UKMLA Cardiology Masterclass: ACS, Arrhythmias & HTN

Cardiology is the single largest clinical chapter on the UKMLA AKT. Between acute coronary syndromes, arrhythmias, heart failure, hypertension, and the cluster of valvular and pericardial conditions, cardiology accounts for roughly 20–25% of the clinical stems on a typical paper. That weighting is not accidental — cardiology maps directly to four of the GMC content map's top presentations (chest pain, breathlessness, palpitations, syncope) and governs most of the prescribing stems the AKT throws at you.

Candidates usually don't lose cardiology marks because the physiology is hard. They lose them because they mix up the three types of ACS on a borderline troponin, because they forget the CHA₂DS₂-VASc scoring rules when an AF patient also has T2DM, because they hit the wrong step on the NICE hypertension ladder for a 56-year-old of Caribbean origin with T2DM, or because they can't reliably read a STEMI territory from a 12-lead. All of these are fixable mistakes — but only if you drill them against the specific formats the UKMLA uses.

This masterclass walks through the twelve cardiology sub-topics the UKMLA tests most aggressively, with exam-focused decision logic, the common distractor patterns, and the NICE-aligned answers UK F1s are expected to know. We'll cover ACS classification and management, AF rate-vs-rhythm and anticoagulation, the hypertension stepwise ladder, heart failure quadruple therapy, valvular disease essentials, pericarditis and myocarditis, the wide-complex vs narrow-complex tachyarrhythmia decision, bradyarrhythmia, and the ECG patterns you must recognise at speed. Each section closes with the specific AKT question patterns you'll see.

Table of contents

1. Why cardiology dominates the AKT
2. Acute coronary syndromes (STEMI, NSTEMI, UA)
3. Atrial fibrillation
4. Hypertension
5. Heart failure
6. Valvular disease
7. Pericarditis and myocarditis
8. Tachyarrhythmias — VT, SVT, torsades
9. Bradyarrhythmias and heart block
10. ECG patterns to recognise
11. Common AKT question patterns
12. Flashcard and drilling strategy
13. FAQ

1. Why cardiology dominates the AKT

Four of the 212 presentations in the GMC content map live squarely in cardiology: chest pain, palpitations, syncope, and (partially) breathlessness. Between them they account for roughly 50 stems across a 200-question AKT paper — once you include the prescribing sub-stems on antiplatelets, anticoagulation, antihypertensives, and heart-failure drugs.

Cardiology also rewards pattern recognition more than any other clinical area. An ECG with tombstoning ST elevation across V1–V4 is anterior STEMI, irrespective of the stem's backstory. A murmur radiating to the carotids in an elderly patient with syncope and chest pain is aortic stenosis. A patient with an irregularly irregular pulse and a CHA₂DS₂-VASc of 3 needs a DOAC. These patterns are drillable in a way that subtler areas (vague abdominal pain, undifferentiated fatigue) aren't.

Your goal for cardiology is a 75%+ subscore in Q-bank practice, because every mark you add in cardiology outperforms almost any other specialty on a marks-per-hour-studied basis. The twelve sections below each map to 3–5 AKT stems in a typical paper.

2. Acute coronary syndromes (STEMI, NSTEMI, UA)

Classification. ACS is a spectrum based on troponin and ECG:

• STEMI — ST elevation ≥1 mm in two contiguous limb leads or ≥2 mm in two contiguous chest leads (or new LBBB with convincing symptoms). Troponin usually rises but diagnosis is ECG-first.
• NSTEMI — troponin rises without ST elevation. May show ST depression, T-wave inversion, or a normal ECG.
• Unstable angina — typical ischaemic symptoms without troponin rise.

Immediate management (MONA-B, modernised):

• Aspirin 300 mg stat (chewed for faster absorption).
• Second antiplatelet — ticagrelor 180 mg or prasugrel if proceeding to PCI; clopidogrel 300 mg if thrombolysis pathway.
• Morphine + antiemetic for analgesia if needed.
• Oxygen only if SpO₂ <94% — routine oxygen is no longer recommended and is often a distractor in AKT stems.
• Nitrates for ongoing pain unless hypotensive, RV infarct, or PDE-5 inhibitor use.

STEMI pathway. Primary PCI within 120 minutes of first medical contact is first-line. Thrombolysis (alteplase, tenecteplase) if PCI not available within that window. Pre-discharge: dual antiplatelet therapy (DAPT) for 12 months, ACE inhibitor, beta-blocker, high-intensity statin (atorvastatin 80 mg).

NSTEMI pathway. GRACE score stratifies risk. High-risk patients (GRACE >140 or recurrent ischaemia) get angiography within 24–72 hours. Fondaparinux or LMWH for anticoagulation. Same secondary prevention package as STEMI.

Post-MI secondary prevention (the "five drugs" answer):

1. Aspirin 75 mg OD indefinitely
2. Second antiplatelet (ticagrelor or clopidogrel) for 12 months
3. Beta-blocker (bisoprolol first-line)
4. ACE inhibitor (ramipril)
5. High-intensity statin (atorvastatin 80 mg)

AKT question pattern. Post-MI patient presents for GP follow-up; stem asks which additional medication should have been started. Answer is usually whichever of the five drugs is missing from the medication list given.

3. Atrial fibrillation

Rate vs rhythm. UK practice (NG196) defaults to rate control for most patients. Rhythm control is offered for: new-onset AF <48 hours, AF with reversible cause, AF causing heart failure, symptomatic AF despite rate control, or where rhythm control is patient-preferred and clinically appropriate.

Rate control agents (in order of preference):

• First-line: beta-blocker (bisoprolol) or rate-limiting calcium channel blocker (diltiazem, verapamil). Choose beta-blocker if heart failure; avoid CCBs in HFrEF.
• Second-line: add digoxin (particularly useful in sedentary elderly patients).
• Third-line: amiodarone (specialist initiation).

Rhythm control: electrical or pharmacological cardioversion. Flecainide (if structurally normal heart) or amiodarone (if structural heart disease). Catheter ablation is increasingly mainstream for paroxysmal AF.

Anticoagulation — CHA₂DS₂-VASc:

• Congestive heart failure — 1
• Hypertension — 1
• Age ≥75 — 2
• Diabetes — 1
• Stroke/TIA history — 2
• Vascular disease — 1
• Age 65–74 — 1
• Sex category (female) — 1

Anticoagulate if score ≥2 in men or ≥3 in women. Consider in men with score 1. DOAC first-line (apixaban 5 mg BD is the typical AKT answer; dose-reduce if 2 of: age ≥80, weight ≤60 kg, creatinine ≥133). Warfarin only for mechanical valves or severe renal impairment.

HAS-BLED assesses bleeding risk but does not override the decision to anticoagulate — it identifies modifiable bleeding risk factors.

AKT question pattern. A 72-year-old woman with AF, hypertension, and T2DM — calculate CHA₂DS₂-VASc. Answer: 5 (age 65–74 = 1 + female = 1 + HTN = 1 + T2DM = 1 + add vascular disease if present). Distractor options usually under-count the female category or miss the age bracket.

4. Hypertension

The hypertension ladder is the single most-tested pathway on the AKT. Memorise it verbatim. See the NICE guidelines post for the full framework — the core summary here:

Step 1:

• ACEi/ARB if age <55 and not Black African/Caribbean origin
• CCB if age ≥55 or Black African/Caribbean origin
• ACEi/ARB regardless of age/ethnicity if T2DM

Step 2: add the other (ACEi + CCB combination).

Step 3: add thiazide-like diuretic (indapamide).

Step 4 (resistant): add spironolactone if K ≤4.5; alpha- or beta-blocker if K >4.5.

Key cautions:

• ACEi contraindicated in bilateral renal artery stenosis, pregnancy, angioedema history.
• CCB (amlodipine) — ankle swelling common; gingival hyperplasia a distractor.
• Thiazides — hyperuricaemia (precipitates gout), hyponatraemia, hypokalaemia.
• Spironolactone — hyperkalaemia, gynaecomastia.

BP targets:

• Clinic BP target <140/90 under 80 years old.
• Clinic BP target <150/90 over 80 years old.
• Clinic BP target <130/80 in T2DM with albuminuria or CKD with significant proteinuria.

AKT question pattern. 58-year-old of Black Caribbean origin with new HTN. Step 1? Answer: CCB (amlodipine). Distractor: ramipril. 58-year-old of Black Caribbean origin with new HTN and T2DM? Answer: ramipril (diabetes override).

5. Heart failure

Classification:

• HFrEF — LVEF <40%. Treated aggressively with four-drug therapy.
• HFpEF — LVEF ≥50% with evidence of diastolic dysfunction. Management focuses on symptoms and comorbidities.
• HFmrEF — LVEF 40–49%. Treated increasingly like HFrEF.

HFrEF quadruple therapy (NG106 + 2021 ESC update, reflected in NICE):

1. ACE inhibitor or ARB (ramipril, candesartan). Sacubitril-valsartan (ARNI) replaces ACEi in those still symptomatic on optimal therapy.
2. Beta-blocker — bisoprolol, carvedilol, or nebivolol (only three licensed for HF).
3. Mineralocorticoid receptor antagonist (MRA) — spironolactone or eplerenone.
4. SGLT2 inhibitor — dapagliflozin or empagliflozin (now standard-of-care in HFrEF regardless of diabetes status).

Additional: loop diuretic (furosemide) for symptomatic fluid overload — does not improve mortality but manages symptoms.

Acute pulmonary oedema management:

• Sit up
• 15L non-rebreather O₂
• IV furosemide 40–80 mg
• GTN infusion if systolic BP adequate
• CPAP if respiratory distress
• Morphine — historically used but evidence now weak; not routinely recommended

AKT question pattern. Stable HFrEF patient on ramipril and bisoprolol, still symptomatic. Next step? Answer: add spironolactone (or SGLT2 inhibitor in modern NICE).

6. Valvular disease

Four valvular lesions cover 95% of AKT valve stems.

Aortic stenosis. Ejection systolic murmur, radiates to carotids, slow-rising pulse, narrow pulse pressure. Triad of syncope, angina, and dyspnoea indicates severe AS. Management: TAVI (increasingly) or surgical AVR. Echocardiography is the diagnostic investigation.

Aortic regurgitation. Early diastolic murmur, best heard leaning forward in expiration. Wide pulse pressure, collapsing (water-hammer) pulse, Corrigan's sign. Causes: rheumatic, infective endocarditis, aortic root dilatation (Marfan's, aortic dissection).

Mitral regurgitation. Pansystolic murmur, radiates to axilla. Causes: MV prolapse, ischaemic, post-MI papillary muscle rupture (acute, severe MR with haemodynamic collapse).

Mitral stenosis. Mid-diastolic rumbling murmur, loud S1, opening snap. Almost always rheumatic origin. AF is a common complication. Management: percutaneous balloon valvotomy or surgical repair.

Infective endocarditis. Duke criteria. Empirical antibiotic for native valve: amoxicillin + gentamicin (UK). Prosthetic valve: vancomycin + gentamicin + rifampicin. Blood cultures ×3 before antibiotics.

AKT question pattern. Elderly patient with syncope, ejection systolic murmur radiating to carotids. Diagnosis? Aortic stenosis. Next investigation? Echocardiogram.

7. Pericarditis and myocarditis

Acute pericarditis. Sharp, pleuritic chest pain, relieved by sitting forward. Pericardial friction rub. ECG: widespread saddle-shaped ST elevation, PR depression. Causes: viral (most common), post-MI (Dressler's), uraemic, malignant, TB, autoimmune.

Management: NSAIDs (ibuprofen 600 mg TDS) + colchicine for 3 months. Steroids only for recurrent or autoimmune pericarditis.

Pericardial effusion and tamponade. Beck's triad: hypotension, muffled heart sounds, raised JVP. Pulsus paradoxus. Echo shows effusion with RV diastolic collapse. Management: urgent pericardiocentesis.

Myocarditis. Usually viral (Coxsackie B, adenovirus, post-COVID). Presents with chest pain, breathlessness, arrhythmias, raised troponin, ECG changes mimicking MI. Cardiac MRI is diagnostic. Supportive treatment; avoid exercise for 6 months.

AKT question pattern. Young patient with pleuritic chest pain relieved sitting forward, saddle-shaped ST elevation. Diagnosis and management? Pericarditis, NSAIDs + colchicine.

8. Tachyarrhythmias — VT, SVT, torsades

Narrow-complex tachycardia (QRS <120 ms):

• Sinus tachycardia — rate usually 100–160, clear P waves. Treat the cause.
• Atrial fibrillation — irregularly irregular, no P waves. Covered above.
• Atrial flutter — sawtooth flutter waves, often 2:1 or 4:1 block. Rate control + anticoagulation as per AF. Cardioversion or ablation.
• SVT (AVNRT/AVRT) — regular, rate 150–220, no visible P waves. Vagal manoeuvres → adenosine 6 mg then 12 mg → synchronised DC cardioversion if unstable.

Wide-complex tachycardia (QRS ≥120 ms):

• Ventricular tachycardia — regular, broad complexes. Unstable: synchronised DC cardioversion. Stable: amiodarone 300 mg IV.
• VT with pulse loss → pulseless VT — defibrillate (unsynchronised). Part of the ALS cardiac arrest algorithm.
• Torsades de pointes — polymorphic VT with long QT. IV magnesium sulphate 2 g. Stop the offending QT-prolonging drug (macrolides, quinolones, antipsychotics, amiodarone itself).

Any tachyarrhythmia with haemodynamic instability (syncope, hypotension, chest pain, heart failure) → synchronised DC cardioversion. This is the universal answer for the "unstable" stem.

AKT question pattern. Regular narrow-complex tachycardia at 180 bpm in a stable patient. Next step? Vagal manoeuvres. If those fail? Adenosine 6 mg.

9. Bradyarrhythmias and heart block

Sinus bradycardia. Often physiological (athletes, beta-blocker use). Treat if symptomatic.

First-degree AV block. PR interval >200 ms. Usually no treatment needed.

Second-degree type I (Wenckebach/Mobitz I). Progressive PR lengthening → dropped beat. Benign. Usually no treatment.

Second-degree type II (Mobitz II). Constant PR → intermittently dropped beats. High risk of progression to complete heart block. Pacemaker indicated.

Third-degree (complete) heart block. Complete AV dissociation — P waves and QRS independent. Junctional or ventricular escape rhythm. Pacemaker urgently; temporary transvenous if symptomatic before permanent.

Acute bradycardia with haemodynamic compromise: atropine 500 mcg IV, up to 3 mg total. Second-line: isoprenaline or transcutaneous pacing.

Sick sinus syndrome. Tachy-brady syndrome in elderly. Symptomatic bradycardia → pacemaker. Often co-exists with AF; anticoagulation still required.

AKT question pattern. ECG shows dissociated P waves and QRS complexes, patient symptomatic. Management? Urgent pacemaker; temporary pacing as bridge.

10. ECG patterns to recognise

Pattern recognition on the 12-lead is genuinely testable at exam speed. The AKT will typically include 3–6 ECG-based stems. Know these cold:

STEMI territories:

• V1–V4: anterior (LAD)
• II, III, aVF: inferior (RCA in 80%, LCx in 20%)
• V5–V6, I, aVL: lateral (LCx or diagonal)
• Reciprocal ST depression in opposite leads is confirmatory
• Posterior MI — ST depression in V1–V3 with tall R waves. Obtain posterior leads (V7–V9) for confirmation.

Hyperkalaemia progression:

1. Tall tented T waves
2. Prolonged PR
3. Loss of P waves
4. Widened QRS
5. Sine wave
6. Asystole

Treatment urgency: K >6.5 or any ECG changes → calcium gluconate 10 mL 10% IV (cardioprotective), insulin-dextrose (shift), nebulised salbutamol (shift), calcium resonium or dialysis (removal).

Hypokalaemia: flattened T waves, U waves, ST depression, prolonged QT.

Long QT (corrected QTc >450 ms men, >470 ms women). Causes: congenital LQTS, drugs (macrolides, antipsychotics, quinolones, amiodarone, ondansetron), electrolytes (low K, low Mg, low Ca), hypothermia. Risk: torsades de pointes.

Left bundle branch block (LBBB). W pattern in V1, M pattern in V6 ("WiLLiaM"). New LBBB with chest pain is a STEMI-equivalent.

Right bundle branch block (RBBB). M pattern in V1, W pattern in V6 ("MaRRoW"). Often benign; pathological if new or with symptoms.

Atrial fibrillation. No P waves, irregularly irregular R-R intervals.

WPW syndrome. Short PR, delta wave (slurred upstroke of QRS). Risk: AF with rapid ventricular response via accessory pathway → SVT.

Brugada syndrome. Coved ST elevation in V1–V2, RBBB pattern. Risk: sudden cardiac death. Implantable defibrillator.

The emergency presentations post expands on the acute decisions triggered by these ECG findings.

11. Common AKT question patterns

Six recurring cardiology stem templates appear on almost every AKT paper. Recognising the template tells you what's being tested.

Template 1 — Acute chest pain triage. Middle-aged patient with chest pain; stem gives ECG findings, troponin, and risk factors. Task: classify (STEMI / NSTEMI / UA / non-cardiac) and pick next step (PCI / angiography within 72h / discharge with safety net). Mistake: picking the maximally invasive option without reading the troponin.

Template 2 — Anticoagulation decision. AF patient with listed comorbidities. Calculate CHA₂DS₂-VASc, decide on anticoagulation, pick the agent. Mistake: forgetting the +1 for female sex (and the +1 for age 65–74 separately from +2 for ≥75).

Template 3 — Hypertension escalation. Patient with HTN on one or two agents, BP still above target. Pick next step on the NICE ladder. Mistake: picking the wrong step 1 based on forgotten ethnicity/age/diabetes overrides.

Template 4 — Heart failure escalation. Patient already on ramipril and bisoprolol; stem asks for next step. Mistake: picking furosemide (symptomatic only) instead of spironolactone or SGLT2 inhibitor (mortality benefit).

Template 5 — Arrhythmia recognition and management. ECG shown or described; pick the rhythm and the first action. Mistake: picking amiodarone in an unstable VT (DC cardioversion is correct) or adenosine in AF (useless).

Template 6 — Post-MI secondary prevention. Post-discharge MI patient; medication list missing one of the five core drugs. Pick the missing one. Mistake: overlooking the statin or the second antiplatelet.

Every cardiology session you do should end by asking: "which template was this?" That meta-tagging accelerates pattern recognition on exam day.

Halfway checkpoint — MLA Prep tags every cardiology question by template (acute chest pain triage, anticoagulation, HTN escalation, HF escalation, arrhythmia, post-MI) and lets you filter by the template you score worst on. Start your free diagnostic and see your per-template breakdown in 20 minutes.

12. Flashcard and drilling strategy

Cardiology rewards spaced-repetition practice more than almost any other specialty because the decision logic is finite and rule-based. Build flashcards for:

• The five post-MI secondary-prevention drugs.
• The CHA₂DS₂-VASc variables and scoring thresholds.
• Each step of the NICE hypertension ladder, with the age/ethnicity/diabetes overrides.
• The four-drug HFrEF package and the order of escalation.
• The four valve lesions — one card per lesion covering murmur, radiation, causes, management.
• Each wide-complex/narrow-complex tachyarrhythmia and first-line action.
• The six bradyarrhythmia rhythms and the pacemaker indication for each.
• The STEMI territories to coronary artery.
• The hyperkalaemia ECG progression.
• The drugs that prolong QT.

Combine the flashcards with daily Q-bank practice filtered to cardiology. Across four weeks, aim for 400–500 cardiology questions with thorough explanation review per the 20-minute protocol. This alone typically lifts cardiology subscores from mid-50s to high-70s.

The active recall and spaced repetition guide explains how to layer these flashcards into your daily review schedule. The 12-week study plan slots cardiology into weeks 2–3 for most candidates.

13. FAQ

How many AKT marks come from cardiology? Approximately 35–50 questions on a 200-question paper touch cardiology content, including prescribing, ECG interpretation, and management stems.

Do I need to interpret raw ECG images? Yes. The AKT shows ECG images on screen and asks for rhythm identification, STEMI territory, or common patterns (hyperkalaemia, LBBB, WPW). Practice with printed or digital 12-leads regularly.

Is BNP useful for heart failure diagnosis? Yes. NT-proBNP <400 ng/L excludes HF; >2000 is diagnostic and triggers specialist referral within 2 weeks. The 400–2000 range triggers echo and routine specialist input within 6 weeks.

Are statins first-line for all post-MI patients? Atorvastatin 80 mg OD is standard unless contraindicated. High-intensity, not moderate. This is a common distractor — simvastatin 40 mg is a lower-intensity alternative and is typically the wrong answer on AKT stems.

What's the role of SGLT2 inhibitors in HFrEF? Dapagliflozin and empagliflozin are now standard-of-care in HFrEF regardless of diabetes status. If a heart-failure stem omits an SGLT2 inhibitor from the medication list, that's often the answer.

How does the AKT test coronary anatomy? Usually via STEMI territory localisation — ST elevation in II, III, aVF maps to RCA inferior territory, and so on. Detailed angiographic knowledge isn't required.

What about pregnancy-related cardiology (peripartum cardiomyopathy, pre-eclampsia HTN)? Covered briefly — peripartum cardiomyopathy presents in late pregnancy or early postpartum, managed like HFrEF but with ACE inhibitor contraindicated during pregnancy. Pre-eclampsia HTN treated with labetalol or nifedipine (never ACEi/ARB).

Do I need to know about TAVI indications? Broad strokes — TAVI is now first-line for severe aortic stenosis in most elderly patients and increasingly offered to younger/lower-surgical-risk groups. Surgical AVR remains appropriate for younger patients with long life expectancy.

What's the place of loop diuretics in HFrEF? Symptomatic control only — no mortality benefit. Furosemide doses escalate as symptoms dictate. Always combine with mortality-modifying agents (ACEi, beta-blocker, MRA, SGLT2).

Is BP over 180/120 always an emergency? Malignant hypertension (BP ≥180/120 with end-organ damage: headache, visual symptoms, papilloedema, renal impairment) needs urgent admission and controlled BP reduction. BP ≥180/120 without end-organ damage triggers same-day clinic review and starting or uptitrating antihypertensives — not necessarily A&E.

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Cardiology done well is the single biggest lever on an AKT subscore. Twelve sub-topics, five or six question templates, and a finite set of decision trees — that's the whole surface area. Drill the hypertension ladder until you can write it from memory. Drill the AF anticoagulation decision until CHA₂DS₂-VASc calculation is automatic. Drill the STEMI territory map until the ECG lead pattern triggers the coronary artery answer in under five seconds. These are low-cognition, high-mark retrievals on exam day.

Pair this masterclass with the content map prioritisation and the NICE guidelines post — those two cover the framework, and cardiology is where you apply it first. The 12-week plan and the Q-bank comparison close the loop on scheduling and practice volume.

MLA Prep's cardiology module covers all 12 sub-topics above with AKT-aligned SBAs, ECG recognition drills, and spaced-repetition cards for every NICE ladder — mapped to the exact question templates the AKT uses. Start the free diagnostic to benchmark your cardiology subscore, or compare plans for full access.