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

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).

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).

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.

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.

What is the inheritance pattern of hypertrophic cardiomyopathy and the typical genes involved?

Autosomal dominant, caused by mutations in sarcomeric protein genes — most commonly beta-myosin heavy chain (MYH7) and myosin-binding protein C (MYBPC3).

In hypertrophic obstructive cardiomyopathy (HOCM), how do the murmur and outflow obstruction respond to Valsalva and to squatting?

Valsalva (reduced preload) INCREASES the LVOT obstruction and intensifies the ejection systolic murmur; squatting/handgrip (increased preload/afterload) DECREASES the murmur. This dynamic behaviour helps distinguish HOCM from aortic stenosis.

Name the high-risk features used to assess sudden cardiac death risk in HCM (which may prompt ICD).

Family history of sudden cardiac death, unexplained syncope, massive LV wall thickness ($\geq 30\,\text{mm}$), non-sustained VT on Holter, and abnormal blood pressure response to exercise. The HCM Risk-SCD score quantifies 5-year risk.

Give three causes of restrictive cardiomyopathy.

Amyloidosis, sarcoidosis, haemochromatosis (iron overload), endomyocardial fibrosis, and storage diseases. Amyloid is the classic cause and shows speckled myocardium on echo with low voltages on ECG despite thickened walls.

What are the standard indications for referral for cardiac transplantation in advanced heart failure?

Refractory end-stage heart failure (NYHA III-IV) despite optimal therapy with poor prognosis, e.g. peak VO2 $<12\text{–}14\,\text{mL/kg/min}$, recurrent hospitalisations, dependence on inotropes, or refractory ventricular arrhythmias, in the absence of major contraindications.

What is an LVAD used for, and what is its most feared complication?

A left ventricular assist device (LVAD) provides mechanical circulatory support as a bridge to transplant, bridge to recovery, or destination therapy. Major complications include thrombosis/pump failure, driveline infection, bleeding (acquired von Willebrand disease) and stroke; lifelong anticoagulation is required.

State the CHA2DS2-VASc components and what total score generally warrants anticoagulation in AF.

Congestive HF (1), Hypertension (1), Age $\geq 75$ (2), Diabetes (1), prior Stroke/TIA/thromboembolism (2), Vascular disease (1), Age 65-74 (1), Sex category female (1). Anticoagulate when score $\geq 2$ in men or $\geq 3$ in women; consider at 1 in men/2 in women.

In AF, when is rhythm control favoured over rate control, and what is the first-line rate-control drug?

Rhythm control is favoured in new-onset AF (<48 h), reversible cause, heart failure thought caused by AF, or symptomatic/young patients. First-line rate control is a beta-blocker or rate-limiting CCB (avoid CCB in HFrEF); digoxin is reserved for sedentary patients or as add-on.

What is the classic ECG appearance and ventricular rate of typical atrial flutter, and the definitive treatment?

Sawtooth flutter (F) waves, best seen in the inferior leads, with an atrial rate ~300/min and 2:1 AV conduction giving a ventricular rate of ~150/min. Definitive treatment is radiofrequency ablation of the cavotricuspid isthmus; anticoagulation follows the same rules as AF.

What is the acute management of a haemodynamically stable narrow-complex regular SVT (e.g. AVNRT)?

Vagal manoeuvres first (Valsalva/carotid sinus massage). If unsuccessful, IV adenosine $6\,\text{mg}$ rapid bolus, then $12\,\text{mg}$, then $18\,\text{mg}$ if needed. If still refractory or unstable, synchronised DC cardioversion.

Describe the resting ECG features of Wolff-Parkinson-White syndrome.

Short PR interval ($<120\,\text{ms}$), a slurred upstroke of the QRS (delta wave), and a widened QRS due to ventricular pre-excitation via an accessory pathway (e.g. bundle of Kent).

Why are AV-nodal blocking drugs (e.g. verapamil, adenosine, digoxin) dangerous in pre-excited (WPW) atrial fibrillation?

Blocking the AV node promotes preferential rapid conduction down the accessory pathway, which can accelerate the ventricular rate and precipitate ventricular fibrillation. Use procainamide/flecainide or DC cardioversion instead.

How do you distinguish ventricular tachycardia from SVT with aberrancy on ECG?

Features favouring VT: AV dissociation, capture/fusion beats, very broad QRS ($>140\,\text{ms}$), extreme axis deviation, concordance across the chest leads, and a history of ischaemic heart disease. When in doubt, treat a broad-complex tachycardia as VT.

What is the management of pulseless VT/VF versus monomorphic VT with a pulse but adverse signs?

Pulseless VT/VF: immediate unsynchronised defibrillation and CPR (shockable ACLS algorithm). VT with a pulse but adverse features (shock, syncope, ischaemia, HF): synchronised DC cardioversion. Stable VT: IV amiodarone.

What is torsades de pointes, its ECG signature, and its emergency treatment?

Polymorphic VT associated with a prolonged QT interval, showing a characteristic 'twisting' of QRS around the baseline. Treat with IV magnesium sulphate, stop QT-prolonging drugs, correct electrolytes; overdrive pacing or isoprenaline if recurrent.

Differentiate Mobitz type I (Wenckebach) from Mobitz type II second-degree AV block.

Mobitz I: progressive PR prolongation until a beat is dropped (cyclical); usually benign, AV-nodal. Mobitz II: constant PR interval with intermittent non-conducted P waves; infranodal, high risk of progression to complete heart block — needs pacing.

What defines complete (third-degree) heart block on ECG and its definitive treatment?

Complete AV dissociation — P waves and QRS complexes are independent, with an escape rhythm (junctional narrow or ventricular broad) at a slow rate. Definitive treatment is permanent pacemaker implantation (atropine/temporary pacing acutely).

Describe the ECG hallmark and inheritance of Long QT syndrome, and a common trigger for each major subtype.

Prolonged corrected QT ($\text{QTc} > 470\,\text{ms}$ men, $>480\,\text{ms}$ women), risk of torsades. Usually autosomal dominant (Romano-Ward). LQT1 (KCNQ1) triggered by exercise/swimming; LQT2 (KCNH2) by emotion/auditory stimuli; LQT3 (SCN5A) during sleep/rest.

What is the ECG pattern of Brugada syndrome and its inheritance/risk?

Coved ST-elevation $\geq 2\,\text{mm}$ with T-wave inversion in V1-V2 (type 1 pattern), due to autosomal dominant SCN5A sodium-channel mutations. It predisposes to polymorphic VT/sudden death, often during sleep or fever; an ICD is the only proven preventive therapy.

How is QT corrected for heart rate (give Bazett's formula)?

$$\text{QTc} = \frac{\text{QT}}{\sqrt{\text{RR}}}$$ where QT and RR are measured in seconds. A QTc above approximately $440\text{–}460\,\text{ms}$ is prolonged.

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.

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 $>4.0\,\text{m/s}$.

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.

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.

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.

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.

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.

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).

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.

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.

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.

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).

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 $\geq 120\,\text{mmHg}$.

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 $\leq 4.5$.

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.

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.

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.

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.

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.

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).

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.

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).

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.

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.