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

24 sample cards from the Cardiology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. List the classic clinical triad and key examination findings of severe aortic stenosis.

   Triad of exertional syncope, angina and dyspnoea/heart failure. Signs: ejection systolic murmur radiating to the carotids, a slow-rising low-volume pulse (pulsus parvus et tardus), narrow pulse pressure, soft/absent S2, and a sustained apex beat.

2. What echocardiographic measurements define severe aortic stenosis?

   Aortic valve area $<1.0\,\text{cm}^2$, mean transvalvular gradient $>40\,\text{mmHg}$, and peak aortic jet velocity $>4.0\,\text{m/s}$.

3. What are the indications for valve intervention (SAVR/TAVI) in aortic stenosis?

   Symptomatic severe AS, or asymptomatic severe AS with LV systolic dysfunction (EF <50%), or undergoing other cardiac surgery. Choice between surgical AVR and transcatheter AVI depends on surgical risk, age and anatomy.

4. Describe the murmur and peripheral signs of chronic aortic regurgitation.

   Early diastolic decrescendo murmur at the left sternal edge (louder sitting forward, in expiration), with a wide pulse pressure causing a collapsing (water-hammer) pulse, Corrigan's sign, Quincke's sign, de Musset's sign and an Austin Flint murmur (mid-diastolic) in severe cases.

5. Compare the murmurs of mitral stenosis and mitral regurgitation.

   Mitral stenosis: low-pitched rumbling MID-DIASTOLIC murmur with an opening snap, loud S1, best heard at the apex in the left lateral position; commonest cause is rheumatic heart disease. Mitral regurgitation: PANSYSTOLIC murmur at the apex radiating to the axilla with a soft S1.

6. What is the modified Duke criteria framework for diagnosing infective endocarditis?

   Diagnosis requires 2 major, OR 1 major + 3 minor, OR 5 minor criteria. Major: positive blood cultures with typical organisms (or persistent bacteraemia) and echocardiographic evidence of endocardial involvement (vegetation/abscess/new valve regurgitation). Minor: predisposing heart condition/IVDU, fever $>38^\circ\text{C}$, vascular phenomena, immunological phenomena, and microbiological evidence not meeting major.

7. Which organisms most commonly cause infective endocarditis in (a) native valves, (b) prosthetic valves <2 months, and (c) IV drug users?

   (a) Native valve: Staphylococcus aureus (acute) and viridans streptococci (subacute); (b) early prosthetic valve: coagulase-negative staphylococci (Staph epidermidis); (c) IV drug users: Staph aureus affecting the tricuspid (right-sided) valve.

8. List the surgical indications in infective endocarditis.

   Heart failure due to valve dysfunction, uncontrolled infection (abscess, persistent bacteraemia, resistant/fungal organisms), and prevention of embolism (large mobile vegetations >10 mm, especially after an embolic event).

9. What are the two main types of prosthetic heart valve and their key trade-off?

   Mechanical valves are durable (last decades) but thrombogenic, requiring lifelong warfarin anticoagulation. Bioprosthetic (tissue) valves need little/no long-term anticoagulation but are less durable (structural degeneration in ~10-15 years), so are favoured in older patients.

10. Name the major complications of prosthetic heart valves.

    Thrombosis/thromboembolism, bleeding from anticoagulation, infective endocarditis, structural valve degeneration (bioprosthetic), paravalvular leak, and haemolytic anaemia (from mechanical shear). A muffled or changed valve click and new murmur suggest dysfunction.

11. Differentiate the four shunt lesions Eisenmenger syndrome arises from and what defines the syndrome.

    Eisenmenger syndrome develops from an uncorrected large left-to-right shunt (VSD, ASD, PDA, or AV septal defect) that causes pulmonary hypertension, eventually reversing the shunt to right-to-left, producing cyanosis, clubbing and erythrocytosis. It contraindicates closure of the defect.

12. Which congenital heart lesion is associated with radio-femoral delay and rib notching, and which valve abnormality coexists?

    Coarctation of the aorta — causing upper-limb hypertension, radio-femoral delay, and rib notching from collateral intercostal vessels. It is commonly associated with a bicuspid aortic valve (and Turner syndrome).

13. State the NICE blood pressure thresholds for stage 1, stage 2 and severe hypertension (clinic readings).

    Stage 1: clinic $\geq 140/90$ (ABPM/HBPM $\geq 135/85$). Stage 2: clinic $\geq 160/100$ (ABPM/HBPM $\geq 150/95$). Severe (stage 3): clinic systolic $\geq 180$ or diastolic $\geq 120\,\text{mmHg}$.

14. Outline the NICE step 1 antihypertensive choice based on age and ethnicity.

    Under 55 and not of Black African/African-Caribbean origin: ACE inhibitor or ARB (A). Aged $\geq 55$, OR of Black African/African-Caribbean origin (any age): calcium channel blocker (C). Step 2 combines A + C; step 3 adds a thiazide-like diuretic (D); step 4 adds spironolactone if potassium $\leq 4.5$.

15. What distinguishes a hypertensive emergency from urgency, and how fast should BP be lowered in emergency?

    A hypertensive emergency is severe hypertension WITH acute end-organ damage (encephalopathy, retinal haemorrhages/papilloedema, AKI, MI, dissection, pulmonary oedema); urgency lacks acute organ damage. In emergencies lower BP gradually with IV agents — by no more than ~25% in the first hour — to avoid cerebral hypoperfusion.

16. Compare the management of Stanford type A versus type B aortic dissection.

    Type A (involves the ascending aorta) is a surgical emergency requiring urgent operative repair. Type B (descending aorta only, distal to the left subclavian) is usually managed medically with aggressive heart-rate and blood-pressure control (IV beta-blockers, e.g. labetalol), with intervention reserved for complications.

17. What is the threshold for elective repair of an abdominal aortic aneurysm and the key surveillance principle?

    Elective repair (EVAR or open) is offered when the AAA reaches $\geq 5.5\,\text{cm}$ in diameter, is symptomatic, or expands rapidly ($>1\,\text{cm/year}$). Smaller aneurysms are monitored by ultrasound surveillance.

18. Describe the ECG findings of acute pericarditis and the first-line treatment.

    Widespread (concave/saddle-shaped) ST-elevation and PR depression across multiple leads, with reciprocal ST-depression and PR elevation in aVR. First-line treatment is NSAIDs (or aspirin) PLUS colchicine; treat the underlying cause.

19. List Beck's triad and the pulsus paradoxus finding of cardiac tamponade.

    Beck's triad: hypotension, raised JVP (distended neck veins), and muffled/quiet heart sounds. Pulsus paradoxus is an exaggerated fall in systolic BP $>10\,\text{mmHg}$ on inspiration. Treatment is urgent pericardiocentesis.

20. Give the WHO clinical classification (5 groups) of pulmonary hypertension.

    Group 1: pulmonary arterial hypertension (idiopathic, heritable, drug-induced, connective tissue disease). Group 2: PH due to left heart disease. Group 3: PH due to lung disease/hypoxia. Group 4: chronic thromboembolic PH (CTEPH). Group 5: multifactorial/unclear mechanisms (e.g. sarcoid, haematological disorders).

21. What is the haemodynamic definition of pulmonary hypertension, and which group is treated with pulmonary vasodilators?

    Mean pulmonary artery pressure $>20\,\text{mmHg}$ at rest on right heart catheterisation (with PCWP $\leq 15\,\text{mmHg}$ and PVR $>2$ Wood units for pre-capillary PH). Targeted pulmonary vasodilators (endothelin antagonists, PDE-5 inhibitors, prostacyclins) are used mainly in Group 1 PAH, NOT in Group 2.

22. In cardiac catheterisation, write the formula for cardiac output by the Fick principle.

    $$\text{CO} = \frac{\text{VO}_2}{(\text{Ca} - \text{Cv}) \times 10}$$ where $\text{VO}_2$ is oxygen consumption (mL/min) and $(\text{Ca}-\text{Cv})$ is the arteriovenous oxygen content difference (mL O2 per 100 mL blood).

23. What ECG changes are characteristic of hyperkalaemia, and in what order do they appear with rising potassium?

    Progressively: tall tented T waves, then flattening/loss of P waves and PR prolongation, then widening of the QRS, finally a sinusoidal pattern and VF/asystole. Urgent treatment is IV calcium gluconate for cardioprotection plus insulin-dextrose to shift potassium.

24. Which echocardiographic and ECG features suggest cardiac amyloidosis?

    Echo: increased LV wall thickness with a 'speckled/granular' sparkling myocardium, biatrial enlargement, and restrictive filling. ECG: LOW QRS voltages despite the thick walls (voltage-mass mismatch), often with a pseudo-infarct pattern. Confirm with cardiac MRI and tissue/DPD-scintigraphy or biopsy.

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