Cardiovascular system examination

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Cardiovascular System Examination

A systematic cardiovascular exam proceeds through general inspection → vital signs → jugular venous pressure → arterial pulse → precordial examination → auscultation. Each step provides distinct hemodynamic information that cannot be replaced by technology alone.

1. General Inspection

Look for signs that suggest underlying cardiac disease before touching the patient:
  • Dyspnoea at rest, orthopnoea - raised JVP, left heart failure
  • Malar flush - mitral stenosis
  • Cyanosis - central (lips, tongue) vs. peripheral (fingertips)
  • Clubbing - congenital cyanotic heart disease, infective endocarditis
  • Splinter haemorrhages, Osler nodes, Janeway lesions - infective endocarditis
  • Xanthelasma / corneal arcus - hyperlipidaemia
  • Marfanoid habitus - aortic root dilatation, mitral valve prolapse
  • Raised BMI, cushingoid features - hypertension risk

2. Blood Pressure

Accurate measurement requires: seated position, arm at heart level, feet flat, 5-10 min rest, appropriately sized cuff (bladder length 80%, width 40% of arm circumference). Inflate 30 mmHg above expected systolic; release at 2-3 mmHg/s. Systolic = first Korotkoff sound (K1); diastolic = disappearance (K5).
Common errors: using a small cuff overestimates BP; a large cuff underestimates it.
Measure both arms. A difference >15 mmHg between arms suggests subclavian stenosis or aortic dissection.
Special patterns:
PatternSignificance
Wide pulse pressureChronic severe AR, hyperthyroidism, anaemia
Narrow pulse pressureSevere AS, tamponade, severe LV dysfunction
Orthostatic drop (>20/10 mmHg)Volume depletion, autonomic neuropathy

3. Jugular Venous Pressure (JVP)

The JVP is the single most important bedside measurement for estimating volume status. The internal jugular vein is preferred (directly in line with SVC and right atrium; the external jugular is valved).
Technique: Position patient at 30-45°; identify the double waveform of the internal jugular. Measure the vertical distance from the sternal angle (angle of Louis) to the top of the pulsation. A distance >4.5 cm at 30° is abnormal. Note: bedside estimates are in cmH₂O - convert to mmHg (1.36 cmH₂O = 1 mmHg).
When elevated JVP is suspected, sit the patient upright with legs dangling - venous pulsation above the clavicle in this position is clearly abnormal.
JVP vs. Carotid:
FeatureJVPCarotid
WaveformBiphasic (sinus rhythm)Monophasic
CompressibleYes (obliterated by pressure)No
Varies with posture/inspirationYesNo

JVP Waveform Components

Jugular venous pulse waveforms showing normal, tricuspid regurgitation, and constrictive pericarditis patterns
Wave/DescentTimingMechanismAbnormality
a wavePre-systole (after P wave, before S1)Right atrial contractionProminent in reduced RV compliance (PS, pulmonary HTN); absent in AF
c waveEarly systoleTricuspid valve pushed into RA during RV contractionUsually not visible clinically
x descentSystoleRA relaxation + tricuspid valve moves toward RV apexAttenuated/abolished in tricuspid regurgitation
v waveLate systoleRA filling while tricuspid valve is closedGiant v wave in tricuspid regurgitation
y descentEarly diastoleTricuspid valve opens; RA emptiesRapid/sharp y descent in constrictive pericarditis (+ pericardial knock)
Cannon a waves (giant a waves) - seen when RA contracts against a closed tricuspid valve - hallmark of AV dissociation (ventricular tachycardia, complete heart block).
Kussmaul's sign - paradoxical rise (or failure to fall) of JVP on inspiration - seen in constrictive pericarditis, restrictive cardiomyopathy, right heart failure.
Abdominojugular reflux (hepatojugular reflux) - sustained JVP rise >3 cm with 10 s of firm abdominal pressure - positive in elevated right or left heart filling pressures.
An elevated JVP (RA pressure >10 mmHg) has an 88% positive predictive value for a pulmonary artery wedge pressure >22 mmHg, and carries independent prognostic significance in heart failure.

4. Arterial Pulse

Assess the radial pulse first (rate, rhythm, volume, character), then the carotid for character/waveform (never compress both simultaneously), then peripheral pulses systematically.
Rate: Normal 60-100 bpm. Bradycardia <60; tachycardia >100.
Rhythm: Regular vs. irregularly irregular (AF) vs. regularly irregular (2nd-degree AV block, bigeminy).
Pulse character (best felt at the carotid):
PulseCharacterCauses
NormalSmooth upstroke, single peak-
Pulsus parvus et tardus (small/slow rising)Weak, delayed, prolonged upstroke; anacrotie notch may be feltSevere aortic stenosis
Collapsing (Corrigan's / water-hammer)Sharp rise, rapid collapseChronic severe AR, PDA, hyperdynamic states
BisferiensTwo systolic peaksSevere AR (±AS), HOCM
Pulsus paradoxusSystolic BP falls >10 mmHg on inspirationCardiac tamponade, massive PE, severe obstructive lung disease
Pulsus alternansBeat-to-beat variation in amplitude, regular rhythmSevere LV systolic dysfunction
Pulsus paradoxus measurement: inflate cuff above systolic; lower slowly; note the pressure at which Korotkoff sounds first appear (expiration only) and the pressure at which they are heard throughout the cycle. Difference >10 mmHg = positive.

5. Precordial Examination

Inspection

  • Visible apex beat - hyperdynamic states, LV enlargement
  • Visible pulsations - right parasternal (RV hypertrophy or ascending aortic aneurysm), pulmonary area (pulmonary HTN)
  • Chest wall deformities - pectus excavatum, scoliosis

Palpation

Apex beat:
  • Normal location: 5th intercostal space, midclavicular line
  • Displaced laterally and/or inferiorly - LV dilation
  • Hyperdynamic/thrusting - volume overload (AR, MR, VSD)
  • Heaving/sustained - pressure overload (AS, hypertension)
  • Tapping - palpable S1 in mitral stenosis
  • Double impulse - HOCM (palpable S4)
Right ventricular heave (parasternal lift): left parasternal area lifts the palm - RV hypertrophy or RV volume overload.
Thrills: palpable murmurs (grade ≥4/6). Systolic thrill at the right upper sternal border = AS or sub-AS; thrill at the left lower sternal border = VSD; apical systolic thrill = MR.
Palpable heart sounds:
  • Palpable P2 at pulmonary area = pulmonary hypertension
  • Palpable S4 at apex = reduced LV compliance

6. Auscultation

Position the patient supine initially; roll to left lateral decubitus for mitral sounds; sit forward, exhale for aortic sounds. Use the diaphragm (high frequencies) and bell lightly applied (low frequencies - S3, S4, MS rumble).
Auscultate in sequence: aortic area (2nd right ICS), pulmonary area (2nd left ICS), tricuspid area (lower left sternal border), mitral area (apex).

Heart Sounds

S1 (first heart sound)
  • Closure of mitral (M1) then tricuspid (T1) valves
  • Loud S1: tachycardia, mitral stenosis (pliable valve), short PR interval, hyperdynamic states
  • Soft S1: long PR interval, severe MR, calcified immobile mitral valve, poor LV function
  • Variable S1: AF (variable RR), complete heart block (PR changes)
S2 (second heart sound)
  • Closure of aortic (A2) then pulmonary (P2) valves
  • Physiological splitting: increases on inspiration (delayed P2 as RV stroke volume increases)
  • Wide fixed splitting: ASD (fixed), RBBB (delayed P2), pulmonary stenosis
  • Wide splitting with respiratory variation: RBBB, RV failure
  • Paradoxical (reversed) splitting: A2 delayed, splits on expiration - LBBB, severe AS, HOCM
  • Loud P2: pulmonary hypertension
  • Soft A2: severe AS
S3 (third heart sound / ventricular gallop)
  • Low-pitched; heard with bell at apex (left-sided) or LLSB (right-sided)
  • Timing: early diastole, just after S2 - rapid filling phase
  • Pathological in adults - indicates elevated filling pressures, reduced LV compliance; seen in HF, dilated cardiomyopathy, MR, VSD
  • Physiological in children, young adults, pregnancy, athletes
S4 (fourth heart sound / atrial gallop)
  • Low-pitched; heard just before S1
  • Produced by atrial contraction into a stiff, non-compliant ventricle
  • Seen in: LVH (hypertension, HCM, AS), ischaemia, acute MI
  • Never heard in AF (no organized atrial contraction)
Additional sounds:
SoundTimingCause
Ejection clickEarly systole, just after S1Bicuspid aortic valve (aortic EC), pulmonary stenosis (pulmonary EC, decreases on inspiration)
Mid-systolic clickMid-late systoleMitral valve prolapse (moves earlier on standing)
Opening snap (OS)Early diastole, after S2Mitral stenosis (pliable valve). Short A2-OS interval = more severe MS
Pericardial knockEarly diastoleConstrictive pericarditis (coincides with rapid y descent of JVP)
Pericardial rubSystolic + diastolic (three-component)Pericarditis (best heard leaning forward, end-expiration)
Prosthetic valve soundsMetallic opening/closing clicksMechanical prostheses

Murmurs

Characterise each murmur by: timing - location - radiation - intensity (Levine grade) - quality - pitch - response to manoeuvres.
Levine grading:
GradeDescription
1/6Heard only with special effort
2/6Soft but heard immediately
3/6Moderately loud, no thrill
4/6Loud + thrill
5/6Heard with stethoscope barely on chest
6/6Heard without stethoscope

Systolic Murmurs

MurmurTimingLocation/RadiationQualityKey Features
Aortic stenosisEjection (mid-systolic)RUSB → carotidHarsh, crescendo-decrescendoSoft/absent A2; slow-rising pulse; Gallavardin phenomenon (musical quality at apex)
HOCMEjection (mid-systolic)LLSB (no carotid radiation)HarshIncreases with Valsalva/standing; decreases with squatting
Pulmonary stenosisEjection (mid-systolic)LUSBHarshEjection click; wide splitting of S2; louder on inspiration
Mitral regurgitationHolosystolicApex → axillaBlowingSoft S1; often S3; radiates to axilla
Tricuspid regurgitationHolosystolicLLSBBlowingLouder on inspiration (Carvallo's sign); giant v wave in JVP
VSDHolosystolicLLSBHarshThrill common; small VSD louder (maladie de Roger)
MVPLate systolicApexMid-systolic click + late systolic murmur; click moves earlier with standing

Diastolic Murmurs (always pathological)

MurmurTimingLocationQualityKey Features
Aortic regurgitationEarly diastolic (decrescendo)Left sternal edgeBlowing, high-pitchedHeard best leaning forward, exhaling; wide pulse pressure; collapsing pulse
Pulmonary regurgitationEarly diastolicLUSBGraham Steell murmur (pulmonary HTN-associated)
Mitral stenosisMid-diastolic (rumble) + presystolic accentuationApex (LLD position, bell)Low-pitched rumbleOpening snap precedes; presystolic accentuation disappears in AF
Tricuspid stenosisMid-diastolicLLSBLow-pitchedAccentuated by inspiration

Continuous Murmurs

  • Patent ductus arteriosus (PDA): machinery murmur, peaks at S2, heard at left infraclavicular area
  • Arteriovenous fistula, venous hum (children; abolished by jugular compression)

Dynamic Auscultation - Manoeuvres

ManoeuvreHaemodynamic effectIncreasesDecreases
Valsalva (straining phase)Decreased venous return, decreased LV sizeHOCM, MVP click (earlier)Most other murmurs
SquattingIncreased venous return + afterloadMost murmursHOCM, MVP
StandingDecreased venous returnHOCM, MVP (earlier click)Most murmurs
InspirationIncreased right heart fillingRight-sided murmurs (TR, PS, TS)Left-sided murmurs
HandgripIncreased afterloadMR, AR, VSDHOCM, AS
Passive leg raiseIncreased venous returnMost murmursHOCM
Amyl nitriteDecreased afterload, tachycardiaAS, HOCM, PS, TSMR, AR, VSD

7. Peripheral Signs of Specific Conditions

SignCondition
Corrigan's pulse (carotid)Severe AR
De Musset's sign (head nodding)Severe AR
Quincke's sign (capillary pulsation in nails)Severe AR
Duroziez's sign (femoral bruit)Severe AR
Hill's sign (popliteal systolic BP >20 mmHg above brachial)Severe AR
Ankle oedemaRight heart failure, venous insufficiency
Sacral oedemaRight heart failure (bed-bound patients)
Hepatomegaly (pulsatile)Tricuspid regurgitation
SplenomegalyInfective endocarditis, congestive cardiac failure

Summary: Systematic Approach

  1. General inspection - habitus, signs of syndromes, peripheral stigmata
  2. Vital signs - HR, BP (both arms), SpO₂, respiratory rate
  3. Hands - clubbing, splinter haemorrhages, peripheral cyanosis, radial pulse
  4. Face/neck - malar flush, corneal arcus, xanthelasma, JVP
  5. Carotid pulse - character and volume
  6. Precordium - inspect, palpate (apex beat, heaves, thrills), percuss (cardiac dullness)
  7. Auscultation - S1, S2, added sounds, murmurs (all areas; dynamic manoeuvres as needed)
  8. Lung bases - bibasal crepitations (pulmonary oedema)
  9. Abdomen - hepatomegaly, splenomegaly, pulsatile aorta, ascites
  10. Lower limbs - peripheral pulses, oedema, signs of peripheral arterial disease

Sources: Harrison's Principles of Internal Medicine, 22nd ed. (2025), pp. 1904-1908 | Fuster and Hurst's The Heart, 15th ed., Ch. 3
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