Membership of the Royal College of Physicians (MRCP UK) Cardiology Syllabus

Cardiology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Cardiology in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Ischaemic Heart Disease and Acute Coronary Syndromes

   5 topics

   • Stable angina assessment and management
     • CT coronary angiography and functional testing
     • Antianginal pharmacotherapy and revascularisation thresholds
   • ST-elevation myocardial infarction (STEMI)
     • Primary PCI pathways and door-to-balloon targets
     • Thrombolysis indications and contraindications
   • NSTEMI and unstable angina
     • GRACE risk stratification
     • Dual antiplatelet therapy regimens
   • Complications of myocardial infarction
     • Mechanical complications: VSD, papillary muscle rupture
     • Post-infarct arrhythmia and pericarditis
   • Secondary prevention after coronary events
2. 2

   Heart Failure and Cardiomyopathy

   5 topics

   • Heart failure with reduced ejection fraction
     • Four-pillar guideline-directed medical therapy
     • Device therapy: CRT and ICD indications
   • Heart failure with preserved ejection fraction
   • Acute decompensated heart failure and cardiogenic shock
   • Dilated, hypertrophic and restrictive cardiomyopathies
     • Hypertrophic cardiomyopathy and sudden death risk
     • Infiltrative disease: amyloid and sarcoid
   • Cardiac transplantation and mechanical support
3. 3

   Arrhythmias and Conduction Disorders

   5 topics

   • Atrial fibrillation and flutter
     • Rate versus rhythm control
     • CHA2DS2-VASc and anticoagulation
   • Supraventricular tachycardias and pre-excitation
   • Ventricular tachyarrhythmias
   • Bradyarrhythmias and heart block
     • Pacemaker indications and modes
   • Inherited channelopathies
     • Long QT syndrome and Brugada syndrome
4. 4

   Valvular and Structural Heart Disease

   5 topics

   • Aortic stenosis and regurgitation
     • TAVI versus surgical valve replacement
   • Mitral stenosis and regurgitation
   • Infective endocarditis
     • Duke criteria and antimicrobial therapy
   • Prosthetic valve assessment and complications
   • Adult congenital heart disease overview
5. 5

   Vascular, Pericardial and Pulmonary Circulation

   5 topics

   • Hypertension and hypertensive emergencies
     • Secondary hypertension screening
   • Aortic dissection and aneurysm
   • Pericarditis and pericardial effusion/tamponade
   • Pulmonary hypertension classification and management
   • Cardiac investigations interpretation
     • ECG interpretation
     • Echocardiography and cardiac MRI principles

Cardiology flashcards for Membership of the Royal College of Physicians (MRCP UK)

24 of 68 cards from the Cardiology deck — real questions with worked answers.

1. What is the first-line antianginal drug therapy for stable angina, and what is added if monotherapy fails?

   First-line: a beta-blocker OR a rate-limiting calcium channel blocker (e.g. diltiazem/verapamil). If one alone fails, combine a beta-blocker with a dihydropyridine CCB (e.g. amlodipine). All patients also receive a short-acting GTN, plus aspirin and a statin for secondary prevention.

2. In stable angina, which non-invasive investigation does NICE recommend first-line when angina is suspected (typical or atypical)?

   CT coronary angiography (CTCA) is the first-line investigation to assess for coronary artery disease in patients with chest pain of suspected cardiac origin.

3. Define the ECG criteria for STEMI in standard leads versus the special threshold in leads V2-V3.

   New ST-elevation $\geq 1\,\text{mm}$ in $\geq 2$ contiguous limb/chest leads, EXCEPT in V2-V3 where the threshold is $\geq 2\,\text{mm}$ in men ($\geq 2.5\,\text{mm}$ in men <40) and $\geq 1.5\,\text{mm}$ in women. New LBBB with ischaemic symptoms is also treated as STEMI.

4. What is the target time window for primary PCI in STEMI, and when is fibrinolysis used instead?

   Primary PCI is preferred if it can be delivered within 120 minutes of when fibrinolysis could have been given, and the patient presents within 12 hours of symptom onset. If PCI is not available within that window, give fibrinolysis, then transfer for angiography.

5. Match the STEMI territory to the culprit coronary artery: inferior, anteroseptal, lateral.

   Inferior (II, III, aVF) = right coronary artery (or left circumflex). Anteroseptal (V1-V4) = left anterior descending. Lateral (I, aVL, V5-V6) = left circumflex. Posterior (tall R/ST depression V1-V3) = RCA or circumflex.

6. In an inferior STEMI, why should you obtain right-sided ECG leads, and what management implication follows?

   To detect right ventricular infarction (ST-elevation in V4R). RV infarction causes preload-dependent hypotension, so nitrates must be avoided and the patient managed with IV fluids to maintain RV filling.

7. What ECG and biomarker findings distinguish NSTEMI from unstable angina?

   Both show ischaemic symptoms without ST-elevation (may have ST-depression/T-inversion). NSTEMI has a RISE in troponin indicating myocardial necrosis; unstable angina has a NORMAL troponin (no necrosis).

8. What risk score guides the timing of invasive angiography in NSTEMI/unstable angina, and what threshold prompts early intervention?

   The GRACE score estimates 6-month mortality. Intermediate-to-high risk (>3% predicted 6-month mortality) warrants coronary angiography, ideally within 72 hours; very high-risk/unstable patients go immediately.

9. Outline the initial drug management of NSTEMI (the antithrombotic and antianginal components).

   Aspirin 300 mg loading then continue; antithrombin (fondaparinux if no immediate angiography, or unfractionated heparin if going to cath lab). Add a second antiplatelet (ticagrelor/prasugrel/clopidogrel). Plus nitrates/opioids for pain, oxygen only if hypoxic, and risk stratify with GRACE.

10. A patient develops a new pansystolic murmur and acute pulmonary oedema 3-5 days after MI. What are the two key differentials and how are they distinguished?

    Acute mitral regurgitation (papillary muscle rupture) versus ventricular septal rupture (VSD). Both cause a pansystolic murmur and shock. Echocardiography distinguishes them; a right heart catheter step-up in oxygen saturation confirms VSD.

11. What complication is suggested by sudden pulseless electrical activity (PEA) and cardiac arrest several days post-MI?

    Free wall (myocardial) rupture causing cardiac tamponade, typically 3-14 days post-MI. It carries a very high mortality and may require emergency pericardiocentesis and surgery.

12. Differentiate early post-MI pericarditis from Dressler syndrome.

    Early infarct-associated pericarditis occurs within the first 1-3 days. Dressler syndrome is an autoimmune pericarditis occurring 2-6 weeks post-MI with fever, pleuritic chest pain, pericardial effusion and raised inflammatory markers; treated with NSAIDs/aspirin (and colchicine).

13. List the five drug classes of secondary prevention given to most patients after an MI.

    1) Dual antiplatelet therapy (aspirin lifelong + a P2Y12 inhibitor for ~12 months), 2) ACE inhibitor, 3) beta-blocker, 4) high-intensity statin (e.g. atorvastatin 80 mg), 5) an aldosterone antagonist (e.g. eplerenone) if there is heart failure with LV dysfunction.

14. What lifestyle and cardiac rehabilitation advice is standard after a coronary event regarding driving?

    After MI with successful PCI, ordinary (group 1) driving may resume after 1 week if LVEF >40% and no other disqualifying condition (4 weeks if no successful PCI). Group 2 (HGV/PSV) licences require re-assessment and are generally barred for at least 6 weeks. Cardiac rehab, smoking cessation, Mediterranean diet and exercise are advised.

15. Define heart failure with reduced ejection fraction (HFrEF) by EF threshold.

    HFrEF is defined as symptomatic heart failure with a left ventricular ejection fraction $\leq 40\%$.

16. Name the four pillars of guideline-directed medical therapy for HFrEF.

    1) ACE inhibitor or ARNI (sacubitril-valsartan), 2) beta-blocker, 3) mineralocorticoid receptor antagonist (spironolactone/eplerenone), 4) SGLT2 inhibitor (dapagliflozin/empagliflozin). These four reduce mortality and hospitalisation.

17. In HFrEF, what EF and QRS criteria qualify a patient for cardiac resynchronisation therapy (CRT)?

    Patients with LVEF $\leq 35\%$ despite optimal medical therapy, in sinus rhythm, with QRS duration $\geq 130\text{–}150\,\text{ms}$ (especially LBBB morphology) benefit from CRT. An ICD is also considered for primary prevention of sudden death.

18. How is heart failure with preserved ejection fraction (HFpEF) defined, and what is its hallmark pathophysiology?

    HFpEF: symptoms/signs of heart failure with LVEF $\geq 50\%$ plus objective evidence of diastolic dysfunction/raised filling pressures (e.g. raised BNP, structural changes like LV hypertrophy or left atrial enlargement). The hallmark is impaired ventricular relaxation/diastolic dysfunction with normal systolic function.

19. Which drug class has shown mortality/hospitalisation benefit in HFpEF, and what is the general management approach?

    SGLT2 inhibitors (empagliflozin, dapagliflozin) reduce HF hospitalisation in HFpEF. Otherwise management is largely symptomatic: diuretics for congestion and aggressive treatment of comorbidities (hypertension, AF, obesity, diabetes).

20. What does an elevated natriuretic peptide (BNP/NT-proBNP) indicate, and what conditions falsely lower it?

    Elevated BNP/NT-proBNP indicates raised ventricular wall stress, supporting a diagnosis of heart failure (and correlating with prognosis). Levels can be falsely LOW in obesity and with treatment using ACE inhibitors, ARBs, beta-blockers, diuretics and MRAs.

21. List the haemodynamic profiles (Forrester/'warm-cold, wet-dry') used to guide management of acute decompensated heart failure.

    Based on perfusion and congestion: Warm & dry (well perfused, no congestion), Warm & wet (congested, perfused — give diuretics/vasodilators), Cold & dry (hypoperfused, dry — fluids/inotropes), Cold & wet (hypoperfused + congested — inotropes ± vasodilators, the highest-risk group).

22. Define cardiogenic shock and give its key haemodynamic criteria.

    Cardiogenic shock is end-organ hypoperfusion due to cardiac dysfunction despite adequate intravascular volume: sustained hypotension (SBP $<90\,\text{mmHg}$ for >30 min or needing support), cardiac index $<2.2\,\text{L/min/m}^2$, and elevated pulmonary capillary wedge pressure ($>15\,\text{mmHg}$), with signs of hypoperfusion (oliguria, cool peripheries, lactataemia).

23. What is the most common cause of cardiogenic shock, and what is the definitive treatment?

    Acute MI with extensive LV failure (or mechanical complication) is the commonest cause. Definitive treatment is urgent revascularisation (primary PCI) of the culprit vessel; supportive measures include inotropes/vasopressors and mechanical circulatory support.

24. Compare the three cardiomyopathy types by their primary functional abnormality and typical ventricular geometry.

    Dilated (DCM): systolic dysfunction with dilated thin-walled ventricles. Hypertrophic (HCM): diastolic dysfunction with asymmetric LV hypertrophy (often septal). Restrictive (RCM): diastolic dysfunction with normal-sized, stiff, non-compliant ventricles and biatrial enlargement.

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