CFB MED06 Cardiovascular (II) Physical Examination
Systematic clinical assessment of the heart and vasculature through inspection, palpation, percussion, and auscultation to evaluate cardiac structure, function, and hemodynamic status.
This lecture by Professor Hung-Fat Tse is the physical examination companion to MED05 (CVS History Taking). The core message — stated on the very first content slide — is that cardiovascular examination is more than just listening to the heart [1]. You systematically evaluate the entire patient from general inspection through to the lungs, abdomen, and blood pressure, because cardiovascular disease causes systemic manifestations and systemic diseases cause cardiovascular manifestations.
Learning Objectives (inferred from slide structure):
- Perform a systematic pre-examination routine (IPPEC).
- Conduct a thorough general inspection for CVS-relevant signs.
- Assess the arterial system (pulses, blood pressure, special tests).
- Examine the jugular venous pressure (JVP) and interpret its waveform.
- Inspect, palpate, and auscultate the precordium correctly.
- Identify, grade, time, and characterise heart murmurs.
- Recognise the effects of dynamic manoeuvres on murmurs.
- Integrate ancillary examinations (lungs, abdomen, fundoscopy, BP).
How this fits into exams:
- OSCE stations on CVS examination are bread-and-butter.
- Written papers commonly test JVP waveform abnormalities, murmur grading/timing, and dynamic manoeuvres (past paper MCQ themes) [2][3].
- The lecture's own embedded MCQs (slides 87–89) are direct exam-style questions — study them verbatim.
"5 Important things to remember before examining a patient: I = Introduce, P = Permission, P = Positioning, E = Exposure adequately, C = Comfortable" [1]
| Letter | Action | Why it Matters |
|---|---|---|
| I | Introduce yourself | Professional rapport; OSCE mark |
| P | Permission | Consent is medico-legal and ethical |
| P | Positioning | CVS exam requires 45° head elevation for JVP; wrong position = wrong JVP reading |
| E | Exposure | Must expose entire chest; miss median sternotomy scar = miss valve replacement |
| C | Comfortable | Patient comfort improves cooperation and sign elicitation |
OSCE Trap
Forgetting IPPEC is an automatic mark deduction. Always state it aloud even if the examiner says "proceed with the examination."
2. General Inspection
"Systemic diseases → CVS manifestations (e.g. congenital syndromes, metabolic disorders) AND CVS diseases → Systemic manifestations (e.g. infective endocarditis, hypertension)" [1]
This bidirectional relationship is the conceptual anchor. You must look at the whole patient before touching the precordium.
| Finding | Condition | CVS Relevance |
|---|---|---|
| Body weight/height | Obesity (BMI > 30) | Major CV risk factor; associated with HT, DM, dyslipidaemia [4] |
| Turner's syndrome facies | Short stature, webbed neck, wide-set nipples | Coarctation of aorta, bicuspid aortic valve |
| Malar flush | Mitral stenosis | Low cardiac output + pulmonary HT → cutaneous vasodilation + chronic hypoxemia [5] |
| Acromegaly | GH excess | Cardiomyopathy, HT, arrhythmias |
| Xanthelasma / xanthomata | Hypercholesterolaemia / hypertriglyceridaemia | Premature atherosclerosis |
| Gynaecomastia | Drug side effects (spironolactone, digoxin) or Cushing's | Relevant to HF medication history |
| Cushing's features | Moon face, buffalo hump, striae | Secondary hypertension |
| Hyperthyroidism | Weight loss, tremor, lid retraction | AF, high-output HF |
| Hypothyroidism | Puffy face, slow relaxing reflexes | Pericardial effusion, bradycardia, dyslipidaemia |
"Pallor, Icterus, Cyanosis, Clubbing, Edema, Lymphadenopathy + Temperature, Pulse, Respiratory rate, BP" [1]
These are the standard "PICCEL" signs plus vital signs. Each has CVS significance:
- Pallor → anaemia → high-output failure
- Icterus → liver congestion from right heart failure, or prosthetic valve haemolysis
- Cyanosis → central (desaturated Hb > 5 g/dL) in cyanotic congenital heart disease; peripheral in low output
- Clubbing → see below
- Edema → right heart failure, fluid overload
- Lymphadenopathy → infective endocarditis (rarely), lymphoma causing SVC obstruction
2.4 Hands and Feet
"Finger clubbing: cyanotic congenital heart disease, infective endocarditis" [1]
Signs of early clubbing [1]:
- Loss of the normal angle between the nail base and proximal skin (the hyponychial angle is obliterated — normally ~160°, in clubbing it becomes ≥180°).
- Increased floating/fluctuation sensation when pressing the nail bed — the nail feels "boggy" because of fibrovascular tissue proliferation beneath.
- Schamroth's window test — when opposing the dorsal surfaces of terminal phalanges of corresponding fingers, a normal diamond-shaped "window" is visible; this window is lost in clubbing.
"Differential clubbing: more severe clubbing of the feet than hands" [1]
High Yield – Lecture MCQ 1
"Which condition is associated with more severe clubbing of the feet than hands? Answer: Patent ductus arteriosus (PDA). PDA connects the pulmonary artery to the aorta distal to the left subclavian artery → deoxygenated blood preferentially reaches the lower limbs → differential cyanosis and differential clubbing of the feet." [1]
This concept is based on the anatomy: the ductus joins the aorta distal to where the left subclavian artery branches off, so the upper limbs receive oxygenated blood from the LV while the lower limbs receive a mixture (with deoxygenated blood from the PA). Hence feet are more cyanosed/clubbed than hands.
"Splinter haemorrhage; Osler's node — painful, tender; Janeway lesion — painless" [1]
| Sign | Pathophysiology | Key Distinguishing Feature |
|---|---|---|
| Splinter haemorrhage | Microemboli to nail bed capillaries | Linear, non-blanching, reddish-brown lines under nails |
| Osler's nodes | Immune complex deposition → vasculitis | Painful, tender, violaceous nodules on finger/toe pads |
| Janeway lesions | Septic microemboli → microabscesses | Painless, erythematous macules on palms/soles |
Exam Discriminator
Students frequently confuse Osler's nodes and Janeway lesions. Osler = Ouch (painful). Janeway = painless. The mnemonic works because "O" for Osler = "O" for ouch.
Other IE signs from senior notes [6]: Roth spots (retinal haemorrhages with pale centres), conjunctival petechiae, splenomegaly, microscopic haematuria.
"Peripheral edema" — pitting oedema of ankles/sacrum indicates right heart failure or fluid overload [1].
3. Arterial System Examination
"All accessible arterial pulses should be assessed and compared bilaterally: radial, brachial, subclavian, carotid, femoral, popliteal, posterior tibial, dorsalis pedis" [1]
Causes of absent or reduced pulses: atherosclerosis, embolic occlusion, dissection, vascular compression, congenital anomaly [1].
"Hypertensive patient → simultaneous palpation of radial and femoral artery → radiofemoral delay → coarctation of aorta" [1]
Why radiofemoral delay? In coarctation, the narrowed aortic segment (usually just distal to the left subclavian artery) means blood reaches the femoral artery later and with reduced pressure. Collateral arteries partially bypass the obstruction but are slow. This sign is most important in a young hypertensive patient — it is a cause of secondary hypertension.
"Rate: 60–100 beats/min. Rhythm: skipped beats (regularly irregular), irregularly irregular → atrial fibrillation. Volume: diminished → poor cardiac output, aortic stenosis (slow rising, anacrotic), pericardial effusion. Increased → 'pounding' pulse. Character: best felt in carotid or brachial arteries." [1]
| Characteristic | What You Assess | Clinical Significance |
|---|---|---|
| Rate | Count for 15s × 4 (or 30s × 2 if irregular) | Tachycardia/bradycardia |
| Rhythm | Regularly irregular vs. irregularly irregular | Irregularly irregular = AF until proven otherwise |
| Volume | Force of pulse wave | Low volume in shock, AS; bounding in AR, sepsis |
| Character | Shape of the pulse waveform (best at carotid) | See table below |
Collapsing pulse: aortic regurgitation, AV fistula, persistent ductus arteriosus, rupture sinus of Valsalva, hyperdynamic circulation. Slow rising: aortic stenosis. Bisferiens: AS + AR combined. HOCM: jerky pulse. [1]
| Pulse Character | Waveform | Conditions | How to Elicit |
|---|---|---|---|
| Collapsing (water-hammer) | Rapid rise, rapid fall | AR, PDA, AV fistula, thyrotoxicosis, severe anaemia, Paget's | Raise patient's arm above heart level while palpating radial → feel a "slapping" pulse against your palm |
| Slow rising (parvus et tardus) | Gradual upstroke, delayed peak | Severe AS | Best felt at carotid; reduced volume + delayed peak |
| Bisferiens | Double systolic peak | Combined AS + AR, HOCM | Best felt at carotid |
| Jerky | Brisk upstroke, rapid collapse | HOCM | Due to dynamic LVOT obstruction |
| Pulsus alternans | Alternating strong/weak beats | Severe LV failure | Pathognomonic of LV failure [7] |
Corrigan's sign = visible pulsation of the carotid arteries in AR (the "dancing carotids") [1].
3.4 Blood Pressure and Special Tests
"Pulsus paradoxus" [1] — an exaggerated fall in systolic BP ( > 10 mmHg) during inspiration.
Mechanism: Normally, inspiration slightly reduces LV output (because increased venous return to RV causes interventricular septum to shift left, reducing LV filling). In cardiac tamponade or severe asthma, this effect is exaggerated.
How to measure: Inflate cuff above systolic pressure → slowly deflate → note pressure at which Korotkoff sounds are first heard only during expiration → continue deflating → note pressure at which sounds are heard throughout the cycle → difference is the pulsus paradoxus.
Causes: Cardiac tamponade (most classic), constrictive pericarditis, severe asthma/COPD, tension pneumothorax.
"Hypertensive retinopathy — Grade III, Grade IV" [1]
| Grade | Findings | Clinical Significance |
|---|---|---|
| I | Arteriolar narrowing, silver/copper wiring | Mild, chronic HT |
| II | AV nipping (arteriovenous crossing changes) | Moderate HT |
| III | Flame haemorrhages, cotton-wool spots, hard exudates | Severe HT, suggests end-organ damage |
| IV | Grade III + papilloedema | Malignant/accelerated HT — medical emergency |
"Orthostatic (postural) hypotension: with position change of supine to sitting, or sitting to standing, BP ↓ > 10 mmHg; HR ↑ > 20 beats/min" [1]
Note: The standard definition from most guidelines (and senior notes [7]) is ≥20 mmHg systolic fall or ≥10 mmHg diastolic fall within 2–5 minutes of standing. The lecture slide uses a slightly simplified threshold. For the exam, use the lecture's numbers first but be aware of the standard definition.
4. Jugular Venous Pressure (JVP)
The internal jugular vein (IJV) is used because it is in direct continuity with the right atrium — there are no valves between them. Therefore, the IJV column of blood acts as a manometer reflecting right atrial pressure.
Table from slide 30 [1]:
| Feature | Internal Jugular Vein (JVP) | Carotid Artery |
|---|---|---|
| Location | Lower and lateral | Deeper and medial |
| Contour | Double peak (a and v waves) | Single peak |
| Character | Not palpable | Forceful and palpable |
| Inspiration | More visible but mean pressure decreases | No change |
| Posture | Decreases with upright posture | No change |
| Compressibility | Obliterated by pressure | Cannot be obliterated |
| Abdominal compression | Transient increase in pressure | No effect |
High Yield Discriminator
If you can palpate it, it's the carotid, not the JVP. If it disappears with gentle pressure or rises with abdominal compression (hepatojugular reflux), it's the JVP.
"Changes in jugular venous pulse during respiration: Inspiration → lower level; Expiration → higher amplitude" [1]
Why? During inspiration, intrathoracic pressure becomes more negative → increased venous return to the right atrium → right atrium empties more effectively → JVP level falls. The reverse occurs during expiration. This is a normal finding.
Kussmaul's sign = paradoxical rise in JVP during inspiration. Seen in constrictive pericarditis, restrictive cardiomyopathy, and severe right heart failure, because the rigid pericardium/myocardium cannot accommodate the increased venous return.
"A wave: right atrial contraction, precedes carotid pulse. X descent: right atrial relaxation + passive pulling during RV systole. C wave: tricuspid valve closure. V wave: filling of RA during ventricular systole with TV closed, roughly synchronous with carotid pulse. Y descent: RA pressure drop during TV opening." [1]
| Wave | Timing | Mechanism | Mnemonic |
|---|---|---|---|
| a | Pre-systolic (before S1) | Atrial contraction | a = atrial |
| c | Early systole | Tricuspid valve closure (bulges into RA) | c = closure |
| x | Systole (descent) | Atrial relaxation + downward pulling of AV ring | |
| v | Late systole | Passive filling of RA against closed TV | v = venous filling |
| y | Early diastole (descent) | TV opens → blood rushes into RV |
"Giant A wave: ↓ RV compliance → forceful RA contraction. Causes: pulmonary hypertension, PV/TV stenosis. Cannon A wave: AV dissociation. Causes: complete heart block, atrial flutter, ventricular pacing, VT. Giant V wave: TV regurgitation. Absent A wave: atrial fibrillation." [1]
| Abnormality | Mechanism | Causes |
|---|---|---|
| Giant a wave | RA contracting against increased resistance | Pulmonary HT, PS, TS, RV hypertrophy |
| Cannon a wave | Atrium contracts against a closed tricuspid valve (AV dissociation) | Complete heart block, VT, ventricular pacing |
| Giant v wave | Blood regurgitates into RA during systole | Tricuspid regurgitation |
| Absent a wave | No coordinated atrial contraction | Atrial fibrillation |
Common Exam Trap
Giant a waves are regular (every beat has an oversized a wave). Cannon a waves are irregular (only occur when atrial contraction happens to coincide with a closed TV — this occurs randomly in complete heart block). Don't confuse them.
"Normal JVP ≤ 4.5 cm above the sternal angle at 45°. ↑ JVP ( > 4.5 cm): right ventricular failure, fluid overload, SVC obstruction. ↓ JVP: hypovolaemia, dehydration." [1]
Why 4.5 cm? The sternal angle is ~5 cm above the centre of the right atrium regardless of patient position. Normal RA pressure is ~5–8 cmH₂O, so the top of the blood column should be roughly at or just below the sternal angle (i.e. ≤3–4 cm above it). The 4.5 cm cutoff is therefore a clinical estimate of the upper limit of normal RA pressure.
"Constrictive pericarditis → sustained rise of venous pressure during hepato-jugular reflux. In the presence of impaired RV/LV filling, pressure applied to the liver causes a sustained rise of the venous pressure as the heart cannot handle the increased venous return." [1]
The test: press firmly on the liver for ≥10 seconds while watching the JVP. A transient rise ( < 3 seconds) is normal. A sustained rise indicates the right heart cannot handle the extra venous return — seen in constrictive pericarditis, right heart failure, and cardiac tamponade.
5. Precordium Examination
"Supine with head elevated 30–45°: Inspection → Palpation. Left lateral decubitus: Palpation (if needed) → Auscultation with bell at apex. Supine with head elevated: Auscultation with bell at LSB for S3/S4, diaphragm at all areas. Sitting, leaning forward with expiration: Auscultation with diaphragm at LSB." [1]
This sequence is designed to optimise detection of specific findings:
- Left lateral decubitus brings the apex closer to the chest wall → better for palpating the apex beat and hearing the low-pitched mid-diastolic rumble of mitral stenosis (using the bell).
- Sitting forward in expiration brings the heart closer to the anterior chest wall and reduces lung volume → better for hearing the early diastolic murmur of aortic regurgitation (using the diaphragm).
"Chest wall abnormalities, visible apex and hepatic pulsation, surgical scars" [1]
Look for:
- Median sternotomy scar → previous CABG or valve surgery
- Left lateral thoracotomy scar → mitral valve surgery, PDA ligation, coarctation repair
- Pacemaker/ICD bulge → usually left infraclavicular area
- Pectus excavatum (may shift the heart and cause a systolic murmur)
5.3 Palpation
"Displaced: > MCL and 5th ICS → cardiac enlargement. Tapping: palpable 1st HS → mitral stenosis. Sustained (heaving): LV hypertrophy. Hyperdynamic (thrusting): ↑ LV volume → volume overload, e.g. aortic regurgitation." [1]
| Apex Character | Mechanism | Condition |
|---|---|---|
| Normal | 5th ICS, MCL; brief, localised | Healthy heart |
| Displaced | LV dilatation pushes apex laterally and inferiorly | Any cause of LV enlargement (AR, DCM, MR) |
| Tapping | Palpable loud S1 | Mitral stenosis |
| Sustained/heaving | Prolonged systolic contraction against high pressure | LV hypertrophy (HT, AS) — "pressure overload" |
| Hyperdynamic/thrusting | Vigorous, non-sustained | Volume overload (AR, MR, high-output states) |
| Double impulse | Two distinct impulses per beat | HOCM |
Why can't you find the apex? Consider COPD (hyperinflation), obesity, pericardial effusion, dextrocardia. If not found in the supine position, turn the patient to the left lateral decubitus [1].
"Parasternal heave → RV volume or pressure overloading: ASD, PR, TR, PS, pulmonary HT; rarely left atrial lift due to MR" [1]
How to feel it: Place the heel of your hand on the left sternal edge. A sustained lift pushing your hand up during systole indicates RV hypertrophy/overload.
A thrill is a palpable murmur (grade ≥4). It indicates significant turbulence and therefore haemodynamically significant valvular disease. Feel at the apex, left sternal edge, and aortic/pulmonary areas.
"Right 2nd interspace — Aortic area. Left 2nd interspace — Pulmonic area. Left sternal border — right ventricular area. Apex — left ventricular area. Epigastric (subxiphoid)." [1]
These areas represent where murmurs from each valve are best heard — they do NOT correspond to the anatomical positions of the valves themselves.
6. Heart Sounds
"↑ S1: tachycardia, mitral stenosis, high cardiac output. ↓ S1: first-degree AV block, impaired LV contraction, mitral regurgitation. Varying S1: complete heart block and atrial fibrillation." [1]
Mechanism: S1 is produced by closure of the mitral and tricuspid valves at the onset of ventricular systole. The intensity depends on:
- Valve position at onset of systole — if valves are wide open (short PR interval, MS where high LA pressure keeps them open), they close with greater force → loud S1. If partially closed already (long PR, first-degree AV block), they close gently → soft S1.
- LV contractility — stronger contraction → louder S1. Impaired contractility → soft S1.
- Valve structure — calcified, immobile valve (late-stage MS) → eventually soft S1 despite previously being loud.
| S1 Change | Mechanism | Conditions |
|---|---|---|
| Loud | Valve wide open at start of systole | MS (pliable valve), tachycardia, short PR |
| Soft | Valve partially closed or poorly mobile | 1st degree AV block, severe MR, calcified MS |
| Variable | Changing PR interval or filling | Complete heart block, AF |
"↑ S2: pulmonary hypertension, ASD, dilated pulmonary artery. ↓ S2: aging, aortic stenosis/regurgitation, pulmonary stenosis." [1]
S2 has two components: A2 (aortic valve closure) and P2 (pulmonary valve closure). Normally A2 precedes P2, and the gap widens during inspiration (physiological splitting).
| Splitting Pattern | Mechanism | Condition |
|---|---|---|
| Normal/physiological | Inspiration → ↑RV filling → delayed P2 | Normal |
| Wide splitting | Delayed RV emptying | RBBB, PS |
| Fixed splitting | Constant RV volume regardless of respiration | ASD (L→R shunt equalises filling) |
| Reversed (paradoxical) | Delayed LV emptying → A2 comes after P2 | LBBB, severe AS, HOCM |
| Single S2 | Only one component heard | Severe AS (no A2), Eisenmenger (loud P2 only) |
| Loud P2 | Increased pulmonary artery pressure | Pulmonary hypertension |
"3rd HS → physiological in young person, rapid LV filling or heart failure (LV volume overload)" [1]
Mechanism: Occurs in early diastole during rapid passive ventricular filling. When the ventricle is distended and non-compliant, the sudden deceleration of blood produces a low-pitched sound. In young people, it is physiological because the ventricle fills rapidly.
- Heard with the bell at the apex in left lateral decubitus.
- Pathological S3 → heart failure, MR, AR, VSD — any cause of volume overload.
- S3 has high specificity ( > 90%) for HF but low sensitivity [8].
"4th HS → always pathological (atrial filling)" [1]
Mechanism: Occurs in late diastole when the atrium contracts forcefully against a stiff, non-compliant ventricle. The atrial "kick" pushes blood into the ventricle, producing a low-frequency sound.
- Always pathological (unlike S3 which can be physiological in the young).
- Causes: LVH (from HT, AS, HOCM), acute MI (stiff ischaemic ventricle), diastolic HF.
- Absent in AF — no coordinated atrial contraction = no S4.
"Gallop rhythm → heart failure" [1]
When S3 (or S4) is present with tachycardia, the three sounds (S1-S2-S3 or S4-S1-S2) produce a rhythm resembling a galloping horse. This is a clinical sign of heart failure.
"Mechanical heart sound — MV replacement, MV + AV replacement" [1]
Prosthetic valves (especially mechanical) produce audible clicks. A metallic click replacing S1 = prosthetic mitral valve. Metallic clicks replacing both S1 and S2 = prosthetic MV + AV.
7. Heart Murmurs
"Mechanism of murmur" — Turbulent blood flow through narrowed or incompetent valves, abnormal communications (septal defects), or increased flow across normal valves [1].
"Grading 1–6. Timing: systolic or diastolic (feel the carotid pulse). Characters: pitch (low, medium, high) & quality (blowing, harsh, musical, rumbling). Site of maximum propagation and radiation (axilla and neck). Effect of posture (left lateral and sitting). Effect of respiration (inspiration and expiration). Effect of manoeuvre (if needed)." [1]
Murmur grading 1–6 [1]:
| Grade | Description | Thrill? |
|---|---|---|
| 1 | Very faint, heard only after "tuning in" | No |
| 2 | Quiet but heard immediately on placing stethoscope | No |
| 3 | Moderately loud | No |
| 4 | Loud, with palpable thrill | Yes |
| 5 | Very loud with thrill, may be heard with stethoscope partly off chest | Yes |
| 6 | Very loud, heard with stethoscope entirely off chest | Yes |
Key Threshold
Grade ≥ 4 = thrill present. This is the discriminating line between grades 3 and 4. Thrills indicate haemodynamically significant disease.
7.4 Systolic Murmurs
"Aortic stenosis — radiate to carotids, slow upstroke, low volume pulse. Pulmonary stenosis. ASD — fixed splitting of S2, loud S2." [1]
ESMs are crescendo-decrescendo (diamond-shaped) and occur in mid-systole because they are generated by blood being ejected through a narrowed valve or across a normal valve with increased flow.
| Condition | Best Heard | Radiation | Key Associated Signs |
|---|---|---|---|
| Aortic stenosis | Aortic area (R 2nd ICS) | Carotids | Slow-rising pulse, narrow pulse pressure, soft A2 |
| Pulmonary stenosis | Pulmonary area (L 2nd ICS) | Left shoulder | RV heave, widely split S2 |
| ASD | Pulmonary area | — | Fixed splitting of S2, loud P2, RV heave |
| Flow murmur | LSE | — | Physiological in children, pregnancy, anaemia |
"Mitral regurgitation — radiate to axilla, loudest at axilla, soft S1. Tricuspid regurgitation — giant V wave, ↑ with inspiration. VSD — widely radiating, loudest at left sternal area, thrill." [1]
PSMs extend from S1 to S2 without a gap because there is a continuous pressure gradient between the chambers throughout systole (e.g. LV → LA in MR).
| Condition | Best Heard | Radiation | Key Associated Signs |
|---|---|---|---|
| MR | Apex | Axilla | Soft S1, displaced apex, S3 if severe |
| TR | Left lower sternal edge | Right sternal edge | Giant v wave in JVP, increases with inspiration (Carvallo's sign) |
| VSD | Left sternal edge (3rd–4th ICS) | Widely radiating | Thrill, loud PSM (small VSD louder than large VSD) |
7.5 Diastolic Murmurs
All diastolic murmurs are pathological — never physiological (unlike some systolic murmurs).
"Aortic regurgitation — blowing and high pitch, loudest at left sternal border, ejection systolic murmur, best with patient exhale and lean forward" [1]
AR produces an EDM because the regurgitant flow from aorta → LV occurs immediately after A2 closure, when the pressure gradient is highest, and then diminishes (decrescendo pattern).
"Mitral stenosis — rumbling and low pitch, loudest at apex, ↑ with exercise. Graham Steell murmur: PR (pulmonary regurgitation from pulmonary HT). Austin Flint murmur: AR (AR jet hits the anterior MV leaflet, mimicking MS)." [1]
The MS murmur is best heard with the bell in the left lateral decubitus position because it is low-pitched and localised to the apex.
| Murmur | Mechanism | How to Differentiate |
|---|---|---|
| Graham Steell | Functional PR from pulmonary HT (often secondary to severe MS) | High-pitched EDM at left upper sternal border; signs of pulmonary HT |
| Austin Flint | AR jet pushes MV leaflet → functional MS | Mid-diastolic rumble at apex in a patient with AR; no opening snap (unlike true MS) |
"PDA — cyanosis, left parasternal heave, collapsing pulse" [1]
A continuous murmur spans systole and diastole because the pressure gradient persists throughout the cardiac cycle (aortic pressure > pulmonary artery pressure in both systole and diastole in PDA).
Also called a "machinery murmur" — heard best at the left infraclavicular area.
| Valve Lesion | Timing | Character | Best Heard | Radiation | Special Features |
|---|---|---|---|---|---|
| AS | ESM | Harsh, crescendo-decrescendo | R 2nd ICS | Carotids | Slow-rising pulse, soft A2, S4 |
| PS | ESM | — | L 2nd ICS | Left shoulder | Wide split S2, RV heave |
| ASD | ESM | — | L 2nd ICS | — | Fixed split S2 |
| MR | PSM | Blowing | Apex | Axilla | Soft S1, displaced apex, S3 |
| TR | PSM | Blowing | LLSE | R sternal edge | Giant v wave, ↑ inspiration |
| VSD | PSM | Harsh | LLSE | Widely | Thrill |
| AR | EDM | Blowing, high-pitched | LLSE | — | Collapsing pulse, wide PP; sit forward, exhale |
| MS | Mid-diastolic | Rumbling, low-pitched | Apex | — | Loud S1, opening snap, malar flush; left lateral, bell |
| PDA | Continuous | Machinery | L infraclavicular | — | Collapsing pulse, differential clubbing (feet > hands) |
| HOCM | ESM | Harsh | LLSE | No radiation | Jerky pulse, double apex, S4, ↑ with Valsalva/standing |
8. Dynamic Manoeuvres
"Manoeuvres: lying, squatting, standing, Valsalva, isometric exercise" [1]
These change preload and/or afterload, modifying the intensity/duration of specific murmurs.
"HOCM: Ejection systolic murmur, no radiation, but increases with Valsalva manoeuvre and during squatting to standing, jerky pulse, double apex beat, S4" [1]
Why Valsalva increases HOCM murmur: Valsalva (straining against a closed glottis) reduces venous return → smaller LV cavity → the thickened interventricular septum is closer to the anterior MV leaflet → worsened LVOT obstruction → louder murmur.
Why squatting-to-standing increases it: Standing reduces preload (blood pools in legs) → same mechanism as above.
Conversely, squatting increases preload AND afterload → LV cavity larger → less obstruction → murmur quieter. This is the opposite of AS (where squatting increases the murmur because more blood flows through the fixed stenosis).
High Yield – Lecture MCQ 2
"Which condition is associated with increasing duration of the systolic murmur when the patient changes from supine to upright posture? Answer: Mitral valve prolapse → ↑ prolapse of mitral valve → ↑ murmur duration. (HOCM: ↑ murmur intensity. AS: ↓ murmur intensity.)" [1]
"Mitral Valve Prolapse" [1] — Classic finding: mid-systolic click followed by a late systolic murmur.
With standing/Valsalva (↓ preload) → LV smaller → MVP occurs earlier in systole → click moves closer to S1 → murmur duration increases (starts earlier, extends to S2).
With squatting (↑ preload) → LV bigger → MVP occurs later → click moves closer to S2 → murmur duration decreases.
Right-sided murmurs increase with inspiration (↑ venous return to right heart → ↑ flow → louder TR/PS murmur). This is Carvallo's sign for TR.
Left-sided murmurs increase with expiration (↑ pulmonary venous return to left heart + heart closer to chest wall).
| Manoeuvre | Effect on Preload | Effect on Afterload | HOCM | AS | MR | MVP |
|---|---|---|---|---|---|---|
| Valsalva (strain) | ↓ | ↓ | ↑ | ↓ | ↓ | Earlier click, longer murmur |
| Standing | ↓ | — | ↑ | ↓ | ↓ | Earlier click, longer murmur |
| Squatting | ↑ | ↑ | ↓ | ↑ | ↑ | Later click, shorter murmur |
| Inspiration | ↑ (R heart) | — | — | — | — | Right-sided murmurs ↑ |
| Isometric exercise (handgrip) | — | ↑ | ↓ | ↓ | ↑ | — |
The HOCM Rule
HOCM is the rebel: it gets louder when most other murmurs get softer (with Valsalva and standing). This is a classic MCQ discriminator. The reason is that HOCM's obstruction is dynamic — it depends on cavity size — whereas AS's obstruction is fixed and depends on flow volume.
9. Ancillary Examinations
"Examination of the lungs: bilateral basal crackles → heart failure. Examination of the abdomen: pulsatile and enlarged liver → TR. Measurement of arterial BP with sphygmomanometer. If indicated, check orthostatic (postural) hypotension." [1]
Bilateral basal fine inspiratory crackles (crepitations) indicate pulmonary oedema from left heart failure. Wheezing ("cardiac asthma") can also occur.
- Hepatomegaly — right heart failure (congestive hepatomegaly).
- Pulsatile liver — tricuspid regurgitation (systolic pulsation transmitted through the hepatic veins).
- Ascites — severe right heart failure.
- Splenomegaly — infective endocarditis.
Always measure in both arms. A disparity > 15 mmHg suggests subclavian stenosis, aortic dissection, or coarctation [4].
Complete the examination by palpating all peripheral pulses (already described in Section 3) to assess for peripheral arterial disease.
As Ryan Ho's notes summarise [9], the aim of the CVS examination is to reach:
- Rhythm diagnosis (e.g. AF)
- Anatomical diagnosis (e.g. mitral stenosis)
- Aetiological diagnosis (e.g. rheumatic heart disease)
- Functional diagnosis (e.g. in right heart failure / NYHA class)
| Related GC Topic | Connection to CVS PE |
|---|---|
| GC 032 / Block A - Chest pain on exertion [4] | PE in IHD: assess risk factors (xanthomata, acanthosis nigricans, Frank sign), complications (S3/S4, displaced PMI, basal crackles), and other causes of angina (AS murmur, HOCM, pulmonary HT) |
| GC 028 - Accelerating chest pain [10] | Same PE table as GC 032; acute setting adds checking for arrhythmias, ischaemic MR, low-output failure |
| GC 058 - High blood pressure [11] | PE for hypertension: BP in both arms, fundoscopy, BMI, peripheral pulses, CVS exam; assess target organ damage |
| GC 050 - Fever and murmur [5] | IE signs (splinter, Osler, Janeway, Roth spots); valvular lesion auscultation; dental exam |
| GC 089 - Syncope and irregular heartbeat [12] | Pulse (rate, rhythm), orthostatic BP, carotid sinus massage, cardiac auscultation for AS/HOCM |
Likely Exam Questions
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A 25-year-old woman with Turner syndrome is found to have BP 165/90 mmHg. On examination, there is radiofemoral delay. What is the most likely diagnosis? → Coarctation of aorta.
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A patient with a systolic murmur is asked to perform a Valsalva manoeuvre. The murmur increases in intensity. What is the most likely diagnosis? → HOCM (the only common murmur that increases with Valsalva).
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A 60-year-old man with AF and breathlessness has a mid-diastolic rumbling murmur best heard at the apex with the patient in the left lateral decubitus position. What is the diagnosis? → Mitral stenosis.
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On JVP examination, cannon a waves are observed. Which rhythm disturbance is most consistent? → Complete heart block (AV dissociation → atrium contracts against closed TV intermittently).
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A patient with known PDA has clubbing of the toes but not the fingers. Why? → Deoxygenated blood from PA enters aorta distal to left subclavian artery → only lower limbs are cyanosed/clubbed.
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What is the most specific physical sign for heart failure? → S3 gallop (specificity > 90%) [8].
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Describe the technique for examining the JVP. How do you distinguish it from the carotid pulse? List 4 causes of raised JVP. (4–5 marks)
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A patient has an early diastolic murmur at the left sternal border. Describe the optimal position for auscultation. What are the expected pulse and blood pressure findings? → Sit forward, exhale. Collapsing pulse, wide pulse pressure (AR).
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Grade the following murmur: loud, with a palpable thrill, heard with the stethoscope on the chest. → Grade 4.
Active Recall - CVS Physical Examination
High Yield Summary
CVS physical examination is a systematic head-to-toe assessment: IPPEC → General Inspection (facies, hands for clubbing and IE signs, oedema) → Arterial system (all pulses bilaterally, rate/rhythm/volume/character, radiofemoral delay for coarctation, collapsing pulse for AR) → JVP (distinguish from carotid via 6 features; height at 45 degrees, normal less than or equal to 4.5 cm; waveform — giant a in pulmonary HT, cannon a in AV dissociation, giant v in TR, absent a in AF) → Precordium (inspect for scars/deformity; palpate apex character and location, heave, thrills; auscultate S1/S2 variations, S3/S4, murmurs) → Murmurs described by grading 1–6, timing, character, site, radiation, posture, respiration, manoeuvres → HOCM is the rebel murmur that increases with Valsalva/standing → MVP click moves earlier and murmur lengthens with standing → Ancillary exams: lung crackles for HF, pulsatile liver for TR, BP both arms, orthostatic BP. Always think bidirectionally: systemic diseases cause CVS signs and CVS diseases cause systemic signs.
[1] Lecture slides: CFB (MED06) Cardiovascular (II) Physical Examination.pdf [2] Past papers: 2023 Fourth Summative MCQ.pdf [3] Past papers: 2024 Fourth Summative MCQ.pdf [4] GC lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (p30) [5] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p437–439) [7] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p317, p362) [8] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf (p7) [9] Senior notes: Ryan Ho Cardiology.pdf (p4); Ryan Ho Fundamentals.pdf (p21) [10] GC lecture slides: GC 028. Accelerating chest pain_Acute coronary.pdf (p19) [11] GC lecture slides: GC 058. High Blood Pressure.pdf (p31) [12] Senior notes: Block A - Syncope and irregular heartbeat_ Cardiac arrhythmia; Heart blocks, Bradycardia.pdf (p7)
CFB MED05 Cardiovascular (i) Physical Examination (history Taking)
Cardiovascular history taking is the systematic collection of a patient's symptoms, risk factors, and relevant medical background—including chest pain, dyspnea, palpitations, syncope, and peripheral edema—to guide the clinical assessment of heart and vascular disease.
CFB MED04 Central Nervous System
The central nervous system comprises the brain and spinal cord, serving as the primary integration and command center for processing sensory information, coordinating motor output, and governing higher cognitive functions.