MRCP PACES Station 3: Mastering Cardiovascular Examination

Admin
Cardiology MRCP PACES
2046 words • 9 min read

Article Content

Published by TalkingCases

Jun 15, 2026

MRCP PACES Station 3: Mastering Cardiovascular Examination

Why Station 3 Cardiology Cases Catch Candidates Out

MRCP PACES Station 3 tests two systems: cardiovascular and neurological. Of the two, cardiology cases are deceptively straightforward in appearance — the patient is sitting up, the examination is familiar, and the signs are often loud. Yet Station 3 is where many otherwise strong candidates stumble because presenting findings at registrar level demands precision, structure, and a clear management plan — not just naming the murmur.

This guide walks you through the high-yield cardiovascular cases, the examination framework that earns marks, and the discussion questions that separate passes from distinctions.


The Station 3 Cardiovascular Framework That Never Fails

Before touching the patient, take 10 seconds at the end of the bed. Look for:

  • Dysmorphic features (Turner syndrome → coarctation; Marfanoid habitus → aortic regurgitation, mitral valve prolapse)

  • Breathing pattern — orthopnoea suggests heart failure

  • Visible pulsations — visible apex beat, suprasternal pulsation (aortic regurgitation)

  • Nebuliser, oxygen, or GTN spray at the bedside

Then proceed systematically:

1. Hands and Pulse

  • Tar staining → ischaemic heart disease

  • Peripheral stigmata — splinter haemorrhages, Osler nodes, Janeway lesions (infective endocarditis)

  • Tendon xanthomata → familial hypercholesterolaemia

  • Radial pulse: rate, rhythm, character. A slow-rising pulse suggests aortic stenosis; a collapsing (water-hammer) pulse suggests aortic regurgitation. An irregularly irregular pulse suggests atrial fibrillation.

  • Radio-radial delay → coarctation of aorta (check femoral pulses simultaneously for radio-femoral delay)

2. Face and Neck

  • Conjunctival pallor (anaemia may exacerbate murmurs)

  • Dental caries → endocarditis risk

  • High arched palate, arachnodactyly → Marfan syndrome

  • JVP: Elevated in right heart failure, tricuspid regurgitation (giant cv waves), constrictive pericarditis (Kussmaul's sign)

  • Carotid pulse: Assess character — slow rising (AS), bounding (AR)

3. Precordium

  • Inspect: Scars (median sternotomy, thoracotomy for mitral valvotomy), visible apex, pacemaker/ICD box

  • Palpate:

    • Apex beat — location (displaced = volume overload; tapping = mitral stenosis; heaving = pressure overload/LVH; thrusting = volume overload)

    • Parasternal heave → right ventricular hypertrophy or volume overload

    • Thrills — palpable murmurs (grade ≥4)

  • Auscultate systematically:

    • Apex (mitral area) with bell for low-pitched sounds (mitral stenosis) and diaphragm for high-pitched

    • Lower left sternal edge (tricuspid area)

    • Upper left sternal edge (pulmonary area)

    • Upper right sternal edge (aortic area)

    • Roll patient left lateral position — listen at apex with bell for mitral stenosis

    • Sit patient forward, breath held in expiration — listen at lower left sternal edge for aortic regurgitation

    • Listen to carotids (radiation of aortic stenosis) and axilla (radiation of mitral regurgitation)

  • Dynamic manoeuvres:

    • Inspiration → increases right-sided murmurs (tricuspid, pulmonary)

    • Hand grip → increases left-sided murmurs (AS, AR, MS, MR)

    • Valsalva (release phase) → increases HOCM murmur, decreases AS and MR

    • Standing from squatting → increases HOCM murmur, decreases AS and MR

4. Back and Legs

  • Sacral/pedal oedema → heart failure

  • Basal crackles → pulmonary oedema

  • Peripheral pulses — check for vascular disease


The Top 10 High-Yield Cardiology Cases

1. Aortic Stenosis (AS)

Murmur: Ejection systolic, heard best at the upper right sternal edge, radiating to carotids.

Key signs:

  • Slow-rising pulse (pulsus parvus et tardus)

  • Heaving, non-displaced apex beat

  • Ejection click (in valvular AS with pliable valve)

  • Soft/absent S2 (due to calcified immobile valve)

  • Reverse splitting of S2 (late A2)

Examiner questions to anticipate:

  • Causes: degenerative calcific (most common in elderly), bicuspid valve, rheumatic

  • Severity assessment: echo criteria (mean gradient >40 mmHg, valve area <1.0 cm², peak velocity >4 m/s)

  • Symptoms: angina, syncope, breathlessness (classical triad)

  • Management: AVR (surgical or TAVI) if symptomatic with severe AS

Clinical pearl: The Carabello sign — a rise in blood pressure after aortic valve catheterisation suggests severe AS. More relevant for written exams, but shows depth.


2. Aortic Regurgitation (AR)

Murmur: Early diastolic, decrescendo, heard best at the lower left sternal edge with patient sitting forward in expiration (Erb's point). May also have an ejection systolic murmur (flow murmur) and Austin Flint murmur (mid-diastolic murmur from fluttering anterior mitral leaflet).

Key signs:

  • Collapsing (water-hammer) pulse

  • Wide pulse pressure (large pulse pressure with low diastolic)

  • Thrusting, displaced apex beat (volume overload)

  • Bounding peripheral pulses

  • Named eponymous signs: Corrigan's pulse (visible carotid pulsation), de Musset's sign (head nodding), Quincke's sign (nailbed pulsation), Duroziez's sign (femoral artery murmur), Traube's sign (pistol-shot over femorals)

Causes to discuss:

  • Valve disease: rheumatic, bicuspid valve, endocarditis

  • Root dilation: Marfan syndrome, aortic dissection, syphilis, ankylosing spondylitis, RA, hypertension

Management: AVR when symptomatic or LV ejection fraction <50% or LV end-systolic diameter >50 mm.


3. Mitral Stenosis (MS)

Murmur: Mid-diastolic, low-pitched rumble at the apex, heard best with the bell in the left lateral position. Opening snap precedes the murmur.

Key signs:

  • Tapping, non-displaced apex (palpable first heart sound)

  • Loud S1

  • Malar flush (mitral facies)

  • Atrial fibrillation common

  • Pulmonary hypertension signs (loud P2, parasternal heave, elevated JVP)

Causes: Rheumatic heart disease (by far the most common), rarely congenital, SLE, carcinoid

Management:

  • Medical: rate control (beta-blockers), anticoagulation if AF

  • Percutaneous mitral balloon valvotomy (PMBV) if pliable, non-calcified valve without LA thrombus or significant MR

  • Surgical: MVR if unsuitable for PMBV

Pearl: The shorter the interval between S2 and the opening snap, the more severe the stenosis.


4. Mitral Regurgitation (MR)

Murmur: Pansystolic murmur at the apex, radiating to the axilla.

Key signs:

  • Thrusting, displaced apex (volume overload)

  • Soft S1

  • S3 gallop (in chronic severe MR)

  • Thrill may be present

Causes:

  • Chronic: mitral valve prolapse, ischaemic (post-MI papillary muscle dysfunction), rheumatic, dilated cardiomyopathy (functional MR), endocarditis

  • Acute: ruptured papillary muscle (post-MI), ruptured chordae, acute endocarditis

Management: MV repair (preferred) or replacement. Indications: symptomatic severe MR, asymptomatic with LV dysfunction (EF <60% or LVESD ≥40 mm).


5. Mitral Valve Prolapse (MVP)

Murmur: Late systolic murmur preceded by a mid-systolic click at the apex. The click and murmur move earlier with standing/Valsalva and later with squatting.

Key signs:

  • May have associated features: Marfanoid habitus, pectus excavatum

  • Often thin, young patient

Management: Reassurance if asymptomatic. Beta-blockers for symptoms. Surgery for severe MR.


6. Hypertrophic Obstructive Cardiomyopathy (HOCM)

Murmur: Ejection systolic at lower left sternal edge, increases with Valsalva/standing (decreased preload → smaller LV → more obstruction) and decreases with squatting/hand grip.

Key signs:

  • Jerky pulse (rapid upstroke)

  • Twin apex beat (double impulse)

  • Reverse split S2

  • May coexist with MR murmur (due to systolic anterior motion of mitral valve)

Management:

  • Beta-blockers or verapamil as first-line

  • Avoid vasodilators, diuretics, and digoxin (worsen gradient)

  • ICD for high-risk patients (family history of sudden death, syncope, NSVT, marked LVH, abnormal BP response to exercise)

  • Septal reduction therapy (myectomy or alcohol septal ablation) if refractory symptoms

Exam favourite: Differentiate HOCM from AS — in HOCM, pulse is jerky/bifid (not slow-rising) and the murmur increases with Valsalva.


7. Tricuspid Regurgitation (TR)

Murmur: Pansystolic at the lower left sternal edge, increased with inspiration (Carvallo's sign).

Key signs:

  • Giant cv waves in JVP

  • Pulsatile liver

  • Parasternal heave

  • Peripheral oedema

Causes: Functional (secondary to pulmonary hypertension/RV dilatation) most common; also endocarditis (IVDU), Ebstein anomaly, rheumatic, carcinoid

Management: Treat underlying cause. Tricuspid valve repair/replacement in selected cases.


8. Ventricular Septal Defect (VSD)

Murmur: Pansystolic at the lower left sternal edge (may radiate widely). Small VSDs have louder, higher-pitched murmurs (Maladadie de Roger).

Key signs:

  • Thrill at lower left sternal edge

  • May have pulmonary hypertension signs with large defects

Management: Most small VSDs close spontaneously in childhood. Surgical closure for large defects, endocarditis, or significant shunting.


9. Prosthetic Heart Valves

Key features:

  • Mechanical valves: Clicking sound (opening/closing), require lifelong anticoagulation (target INR depends on valve position and type)

  • Bioprosthetic valves: Softer sounds, no routine anticoagulation required unless other indications

  • Listen for new murmurs → valve dysfunction (regurgitation, dehiscence, endocarditis)

  • Median sternotomy scar is the clue

Anticoagulation targets (NICE):

  • Mechanical mitral: INR 3.0–4.0 (target 3.5)

  • Mechanical aortic: INR 2.5–3.5 (target 3.0) — varies by valve type


10. Congestive Cardiac Failure

Key signs:

  • Displaced apex (LV dilatation)

  • S3 gallop

  • Bilateral basal crackles

  • Elevated JVP

  • Peripheral/sacral oedema

  • Signs of underlying cause: murmurs, prosthetic valve, pacemaker

Discussion points:

  • BNP/NT-proBNP for diagnosis

  • Echo: LVEF, wall motion abnormalities, valve function

  • Management: GDMT for HFrEF — ACE inhibitor/ARNI, beta-blocker, MRA, SGLT2 inhibitor (the "fantastic four" quadruple therapy)

  • Device therapy: CRT or ICD as appropriate


How to Present Your Findings — The Registrar-Level Template

Examiners reward structured, complete presentations. Use this template:

"Sir/Madam, my clinical findings are in keeping with a diagnosis of [valve lesion].

At the end of the bed, the patient is comfortable at rest. There is a median sternotomy scar consistent with previous cardiac surgery.

In the hands, there is no stigmata of infective endocarditis. The radial pulse is regular, rate 72, with a slow-rising character. Blood pressure is 120/80.

The JVP is not elevated. On examination of the precordium, the apex beat is heaving and non-displaced in the 5th intercostal space, mid-clavicular line. There is a systolic thrill palpable at the upper right sternal edge.

On auscultation, there is an ejection systolic murmur, loudest at the upper right sternal edge, radiating to the carotids. The second heart sound is soft. There are no signs of heart failure — the patient is euvolaemic with no peripheral oedema and clear lung bases.

In summary, my findings are consistent with severe aortic stenosis. I would like to complete my examination by checking the remaining peripheral pulses, examining for carotid bruits, performing a 12-lead ECG, and requesting an echocardiogram to confirm the diagnosis and assess severity."


The Three-Layer Answer for Examiner Questions

When the examiner asks a follow-up, structure your answer:

  1. Immediate management — stabilise the patient, treat acute symptoms

  2. Investigations — bedside, bloods, imaging (always specify echo)

  3. Definitive management — medical, interventional, surgical; mention MDT discussion


Common Mistakes That Cost Marks

Mistake Consequence
Not performing dynamic manoeuvres Misses HOCM vs AS differentiation — a classic examiner trap
Calling a murmur 'systolic' without specifying Pansystolic vs ejection systolic changes the differential entirely
Not checking for signs of heart failure Even if the primary lesion is a murmur, heart failure signs change management
Forgetting to mention the apex character Tapping (MS), heaving (AS), thrusting (AR/MR) — this is a key discriminator
Not asking about the patient's symptoms In Station 5 especially, clinical context matters
Overlooking scars Median sternotomy, thoracotomy, pacemaker — these are diagnostic anchors

Study Resources for PACES Cardiology

  1. PACES cases at your hospital — examine as many patients with murmurs as possible

  2. Douglas et al., Macleod's Clinical Examination — the cardiovascular chapter is gold

  3. Ryder et al., PACES for the MRCP — case-based scenarios with presentation scripts

  4. Online murmur libraries — the Blaufuss Medical Multimedia and Washington University heart sound simulators are excellent

  5. Echo images — familiarise yourself with basic echo findings of common valve lesions


Practice Strategy for Station 3

  • Examine 2–3 cardiology patients per week during your PACES preparation

  • Practise presentations aloud — record yourself and review against the template above

  • Learn the manoeuvres — you must perform at least one dynamic manoeuvre in every cardiology case

  • Master the murmur differentials — know the table below cold

Feature Aortic Stenosis HOCM Mitral Regurgitation Mitral Valve Prolapse
Murmur type Ejection systolic Ejection systolic Pansystolic Late systolic + click
Location Upper RSE Lower LSE Apex Apex
Radiation Carotids None Axilla None
Valsalva Earlier click/murmur
Squatting Later click/murmur
Hand grip
Pulse Slow-rising Jerky/bifid Normal Normal
Apex Heaving, non-displaced Twin/jerky Thrusting, displaced May be normal

Final Thoughts

Cardiology cases in PACES Station 3 reward candidates who examine methodically, present with confidence, and think like a registrar. The key is not just identifying the murmur but contextualising it — Does the patient have heart failure? What are the management options? What are the risks of this lesion if left untreated?

Practise your presentations until they flow naturally. Remember: the examiner has heard hundreds of candidates name murmurs. What earns you the pass is demonstrating that you understand the patient as a whole, not just the sound.

Good luck with your PACES preparation.


This guide is based on standard PACES examination techniques and current cardiology guidelines. Always refer to the latest NICE and ESC guidelines for management decisions.

Share

Keep your MRCP PACES reading path deliberate

This article belongs to the MRCP PACES consultation and communication cluster. Move back to the PACES hub for scope, browse only PACES articles, or switch into deliberate rehearsal inside TalkingCases.

Related Articles

Continue your medical education journey with these carefully curated insights

11 min read

MRCP PACES Station 1: High-Yield Respiratory Examination Guide

MRCP PACES Station 1: High-Yield Respiratory Examination GuideWhy Station 1 Respiratory Cases Trip Up Good CandidatesStation 1 of MRCP PACES is the first clinical encounter …

8 min read

MRCP PACES Endocrinology: Smarter Online Practice for High-Yield Cases

MRCP PACES Endocrinology: Smarter Online Practice for High-Yield CasesEndocrinology is one of the most commonly tested specialties in MRCP PACES, yet many candidates underestimate it. …

6 min read

MRCP PACES to Consultant: UK Career Roadmap

From MRCP PACES to Consultant: Your UK Career RoadmapCongratulations on passing MRCP PACES — or on working towards it. The examination itself is often described …

Join the Discussion

Share your thoughts and insights with the medical community

Comments