📋 Key Information Summary
- Cardiac murmurs arise from turbulent blood flow and require systematic characterisation by timing (systolic vs diastolic vs continuous), intensity (Levine I–VI/6), quality, radiation, and response to dynamic manoeuvres.
- Innocent (functional) murmurs are common in children (up to 80%) and young adults; they are always systolic, grade ≤ III/6, non-radiating, and disappear with positional change or Valsalva.
- Any diastolic murmur is pathological until proven otherwise and mandates echocardiography.
- Systolic murmurs are classified as ejection (crescendo–decrescendo) or pansystolic (holosystolic); ejection murmurs may be innocent or pathological, while pansystolic murmurs are always pathological.
- The most common pathological murmurs in Australia are aortic stenosis in the elderly, mitral regurgitation, and hypertrophic obstructive cardiomyopathy in young athletes.
- Bedside dynamic manoeuvres — Valsalva, squat-to-stand, passive leg elevation, and amyl nitrite inhalation — can differentiate murmurs when echocardiography is not immediately available.
- Transthoracic echocardiography (TTE) is the gold-standard investigation (MBS item 55124) and should be performed for any murmur graded ≥ III/6, any diastolic murmur, or any systolic murmur with symptoms.
- A 12-lead ECG (MBS item 11700) is essential for assessing chamber enlargement, conduction abnormalities, and arrhythmias associated with valvular disease.
- Continuous murmurs (e.g., patent ductus arteriosus, arteriovenous fistula) are always pathological and require urgent investigation.
- Rheumatic heart disease remains disproportionately prevalent in Aboriginal and Torres Strait Islander communities — echocardiographic screening programmes are in place across Northern Territory, Queensland, and Western Australia.
- Endocarditis prophylaxis (Australian Dental Association / Cardiac Society consensus) is indicated for prosthetic valves, previous infective endocarditis, and certain congenital heart diseases — NOT for native valvular disease alone.
- Red-flag features warranting urgent referral: new murmur with haemodynamic instability, syncope, chest pain, signs of heart failure, or sepsis.
Introduction & Australian Epidemiology
Cardiac murmurs are audible vibrations produced by turbulent blood flow within the heart or great vessels. While many murmurs are benign, others signify significant structural heart disease that may require medical or surgical intervention. A systematic approach to murmur characterisation — incorporating timing, character, radiation, dynamic manoeuvres, and associated clinical findings — is essential for accurate bedside diagnosis.
Australian epidemiology: Innocent murmurs are detected in up to 80% of healthy children and 10–15% of adults during routine examination. Degenerative calcific aortic stenosis affects approximately 3% of Australians aged >75 years, making it the most common valvular lesion requiring intervention in the elderly. Rheumatic heart disease (RHD) persists as a major health burden in Aboriginal and Torres Strait Islander communities, with notification rates exceeding 100 per 100,000 in some Northern Territory communities compared with <1 per 100,000 in the non-Indigenous population. Mitral valve prolapse affects 2–3% of the general population, while bicuspid aortic valve (present in 1–2% of Australians) is the most common congenital cardiac abnormality.
This guideline provides a structured approach to murmur classification, bedside differentiation of innocent from pathological murmurs, key murmur features, and appropriate investigation pathways within the Australian healthcare context.
Pathophysiology of Cardiac Murmurs
Murmur generation requires two conditions: (1) a pressure gradient across an orifice and (2) sufficient blood flow velocity to produce laminar flow disruption. The physical determinants are described by the simplified Bernoulli equation (ΔP = 4V²), where the pressure gradient is proportional to the square of flow velocity.
Mechanisms of Murmur Generation
- Valvular stenosis: Narrowing of a valve orifice accelerates flow, producing turbulence distal to the obstruction (e.g., aortic stenosis produces a systolic ejection murmur).
- Valvular regurgitation: Incomplete valve closure permits retrograde flow across a pressure gradient (e.g., mitral regurgitation produces a pansystolic murmur).
- Increased flow volume: Conditions such as anaemia, thyrotoxicosis, pregnancy, and arteriovenous fistulae increase cardiac output and flow velocity through normal valves.
- Structural abnormalities: Ventricular septal defects, patent ductus arteriosus, and hypertrophic cardiomyopathy create abnormal flow pathways.
- Tethering or prolapse: Elongated chordae tendineae or myxomatous degeneration alter valve geometry, causing regurgitation.
Clinical pearl: The intensity of a murmur does not always correlate with severity of disease. A soft murmur may indicate severe aortic stenosis when cardiac output is low (e.g., heart failure), while a loud murmur may indicate trivial regurgitation with high flow states.
Classification (Systolic, Diastolic, Continuous)
The first step in murmur assessment is timing within the cardiac cycle. Palpation of the carotid upstroke simultaneously with auscultation helps identify the first heart sound (S1) and hence the onset of systole.
| Timing | Subtype | Character | Causes |
|---|---|---|---|
| Systolic | Ejection (crescendo–decrescendo) | Diamond-shaped; begins after S1, peaks mid-systole, ends before S2 | Aortic stenosis, pulmonary stenosis, bicuspid aortic valve, innocent flow murmur, HOCM, aortic sclerosis |
| Pansystolic (holosystolic) | Flat intensity from S1 to S2 (or beyond) | Mitral regurgitation, tricuspid regurgitation, ventricular septal defect | |
| Diastolic | Early diastolic (decrescendo) | High-pitched, blowing; begins with S2, diminishes | Aortic regurgitation, pulmonary regurgitation |
| Mid-to-late diastolic (low-pitched rumble) | Best heard with bell at apex in left lateral decubitus | Mitral stenosis, Austin Flint murmur, Carey–Coombs murmur (acute rheumatic fever) | |
| Continuous | Throughout systole and diastole | Machinery-like; present in both phases | Patent ductus arteriosus, ruptured sinus of Valsalva, arteriovenous fistula, mammary soufflé (pregnancy) |
Key rule: All diastolic and continuous murmurs are pathological. They require echocardiography regardless of the clinical context. Do not dismiss these as benign.
Murphy Classification of Systolic Murmurs (Australian teaching standard)
- Group 1 — Early systolic: Begins with S1 and fades before S2. Causes: small muscular VSD, tricuspid regurgitation in the absence of pulmonary hypertension.
- Group 2 — Ejection systolic: Begins after S1, ends before S2. A gap exists at both ends. Causes: aortic stenosis, pulmonary stenosis, innocent murmur, HOCM, aortic sclerosis.
- Group 3 — Pansystolic: Begins with S1 and continues to or beyond S2. No gap. Causes: mitral regurgitation, tricuspid regurgitation, VSD.
- Group 4 — Late systolic: Begins mid-to-late systole, extends to S2. Causes: mitral valve prolapse, HOCM with late peaking.
Innocent vs Pathological Murmurs
Differentiating innocent (functional/benign) murmurs from pathological murmurs is one of the most important clinical skills in cardiology. Misclassification may lead to unnecessary anxiety and investigation, or conversely, missed serious pathology.
| Feature | Innocent Murmur | Pathological Murmur |
|---|---|---|
| Timing | Systolic only | Any timing (systolic, diastolic, continuous) |
| Grade | ≤ III/6 | Any grade; ≥ III/6 often pathological |
| Quality | Soft, musical, vibratory, blowing | Harsh, rough, rumbling |
| Radiation | Localised, no radiation to neck/axilla | Radiates to carotids (AS), axilla (MR), back (coarctation) |
| S1 / S2 | Normal S1 and S2; no added sounds | May have abnormal splitting, S3, S4, ejection click, opening snap |
| Positional change | Disappears or markedly changes with position | Persists across positions |
| Val manoeuvre | Diminishes | HOCM increases; AS and MR decrease |
| Symptoms | Asymptomatic; normal growth/development | Dyspnoea, syncope, chest pain, exercise intolerance, failure to thrive (paediatric) |
| Thrill | Absent (thrill = grade ≥ IV/6) | May be present |
Common Innocent Murmurs
| Murmur | Population | Features |
|---|---|---|
| Still's murmur | Children 3–8 years | Grade I–III/6, vibratory/groaning, lower left sternal border, supine → disappears sitting/standing |
| Pulmonary flow murmur | Children and young adults | Ejection systolic, left upper sternal border, accentuated by expiration |
| Venous hum | Children 3–10 years | Continuous, supraclavicular, abolished by turning head or compressing jugular vein |
| Mammary soufflé | Pregnant/postpartum women | Continuous, overbreast area, abolished by stethoscope pressure |
| Physiological flow murmur | All ages (fever, anaemia, pregnancy) | Soft ejection systolic, base, resolves when underlying condition treated |
Decision pathway: If a murmur is systolic, grade ≤ II/6, non-radiating, with no added heart sounds, no symptoms, and no thrill — it is very likely innocent. A cardiology referral is not mandatory, but documentation of the findings and clinical reasoning is essential. If any doubt exists, refer for echocardiography.
Key Murmurs & Their Features
The following table summarises the hallmark auscultatory findings, dynamic manoeuvre responses, and associated signs for the most clinically important murmurs encountered in Australian practice.
| Murmur | Location & Radiation | Pitch / Quality | Dynamic Response | Associated Signs |
|---|---|---|---|---|
| Aortic stenosis | Right upper sternal border → carotids (both); apex (Gallavardin phenomenon) | Harsh, rough, crescendo–decrescendo | ↓ Valsalva, ↓ squatting; ↑ handgrip may paradoxically soften | Slow-rising carotid upstroke (pulsus parvus et tardus), S4, narrow S2 splitting, ejection click if bicuspid valve |
| Mitral regurgitation | Apex → axilla; may radiate to left sternal border if posterior leaflet | Blowing, high-pitched, pansystolic | ↑ Handgrip; ↓ Valsalva; ↑ squatting; ↑ leg elevation | Displaced apex beat, S3, wide-apart S2 (early P2), AF common in chronic severe MR |
| Aortic regurgitation | Left lower sternal border (Erb's point); best heard sitting forward, end-expiration | High-pitched, blowing, decrescendo early diastolic | ↑ Sitting/leaning forward, end-expiration; ↑ handgrip increases murmur | Wide pulse pressure, collapsing (water-hammer) pulse, de Musset sign, Quincke sign, Duroziez sign, Austin Flint murmur at apex |
| Mitral stenosis | Apex (bell), left lateral decubitus; no radiation | Low-pitched rumbling, mid-diastolic ± presystolic crescendo | ↑ Exercise; ↑ left lateral decubitus; best heard with bell | Loud S1, opening snap (shorter OS–S2 interval = more severe stenosis), tapping apex beat, AF, signs of pulmonary hypertension |
| Hypertrophic obstructive cardiomyopathy (HOCM) | Left lower sternal border; no radiation to carotids | Harsh, crescendo–decrescendo, ejection systolic | ↑ Valsalva (classical distinguishing feature); ↓ squatting; ↑ standing from squat | Bifid pulse, double-apex beat, S4, associated with systolic anterior motion (SAM) of mitral valve on echo |
| Ventricular septal defect (VSD) | Left lower sternal border; may be localised or diffuse | Harsh, loud, pansystolic (small defects = louder) | Minimal dynamic change | Palpable thrill at left sternal border; large VSD → S3, displaced apex, signs of heart failure |
| Patent ductus arteriosus (PDA) | Left infraclavicular / upper left sternal border | Machinery-like continuous murmur | Minimal; may accentuate with inspiration | Bounding pulse, widened pulse pressure, displaced apex, S3 if large |
| Mitral valve prolapse (MVP) | Apex; may radiate to axilla if significant MR | Mid-to-late systolic click ± late systolic crescendo murmur | ↑ Valsalva/standing (click and murmur move earlier); ↓ squatting (click and murmur move later) | Click timing varies with preload; associated with Marfan syndrome, Ehlers–Danlos |
Grading Murmur Intensity (Levine Scale)
Grade I–II
Soft
I = barely audible; II = faint but immediately audible. Often innocent; may be pathological if low cardiac output.
Setting: GP review, consider echo if risk factors
Grade III–IV
Moderate–Loud
III = easily heard; IV = associated with a thrill. Almost always pathological. Echocardiography indicated.
Setting: Cardiology referral, echocardiography
Grade V–VI
Very Loud
V = audible with stethoscope partly off chest; VI = audible without stethoscope. Always pathological; often severe valvular disease.
Setting: Urgent cardiology, echocardiography, possible surgical assessment
Clinical Presentation & Diagnostic Approach
Bedside Assessment Protocol
- Confirm presence and timing: Palpate carotid pulse while auscultating; synchronise S1 with pulse upstroke. Determine if murmur is systolic, diastolic, or continuous.
- Characterise intensity: Grade I–VI using the Levine scale. Note presence of a palpable thrill (≥ grade IV).
- Describe quality: Harsh, blowing, musical, rumbling, rough, high-pitched vs low-pitched.
- Map radiation: Carotids (aortic stenosis), axilla (mitral regurgitation), back (coarctation), neck (pulmonary stenosis).
- Listen for associated sounds: S3, S4, ejection click, opening snap, fixed splitting of S2 (ASD), wide paradoxical splitting (aortic stenosis).
- Perform dynamic manoeuvres: Valsalva, squat-to-stand, passive leg elevation, handgrip, amyl nitrite inhalation (where available).
- Assess for signs of haemodynamic consequence: Pulse character and volume, blood pressure (both arms if coarctation suspected), JVP, apex beat location and character, peripheral oedema, hepatomegaly.
- Evaluate symptoms: Exertional dyspnoea, syncope or presyncope, anginal chest pain, palpitations, exercise intolerance, orthopnoea, paroxysmal nocturnal dyspnoea.
Red Flags Warranting Urgent Investigation
- New murmur with haemodynamic instability (hypotension, tachycardia, poor perfusion)
- New murmur in the setting of fever, rigors, or positive blood cultures — suspect infective endocarditis
- Acute severe mitral regurgitation (papillary muscle rupture post-MI, ruptured chordae tendineae) — loud, often short pansystolic murmur with pulmonary oedema
- Aortic dissection with new aortic regurgitation — early diastolic murmur, pulse deficits, unequal arm pressures
- Any diastolic murmur — always pathological
- Murmur with syncope — may indicate critical aortic stenosis or HOCM
Investigations
First-Line Investigations
Essential
12-Lead Electrocardiogram (ECG)
MBS item 11700. Assess for chamber hypertrophy (LVH voltage criteria: Sokolow–Lyon or Cornell), atrial enlargement (P mitrale, P pulmonale), conduction abnormalities (LBBB/RBBB, first-degree AV block), arrhythmias (AF), and ischaemic changes. In aortic stenosis, look for LVH with strain pattern.
Essential
Transthoracic Echocardiography (TTE)
MBS item 55124 (adult), 55127 (paediatric). Gold-standard non-invasive assessment. Provides valve morphology, haemodynamic severity (pressure gradients, valve area, regurgitant fraction), chamber dimensions, ejection fraction, and associated structural abnormalities. Indicated for all murmurs graded ≥ III/6, all diastolic murmurs, any murmur with symptoms, and any murmur in pregnancy.
Available
Chest X-Ray (CXR)
MBS item 58500. Assess cardiac silhouette size, chamber enlargement, pulmonary oedema, calcification of the aortic valve or mitral annulus, and rib notching (coarctation of the aorta). Less sensitive than echo but useful as initial screen.
Second-Line / Specialist Investigations
Specialist
Transoesophageal Echocardiography (TOE)
MBS item 55126. Superior visualisation of posterior cardiac structures (mitral valve, left atrial appendage, aortic root). Indicated when TTE is inconclusive, suspected endocarditis with negative TTE, pre-cardioversion assessment for AF, and assessment of prosthetic valve dysfunction.
Specialist
Stress Echocardiography
MBS item 55133. Exercise or dobutamine stress to assess valve haemodynamics under exertion. Useful for asymptomatic severe aortic stenosis (exercise testing is contraindicated in symptomatic severe AS) and dynamic assessment of HOCM.
Specialist
Cardiac MRI
MBS item 63342 (with Medicare rebate for selected indications). Provides precise ventricular volumes, regurgitant volumes, tissue characterisation (fibrosis, infiltration). Increasingly used for complex congenital heart disease and AR quantification when echo is discordant.
Specialist
Cardiac Catheterisation
Invasive haemodynamic assessment. Reserved for when non-invasive data is insufficient, pre-surgical planning (coronary angiography before valve surgery), and transcatheter valve interventions (TAVI, MitraClip).
Laboratory Investigations (Supportive)
| Test | Indication |
|---|---|
| Full blood count (FBC) | Anaemia (flow murmur), infective endocarditis (↑ WCC, ↓ Hb) |
| Inflammatory markers (CRP, ESR) | Infective endocarditis, acute rheumatic fever |
| Blood cultures (3 sets) | Suspected infective endocarditis — before antibiotics |
| BNP / NT-proBNP | Assess heart failure severity; serial monitoring in valvular disease |
| Iron studies, TFT | Exclude high-output causes (iron deficiency anaemia, thyrotoxicosis) |
| ASO titre, anti-DNase B | Confirm acute rheumatic fever (revised Jones criteria) |
Special Populations
Paediatric
Innocent murmurs are extremely common in children (up to 80%). Still's murmur is the most frequent benign murmur in children aged 3–8 years. Venous hums are common and must not be confused with PDA.
Any murmur present from birth or detected in the neonatal period should be evaluated promptly — consider structural congenital heart disease.
Paediatric echocardiography (MBS item 55127) should be performed if murmur is grade ≥ III/6, diastolic, continuous, or associated with symptoms (failure to thrive, cyanosis, poor feeding, excessive sweating).
Red flags in neonates/infants: central cyanosis, differential cyanosis, absent femoral pulses (coarctation), hepatomegaly, tachypnoea at rest.
Pregnancy
Physiological flow murmurs are common in pregnancy due to increased cardiac output (up to 50% increase) and expanded blood volume. Grade I–II ejection systolic murmurs are usually innocent.
Mammary soufflé is a continuous murmur heard over the breast area in late pregnancy and lactation — abolished by stethoscope pressure. Do not mistake for PDA.
Any diastolic murmur, pansystolic murmur, or murmur with haemodynamic significance requires echocardiography during pregnancy.
Rheumatic mitral stenosis is the most commonly encountered pathological valvular lesion in pregnant women in Australia. WHO risk classification (1–4) guides management and delivery planning.
Elderly
Calcific degenerative aortic stenosis is the most common valvular pathology in Australians aged >75 years. The murmur may be softer in low-output states — do not be falsely reassured by a quiet murmur.
Sclerotic changes (aortic sclerosis) produce a soft ejection systolic murmur without haemodynamic obstruction — present in up to 30% of those >65 years.
Atrial fibrillation is common and may alter the auscultatory findings (variable S1 intensity, absent presystolic component of mitral stenosis murmur).
Transcatheter aortic valve implantation (TAVI) is available across Australian metropolitan centres and selected regional sites for patients at intermediate to high surgical risk.
Renal Impairment
Patients on haemodialysis have accelerated valvular calcification, particularly of the aortic and mitral valves. Regular echocardiographic surveillance is recommended.
Anaemia of chronic kidney disease may cause or exacerbate flow murmurs. Target haemoglobin per KHA-CARI guidelines (100–115 g/L).
Immunocompromised
Higher risk of infective endocarditis with unusual or resistant organisms. Lower threshold for blood cultures and echocardiography when a new murmur is detected.
Consider fungal endocarditis (Candida, Aspergillus) in patients with prolonged neutropenia, central venous catheters, or prior broad-spectrum antibiotics.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Management Principles
Management of cardiac murmurs depends entirely on the underlying aetiology. The following provides a framework for initial management and referral.
Innocent Murmurs
- Reassurance — explain the benign nature to the patient/parents.
- Document findings clearly in the medical record (grade, location, character, absence of associated abnormalities).
- Echocardiography is NOT required unless there is clinical doubt or parental/patient anxiety.
- Repeat auscultation at subsequent visits — innocent murmurs may vary with physiological state.
Pathological Murmurs — Referral Criteria
1
Any diastolic or continuous murmur
Urgent cardiology referral and echocardiography. Do not wait.
2
Systolic murmur ≥ grade III/6
Refer for echocardiography. Non-urgent if asymptomatic; urgent if symptomatic.
3
Any murmur with symptoms
Dyspnoea, syncope, chest pain, exercise intolerance, heart failure signs — urgent referral.
4
New murmur in pregnancy
Echocardiography indicated. Liaise with obstetric and cardiology teams. WHO risk stratification.
Endocarditis Prophylaxis
Australian guidelines (Cardiac Society / Dental Association consensus): Antibiotic prophylaxis for dental procedures is recommended ONLY for patients at highest risk:
- Prosthetic cardiac valves (including transcatheter)
- Previous infective endocarditis
- Certain congenital heart diseases (unrepaired cyanotic CHD, completely repaired CHD with prosthetic material within 6 months, repaired CHD with residual defects at or adjacent to prosthetic material)
- Cardiac transplant recipients with valvulopathy
Amoxicillin
Amoxil® · Penicillin antibiotic
Adult dose
2 g PO, 30–60 minutes before dental procedure
Paediatric dose
50 mg/kg (max 2 g) PO, 30–60 minutes before procedure
Route
Oral
Renal adjustment
eGFR <30: reduce dose or extend interval
PBS status
✔ PBS General Benefit
Cefazolin
Cefazolin · Cephalosporin (penicillin allergy)
Adult dose
1 g IV/IM, 30–60 minutes before dental procedure
Paediatric dose
50 mg/kg (max 1 g) IV/IM, 30–60 minutes before procedure
Route
IV or IM
Renal adjustment
eGFR <30: reduce dose
PBS status
✔ PBS General Benefit
Clindamycin
Dalacin C® · Lincosamide (severe penicillin allergy)
Adult dose
600 mg PO, 30–60 minutes before dental procedure
Paediatric dose
20 mg/kg (max 600 mg) PO, 30–60 minutes before procedure
Route
Oral (or IV if unable to take PO)
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Monitoring & Follow-Up
The frequency of clinical and echocardiographic follow-up depends on valve lesion severity and symptoms. The following intervals align with Australian Cardiac Society and ESC/AHA recommendations:
| Valve Lesion | Severity | Clinical Review | Echo Interval |
|---|---|---|---|
| Aortic stenosis | Mild (Vmax 2.0–2.9 m/s) | Every 12 months | Every 3–5 years |
| Aortic stenosis | Moderate (Vmax 3.0–3.9 m/s) | Every 6–12 months | Every 1–2 years |
| Aortic stenosis | Severe (Vmax ≥4.0 m/s) | Every 6 months | Every 6–12 months (or sooner if symptomatic) |
| Mitral regurgitation | Severe (primary) | Every 6 months | Every 6–12 months; annual if asymptomatic with preserved LV |
| Mitral stenosis | Moderate–severe | Every 6–12 months | Every 1–2 years |
| Aortic regurgitation | Severe | Every 6 months | Every 6–12 months; annual if asymptomatic with preserved LV |
Exercise testing: Symptom-limited exercise testing is recommended for asymptomatic severe aortic stenosis (with continuous ECG and BP monitoring). Development of symptoms, hypotension, or ST changes during exercise indicates need for intervention. Exercise testing is contraindicated in symptomatic severe aortic stenosis.
📚 References
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- 4. RHDAustralia (ARF/RHD writing group). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease (3rd edition). Menzies School of Health Research, Darwin.
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