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Auscultation of Heart Valves: Clinical Anatomy

The Five Classic Auscultatory Areas

Key concept: Auscultatory areas do NOT correspond to the anatomical location of the valves. They are the sites on the chest wall where sounds from each valve are best conducted and heard.

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Why Sounds Are Heard Where They Are

• Aortic stenosis murmur: heard at the base (right 2nd ICS) and radiates to the carotid arteries
• Mitral regurgitation murmur: heard at the apex and radiates to the left axilla
• Aortic regurgitation murmur: heard along the left sternal border (3rd-4th ICS) when caused by valve disease; when caused by aortic root dilation, it may be more audible along the right sternal border
• Tricuspid regurgitation: can radiate to the right sternal border; increases with inspiration (Carvallo's sign)

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Technique

1. Sitting up, leaning forward - best for aortic regurgitation and pericardial rubs; base of heart sounds
2. Supine - standard for most heart sounds
3. Left lateral decubitus - brings the apex closer to the chest wall; best for mitral murmurs (especially the low-pitched MS rumble) and S3/S4 gallops

• Diaphragm (firm pressure): high-pitched sounds - most murmurs, S1, S2, aortic regurgitation, ejection clicks, opening snaps
• Bell (light pressure): low-pitched sounds - S3, S4, mitral stenosis diastolic rumble, vascular bruits. If excessive pressure is applied to the bell, it acts like a diaphragm and low-pitched sounds are lost

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Heart Sounds and Their Valve Origins

S1 (First Heart Sound)

• Produced by closure of the mitral and (to a lesser extent) tricuspid valves - marks the end of diastole/start of systole
• Louder in mitral stenosis (when leaflets are mobile)
• Softer in mitral regurgitation (poor leaflet coaptation)

S2 (Second Heart Sound)

• Produced by closure of the aortic valve (A2) followed by the pulmonic valve (P2)
• Physiologic splitting: On inspiration - increased RV filling delays P2, causing audible splitting (A2 then P2). On expiration - both coincide and S2 is single
• Fixed splitting: A2-P2 interval unchanged with respiration - seen in atrial septal defect and right bundle branch block
• Paradoxical splitting: S2 splits on expiration and becomes single on inspiration - delayed A2 (e.g., severe AS, HOCM, LBBB)
• Loud A2: systemic hypertension
• Soft/absent A2: severe calcific aortic stenosis
• Loud P2: pulmonary hypertension

Opening Snap

• High-pitched sound in early diastole - heard before rapid filling begins
• Mitral opening snap: heard best at the apex
• Tricuspid opening snap: left 3rd-4th ICS
• Distinguished from a loud P2 by its longer interval from S2 and its location

S3 (Third Heart Sound)

• Low-pitched sound in early diastole - corresponds to rapid ventricular filling
• Normal in children and young adults; pathological after age ~40
• Causes: mitral regurgitation (increased filling volume), heart failure (elevated filling pressures)
• Left ventricular S3: heard at the apex with the bell
• Right ventricular S3: heard at the 4th ICS, left parasternal border with the bell

S4 (Fourth Heart Sound)

• Low-pitched sound in late diastole - from atrial contraction against a stiff ventricle
• Nearly ubiquitous in hypertension, heart failure, ischemic heart disease

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Murmur Characteristics at Each Valve

Aortic Stenosis (AS)

• Harsh systolic ejection murmur, late-peaking
• Best heard at the right 2nd ICS, radiates to carotids
• Gallavardin phenomenon: high-frequency components radiate to apex and can mimic MR
• Louder and later-peaking = more severe
• Decreases with standing/Valsalva; increases with squatting

Aortic Regurgitation (AR)

• High-pitched, blowing diastolic murmur, begins immediately after A2
• Best heard at the left sternal border (3rd-4th ICS), with patient sitting up and leaning forward in deep exhalation
• Duration correlates better with severity than intensity
• Austin Flint murmur: a mid-to-late diastolic low-pitched rumble at the apex in severe AR (AR jet impinging on the mitral valve)

Mitral Stenosis (MS)

• Low-pitched diastolic rumble with pre-systolic accentuation (in sinus rhythm)
• Best heard at the apex, with patient in left lateral decubitus, using the bell
• Preceded by an opening snap
• Louder S1 when leaflets remain mobile

Mitral Regurgitation (MR)

• High-pitched, blowing pansystolic murmur
• Best heard at the apex, radiates to the left axilla
• Intensity unaffected by beat-to-beat variation (unlike AS)

Tricuspid Regurgitation (TR)

• Pansystolic murmur at the lower left sternal border (tricuspid area)
• Increases with inspiration (Carvallo's sign) - distinguishes TR from MR

Pulmonic Stenosis (PS)

• Systolic ejection murmur at the left 2nd ICS
• Often preceded by an ejection click

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Murmur Grading (Levine Scale)

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Prosthetic Valve Sounds

• All mechanical valves produce a crisp high-pitched closing click
• Older ball-cage and tilting-disk prostheses also produce an opening click
• Newer bileaflet valves are typically silent on opening
• Any regurgitant murmur from a prosthetic valve is pathological (paravalvular leak, leaflet dysfunction)
• Normal prostheses have an intrinsic mild ejection murmur (aortic/pulmonic position) or a soft diastolic rumble (mitral/tricuspid position)

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Auscultation of Heart Valves - Summary

5 Auscultatory Areas

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Heart Sounds - Origins

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Key Murmurs

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3 Patient Positions

• Supine - standard
• Left lateral decubitus - mitral murmurs, S3/S4
• Sitting, leaning forward - aortic regurgitation, pericardial rub

Stethoscope

• Diaphragm - high-pitched sounds (most murmurs, S1, S2, AR)
• Bell (light pressure) - low-pitched sounds (S3, S4, MS rumble)

Murmur Grading

• I-III: no thrill | IV-VI: thrill present | Grade VI heard without stethoscope

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Hemoptysis

Definition

Massive hemoptysis = >150-200 mL in 24 hours OR a rate ≥100 mL/h. Patients rarely die of exsanguination - they die of asphyxiation from blood filling the airways.

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Hemoptysis vs. Pseudohemoptysis

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Anatomy of Bleeding

• Most hemoptysis arises from the bronchial circulation (high-pressure, originates from the aorta)
• The pulmonary circulation is low-pressure; massive bleeding from it is less common
• Bronchial arteries neovascularize tumors, dilated airways (bronchiectasis), and cavitary lesions - making these vulnerable to rupture

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Causes (Etiology)

Infections (Most common globally)

Malignancy

• Bronchogenic carcinoma (any histology) - common cause, both massive and non-massive
• Squamous cell / small cell carcinoma - central tumors that erode into major pulmonary vessels
• Carcinoid tumors - highly vascular, arise in proximal airways
• Pulmonary metastases - melanoma, sarcoma, breast, colon
• Kaposi's sarcoma in HIV/AIDS

Age clue: Hemoptysis before age 40 - think infections. After age 40-45 or with smoking history - think bronchogenic carcinoma.

Vascular

Autoimmune / Pulmonary-Renal Syndromes

• Granulomatosis with polyangiitis (GPA) - formerly Wegener's
• Anti-GBM (Goodpasture) disease - hemoptysis + hematuria
• Both can cause DAH

Other / Mechanical

• Catamenial hemoptysis - pulmonary endometriosis; cyclical, with menses
• Foreign body aspiration
• Iatrogenic: pulmonary artery catheter rupture, post-lung biopsy, post-pulmonary vein isolation
• Coagulopathy / anticoagulation / antiplatelet therapy
• COPD - unexplained, usually not recurrent

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Management Algorithm

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Evaluation

History

• Volume and frequency (quantify with references: 1 cup = 236 mL)
• Smoking history, weight loss (malignancy)
• Fever, productive cough (infection)
• Prior lung disease (bronchiectasis, CF, TB, cancer)
• Immobilization (PE), anticoagulants, autoimmune history
• Cyclical pattern with menses (catamenial)

Physical Examination

• Assess for life threat: hypoxemia, tachycardia, hemodynamic instability
• Examine nasal/oral cavities (rule out epistaxis)
• Lung auscultation: lateralizing crackles, wheeze
• Cardiac: murmurs (mitral stenosis)
• Skin: telangiectasias (HHT), purpura (vasculitis), ecchymoses (coagulopathy), clubbing

Laboratory

• CBC, coagulation studies (PT/INR, aPTT), BMP, urinalysis
• Sputum cultures, AFB smear/culture (if TB suspected)
• ANA, ANCA, anti-GBM antibodies (if vasculitis/Goodpasture suspected)
• D-dimer / BNP if PE or CHF suspected

Imaging

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Management

Non-Massive Hemoptysis

• No risk factors (young, non-smoker, normal CXR): treat underlying infection, close follow-up
• With risk factors (age >40, smoker, abnormal CXR): CT chest + bronchoscopy + treat underlying cause

Massive Hemoptysis - Emergency Approach

• Place patient in lateral decubitus, bleeding side DOWN - prevents blood spilling into the unaffected lung
• Supplemental oxygen
• Avoid aggressive sedation - cough reflex is the patient's own airway clearance mechanism

• Single-lumen ET tube (≥8 Fr) - easier placement, allows bronchoscopy
• Double-lumen ET tube (DLT) - isolates each hemithorax independently; requires expertise
• Endobronchial blocker - balloon tamponade of bleeding segment via bronchoscope

• First-line definitive procedure for massive hemoptysis
• Controls bleeding in 75-90% of patients
• Rebleeding rate: 20-50% without definitive surgery
• Complications: post-embolization syndrome (fever, pleuritic pain, dysphagia - resolves in 5-7 days), rare: spinal cord infarction, esophageal/bronchial necrosis

• Salvage strategy after failed embolization
• Better outcomes in elective (non-urgent) setting

• Nd:YAG laser, argon plasma coagulation, electrocautery - for localized endobronchial lesions
• Cryoprobe - for clot removal

Specific Therapies

• Anticoagulation reversal if on anticoagulants
• Blood products: FFP, platelets for coagulopathy/thrombocytopenia
• Desmopressin (DDAVP) - for platelet dysfunction in renal failure
• Immunosuppression - for vasculitis/DAH
• Tranexamic acid - antifibrinolytic; used increasingly but evidence still evolving
• Bevacizumab/VEGF inhibitors - associated with life-threatening hemoptysis in squamous NSCLC - use with caution or avoid

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Key Points

• Death from hemoptysis = asphyxiation, not exsanguination
• Bronchial (high-pressure) circulation = source of most massive hemoptysis
• Life-threatening hemoptysis = only 5-15% of all hemoptysis cases
• CT chest identifies the source in ~70-88% of cases; superior to bronchoscopy for parenchymal causes
• BAE is the first-line intervention; surgery is reserved for failure/recurrence
• Always rule out pseudohemoptysis (epistaxis, hematemesis) before workup

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