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Life-threatening causes: acute coronary syndrome, pulmonary embolism, aortic dissection, tension pneumothorax, oesophageal rupture and cardiac tamponade. Other causes: pericarditis (pleuritic, relieved leaning forward), pneumonia and pleurisy, gastro-oesophageal reflux, musculoskeletal pain, anxiety, herpes zoster. Assessment: character (pressure, radiation, exertional, relief by rest or nitrates), associated symptoms (dyspnoea, sweating, syncope), risk factors, examination (blood pressure in both arms, murmurs, signs of heart failure), ECG within 10 minutes and serial high-sensitivity troponin.

STEMI: ST elevation (at least 1 mm in two contiguous leads; 2 mm in V2-V3 in men) or new left bundle branch block: primary PCI within 120 minutes (thrombolysis if PCI is not available). NSTE-ACS: ST depression or T inversion, troponin raised (NSTEMI) or normal (unstable angina); risk stratification (GRACE) determines timing of angiography. Treatment: aspirin plus P2Y12 inhibitor, anticoagulation, nitrates and analgesia, beta-blocker, high-intensity statin, ACE inhibitor. Complications: arrhythmias (VF), cardiogenic shock, mechanical complications, pericarditis. Secondary prevention and cardiac rehabilitation.

Steps: rate, rhythm (P before each QRS?), axis, intervals (PR 120-200 ms, QRS below 120 ms, QTc below about 450 ms in men and 460 in women), P wave, QRS morphology (Q waves, bundle branch block, hypertrophy), ST segment and T waves. Localisation of infarction: anterior (V1-V4, LAD), lateral (I, aVL, V5-V6, circumflex), inferior (II, III, aVF, RCA). Other patterns: hyperkalaemia (peaked T waves, wide QRS), pericarditis (diffuse concave ST elevation, PR depression), pulmonary embolism (sinus tachycardia, S1Q3T3), atrial fibrillation (irregularly irregular, no P waves).

1. Name six life-threatening causes of chest pain. 2. What is the reperfusion target for STEMI? 3. Which leads show inferior infarction and which artery is involved? 4. What ECG changes occur in pericarditis?

1. ACS, pulmonary embolism, aortic dissection, tension pneumothorax, oesophageal rupture, cardiac tamponade. 2. Primary PCI within 120 minutes of first medical contact. 3. II, III and aVF; usually the right coronary artery. 4. Diffuse concave ST elevation and PR depression.

Types: HFrEF (EF 40 percent or less), HFmrEF (41-49 percent) and HFpEF (50 percent or more). Causes: coronary disease, hypertension, cardiomyopathy, valve disease, arrhythmia. Diagnosis: symptoms and signs, NT-proBNP, echocardiography. Treatment of HFrEF: ACE inhibitor or ARNI, beta-blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor (each reduces mortality), loop diuretics for congestion, ICD for primary prevention if EF stays at or below 35 percent, cardiac resynchronisation therapy for wide QRS. SGLT2 inhibitors also help HFpEF. Acute decompensation: oxygen, intravenous diuretics, vasodilators, and inotropes or mechanical support in shock.

- Dilated cardiomyopathy: ventricular dilation and reduced EF; causes genetic (titin), alcohol, viral, chemotherapy (anthracyclines), peripartum. - Hypertrophic cardiomyopathy: sarcomeric gene mutations, asymmetric septal hypertrophy, dynamic outflow obstruction, diastolic dysfunction; leading cause of sudden death in young athletes; treated with beta-blockers, avoiding dehydration and vasodilators, septal reduction, ICD for high risk. - Restrictive cardiomyopathy: stiff ventricles, amyloidosis, sarcoidosis. - Arrhythmogenic cardiomyopathy: fibro-fatty replacement of right ventricular myocardium, ventricular arrhythmias, desmosomal gene mutations.

Acute pericarditis: sharp pleuritic chest pain relieved by sitting forward, pericardial friction rub, diffuse ST elevation; treated with NSAIDs plus colchicine; complications: effusion, tamponade (Beck triad: hypotension, raised jugular venous pressure, muffled heart sounds) and constriction. Myopericarditis: troponin rise with pericarditis features. Infective endocarditis: fever, new murmur, embolic phenomena (splinter haemorrhages, Janeway lesions, Osler nodes, Roth spots); organisms Staphylococcus aureus, viridans streptococci, enterococci; Duke criteria; blood cultures before antibiotics; echocardiography; prolonged intravenous antibiotics and surgery for complications. Mitral valve prolapse: systolic click and late systolic murmur; usually benign; complications include mitral regurgitation and rarely arrhythmias or endocarditis.

1. List the four drug classes that reduce mortality in HFrEF. 2. Why are vasodilators and dehydration avoided in hypertrophic cardiomyopathy? 3. What is Beck triad? 4. Give the classic signs of infective endocarditis.

1. ACE inhibitor/ARNI, beta-blocker, mineralocorticoid antagonist, SGLT2 inhibitor. 2. They worsen dynamic outflow obstruction. 3. Hypotension, raised jugular venous pressure and muffled heart sounds in tamponade. 4. Fever, new murmur, splinter haemorrhages, Osler nodes, Janeway lesions, Roth spots.

Sinus bradycardia, sick sinus syndrome (tachy-brady), and atrioventricular block: first degree (PR above 200 ms), second degree Mobitz I (Wenckebach, progressive PR prolongation, usually benign) and Mobitz II (sudden non-conducted P waves, risk of complete block), and third degree (complete AV dissociation). Causes: ageing fibrosis, ischaemia (inferior infarction), drugs (beta-blockers, verapamil, digoxin), Lyme disease. Treatment: remove reversible causes; atropine acutely; permanent pacemaker for symptomatic bradycardia, Mobitz II and complete block.

Ventricular tachycardia (wide-complex, at least three beats above 100/min): most often with scar from myocardial infarction or cardiomyopathy. Monomorphic VT is scar-related; polymorphic VT (torsades de pointes) accompanies a long QT interval. Ventricular fibrillation: chaotic activity with no output. Management: unstable patients need immediate DC cardioversion or defibrillation; stable VT can be treated with amiodarone or procainamide. Long-term: treat the cause, beta-blockers, ablation and implantable cardioverter-defibrillator.

Long QT syndrome (potassium or sodium channel mutations; torsades; triggered by exercise or drugs; beta-blockers), Brugada syndrome (SCN5A; coved ST elevation in V1-V3; ventricular fibrillation during rest or fever; ICD in high-risk patients; avoid sodium channel blocking drugs and treat fever), catecholaminergic polymorphic VT (exercise-induced) and short QT syndrome. Sudden cardiac death: most in adults from coronary disease; in the young from cardiomyopathies and channelopathies. Prevention: risk stratification, ICD, screening of family members.

Types: reflex (vasovagal, situational, carotid sinus), orthostatic hypotension (drugs, volume depletion, autonomic failure) and cardiac (arrhythmia, structural disease such as aortic stenosis and hypertrophic cardiomyopathy). Evaluation: history (prodrome, triggers, posture, exertion), examination including orthostatic blood pressure, ECG, and echocardiography when structural disease is suspected. High-risk features: syncope on exertion or supine, abnormal ECG, structural heart disease, family history of sudden death.

1. Compare Mobitz I and Mobitz II. 2. Which arrhythmia accompanies long QT syndrome? 3. Describe the ECG in Brugada syndrome. 4. List high-risk features of syncope.

1. Mobitz I: progressive PR lengthening before a dropped beat, usually benign. Mobitz II: sudden dropped beats with constant PR, risk of complete block, needs pacing. 2. Torsades de pointes (polymorphic ventricular tachycardia). 3. Coved ST elevation in V1-V3 with right bundle branch block pattern. 4. Exertional or supine onset, abnormal ECG, structural heart disease, family history of sudden death.