Here is a comprehensive guide to the Cardiovascular System Examination, synthesized from Harrison's and Goldman-Cecil Medicine.
Cardiovascular System Examination
1. General Approach & Vital Signs
Before the focused cardiac exam, note:
- Pulse rate and rhythm — tachycardia, bradycardia, or irregularity
- Blood pressure (both arms) — a discrepancy suggests aortic dissection or atherosclerotic disease of the great vessels; if coarctation is suspected, measure in a leg as well
- Pulsus paradoxus — >10 mmHg drop in systolic BP on inspiration is typical of pericardial tamponade
- Respiratory rate — tachypnoea and laboured breathing suggest pulmonary oedema; Cheyne-Stokes respirations indicate advanced heart failure
General appearance may reveal clues: Marfan syndrome, Turner syndrome, Down syndrome, or systemic conditions like hyperthyroidism (exophthalmos), myotonic dystrophy (ptosis, AV block), or scleroderma.
2. Ophthalmologic Examination
| Finding | Association |
|---|
| Diabetic/hypertensive retinopathy | Diabetes, hypertension |
| Roth spots | Infective endocarditis |
| Retinal artery beading | Severe hypercholesterolaemia |
| Blue sclerae | Osteogenesis imperfecta → aortic dilation, MVP |
| Retinal artery occlusion | Left atrial thrombus, myxoma, atherosclerotic emboli |
| Exophthalmos | Hyperthyroidism |
3. Jugular Venous Pressure (JVP) & Waveform
The JVP is the single most important bedside measurement for estimating volume status. The internal jugular vein is preferred (the external jugular is valved and not directly in line with the SVC/RA). Venous pulsations above the clavicle in the sitting position are clearly abnormal (the clavicle-to-RA distance is ≥10 cm).
A distance >4.5 cm above the sternal angle (angle of Louis) at 30° elevation is considered elevated. Note: bedside estimates are in cmH₂O; convert to mmHg by dividing by 1.36.
JVP Waveform Components
| Component | Mechanism | Clinical pearl |
|---|
| a wave | Right atrial presystolic contraction (after P wave, before S1) | Absent in AF; cannon a wave = AV dissociation (VT vs SVT discriminator) |
| c wave | Tricuspid valve pushed into RA during early systole | Small, often not visible |
| x descent | Fall in RA pressure after tricuspid opens | Prominent in tamponade |
| v wave | Atrial filling during ventricular systole | Accentuated in tricuspid regurgitation |
| y descent | Tricuspid opens → ventricular filling | Rapid y descent in constrictive pericarditis; absent/blunted in tamponade |
Distinguishing venous from arterial pulsation: The venous waveform is usually biphasic (vs monophasic carotid), changes with posture and inspiration, and is obliterable with gentle pressure.
4. Arterial Pulse
Assess the carotid pulse for volume, contour, and timing:
| Pulse character | Significance |
|---|
| Pulsus bisferiens (double peak in systole) | Severe AR ± AS, HOCM |
| Pulsus alternans | Severe LV dysfunction |
| Pulsus paradoxus (>10 mmHg inspiratory drop) | Cardiac tamponade, severe asthma |
| Small, slow-rising (parvus et tardus) | Aortic stenosis |
| Bounding, collapsing | Aortic regurgitation, hyperdynamic states |
| Pulsus bigeminus | Bigeminal ectopy |
5. Precordial Inspection & Palpation
- Apex beat (Point of Maximal Impulse, PMI): Normally in the 5th intercostal space, mid-clavicular line. A laterally displaced impulse indicates LV dilatation; a sustained impulse suggests LV hypertrophy.
- Right ventricular heave/lift at the lower left sternal border suggests RV enlargement (e.g., pulmonary hypertension, RV failure).
- Thrills are palpable murmurs (grade ≥4/6) — felt over aortic/pulmonary areas or at the apex.
- A loud P2 that can be palpated at the 2nd left interspace suggests pulmonary hypertension.
6. Auscultation
Auscultatory Areas
- Aortic area — 2nd right intercostal space
- Pulmonary area — 2nd left intercostal space
- Tricuspid area — lower left sternal border
- Mitral area (apex) — 5th ICS, mid-clavicular line
First Heart Sound (S1)
- Caused by mitral (M1) and tricuspid (T1) valve closure
- Loud S1 → MS with pliable leaflets, hyperdynamic states
- Soft S1 → Long PR interval, severe MS with calcified leaflets, LV dysfunction
- Variable S1 → AF, complete heart block (cannon beat)
Second Heart Sound (S2)
- A2 (aortic closure) precedes P2 (pulmonary closure)
- Physiologic splitting: widens on inspiration (increased RV filling delays P2); narrows on expiration
| S2 Pattern | Cause |
|---|
| Fixed splitting | Atrial septal defect (ASD) |
| Wide splitting | RBBB, pulmonary stenosis |
| Reversed/paradoxical splitting | LBBB, RV pacing, severe AS, HOCM, acute ischaemia (components audible on expiration, narrow on inspiration) |
| Narrow/single S2 | Pulmonary hypertension (loud P2 ≥ A2) |
| Absent P2 | Severe pulmonary stenosis |
Added Sounds
Systolic:
- Ejection click (early systolic, high-pitched) → bicuspid aortic or pulmonary valve; pulmonic ejection sound is the only right-sided event that decreases with inspiration
- Non-ejection click (mid-systolic click) → MVP; click-murmur complex moves away from S1 on squatting (increased preload) and toward S1 on standing
Diastolic:
| Sound | Timing | Cause | Key feature |
|---|
| Opening snap (OS) | Early diastole, after S2 | Mitral stenosis | A2-OS interval inversely proportional to severity (shorter = higher LAP) |
| S3 (ventricular gallop) | Early diastole | Elevated LVEDP, severe LV dysfunction | Low-pitched, at apex; normal in young adults; correlated with poor prognosis |
| S4 (atrial gallop) | Late diastole (presystolic) | Reduced LV compliance (HTN, ischaemia) | Low-pitched; indicates diastolic dysfunction; absent in AF |
| Pericardial knock | Early diastole, after OS | Constrictive pericarditis | High-pitched; exaggerated y descent in JVP |
| Tumour plop | Diastolic | Atrial myxoma | Positional |
Heart Murmurs
Systolic murmurs:
| Murmur | Character | Best heard | Radiation | Dynamic clues |
|---|
| Aortic stenosis (AS) | Harsh, crescendo-decrescendo | 2nd RSB | Neck (carotids) | Louder with squatting; softer with Valsalva |
| HOCM | Crescendo-decrescendo | LLSB | — | Louder with Valsalva/standing; softer with squatting |
| Mitral regurgitation (MR) | Holosystolic, blowing | Apex | Axilla/back | — |
| Tricuspid regurgitation (TR) | Holosystolic | LLSB | — | Increases with inspiration (Carvallo's sign) |
| MVP | Late systolic ± click | Apex | — | Click moves to S1 on standing |
| VSD | Holosystolic, harsh | LLSB | — | — |
| Pulmonary stenosis | Ejection systolic | 2nd LSB | — | Ejection click that softens on inspiration |
Diastolic murmurs (always pathological):
| Murmur | Character | Best heard | Radiation | Dynamic clues |
|---|
| Aortic regurgitation (AR) | Early diastolic, blowing, decrescendo | 3rd LSB (leaning forward, expiration) | — | Austin Flint murmur at apex |
| Mitral stenosis (MS) | Mid-diastolic, low-pitched rumble | Apex (bell) | — | Louder with left lateral decubitus + exercise |
| Tricuspid stenosis (TS) | Mid-diastolic | LLSB | — | Increases with inspiration |
| Pulmonary regurgitation | Early diastolic | 2nd/3rd LSB | — | Graham Steell murmur in PAH |
Dynamic auscultation manoeuvres:
| Manoeuvre | Effect | Useful for |
|---|
| Valsalva (strain phase) | ↓ preload | HOCM louder; MVP click earlier; others softer |
| Squatting | ↑ preload + afterload | HOCM softer; MVP click later |
| Standing | ↓ preload | HOCM louder; MVP click earlier |
| Inspiration | ↑ RV filling | Right-sided murmurs louder (TR, TS, PS) |
| Leg raising | ↑ preload | Similar to squatting |
| Amyl nitrite | ↓ afterload | AS louder; AR softer |
| Handgrip | ↑ afterload | MR, AR, VSD louder; HOCM softer |
7. Peripheral Examination
Abdomen
- Hepatomegaly — right heart failure; an enlarged pulsatile liver = severe tricuspid regurgitation / markedly elevated right heart pressure
- Ascites — advanced right heart failure
- Abdominal aorta pulsation — screen for AAA in appropriate patients
Extremities
- Pitting oedema — dependent; graded 0–3+; from elevated right-sided filling pressures → increased hydrostatic pressure → transudation; must exclude other causes (calcium channel blockers, venous insufficiency, hypoproteinaemia)
- Cool extremities → low cardiac output or peripheral arterial disease
- Clubbing → cyanotic congenital heart disease, infective endocarditis
- Peripheral cyanosis → low cardiac output; central cyanosis (tongue) → right-to-left shunt, respiratory failure
- Splinter haemorrhages, Osler nodes, Janeway lesions → infective endocarditis
- Xanthelasma, corneal arcus → hyperlipidaemia
Summary: Structured Examination Sequence
- General appearance (dyspnoea, cyanosis, pallor, syndromic features)
- Vital signs (HR, BP both arms, RR, SpO₂)
- Hands (clubbing, cyanosis, splinters, peripheral pulses)
- Face/eyes (retinal changes, malar flush of MS, xanthelasma)
- Neck (JVP waveform and height, carotid pulse character)
- Precordium — inspect, palpate (apex, heaves, thrills), auscultate (S1, S2, added sounds, murmurs) with dynamic manoeuvres
- Lung bases (bibasal crepitations → pulmonary oedema; pleural effusion → heart failure)
- Abdomen (hepatomegaly, ascites, aortic pulsation)
- Legs (oedema, temperature, peripheral pulses)
- Completion: request BP lying/standing, 12-lead ECG, CXR, bedside echo
Sources: Harrison's Principles of Internal Medicine 22E (2025), p. 1904–1908; Goldman-Cecil Medicine, International Edition, p. 391