Pediatric Heart Murmurs

This table summarizes common pediatric heart murmurs, with emphasis on distinguishing innocent from pathologic murmurs. It is intended as a study and review aid, not a substitute for clinical judgment.

Urgent Action Required (Red Flags)

Before reviewing the murmurs, it is critical to recognize the signs that demand immediate action. If a child with a heart murmur presents with any of the following, it constitutes a medical emergency requiring prompt evaluation and referral to a pediatric cardiologist.

Infants:

Cyanosis (bluish skin, lips, or nails)
Poor feeding, sweating or breathing hard with feeds
Failure to thrive or poor weight gain
Tachypnea (rapid breathing) or increased work of breathing

Older Children:

Chest pain, especially with exertion
Syncope (fainting) or dizziness, particularly with exercise
Reduced exercise tolerance compared to peers
Palpitations

Any Age:

A harsh, loud murmur (Grade 3/6 or higher)
A palpable thrill (vibration felt on the chest)
Abnormal heart sounds (e.g., a single or widely split fixed S2)
Weak or absent femoral pulses

Summary Table of Pediatric Murmurs

Murmur / Lesion	Type	Timing	Location & Radiation	Quality / Pitch	Position & Maneuvers	Key Associated Features / Notes	Treatment
Innocent (Physiologic) Murmurs
Still’s murmur	Innocent	Midsystolic, early–mid systolic; short; grade I–II (occasionally III).	Left lower sternal border (LLSB) and/or apex; no significant radiation.	Vibratory, musical, “twanging string”; low–medium pitch.	Louder in the supine position and with increased cardiac output (fever, anxiety, anemia); softer or disappears when sitting or standing.	Common between ~3–7 years; normal S2; no clicks, no thrill, normal pulses and growth. One of the classic “seven S’s” of innocent murmurs (systolic, soft, short, small area, single, sweet, sensitive to position).	Reassurance only
Innocent pulmonary flow murmur	Innocent	Midsystolic ejection; grade I–III.	Left upper sternal border (LUSB), pulmonic area; minimal or no radiation.	Soft, blowing, non-harsh.	Louder supine and with increased flow (fever, exercise); decreases with standing or Valsalva.	Normal S2; no clicks; normal pulses and exam. Must be distinguished from pulmonary valve stenosis (which is harsher, may have a click, and can radiate).	Reassurance
Venous hum	Innocent	Continuous (systolic & diastolic), often louder in diastole; low grade.	Infraclavicular and supraclavicular areas, especially right side; best heard over the neck near the clavicle.	Soft, humming; low pitch.	Disappears or diminishes when the child is supine, when the neck is flexed or turned, or with gentle jugular vein compression; loudest sitting or standing.	Only common innocent murmur with a diastolic component; due to venous flow in jugular/subclavian veins; normal cardiac exam otherwise.	Reassurance
Supraclavicular / carotid systolic bruit	Innocent	Brief early systolic; grade I–III.	Supraclavicular fossae and over carotid arteries; may radiate to neck.	Harsh but very short; high frequency.	Louder with head extension; may decrease with gentle carotid compression.	Due to turbulent flow in great vessels; normal S2, pulses, and blood pressure; distinguish from aortic stenosis (which is longer, radiates widely, and often has a thrill).	Reassurance
Peripheral pulmonary flow murmur of the newborn	Innocent	Midsystolic ejection; soft, low grade.	LUSB with radiation to axillae and back.	Soft, blowing.	Often heard in premature or small infants; typically resolves by 3–6 months of age.	Due to relative narrowing of peripheral pulmonary arteries; normal pulses, saturations, and growth; must be distinguished from true branch pulmonary artery stenosis in syndromic infants.	Follow up to ensure resolution
Pathologic Murmurs – Septal Defects & Shunts
Ventricular septal defect (VSD)	Pathologic	Classically holosystolic (pansystolic); may be early systolic if very small; grade II–IV, often with thrill.	LLSB; may radiate across precordium; small muscular VSDs often very localized.	Harsh, blowing.	Intensity often inversely related to defect size (small VSD → louder murmur); may soften as pulmonary vascular resistance rises or with very large defects and heart failure.	Large VSDs: tachypnea, poor feeding, failure to thrive, hepatomegaly; possible mid-diastolic rumble at apex from increased flow across mitral valve; risk of pulmonary hypertension and Eisenmenger if untreated.	Urgent if heart failure; may close spontaneously; otherwise medical or surgical repair
Atrial septal defect (ASD – secundum)	Pathologic	Systolic ejection murmur; mid-systolic; grade II–III.	LUSB (pulmonic area); may have wide radiation but usually not harsh.	Soft, blowing ejection murmur from increased flow across pulmonary valve; not from the defect itself.	Fixed, widely split S2 is classic; murmur intensity may increase with increased pulmonary blood flow.	Often asymptomatic in childhood; large defects → exercise intolerance, frequent respiratory infections; right ventricular heave; risk of pulmonary hypertension in adulthood if unrepaired. Holt-Oram Syndrome	Elective closure to prevent long-term complications
Atrioventricular septal defect (AVSD / AV canal)	Pathologic	Holosystolic murmur (VSD component) ± mid-diastolic rumble (increased AV valve flow).	LLSB and apex; may radiate widely.	Harsh holosystolic plus low-frequency diastolic rumble.	Murmur appears as pulmonary vascular resistance falls in early infancy; may be softer in very large defects with severe heart failure.	Strongly associated with Down syndrome; early congestive heart failure, poor growth, tachypnea; often requires early surgical repair.	Requires early surgical repair
Patent ductus arteriosus (PDA)	Pathologic	Classically continuous “machinery” murmur (systolic–diastolic), often louder in systole; grade II–IV.	Left infraclavicular area and LUSB; may radiate to back.	Rough, “machinery-like,” continuous.	Murmur may diminish if pulmonary vascular resistance becomes very high; bounding pulses and wide pulse pressure are typical.	Large PDA: tachypnea, poor feeding, failure to thrive; risk of pulmonary hypertension and Eisenmenger; in preterm infants, may present with respiratory distress and feeding intolerance. Prematurity & congenital rubella	Urgent if heart failure; medical closure (preemies), catheter device, or surgery
Other continuous murmurs (e.g., aortopulmonary window, coronary fistula)	Pathologic	Continuous or systolic-dominant.	Variable; often along LUSB or precordium.	Harsh, machinery-like or blowing.	Do not disappear with position changes (unlike venous hum).	Always consider pathologic continuous murmurs if not clearly a venous hum or PDA; often require imaging for diagnosis.
Pathologic Murmurs – Outflow Tract Obstruction
Pulmonary valve stenosis	Pathologic	Systolic ejection murmur; crescendo–decrescendo; grade II–IV.	LUSB; radiates to back; may have a systolic ejection click best at LUSB that decreases with inspiration.	Harsh ejection quality.	Murmur intensity and duration increase with severity; wide splitting of S2; click may vary with respiration.	Severe stenosis: exertional dyspnea, fatigue, cyanosis in infants with critical obstruction; right ventricular heave; may be isolated or part of syndromes (e.g., Noonan).	Urgent in newborns with cyanosis; balloon valvuloplasty
Aortic valve stenosis (valvar)	Pathologic	Systolic ejection murmur; crescendo–decrescendo; grade II–IV, often with thrill.	Right upper sternal border (RUSB); radiates to carotids and sometimes apex.	Harsh, rough ejection murmur; may have systolic ejection click at apex or RUSB.	Murmur louder with increased preload; may decrease with Valsalva; paradoxical splitting of S2 in severe disease.	Symptoms: exertional chest pain, syncope, dyspnea; diminished or delayed carotid upstroke; may be due to bicuspid aortic valve; risk of sudden death with severe obstruction. WIlliams Syndrome	Urgent if syncope, chest pain, or HF; balloon valvuloplasty or surgery
Subvalvar / supravalvar aortic stenosis	Pathologic	Systolic ejection murmur similar to valvar AS.	RUSB or mid-left sternal border; radiates to neck.	Harsh ejection.	Often indistinguishable from valvar AS by auscultation alone.	Supravalvar AS associated with Williams syndrome; may have systemic hypertension and characteristic facies; imaging required for precise diagnosis.
Coarctation of the aorta	Pathologic	Systolic murmur; may extend into early diastole; grade II–III.	Left infrascapular area (back) and LSB; may be heard at LUSB.	Blowing, medium pitch.	Murmur may be subtle; check four-limb blood pressures and femoral pulses (diminished or delayed).	Upper extremity hypertension, lower extremity hypotension; differential cyanosis in ductal-dependent lesions; in neonates, may present in shock when ductus closes; often associated with bicuspid aortic valve. Turner Syndrome	Critical in newborns; prostaglandin + surgical/balloon repair
Hypertrophic cardiomyopathy (HCM)	Pathologic	Systolic ejection murmur; crescendo–decrescendo; mid to late systolic.	LLSB and apex; may radiate to base.	Harsh, medium–high pitch.	Increases with maneuvers that decrease preload or afterload (standing, Valsalva, amyl nitrite); decreases with squatting or handgrip (increased afterload/preload).	May have S4, bisferiens carotid pulse; family history of sudden death; exertional syncope or chest pain; always consider in athletic adolescents with murmurs.	Urgent if syncope or exertional symptoms; activity restriction; cardiology management
Pathologic Murmurs – Regurgitant & Valvular Lesions
Mitral regurgitation (MR)	Pathologic	Holosystolic; grade II–IV.	Apex; radiates to left axilla (classic) and sometimes to back.	Blowing, high-pitched.	Intensity may increase with handgrip (increased afterload); may be softer in acute severe MR.	Causes: rheumatic disease, congenital lesions, endocarditis, cardiomyopathy; may have S3, displaced apical impulse, signs of left-sided heart failure.	Medical therapy; surgery if severe
Mitral valve prolapse (MVP)	Pathologic (though often benign course)	Mid-to-late systolic murmur following a midsystolic click.	Apex; limited radiation.	Late systolic, blowing; click is high-pitched.	Click and murmur move earlier and become louder with decreased preload (standing, Valsalva); move later with squatting or handgrip.	May be associated with chest pain, palpitations; can progress to significant MR; sometimes associated with connective tissue disorders (e.g., Marfan).	Usually benign; treat MR if present
Tricuspid regurgitation (TR)	Pathologic	Holosystolic; grade II–IV.	LLSB; may radiate to right lower sternal border or epigastrium.	Blowing, high-pitched.	Increases with inspiration (Carvallo sign); may decrease with expiration.	Often secondary to pulmonary hypertension or right ventricular dilation; may have hepatomegaly, peripheral edema, prominent jugular venous pulsations in older patients.	Treat underlying cause
Aortic regurgitation (AR)	Pathologic	Early diastolic, decrescendo; high-pitched; grade II–III.	Left sternal border (3rd–4th intercostal space) or RUSB; may radiate along LSB.	Blowing, high-frequency.	Best heard with diaphragm, patient sitting up, leaning forward, in end-expiration.	Wide pulse pressure, bounding pulses; may have Austin Flint mid-diastolic rumble at apex; causes include bicuspid aortic valve, rheumatic disease, aortic root dilation.	Urgent if HF; valve replacement if severe
Pulmonary regurgitation (e.g., Graham Steell murmur)	Pathologic	Early diastolic, decrescendo; high-pitched.	LUSB; may radiate down LSB.	Blowing, high-frequency.	Best heard with diaphragm, patient sitting up; often associated with loud P2.	Common in patients with pulmonary hypertension or after repair of tetralogy of Fallot; may contribute to right ventricular dilation and dysfunction.	Usually not urgent; valve replacement later if needed
Mitral stenosis (MS)	Pathologic	Mid-diastolic rumble with presystolic accentuation (if sinus rhythm); low-pitched.	Apex; localized.	Rumbling, low-frequency; opening snap after S2 in rheumatic MS.	Best heard with bell at apex in left lateral decubitus position.	Rare in children in high-income settings; usually rheumatic; associated with pulmonary hypertension, loud S1, and signs of left atrial enlargement.
Pathologic Murmurs – Cyanotic Congenital Heart Disease
Tetralogy of Fallot (TOF)	Pathologic	Systolic ejection murmur; crescendo–decrescendo; grade II–IV.	LSB (mid to upper); may radiate widely.	Harsh ejection murmur from right ventricular outflow tract obstruction.	Murmur intensity often inversely related to degree of right-to-left shunt (very severe obstruction → softer murmur but more cyanosis).	Cyanosis, clubbing, “tet spells” (hypercyanotic episodes), single S2; boot-shaped heart on imaging; requires surgical repair.	Tet spells are emergencies; surgical repair required
Transposition of the great arteries (TGA)	Pathologic	Often no characteristic murmur or only a soft nonspecific systolic murmur.	Variable; may be LSB or LUSB if associated VSD or outflow obstruction.	Soft systolic if present.	Murmur not a reliable feature; focus on saturations and clinical status.	Profound cyanosis in the newborn period; may have single loud S2; ductal and septal patency critical for mixing; emergent diagnosis and management required.	Emergent diagnosis; prostaglandin + surgery
Truncus arteriosus	Pathologic	Systolic ejection murmur ± diastolic regurgitant murmur.	LSB or LUSB.	Harsh systolic from increased flow; possible early diastolic murmur of truncal valve regurgitation.	Murmur appears as pulmonary vascular resistance falls; may be accompanied by bounding pulses.	Early heart failure, tachypnea, poor feeding; single S2; requires early surgical repair.	Early surgical repair
Total anomalous pulmonary venous return (TAPVR)	Pathologic	Often soft systolic ejection murmur; may be absent.	LUSB if present.	Soft ejection.	Fixed split S2 may be present due to increased right-sided flow.	Cyanosis, respiratory distress in newborn; may have signs of pulmonary venous obstruction (tachypnea, pulmonary edema); murmur is not a prominent feature.	Emergent repair if obstructed
Tricuspid atresia / single ventricle physiology	Pathologic	Often holosystolic murmur from VSD or AV valve regurgitation; may have continuous or diastolic components depending on associated lesions.	LLSB or apex; variable.	Harsh or blowing.	Murmur pattern depends on associated shunts and outflow obstruction.	Cyanosis, heart failure, abnormal pulses; diagnosis relies heavily on imaging; murmur alone is not specific.
Global Red Flags & Innocent vs Pathologic Clues
Innocent vs pathologic – key auscultatory clues	Summary	Innocent: always systolic (except venous hum); short; low grade (≤ II–III); no diastolic component. Pathologic: any diastolic murmur, holosystolic, or continuous (non–venous hum) is pathologic until proven otherwise.	Innocent: localized, no significant radiation. Pathologic: often radiates to back, neck, or axilla.	Innocent: “soft,” “sweet,” musical, non-harsh. Pathologic: harsh, blowing, or rough; may have clicks, gallops, or abnormal S2.	Innocent: often change with position (softer standing) and with physiologic state; pathologic: usually persistent and less position-dependent.	Red flags: grade ≥ III, thrill, abnormal S2 (single, fixed split, paradoxical), clicks, diastolic murmurs, symptoms (cyanosis, syncope, chest pain with exertion, poor feeding, failure to thrive), abnormal pulses or blood pressures, family history of sudden death or cardiomyopathy.