Heart Murmurs by Condition

Murmur Grading (Levine Scale)

1. Systolic Murmurs

Holosystolic (Pansystolic) Murmurs

Mitral Regurgitation (MR)

• Murmur: High-pitched, blowing, holosystolic murmur at the apex, radiating to the axilla or left scapula
• Chronic MR: The murmur begins with S1 and persists through and may obscure S2
• Acute MR (e.g. papillary muscle rupture post-MI): Harsh apical systolic murmur that may end before S2 because the acute rise in left atrial pressure equalizes LV-LA pressure early
• Why: The mitral valve fails to coapt properly during systole. Blood flows backwards from the high-pressure LV into the low-pressure LA throughout the entire systolic period, creating sustained turbulence. The regurgitant jet against the LA wall generates the characteristic high-frequency sound
• Associated findings: Soft or absent S1 (poor leaflet closure), S3 gallop (increased LV filling), displaced apical impulse

Tricuspid Regurgitation (TR)

• Murmur: Holosystolic at the lower left sternal border (LLSB); increases with inspiration (Carvallo's sign - increased venous return to the right heart augments the murmur)
• Why: Similar mechanism to MR but in the right heart - the RV ejects blood back into the RA. The Carvallo's sign is pathognomonic because inspiration increases right-sided filling and therefore more blood regurgitates
• Associated: Prominent CV waves in the JVP, pulsatile hepatomegaly

Ventricular Septal Defect (VSD)

• Murmur: Harsh holosystolic murmur, left sternal border, grade 4-5/6, with a palpable thrill
• Why: During systole, the high-pressure LV shunts blood left-to-right through the defect into the lower-pressure RV, generating turbulence throughout systole
• Important exception: In large VSDs with pulmonary hypertension (Eisenmenger syndrome), the RV pressure rises to match LV, the pressure gradient diminishes, and the murmur becomes shorter (early systolic only) or disappears entirely - replaced by signs of pulmonary hypertension

Midsystolic (Ejection) Murmurs

Aortic Stenosis (AS)

• Murmur: Harsh, rough, crescendo-decrescendo (diamond-shaped) midsystolic murmur, loudest at the right 2nd intercostal space (aortic area), radiating into the carotids
• Gallavardin effect: The murmur transmits to the apex where it sounds higher-pitched and more musical - can be mistaken for MR
• Why: The calcified/fused aortic valve leaflets create a narrowed orifice. Blood must accelerate through this stenotic orifice during ejection, producing turbulence that peaks at mid-systole when flow velocity is highest. The crescendo-decrescendo shape mirrors the ventricular ejection profile
• Associated: Slow-rising, sustained, small-amplitude carotid pulse (pulsus parvus et tardus); paradoxical split of S2 (delayed A2 due to prolonged LV ejection); loss of A2 in severe disease; S4 gallop

Pulmonary Stenosis (PS)

• Murmur: Crescendo-decrescendo at the left 2nd intercostal space (pulmonic area); murmur spills through A2 and ends at the delayed P2 (because RV takes longer to eject through the stenotic pulmonic valve)
• Why: Same mechanism as AS but on the right side. The delay in P2 is a key distinguishing feature - pulmonic valve closure is pushed later in time because the RV empties slowly through the stenosis
• Associated: Wide splitting of S2 (delayed P2), ejection click (in mild PS), RV heave

Hypertrophic Obstructive Cardiomyopathy (HOCM)

• Murmur: Harsh midsystolic murmur at the LLSB and apex, does NOT radiate to the carotids (unlike AS)
• Why: The hypertrophied interventricular septum obstructs the LV outflow tract (LVOT) during systole. The systolic anterior motion (SAM) of the mitral valve also contributes. The outflow gradient is dynamic - it worsens when the LV is smaller (preload reduction) and improves when the LV is larger (increased preload)
• Maneuvers (critical for HOCM):
  • Valsalva (strain phase) / Standing up: Increases murmur (reduces preload, smaller LV, more obstruction)
  • Squatting / Leg raise: Decreases murmur (increases preload, larger LV, less obstruction)
  • This is opposite to AS, where Valsalva decreases the murmur

Late Systolic Murmurs

Mitral Valve Prolapse (MVP)

• Murmur: Mid-to-late systolic murmur preceded by a non-ejection mid-systolic click, both heard best at the apex; the murmur crescendos into S2
• Why: The redundant mitral leaflets billow into the LA in mid-systole. When leaflet coaptation fails, a regurgitant jet begins - hence the murmur starts late. The click represents the sudden tensing of the chordae tendineae as the leaflets reach maximal prolapse
• Maneuver trick: With Valsalva or standing (reduced preload, smaller LV), the LV reaches its critical volume earlier - the click and murmur move toward S1. With squatting (increased preload, larger LV), they move toward S2

2. Diastolic Murmurs

Early Diastolic Murmurs

Aortic Regurgitation (AR)

• Murmur: High-pitched, blowing, decrescendo diastolic murmur beginning immediately after A2, heard best at the left sternal border 3rd/4th intercostal space (Erb's point) with the patient leaning forward and breath held in expiration
• Why: The incompetent aortic valve allows blood to flow back from the high-pressure aorta into the LV throughout diastole. The murmur is loudest at the beginning of diastole when the aorto-ventricular pressure gradient is greatest, then decrescendos as the gradient diminishes over diastole
• Austin Flint murmur: In severe AR, the regurgitant jet streams across the open anterior mitral leaflet, causing it to flutter and creating a mid-diastolic rumble (mimics MS but without the opening snap)
• Peripheral signs of severe AR: Wide pulse pressure, collapsing ("water-hammer") pulse, Corrigan's pulse, Quincke's sign, Duroziez's sign, de Musset's sign (head nodding)

Pulmonary Regurgitation (PR)

• Graham Steell murmur: High-pitched, blowing, early diastolic decrescendo at the left 2nd ICS, associated with pulmonary hypertension
• Why: Pulmonary hypertension dilates the pulmonary artery and the annulus, preventing leaflet coaptation. The high diastolic pressure in the pulmonary artery drives blood back into the RV

Mid-to-Late Diastolic Murmurs

Mitral Stenosis (MS)

• Murmur: Low-pitched, rumbling, mid-diastolic murmur (best heard with the bell of the stethoscope) at the apex with the patient in the left lateral decubitus position; presystolic accentuation in sinus rhythm (due to atrial contraction augmenting flow)
• Preceded by: An opening snap (OS) - a high-pitched clicking sound shortly after S2 when the stenotic but pliable valve is forced open by LA pressure. The shorter the S2-OS interval, the more severe the stenosis (high LA pressure opens the valve earlier)
• Why: The thickened/fused mitral leaflets (usually rheumatic) create a narrow orifice. Blood flows from the high-pressure LA into the LV throughout diastole, but the gradient drives turbulent flow that produces the rumble. Presystolic accentuation occurs because atrial contraction squeezes the last bolus of blood through the narrow valve
• Associated: Loud S1 (pliable leaflet snaps shut with force); small, tapping apical impulse (underfilled LV); signs of pulmonary congestion

Tricuspid Stenosis (TS)

• Murmur: Low-pitched mid-diastolic rumble at the LLSB; increases with inspiration (Carvallo's sign - more RA-RV gradient with increased venous return)
• Why: Same mechanism as MS on the right side - narrowed tricuspid orifice creates a diastolic RA-RV gradient

3. Continuous Murmurs

Patent Ductus Arteriosus (PDA)

• Murmur: Continuous, "machinery" murmur peaking at S2, heard best at the left infraclavicular area / left 2nd ICS - the Gibson murmur
• Why: There is a pressure gradient from the aorta to the pulmonary artery in both systole AND diastole. Aortic pressure exceeds pulmonary artery pressure throughout the entire cardiac cycle, so blood flows continuously from aorta to pulmonary artery, generating non-stop turbulence that peaks at the time of greatest aorto-pulmonary gradient (around S2, when aortic pressure is high and the pulmonary artery has just received its last systolic bolus)

Other Causes of Continuous Murmurs

Quick Reference Table

Key Bedside Maneuvers Summary

Breath Sounds: Types, Mechanisms, and Clinical Significance

Important Note on Terminology

Part 1: Normal Breath Sounds

1. Normal Breath Sounds (previously "Vesicular")

• Where heard: Over most of the lung periphery
• Character: Soft, low-pitched (200-600 Hz), non-musical; inspiratory phase is longer and louder than expiratory; expiratory sounds may be barely audible
• Why they sound this way:
  • The inspiratory component is generated by turbulent airflow in the lobar and segmental bronchi as air accelerates inward
  • The expiratory component originates in the larger, more central airways - by the time those sounds reach the chest wall, they have been dampened and filtered by the large air-filled lung volume, making them soft or absent
  • Intensity varies with regional ventilation - diminishes in hypoventilated zones
• Clinical pearl: Diminished or absent normal breath sounds = reduced airflow through that region (obstruction, effusion, pneumothorax, emphysema)

2. Tracheal Breath Sounds

• Where heard: Over the trachea, just below the sternal notch
• Character: Loud, hollow, harsh, non-musical (75-1600 Hz); equal in inspiration and expiration with a brief pause between phases
• Why: Air passes through the wide, rigid tracheal tube at high velocity with pronounced turbulence. There is minimal lung parenchyma to dampen the sound, so both phases are equally loud
• Normal only here - if heard in the lung periphery, they become pathological (see bronchial breath sounds below)

3. Bronchovesicular Breath Sounds

• Where heard: Over the 1st and 2nd intercostal spaces anteriorly, and between the scapulae posteriorly (near the main bronchi)
• Character: Intermediate intensity; inspiration and expiration roughly equal in length and loudness
• Why: These zones overlie large bronchi but also have surrounding alveolar tissue, creating a blend of tracheal-quality and peripheral dampening

Part 2: Adventitious (Abnormal) Breath Sounds

Continuous Adventitious Sounds

Bronchial (Tubular) Breath Sounds

• Character: Loud, harsh, high-pitched; expiratory phase is longer and louder than inspiratory (the reverse of normal); a distinct gap exists between inspiration and expiration
• Where pathologically heard: Peripheral lung zones where vesicular sounds should be present
• Why this happens: In normal lungs, the large central airway sounds are filtered and dampened by air-filled alveoli before reaching the chest wall. When alveoli become consolidated (filled with fluid, pus, or blood - as in pneumonia) or collapsed (atelectasis), they lose their air cushion but remain connected to a patent bronchus. They now transmit large-airway sounds directly to the chest wall without filtering - like listening through a solid medium instead of air
• Conditions: Lobar pneumonia (classic), pulmonary infarction, compression atelectasis adjacent to a large effusion (Skodaic resonance zone)
• Associated signs: Increased vocal fremitus, bronchophony, egophony ("E to A" change), whispered pectoriloquy

Wheezes

• Character: Continuous musical sound lasting >250 ms; high-pitched (dominant frequency ≥400 Hz); hissing quality; predominantly expiratory but can be bi-phasic in severe airflow obstruction
• Mechanism: Generated by two mechanisms acting together in a narrowed airway:
  1. Limitation of airflow - narrowed lumen creates a velocity gradient
  2. Airway wall vibration - the walls flutter like a reed instrument as high-velocity air flows past them (the "flutter mechanism")
• Expiration is more commonly affected because during expiration, dynamic airway compression adds to any existing narrowing, causing walls to appose and vibrate
• Conditions producing wheezes:
  • Asthma: Diffuse bronchospasm + mucosal edema + mucus plugging; can be bi-phasic in a severe attack. A "silent chest" in severe asthma is ominous - so little air movement that no wheeze is generated
  • COPD: Chronic airway narrowing from inflammation, loss of elastic recoil, and mucus; typically diffuse, expiratory
  • Cardiac asthma: Left heart failure floods peribronchial tissue, compressing airways from the outside
  • Anaphylaxis: Massive bronchospasm
  • Focal/fixed wheeze: A single persistent wheeze at the same location = partial bronchial obstruction by a tumour, foreign body, or lymph node pressing on airway; does not clear with coughing

Rhonchi

• Character: Continuous, low-pitched (dominant frequency <200 Hz); snoring or gurgling quality; lasting >250 ms; heard in expiration (occasionally both phases)
• Mechanism: Caused by secretions (liquid or mucus) in large airways partially blocking the lumen. As airflow passes through or around mucus, it causes the secretions and the airway walls to oscillate
• Key distinguishing feature: Rhonchi change or clear after coughing (the cough repositions or expels the secretions, altering or eliminating the sound). Wheezes do NOT clear with coughing
• Conditions: Bronchitis, COPD with mucus hypersecretion, bronchiectasis, retained secretions post-operatively

Stridor

• Character: High-pitched, continuous, predominantly inspiratory musical sound; best heard over the neck and upper trachea, not the chest
• Mechanism: Turbulent airflow through a significantly narrowed extrathoracic (upper) airway. During inspiration, negative intraluminal pressure causes the already-narrowed extrathoracic airway to collapse further, generating intense turbulence and the characteristic sound. During expiration, positive intraluminal pressure stents the airway open, so the sound is less prominent
• Fixed lesions (not dynamic) produce stridor in both inspiration and expiration
• Conditions: Croup (in children - subglottic edema), epiglottitis, anaphylaxis (laryngeal edema), foreign body, laryngeal tumour, postintubation subglottic stenosis, tracheal compression by a goitre or mediastinal mass
• Clinically critical: Stridor signals a potentially life-threatening upper airway obstruction and demands urgent assessment. It is sometimes mistaken for a wheeze - the key difference is that stridor is inspiratory, over the neck, while wheeze is expiratory, over the chest

Discontinuous Adventitious Sounds

Fine Crackles (Fine Rales / Crepitations)

• Character: Soft, high-pitched, short-duration explosive pops; mid-to-late inspiratory (heard toward the end of inspiration); not altered by coughing; sound like rubbing strands of hair together near the ear, or the sound of pulling velcro apart
• Mechanism: During expiration, small airways and alveoli in dependent lung zones close prematurely under the weight of the lung and increased surface tension. On the next inspiration, when airway opening pressure is reached, these collapsed airways snap open explosively - the rapid release of stored pressure creates the crackling pop. The sound occurs late in inspiration because the terminal airways open last, after the larger airways have already opened
• Conditions:
  • Pulmonary fibrosis / Interstitial lung disease: Stiff, inelastic alveoli and airways collapse and snap open repeatedly; classic bilateral basal fine crackles, sometimes described as "Velcro rales"
  • Pulmonary oedema (heart failure): Fluid in alveoli increases surface tension, causing premature airway closure; bilateral basal fine crackles, may become more widespread as oedema worsens
  • Early pneumonia: Alveolar fluid causes the same mechanism as oedema
  • Atelectasis: Crackles from re-expansion of collapsed segments; may clear with deep breathing

Coarse Crackles

• Character: Louder, lower-pitched, longer-duration explosive pops; early inspiratory (and sometimes expiratory); often change or clear with coughing
• Mechanism: Opening of larger, more proximal airways (bronchi) that have collapsed due to secretions or loss of structural support. The larger airway generates a louder, lower-frequency pop
• Conditions: Bronchiectasis (classic), chronic bronchitis, COPD with secretions, resolving pneumonia with retained secretions. The fact that they change with coughing distinguishes them from fine crackles

Clinical distinction - Fine vs. Coarse Crackles

Extrapulmonary Sounds

Pleural Friction Rub

• Character: Coarse, leathery, creaking, or grating sound; heard in both inspiration and expiration (biphasic); typically loudest at the lung base; sounds "close to the ear"; does NOT change with coughing; may be exaggerated by pressing the stethoscope firmly
• Mechanism: Normally the visceral and parietal pleural surfaces slide smoothly over each other, lubricated by a thin film of pleural fluid. When pleural surfaces are thickened and roughened by inflammation or tumour, sliding is impaired and friction generates the sound - like two pieces of leather rubbing together. The sound is generated by the change in shape of thickened pleura itself (even a small amount of fluid remains between surfaces)
• Conditions: Pleuritis (pleurisy) from pneumonia, pulmonary embolism/infarction, viral pleuritis, tuberculosis, mesothelioma, uraemic pleuritis
• Important: A rub may temporarily disappear if a large effusion develops (fluid separates the surfaces) - but can reappear at the effusion margins

Mediastinal Crunch (Hamman's Sign)

• Character: Crunching, crackling sounds synchronous with cardiac contraction (not respiration); heard over the precordium
• Mechanism: Air in the mediastinum (pneumomediastinum) is compressed by each heartbeat, creating the crunching sound
• Conditions: Spontaneous pneumomediastinum, oesophageal rupture (Boerhaave syndrome), barotrauma

Part 3: Voice Sounds

Part 4: Complete Clinical Reference Table

Summary: Why Each Sound Occurs