Make notes on cardiovascular system examinations in detailed from Hutchison clinical book (like all the of pulse and heave with demonstration images , how to perform) correlate with the disease

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Note on sources: Hutchison's Clinical Methods is not currently in the available library. The notes below are compiled from the three most authoritative alternatives available: Harrison's Principles of Internal Medicine 22E, Fuster and Hurst's The Heart 15th Edition, and Goldman-Cecil Medicine - all of which cover the same Hutchisonian physical examination framework in even greater depth.

Cardiovascular System Examination - Comprehensive Notes

OVERVIEW: SEQUENCE OF EXAMINATION

Step	Component
1	General inspection - appearance, cyanosis, clubbing, edema
2	Blood pressure measurement (both arms)
3	Arterial pulse - rate, rhythm, volume, character
4	Jugular venous pressure (JVP) and waveform analysis
5	Precordial inspection and palpation (apex beat, heaves, thrills)
6	Cardiac auscultation (heart sounds, added sounds, murmurs)
7	Peripheral vascular assessment

PART 1: GENERAL INSPECTION

Before touching the patient, observe:

Cyanosis - central (lips, tongue) vs peripheral (fingers)
- Central: Eisenmenger's, Fallot's, pulmonary hypertension
- Peripheral: low cardiac output, heart failure
Clubbing - infective endocarditis, cyanotic congenital heart disease
Malar flush - mitral stenosis (MS) with low cardiac output
Pallor - anaemia (high-output states), cardiogenic shock
Xanthelasma / xanthomata - hypercholesterolaemia, premature IHD
Corneal arcus - if <50 years, suggests dyslipidaemia
Marfanoid habitus - tall, arachnodactyly, high arched palate - aortic root dilatation, AR, MVP
Edema - bilateral pitting pedal edema + elevated JVP = right heart failure / cor pulmonale

PART 2: BLOOD PRESSURE

Technique

Patient seated, arm at heart level, supported, back supported, feet on floor
Wait 5-10 minutes before measuring
Cuff bladder: length 80%, width 40% of arm circumference (use correct cuff size - too small overestimates BP)
Inflate 30 mmHg above expected systolic, deflate at 2-3 mmHg/sec
Systolic = first Korotkoff sound (Phase I); Diastolic = disappearance (Phase V)
Measure both arms - normal difference <10 mmHg

Abnormal Findings

Finding	Disease Correlation
Both arms differ >10 mmHg	Subclavian artery stenosis, aortic dissection, coarctation of aorta
Wide pulse pressure	Severe AR, hypertension (elderly), PDA, AV fistula
Narrow pulse pressure	Shock, severe AS, cardiac tamponade
Leg BP lower than arm	Coarctation of aorta (normally legs are 20 mmHg higher)

Pulsus Paradoxus

A fall in systolic BP >10 mmHg on inspiration.

How to measure:

Inflate cuff 15-20 mmHg above systolic
Deflate slowly while patient breathes normally
Note the pressure at which sounds first appear (expiratory) and the pressure at which sounds are heard continuously through both phases
Difference >10 mmHg = pulsus paradoxus

Diseases: Cardiac tamponade (classic), constrictive pericarditis, massive PE, severe asthma, tension pneumothorax, hemorrhagic shock

Pulsus Alternans

Beat-to-beat variation in pulse amplitude - every other Korotkoff sound is audible as the cuff is slowly deflated.

Disease: Severe LV systolic dysfunction (heart failure)

PART 3: ARTERIAL PULSE

Technique

Palpate the carotid artery for character and contour (most reliable). Alternatively palpate the brachial artery - rest the patient's elbow on your palm, palpate the vessel with your thumb; brachial pulse is deeper.

Assess simultaneously:

Rate and rhythm
Volume (amplitude)
Character (upstroke velocity, waveform contour)
Peripheral pulse equality

Normal and abnormal arterial pulse waveform patterns in various disease states

Figure: Normal arterial pulse waveform and abnormal patterns seen in various diseases - Fuster and Hurst's The Heart, 15th Edition

Named Pulse Abnormalities and Disease Correlations

Carotid pulse waveform configurations and differential diagnoses with heart sounds

Figure: Carotid pulse waveform configurations - A. Normal, B. Aortic stenosis (anacrotic/parvus et tardus), C. Bisferiens (severe AR), D. Bisferiens in HOCM (spike-and-dome), E. Dicrotic pulse (sepsis, shock) - Harrison's Principles 22E

Pulse Type	Character	Disease
Pulsus parvus et tardus	Weak volume + slow delayed upstroke	Severe aortic stenosis (AS)
Anacrotic pulse	Notch on ascending limb; slow interrupted upstroke	Severe aortic stenosis
Corrigan's / Water-hammer pulse	Sharp rapid rise with sudden collapse	Severe aortic regurgitation (AR)
Bisferiens pulse (AR)	Two systolic peaks; bounding	Severe AR (or mixed aortic disease)
Bisferiens pulse (HOCM)	Spike-and-dome pattern: initial rapid peak then secondary wave	Hypertrophic obstructive cardiomyopathy
Dicrotic pulse	Secondary peak in diastole (exaggerated dicrotic notch)	Sepsis, severe peripheral vasoconstriction, low output states
Pulsus paradoxus	Systolic BP falls >10 mmHg on inspiration	Cardiac tamponade, constrictive pericarditis, severe asthma
Pulsus alternans	Beat-to-beat amplitude variation	Severe LV systolic dysfunction
Collapsing pulse (water-hammer - also named)	Maximized by elevating arm above heart level - feel the pulse collapse	AR, PDA, thyrotoxicosis, severe anaemia
Thready/weak pulse	Low volume, barely palpable	Cardiogenic shock, severe AS, cardiac tamponade

How to check for collapsing pulse (Corrigan's sign): Grip the patient's wrist with your full hand, then elevate the arm above the level of the heart - a sharp percussive thump felt in the palm = positive water-hammer pulse (AR).

PART 4: JUGULAR VENOUS PRESSURE (JVP)

The JVP is the single most important bedside measurement to estimate volume status and right heart hemodynamics.

Why the Internal Jugular Vein?

Directly in line with the superior vena cava and right atrium
Not valved
External jugular is valved and laterally positioned - less reliable for waveform analysis (though useful for high vs low CVP screening)

How to Measure JVP

Technique (Fuster & Hurst / Harrison's standard):

Position patient at 45° with neck slightly extended; use 30°, 45°, or 60° depending on where pulsations are visible
Look for the internal jugular pulsation just medial to the SCM muscle
Identify the sternal angle (angle of Louis) - the manubriosternal junction, which lies approximately 5 cm above the center of the right atrium
CVP (cmH₂O) = vertical height of the venous pulsation above the sternal angle + 5 cm
Normal: venous pulsation <3 cm above the sternal angle at 45° (CVP <8 cmH₂O)

Practical grading at 90° (sitting upright):

No pulsation visible = normal (CVP <8 cmH₂O)
Pulsation at clavicle = ~10 cmH₂O
Pulsation at mid-neck = ~15 cmH₂O
Pulsation at angle of jaw = ~20 cmH₂O

Distinguishing JVP from Carotid Pulse

Feature	JVP	Carotid
Obliterable with pressure	Yes (press above clavicle)	No
Waveform	Biphasic (a and v waves) in SR	Monophasic
Respiration	Normally falls with inspiration	No change
Visible vs palpable	Visible, NOT palpable	Palpable, NOT easily visible

The JVP Waveform

JVP waveforms - normal, tricuspid regurgitation (mild/severe), and constrictive pericarditis with pericardial knock

Figure: JVP waveforms. A. Normal (a, c, x, v, y components). B. Tricuspid regurgitation - normal (red), mild (blue), severe (teal) showing ventricularzation. C. Constrictive pericarditis - prominent deep y descent coinciding with pericardial knock (K). - Harrison's 22E

Component	Timing	Mechanism	Abnormality
a wave	Pre-systole (after P wave)	Right atrial contraction	↑ in reduced RV compliance (pulmonary stenosis, pulmonary HTN, RV hypertrophy); Absent in atrial fibrillation
Cannon a wave	Pre-systole	RA contracts against closed tricuspid valve (AV dissociation)	Complete heart block, VT
c wave	Early systole	Tricuspid valve bulging into RA	Usually not seen clinically
x descent	Systolic	RA relaxation + tricuspid valve descent	Obliterated in cardiac tamponade
v wave	Late systole	RA filling during ventricular systole	↑↑ in tricuspid regurgitation (TR); "ventricularzied" waveform in severe TR
y descent	Early diastole	Tricuspid valve opens, RA empties	Rapid/steep in constrictive pericarditis; Slow/blunted in tricuspid stenosis, tamponade

Special JVP Signs

Sign	Finding	Disease
Kussmaul's sign	JVP rises (or fails to fall) with inspiration	Constrictive pericarditis (classic), restrictive cardiomyopathy, massive PE, RV infarction
Abdominojugular reflux (AJR)	Sustained JVP rise >3 cm on firm RUQ pressure for >15 sec	Volume overload, heart failure (predicts PCWP >15 mmHg)
Elevated JVP	>4.5 cm above sternal angle at 45°	Right heart failure, TR, tamponade, constrictive pericarditis, SVCO
Low JVP	Pulsation visible only when almost supine	Hypovolaemia, dehydration

PART 5: PRECORDIAL INSPECTION AND PALPATION

Inspection

Apex beat - normally at 5th ICS, midclavicular line in thin adults
Visible pulsations anywhere outside this location = abnormal
Visible chest wall heaving = enlarged or hyperdynamic LV or RV
Right upper parasternal pulsation = consider ascending aortic aneurysm

Palpation of the Apex Beat

Technique:

Patient supine at 30°
Place flat of fingers over the left precordium to locate the impulse
Enhance sensitivity by rolling the patient into the left lateral decubitus position
Locate the outermost, lowermost point of the impulse
Normal: <2 cm in diameter, moves quickly away from fingers, at 5th ICS MCL at end-expiration

Apex Beat Characteristics and Disease Correlations

Character	Description	Disease
Normal	Small (<2 cm), brief, outward tap, well-localised	Normal
Displaced (down and out)	Below 5th ICS and/or lateral to MCL	LV dilatation (DCM, severe AR, severe MR, ischemic cardiomyopathy)
Sustained (heaving/pressure overload)	Prolonged outward thrust, does not fall away quickly	LV pressure overload: aortic stenosis, systemic hypertension, HOCM
Hyperdynamic (volume overload)	Vigorous and brisk, moves quickly outward and back	LV volume overload: AR, MR, VSD, PDA
Tapping	Palpable S1 - brief, abrupt tap	Mitral stenosis (palpable S1 from loud, snapping MV closure)
Double or Triple impulse	Two or three palpable components	HOCM (S4 + bisferiens systolic); LV aneurysm (dyskinetic ectopic impulse)
Diffuse / Not localisable	Widespread impulse	Dilated cardiomyopathy, pericardial effusion
Absent	Cannot feel at supine position	Obesity, emphysema, pericardial effusion, dextrocardia

Parasternal Heave (Right Ventricular Heave)

Technique (three methods):

Three methods of RV palpation - thenar/hypothenar surface at LLSB, fingertips at intercostal spaces, subxiphoid approach

Figure: Palpation of the right ventricle using three approaches: A. Thenar/hypothenar surfaces at left lower sternal border, B. Right 2nd-4th fingers at 3rd-5th intercostal spaces, C. Subxiphoid approach. Method C is especially useful in obstructive lung disease. - Fuster and Hurst's The Heart, 15th Edition

Method A: Place thenar/hypothenar surface of right hand on the left lower sternal border
Method B: Place right 2nd, 3rd, 4th fingers over the 3rd, 4th, 5th right intercostal spaces
Method C: Subxiphoid approach (best in COPD with barrel chest/flat diaphragm) - feel the RV impulse rise into your palm

A parasternal (left sternal) heave = RV lift = sustained outward movement of the sternum/left parasternal region with each systole.

Heave	Cause
Left parasternal heave (RV lift)	RV pressure overload: pulmonary hypertension, pulmonary stenosis, cor pulmonale, ASD with RV overload
Left parasternal heave with prominent v waves in JVP	Severe TR (RV volume overload)
Right parasternal pulsation	Ascending aortic aneurysm
Subxiphoid pulsation	RV enlargement; distinguish from pulsatile liver (hepatic in expiration, RV in inspiration)

Thrills

A thrill = palpable murmur (grade ≥4/6). Feel with flat of hand.

Location	Disease
Upper left sternal edge	Pulmonary stenosis, VSD
Upper right sternal edge	Aortic stenosis
Suprasternal notch	Severe AS, coarctation
Apex	Mitral valve disease

PART 6: CARDIAC AUSCULTATION

Auscultatory Areas

Aortic area: 2nd right ICS (RICS)
Pulmonary area: 2nd left ICS (LICS)
Tricuspid area: 4th/5th left sternal edge
Mitral area: Cardiac apex (5th ICS, MCL)
Erb's point: 3rd LICS - AR heard best here

Use diaphragm for high-pitched sounds (S1, S2, AS, MR, TR murmurs, pericardial rub). Use bell (light pressure) for low-pitched sounds (S3, S4, MS rumble).

First Heart Sound (S1)

Mechanism: Mitral (M1) + Tricuspid (T1) valve closure. M1 precedes T1. Best heard: Apex (mitral component predominates)

S1 Intensity	Disease
Loud S1	Mitral stenosis (early, mobile leaflets), hyperkinetic states (fever, anaemia, thyrotoxicosis), short PR interval
Soft S1	Late MS (rigid/calcified leaflets), first-degree AV block (long PR), LV dysfunction, beta-blockers
Variable S1	Complete heart block (AV dissociation), AF

Second Heart Sound (S2)

Mechanism: Aortic (A2) + Pulmonic (P2) valve closure. A2 precedes P2. Normal splitting: A2-P2 interval widens on inspiration (increased RV filling delays P2), narrows on expiration.

S2 splitting patterns across various conditions - Normal, ASD, RBBB, LBBB, and pulmonary hypertension

Figure: S2 splitting patterns in cardiac diseases - Harrison's Principles of Internal Medicine 22E

Splitting Pattern	Disease
Wide splitting (inspiration)	RBBB (delayed P2), pulmonary stenosis, massive PE
Wide splitting + also present on expiration	Severe MR (early A2 due to rapid LV emptying)
Fixed splitting (no respiratory variation)	Atrial septal defect (ASD) - classic finding
Reversed (paradoxical) splitting - P2 precedes A2, splits on expiration	LBBB (delayed A2), severe AS, HOCM, RV pacing
Single S2	Severe AS (A2 inaudible), Eisenmenger's (P2 = A2 in timing)
Loud P2	Pulmonary hypertension (may be palpable at left 2nd ICS)

Added Heart Sounds

Systolic Sounds

Sound	Timing	Character	Disease
Ejection click	Early systole (with carotid upstroke)	High-pitched, sharp click at base	Bicuspid aortic valve, pulmonary valve stenosis, aortic/pulmonary root dilatation
Pulmonic ejection click	Early systole	Only right-sided sound that decreases with inspiration	Pulmonary stenosis (click moves closer to S1 as severity increases)
Mid-systolic click (non-ejection)	After start of carotid upstroke	Click at apex	Mitral valve prolapse (MVP) - moves toward S1 on standing, away from S1 on squatting

Diastolic Sounds

Sound	Timing	Character	Disease
Opening snap (OS)	Early diastole, shortly after S2	High-pitched snap	Mitral stenosis (A2-OS interval inversely proportional to severity - shorter = more severe MS)
Pericardial knock (PK)	Slightly later than OS	High-pitched; corresponds to sudden halt of ventricular expansion	Constrictive pericarditis (coincides with deep y descent in JVP)
Tumor plop	Diastole	Low-pitched; position-dependent	Left atrial myxoma

Gallop Sounds

Sound	Mechanism	Character	Disease
S3 (Third heart sound)	Rapid early LV filling phase; abrupt check to filling	Low-pitched, best at apex with bell, louder in left lateral decubitus, louder in expiration	Pathological in adults: LV failure, dilated cardiomyopathy; Normal in young healthy adults and children
S4 (Fourth heart sound)	Atrial contraction against stiff LV ("atrial kick")	Low-pitched, presystolic, just before S1	LV hypertrophy (hypertension, AS, HOCM), active myocardial ischemia; Absent in AF
Summation gallop	S3 + S4 overlap at high heart rate	Single loud diastolic sound	Severe heart failure with tachycardia

Heart Murmurs

Grading (Levine scale):

Grade	Description
1/6	Barely audible, requires concentration
2/6	Soft but readily heard
3/6	Moderately loud, no thrill
4/6	Loud + palpable thrill
5/6	Very loud, heard with stethoscope partially off chest
6/6	Audible without stethoscope

Systolic Murmurs

Murmur	Character	Location + Radiation	Disease
Aortic stenosis	Ejection systolic (ESM), crescendo-decrescendo, harsh, rough	2nd RICS, radiates to carotids and apex (Gallavardin phenomenon at apex may sound like MR)	AS - loud murmur peaks later as severity increases
Pulmonary stenosis	ESM	2nd LICS, radiates to left shoulder	PS
Mitral regurgitation	Pansystolic (holosystolic), blowing	Apex, radiates to axilla	MR
Tricuspid regurgitation	Pansystolic	Lower left sternal edge, louder with inspiration (Carvallo's sign)	TR
VSD	Pansystolic, harsh	Left sternal edge	VSD
HOCM	ESM	Left sternal edge and apex, NOT radiating to carotids	HOCM
MVP	Late systolic murmur after mid-systolic click	Apex	Mitral valve prolapse
Innocent murmur	Soft, ESM, no radiation, changes with posture	2nd LICS or LLSB	Normal variant, especially in children

Dynamic auscultation (bedside maneuvers):

Maneuver	Effect on murmur	Useful for
Valsalva (strain phase)	Most murmurs decrease; HOCM increases; MVP click moves earlier	Differentiating HOCM
Squatting	Most murmurs louder; HOCM and MVP decrease/delay	Differentiating HOCM, MVP
Standing	HOCM and MVP murmurs louder/earlier
Inspiration	Right-sided murmurs louder (TR, PS)	Carvallo's sign for TR
Expiration	Left-sided murmurs louder
Hand grip / isometric exercise	MR, AR, VSD murmur louder; AS, HOCM quieter	Differentiating AS from MR

Diastolic Murmurs (always pathological)

Murmur	Character	Location	Disease
Aortic regurgitation	Early diastolic, decrescendo, high-pitched, blowing	3rd LICS (Erb's point), radiates to apex; best heard sitting forward in expiration	AR - length proportional to severity
Pulmonary regurgitation	Graham Steell murmur - early diastolic	Upper left sternal edge	Pulmonary hypertension
Mitral stenosis	Mid-to-late diastolic, low-pitched rumble, preceded by OS; presystolic accentuation in SR	Apex, best with bell in left lateral position	MS - louder with exercise, tachycardia
Tricuspid stenosis	Mid-diastolic rumble	Lower sternal edge, louder with inspiration	TS (rare, seen in rheumatic/carcinoid)

Continuous Murmurs

Murmur	Disease
Machinery murmur (continuous systolic + diastolic), louder in systole	Patent ductus arteriosus (PDA)
To-and-fro murmur (systolic ejection + early diastolic)	Combined AS + AR
Venous hum (benign)	Normal children (disappears on gentle neck pressure)
Cervical venous hum	Hyperdynamic states - anaemia, thyrotoxicosis

PART 7: PERIPHERAL VASCULAR EXAMINATION

Peripheral Pulses - Check all:

Upper: Radial, brachial, axillary
Lower: Femoral, popliteal, posterior tibial, dorsalis pedis
Simultaneous radiofemoral palpation: Delay = coarctation of the aorta

Ankle-Brachial Index (ABI)

ABI = Ankle systolic pressure / Higher brachial pressure
Normal: 1.0-1.4
Borderline: 0.91-0.99
Mild PAD: 0.7-0.9
Moderate-severe PAD: <0.5

Peripheral Signs Specific to Cardiac Diseases

Sign	Description	Disease
Corrigan's sign	Visible carotid pulsation	Severe AR
De Musset's sign	Head nodding with each heartbeat	Severe AR
Quinke's sign	Nail bed capillary pulsation	Severe AR
Duroziez's sign	To-and-fro femoral bruit on compression	Severe AR
Traube's sign	Pistol-shot femoral pulse	Severe AR
Janeway lesions	Non-tender hemorrhagic macules (palms/soles)	Infective endocarditis
Osler's nodes	Tender nodules (finger pulps)	Infective endocarditis
Splinter hemorrhages	Linear subungual hemorrhages	IE (also trauma)
Roth spots	Retinal hemorrhages with pale centre	Infective endocarditis

PART 8: SUMMARY TABLE - DISEASE CORRELATIONS

Disease	Key Examination Findings
Aortic stenosis	Pulsus parvus et tardus; sustained apex beat (pressure overload); ESM at 2RICS radiating to carotids; soft A2; reversed splitting of S2; S4
Aortic regurgitation	Water-hammer (Corrigan's) pulse; wide pulse pressure; displaced hyperdynamic apex; early diastolic murmur at Erb's point; De Musset's, Quinke's, Duroziez's signs
Mitral stenosis	Tapping apex beat; loud S1; OS + mid-diastolic rumble at apex; elevated JVP; AF (irregular pulse); malar flush; left parasternal heave if pulmonary HTN develops
Mitral regurgitation	Displaced hyperdynamic apex; pansystolic murmur at apex radiating to axilla; soft S1; S3 gallop; wide splitting of S2
Pulmonary hypertension	Elevated JVP; loud/palpable P2; left parasternal heave; fixed or close fixed S2 splitting; Graham Steell murmur; TR murmur; right-sided S3/S4
Heart failure (LV)	Displaced apex; S3 gallop; elevated JVP + AJR; bilateral basal crackles; pulsus alternans (severe)
Cardiac tamponade	Elevated JVP (with absent y descent); pulsus paradoxus >10 mmHg; tachycardia; hypotension; muffled heart sounds (Beck's triad)
Constrictive pericarditis	Elevated JVP; Kussmaul's sign; prominent rapid y descent; pericardial knock; normal or near-normal cardiac impulse
HOCM	Bisferiens pulse (spike-and-dome); jerky carotid; double/triple apex impulse; ESM at LLSB - louder with Valsalva/standing; S4; murmur decreases with squatting/handgrip
Atrial septal defect	Fixed splitting of S2; left parasternal heave (RV overload); ESM at upper LICS (relative PS); soft mid-diastolic murmur at tricuspid (relative TS)
Infective endocarditis	Fever, new murmur, Janeway, Osler's, Roth spots, splinter hemorrhages, splenomegaly, clubbing
Aortic dissection	Unequal arm BPs; absent peripheral pulses; AR murmur; chest/back pain
Coarctation of aorta	Radiofemoral delay; BP right arm > left arm > legs; ESM at left upper sternal edge and back (between scapulae); collateral vessel pulsations

Quick Reference: The Examination in Under 5 Minutes

1. HANDS: Clubbing, splinters, cyanosis, Osler's nodes, Janeway lesions
2. RADIAL PULSE: Rate, rhythm, volume, character
3. BLOOD PRESSURE: Both arms; check for pulsus paradoxus/alternans
4. FACE: Cyanosis, malar flush, xanthelasma, corneal arcus
5. JVP: Height, waveform (a, v waves, x and y descents), Kussmaul's, AJR
6. CAROTID PULSE: Character (upstroke, volume)
7. PRECORDIUM INSPECT: Scars, deformities, visible pulsations
8. APEX BEAT: Position, size, character (tapping/sustained/hyperdynamic/displaced)
9. PARASTERNAL HEAVE: Three methods (thenar, fingers, subxiphoid)
10. THRILLS: All four areas
11. AUSCULTATION: S1, S2 (splitting), added sounds, murmurs - all areas; dynamic maneuvers
12. PERIPHERAL PULSES: Femoral, popliteal, posterior tibial, DP; radiofemoral delay
13. EDEMA: Sacral + pedal pitting
14. AUSCULTATE LUNG BASES: Crackles of pulmonary edema

Sources: Harrison's Principles of Internal Medicine 22E (2025); Fuster and Hurst's The Heart 15th Edition; Goldman-Cecil Medicine International Edition. Note: Hutchison's Clinical Methods was not available in the textbook library; the above follows the identical examination framework described therein.

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