# Heart Murmurs USMLE: Chart, Valsalva & Squatting

> How do you match a murmur to a diagnosis on USMLE?

Match any murmur to its lesion by timing, site, radiation and maneuver response, then stage it and time valve replacement under the 2020 ACC/AHA guideline.

Match murmurs in three steps. Timing first: diastolic murmurs such as aortic regurgitation and mitral stenosis are always pathologic; a continuous machine-like murmur is usually a PDA. Then location and radiation: right upper sternal border to carotids is aortic stenosis; apex to axilla is mitral regurgitation. Maneuvers break ties: only HCM and mitral valve prolapse grow louder with Valsalva.

## How do you match a murmur to a diagnosis on USMLE?

Murmur stems hand over four clues in a fixed order, each one removing answer choices.

1. **Timing.** Systolic murmurs fall between S1 and S2 and keep the list long: AS, HCM, MR, MVP, VSD, TR, PS and the ASD flow murmur. Diastolic murmurs point to AR or MS, or their right-sided counterparts, pulmonic regurgitation and tricuspid stenosis. A murmur that carries through S2 is continuous: a PDA, coarctation collaterals or an innocent venous hum.
2. **Location and radiation.** Turbulence is loudest where the jet lands and travels with it: AS from the right upper sternal border into the carotids, MR from the apex to the left axilla, coarctation to the back.
3. **The company it keeps.** A single S2 with a slow-rising carotid pulse means AS, a midsystolic click MVP, an opening snap MS, a wide fixed split S2 ASD, and bounding pulses AR or a large PDA.
4. **Maneuvers.** Bedside maneuvers decide between two survivors, classically HCM against AS.

The ECG in the stem often confirms the lesion, from left atrial enlargement in MS to left ventricular hypertrophy with deep T-wave inversions in HCM, so pair this page with [how to read an ECG on the USMLE](/blog/how-to-read-ecg-usmle) and the [Cardiology](/topics/cardiology) hub.

## Heart murmur chart: timing, location, radiation and clinching clue

The chart lists 13 lesions; a dash in the radiation column means radiation does not help identify the lesion.

| Lesion | Timing and character | Loudest at | Classic radiation | Clinching clue |
| --- | --- | --- | --- | --- |
| Aortic stenosis | Systolic crescendo-decrescendo; peaks later as it worsens | Right upper sternal border | Both carotids | Pulsus parvus et tardus, single S2, S4 |
| Hypertrophic cardiomyopathy | Harsh, late-peaking systolic | Left sternal border, 3rd-4th space | -- | Louder with Valsalva or standing; brisk, bifid carotid pulse |
| Mitral regurgitation | Holosystolic, blowing | Apex | Left axilla | S3 when severe; acute after inferoposterior MI |
| Mitral valve prolapse | Midsystolic click, late systolic murmur | Apex | Left axilla once MR develops | Click moves toward S1 with standing or Valsalva |
| Ventricular septal defect | Harsh holosystolic | Left lower sternal border | -- | Possible thrill; new after MI suggests septal rupture |
| Tricuspid regurgitation | Holosystolic | Left lower sternal border | -- | Louder on inspiration (Carvallo sign); large c-v waves |
| Pulmonic stenosis | Harsh systolic ejection | Left 2nd intercostal space | -- | Wide split S2 that still moves; louder on inspiration |
| Atrial septal defect | Systolic ejection murmur from pulmonic flow | Left upper sternal border | -- | Wide fixed split S2 |
| Coarctation of the aorta | Systolic ejection; continuous collateral murmurs | Left upper sternal border | Left interscapular back | Arm pressure above leg pressure; weak, delayed femoral pulses |
| Aortic regurgitation | Early diastolic, blowing decrescendo | Left sternal border 3rd-4th space, leaning forward | -- | Wide pulse pressure, water-hammer pulse; Austin Flint rumble |
| Mitral stenosis | Opening snap, then diastolic rumble | Apex, left lateral decubitus | -- | Loud S1; snap nearer S2 as it worsens; atrial fibrillation |
| Patent ductus arteriosus | Continuous, machine-like | Left upper sternal border | -- | Bounding pulses; preterm infant |
| Still murmur (innocent) | Early systolic, vibratory, grade 1-3 | Left lower sternal border | -- | Healthy child, normal S2 |

HCM and AS sound alike, but HCM sits lower on the left sternal border with a brisk carotid upstroke, while AS gives a weak, delayed pulse.

## Which murmurs increase with Valsalva?

Hypertrophic cardiomyopathy and mitral valve prolapse are the murmurs that get louder during the strain phase of the Valsalva maneuver; almost every other murmur gets softer because less blood crosses the lesion.

Straining cuts venous return, so the left ventricle fills less and shrinks: in HCM the smaller cavity worsens the outflow obstruction from systolic anterior motion of the mitral leaflet, and in MVP the redundant leaflet buckles sooner, moving the click toward S1 and lengthening the murmur.

| Maneuver | Hemodynamic change | Louder | Softer |
| --- | --- | --- | --- |
| Valsalva, strain phase | ↓ venous return, smaller left ventricle | HCM; MVP (click earlier, murmur longer) | AS, MS, AR, MR, VSD, TR |
| Standing from a squat | ↓ venous return | HCM, MVP | AS, MS, AR, MR, VSD |
| Squatting | ↑ venous return and ↑ afterload | AS, MS, AR, MR | HCM; MVP (click later) |
| Passive leg raise | ↑ venous return | AS | HCM |
| Sustained handgrip | ↑ afterload | MR, AR, VSD | AS, HCM; MVP (click later) |
| Inspiration | ↑ right-heart filling | TR (Carvallo sign), tricuspid stenosis, PS, pulmonic regurgitation | Left-sided murmurs |
| Amyl nitrite (classic exam maneuver) | ↓ afterload, venodilation | AS, HCM, MVP | MR, AR, VSD |

Squatting and passive leg raising add venous return, softening the HCM murmur while the AS murmur grows; Valsalva and standing reverse both. Handgrip cannot separate them: its rise in afterload softens both outflow murmurs while driving more blood backward through a leaking mitral or aortic valve or a VSD. Amyl nitrite works the opposite way, separating MR, which softens, from AS, which grows. The [HOCM memory palace](/blog/2026-05-26-memory-palace-technique-for-hypertrophic-cardiomyopathy-hocm) adds hooks for the HCM pattern.

## Which murmurs are heard at the left lower sternal border?

Six murmurs sit at or near the left lower sternal border: VSD, tricuspid regurgitation and the innocent Still murmur in systole, tricuspid stenosis in diastole, and, slightly higher at the third or fourth interspace, HCM in systole and aortic regurgitation in diastole.

| Listening post | Systolic murmurs | Diastolic or continuous murmurs |
| --- | --- | --- |
| Right upper sternal border | Aortic stenosis | -- |
| Left upper sternal border | Pulmonic stenosis, ASD flow murmur, coarctation | PDA (continuous) |
| Left sternal border, 3rd-4th space | HCM | Aortic regurgitation |
| Left lower sternal border | VSD, tricuspid regurgitation, Still murmur | Tricuspid stenosis |
| Apex | Mitral regurgitation, MVP | Mitral stenosis, Austin Flint rumble |
| Left interscapular back | Coarctation | -- |

A holosystolic murmur here that swells on inspiration, with large c-v waves, is tricuspid regurgitation; a harsh one with a thrill that does not is more likely a VSD. Ebstein anomaly adds a widely split S1 to its tricuspid regurgitation murmur and is linked to maternal lithium and Wolff-Parkinson-White syndrome; see this [Ebstein anomaly question breakdown](/blog/2026-05-28-q-bank-breakdown-ebstein-anomaly-why-every-answer-choice-matters).

## Why each murmur sounds the way it does

A murmur is turbulent flow across a pressure gradient, so its shape traces that gradient through the cardiac cycle.

- **Ejection murmurs** (AS, PS, HCM, ASD flow) start after S1 and rise and fall with ejection; worsening AS delays the peak, and failing contractility in critical AS makes the murmur softer and shorter.
- **Holosystolic murmurs** (MR, TR, VSD) run from S1 to S2 because ventricular pressure exceeds that of the receiving chamber for all of systole.
- **Aortic regurgitation** is loudest just after S2, when the aortic-to-ventricular gradient is widest.
- **Mitral stenosis** opens with a snap; the higher the atrial pressure, the sooner the snap follows S2.
- **A PDA** is continuous because aortic pressure exceeds pulmonary artery pressure throughout the cycle.

A paradoxical split, heard in expiration, means delayed aortic closure from AS or left bundle branch block; a wide split that still widens on inspiration means right bundle branch block or PS; a split that never moves is ASD. Outside childhood and pregnancy, an S3 usually signals a dilated, failing ventricle and an S4 a stiff one, as in AS or HCM. Chronic AR and MR dilate the left ventricle while AS thickens it; once it fails, classify it as in [HFrEF vs HFpEF](/blog/hfref-vs-hfpef-usmle).

## Innocent or pathologic: which murmurs need an echocardiogram?

Systolic murmurs can be innocent, but a diastolic murmur is always abnormal and needs echocardiography.

Innocent murmurs come from normal flow through normal structures and are common in children and in pregnancy; the vibratory Still murmur and the venous hum, a continuous hum low in the neck, are the classic childhood examples. In children, red flags are a holosystolic or diastolic murmur, grade 3 or louder, a harsh quality, maximal intensity at the left upper sternal border, a murmur louder on standing, a systolic click or an abnormal S2. On the Levine scale a palpable thrill first appears at grade 4, and diastolic murmurs are graded only from 1 to 4.

## Causes and associations behind each valve lesion

Vignettes rarely name the lesion; they name a disease, a drug or a syndrome that implies it.

| Clue in the stem | Lesion to expect | Why |
| --- | --- | --- |
| Rheumatic fever years earlier | Mitral stenosis; MR in the acute attack | Rheumatic valvulitis hits the mitral valve, less often the aortic |
| Older adult, calcified valve | Calcific aortic stenosis | Calcium deposits on the leaflets with age |
| Aortic stenosis before about age 70 | Bicuspid aortic valve | Present in 0.5-2% of live births; also AR and aortic dilation |
| Turner syndrome | Bicuspid valve, coarctation, aortic dilation | Coarctation affects 10-20% of patients |
| Marfan syndrome | Aortic root dilation with AR; MVP | FBN1 variants disrupt fibrillin-1, weakening the root and valve tissue |
| Injection drug use with fever | Tricuspid regurgitation | Right-sided endocarditis |
| Flushing, diarrhea, liver metastases | Tricuspid regurgitation plus pulmonic stenosis | Serotonin-driven fibrosis; the lungs inactivate serotonin, sparing the left heart |
| Lithium exposure in pregnancy | Ebstein anomaly | Apically displaced tricuspid leaflets atrialize part of the right ventricle |
| Prematurity or congenital rubella | Patent ductus arteriosus | Rubella also causes pulmonary artery stenosis |
| Noonan syndrome | Pulmonic stenosis | Congenital valve narrowing |
| Inferoposterior MI | Acute MR | Papillary muscle rupture, usually the posteromedial muscle |
| Aortic dissection or endocarditis | Acute aortic regurgitation | Sudden failure of the root or leaflets |

Rheumatic MS often surfaces 15 years or more after the acute attack, or in pregnancy as blood volume rises; drill it with this [rheumatic heart disease question breakdown](/blog/2026-05-27-q-bank-breakdown-rheumatic-heart-disease-why-every-answer-choice-matters).

## Severity stages and valve replacement under the 2020 ACC/AHA guideline

The 2020 ACC/AHA valvular heart disease guideline is still the current US guideline in October 2026; the AHA publication schedule anticipates the next one in the first quarter of 2027.

Every lesion is staged A (at risk), B (progressive), C (asymptomatic severe: C1 with a compensated ventricle, C2 with a decompensating one) or D (symptomatic severe), and most intervention decisions turn on the move into C2 or D.

Severe aortic stenosis means a peak velocity of at least 4.0 m/s or a mean gradient of at least 40 mm Hg, usually with a valve area of 1.0 cm² or less; 5.0 m/s or more is very severe. A valve area of 1.0 cm² or less with a lower gradient is low-flow, low-gradient severe AS, from an LVEF under 50% or a small stroke volume. Mean survival drops to about 3 years once symptoms begin. Statins do not slow progression, nitrates can drop blood pressure, and balloon valvuloplasty gives older adults only temporary relief.

| Lesion | Intervene when | Procedure notes |
| --- | --- | --- |
| Severe aortic stenosis | Symptoms, or LVEF below 50% without symptoms | Surgical (SAVR) or transcatheter (TAVI) replacement by age, life expectancy and risk |
| Severe aortic regurgitation | Symptoms or LVEF 55% or less; reasonable with LV end-systolic diameter above 50 mm | Valve replacement; the old LVEF cut-off was 50% |
| Severe primary mitral regurgitation | Symptoms, LVEF 60% or less, or LV end-systolic diameter 40 mm or more | Repair preferred over replacement; transcatheter edge-to-edge repair if surgery is unsuitable |
| Secondary mitral regurgitation | Symptoms despite guideline-directed heart failure therapy | Treat the ventricle first; edge-to-edge repair in selected patients |
| Severe rheumatic mitral stenosis (area 1.5 cm² or less) | Symptoms | Balloon commissurotomy if the valve is suitable; warfarin, not a DOAC, for atrial fibrillation |

SAVR is preferred under 65 or with more than 20 years of life expectancy, SAVR or transfemoral TAVI (also called TAVR) after shared decision-making from 65 to 80, and transfemoral TAVI over 80 or with less than 10 years expected; at high or prohibitive surgical risk, TAVI is preferred if survival beyond 12 months is expected. Asymptomatic patients at low surgical risk may also be offered replacement for very severe AS, falling exercise tolerance, a BNP above three times normal or rapid progression.

## Endocarditis prophylaxis: who still gets antibiotics before dental work

Antibiotic prophylaxis before dental work is limited to four highest-risk groups under the 2021 AHA scientific statement:

- A prosthetic valve, including a transcatheter valve, or prosthetic material used for valve repair
- Previous infective endocarditis
- Unrepaired cyanotic congenital heart disease, the first 6 months after complete repair with prosthetic material or a device, or a residual shunt or regurgitation at or next to a prosthetic patch or device
- A heart transplant with valvulopathy

Only dental procedures that manipulate gingival tissue or the periapical region of teeth, or perforate the oral mucosa, qualify. The usual regimen is a single dose of amoxicillin 30 to 60 minutes beforehand; clindamycin was dropped in 2021 because of more frequent and severe reactions, including *C. difficile* infection. MVP, a native bicuspid valve, rheumatic disease without a prosthesis and HCM do not qualify, since a higher lifetime risk alone is not an indication. Active endocarditis is covered in this [infective endocarditis question breakdown](/blog/2026-05-27-q-bank-breakdown-infective-endocarditis-why-every-answer-choice-matters).

> **10-second murmur ID:** 1) Diastolic: AR or MS; continuous: PDA. 2) Right upper sternal border to the carotids, slow weak pulse: AS. 3) Left sternal border, louder on standing or Valsalva: HCM. 4) Apex to axilla: MR; click first: MVP. 5) Left lower sternal border, louder on inspiration: TR; harsh with a thrill: VSD. 6) Fixed split S2: ASD. 7) Arm pressure above leg pressure: coarctation.

## How USMLE tests murmurs

Most murmur items hide one discriminating detail and ask for the lesion, the mechanism or the next step.

- **Exertional syncope at 78, a late-peaking right upper sternal border murmur and a slow-rising pulse:** symptomatic severe AS; replace the valve, choosing SAVR or transfemoral TAVI with the patient.
- **Loud new apical holosystolic murmur and pulmonary edema after an inferoposterior MI:** papillary muscle rupture; nitroprusside and an intra-aortic balloon pump bridge to surgery.
- **Hoarseness, an opening snap and a diastolic rumble:** MS, with a large left atrium compressing the left recurrent laryngeal nerve (Ortner syndrome).

## Worked vignette: the athlete whose murmur grows on standing

A 19-year-old basketball player faints during a sprint drill. His uncle died suddenly at age 30. He has a grade 3/6 harsh systolic murmur at the left sternal border, fourth intercostal space, that grows louder when he stands up from a squat, and a brisk carotid upstroke with a double peak. The ECG shows left ventricular hypertrophy with deep T-wave inversions. Which of the following would most likely make this murmur softer?

- A. Strain phase of the Valsalva maneuver
- B. Standing quickly from a squat
- C. Sustained isometric handgrip
- D. Inhaled amyl nitrite
- E. Sublingual nitroglycerin

**Answer: C.** Exertional syncope, a family history of sudden death, a left sternal border murmur that rises on standing and a brisk, bifid carotid pulse point to hypertrophic cardiomyopathy with dynamic outflow obstruction. Handgrip raises afterload, keeping the ventricle fuller and lowering the outflow gradient, so the murmur softens, as it would with prolonged squatting or a passive leg raise. Valsalva strain (A) and standing (B) cut venous return and worsen the obstruction. Amyl nitrite (D) and nitroglycerin (E) lower afterload or preload and intensify the murmur, which is why drugs that do so, such as nitrates and diuretics, are generally avoided in obstructive HCM. AS would sit at the right upper sternal border with a weak, slow-rising pulse. First-line therapy is a beta-blocker or a nondihydropyridine calcium channel blocker.

## Common wrong-answer traps

- **Using handgrip to separate HCM from AS.** Handgrip softens both; Valsalva, standing, squatting and leg raising move them in opposite directions.
- **Choosing clindamycin for dental prophylaxis in penicillin allergy.** The 2021 AHA regimens dropped it; use azithromycin, clarithromycin or doxycycline, or cephalexin unless penicillin caused anaphylaxis, angioedema or urticaria.
- **Anticoagulating rheumatic MS with atrial fibrillation using a DOAC.** Warfarin is the drug.
- **Using an LVEF of 50% as the AR surgery trigger.** The 2020 guideline moved the cut-off to 55%.

## Sources

- ACC: [2020 ACC/AHA valve guideline key perspectives, part 1](https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2020/12/16/21/58/2020-ACC-AHA-VHD-GL-Pt-1-GL-VHD), [part 2](https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2020/12/16/22/00/2020-ACC-AHA-VHD-GL-Pt-2-GL-VHD)
- AHA: [guideline publication schedule](https://professional.heart.org/en/guidelines-and-statements/guideline-publication-schedule), [2021 endocarditis prevention statement slides](https://professional.heart.org/-/media/PHD-Files-2/Science-News/p/prevention_of_viridans_group_streptococcal_infective_endocarditis_slides.pdf), [top things to know](https://professional.heart.org/en/science-news/prevention-of-viridans-group-streptococcal-infective-endocarditis/top-things-to-know)
- StatPearls (NCBI Bookshelf): [Physiology, cardiovascular murmurs](https://www.ncbi.nlm.nih.gov/books/NBK525958/), [Hypertrophic cardiomyopathy](https://www.ncbi.nlm.nih.gov/books/NBK430788/)
- CDC: [Acute rheumatic fever clinical guidance](https://www.cdc.gov/group-a-strep/hcp/clinical-guidance/acute-rheumatic-fever.html)

Turn timing, site and maneuver response into one reflex before test day: [Practice valvular disease questions on StepGenie](https://dashboard.stepgenie.app/sign-up).

## Frequently asked questions

### Which murmurs get louder with the Valsalva maneuver?

Hypertrophic cardiomyopathy and mitral valve prolapse are the two classic murmurs that get louder during the strain phase of Valsalva. Straining cuts venous return and shrinks the left ventricle, which worsens dynamic outflow obstruction in HCM and lets the prolapsing mitral leaflet buckle sooner, moving the click toward S1 and lengthening the murmur. Aortic stenosis, mitral regurgitation, aortic regurgitation, mitral stenosis, VSD and tricuspid regurgitation all get softer because less blood crosses the lesion.

### Why does the HOCM murmur decrease with squatting?

Squatting increases venous return and afterload at the same time, so the left ventricle fills more and stays larger through systole. A bigger cavity holds the thickened septum and the anterior mitral leaflet farther apart, which lessens the dynamic outflow obstruction, so the murmur softens. Passive leg raising and sustained handgrip soften it too. Standing up from a squat does the opposite: venous return falls, the cavity shrinks and the murmur gets louder.

### What does pulsus parvus et tardus mean?

Pulsus parvus et tardus is Latin for a pulse that is small and late: a carotid or peripheral pulse with reduced amplitude and a slow, delayed upstroke. It is the classic pulse of severe aortic stenosis, because the narrowed valve limits how much blood the left ventricle can eject and how fast. Hypertrophic cardiomyopathy gives the opposite carotid pulse, with a brisk upstroke and often a double, bifid peak.

### Which murmurs are heard at the left lower sternal border?

The left lower sternal border is the site of the holosystolic murmurs of ventricular septal defect and tricuspid regurgitation, the innocent vibratory Still murmur of childhood and the diastolic murmur of tricuspid stenosis. Slightly higher, at the third or fourth intercostal space, sit the systolic murmur of hypertrophic cardiomyopathy and the early diastolic murmur of aortic regurgitation. A murmur here that grows on inspiration is right-sided, usually tricuspid regurgitation.

### Who still needs antibiotic prophylaxis for endocarditis before dental work?

Under the 2021 American Heart Association statement, only patients at the highest risk of a bad outcome qualify: those with a prosthetic valve or prosthetic material used for valve repair, previous infective endocarditis, unrepaired cyanotic congenital heart disease, the first 6 months after complete repair with prosthetic material or a device, or a residual defect at or next to a patch or device, and heart transplant recipients with valvulopathy. Mitral valve prolapse, a native bicuspid valve and rheumatic disease without a prosthesis do not qualify.

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