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Cardiovascular System Examination - Complete Guide

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ORDER OF EXAMINATION

1. General Appearance
2. Vital Signs (BP, HR, RR)
3. Ophthalmologic Exam
4. Jugular Venous Pressure (JVP)
5. Carotid Pulse
6. Precordial Inspection and Palpation
7. Cardiac Auscultation
8. Abdominal and Peripheral Exam

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1. GENERAL APPEARANCE

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2. VITAL SIGNS

Blood Pressure

Pulsus Paradoxus

Pulsus Alternans

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3. OPHTHALMOLOGIC EXAM

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4. JUGULAR VENOUS PRESSURE (JVP)

• JVP: biphasic (two peaks), not palpable, changes with posture and respiration
• Carotid: monophasic, palpable, does not change with respiration

JVP Waveform Components and Their Abnormalities

Elevated JVP: Differential Diagnosis

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5. CAROTID PULSE (CHARACTER OF PULSE)

Differentiating Aortic Stenosis vs Aortic Regurgitation by Pulse

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6. PRECORDIAL INSPECTION AND PALPATION

Inspection

Palpation (Technique: supine at 30°, left lateral decubitus to enhance)

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7. CARDIAC AUSCULTATION

Heart Sounds

First Heart Sound (S1)

Second Heart Sound (S2)

Third Heart Sound (S3) - Early Diastolic Gallop

Fourth Heart Sound (S4) - Presystolic Gallop

Differentiating S3 vs S4

Additional Sounds

Heart Murmurs

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SYSTOLIC MURMURS

Holosystolic (Pansystolic) Murmurs

Midsystolic (Ejection) Murmurs

Differentiating AS vs MR vs HOCM (all are systolic murmurs)

Late Systolic Murmur

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DIASTOLIC MURMURS (always pathological)

Early Diastolic (Decrescendo)

Mid-Diastolic (Rumbling)

Differentiating MS vs Austin Flint Murmur

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CONTINUOUS MURMURS (systole + diastole)

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8. ABDOMINAL AND PERIPHERAL EXAMINATION

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DISEASE-BY-DISEASE SUMMARY: SIGNS IN ORDER

Aortic Stenosis

1. General: symptoms on exertion (angina, syncope, dyspnea = classic triad)
2. Pulse: parvus et tardus; narrow pulse pressure
3. JVP: may show prominent a wave (if pulmonary hypertension develops)
4. Apex: sustained (heaving), not displaced (unless LV dilation in late disease)
5. Palpation: systolic thrill at 2nd right ICS
6. S1: normal; S2: single or paradoxically split (P2 soft/absent A2)
7. S4 gallop present
8. Murmur: midsystolic ejection crescendo-decrescendo at right 2nd ICS, radiating to carotids

Aortic Regurgitation (Chronic)

1. Pulse: water-hammer (Corrigan's); wide pulse pressure; bisferiens if severe
2. BP: high systolic, very low diastolic
3. Apex: displaced laterally and inferiorly (volume overloaded LV)
4. S1: normal; early diastolic decrescendo murmur at left sternal border
5. Austin Flint murmur at apex (in severe AR)
6. S3 in decompensated AR
7. Peripheral signs: pistol-shot femoral pulse (Traube's), Duroziez sign, Quincke pulses, de Musset's sign (head nodding)

Mitral Stenosis

1. General: dyspnea, hemoptysis, AF, systemic emboli
2. Pulse: irregular if AF
3. JVP: elevated if pulmonary hypertension present
4. Apex: not displaced; "tapping" quality (palpable S1)
5. S1: loud (pliable leaflets); S2: loud P2 if pulmonary hypertension
6. Opening snap (shortly after S2)
7. Mid-diastolic rumble at apex (bell of stethoscope, left lateral decubitus)
8. Presystolic accentuation (in sinus rhythm)

Mitral Regurgitation (Chronic)

1. Pulse: brisk, hyperdynamic
2. Apex: displaced laterally (volume overload); palpable S3
3. S1: soft; S2: wide splitting (early A2 due to rapid LV emptying); S3 present
4. Holosystolic blowing murmur at apex, radiating to axilla
5. If posterior leaflet: murmur radiates anteriorly to base (mimics AS)

Hypertrophic Obstructive Cardiomyopathy (HOCM)

1. General: dyspnea, syncope, chest pain, palpitations in young patient; family history of sudden death
2. Pulse: bisferiens; spike-and-dome character
3. Apex: triple cadence (S4 + bisferiens); sustained but not displaced
4. S4 prominent
5. Midsystolic murmur at left lower sternal border
6. Dynamic character is key: increases with Valsalva and standing; decreases with squatting and handgrip
7. Coexistent MR murmur often present

Constrictive Pericarditis

1. General: fatigue, peripheral edema, ascites - often misdiagnosed as liver disease
2. JVP: elevated with prominent/rapid y descent; Kussmaul sign (JVP rises with inspiration)
3. Pulse: may have pulsus paradoxus (mild)
4. Precordium: quiet precordium (no heave)
5. S3 equivalent = pericardial knock (high-pitched early diastolic sound; earlier than usual S3, occurs at nadir of rapid Y descent)
6. Hepatomegaly, ascites, peripheral edema

Cardiac Tamponade

1. General: Beck's triad - Hypotension + Elevated JVP + Muffled heart sounds
2. JVP: elevated; blunted/absent Y descent (impaired diastolic filling)
3. Pulse: pulsus paradoxus >10 mmHg (may be palpable >15 mmHg)
4. Precordium: quiet, no heave, heart sounds muffled
5. No Kussmaul sign

Differentiating Tamponade vs Constrictive Pericarditis

Pulmonary Hypertension

1. Pulse: normal or reduced volume
2. JVP: elevated; prominent a wave; if TR develops - prominent v wave
3. RV heave at left parasternal area
4. Palpable P2 at left 2nd ICS
5. S2: loud P2, narrow or single splitting
6. Right-sided S4; then right-sided S3 if RV fails
7. Ejection click in pulmonic area
8. TR murmur (holosystolic, left lower sternal border, increases with inspiration) develops late
9. PR murmur (Graham Steell) - high-pitched early diastolic decrescendo at left 2nd-3rd ICS

Infective Endocarditis

1. General: fever, weight loss, fatigue, embolic phenomena
2. Eyes: Roth spots (fundus), petechiae
3. Hands: Osler nodes (painful tender nodules - fingertips), Janeway lesions (non-tender hemorrhagic macules - palms/soles), splinter hemorrhages (nails)
4. New or changing murmur (most commonly MR or AR)
5. Splenomegaly
6. Signs of heart failure if severe valvular destruction

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NYHA FUNCTIONAL CLASSIFICATION (Summary)

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Coarctation of the Aorta: Why Arm BP > Leg BP

The Anatomy - This is the Key

Heart → Ascending Aorta
         ↓
    Brachiocephalic artery → Right arm
    Left common carotid artery → Brain
    Left subclavian artery → Left arm
         ↓
    *** COARCTATION HERE ***  ← narrowing at this point
         ↓
    Descending aorta → Legs, abdomen

Why Arms Have HIGH BP

• Chronic increased afterload → LV hypertrophy
• Activation of renin-angiotensin-aldosterone system (kidneys sense reduced perfusion downstream) → further raises BP systemically (arms)

Why Legs Have LOW BP

• Femoral pulses are weak and delayed (brachial-femoral pulse delay - you feel the radial pulse before the femoral pulse in the same patient)
• Systolic BP gradient between right arm and lower limb ≥20 mmHg = significant coarctation (Braunwald's Heart Disease)
• Legs may be cool, pale, and the patient may have leg claudication

Important Clinical Nuance: WHICH ARM to Use

Summary Table

Associated Radiological Signs (Chest X-ray)

• Rib notching (erosion of undersurfaces of ribs 3-8) - caused by dilated intercostal collateral arteries that form to bypass the obstruction and supply the lower body
• Figure-of-3 sign - the aortic silhouette shows pre-stenotic dilation + the coarctation notch + post-stenotic dilation, forming a "3" shape
• E sign on barium swallow (reverse figure-3)

Collateral Circulation

• Continuous interscapular murmur (collateral flow)
• Rib notching on CXR
• Braunwald's Heart Disease, Cardiovascular Medicine 2-Vol Set
• The Developing Human: Clinically Oriented Embryology

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Constrictive Pericarditis vs Restrictive Cardiomyopathy

The Core Concept First

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Causes

Constrictive Pericarditis

1. Post-cardiac surgery (most common today - ~29% of cases; previously rare)
2. Idiopathic / post-viral pericarditis (~22%)
3. Radiation therapy (breast cancer, Hodgkin disease - increasingly common)
4. Tuberculous pericarditis (most common cause in Africa/Asia)
5. Connective tissue disease (SLE, RA)
6. Uremia
7. Purulent (bacterial) pericarditis
8. Neoplasm, trauma, drugs (procainamide, methylsergide)

Restrictive Cardiomyopathy

1. Amyloidosis (most common secondary cause)
2. Sarcoidosis
3. Radiation-induced myocardial fibrosis
4. Hemochromatosis
5. Glycogen storage diseases
6. Endomyocardial fibrosis (tropical Africa/Asia - most common cause worldwide)
7. Loeffler endomyocarditis (hypereosinophilia)
8. Metastatic tumors
9. Idiopathic (interstitial fibrosis)

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Pathophysiology

Constrictive Pericarditis

• Visceral and parietal pericardium fuse into a rigid, inextensible fibro-calcific rind
• This shell restricts ventricular filling from outside but the myocardium itself is normal
• Key concept: ventricular interdependence - because total cardiac volume is fixed by the rigid shell, when the RV fills more (on inspiration), it physically shifts the septum into the LV, reducing LV filling. This respiratory reciprocity between the two ventricles is the defining feature.
• Filling pressures equalize across all four chambers (LVEDP = RVEDP within 5 mmHg)
• Early diastolic filling is rapid (open tricuspid/mitral) then abruptly halted when cardiac volume hits the rigid pericardial shell → produces the square-root sign / pericardial knock

Restrictive Cardiomyopathy

• The myocardium itself is stiff due to infiltration or fibrosis
• Impaired relaxation throughout diastole (not just a mid-diastolic halt)
• Both ventricles cannot relax; both atria dilate markedly trying to push blood in
• No ventricular interdependence - the pericardium is normal, so each ventricle operates independently
• Filling pressures are elevated but do not equalize as strictly; LVEDP often > RVEDP

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Clinical Features - Comparison Table

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Differentiating Features (Key Points)

1. Orthopnea/PND

• Absent in CP - because the pericardium equally restricts all positions; left atrial pressure is not dramatically higher than right
• Present in RCM - especially when LV disease is dominant

2. Ascites out of proportion

• In CP, ascites is often the most striking finding, more than leg edema - frequently misdiagnosed as liver cirrhosis
• In RCM, peripheral edema and ascites are more proportionate

3. Pericardial Knock vs S3

4. BNP Levels

• CP: Low BNP (myocardium is not under stretch/stress; it's the pericardium at fault)
• RCM: High BNP (myocardium itself is diseased and stressed)
• This is an important and practical differentiator

5. History

• Prior cardiac surgery, radiation, TB infection → think CP
• Amyloidosis (carpal tunnel, peripheral neuropathy, proteinuria), sarcoidosis → think RCM

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ECG

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Chest X-Ray

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Echocardiography

Doppler - The Most Specific Echo Differentiator

1. Diastolic respirophasic shift of ventricular septum
2. Medial mitral annulus e' ≥9 cm/s
3. Diastolic expiratory hepatic vein flow reversal ratio >0.8

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Cardiac Catheterization (Gold Standard)

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CT / MRI

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Treatment

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Quick Memory Summary

CP = Outside problem (pericardium). Normal myocardium. Surgically curable. Ventricular interdependence. Expiratory hepatic reversals. High e'. Low BNP. Pericardial knock. Septal bounce. Calcification on CXR.

RCM = Inside problem (myocardium). Stiff muscle. Not curable. No interdependence. Inspiratory hepatic reversals. Low e'. High BNP. No pericardial knock. No septal bounce. Thick walls/granular texture (amyloid).

• Fuster and Hurst's The Heart, 15th Ed
• Braunwald's Heart Disease, Cardiovascular Medicine
• Robbins & Kumar Pathologic Basis of Disease
• Grainger & Allison's Diagnostic Radiology

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Constrictive Pericarditis (CP) vs Restrictive Cardiomyopathy (RCM) vs HOCM - Complete Comparison

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THE FUNDAMENTAL CONCEPT: WHAT IS THE PROBLEM?

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CAUSES / ETIOLOGY

Constrictive Pericarditis

• Post-cardiac surgery (#1 today ~29%)
• Idiopathic/post-viral (~22%)
• Radiation therapy (breast cancer, Hodgkin lymphoma)
• Tuberculosis (#1 in Africa/Asia)
• Connective tissue disease (SLE, RA)
• Uremia, purulent pericarditis, neoplasm

Restrictive Cardiomyopathy

• Amyloidosis (most common secondary cause - AL or TTR)
• Sarcoidosis
• Hemochromatosis
• Radiation-induced myocardial fibrosis
• Endomyocardial fibrosis (tropical regions - most common worldwide)
• Loeffler endomyocarditis (hypereosinophilia)
• Glycogen storage diseases, mucopolysaccharidoses
• Metastatic tumors, idiopathic fibrosis

HOCM

• Autosomal dominant genetic disorder (1 in 500 people - most common genetic cardiovascular disease)
• Mutations in sarcomeric proteins: beta-myosin heavy chain (most common), myosin-binding protein C, troponin T

• 400 causative mutations identified; all are gain-of-function mutations

• Most common cause of sudden cardiac death in athletes under 35 years

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PATHOPHYSIOLOGY SUMMARY

CP

• Visceral + parietal pericardium fuse into a rigid fibro-calcific shell
• Myocardium is completely normal
• Total cardiac volume is fixed by the rigid shell → ventricular interdependence: when RV fills more (inspiration), it physically shifts the septum into LV → LV filling falls (and vice versa)
• All chamber pressures equalize (LVEDP ≈ RVEDP within 5 mmHg)
• Early diastolic filling is rapid then abruptly halted mid-diastole (hits the rigid pericardial wall) → square-root sign (dip and plateau)

RCM

• Myocardium itself is stiff due to infiltration (amyloid deposits) or fibrosis
• Impaired relaxation throughout all of diastole - not just mid-diastole
• Both ventricles stiff → massive biatrial dilation (atria work harder to push blood in)
• No ventricular interdependence (pericardium is normal)
• LVEDP often > RVEDP (asymmetric - LV usually more affected)
• BNP is high (myocardium is stressed)

HOCM

• Massive asymmetric septal hypertrophy (90% of cases) → septum bulges into LVOT ("banana-shaped" LV cavity)
• During systole, high-velocity blood flow across narrow LVOT → Venturi effect → systolic anterior motion (SAM) of anterior mitral leaflet → MR + further worsening of obstruction
• Result: dynamic LVOT gradient that increases when cavity is smaller (less blood in LV) or when heart contracts harder
• Myocardium is hypercontractile but does not relax properly → diastolic dysfunction + high filling pressures
• Massive hypertrophy + compromised intramural coronaries → ischemia even without CAD
• Risk of VF → sudden death (myocyte disarray, interstitial fibrosis are arrhythmogenic)

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CLINICAL FEATURES - THREE-WAY COMPARISON TABLE

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PHYSICAL EXAMINATION - THREE-WAY COMPARISON

Pulse

JVP

Precordium

Heart Sounds

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THE CARDINAL DIFFERENTIATING FEATURE: MURMUR BEHAVIOR IN HOCM

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ECG COMPARISON

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IMAGING COMPARISON

Chest X-Ray

Echocardiography

Tissue Doppler (e' velocity - most important differentiator between CP and RCM)

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CARDIAC CATHETERIZATION COMPARISON

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MRI / CT COMPARISON

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BNP (Brain Natriuretic Peptide)

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TREATMENT COMPARISON

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THE CLASSIC "CANNOT MISS" DIFFERENTIATORS - SUMMARY

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Pre-Systolic Accentuation - Meaning

Simple Definition

• Pre = before
• Systolic = systole (ventricular contraction)
• Accentuation = getting louder / intensified

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Why Does It Happen? (Mechanism)

DIASTOLE (relaxation phase)
|
|--- Early diastole: Mitral valve opens → blood rushes from LA to LV (rapid filling)
|       ↓  (mid-diastolic rumble starts here after opening snap)
|--- Mid diastole: Flow slows → murmur gets softer (decrescendo)
|
|--- Late diastole: LEFT ATRIUM CONTRACTS ← this is the KEY moment
|       ↓
|   Atrial contraction forces more blood through the narrowed mitral valve orifice
|   → Turbulent flow suddenly INCREASES again
|   → Murmur becomes louder just before S1
|
PRE-SYSTOLIC ACCENTUATION here ↑
|
S1 (mitral valve closes → systole begins)

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The Cardinal Rule: Only Present in Sinus Rhythm

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Where Does It Fit in the Full MS Murmur?

S1 ——— systole ——— S2 — [Opening Snap] — mid-diastolic rumble (decrescendo)
                                                              ↘
                                                   [crescendo] → S1
                                                   ↑
                                          PRE-SYSTOLIC ACCENTUATION

• Loud S1 (pliable leaflets closing)
• Opening snap (shortly after A2; short A2-OS interval = more severe MS)
• Mid-diastolic low-pitched rumble (best with bell; left lateral decubitus)
• Pre-systolic crescendo (atrial contraction) → then S1

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Clinical Significance - What Does It Tell You?

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How to Best Hear the Murmur (Including Presystolic Component)

• Patient in left lateral decubitus position (brings apex to chest wall)
• Use the bell of the stethoscope (low pitch)
• Apply light pressure (heavy pressure converts bell to diaphragm - loses low frequencies)
• Quiet room - this is a very soft murmur
• Exercise the patient briefly (sit-ups, leg raises) - increases heart rate and gradient → murmur louder
• Listen specifically for the crescendo just before S1

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Conditions Where Presystolic Accentuation is Absent Even with MS

1. Atrial fibrillation (most common - no coordinated atrial contraction)
2. Complete AV block with long PR (atrial contraction so far from ventricular systole that the crescendo dissipates)
3. Severe MS with calcified, immobile valve (very little flow even with atrial contraction)

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Austin Flint Murmur - Does It Have Pre-Systolic Accentuation?

• Fuster & Hurst's The Heart, 15th Ed
• Braunwald's Heart Disease, Cardiovascular Medicine
• Frameworks for Internal Medicine

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Pulsus Paradoxus - Complete Guide

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Definition

• Normal: systolic BP falls slightly (<10 mmHg) on inspiration - this is physiological
• Abnormal (pulsus paradoxus): systolic BP falls >10 mmHg on inspiration

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Normal Physiology First (to understand the pathology)

• Intrathoracic pressure falls (diaphragm descends)
• Pulmonary vasculature expands → temporarily pools more blood in lungs
• Right heart: venous return increases (RV fills more)
• Left heart: less blood returns from pulmonary veins → LV fills slightly less
• Net result: small fall in systolic BP (~5-10 mmHg) - this is normal

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Mechanism of Pulsus Paradoxus

Mechanism 1: Ventricular Interdependence (Dominant)

INSPIRATION
  ↓
Intrathoracic pressure falls → RV venous return INCREASES → RV fills MORE
  ↓
Total pericardial volume is FIXED (by rigid effusion / pericardium)
  ↓
RV expands → physically pushes interventricular septum LEFT into LV
  ↓
LV cavity becomes SMALLER → LV stroke volume DECREASES
  ↓
Aortic output FALLS → Systolic BP DROPS on inspiration

Mechanism 2: Pulmonary Vascular Pooling (Contributing)

INSPIRATION
  ↓
Intrathoracic pressure falls → Pulmonary veins also fall in pressure
  ↓
But: intracardiac pressure (LA) is buffered by pericardial effusion
     so it does NOT fall as much
  ↓
Diastolic filling gradient (pulmonary veins → LA) DECREASES
  ↓
Less blood enters LV → LV stroke volume FALLS further

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Causes - Ordered by Importance

Cardiac Causes

Pulmonary/Respiratory Causes

Other Causes

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Differentiating the Causes

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How to Measure Pulsus Paradoxus (Step-by-Step)

1. Inflate cuff well above systolic pressure (e.g., 30 mmHg above expected)
2. Slowly deflate at 2-3 mmHg/second
3. Note the pressure at which Korotkoff sounds are first heard - they will only appear during expiration at first - record this pressure (A)
4. Continue slowly deflating
5. Note the pressure at which Korotkoff sounds are heard throughout the entire respiratory cycle (both inspiration and expiration) - record this pressure (B)
6. Pulsus paradoxus = A - B (in mmHg)

• Palpate the radial pulse while watching the patient breathe
• If the pulse disappears or markedly weakens on inspiration, pulsus paradoxus is present
• A palpable pulsus paradoxus at the radial or femoral artery indicates the difference is >15-20 mmHg

• Watch the pulse oximetry waveform
• If the waveform amplitude visibly decreases during inspiration → suggests pulsus paradoxus

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When Pulsus Paradoxus May Be Falsely ABSENT in Tamponade

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Pulsus Paradoxus vs Pulsus Alternans - Don't Confuse!

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Pulsus Paradoxus vs Kussmaul Sign - Related but Different

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Quick Memory Summary

Pulsus paradoxus = systolic BP drops >10 mmHg on inspiration = exaggerated normal physiology

Mechanism = ventricular interdependence (RV fills more → LV fills less) + pulmonary vascular pooling

Classic cause = cardiac tamponade (>20 mmHg)

Also in = severe asthma, COPD, massive PE, tension pneumothorax

Absent in tamponade when = AR, ASD, severe LVH, positive pressure ventilation

Paradoxus = arterial problem; Kussmaul = venous problem - opposite findings in tamponade vs constrictive pericarditis

• Roberts & Hedges' Clinical Procedures in Emergency Medicine
• Braunwald's Heart Disease, Cardiovascular Medicine
• Fuster & Hurst's The Heart, 15th Ed