Causes of different murmers and their features

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Heart Murmurs: Causes and Features

What Produces a Murmur?

Murmurs arise from audible turbulence due to:
  • Accelerated flow through normal or abnormal orifices
  • Flow through a narrowed/irregular orifice into a dilated vessel/chamber
  • Backward (regurgitant) flow through an incompetent valve, VSD, or PDA
Grading (I–VI): Grade 1 = barely audible; Grade 3+ = loud (structurally significant); Grade 4+ = palpable thrill; Grade 5 = heard with stethoscope edge only; Grade 6 = heard off chest.

Murmur Timing Diagrams

Principal heart murmurs diagram
A = presystolic (MS/TS in sinus rhythm); B = holosystolic (MR/TR/VSD); C = ejection murmur with ejection click (AS); D = PS murmur spilling past A2; E = AR diastolic murmur; F = MS after opening snap; G = short mid-diastolic after S3; H = continuous murmur (PDA)

SYSTOLIC MURMURS

Mechanism Comparison

MR vs AS murmur mechanism
AV regurgitation (MR) → holosystolic plateau murmur from MVC to MVO. Semilunar valve obstruction (AS) → ejection murmur from AVO to AVC, with crescendo-decrescendo (diamond) shape.

1. Holosystolic (Pansystolic) Murmurs

Extend from S1 to S2 — caused by a sustained pressure gradient between two chambers throughout systole.
ConditionCauseBest HeardKey Features
Mitral regurgitation (MR)Mitral prolapse, rheumatic, flail leaflet, ischemia, dilated CMPApexHigh-pitched, blowing, plateau quality; radiates to axilla (posterior jet) or LSB (anterior jet). "Honking" quality in MVP.
Tricuspid regurgitation (TR)Functional RV dilation, endocarditis, carcinoidLower LSBIncreases with inspiration (Carvallo's sign); regurgitant CV waves in JVP
VSD (large)Congenital / acquiredLSB 3rd–4th ICSHarsh; loud (grade 4–5) in small restrictive VSDs; becomes limited to early systole if pulmonary HTN develops

2. Early Systolic Murmurs

Begin at S1, end before midsystole.
ConditionCauseFeatures
Acute severe MRPapillary muscle rupture, chordal tearEarly decrescendo; into a normal-sized, non-compliant LA; best heard medial to apex
Small muscular VSDCongenital; defect closes during contractionLocalized to LSB, grade 4–5; absent signs of pulmonary HTN
TR with normal PA pressureInfective endocarditisSoft (grade 1–2), LSB, increases with inspiration; no right heart failure signs

3. Midsystolic (Ejection) Murmurs

Begin after S1, end before S2 — crescendo-decrescendo shape.
ConditionCauseBest HeardKey Features
Aortic stenosis (AS)Calcific (elderly), bicuspid AV, rheumaticRight 2nd ICS → carotidsHarsh, radiates to carotids; Gallavardin effect (purer/higher at apex); associated with slow-rising pulse, narrow PP, absent A2 in severe disease
Pulmonic stenosis (PS)CongenitalLeft 2nd ICSPreceded by ejection click; murmur peaks later and spills past A2; wide split S2; P2 delayed/soft
HOCMDynamic LV outflow obstructionLSB / apexIncreases with Valsalva and standing (reduced preload); decreases with squatting; does NOT radiate to carotids
Aortic sclerosisThickened non-obstructive AV leafletsRight 2nd ICSGrade 1–2; normal A2; no carotid radiation; normal carotid upstroke
High-flow statesAnemia, fever, pregnancy, hyperthyroidism, AV fistulaVariableSoft, grade 1–2, no associated abnormal heart sounds
ASDIncreased flow across PVLeft 2nd ICSFixed wide split S2 is the key finding; murmur itself is often soft

4. Late Systolic Murmurs

ConditionCauseFeatures
Mitral valve prolapse (MVP)Myxomatous degenerationPreceded by a mid-systolic click; murmur moves earlier with standing/Valsalva (reduces preload, earlier prolapse); moves later with squatting

DIASTOLIC MURMURS

1. Diastolic Rumbles (Low-pitched, best with bell)

ConditionCauseBest HeardKey Features
Mitral stenosis (MS)Rheumatic fever (most common)Apex (left lateral decubitus)Low-pitched, rumbling; opening snap (OS) precedes it; presystolic accentuation in sinus rhythm; duration ∝ severity
Tricuspid stenosis (TS)Rheumatic (usually with MS), carcinoidLower LSBRare; increases with inspiration
Austin-Flint murmurAortic regurgitation jet strikes anterior MV leafletApexMid-diastolic rumble; mimics MS but no opening snap, no loud S1
Flow rumbleIncreased AV valve flow (severe MR/TR, ASD, VSD)Apex or LSBDue to volume overload causing relative stenosis across AV valve

2. Diastolic Decrescendo Murmurs (High-pitched, use diaphragm)

ConditionCauseBest HeardKey Features
Aortic regurgitation (AR)Bicuspid AV, rheumatic, endocarditis, aortic root dilation, aortitisLeft sternal border (3rd ICS)High-pitched blowing; heard leaning forward + breath held; murmur at right 2nd ICS → root dilation; duration and intensity ∝ severity. Wide pulse pressure, collapsing pulse, Corrigan's, water-hammer signs
Pulmonary regurgitation (PR)Functional (pulmonary HTN) — Graham Steell murmurLeft 2nd ICSLow-pitched (primary PR); high-pitched in Graham Steell (follows loud P2); increases with inspiration (differentiates from AR)

CONTINUOUS MURMURS

Begin in systole, continue through S2 into diastole — caused by a persistent pressure gradient across both phases of the cardiac cycle.
ConditionNotes
Patent ductus arteriosus (PDA)Classic "machinery" murmur; loudest at left infraclavicular/2nd ICS; peaks at S2
Ruptured sinus of Valsalva aneurysmSudden onset; aorta → RV/RA
Coronary/systemic AV fistulaContinuous over affected area
Cervical venous humBenign; disappears with neck compression or supine position
Mammary souffle of pregnancyBenign; disappears with pressure on stethoscope
Aortopulmonary septal defectRare congenital
Pulmonary artery branch stenosisPeripheral; radiates to both lung fields

Summary: Key Differentiating Maneuvers

ManeuverEffectUse
Valsalva / Standing↓ preload → louder HOCM/MVP; softer AS/MRHOCM vs AS
Squatting↑ preload → softer HOCM/MVP; louder AS/MRHOCM vs AS
Inspiration↑ right heart filling → louder TR, PR, TSRight-sided murmurs
Handgrip↑ afterload → louder MR, AR; softer HOCMMR vs HOCM
Leaning forwardBetter transmission of ARAR detection
Left lateral decubitusBetter MS detectionMS

Sources: Harrison's Principles of Internal Medicine 22E, pp. 326–334; Fuster & Hurst's The Heart 15th Ed., pp. 95–100

Examination findings in aortic regurgitation

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Examination Findings in Aortic Regurgitation

Causes (for context)

ValvularAortic RootCombined
Bicuspid AV, rheumatic, infective endocarditis, calcific degenerationHypertension, Marfan syndrome, aortic dissection, syphilitic aortitis, Ehlers-Danlos, Takayasu, giant cell aortitis, atherosclerotic aneurysmBicuspid AV + root dilation, ankylosing spondylitis

General Inspection

SignDescription
de Musset's signHead nodding/bobbing with each heartbeat — from large stroke volume
Awareness of heartbeatPatient notices pounding in chest, especially supine on left side

Pulse & Blood Pressure

SignDescription
Corrigan's pulse (water-hammer pulse)Abrupt distension then rapid collapse of the arterial pulse; best felt by elevating the patient's arm and palpating the radial artery
Bisferiens pulseDouble-peak systolic pulse; best appreciated in the brachial and femoral arteries
Wide pulse pressureElevated systolic (increased stroke volume) + reduced diastolic (runoff into LV); e.g. 160/40 mmHg
Hill's signPopliteal systolic BP exceeds brachial by >20 mmHg in moderate AR, >60 mmHg in severe AR
Duroziez's signSystolic and diastolic bruit heard over the femoral artery when partially compressed with stethoscope
Müller's signPulsation of the uvula
Quincke's signCapillary pulsation visible at the nail bed on gentle pressure
Traube's sign"Pistol-shot" (booming systolic and diastolic sounds) over the femoral artery
Note: Diastolic BP measured at phase IV Korotkoff (muffling), not disappearance, as sounds may persist to zero in severe AR.

Precordium

FindingDescription
Displaced apex beatLaterally and inferiorly displaced — reflecting LV dilation (cor bovinum in severe chronic disease)
Hyperdynamic apexDiffuse, forceful, volume-overloaded character
Palpable rapid filling waveFelt at apex
Systolic thrillAt the base of heart or suprasternal notch due to augmented stroke volume
Carotid shudderPalpable vibratory sensation in the carotid arteries

Auscultation

The Murmur

  • Character: High-pitched, blowing, decrescendo diastolic murmur beginning immediately after A2
  • Best heard: Sitting forward, leaning forward, breath held in deep expiration, using the diaphragm firmly at the left sternal border (3rd–4th ICS)
  • Location clue:
    • Left sternal border → primary valvular disease
    • Right sternal border (upper) → aortic root dilation
  • Severity correlates with duration (not intensity):
    • Mild AR → early diastolic only, soft, high-pitched blowing
    • Severe AR → holodiastolic, may have rough/musical quality
    • "Cooing dove" or musical quality → eversion or perforation of an aortic cusp
    • In severe AR with LV decompensation: late diastolic component disappears as LV and aortic pressures equalize

Other Auscultatory Findings

FindingSignificance
Austin Flint murmurMid-diastolic/pre-systolic low-pitched apical rumble in severe AR — AR jet strikes anterior MV leaflet causing it to vibrate; mimics MS but without opening snap
Systolic ejection murmur (harsh, at base, radiating to carotids)Due to greatly increased LV stroke volume and ejection rate — does not indicate concurrent AS; carotid palpation differentiates
S3 gallopIndicates elevated LV end-diastolic volume; suggests impaired LV function in severe AR
Soft or absent A2Severe valvular AR (leaflet destruction)

Summary: Key Named Signs

EponymSign
Corrigan's / water-hammer pulseCollapsing pulse
de Musset's signHead bobbing
Duroziez's signFemoral double bruit
Hill's signPopliteal BP > brachial BP
Traube's signPistol-shot femorals
Quincke's signNail-bed capillary pulsation
Müller's signUvular pulsation
Austin Flint murmurApical diastolic rumble (no MS)
Gallavardin effect (if concurrent AS)Systolic murmur sounds purer at apex

Acute vs Chronic AR — Key Differences on Exam

FeatureChronic ARAcute AR (e.g. endocarditis, dissection)
Pulse pressureWideMay be normal/only mildly elevated
Apex beatDisplaced, hyperdynamicNot displaced (LV not yet dilated)
Diastolic murmurLong, holodiastolicShort, early diastolic only (rapid LV/Ao pressure equalization)
S1NormalSoft or absent (premature mitral valve closure)
Signs of LV failureLateEarly and prominent (pulmonary oedema, shock)
Wide pulse pressure signs (Corrigan etc.)PresentMay be absent

Sources: Braunwald's Heart Disease 11E, pp. 718–720; Fuster & Hurst's The Heart 15th Ed., pp. 97–98; Harrison's Principles of Internal Medicine 22E
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