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Cardiology Topic Index — every topic, tiered: Core · Important · Rare
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Prevention & Investigations

Primary prevention (CVD risk)Coretap to open ▾
Estimate 10-year risk with QRISK3; offer atorvastatin 20 mg if ≥10%. Always offered regardless of QRISK: familial hypercholesterolaemia, established CVD, T1DM >10y/age>40, CKD.
Tool: QRISK3 (adds SLE, severe mental illness, steroids, atypical antipsychotics, migraine, ED, BP variability).
Threshold: QRISK ≥10% → offer atorvastatin 20 mg.
No QRISK needed: FH, established CVD, T1DM (>10y or >40), CKD stage ≥3.
Also: Optimise BP, smoking, diabetes, weight.
A well 56-year-old has a QRISK3 of 12% and no established disease. What is the appropriate primary-prevention drug?
  • AAtorvastatin 80 mg
  • BAtorvastatin 20 mg
  • CAspirin 75 mg
  • DNo drug
  • EEzetimibe
Correct: B — Atorvastatin 20 mg
Why: For primary prevention with QRISK ≥10%, offer atorvastatin 20 mg; 80 mg is for secondary prevention. Aspirin is not used for primary prevention.
Options:
  • That’s secondary.
  • (correct)
  • Not for primary prevention.
  • Statin indicated.
  • Not first-line.
Lifestyle modificationCoretap to open ▾
Core of all cardiovascular prevention: stop smoking, Mediterranean-style diet, ≥150 min/week moderate activity, alcohol ≤14 units/week, weight/waist reduction, salt <6 g/day.
Smoking: Cessation is the single highest-impact intervention; offer support + pharmacotherapy.
Diet & activity: Mediterranean diet; ≥150 min/week moderate exercise; salt <6 g/day.
Alcohol/weight: ≤14 units/week spread over ≥3 days; reduce weight/waist.
Which single lifestyle change gives the greatest cardiovascular benefit in a smoker with stable angina?
  • AReducing salt
  • BSmoking cessation
  • CTaking vitamins
  • DReducing caffeine
  • EStanding desk
Correct: B — Smoking cessation
Why: Smoking cessation is the highest-impact lifestyle intervention for cardiovascular risk.
Options:
  • Helpful but lesser.
  • (correct)
  • No benefit.
  • Minimal.
  • Minimal.
Cardiac chest pain: assessmentCoretap to open ▾
Typical angina = constricting, provoked by exertion, relieved by rest/GTN in ~5 min (all 3 = typical). First-line investigation for stable chest pain is CT coronary angiography. Acute: <12h admit, 12–72h same-day, >72h ECG+troponin.
Typicality: 3 features = typical; 2 = atypical; 0–1 = non-anginal.
Investigate stable: CT coronary angiography first-line (exercise ECG no longer recommended for diagnosis).
Acute timing: <12h emergency; 12–72h same-day; >72h ECG+troponin.
Emergency: Ongoing pain + ST elevation → STEMI pathway.
A 55-year-old has exertional constricting chest pain relieved by rest, with a normal resting ECG. What is the first-line investigation?
  • AExercise ECG
  • BCT coronary angiography
  • CInvasive angiography
  • DEchocardiogram
  • EChest X-ray
Correct: B — CT coronary angiography
Why: NICE recommends CT coronary angiography first-line for suspected stable angina; the exercise ECG is no longer used for diagnosis.
Options:
  • No longer first-line.
  • (correct)
  • Third-line.
  • Not diagnostic for angina.
  • Not diagnostic.
Broad-complex tachycardiaImportanttap to open ▾
Regular broad-complex = VT until proven otherwise → amiodarone 300 mg IV (if stable) or synchronised DC shock (if unstable). Irregular broad-complex + long QT = torsades → IV magnesium.
Regular: Treat as VT: amiodarone 300 mg IV over 20–60 min if stable; DC cardioversion if adverse features.
Irregular: AF with bundle branch block, or torsades (polymorphic VT) → magnesium for torsades.
Unstable: Synchronised DC cardioversion.
A stable patient has a regular broad-complex tachycardia. Assuming it is VT, what is the appropriate drug?
  • AAdenosine
  • BAmiodarone 300 mg IV
  • CVerapamil
  • DDigoxin
  • EAtropine
Correct: B — Amiodarone 300 mg IV
Why: A regular broad-complex tachycardia is treated as VT; amiodarone is the drug of choice when the patient is stable (DC cardioversion if unstable).
Options:
  • For narrow-complex SVT.
  • (correct)
  • Dangerous in VT.
  • Not indicated.
  • For bradycardia.
Bradycardia: managementImportanttap to open ▾
If adverse features (shock, syncope, ischaemia, heart failure): atropine 500 mcg IV up to 3 mg; then transcutaneous pacing / isoprenaline / adrenaline. No adverse features + no asystole risk → observe.
Adverse features: Shock, syncope, myocardial ischaemia, heart failure.
First drug: Atropine 500 mcg IV, repeat to a maximum of 3 mg.
If unresponsive/high risk: Transcutaneous pacing, isoprenaline or adrenaline infusion; expert help.
A patient with complete heart block is hypotensive and syncopal with a rate of 35. What is the immediate first drug?
  • AAdenosine
  • BAtropine 500 mcg IV
  • CAmiodarone
  • DDigoxin
  • EBisoprolol
Correct: B — Atropine 500 mcg IV
Why: Symptomatic bradycardia with adverse features is treated first with atropine 500 mcg IV (up to 3 mg), then pacing if needed.
Options:
  • Wrong indication.
  • (correct)
  • Wrong indication.
  • Slows further.
  • Slows further.
Cardiac investigations: exercise & ambulatory ECGImportanttap to open ▾
Exercise ECG: assesses inducible ischaemia/functional capacity (no longer first-line to diagnose angina). Ambulatory (Holter/loop) ECG: captures intermittent arrhythmia during symptoms.
Exercise ECG: Now mainly for functional assessment/risk, not first-line angina diagnosis (CTCA replaced it).
Ambulatory ECG: 24-hour Holter for frequent symptoms; external/implantable loop recorder for infrequent ones.
First for palpitations: 12-lead ECG + bloods, then ambulatory monitoring.
A patient has infrequent palpitations (once a month) with a normal resting ECG. Which is the best monitoring choice?
  • A24-hour Holter
  • BImplantable/external loop recorder
  • CExercise ECG
  • DEchocardiogram
  • ERepeat 12-lead
Correct: B — Implantable/external loop recorder
Why: Infrequent symptoms are best captured with a loop recorder; a 24-hour Holter suits frequent (near-daily) symptoms.
Options:
  • Misses infrequent events.
  • (correct)
  • Not for arrhythmia capture.
  • Structural, not rhythm.
  • Low yield.
Cardiac imaging: echo, catheterisation, nuclearImportanttap to open ▾
Echocardiography: first-line for valve disease, HF (EF), cardiomyopathy. Coronary angiography (catheterisation): gold standard for coronary anatomy/intervention. Myocardial perfusion (nuclear/SPECT): functional ischaemia when CTCA inconclusive.
Echo: Structure/function — EF, valves, cardiomyopathy, effusion; first-line in HF diagnosis after NT-proBNP.
Catheterisation: Invasive coronary angiography — definitive anatomy + PCI; used when non-invasive tests inconclusive or high-risk.
Nuclear/SPECT: Myocardial perfusion imaging for functional ischaemia (2nd-line after CTCA).
Which investigation is first-line to assess left-ventricular function and valves in suspected heart failure (after NT-proBNP)?
  • ACoronary angiography
  • BEchocardiography
  • CMyocardial perfusion scan
  • DExercise ECG
  • EChest X-ray
Correct: B — Echocardiography
Why: Echocardiography is first-line for assessing ejection fraction, valves and structure in heart failure once NT-proBNP indicates the need.
Options:
  • Invasive, for coronaries.
  • (correct)
  • For ischaemia, not structure.
  • Not structural.
  • Non-specific.

Hypertension

Hypertension: diagnosisCoretap to open ▾
Clinic ≥140/90 → confirm with ABPM/HBPM. Stage 1 ABPM ≥135/85; Stage 2 ≥150/95; severe ≥180/120.
Confirm: A raised clinic reading needs ABPM (or HBPM) before diagnosis — unless ≥180/120 or end-organ damage.
HBPM: Twice daily, 7 days, discard day 1; average the rest.
Stages: Stage 1 ABPM ≥135/85 · Stage 2 ≥150/95 · Severe clinic ≥180/120.
A clinic BP is 148/94 with no symptoms or end-organ damage. What is the next step?
  • AStart an ACE inhibitor
  • BOffer ABPM or HBPM to confirm
  • CAdmit for assessment
  • DRepeat in 12 months
  • EStart two agents
Correct: B — Offer ABPM or HBPM to confirm
Why: A raised clinic reading is confirmed with ambulatory or home monitoring before diagnosis and treatment.
Options:
  • Don’t treat before confirming.
  • (correct)
  • Admission is for ≥180/120 with red flags.
  • Too long a delay.
  • Not without confirmation.
Hypertension: managementCoretap to open ▾
A/C/D ladder: <55 or T2DM → ACEi/ARB; ≥55 or Black → CCB. Then A+C, A+C+D. Step 4 by K⁺ (≤4.5 spironolactone; >4.5 alpha/beta-blocker).
Step 1: <55 or T2DM → ACEi/ARB · ≥55 or African/Caribbean → CCB.
Steps 2–3: A+C, then A+C+thiazide-like diuretic (indapamide).
Step 4: K⁺ ≤4.5 → spironolactone · K⁺ >4.5 → alpha- or beta-blocker.
Targets: <80: 140/90 clinic (135/85 ABPM). ≥80: 150/90 (145/85). T2DM/ACR≥70/stroke: 130/80.
A 62-year-old of African-Caribbean origin, no diabetes, needs first-line antihypertensive. Which drug?
  • AACE inhibitor
  • BCalcium-channel blocker
  • CBeta-blocker
  • DThiazide-like diuretic
  • ESpironolactone
Correct: B — Calcium-channel blocker
Why: For ≥55 or Black African/Caribbean patients without diabetes, a CCB is first-line; ACEi is less effective as monotherapy here.
Options:
  • Less effective here.
  • (correct)
  • Not first-line.
  • Step 3.
  • Step 4.
Isolated systolic hypertensionImportanttap to open ▾
Treat the same as standard hypertension (usually CCB or thiazide-like if >55); target systolic <140 (<150 if >80).
Definition: Systolic ≥140 with normal diastolic — common in the elderly (arterial stiffness).
Treat: Same pathway as standard hypertension; watch for excessive diastolic drop.
An 82-year-old has a clinic BP of 168/78. What is the appropriate approach?
  • ANo treatment — diastolic is normal
  • BTreat as hypertension; CCB or thiazide-like, target <150 systolic
  • CBeta-blocker first-line
  • DOnly treat if symptomatic
  • EHalve to 130 systolic quickly
Correct: B — Treat as hypertension; CCB or thiazide-like, target <150 systolic
Why: Isolated systolic hypertension is treated like standard hypertension; the systolic target is <150 in the over-80s.
Options:
  • Systolic still matters.
  • (correct)
  • Not first-line.
  • Treat regardless of symptoms.
  • Avoid over-aggressive lowering.
Hypertension: secondary causesImportanttap to open ▾
Consider in young/resistant/severe HTN: renal artery stenosis, Conn’s, phaeochromocytoma, Cushing’s, coarctation, hyper/parathyroid, hyperthyroid.
Screen when: Young, resistant to 3 drugs, or severe/accelerated.
Surgically-correctable: Renal artery stenosis, coarctation, phaeo, Conn’s, Cushing’s, unilateral renal disease, hyperthyroid, hyperparathyroid.
Clues: Hypokalaemia → Conn’s; episodic sweating/headache → phaeo; arm-leg BP gap → coarctation.
A 30-year-old with resistant hypertension has a low potassium and metabolic alkalosis. Which secondary cause is most likely?
  • APhaeochromocytoma
  • BPrimary hyperaldosteronism (Conn’s)
  • CCushing’s
  • DCoarctation
  • ERenal artery stenosis
Correct: B — Primary hyperaldosteronism (Conn’s)
Why: Hypertension with hypokalaemic alkalosis suggests primary hyperaldosteronism (Conn’s). Screen with an aldosterone:renin ratio.
Options:
  • Phaeo gives episodic surges.
  • (correct)
  • Cushing’s has other features.
  • Coarctation gives arm-leg gap.
  • RAS worsens on ACEi.
Diabetes mellitus: hypertension managementCoretap to open ▾
ACE inhibitor/ARB first-line regardless of age. Target <140/90 (T2DM); <135/85 T1DM; <130/80 if end-organ damage.
First-line: ACE inhibitor or ARB regardless of age (renoprotective).
Targets: <140/90 clinic in T2DM; <130/80 if end-organ damage/ACR≥70.
Add-on: Then CCB or thiazide-like diuretic as per standard steps.
A 58-year-old with type 2 diabetes and no proteinuria has hypertension. First-line drug?
  • AAmlodipine
  • BAn ACE inhibitor
  • CBendroflumethiazide
  • DBisoprolol
  • EDoxazosin
Correct: B — An ACE inhibitor
Why: In diabetics, ACE inhibitors (or ARBs) are first-line at any age for renoprotection.
Options:
  • CCB is add-on.
  • (correct)
  • Diuretic is add-on.
  • Not first-line.
  • Later step.
Postural hypotensionImportanttap to open ▾
Drop ≥20 systolic / 10 diastolic on standing. Treat based on standing BP; review vasodilators/diuretics; midodrine/fludrocortisone if needed.
Definition: Fall ≥20 systolic or ≥10 diastolic within 3 min of standing.
Causes: Drugs (diuretics, vasodilators, alpha-blockers), autonomic failure, dehydration.
Manage: Treat on standing BP; review drugs; midodrine/fludrocortisone if persistent.
An elderly man on several antihypertensives has dizziness on standing with a 30 mmHg systolic drop. Best approach?
  • AIncrease his antihypertensives
  • BReview/reduce culprit drugs and treat based on standing BP
  • CIgnore it
  • DStart a beta-blocker
  • EAdd a diuretic
Correct: B — Review/reduce culprit drugs and treat based on standing BP
Why: Postural hypotension is managed by reviewing culprit drugs and titrating to the standing blood pressure.
Options:
  • Would worsen it.
  • (correct)
  • Falls risk.
  • May worsen.
  • May worsen.

AF & Arrhythmias

Atrial fibrillation: anticoagulationCoretap to open ▾
CHA₂DS₂-VASc ≥2 (or ≥1 men) → anticoagulate; DOAC first-line, warfarin if DOAC unsuitable/valvular. Bleeding risk: ORBIT (HAS-BLED still known).
Score: CHA₂DS₂-VASc: CHF, HTN, Age≥75 (2), Diabetes, Stroke/TIA (2), Vascular, Age 65–74, Sex (female).
Offer: Men ≥1, women ≥2 → anticoagulate. DOAC first-line.
Bleeding: NICE now uses ORBIT (replaced HAS-BLED). A high score modifies risk factors, doesn’t stop anticoagulation.
Valvular AF: Mechanical valve / moderate–severe mitral stenosis → warfarin, not DOAC.
An 83-year-old woman with hypertension and diabetes has new AF. Her CHA₂DS₂-VASc and management?
  • AScore 2, no treatment
  • BScore 4, offer a DOAC
  • CScore 1, aspirin
  • DScore 6, warfarin only
  • EScore 3, aspirin+clopidogrel
Correct: B — Score 4, offer a DOAC
Why: Age≥75 (2)+female (1)+HTN (1)+diabetes (1)=4 → anticoagulate with a DOAC. Antiplatelets are not used for AF stroke prevention.
Options:
  • Underestimate.
  • (correct)
  • Aspirin not used.
  • DOAC first-line, not warfarin.
  • Antiplatelets not used.
Atrial fibrillation: rate control and rhythmCoretap to open ▾
Rate control first-line for most (beta-blocker or rate-limiting CCB; digoxin if sedentary/HF). Rhythm control if <65, first presentation, precipitant, or HF.
Rate first: Beta-blocker or rate-limiting CCB; digoxin only if sedentary or heart failure.
Rhythm control: Consider if younger, reversible cause, new-onset, or heart failure. Flecainide/sotalol (no structural disease); amiodarone if structural/HF.
A 70-year-old with permanent AF, HR 100, no HF, asymptomatic. First-line rate control?
  • ADigoxin
  • BBisoprolol
  • CAmiodarone
  • DFlecainide
  • ESotalol
Correct: B — Bisoprolol
Why: Rate control is first-line; a beta-blocker (or rate-limiting CCB). Digoxin is reserved for sedentary/HF patients.
Options:
  • Sedentary/HF only.
  • (correct)
  • Rhythm drug.
  • Rhythm drug.
  • Rhythm drug.
Atrial fibrillation: cardioversionImportanttap to open ▾
Onset <48 h: heparinise then cardiovert. >48 h/unknown: anticoagulate 3 weeks first (or TOE-guided). High recurrence: amiodarone/sotalol 4 weeks first.
<48 h: Heparinise then cardiovert (electrical or pharmacological).
>48 h / unknown: Anticoagulate 3 weeks before, or do TOE to exclude thrombus.
After ablation: Continue anticoagulation per CHA₂DS₂-VASc long-term.
A patient with AF of uncertain duration (probably >48h) needs cardioversion but is stable. What is required first?
  • AImmediate DC cardioversion
  • B3 weeks of anticoagulation or a TOE
  • CAspirin only
  • DDigoxin loading
  • ENo preparation
Correct: B — 3 weeks of anticoagulation or a TOE
Why: With onset over 48 hours or unknown, anticoagulate for 3 weeks before cardioversion, or use TOE to exclude atrial thrombus.
Options:
  • Risks embolic stroke.
  • (correct)
  • Aspirin insufficient.
  • Doesn’t address clot risk.
  • Unsafe.
Atrial fibrillation: post-strokeImportanttap to open ▾
After a stroke in AF, start/continue anticoagulation — but delay initiation (often ~2 weeks after a disabling stroke) to reduce haemorrhagic transformation.
Principle: AF-related stroke needs anticoagulation, not antiplatelets, long-term.
Timing: Delay anticoagulation after a large/disabling stroke (haemorrhagic transformation risk); shorter delay for TIA/small stroke.
A patient with AF has an acute ischaemic stroke. What is the long-term antithrombotic?
  • AAspirin lifelong
  • BAnticoagulation (DOAC), timing guided by stroke size
  • CClopidogrel
  • DDipyridamole
  • ENo treatment
Correct: B — Anticoagulation (DOAC), timing guided by stroke size
Why: AF-related stroke requires anticoagulation for secondary prevention; initiation is delayed after larger strokes to avoid haemorrhagic transformation.
Options:
  • Antiplatelet under-treats AF.
  • (correct)
  • Antiplatelet under-treats.
  • Antiplatelet under-treats.
  • Under-treats.
Supraventricular tachycardiaImportanttap to open ▾
Regular narrow-complex tachycardia. Acute: vagal manoeuvres → adenosine 6→12→18 mg (avoid in asthma; use verapamil).
Acute: Modified Valsalva first, then IV adenosine 6→12→18 mg (transient flatline warning).
Asthma: Avoid adenosine — use verapamil.
Unstable: Synchronised DC cardioversion.
A stable 30-year-old with a regular narrow-complex tachycardia at 180 fails vagal manoeuvres. Next step?
  • AIV adenosine 6 mg
  • BIV amiodarone
  • CDC cardioversion
  • DIV digoxin
  • EOral bisoprolol
Correct: A — IV adenosine 6 mg
Why: For stable regular narrow-complex SVT, IV adenosine (6→12→18 mg) is next after vagal manoeuvres. DC cardioversion is for instability.
Options:
  • (correct)
  • Amiodarone is for broad-complex.
  • For unstable patients.
  • Too slow.
  • Not acute.
Atrial flutterImportanttap to open ▾
Sawtooth flutter waves; rate often ~150 (2:1 block). Manage like AF (rate/rhythm + anticoagulation); catheter ablation is very effective.
ECG: Sawtooth flutter waves, atrial rate ~300, often 2:1 block → ventricular ~150.
Manage: Rate/rhythm control and anticoagulation as for AF.
Cure: Catheter ablation of the cavotricuspid isthmus is highly effective.
A regular narrow-complex tachycardia at exactly 150/min with sawtooth baseline. Diagnosis?
  • AAtrial fibrillation
  • BAtrial flutter
  • CSinus tachycardia
  • DVT
  • ESVT
Correct: B — Atrial flutter
Why: A regular rate near 150 with sawtooth waves is atrial flutter with 2:1 block; anticoagulate as for AF.
Options:
  • AF is irregular.
  • (correct)
  • Has normal P waves.
  • Broad complex.
  • No flutter waves.
Atrioventricular blockImportanttap to open ▾
1st degree (long PR, benign). Mobitz I (Wenckebach, progressive PR then dropped, usually benign). Mobitz II / complete → pacing.
First-degree: PR >200 ms, every P conducts — usually benign.
Mobitz I (Wenckebach): Progressive PR lengthening then a dropped beat — usually benign.
Mobitz II: Constant PR with intermittent dropped beats — risk of progression → pacing.
An ECG shows progressive PR lengthening then a dropped QRS, repeating. What is this?
  • AFirst-degree block
  • BMobitz type I (Wenckebach)
  • CMobitz type II
  • DComplete heart block
  • ESinus arrhythmia
Correct: B — Mobitz type I (Wenckebach)
Why: Progressive PR prolongation then a dropped beat is Mobitz I (Wenckebach), usually benign.
Options:
  • PR fixed/long.
  • (correct)
  • PR constant with drops.
  • P and QRS dissociated.
  • Rate varies with respiration.
Complete heart blockImportanttap to open ▾
P waves and QRS independent; risk of syncope/asystole. Needs permanent pacemaker. Common after inferior MI.
ECG: P waves and QRS independent (AV dissociation); slow escape rhythm.
Symptoms: Syncope, dizziness; risk of asystole. Common after inferior MI.
Treat: Permanent pacemaker (atropine/temporary pacing acutely).
An ECG shows P waves and QRS complexes with no relationship, ventricular rate 38. Definitive treatment?
  • AObservation
  • BPermanent pacemaker
  • CBeta-blocker
  • DAdenosine
  • EAmiodarone
Correct: B — Permanent pacemaker
Why: Complete (third-degree) heart block with symptoms/slow escape needs a permanent pacemaker.
Options:
  • Unsafe.
  • (correct)
  • Worsens it.
  • No role.
  • No role.
Brugada syndromeRare · recognise
Autosomal dominant sodium channelopathy; coved ST elevation V1–V3; risk of sudden death → ICD.
Long QT syndromeImportanttap to open ▾
Prolonged QTc → torsades/sudden death. Causes: congenital, hypokalaemia/magnesaemia/calcaemia, drugs (macrolides, antipsychotics, citalopram). Avoid QT-prolonging drugs; beta-blockers.
Risk: Prolonged QTc predisposes to torsades de pointes and sudden death.
Causes: Congenital; hypokalaemia/magnesaemia/calcaemia; drugs (macrolides, antipsychotics, citalopram, ondansetron).
Manage: Stop offending drugs, correct electrolytes; beta-blockers; ICD in high risk.
A patient on citalopram and clarithromycin collapses; ECG shows a long QT and polymorphic VT. Immediate drug?
  • AAmiodarone
  • BIV magnesium sulphate
  • CAdenosine
  • DDigoxin
  • EFlecainide
Correct: B — IV magnesium sulphate
Why: Torsades de pointes from a long QT is treated with IV magnesium; also stop QT-prolonging drugs and correct electrolytes.
Options:
  • Can prolong QT.
  • (correct)
  • Wrong rhythm.
  • No role.
  • Prolongs QT.
Wolff-Parkinson-WhiteImportanttap to open ▾
Short PR + delta wave (accessory pathway). Avoid AV-node blockers if AF+WPW; definitive treatment is ablation.
ECG: Short PR + delta wave (slurred QRS upstroke) from an accessory pathway.
Danger: AF with WPW → avoid AV-node blockers (digoxin, verapamil) — can accelerate conduction.
Cure: Radiofrequency ablation of the accessory pathway.
A young patient has palpitations; ECG shows a short PR interval and a delta wave. Which drug is dangerous if they develop AF?
  • AFlecainide
  • BDigoxin (AV-node blocker)
  • CAmiodarone
  • DSotalol
  • EProcainamide
Correct: B — Digoxin (AV-node blocker)
Why: In WPW with AF, AV-node blockers such as digoxin/verapamil can accelerate conduction down the accessory pathway → VF. Ablation is definitive.
Options:
  • Can be used.
  • (correct)
  • Can be used.
  • Not the classic danger.
  • Can be used.
Premature ventricular complexesRare · recognise
Common, often benign 'skipped beats'. Beta-blockers if symptomatic; investigate if frequent or structural disease.
Investigating palpitationsCoretap to open ▾
First-line 12-lead ECG + bloods (FBC, TFT, U&E); then Holter/ambulatory monitor; loop recorder for infrequent symptoms.
First-line: 12-lead ECG + bloods (FBC, TFT, U&E).
Next: Ambulatory (Holter) monitor; loop recorder for infrequent symptoms.
Red flags: Syncope, family history of sudden death, structural disease → refer.
A patient with intermittent palpitations has a normal resting ECG and bloods. Best next investigation?
  • AEchocardiogram
  • BAmbulatory ECG (Holter) monitor
  • CCoronary angiography
  • DChest X-ray
  • EExercise test
Correct: B — Ambulatory ECG (Holter) monitor
Why: After a normal resting ECG and bloods, capture the rhythm during symptoms with an ambulatory/Holter monitor (loop recorder if infrequent).
Options:
  • Not first for rhythm.
  • (correct)
  • Not indicated.
  • Unhelpful.
  • Not for palpitations.

Angina, ACS & MI

Angina pectoris: drug managementCoretap to open ▾
First-line beta-blocker OR CCB (titrate before adding). Combine BB + dihydropyridine CCB (never BB+verapamil/diltiazem). Then nitrate/ivabradine/nicorandil/ranolazine. All get aspirin + statin + GTN.
First-line: Beta-blocker or CCB; titrate to max before adding a second.
Combining: BB + a dihydropyridine CCB (e.g. amlodipine). Never BB + verapamil/diltiazem.
If mono not tolerated: Long-acting nitrate, ivabradine, nicorandil or ranolazine.
Secondary prevention: Aspirin, statin, GTN for attacks; address risk factors.
A patient on maximum bisoprolol still has angina and no heart failure. Best next step?
  • AAdd verapamil
  • BAdd amlodipine (dihydropyridine CCB)
  • CAdd diltiazem
  • DStop the beta-blocker
  • EAdd ivabradine monotherapy
Correct: B — Add amlodipine (dihydropyridine CCB)
Why: Add a dihydropyridine CCB to a beta-blocker. Verapamil/diltiazem with a beta-blocker risks heart block.
Options:
  • Heart-block risk.
  • (correct)
  • Heart-block risk.
  • Don’t stop effective drug.
  • Not monotherapy here.
Acute coronary syndrome: initial managementCoretap to open ▾
MONA-style: aspirin 300 mg + analgesia + oxygen only if hypoxic. STEMI → primary PCI (<120 min) or thrombolysis. NSTEMI → GRACE risk → angiography. Second antiplatelet: ticagrelor/prasugrel.
Immediate: Aspirin 300 mg; oxygen only if SpO₂ low; GTN/analgesia; ECG.
STEMI: Primary PCI within 120 min of when thrombolysis could be given; else thrombolysis.
NSTEMI: Fondaparinux if no early angiography; risk-stratify (GRACE) for angiography timing.
Second antiplatelet: Ticagrelor (or prasugrel if PCI planned).
A patient has a STEMI 90 minutes from a PCI centre. What is the priority treatment?
  • AThrombolysis now
  • BPrimary PCI
  • CAspirin then discharge
  • DWarfarin
  • EBeta-blocker only
Correct: B — Primary PCI
Why: Primary PCI is preferred if achievable within 120 minutes; otherwise thrombolysis. Aspirin 300 mg is given regardless.
Options:
  • PCI preferred if in time.
  • (correct)
  • Inadequate.
  • Not acute treatment.
  • Insufficient.
Myocardial infarction: secondary preventionCoretap to open ▾
The 6 A's: Aspirin (lifelong) + second Antiplatelet (12 mo) + ACE inhibitor + Atenolol/beta-blocker + Atorvastatin 80 + Aldosterone antagonist (if HF). Cardiac rehab; no sex 4 weeks; no sildenafil 6 months.
Drugs that improve mortality: Dual antiplatelets, ACE inhibitor, beta-blocker, spironolactone (if LV dysfunction).
Statin: Atorvastatin 80 mg.
Lifestyle: Cardiac rehab, smoking cessation, diet; sexual activity after 4 weeks.
Which combination best reflects mortality-improving secondary prevention after an MI with LV dysfunction?
  • AAspirin alone
  • BDAPT + ACE inhibitor + beta-blocker + spironolactone
  • CWarfarin + statin
  • DCCB + nitrate
  • EAspirin + CCB
Correct: B — DAPT + ACE inhibitor + beta-blocker + spironolactone
Why: Post-MI mortality is reduced by dual antiplatelets, an ACE inhibitor, a beta-blocker and (with LV dysfunction) an aldosterone antagonist.
Options:
  • Under-treats.
  • (correct)
  • Not the standard.
  • No mortality benefit.
  • No mortality benefit.
Myocardial infarction: complicationsImportanttap to open ▾
Persistent ST elevation + HF = LV aneurysm. VSD/free-wall rupture, acute MR (papillary rupture), Dressler’s (2–6 wk autoimmune pericarditis), arrhythmia, heart block (inferior MI), cardiogenic shock.
LV aneurysm: Persistent ST elevation weeks later + HF → thrombus risk → anticoagulate.
Mechanical: VSD (pansystolic, LLSE), acute MR (pansystolic→axilla, papillary rupture), free-wall rupture → tamponade.
Dressler’s: 2–6 weeks: fever, pleuritic pain, effusion, ↑ESR → NSAIDs.
Three weeks after an MI a patient has fever, pleuritic chest pain, a pericardial rub and raised ESR. Diagnosis?
  • AAcute pericarditis
  • BDressler’s syndrome
  • CRe-infarction
  • DPulmonary embolism
  • ELV aneurysm
Correct: B — Dressler’s syndrome
Why: Dressler’s syndrome is an autoimmune pericarditis 2–6 weeks post-MI with fever, pleuritic pain, effusion and raised ESR; treat with NSAIDs.
Options:
  • Acute pericarditis is <48h.
  • (correct)
  • Different picture.
  • No rub/ESR pattern.
  • No fever/rub.
Acute pericarditisImportanttap to open ▾
Pleuritic chest pain relieved by sitting forward; saddle-shaped/widespread ST elevation + PR depression; pericardial rub. Treat NSAIDs + colchicine.
Features: Pleuritic chest pain relieved by sitting forward; pericardial rub.
ECG: Widespread saddle-shaped ST elevation + PR depression.
Treat: NSAID + colchicine; investigate cause.
A young man has sharp chest pain relieved by leaning forward, a rub, and widespread saddle ST elevation. Treatment?
  • AAspirin 300 mg + PCI
  • BNSAID plus colchicine
  • CThrombolysis
  • DBeta-blocker
  • EAntibiotics
Correct: B — NSAID plus colchicine
Why: Acute pericarditis is treated with an NSAID plus colchicine; the widespread ST elevation distinguishes it from a STEMI.
Options:
  • That’s for STEMI.
  • (correct)
  • Not indicated.
  • Not first-line.
  • Only if bacterial.
Cardiac tamponadeImportanttap to open ▾
Beck’s triad: hypotension, muffled heart sounds, raised JVP; pulsus paradoxus. Urgent pericardiocentesis.
Beck’s triad: Hypotension, muffled heart sounds, raised JVP.
Sign: Pulsus paradoxus (>10 mmHg inspiratory systolic fall).
Treat: Urgent pericardiocentesis.
A patient is hypotensive with muffled heart sounds, raised JVP and pulsus paradoxus. Immediate management?
  • AIV fluids only
  • BUrgent pericardiocentesis
  • CThrombolysis
  • DBeta-blocker
  • EAspirin
Correct: B — Urgent pericardiocentesis
Why: Beck’s triad with pulsus paradoxus is cardiac tamponade — relieve with urgent pericardiocentesis.
Options:
  • Temporising only.
  • (correct)
  • Contraindicated.
  • Harmful.
  • No role.
Takotsubo cardiomyopathyRare · recognise
Stress ('broken heart') cardiomyopathy; apical ballooning, mimics ACS after emotional stress; supportive treatment, usually recovers.
MyocarditisRare · recognise
Viral (e.g. Coxsackie) inflammation; chest pain, dyspnoea, arrhythmia, raised troponin with normal coronaries; may follow a viral illness. Supportive care; avoid exercise; treat complications/heart failure.

Heart Failure

Chronic heart failure: diagnosisCoretap to open ▾
NT-proBNP first-line → echo. >2000 ng/L: specialist+echo within 2 weeks; 400–2000: within 6 weeks; <400 makes HF unlikely.
First test: NT-proBNP for all suspected chronic HF.
Thresholds: BNP >400 / NT-proBNP >2000 → 2 weeks. BNP 100–400 / NT-proBNP 400–2000 → 6 weeks.
Raises BNP: LVH, ischaemia, tachycardia, hypoxaemia/PE, GFR<60, sepsis, age>70. Lowers: obesity, ACEi/BB/ARB/diuretic/MRA.
A breathless patient has an NT-proBNP of 2400 ng/L. How urgently should echo and specialist review occur?
  • A6 weeks
  • B2 weeks
  • C24 hours
  • DRoutine
  • ENot needed
Correct: B — 2 weeks
Why: NT-proBNP above 2000 mandates specialist review and echo within 2 weeks.
Options:
  • 6 weeks is for 400–2000.
  • (correct)
  • Not unless unstable.
  • Delay inappropriate.
  • Action needed.
Chronic heart failure: drug managementCoretap to open ▾
Four pillars for HFrEF, started together and titrated: ACE inhibitor (→ARNI if still symptomatic) + beta-blocker + MRA + SGLT2 inhibitor. Loop diuretic for congestion. HFpEF: SGLT2i + manage comorbidities.
Four pillars: ACEi/ARNI + beta-blocker + MRA + SGLT2 inhibitor — to maximum tolerated dose.
Symptoms: Loop diuretic for congestion (no mortality benefit).
Add-ons: Ivabradine (sinus HR>75, EF<35%); digoxin (esp. AF); CRT/ICD selected.
Licensed BBs: Bisoprolol, carvedilol, nebivolol.
A patient with HFrEF is symptomatic on ramipril and bisoprolol. Which addition is most appropriate?
  • ADigoxin
  • BSpironolactone + an SGLT2 inhibitor
  • CAmlodipine
  • DIvabradine monotherapy
  • EDiuretic only
Correct: B — Spironolactone + an SGLT2 inhibitor
Why: The four pillars include an MRA and an SGLT2 inhibitor added to the ACE inhibitor and beta-blocker in HFrEF.
Options:
  • Later-line.
  • (correct)
  • No mortality benefit.
  • Add-on with criteria.
  • Symptom relief only.
Chronic heart failure: NYHA classificationImportanttap to open ▾
I: no limitation. II: slight (ordinary activity). III: marked (less-than-ordinary activity). IV: symptoms at rest.
I: No limitation of activity.
II: Slight limitation — symptoms on ordinary activity.
III: Marked limitation — symptoms on less-than-ordinary activity.
IV: Symptoms at rest.
A patient with heart failure is breathless only on climbing two flights of stairs but comfortable at rest and on the flat. NYHA class?
  • AI
  • BII
  • CIII
  • DIV
  • EUnclassifiable
Correct: B — II
Why: Symptoms on ordinary exertion with comfort at rest is NYHA class II.
Options:
  • No symptoms would be I.
  • (correct)
  • III is less-than-ordinary activity.
  • IV is at rest.
  • Classifiable.
Prescribing in patients with heart failureImportanttap to open ▾
Avoid worsening drugs: NSAIDs, non-dihydropyridine CCBs (verapamil/diltiazem) in HFrEF, glitazones. Start beta-blockers low and slow, never in decompensation.
Avoid: NSAIDs (fluid retention/renal), verapamil/diltiazem in HFrEF, glitazones.
Beta-blockers: Start low, go slow; never in acute decompensation.
Watch: Monitor U&E on ACEi/ARB/MRA; risk of hyperkalaemia.
Which drug should generally be avoided in a patient with HFrEF?
  • ARamipril
  • BVerapamil
  • CBisoprolol
  • DDapagliflozin
  • ESpironolactone
Correct: B — Verapamil
Why: Non-dihydropyridine CCBs such as verapamil are negatively inotropic and avoided in HFrEF; the others are guideline therapy.
Options:
  • Pillar drug.
  • (correct)
  • Pillar drug.
  • Pillar drug.
  • Pillar drug.
Dilated cardiomyopathyRare · recognise
Dilated, poorly-contracting ventricle; causes ischaemia, alcohol, viral, peripartum, haemochromatosis. Manage as HF.
Hypertrophic obstructive cardiomyopathy: featuresImportanttap to open ▾
Autosomal dominant; jerky pulse, ejection systolic murmur louder on Valsalva, S4; sudden death in young athletes. Echo: asymmetric septal hypertrophy + SAM. Beta-blockers; avoid ACEi/nitrates/diuretics; screen relatives.
Inheritance: Autosomal dominant sarcomere mutation; cause of sudden death in young athletes.
Signs: Jerky pulse, ejection systolic murmur louder on Valsalva (↓preload), S4.
Echo: Asymmetric septal hypertrophy + systolic anterior motion of mitral valve. Beta-blockers; avoid nitrates/ACEi/diuretics; screen relatives.
A young athlete has exertional syncope and an ejection systolic murmur that gets louder on Valsalva. Most likely diagnosis?
  • AAortic stenosis
  • BHypertrophic obstructive cardiomyopathy
  • CMitral regurgitation
  • DInnocent murmur
  • EVSD
Correct: B — Hypertrophic obstructive cardiomyopathy
Why: A murmur that increases with reduced preload (Valsalva) in a young person with syncope is HOCM; aortic stenosis decreases with Valsalva.
Options:
  • AS softens on Valsalva.
  • (correct)
  • Pansystolic to axilla.
  • No syncope.
  • Different murmur.
Cardiomyopathies: key pointsRare · recognise
Dilated (systolic failure), hypertrophic (outflow obstruction, sudden death), restrictive (amyloid/sarcoid, Kussmaul’s, low-voltage ECG).

Valves & Structural

Cardiac murmurs: quick guideImportanttap to open ▾
Systolic: aortic stenosis (ejection, to carotids), mitral regurgitation (pansystolic to axilla), HOCM (louder on Valsalva), VSD (LLSE). Diastolic: aortic regurgitation (early), mitral stenosis (mid + snap).
Systolic: AS ejection→carotids; MR pansystolic→axilla; HOCM louder on Valsalva; VSD at left lower sternal edge.
Diastolic: AR early diastolic (collapsing pulse); MS mid-diastolic + opening snap.
Manoeuvres: ↑afterload (handgrip)→louder AR/MR; ↓preload (Valsalva)→louder HOCM.
A pansystolic murmur heard best at the apex and radiating to the axilla is characteristic of which lesion?
  • AAortic stenosis
  • BMitral regurgitation
  • CAortic regurgitation
  • DMitral stenosis
  • EHOCM
Correct: B — Mitral regurgitation
Why: A pansystolic murmur radiating to the axilla is mitral regurgitation; aortic stenosis is ejection systolic to the carotids.
Options:
  • Ejection to carotids.
  • (correct)
  • Early diastolic.
  • Mid-diastolic.
  • Louder on Valsalva.
Aortic stenosisCoretap to open ▾
Ejection systolic murmur radiating to carotids; slow-rising pulse, narrow pulse pressure. Triad: syncope, angina, dyspnoea. Collapse on ACEi. Severe symptomatic → valve replacement.
Signs: ESM → carotids; slow-rising pulse; narrow pulse pressure; soft/absent S2.
ACEi caution: Moderate–severe AS is a contraindication to ACE inhibitors (severe hypotension).
Management: Symptomatic or severe → aortic valve replacement (surgical or TAVI).
An elderly man has exertional syncope and angina, a slow-rising pulse and an ejection systolic murmur to the carotids. Diagnosis?
  • AAortic regurgitation
  • BAortic stenosis
  • CMitral regurgitation
  • DMitral stenosis
  • EHOCM
Correct: B — Aortic stenosis
Why: Syncope + angina + dyspnoea with a slow-rising pulse and ESM to the carotids is aortic stenosis — and a contraindication to ACE inhibitors when moderate-to-severe.
Options:
  • Collapsing pulse/diastolic.
  • (correct)
  • Radiates to axilla.
  • Mid-diastolic + snap.
  • Louder on Valsalva.
Mitral regurgitationImportanttap to open ▾
Pansystolic murmur radiating to the axilla; may cause LV failure and AF. Causes: prolapse, ischaemia (papillary rupture), rheumatic, endocarditis.
Murmur: Pansystolic at apex → axilla; soft S1, may have S3.
Acute MR: Papillary muscle rupture post-MI → sudden pulmonary oedema — surgical emergency.
Manage: Treat HF; surgery for severe/symptomatic.
Two days after an inferior MI a patient develops acute pulmonary oedema and a new pansystolic murmur radiating to the axilla. Cause?
  • AVentricular septal defect
  • BAcute mitral regurgitation (papillary muscle rupture)
  • CDressler’s
  • DAortic stenosis
  • EFree-wall rupture
Correct: B — Acute mitral regurgitation (papillary muscle rupture)
Why: A new pansystolic murmur to the axilla with acute pulmonary oedema after MI is acute mitral regurgitation from papillary muscle rupture.
Options:
  • VSD is at the left sternal edge.
  • (correct)
  • Dressler’s is later/pericarditic.
  • AS is ejection systolic.
  • Free-wall rupture → tamponade.
Aortic regurgitationImportanttap to open ▾
Early diastolic murmur; collapsing (water-hammer) pulse, wide pulse pressure. Causes: bicuspid valve, Marfan, endocarditis, rheumatic. Surgery for symptoms/LV dilatation.
Murmur: Early diastolic, at the left sternal edge, patient sitting forward.
Pulse: Collapsing (water-hammer) pulse, wide pulse pressure.
Causes: Bicuspid valve, Marfan, endocarditis, rheumatic, dissection. Surgery for symptoms/LV dilatation.
A patient has a collapsing pulse, wide pulse pressure and an early diastolic murmur. Diagnosis?
  • AAortic stenosis
  • BAortic regurgitation
  • CMitral stenosis
  • DMitral regurgitation
  • EPulmonary stenosis
Correct: B — Aortic regurgitation
Why: A collapsing pulse with wide pulse pressure and an early diastolic murmur is aortic regurgitation.
Options:
  • Slow-rising pulse.
  • (correct)
  • Mid-diastolic + snap.
  • Pansystolic.
  • Different.
Mitral stenosisImportanttap to open ▾
Mid-diastolic murmur + opening snap, loud S1; malar flush, AF, haemoptysis; rheumatic. Balloon valvotomy/surgery.
Murmur: Mid-diastolic rumble + opening snap, loud S1; heard at apex in left lateral position.
Associations: Rheumatic heart disease; AF, malar flush, haemoptysis.
Manage: Rate control/anticoagulation for AF; balloon valvotomy or surgery.
A woman with AF has a malar flush, a loud S1 and a mid-diastolic murmur with an opening snap. Diagnosis?
  • AMitral regurgitation
  • BMitral stenosis
  • CAortic stenosis
  • DTricuspid regurgitation
  • EAortic regurgitation
Correct: B — Mitral stenosis
Why: Mid-diastolic murmur with opening snap, loud S1, malar flush and AF is mitral stenosis (usually rheumatic).
Options:
  • Pansystolic.
  • (correct)
  • Ejection systolic.
  • IVDU/pansystolic.
  • Early diastolic.
Heart soundsImportanttap to open ▾
S1 mitral/tricuspid closure; S2 aortic/pulmonary; S3 (HF/volume), S4 (stiff ventricle). Fixed split S2 = ASD.
S1/S2: S1 = mitral/tricuspid closure; S2 = aortic/pulmonary closure.
S3: Rapid ventricular filling — HF/volume overload (can be normal in young).
S4: Atrial contraction against a stiff ventricle. Fixed split S2 = ASD.
A fixed, widely split second heart sound that does not vary with respiration suggests which lesion?
  • AAortic stenosis
  • BAtrial septal defect
  • CMitral regurgitation
  • DPDA
  • ENormal finding
Correct: B — Atrial septal defect
Why: Fixed splitting of S2 is the classic sign of an atrial septal defect.
Options:
  • No fixed split.
  • (correct)
  • No fixed split.
  • Continuous murmur.
  • Fixed split is abnormal.
Jugular venous pulseRare · recognise
Large a-wave (tricuspid stenosis/pulmonary HTN); cannon a-waves (complete block); giant CV waves (tricuspid regurgitation); absent pulsation (SVC obstruction).
Prosthetic heart valvesImportanttap to open ▾
Mechanical: warfarin (+aspirin), last longer, for younger patients (target INR aortic 3.0, mitral 3.5). Bioprosthetic: aspirin, shorter-lived, older patients.
Mechanical: Warfarin (+ aspirin); durable, for younger patients. INR aortic 3.0, mitral 3.5.
Bioprosthetic: Aspirin; less durable, for older patients.
Complications: Thrombosis, endocarditis, haemolysis, failure.
A 40-year-old needs valve replacement and wants the most durable option. Which valve and what anticoagulation?
  • ABioprosthetic + aspirin
  • BMechanical + warfarin
  • CMechanical + aspirin only
  • DBioprosthetic + warfarin
  • ENo anticoagulation
Correct: B — Mechanical + warfarin
Why: Mechanical valves are most durable (suited to younger patients) but require lifelong warfarin.
Options:
  • Less durable.
  • (correct)
  • Needs warfarin.
  • Aspirin usually.
  • Mechanical needs warfarin.
Rheumatic feverRare · recognise
Post-strep (Jones criteria); can cause mitral stenosis years later. Treat strep + anti-inflammatories.
Infective endocarditis: prophylaxisImportanttap to open ▾
Antibiotic prophylaxis NOT routine in UK for dental/other procedures; emphasise oral hygiene. Acute IE → Staph aureus; subacute → Strep viridans; Strep bovis → colonoscopy.
Prophylaxis: Routine antibiotic prophylaxis NOT recommended in the UK for dental/other procedures.
Instead: Emphasise oral hygiene; treat infections promptly.
Organisms: Acute → Staph aureus; subacute → Strep viridans; Strep bovis → colonoscopy.
A patient with a prosthetic valve is due dental extraction. What antibiotic prophylaxis is recommended in the UK?
  • AAmoxicillin 3 g
  • BNo routine antibiotic prophylaxis
  • CClindamycin
  • DVancomycin
  • EGentamicin
Correct: B — No routine antibiotic prophylaxis
Why: NICE does not recommend routine antibiotic prophylaxis for dental procedures; the emphasis is on oral hygiene.
Options:
  • Not routine.
  • (correct)
  • Not routine.
  • Not routine.
  • Not routine.

Aorta, PAD & Venous

Peripheral arterial disease: managementCoretap to open ▾
Claudication + ABPI 0.5–0.9. Best medical therapy: stop smoking, atorvastatin 80, clopidogrel 75 (aspirin if intolerant), supervised exercise. Critical ischaemia (rest pain, ulcers, ABPI<0.5) → urgent vascular referral.
Diagnose: Intermittent claudication; ABPI 0.5–0.9 (normal 0.9–1.2; falsely high >1.3 if calcified).
Best medical therapy: Smoking cessation, atorvastatin 80 mg, clopidogrel 75 mg, supervised exercise, treat comorbidities.
Critical limb ischaemia: Rest pain, ulcers/gangrene, ABPI <0.5 → urgent vascular referral for revascularisation.
Declines surgery, exercise fails: Naftidrofuryl oxalate.
A 66-year-old with calf claudication has an ABPI of 0.7. Besides supervised exercise and stopping smoking, what drug therapy is first-line?
  • AAspirin 75 + atorvastatin 20
  • BClopidogrel 75 + atorvastatin 80
  • CWarfarin + simvastatin
  • DCilostazol only
  • ENo drugs
Correct: B — Clopidogrel 75 + atorvastatin 80
Why: PAD best medical therapy is clopidogrel 75 mg and atorvastatin 80 mg, with supervised exercise and smoking cessation.
Options:
  • Aspirin 2nd-line; statin dose low.
  • (correct)
  • Not standard.
  • Second-line only.
  • Medical therapy essential.
Abdominal aortic aneurysm: screening & managementCoretap to open ▾
Screening: single abdominal ultrasound for men at 65. <5.5 cm surveillance; ≥5.5 cm or symptomatic/rapidly growing → refer for repair. Rupture (pain + hypotension + pulsatile mass) = emergency.
Screening: Men at 65 — one-off abdominal ultrasound.
Surveillance: 3–4.4 cm yearly; 4.5–5.4 cm 3-monthly.
Repair: ≥5.5 cm, symptomatic, or growing >1 cm/yr → vascular referral.
Rupture: Sudden abdominal/back pain + hypotension + pulsatile mass → emergency surgery.
An asymptomatic 65-year-old man is found to have a 4.0 cm abdominal aortic aneurysm on screening. Management?
  • AImmediate surgery
  • BYearly ultrasound surveillance
  • C3-monthly ultrasound
  • DDischarge
  • EStart warfarin
Correct: B — Yearly ultrasound surveillance
Why: AAAs of 3–4.4 cm are monitored with yearly ultrasound; 4.5–5.4 cm 3-monthly; ≥5.5 cm referred for repair.
Options:
  • Not yet.
  • (correct)
  • That’s for 4.5–5.4 cm.
  • Needs surveillance.
  • No role.
Aortic dissection: featuresImportanttap to open ▾
Tearing chest pain radiating to the back; unequal arm pulses/BP; widened mediastinum on CXR. Type A (ascending) → surgery; Type B → medical (BP control).
Features: Sudden tearing chest/back pain; pulse/BP asymmetry; may cause AR, tamponade, stroke.
Investigate: CT angiography (or MRI); widened mediastinum on CXR.
Type A vs B: A (ascending) → surgery; B (descending) → medical BP control.
A hypertensive man has sudden tearing chest pain radiating to the back, unequal radial pulses and a widened mediastinum. Diagnosis?
  • ASTEMI
  • BAortic dissection
  • CPulmonary embolism
  • DPericarditis
  • EPneumothorax
Correct: B — Aortic dissection
Why: Tearing pain to the back with unequal pulses and a widened mediastinum is aortic dissection — confirm with CT angiography.
Options:
  • No pulse asymmetry.
  • (correct)
  • Different picture.
  • Pleuritic, not tearing.
  • Different picture.
Varicose veinsImportanttap to open ▾
Refer to vascular for skin changes, superficial thrombophlebitis with incompetence, or venous ulcer. First-line endothermal ablation, then foam sclerotherapy, then surgery.
Refer to vascular: Skin changes (pigmentation/eczema), superficial thrombophlebitis with incompetence, bleeding, or venous ulcer (healed or not).
First-line: Endothermal ablation / endovenous laser.
Then: Foam sclerotherapy, then surgery. Compression only if intervention unsuitable.
A patient has symptomatic varicose veins with ankle skin pigmentation and eczema. Appropriate action?
  • AReassure only
  • BRefer to vascular services
  • CCompression hosiery only
  • DAspirin
  • EDiuretic
Correct: B — Refer to vascular services
Why: Skin changes from chronic venous insufficiency are an indication to refer to vascular services.
Options:
  • Skin changes warrant referral.
  • (correct)
  • Only if intervention unsuitable.
  • No role.
  • No role.
Superficial thrombophlebitisImportanttap to open ▾
Tender, hard, red superficial vein; check for underlying DVT if extensive. Analgesia; consider anticoagulation if near saphenofemoral junction.
Features: Tender, hard, red superficial vein.
Check: Exclude/assess for underlying DVT, especially if extensive or near the saphenofemoral junction.
Manage: Analgesia, compression; consider anticoagulation if extensive/near junction.
A patient has a tender, hard, erythematous long saphenous vein extending toward the groin. Key concern?
  • ACellulitis only
  • BPropagation to DVT — assess and consider anticoagulation
  • CArterial disease
  • DLymphoedema
  • ENothing
Correct: B — Propagation to DVT — assess and consider anticoagulation
Why: Extensive superficial thrombophlebitis near the saphenofemoral junction can propagate to DVT; assess and consider anticoagulation.
Options:
  • Not just cellulitis.
  • (correct)
  • Venous, not arterial.
  • Different.
  • Needs assessment.
Ankle-brachial pressure indexImportanttap to open ▾
Highest ankle systolic ÷ highest arm systolic. Normal 0.9–1.2; PAD 0.5–0.9; critical <0.5; falsely high >1.3 (calcification, diabetes).
Calculation: Highest ankle systolic ÷ highest arm systolic.
Values: Normal 0.9–1.2; PAD 0.5–0.9; critical <0.5.
Falsely high: >1.3 with calcified vessels (diabetes, CKD).
A diabetic with leg pain has an ABPI of 1.4. How should this be interpreted?
  • ANormal, excludes PAD
  • BFalsely elevated due to arterial calcification
  • CCritical ischaemia
  • DVenous disease
  • EMeasurement error only
Correct: B — Falsely elevated due to arterial calcification
Why: An ABPI above 1.3 suggests incompressible, calcified vessels (common in diabetes/CKD) and can mask PAD.
Options:
  • Doesn’t exclude PAD.
  • (correct)
  • That’s <0.5.
  • ABPI is arterial.
  • Reflects calcification.
Buerger's diseaseRare · recognise
Thromboangiitis obliterans; young male smokers; distal ischaemia/ulcers. Stop smoking is essential.
Takayasu's arteritisRare · recognise
Large-vessel vasculitis in young women; absent/weak pulses, BP asymmetry, bruits. Steroids.
Coarctation of the aortaRare · recognise
Radio-femoral delay; BP higher in arms than legs; may have bicuspid valve. Repair.
Raynaud's phenomenonRare · recognise
Episodic digital vasospasm — white→blue→red with cold/stress. Primary (young women, benign) vs secondary (connective-tissue disease, e.g. scleroderma — check autoantibodies). Keep warm, stop smoking; nifedipine first-line drug.

VTE & PE

Deep vein thrombosisCoretap to open ▾
Two-level DVT Wells: ≥2 → proximal leg vein ultrasound within 4 h (D-dimer if delay); ≤1 → D-dimer. First-line treatment apixaban or rivaroxaban. Provoked 3 months; unprovoked ≥3–6 months.
Wells ≥2: Proximal leg vein ultrasound within 4 hours (interim anticoagulation if delayed); D-dimer if ≤1.
Treat: Apixaban or rivaroxaban first-line (DOAC).
Duration: Provoked 3 months; unprovoked ≥3–6 months; cancer/recurrent longer.
A patient has a two-level DVT Wells score of 3. What is the appropriate initial investigation?
  • AD-dimer
  • BProximal leg vein ultrasound within 4 hours
  • CVenography
  • DCT abdomen
  • EReassure
Correct: B — Proximal leg vein ultrasound within 4 hours
Why: A DVT Wells score of 2 or more means DVT is likely — arrange a proximal leg vein ultrasound within 4 hours (interim anticoagulation if delayed).
Options:
  • D-dimer is for ≤1.
  • (correct)
  • Rarely used now.
  • Not first-line.
  • Needs imaging.
Pulmonary embolism: investigation & managementCoretap to open ▾
Two-level Wells: >4 → CTPA; ≤4 → D-dimer. First-line treatment apixaban or rivaroxaban. Provoked 3 months; unprovoked ≥3–6 months; massive PE with instability → thrombolysis.
Wells >4: CTPA (V/Q if renal impairment/pregnancy/contrast allergy).
Wells ≤4: D-dimer; if positive → CTPA.
Treat: Apixaban or rivaroxaban first-line; LMWH bridge if needed.
Massive PE: Haemodynamic instability → thrombolysis.
A patient with a two-level PE Wells score of 5 needs investigation. What is appropriate?
  • AD-dimer
  • BCTPA
  • CChest X-ray only
  • DRepeat ECG
  • EReassure
Correct: B — CTPA
Why: A PE Wells score above 4 means PE is likely; proceed directly to CTPA (V/Q if CTPA contraindicated).
Options:
  • D-dimer is for ≤4.
  • (correct)
  • Insufficient.
  • Not diagnostic.
  • Unsafe.
Pulmonary embolism: ECGImportanttap to open ▾
Most common finding is sinus tachycardia. Classic (rare) S1Q3T3; right axis deviation, RBBB, T-wave inversion V1–3.
Most common: Sinus tachycardia.
Classic (rare): S1Q3T3 pattern.
Others: Right axis deviation, RBBB, T-wave inversion V1–3.
What is the most common ECG finding in pulmonary embolism?
  • AS1Q3T3
  • BSinus tachycardia
  • CRight bundle branch block
  • DAtrial fibrillation
  • EST elevation
Correct: B — Sinus tachycardia
Why: Sinus tachycardia is the commonest ECG finding in PE; S1Q3T3 is classic but uncommon.
Options:
  • Classic but rare.
  • (correct)
  • Possible, not commonest.
  • Possible, not commonest.
  • Not typical.
Travel-related thrombosisRare · recognise
Long-haul flights increase VTE risk; advise mobilisation/hydration; compression stockings if higher risk.

Cardiac Drugs

ACE inhibitorsCoretap to open ▾
First-line in HTN (<55/T2DM), HF, diabetic nephropathy. Stop if creatinine ↑>30% / eGFR ↓>25% / K⁺ ≥6. Bilateral renal artery stenosis suspected if renal function worsens. Side effects: cough, hyperkalaemia, angioedema, first-dose hypotension.
Monitoring: Check U&E before and 1–2 weeks after starting/uptitration.
Stop rules: Creatinine rise >30%, eGFR fall >25%, or K⁺ ≥6.
Renal artery stenosis: Marked renal decline after starting → suspect bilateral RAS.
Adverse: Dry cough, hyperkalaemia, angioedema, first-dose hypotension (worse with diuretics).
A patient on ramipril 6 months has a creatinine risen 35% from baseline and potassium 5.6. Action?
  • AContinue
  • BStop the ACE inhibitor
  • CIncrease the dose
  • DAdd a potassium supplement
  • EAdd an MRA
Correct: B — Stop the ACE inhibitor
Why: A creatinine rise over 30% or K⁺ ≥5.5 warrants stopping the ACE inhibitor.
Options:
  • Unsafe.
  • (correct)
  • Worsens it.
  • K⁺ already high.
  • Raises K⁺ further.
StatinsCoretap to open ▾
Inhibit HMG-CoA reductase. Atorvastatin 20 mg primary prevention (QRISK≥10%), 80 mg secondary prevention. Contraindicated in pregnancy. Interact with macrolides. Stop if CK ≥5–10× ULN or LFTs >3× ULN.
Doses: Primary prevention atorvastatin 20 mg (QRISK≥10%); secondary 80 mg.
Monitor: LFTs at baseline, 3 and 12 months; recheck lipids at 3 months (target >40% non-HDL fall).
Cautions: Pregnancy (contraindicated); clarithromycin/erythromycin interaction; myopathy.
For primary prevention in a patient with a QRISK3 of 14%, which statin regimen is correct?
  • AAtorvastatin 80 mg
  • BAtorvastatin 20 mg
  • CSimvastatin 10 mg
  • DNo statin
  • ERosuvastatin 40 mg
Correct: B — Atorvastatin 20 mg
Why: Primary prevention with QRISK ≥10% uses atorvastatin 20 mg; 80 mg is for secondary prevention.
Options:
  • That’s secondary.
  • (correct)
  • Under-dosed/low intensity.
  • Indicated here.
  • Not first-line.
AmiodaroneImportanttap to open ▾
Baseline: TFT, LFT, U&E, CXR. Monitor TFT+LFT every 6 months. Many effects: thyroid (hypo/hyper), pneumonitis, hepatotoxicity, slate-grey skin, photosensitivity, corneal deposits. Long half-life; many interactions.
Monitoring: Baseline TFT/LFT/U&E/CXR; then TFT + LFT 6-monthly.
Thyroid: Hypothyroid → continue amiodarone + levothyroxine. Hyperthyroid → stop + refer.
Other: Pneumonitis, grey skin, photosensitivity, corneal microdeposits.
A patient on amiodarone develops a raised TSH and low free T4. Management?
  • AStop amiodarone
  • BContinue amiodarone and add levothyroxine
  • CStart carbimazole
  • DThyroidectomy
  • EHalve the dose
Correct: B — Continue amiodarone and add levothyroxine
Why: Amiodarone-induced hypothyroidism: continue the drug and add levothyroxine. Hyperthyroidism requires stopping it.
Options:
  • That’s for hyperthyroid.
  • (correct)
  • Treats hyperthyroid.
  • Not indicated.
  • Not the answer.
Beta-blockersCoretap to open ▾
Angina, HF (bisoprolol/carvedilol/nebivolol), arrhythmia. Avoid in asthma, with verapamil/diltiazem, in sick sinus. Side effects: insomnia, cold peripheries, ED, reduced hypoglycaemia awareness.
Uses: Angina, heart failure (bisoprolol/carvedilol/nebivolol), arrhythmia, post-MI.
Avoid: Asthma, with verapamil/diltiazem, sick sinus syndrome.
Side effects: Insomnia/nightmares, cold peripheries, ED, reduced hypoglycaemia awareness.
Which combination should never be co-prescribed because of the risk of complete heart block?
  • ABisoprolol + amlodipine
  • BBisoprolol + verapamil
  • CBisoprolol + ramipril
  • DBisoprolol + atorvastatin
  • EBisoprolol + aspirin
Correct: B — Bisoprolol + verapamil
Why: A beta-blocker plus verapamil (or diltiazem) risks severe bradycardia and complete heart block.
Options:
  • Safe combination.
  • (correct)
  • Safe.
  • Safe.
  • Safe.
Calcium channel blockersCoretap to open ▾
Dihydropyridines (amlodipine): vasodilation, ankle oedema. Rate-limiting (verapamil/diltiazem): avoid with beta-blockers and in HF.
Dihydropyridines: Amlodipine/nifedipine — vasodilate; cause ankle oedema, flushing.
Rate-limiting: Verapamil/diltiazem — slow the heart; avoid with beta-blockers and in HFrEF.
Uses: Hypertension, angina, rate control.
A patient develops bilateral ankle swelling after starting amlodipine for hypertension, with normal renal/cardiac function. Cause?
  • AHeart failure
  • BDihydropyridine-induced peripheral oedema
  • CNephrotic syndrome
  • DDVT
  • ELymphoedema
Correct: B — Dihydropyridine-induced peripheral oedema
Why: Amlodipine commonly causes dose-related peripheral (ankle) oedema through precapillary vasodilation; it is not fluid overload.
Options:
  • Not HF here.
  • (correct)
  • No proteinuria.
  • Bilateral, not DVT.
  • Different.
NitratesImportanttap to open ▾
Angina/ACS/HF. Cause headache, flushing, hypotension, tachycardia. Use asymmetric dosing to avoid tolerance.
Uses: Angina (GTN for attacks), ACS, acute heart failure.
Side effects: Headache, flushing, hypotension, reflex tachycardia.
Tolerance: Use asymmetric dosing of standard-release ISMN to avoid tolerance.
Why is a nitrate-free interval advised with standard-release isosorbide mononitrate?
  • ATo reduce headache
  • BTo prevent nitrate tolerance
  • CTo improve absorption
  • DTo lower cost
  • ETo reduce flushing
Correct: B — To prevent nitrate tolerance
Why: An asymmetric dosing schedule provides a daily nitrate-free interval to prevent tolerance.
Options:
  • Not the main reason.
  • (correct)
  • Not the reason.
  • Irrelevant.
  • Not the reason.
NicorandilImportanttap to open ▾
K-channel activator for angina; causes anal/mucosal ulceration and headache.
Class: Potassium-channel activator with nitrate-like action; used in angina.
Key side effect: Anal, oral and GI ulceration (can mimic other pathology).
Also: Headache, flushing.
A patient on a drug for angina develops persistent painful anal ulceration. Which drug is responsible?
  • ABisoprolol
  • BNicorandil
  • CAmlodipine
  • DIsosorbide mononitrate
  • EAspirin
Correct: B — Nicorandil
Why: Nicorandil characteristically causes anal (and other mucosal) ulceration.
Options:
  • Not typical.
  • (correct)
  • Causes oedema.
  • Causes headache.
  • Causes GI bleeding, not ulcers here.
IvabradineRare · recognise
Reduces heart rate (funny channel); for angina and HFrEF (sinus HR>75, EF<35%). Side effects: luminous visual phenomena, headache, heart block.
Digoxin and digoxin toxicityImportanttap to open ▾
Rate control (esp. AF+HF); narrow therapeutic index. Toxicity worse with hypokalaemia: nausea, xanthopsia (yellow vision), arrhythmia; reverse with Digibind.
Use: Rate control in AF, especially with heart failure; narrow therapeutic index.
Toxicity: Nausea, xanthopsia (yellow vision), confusion, arrhythmia; worse with hypokalaemia.
Reverse: Digoxin-specific antibody fragments (Digibind).
A patient on digoxin and a thiazide presents with nausea and yellow-tinged vision. What most likely precipitated toxicity?
  • AHyperkalaemia
  • BHypokalaemia (from the thiazide)
  • CHypernatraemia
  • DHypercalcaemia
  • EHypoglycaemia
Correct: B — Hypokalaemia (from the thiazide)
Why: Hypokalaemia (e.g. from a thiazide) potentiates digoxin toxicity; xanthopsia is characteristic.
Options:
  • Hypokalaemia is the risk.
  • (correct)
  • Not the trigger.
  • Not the trigger.
  • Unrelated.
Loop diureticsCoretap to open ▾
Furosemide for HF congestion; cause hypokalaemia, hypocalcaemia, ototoxicity, gout.
Use: Furosemide for heart-failure congestion and fluid overload.
Electrolytes: Cause hypokalaemia, hyponatraemia, hypocalcaemia.
Other: Ototoxicity (high dose), gout, dehydration/AKI.
Which electrolyte disturbance is characteristic of furosemide?
  • AHyperkalaemia
  • BHypokalaemia
  • CHypercalcaemia
  • DHypernatraemia
  • EHyperphosphataemia
Correct: B — Hypokalaemia
Why: Loop diuretics cause potassium (and calcium) loss — hypokalaemia and hypocalcaemia.
Options:
  • Opposite.
  • (correct)
  • Thiazides raise calcium.
  • No.
  • No.
Thiazide and thiazide-like diureticsCoretap to open ▾
Indapamide/bendroflumethiazide for HTN; cause hypokalaemia, hyponatraemia, hypercalcaemia, hyperuricaemia (gout), impaired glucose, pancreatitis.
Use: Indapamide/bendroflumethiazide for hypertension.
Electrolytes: Hypokalaemia, hyponatraemia, hyperCALCaemia (contrast loops).
Metabolic: Hyperuricaemia (gout), impaired glucose tolerance, pancreatitis.
A patient on indapamide develops an acutely painful, swollen first toe. Which side effect explains this?
  • AHypokalaemia
  • BHyperuricaemia causing gout
  • CHypercalcaemia
  • DHyponatraemia
  • EPancreatitis
Correct: B — Hyperuricaemia causing gout
Why: Thiazides raise urate and can precipitate gout; they also cause hypokalaemia and hypercalcaemia.
Options:
  • Doesn’t cause gout.
  • (correct)
  • Not this presentation.
  • Different.
  • Different presentation.
Potassium-sparing diureticsImportanttap to open ▾
Spironolactone/eplerenone (MRA) in HF/resistant HTN; amiloride. Risk of hyperkalaemia; spironolactone → gynaecomastia.
MRA: Spironolactone/eplerenone — HF and resistant hypertension (step 4 if K⁺ ≤4.5).
Risk: Hyperkalaemia (especially with ACEi/ARB); monitor U&E.
Spironolactone: Can cause gynaecomastia (eplerenone less so).
A man on ramipril and spironolactone for heart failure develops tender breast enlargement and a potassium of 5.8. Best action?
  • AContinue both
  • BSwitch spironolactone to eplerenone and recheck potassium
  • CIncrease spironolactone
  • DAdd another ACE inhibitor
  • EIgnore
Correct: B — Switch spironolactone to eplerenone and recheck potassium
Why: Spironolactone causes gynaecomastia and hyperkalaemia; switching to eplerenone reduces gynaecomastia, and the high potassium needs addressing.
Options:
  • Unsafe/uncomfortable.
  • (correct)
  • Worsens both.
  • Raises K⁺ more.
  • Needs action.
AspirinCoretap to open ▾
Antiplatelet (irreversible COX). Secondary prevention; not routine for primary prevention. Avoid under 16 (Reye’s).
Action: Irreversible COX inhibitor → antiplatelet.
Use: Secondary prevention (post-MI/stroke); not routine for primary prevention.
Caution: Avoid under 16 (Reye’s syndrome); GI bleeding risk.
For which indication is aspirin routinely recommended?
  • APrimary prevention in everyone over 50
  • BSecondary prevention after myocardial infarction
  • CAll hypertensives
  • DAll diabetics
  • EIsolated high cholesterol
Correct: B — Secondary prevention after myocardial infarction
Why: Aspirin is standard for secondary prevention after MI/stroke; it is not recommended for routine primary prevention.
Options:
  • Not routine primary prevention.
  • (correct)
  • No.
  • No.
  • No.
ClopidogrelCoretap to open ▾
P2Y12 inhibitor; reduced efficacy with omeprazole/esomeprazole — use lansoprazole.
Class: P2Y12 inhibitor; first-line long-term antiplatelet after ischaemic stroke and in PAD.
Interaction: Omeprazole/esomeprazole reduce its activation — use lansoprazole.
ACS: Used in DAPT when ticagrelor/prasugrel unsuitable.
A patient on clopidogrel needs a PPI for dyspepsia. Which PPI is preferred?
  • AOmeprazole
  • BLansoprazole
  • CEsomeprazole
  • DAny PPI is equal
  • EAvoid all PPIs
Correct: B — Lansoprazole
Why: Omeprazole and esomeprazole inhibit clopidogrel activation; lansoprazole is preferred.
Options:
  • Reduces efficacy.
  • (correct)
  • Reduces efficacy.
  • Not equal.
  • PPI can be used.
Ticagrelor / PrasugrelImportanttap to open ▾
Potent P2Y12 inhibitors for ACS DAPT (12 months). Prasugrel favoured if PCI; avoid prasugrel after stroke/TIA.
Use: Potent P2Y12 inhibitors for ACS dual antiplatelet therapy (12 months).
Prasugrel: Favoured when PCI planned; avoid after stroke/TIA (bleeding).
Ticagrelor: Causes dyspnoea in some; twice-daily dosing.
Which potent antiplatelet is generally avoided in a patient with a prior stroke undergoing ACS management?
  • ATicagrelor
  • BPrasugrel
  • CClopidogrel
  • DAspirin
  • EDipyridamole
Correct: B — Prasugrel
Why: Prasugrel is contraindicated after stroke/TIA due to bleeding risk; ticagrelor or clopidogrel are alternatives.
Options:
  • Not specifically contraindicated.
  • (correct)
  • Safe.
  • Standard.
  • Not relevant.
WarfarinCoretap to open ▾
Vitamin-K antagonist (factors 2,7,9,10 + protein C/S). Reverse with vitamin K ± PCC. Target INR 2.5 (mechanical valves higher).
Action: Vitamin-K antagonist — inhibits factors II, VII, IX, X (and protein C/S).
Monitoring: INR; target 2.5 (mechanical valves higher).
Reverse: Vitamin K ± prothrombin complex concentrate for major bleeding.
What is the usual target INR for a patient on warfarin for atrial fibrillation?
  • A1.5
  • B2.5
  • C3.5
  • D4.5
  • ENo target
Correct: B — 2.5
Why: The standard target INR for AF is 2.5 (range 2–3); mechanical valves require higher targets.
Options:
  • Too low.
  • (correct)
  • That’s for mechanical valves.
  • Too high.
  • There is a target.
Warfarin: interactions & high INRCoretap to open ▾
Enzyme inhibitors (fluconazole, macrolides, cranberry/grapefruit) raise INR; inducers lower it. INR>8 no bleed → stop + oral vitamin K 1–5 mg; INR 5–8 → withhold 1–2 doses.
Raise INR: Enzyme inhibitors — fluconazole, macrolides, cranberry/grapefruit juice.
Lower INR: Enzyme inducers — rifampicin, carbamazepine, phenytoin, St John’s wort.
High INR: INR>8 no bleed → stop + oral vitamin K 1–5 mg; INR 5–8 → withhold 1–2 doses.
A patient on warfarin has an INR of 9 with no bleeding. What is the correct management?
  • AContinue unchanged
  • BStop warfarin and give oral vitamin K 1–5 mg
  • CGive IV vitamin K + PCC
  • DWithhold one dose only
  • EGive fresh frozen plasma
Correct: B — Stop warfarin and give oral vitamin K 1–5 mg
Why: INR above 8 without bleeding: stop warfarin and give oral vitamin K 1–5 mg, rechecking INR. IV vitamin K + PCC is for major bleeding.
Options:
  • Unsafe.
  • (correct)
  • That’s for major bleeding.
  • Insufficient at INR 9.
  • For active major bleed.
DabigatranImportanttap to open ▾
Direct thrombin inhibitor; reversed by idarucizumab. Contraindicated in mechanical valves.
Class: Direct thrombin (factor IIa) inhibitor DOAC.
Reverse: Idarucizumab.
Caution: Contraindicated in mechanical heart valves; dose-reduce in renal impairment.
Which agent specifically reverses dabigatran?
  • AAndexanet alfa
  • BIdarucizumab
  • CVitamin K
  • DProtamine
  • ETranexamic acid
Correct: B — Idarucizumab
Why: Idarucizumab reverses dabigatran; andexanet alfa reverses factor Xa inhibitors (apixaban/rivaroxaban).
Options:
  • Reverses Xa inhibitors.
  • (correct)
  • Reverses warfarin.
  • Reverses heparin.
  • Adjunct only.
HeparinRare · recognise
Unfractionated (APTT-monitored, reversible with protamine) vs LMWH (anti-Xa). Risk of HIT.
AdrenalineImportanttap to open ▾
Cardiac arrest 1 mg IV (after 3rd shock if shockable; ASAP if non-shockable), anaphylaxis 500 mcg IM.
Cardiac arrest: 1 mg IV — after the 3rd shock if shockable; as soon as possible if non-shockable, then every 3–5 min.
Anaphylaxis: 500 micrograms IM (1:1000) into the anterolateral thigh.
Action: Alpha and beta agonist.
In an adult with anaphylaxis, what is the correct adrenaline dose and route?
  • A1 mg IV of 1:10,000
  • B500 micrograms IM of 1:1000
  • COral
  • D300 micrograms IM
  • E1 mg IM
Correct: B — 500 micrograms IM of 1:1000
Why: Anaphylaxis is treated with IM adrenaline 500 micrograms of 1:1000; IV 1:10,000 is for cardiac arrest.
Options:
  • That’s arrest dosing.
  • (correct)
  • Not a route.
  • Paediatric-ish underdose.
  • Wrong strength/dose.
B-type natriuretic peptideImportanttap to open ▾
Raised by ventricular stretch/HF; also LVH, ischaemia, PE, sepsis, age, low GFR. Lowered by obesity, ACEi/BB/ARB/MRA/diuretics.
Released: By ventricular stretch — a marker in heart failure.
Raised by: LVH, ischaemia, tachycardia, hypoxaemia/PE, GFR<60, sepsis, age>70, cirrhosis.
Lowered by: Obesity, ACEi/ARB/beta-blocker/MRA/diuretics.
Which factor lowers BNP and may cause a falsely reassuring level in heart failure?
  • AAge over 70
  • BObesity
  • CRenal impairment
  • DSepsis
  • ELeft ventricular hypertrophy
Correct: B — Obesity
Why: Obesity lowers BNP (as do ACEi/ARB/BB/MRA/diuretics), risking a falsely low result; the others raise it.
Options:
  • Raises BNP.
  • (correct)
  • Raises BNP.
  • Raises BNP.
  • Raises BNP.
Angiotensin II receptor blockersCoretap to open ▾
Use where ACE inhibitors not tolerated (e.g. cough); similar cautions (hyperkalaemia, renal).
Use: Where ACE inhibitors aren’t tolerated (e.g. cough).
Cautions: Hyperkalaemia, renal impairment, pregnancy (contraindicated).
Note: Don’t combine ACEi + ARB routinely.
A patient needs an ACE inhibitor but develops an intolerable dry cough. Best alternative?
  • AA beta-blocker
  • BAn angiotensin-receptor blocker
  • CA thiazide
  • DA calcium-channel blocker
  • EStop all treatment
Correct: B — An angiotensin-receptor blocker
Why: An ARB provides similar benefits without the bradykinin-mediated cough of ACE inhibitors.
Options:
  • Different class/indication.
  • (correct)
  • Different mechanism.
  • Different mechanism.
  • Treatment still needed.
Nicotinic acidRare · recognise
Lipid-lowering; causes flushing and pruritus, impaired glucose tolerance, myopathy.

ECG & Signs

ECG: coronary territoriesCoretap to open ▾
Inferior II/III/aVF (right coronary); anteroseptal V1–4 (LAD); lateral I/aVL/V5–6 (circumflex). Match ST changes to territory.
Inferior: Leads II, III, aVF → right coronary artery.
Anteroseptal: V1–V4 → left anterior descending.
Lateral: I, aVL, V5–V6 → left circumflex.
An ECG shows ST elevation in II, III and aVF. Which artery is occluded?
  • ALeft anterior descending
  • BRight coronary artery
  • CLeft circumflex
  • DLeft main stem
  • EPulmonary artery
Correct: B — Right coronary artery
Why: Inferior leads II, III and aVF correspond to the right coronary artery territory.
Options:
  • Anteroseptal.
  • (correct)
  • Lateral.
  • Widespread.
  • Not coronary.
ECG: ST elevationCoretap to open ▾
Causes: STEMI (regional), pericarditis (widespread saddle + PR depression), LV aneurysm (persistent), early repolarisation, LBBB.
STEMI: Regional ST elevation matching a coronary territory → emergency reperfusion.
Pericarditis: Widespread saddle ST elevation + PR depression.
Other: Persistent ST elevation = LV aneurysm; also early repolarisation, LBBB.
Regional ST elevation in leads V1–V4 in a patient with chest pain indicates infarction in which territory?
  • AInferior
  • BAnteroseptal (LAD)
  • CLateral
  • DPosterior
  • ERight ventricle
Correct: B — Anteroseptal (LAD)
Why: V1–V4 ST elevation is anteroseptal, supplied by the left anterior descending artery.
Options:
  • Inferior is II/III/aVF.
  • (correct)
  • Lateral is I/aVL/V5–6.
  • Posterior is V7–9.
  • RV leads differ.
ECG: ST depressionImportanttap to open ▾
Ischaemia, digoxin ('reverse tick'), hypokalaemia, posterior MI (V1–3).
Ischaemia: Horizontal/down-sloping ST depression.
Digoxin: ‘Reverse-tick’ ST depression (effect, not toxicity).
Other: Hypokalaemia; posterior MI shows ST depression V1–3.
A patient on digoxin has down-sloping ‘reverse-tick’ ST depression and is asymptomatic with a normal level. What does this represent?
  • ADigoxin toxicity
  • BDigoxin effect (not toxicity)
  • CIschaemia
  • DHypokalaemia
  • ENormal variant
Correct: B — Digoxin effect (not toxicity)
Why: The ‘reverse-tick’ ST depression is the expected digoxin effect and does not by itself indicate toxicity.
Options:
  • Effect ≠ toxicity.
  • (correct)
  • Not necessarily ischaemia.
  • Different pattern.
  • It is drug-related.
ECG: T wave changesImportanttap to open ▾
Peaked (hyperkalaemia, hyperacute MI); inverted (ischaemia, PE with S1Q3T3, digoxin).
Peaked: Hyperkalaemia; hyperacute MI.
Inverted: Ischaemia; PE (with S1Q3T3); digoxin.
Flattened/U waves: Hypokalaemia.
Tall, tented T waves on the ECG should prompt urgent assessment for which abnormality?
  • AHypokalaemia
  • BHyperkalaemia
  • CHypocalcaemia
  • DHypernatraemia
  • EDigoxin toxicity
Correct: B — Hyperkalaemia
Why: Peaked (tented) T waves are the early ECG sign of hyperkalaemia — check potassium and treat urgently.
Options:
  • Gives flat T/U waves.
  • (correct)
  • Prolongs QT.
  • No typical change.
  • Reverse-tick pattern.
ECG: hypokalaemiaImportanttap to open ▾
Small/inverted T waves, prominent U waves, long QT, ST depression.
Signs: Small/flattened or inverted T waves, prominent U waves.
Also: ST depression, long QT (torsades risk).
Mnemonic: ‘No Pot, No T, but a U’.
Which set of ECG changes is characteristic of hypokalaemia?
  • ATall tented T waves
  • BFlattened T waves with prominent U waves
  • CWidespread saddle ST elevation
  • DDelta waves
  • ESawtooth waves
Correct: B — Flattened T waves with prominent U waves
Why: Hypokalaemia flattens T waves and produces prominent U waves, with ST depression and QT prolongation.
Options:
  • That’s hyperkalaemia.
  • (correct)
  • Pericarditis.
  • WPW.
  • Flutter.
ECG: left/right bundle branch blockImportanttap to open ▾
LBBB (WiLLiaM) — never normal, think ischaemia/aortic disease. RBBB (MaRRoW) — can be normal or PE/ASD.
LBBB: ‘WiLLiaM’ — never assume normal; think ischaemia/aortic disease. New LBBB + chest pain = treat as STEMI.
RBBB: ‘MaRRoW’ — can be normal or PE/ASD/cor pulmonale.
Key: New LBBB with chest pain is an ACS until proven otherwise.
A patient with chest pain has a new left bundle branch block. How should this be managed?
  • AReassure — LBBB is benign
  • BTreat as an acute STEMI-equivalent
  • CDischarge with outpatient echo
  • DGive a beta-blocker only
  • ERepeat ECG in a week
Correct: B — Treat as an acute STEMI-equivalent
Why: New LBBB with chest pain is treated as a STEMI-equivalent — urgent reperfusion pathway.
Options:
  • Not benign here.
  • (correct)
  • Unsafe.
  • Insufficient.
  • Unsafe delay.
ECG: axis deviationRare · recognise
Left axis (lead I +, II −); right axis (I −, II +). RAD in PE/RVH; LAD in LAFB.
ECG: P wave changesRare · recognise
Bifid P (P mitrale, mitral stenosis); peaked P (P pulmonale, cor pulmonale).
ECG: normal variantsImportanttap to open ▾
Sinus bradycardia, junctional rhythm, first-degree block, Wenckebach, T inversion in III/aVR/V1 — often benign in athletes.
Often benign: Sinus bradycardia, junctional rhythm, first-degree block, Wenckebach.
Athletes: Sinus bradycardia, LVH by voltage, some T changes.
Caution: Distinguish from pathology by symptoms/context.
Which ECG finding is most likely a benign normal variant in a fit young athlete?
  • ASinus bradycardia
  • BNew left bundle branch block
  • CDelta wave
  • DComplete heart block
  • EWidespread ST elevation with pain
Correct: A — Sinus bradycardia
Why: Sinus bradycardia is a common benign finding in athletes; the others suggest pathology.
Options:
  • (correct)
  • Pathological.
  • WPW.
  • Needs pacing.
  • Suggests pericarditis/STEMI.
ECG: hypothermiaRare · recognise
Bradycardia, J (Osborn) waves, prolonged intervals, arrhythmia.
Hyperlipidaemia: xanthomataImportanttap to open ▾
Tendon xanthomata & xanthelasma (familial hypercholesterolaemia); eruptive (hypertriglyceridaemia); corneal arcus (age/lipids).
Tendon xanthomata / xanthelasma: Familial hypercholesterolaemia.
Eruptive xanthomata: Hypertriglyceridaemia.
Corneal arcus: Common with age; significant if young.
A 35-year-old has tendon xanthomata and a very high LDL. Which diagnosis should be considered?
  • AHypertriglyceridaemia
  • BFamilial hypercholesterolaemia
  • CNormal ageing
  • DHypothyroidism only
  • EDiabetes
Correct: B — Familial hypercholesterolaemia
Why: Tendon xanthomata with markedly raised LDL at a young age suggest familial hypercholesterolaemia — refer to a lipid clinic and cascade-test relatives.
Options:
  • Gives eruptive xanthomata.
  • (correct)
  • Not at 35 with xanthomata.
  • Secondary cause, less specific.
  • Not specific.