{"title": "Chapter 3: Cardiovascular Disorders", "flashcards": [{"q": "What ECG criteria define STEMI?", "a": "ST elevation ≥1 mm in ≥2 contiguous limb leads, OR ≥2 mm in ≥2 contiguous precordial leads. New LBBB in appropriate clinical context is treated as STEMI-equivalent. Posterior MI shows ST depression in V1–V3 (confirmed by ST elevation in V7–V9)."}, {"q": "Name the GRACE score variables for ACS risk stratification.", "a": "Age, heart rate, systolic BP, serum creatinine, Killip class at presentation, cardiac arrest at admission, ST-segment deviation, and elevated cardiac biomarkers. The GRACE 2.0 score predicts in-hospital and 6-month mortality in NSTEMI/UA."}, {"q": "What are the four pillars of GDMT for HFrEF?", "a": "ACE inhibitor/ARB/ARNI (sacubitril-valsartan); beta-blocker (bisoprolol, carvedilol, metoprolol succinate); mineralocorticoid receptor antagonist (spironolactone, eplerenone); SGLT2 inhibitor (dapagliflozin, empagliflozin). Each pillar independently reduces all-cause mortality."}, {"q": "What is the CHA₂DS₂-VASc score used for?", "a": "Estimating annual stroke risk in non-valvular AF to guide anticoagulation. Score ≥2 in men or ≥3 in women warrants anticoagulation. Individual components: CHF (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA (2), Vascular disease (1), Age 65–74 (1), Sex female (1)."}, {"q": "Define Killip classification in acute MI.", "a": "Killip I: no heart failure signs; II: mild-moderate HF (S3, basal crackles, raised JVP); III: severe HF (acute pulmonary oedema); IV: cardiogenic shock (BP <90, oliguria, cyanosis, impaired consciousness). Higher Killip class at presentation correlates with increasing in-hospital mortality."}, {"q": "What is the mechanism of action of adenosine in SVT?", "a": "Adenosine binds A1 receptors in the AV node, causing transient AV block (hyperpolarisation via G-protein-coupled K⁺ channel opening), interrupting re-entrant tachycardia circuits dependent on AV nodal conduction. Half-life is <10 seconds. Initial dose 6 mg rapid IV; repeat with 12 mg if ineffective."}, {"q": "Name three indications for permanent pacemaker implantation.", "a": "Symptomatic sinus node dysfunction (sick sinus syndrome); complete heart block (third-degree AV block) regardless of symptoms; Mobitz type II second-degree AV block; bifascicular block with syncope; chronotropic incompetence limiting function. ESC/NICE guidelines govern specific indications."}, {"q": "What is Beck's triad in cardiac tamponade?", "a": "Hypotension, raised JVP (distended neck veins), and muffled heart sounds. Beck's triad reflects pericardial fluid compression impairing cardiac filling. Pulsus paradoxus (>10 mmHg inspiratory SBP fall), tachycardia, and pulsus alternans may also be present. Urgent pericardiocentesis is required."}, {"q": "Define the term 'electrical storm' in ICD recipients.", "a": "Three or more separate sustained VT/VF episodes within 24 hours, each requiring ICD therapy (ATP or shock). It is a medical emergency associated with high mortality. Management: IV amiodarone, beta-blockade, correction of metabolic triggers, sedation, and cardiology input for catheter ablation consideration."}, {"q": "What physical sign differentiates mitral stenosis from mitral regurgitation on auscultation?", "a": "Mitral stenosis: low-pitched mid-diastolic rumble with opening snap at the apex (heard with bell in left lateral decubitus); loudest in expiration. Mitral regurgitation: pansystolic murmur radiating to axilla. MS also features a loud S1 (if mobile leaflets) and signs of pulmonary hypertension in advanced disease."}], "quiz": [{"q": "Primary PCI for STEMI should ideally be performed within what timeframe from first medical contact?", "opts": ["60 minutes", "90 minutes", "120 minutes", "180 minutes"], "ans": 2, "exp": "ESC 2023 STEMI guidelines recommend primary PCI within 120 minutes of first medical contact for all STEMI patients. The door-to-balloon time target is ≤60 minutes when the patient presents directly to a PCI centre. Thrombolysis is given if PCI cannot be performed within 120 minutes."}, {"q": "Which drug class is contraindicated in HFrEF with decompensation?", "opts": ["Loop diuretics", "Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)", "SGLT2 inhibitors", "Nitrates"], "ans": 1, "exp": "Non-dihydropyridine CCBs have significant negative inotropic effects and worsen acute decompensated HF. They are contraindicated in HFrEF. Dihydropyridine CCBs (amlodipine, felodipine) are safe in HFrEF for hypertension or angina."}, {"q": "What does AV dissociation on ECG indicate in the context of wide-complex tachycardia?", "opts": ["SVT with aberrant conduction", "Ventricular tachycardia", "Torsades de Pointes", "Supraventricular tachycardia"], "ans": 1, "exp": "AV dissociation — independent P wave activity at a different rate from the QRS — is pathognomonic of ventricular tachycardia. Capture beats and fusion beats also confirm VT. All wide-complex tachycardias in haemodynamically unstable patients should be treated as VT until proved otherwise."}, {"q": "Which scoring system identifies patients with AF suitable for rhythm control?", "opts": ["CHA₂DS₂-VASc", "EHRA symptom score (class II–IV)", "HAS-BLED", "GRACE score"], "ans": 1, "exp": "The EHRA (European Heart Rhythm Association) symptom score classifies AF-related symptoms I–IV: I = no symptoms; II = mild (normal daily activities not affected); III = severe (normal activities affected); IV = disabling. Patients with EHRA ≥II symptoms are candidates for rhythm control strategy."}, {"q": "What is the most common cause of chronic heart failure in developed countries?", "opts": ["Dilated cardiomyopathy", "Ischaemic heart disease (coronary artery disease)", "Hypertensive heart disease", "Valvular heart disease"], "ans": 1, "exp": "Ischaemic heart disease (coronary artery disease with prior MI) is the most common underlying aetiology of heart failure with reduced ejection fraction (HFrEF) in Western countries, accounting for approximately 60–70% of cases. Hypertension is the most common risk factor."}, {"q": "A patient develops a new pansystolic murmur and cardiogenic shock 3 days after anterior STEMI. What is the most likely diagnosis?", "opts": ["Pericarditis", "Ventricular septal defect (VSD) from septal rupture", "Papillary muscle dysfunction", "Dressler syndrome"], "ans": 1, "exp": "Mechanical complications of MI occurring 2–7 days after the event include free wall rupture, papillary muscle rupture (causing acute MR), and ventricular septal rupture (causing VSD). An acute VSD produces a harsh pansystolic murmur loudest at the left sternal edge with a systolic thrill, and rapid haemodynamic deterioration."}, {"q": "What is the correct sequence of DC cardioversion energy for AF?", "opts": ["50J → 100J → 200J", "120–150J biphasic initial shock, increasing if unsuccessful", "360J monophasic immediately", "10J → 50J → 100J"], "ans": 1, "exp": "Synchronised DC cardioversion for AF typically starts at 120–150J (biphasic), increasing to 200J and then 360J if previous shocks were unsuccessful. Synchronisation to the R wave is essential to avoid delivering energy during the T wave (which could precipitate VF). Anticoagulation rules must be followed before elective cardioversion."}, {"q": "Which antiplatelet drug irreversibly inhibits P2Y12 ADP receptors on platelets?", "opts": ["Aspirin", "Clopidogrel", "Ticagrelor", "Tirofiban"], "ans": 1, "exp": "Clopidogrel is a thienopyridine prodrug that irreversibly inhibits P2Y12 ADP receptors on platelets, reducing ADP-mediated platelet aggregation for the platelet's lifetime (~7–10 days). Ticagrelor also blocks P2Y12 but reversibly, with faster onset and offset. Aspirin irreversibly inhibits COX-1."}, {"q": "What is the most appropriate management of stable angina refractory to two anti-anginal drugs?", "opts": ["Increase beta-blocker dose indefinitely", "Refer for coronary angiography with a view to revascularisation", "Add a third anti-anginal drug", "Reassure and discharge"], "ans": 1, "exp": "Stable angina uncontrolled on two anti-anginal agents warrants coronary angiography to assess anatomy for PCI or CABG. Revascularisation improves symptoms but has not been shown to reduce death or MI in stable coronary artery disease vs optimal medical therapy (ISCHEMIA trial), so patient preference and functional limitation guide the decision."}, {"q": "What echocardiographic finding defines heart failure with preserved ejection fraction (HFpEF)?", "opts": ["EF <40% with diastolic dysfunction", "EF ≥50% with symptoms/signs of HF and evidence of diastolic dysfunction or elevated filling pressures", "EF 40–49% exclusively", "Wall motion abnormality in a coronary territory"], "ans": 1, "exp": "HFpEF (formerly 'diastolic heart failure') requires: symptoms/signs of heart failure, LVEF ≥50%, and objective evidence of cardiac structural/functional abnormality (LV hypertrophy, LAE) or elevated natriuretic peptides and elevated filling pressures on echo or catheterisation."}, {"q": "Which statin has the greatest LDL-lowering potency?", "opts": ["Simvastatin 40 mg", "Atorvastatin 80 mg", "Rosuvastatin 40 mg", "Pravastatin 40 mg"], "ans": 2, "exp": "Rosuvastatin 40 mg produces the greatest LDL-C reduction (~55–63%), slightly exceeding atorvastatin 80 mg (~50–55%). Both are high-intensity statins per AHA/ACC classification. Rosuvastatin has the additional benefit of being less hepatically metabolised and fewer drug interactions via CYP450."}, {"q": "What is the haemodynamic target for managing acute pulmonary embolism with haemodynamic compromise?", "opts": ["Systolic BP >130 mmHg", "Systolic BP >90 mmHg and maintaining right heart function", "HR <60 bpm", "CVP <8 mmHg"], "ans": 1, "exp": "In massive PE with haemodynamic collapse, the target is systolic BP >90 mmHg. Systemic thrombolysis (alteplase) is first-line for haemodynamically unstable massive PE. Fluid resuscitation is cautious (250–500 mL maximum) as excessive preload can worsen right ventricular distension and septal shift."}, {"q": "Which drug is used for rhythm control in AF in a patient with structural heart disease?", "opts": ["Flecainide", "Propafenone", "Amiodarone", "Sotalol"], "ans": 2, "exp": "Amiodarone is the only anti-arrhythmic agent safe and effective for rhythm control in AF with significant structural heart disease (reduced EF, LVH, prior MI). Flecainide and propafenone are class IC agents contraindicated in structural heart disease due to pro-arrhythmic risk. Sotalol requires normal LV function and QTc monitoring."}, {"q": "What is the role of BNP/NT-proBNP in heart failure management?", "opts": ["Confirms the aetiology of heart failure", "Diagnoses and monitors disease severity; guides treatment decisions", "Identifies coronary artery disease", "Replaces echocardiography"], "ans": 1, "exp": "BNP and NT-proBNP are released from ventricular myocytes in response to wall stress. Elevated levels support a diagnosis of heart failure and correlate with severity. NT-proBNP <125 pg/mL effectively excludes HF in outpatients. BNP-guided therapy may reduce hospitalisation in some patient groups."}, {"q": "Which intervention reduces risk of sudden cardiac death most effectively in secondary prevention after sustained VT/VF?", "opts": ["Amiodarone alone", "Implantable cardioverter-defibrillator (ICD)", "Beta-blocker alone", "Ablation alone"], "ans": 1, "exp": "ICD implantation is the most effective intervention for secondary prevention of sudden cardiac death following haemodynamically significant VT or VF (AVID, CASH, CIDS trials). Beta-blockers and amiodarone reduce recurrence but are inferior to ICD for mortality reduction."}, {"q": "What is the most common arrhythmia precipitating cardiac arrest in adults?", "opts": ["Pulseless electrical activity", "Ventricular fibrillation (VF)", "Asystole", "Pulseless VT"], "ans": 1, "exp": "VF is the most common initial rhythm in witnessed out-of-hospital cardiac arrest, present in approximately 40–60% of cases. It is the most 'shockable' rhythm with the best prognosis if defibrillated promptly. Survival decreases by ~10% for every minute of VF without defibrillation."}, {"q": "In hypertensive emergency, how rapidly should blood pressure be lowered?", "opts": ["To normal immediately (<1 hour)", "By no more than 20–25% in the first hour, then gradually over 24–48 hours", "To <120/80 within 6 hours", "Immediate reduction to 100/60"], "ans": 1, "exp": "Rapid BP normalisation in hypertensive emergency risks cerebral, renal, and coronary hypoperfusion. The target is no more than 20–25% reduction in mean arterial pressure in the first hour, then to ~160/100 over the next 2–6 hours. Exception: aortic dissection requires more aggressive reduction (SBP <120 within 20 min)."}, {"q": "What is the mechanism of digoxin toxicity in hypokalaemia?", "opts": ["Increased digoxin absorption", "Hypokalaemia increases digoxin's effect on Na/K-ATPase, potentiating toxicity even at therapeutic levels", "Reduced renal digoxin clearance", "Increased protein binding"], "ans": 1, "exp": "Potassium and digoxin compete for the same binding site on Na/K-ATPase. In hypokalaemia, there is less potassium competing, so digoxin binds more avidly — even at therapeutic serum levels, toxicity can occur. Classic toxicity signs: nausea, yellow-green visual halos, bradycardia, AV block, ventricular arrhythmias."}, {"q": "Which condition causes a loud P2 on auscultation?", "opts": ["Aortic stenosis", "Pulmonary hypertension", "Mitral stenosis", "Pericardial effusion"], "ans": 1, "exp": "A loud pulmonary component of the second heart sound (P2) reflects elevated pulmonary artery pressure (pulmonary hypertension). It is best heard at the upper left sternal edge. Other signs include parasternal heave (RVH), tricuspid regurgitation murmur, and elevated JVP with prominent 'v' waves."}, {"q": "What is the first-line treatment for stable angina due to coronary artery disease?", "opts": ["PCI", "Sublingual GTN + beta-blocker or calcium channel blocker + optimise CVD risk factors", "Long-acting nitrate alone", "CABG"], "ans": 1, "exp": "Stable angina management: sublingual GTN for acute relief; regular anti-anginal therapy (beta-blocker first-line or rate-limiting CCB if contraindicated) for prophylaxis; plus optimisation of cardiovascular risk factors (statin, antiplatelet, BP control, lifestyle). Revascularisation for refractory symptoms or high-risk anatomy."}]}