day; ↑ to ~4% with high-flow O₂)
Symptomatic or > 2 cm PSP; asymptomatic 1–2 cm SSP	Aspiration ^[7]	Insert 14G needle/angiocath under LA. Withdraw air by syringe until resistance felt. Aspirate < 2.5 L. Repeat CXR in 4h
Symptomatic or > 2 cm PSP/SSP; failed aspiration	Chest drain insertion ^[7]	Inserted at safety triangle ± USG guidance. Connected to underwater seal without suction. Small bore ( < 14Fr) drains have similar success to larger drains while being less painful

Preventing recurrence ^[7]:

Risk of recurrence: 10–30% at 1–5y (1st PSP), 50% at 3y (SSP)
Indications for surgical opinion: 2nd ipsilateral PTX, 1st contralateral PTX, bilateral PTX, persistent air leak > 5–7 days, spontaneous haemothorax, at-risk professions (pilots, divers), pregnancy
Surgical treatment: resection of bullae/blebs + pleurectomy or pleurodesis via VATS (5% recurrence) or open (1% recurrence)
Medical chemical pleurodesis if unfit for surgery: tetracyclines or talc
Avoid air travel until ≥ 1 week after full resolution; avoid diving permanently unless bilateral pleurodesis with normal post-op lung function
Stop smoking

Severity	Treatment	Rationale
Acute pericarditis	NSAIDs (ibuprofen 600 mg TDS or aspirin 750–1000 mg TDS) × 1–2 weeks, tapered over weeks + colchicine (0.5 mg BD × 3 months)	NSAIDs ↓inflammation. Colchicine inhibits microtubule assembly → ↓neutrophil chemotaxis and inflammasome activation → ↓recurrence by ~50% (COPE, ICAP trials). Colchicine is the single most important addition — halves recurrence rate
Post-MI pericarditis (Dressler syndrome)	Aspirin preferred over other NSAIDs (avoid ibuprofen as it may interfere with aspirin's antiplatelet effect). Colchicine added	Avoid corticosteroids if possible — impair myocardial scar healing → ↑risk of ventricular rupture
Pericarditis with effusion + tamponade	Pericardiocentesis (echo-guided subxiphoid approach)	Relieves life-threatening haemodynamic compromise. Send fluid for biochemistry, cytology, microbiology, ADA (TB)
Recurrent pericarditis	Colchicine long-term (≥ 6 months); if refractory: low-dose corticosteroids, azathioprine, anakinra (IL-1 receptor antagonist)	Anakinra targets the autoinflammatory component — very effective in recurrent/refractory cases (AIRTRIP trial)
Constrictive pericarditis	Pericardiectomy if haemodynamically significant	Removal of thickened, fibrosed pericardium to relieve diastolic restriction

C/I for corticosteroids in pericarditis: increase recurrence rate (COPE trial showed ↑recurrence with steroids), and in post-MI setting they impair scar formation. Use only as last resort.

Management follows CURB-65 severity assessment and empirical antibiotic guidelines (local protocols prevail):

CURB-65 Score	Severity	Management
0–1	Low severity	Outpatient oral antibiotics (amoxicillin ± macrolide)
2	Moderate	Hospital admission; IV amoxicillin/co-amoxiclav + macrolide
3–5	Severe	ICU consideration; IV co-amoxiclav + macrolide (or piperacillin-tazobactam ± macrolide)

Key principle: always cover typical organisms (S. pneumoniae) AND atypical organisms (Mycoplasma, Legionella) in moderate-severe CAP.

Patients with chest pain suspected due to GERD should exclude ischaemic heart disease before initiation of empirical PPIs ^[21].

Component	Treatment	Details
Lifestyle	Weight loss, smoking cessation, ↓alcohol, avoid late meals, elevate head of bed, avoid trigger foods ^[21]	These address the mechanical causes of reflux (↓LES tone, ↑intra-abdominal pressure)
PPI	Empirical PPI trial (e.g., omeprazole 20 mg BD × 2–4 weeks) ^[21]	Only changes acidic reflux into non-acidic reflux (changes the pH) but does NOT prevent reflux itself. Relieves heartburn and oesophagitis by reducing acidity. Regurgitation usually remains uncorrected ^[21]. Administer 30–60 min before meals for maximal efficacy
H₂RA	Famotidine, cimetidine	Regular use leads to tolerance → use intermittently only ^[21]. Indicated for mild oesophagitis or NERD
Anti-reflux surgery	Laparoscopic Nissen fundoplication ^[21]	Indicated for refractory symptoms despite maximal medical therapy, or patient preference to avoid lifelong PPI
Oesophageal spasm	PPI when gastroesophageal reflux is present; oral/sublingual nitrates or nifedipine to relieve attacks	Smooth muscle relaxants ↓oesophageal spasm. Nitrates work by releasing NO → smooth muscle relaxation

Treatment	Rationale
Reassurance	Most important step — explain the benign nature. Many patients fear cardiac disease
Simple analgesia (paracetamol, NSAIDs)	↓Inflammation and pain at costochondral junctions or muscle strain sites
Physiotherapy	Stretching, postural correction for chronic musculoskeletal pain / spinal dysfunction
Avoid provocating activities temporarily	Allows healing of strained structures

Treatment	Rationale
Rule out organic causes first	One must be careful to attribute chest pain to psychogenic causes merely basing on features of anxiety ^[1]
Reassurance + psychoeducation	Explaining the mechanism (hyperventilation → alkalosis → paraesthesia → more panic → vicious cycle) helps patients understand and break the cycle
CBT (Cognitive Behavioural Therapy)	To target underlying health beliefs and expectations ^[14]; first-line psychological treatment for panic disorder and somatic symptom disorder. Note: 70–90% decline psychotherapy ^[14]
SSRI (escitalopram, sertraline)	First-line pharmacotherapy for panic disorder. Modulates serotonin → ↓amygdala reactivity → ↓panic response. Takes 2–4 weeks for effect; may transiently worsen anxiety initially — warn patient
Relaxation training	Progressive muscle relaxation, diaphragmatic breathing ^[14]
Avoid benzodiazepines long-term	Risk of dependence. Short-term (PRN) may be used for acute panic attacks while waiting for SSRI to take effect

This is high-yield for exams because arrhythmias are the most common early complication of MI.

Type	Management
Symptomatic sinus bradycardia	Atropine 0.3–0.6 mg IV bolus; pacing if unresponsive ^[1]
AV block: 1° or Mobitz I (Wenckebach)	Conservative ^[1] — usually resolves spontaneously
AV block: Mobitz II or 3° (complete HB)	Pacing ^[1]. Conservative under monitoring as alternative if inferior MI with narrow QRS escape rhythm and adequate rate
PSVT	Cardioversion if haemodynamic compromise; ATP 10–20 mg IV bolus → verapamil 5–15 mg IV ^[1]
AF/AFl	Digoxin, diltiazem, or amiodarone for rate/rhythm control ^[1]. Common and frequently transient
Wide complex tachycardia (treat as VT)	Cardioversion if unstable; amiodarone 150 mg IV over 10 min for stable monomorphic VT; defibrillation for polymorphic VT/VF ^[1]
VF	Prompt defibrillation per ACLS algorithm ^[1]

Diagnosis	Time-Critical Action	Target
STEMI	Primary PCI	Door-to-balloon ≤ 90 min
STEMI	Fibrinolysis (if PCI unavailable)	Door-to-needle ≤ 30 min
Tension PTX	Needle decompression	Immediate — clinical diagnosis, no imaging
Cardiac tamponade	Pericardiocentesis	Immediate
Massive PE	Thrombolysis + anticoagulation	Immediate
Aortic dissection Type A	Anti-impulse therapy + emergency surgery	Surgery within hours
NSTE-ACS very high risk	Invasive angiography	Within 2 hours

High Yield Summary

ACS initial Mx: MONA-B-SACH — Morphine, O₂ (if needed), Nitrates, Aspirin + Beta-blocker + Statin, ACEI, Clopidogrel/ticagrelor, Heparin (LMWH).

STEMI reperfusion: Primary PCI preferred (door-to-balloon ≤ 90 min). Fibrinolysis if PCI unavailable (door-to-needle ≤ 30 min). Aortic dissection is an absolute contraindication to fibrinolysis.

Aortic dissection: Anti-impulse therapy (β-blocker FIRST, then vasodilator; target HR 60–70, SBP 100–120). Type A = emergency surgery. Type B = medical unless complicated (→ TEVAR).

PE: Massive → thrombolysis + anticoagulation. Non-massive → anticoagulation (LMWH → DOAC or warfarin ≥ 3 months). Treat shock as hypovolaemic (IV fluid, avoid vasodilators).

Pneumothorax: Tension → needle decompression (clinical diagnosis, don't wait for CXR). Small asymptomatic → conservative. Large/symptomatic → aspiration or chest drain. Recurrence prevention: surgical pleurectomy/pleurodesis for 2nd ipsilateral or 1st contralateral PTX.

Pericarditis: NSAIDs + colchicine (↓recurrence by 50%). Avoid steroids (↑recurrence, impair scar healing post-MI). Tamponade → pericardiocentesis.

GERD: Exclude IHD first → PPI trial. PPI changes pH but does not prevent reflux. Anti-reflux surgery if refractory.

Psychogenic: Rule out organic causes → reassurance → CBT ± SSRI. Never attribute to anxiety without excluding life-threatening causes.

Active Recall - Management of Chest Pain by Aetiology

Complications of Chest Pain Aetiologies

This section addresses the major complications arising from the life-threatening and common causes of chest pain. Understanding complications requires thinking about them as the downstream consequences of the underlying pathophysiology — each complication is not a random event but a predictable extension of the disease process.

1. Complications of Acute Coronary Syndrome (ACS) / Myocardial Infarction

MI complications are the single highest-yield topic in this category. They can be organised by timing and mechanism.

Why? Infarcted myocardium is electrically unstable — the border zone between dead and viable tissue creates regions of heterogeneous refractoriness, re-entry circuits, and abnormal automaticity. Additionally, acidosis in ischaemic tissue causes K⁺ efflux and Ca²⁺ influx, further destabilising membrane potential ^[1].

Arrhythmia	Mechanism	Notes
Ventricular fibrillation (VF)	Re-entry circuits at border zone of infarct; acidotic tissue with K⁺/Ca²⁺ derangement	Commonest cause of death in the first hour of MI. Prompt defibrillation is life-saving ^[1]
Ventricular tachycardia (VT)	Same re-entrant mechanisms; can degenerate to VF	Sustained monomorphic VT → amiodarone or cardioversion if unstable ^[1]
AF / Atrial flutter	Common and frequently transient; can be a sign of impending or overt LVF ^[1]	Atrial distension from ↑LA pressure (due to LV failure) → triggers AF
Sinus bradycardia	Vagal stimulation (especially in inferior MI, where the diaphragmatic surface is close to vagal fibres)	Atropine if symptomatic; pacing if refractory ^[1]
AV block	1° or Mobitz I: conservative ^[1] — usually reflects vagal tone (inferior MI) and is reversible. Mobitz II or complete HB: pacing ^[1] — reflects structural damage to His-Purkinje system (anterior MI) and may be permanent	Anterior MI with high-degree AV block has worse prognosis because it implies extensive septal necrosis
PSVT	Re-entry involving AV node	Cardioversion if haemodynamic compromise; ATP then verapamil ^[1]

Mechanism: downward spiral exacerbating myocardial ischaemia ^[1]:

↓Systolic function → ↓coronary perfusion → ↓supply → more ischaemia
↓Diastolic function → ↑pulmonary congestion → hypoxaemia → more ischaemia

Indicates extensive myocardial damage → poor prognosis ^[1].

Manifestation	Mechanism	Management
LV dysfunction (95%)	Loss of contractile myocardium → ↓EF → ↑LVEDP → pulmonary oedema	Vasodilators (esp ACEI) if BP stable; inotropes (dopamine then dobutamine) if ↓BP; IABP with view for catheterisation ± revascularisation ^[1]
RV dysfunction (5%)	Usually occurs in inferior MI ^[1]; RV infarction → ↓RV output → underfilling of LV → ↓CO without pulmonary oedema	Volume expansion with colloids/crystalloids ^[1] (the RV needs more preload to push blood through). Bedside echo shows non-compressible IVC ^[1]. Avoid diuretics and vasodilators as they reduce preload further
Cardiogenic shock	Loss of > 40% of LV myocardium; or acute mechanical complication	Inotropes + IABP + urgent revascularisation; consider mechanical circulatory support (Impella, ECMO)

Why RV Infarction Is Managed with Fluids, Not Diuretics

In RV infarction, the failing RV cannot pump blood into the pulmonary circulation → LV is under-filled. The patient appears "dry" on the left side (no pulmonary oedema) but "wet" on the right (↑JVP). Giving diuretics or nitrates would reduce preload to the already struggling RV → worsening of shock. Instead, IV fluids expand the RV preload, helping it push blood forward. This is a classic exam trap.

Complication	Timing	Mechanism	Features	Management
Peri-infarction pericarditis (PIP)	Common on 2nd/3rd day post-MI; 1.2% of MI patients ^[1]	Direct inflammation of pericardium overlying the infarcted myocardium (transmural MI extends to epicardium → irritates adjacent pericardium)	Development of a different pain: positional, sharp pleuritic, esp at trapezius ridge; pericardial rub (diagnostic) ^[1]; ECG: widespread ST↑ or PR↓ beyond anatomic boundary ^[1]	Paracetamol ± aspirin (650 mg Q6–8h) ± opiate analgesia; avoid NSAIDs/steroids 7–10 days after acute MI due to ↑risk of aneurysm/rupture ^[1]
Post-MI pericardial effusion	Common, ~1/3 of acute STEMI ^[1]	Blood/inflammatory fluid seeps into pericardial space from transmural necrosis	Usually asymptomatic, detected incidentally ^[1]	None unless tamponade → drainage ^[1]
Post cardiac injury (Dressler) syndrome	Weeks to months post-MI ^[1]	Probably autoimmunity due to release of cardiac antigens into pericardial space ^[1] — exposed intracellular proteins trigger immune response	Persistent fever, pericarditis, pleurisy; ↑WCC, CRP/ESR; pericardial ± pleural effusion ^[1]	High-dose aspirin/NSAID (indomethacin 25–50 mg TDS × 1–2d), colchicine ± steroid ^[1]

These are devastating complications caused by structural failure of necrotic myocardium. They typically occur when softened, necrotic tissue cannot withstand ventricular pressure.

Complication	Timing	Mechanism	Presentation	Management
IV septal rupture	~24h from MI (up to 2 weeks); ~0.1% of MI ^[1]	Usually complicates anterior MI (LAD); rupture occurs at margin of necrotic and non-necrotic myocardium ^[1] → blood shunts from LV to RV through defect	Sudden haemodynamic deterioration + new pansystolic murmur (to RLSB) ^[1]; usually develops RV failure (d/dx LVF with APO in acute MR) ^[1]	Observe with delayed surgery if stable; emergency cardiac catheterisation + repair if unstable ^[1]
LV free wall rupture	50% occurs ≤ 5 days; > 90% ≤ 2 weeks; < 1% ^[1]	Complete transmural necrosis → ventricular wall cannot withstand systolic pressure → tears	Complete rupture → blood pumps into pericardial cavity → cardiac tamponade → sudden Rt HF + shock → PEA and death ^[1]. Incomplete rupture → sealed by pericardium and thrombus → persistent/recurrent pleuritic chest pain ^[1]	Emergency percutaneous pericardiocentesis → surgical repair ^[1]
Acute papillary muscle rupture → acute MR	Days 2–7 post-MI	Papillary muscle necrosis (especially posteromedial papillary muscle in inferior MI, which has single blood supply from PDA) → rupture → flail mitral leaflet → severe acute MR	Sudden pulmonary oedema + new loud pansystolic murmur at apex radiating to axilla; haemodynamic collapse. D/dx: VSD (murmur at RLSB with RV failure rather than LV failure)	Emergency surgical MV repair/replacement ± IABP stabilisation

How to Distinguish New Murmurs Post-MI: VSD vs Acute MR

Both present with sudden haemodynamic deterioration and a new pansystolic murmur. The key distinction:

VSD: Murmur loudest at left sternal border; causes RV failure (L→R shunt overloads RV); step-up in O₂ saturation in RV on catheterisation
Acute MR: Murmur loudest at apex radiating to axilla; causes LV failure / APO (blood regurgitates into LA → ↑pulmonary venous pressure); large V waves on PCWP tracing

Bedside echocardiography is the fastest way to differentiate.

Category	Complications
Coronary artery related	Dissection and abrupt closure (rare with stenting); intramural haematoma (6.7%); perforation (0.2–0.6%); side branch occlusion (up to 19%) — all can cause myocardial ischaemia/infarction
Stent-related	Stent thrombosis (1–2%): acute event, usually presents with severe STEMI or cardiac death. Due to thrombus at exposed stent surface before endothelialisation. Prevention: DAPT ^[1]. In-stent restenosis (ISR): chronic event (≥ 6–9 months), presents with recurrent stable angina. Due to intimal proliferation. Prevention: DES ^[1]
Access-related	Bleeding, infection, atheroembolism
Systemic	AKI (contrast, haemodynamic instability, atheroembolism); stroke (mural thrombus); bacteraemia

Complication	Mechanism	Features
Haemodynamic collapse / Obstructive shock	Massive PE → acute RV pressure overload → RV dilatation → RV failure → ↓LV filling → ↓CO	Hypotension, syncope, PEA arrest, sudden death
Pulmonary infarction	Complete obstruction of segmental/subsegmental artery → distal lung tissue necrosis (only ~10% of PE cause infarction because of dual blood supply from bronchial arteries)	Pleuritic chest pain, haemoptysis, peripheral wedge-shaped opacity (Hampton hump)
Right heart failure	Acute or chronic RV pressure overload → RV dilatation + TR → systemic venous congestion	↑JVP, hepatic congestion, peripheral oedema, exercise intolerance
Chronic thromboembolic pulmonary hypertension (CTEPH)	~3–4% of PE patients. Organised thrombus fails to resolve → permanent obstruction of pulmonary arteries → progressive ↑PVR → fixed pulmonary hypertension → RV failure	Progressive dyspnoea, exercise intolerance, RV failure. Diagnosed by V/Q scan (mismatched defects) + right heart catheterisation. Treated by pulmonary endarterectomy (PEA) or balloon pulmonary angioplasty
Recurrent PE	Ongoing risk factors (immobilisation, malignancy, thrombophilia) → recurrent DVT and embolisation	New pleuritic pain, dyspnoea; may present as CTEPH if multiple subclinical episodes
Post-PE syndrome	Persistent functional limitation after PE despite treatment — ?residual obstruction, RV dysfunction, or deconditioning	Exercise intolerance, dyspnoea, ↓QoL

Complication	Mechanism	Management
Tension pneumothorax	One-way valve → progressive air accumulation → mediastinal shift → compression of contralateral lung + impaired venous return → obstructive shock	Emergency needle decompression → chest drain
Recurrence	10–30% at 1–5 years for 1st PSP; 50% at 3 years for SSP ^[7]. Residual blebs/bullae predispose to repeat rupture	Surgical pleurodesis/pleurectomy + bullectomy for 2nd ipsilateral or 1st contralateral PTX
Re-expansion pulmonary oedema (RPO, 0–1%) ^[7]	Rapid re-expansion with restoration of blood flow into compressed capillaries → capillary damage with leakage ^[7]	S/S: cough, SOB, desaturation improving upon clamping drain ^[7]. RFs: lung collapse > 3 days, high-volume drainage, early suction use ^[7]. Mx: supportive + clamp drain
Haemopneumothorax	Torn pleural adhesion or intercostal vessel → blood + air in pleural space	Chest drain ± surgical intervention if ongoing haemorrhage
Empyema	Secondary infection of retained pleural fluid/blood	Antibiotics + chest drain ± surgical decortication
Subcutaneous/surgical emphysema	Air tracks from pleural space into subcutaneous tissues via chest wall injury or drain site	Usually self-resolving; ensure drain is functioning

Complication	Mechanism	Features
Pericardial effusion	Inflammatory exudate accumulates in pericardial space	May be asymptomatic; large effusions cause dyspnoea, muffled heart sounds
Cardiac tamponade	Rapid accumulation of fluid (or slow accumulation exceeding pericardial compliance) → ↑intrapericardial pressure → impaired diastolic filling → ↓CO	Beck's triad (hypotension, distended neck veins, muffled heart sounds); pulsus paradoxus; electrical alternans on ECG
Constrictive pericarditis	Chronic inflammation → fibrosis and calcification of pericardium → rigid "shell" encasing heart → restricted diastolic filling	Kussmaul sign (↑JVP on inspiration — because rigid pericardium cannot accommodate ↑venous return), pericardial knock, hepatomegaly, ascites (out of proportion to peripheral oedema). CXR may show pericardial calcification. Treatment: pericardiectomy
Recurrence	~30% recurrence rate without colchicine; autoimmune mechanism	Recurrent episodes of pericarditic chest pain, fever, ↑inflammatory markers. Prevention: colchicine × 3 months
Myopericarditis	Inflammation extends from pericardium into adjacent myocardium	↑Troponin, regional wall motion abnormalities; risk of LV dysfunction

Complication	Mechanism
Oesophagitis	Chronic acid exposure → inflammation of squamous epithelium → erosions, ulcers
Oesophageal stricture	Chronic oesophagitis → fibrosis → luminal narrowing → dysphagia
Barrett's oesophagus	Chronic acid injury → intestinal metaplasia (squamous → columnar epithelium with goblet cells) as a protective adaptation → pre-malignant condition
Oesophageal adenocarcinoma	Barrett's → dysplasia → adenocarcinoma (the metaplasia–dysplasia–carcinoma sequence)
Aspiration	Reflux reaches larynx/pharynx → aspiration into airways → recurrent pneumonia, chronic cough, laryngitis

8. Complications Arising from Treatment of Chest Pain Aetiologies

Complication	Mechanism
Bleeding (most common)	All anticoagulants/antiplatelets impair haemostasis → ↑risk of GI haemorrhage, intracranial haemorrhage, access-site bleeding
Heparin-induced thrombocytopenia (HIT)	Antibodies against heparin-PF4 complexes → platelet activation → paradoxical thrombosis + thrombocytopenia. Type II HIT is immune-mediated and dangerous → must stop all heparin → switch to non-heparin anticoagulant (argatroban)

Complication	Mechanism
Intracranial haemorrhage (~1%)	Plasmin dissolves fibrin indiscriminately → bleeding at vulnerable sites (especially if pre-existing cerebrovascular disease)
Reperfusion arrhythmias	Washout of metabolites from ischaemic tissue → transient electrical instability → accelerated idioventricular rhythm (AIVR), VT, VF. AIVR is usually benign and self-limiting — it is actually a sign of successful reperfusion
Reperfusion injury	Paradoxical myocardial damage upon restoration of blood flow — mechanisms include reactive oxygen species (ROS) generation, calcium overload, mitochondrial dysfunction, inflammation

High Yield Summary

MI complications by timing:

Immediate (hours): Arrhythmias (VF/VT — commonest cause of early death; sinus bradycardia in inferior MI; AV block)
Early (days 1–7): Pump failure (LV dysfunction → APO/cardiogenic shock; RV infarction → manage with fluids NOT diuretics); peri-infarction pericarditis (day 2–3); mechanical complications (septal rupture, free wall rupture → tamponade, papillary muscle rupture → acute MR)
Late (weeks–months): Ventricular aneurysm (anterior wall, persistent ST elevation, mural thrombus); Dressler syndrome (autoimmune pericarditis); thromboembolism (stroke, ischaemic limb 1–3 weeks post-MI); ventricular remodelling → chronic HFrEF

Aortic dissection complications: Type A → AR, tamponade (commonest cause of death), MI, stroke. Type B → visceral/renal/limb ischaemia, spinal cord ischaemia → paraplegia. Both → rupture (haemothorax, haemoperitoneum).

PE complications: Obstructive shock (massive), pulmonary infarction, RV failure, CTEPH (3–4%).

Pneumothorax complications: Tension PTX (obstructive shock), recurrence (10–50%), re-expansion pulmonary oedema.

Key exam trap: RV infarction = give fluids, avoid diuretics/vasodilators. New PSM post-MI = distinguish VSD (RLSB, RV failure) from acute MR (apex, APO).

Active Recall - Complications of Chest Pain Aetiologies

References

^[1] Senior notes: Ryan Ho Cardiology.pdf (p124, p139–142, p144, "PCI complications", "Arrhythmias post-MI", "Pump failure", "Pericardial complications", "Mechanical complications", "Embolism", "Ventricular aneurysm", "Secondary prevention") ^[5] Senior notes: felixlai.md (Aortic Dissection — complications and prognosis) ^[7] Senior notes: Ryan Ho Respiratory.pdf (p153–155, "Pneumothorax — management and re-expansion pulmonary oedema") ^[22] Senior notes: Ryan Ho Respiratory.pdf (p65, "Pneumonia — complications")