Rapid Review·Cardiovascular
Select any text to highlight it or add a note.
PHYSIOLOGY
T1Must knowAuscultation, Maneuvers & Murmurs
FA P294-295
Videos
1 to play here
Play 1 here
Focus on
Where to listen, the maneuvers that separate HCM and MVP from everything else, and the murmur each lesion makes.
Key takeaways
Where to listen
The four areas, by "APT M"
Aortic, Pulmonic, Tricuspid, Mitral. Each area and its differential is mapped on the auscultation areas diagram.- Aortic area: systolic murmurs, i.e. aortic stenosis, flow murmur, aortic valve sclerosis.
- Pulmonic area: systolic ejection murmurs, i.e. pulmonic stenosis, ASD, flow murmur.
- Tricuspid area: holosystolic (tricuspid regurgitation, VSD) or diastolic (tricuspid stenosis).
- Mitral area, the apex: systolic (mitral regurgitation, MVP) or diastolic (mitral stenosis).
- Left sternal border: systolic (hypertrophic cardiomyopathy) or diastolic (aortic regurgitation, pulmonic regurgitation).
| Location | Systolic | Diastolic |
|---|---|---|
| Aortic area | Aortic stenosis, flow murmur, sclerosis | |
| Pulmonic area | Pulmonic stenosis, ASD, flow murmur | |
| Tricuspid area | Tricuspid regurgitation, VSD | Tricuspid stenosis |
| Mitral area (apex) | Mitral regurgitation, MVP | Mitral stenosis |
| Left sternal border | Hypertrophic cardiomyopathy | Aortic regurgitation, pulmonic regurgitation |
Maneuvers
Mehlman's right-sided rule
right-sided murmurs worsen with inspiration, because the diaphragm descends, intrathoracic pressure falls, and right heart filling rises.| Maneuver | Hemodynamic change | Murmurs that INCREASE | Murmurs that DECREASE |
|---|---|---|---|
| Standing, Valsalva (strain) | Lower preload, smaller LV volume | MVP (earlier click), HCM | Most murmurs |
| Passive leg raise, squatting | Raise preload (squatting also raises afterload) | Most murmurs | MVP (later click), HCM |
| Hand grip | Raise afterload, more reverse flow, larger LV volume | Most left-sided murmurs: AR, MR, VSD | AS (lower transaortic gradient), HCM |
| Inspiration | Raise venous return to the right heart | Most right-sided murmurs | Left-sided murmurs (these rise with expiration) |
| Lesion | Mechanism | A smaller LV cavity means |
|---|---|---|
| Hypertrophic cardiomyopathy | Septal hypertrophy plus systolic anterior motion of the mitral valve obstructs outflow | More obstruction, louder murmur |
| Mitral valve prolapse | Redundant leaflets prolapse into the LA | Prolapse happens sooner: earlier click, longer murmur |
The murmurs
Aortic stenosis
LV pressure exceeds aortic pressure through systole.- Crescendo-decrescendo ejection murmur, loudest at the base, radiating to the carotids, with a soft S2 and sometimes an ejection click.
- "Pulsus parvus et tardus", weak pulses with a delayed peak.
- Causes "SAD": Syncope, Angina, Dyspnea on exertion, all from underperfusion of the myocardium and brain.
- From age-related calcification (over 60), which shares its biology with atherosclerosis, or early calcification of a bicuspid valve at roughly 50 to 60.
- Complications: concentric LVH that can progress to heart failure; atrial fibrillation late in the disease, which removes the atrial kick these stiff ventricles depend on, so preload drops and the patient becomes hypotensive with pulmonary edema; and microangiopathic hemolytic anemia.
Mitral and tricuspid regurgitation
holosystolic, high-pitched "blowing."- MR is loudest at the apex and radiates to the axilla; TR is loudest at the tricuspid area. An audible S3 marks the MR as severe.
- MR follows ischemic heart disease, MVP, LV dilatation, or rheumatic fever. TR follows RV dilatation. Infective endocarditis can cause either.
Mitral valve prolapse
late crescendo murmur with a midsystolic click, best at the apex, loudest just before S2. The click comes after the carotid upstroke, from the chordae tendineae snapping taut as the leaflets prolapse into the LA. Mostly idiopathic; otherwise from myxomatous degeneration (ground substance piling up, as in Marfan or Ehlers-Danlos), rheumatic fever, or chordae rupture. Usually benign, but predisposes to infective endocarditis.VSD
holosystolic and harsh, loudest at the tricuspid area. Larger VSDs are quieter than smaller ones, because a small hole generates more turbulence.Aortic regurgitation
early diastolic, decrescendo, high-pitched "blowing," loudest at S2. Heard at the base when the root is dilated and at the left sternal border when the valve itself is diseased.- Causes by "BEAR": Bicuspid aortic valve, Endocarditis, Aortic root dilation (syphilitic aneurysm, aortic dissection), Rheumatic fever. Transcatheter aortic valve implantation also raises the risk.
- Hyperdynamic circulation: a wide pulse pressure (diastolic falls as blood leaks back, systolic rises with the bigger stroke volume), a water-hammer pulse, the pistol-shot femoral pulse (Traube sign), a pulsating nail bed (Quincke pulse), and head bobbing when severe and chronic (de Musset sign).
- Complications: LV dilation and eccentric hypertrophy.
Mitral stenosis
LA pressure far exceeds LV pressure through diastole. An opening snap followed by a delayed rumbling mid-to-late diastolic murmur. A shorter S2-to-opening-snap interval means more severe disease.- The opening snap: the fused leaflet tips open fast and then halt abruptly.
- Causes: a late and highly specific sequela of rheumatic fever, which thickens the leaflets with fibrosis and fuses the commissures; infective endocarditis instead destroys the leaflets under large friable vegetations, without fibrosis.
- Complications of chronic MS: the LA dilates (and can compress the recurrent laryngeal nerve, Ortner syndrome), atrial fibrillation, pulmonary congestion with hemoptysis, and right heart failure.
PDA
continuous machine-like murmur, best at the left infraclavicular area, loudest at S2. Often from congenital rubella or prematurity.| Murmur | Timing and quality | Best heard / radiates | Signature finding |
|---|---|---|---|
| Aortic stenosis | Crescendo-decrescendo systolic | Base, to the carotids | Pulsus parvus et tardus; SAD |
| Mitral regurgitation | Holosystolic blowing | Apex, to the axilla | Post-MI papillary rupture |
| Tricuspid regurgitation | Holosystolic, louder on inspiration | Tricuspid area | Pulsatile liver; from pulmonary hypertension |
| Mitral valve prolapse | Midsystolic click then late crescendo | Apex | Myxomatous degeneration |
| VSD | Holosystolic, harsh | Tricuspid area | Smaller defect gives a louder murmur |
| Aortic regurgitation | Early diastolic decrescendo | Base or left sternal border | Wide pulse pressure, head bobbing |
| Mitral stenosis | Opening snap then rumbling diastolic | Apex | Shorter S2-to-OS means worse |
| PDA | Continuous machine-like | Left infraclavicular | Congenital rubella |
What the exam actually builds vignettes on
| Pulse | Lesion | Mechanism |
|---|---|---|
| Pulsus parvus et tardus (weak, delayed) | Aortic stenosis | Fixed obstruction to ejection |
| Bounding, "brisk upstroke with precipitous downstroke" | Aortic regurgitation (4/5), PDA or AV fistula (1/5) | Blood leaves the arterial circulation rapidly |
| Pulsus paradoxus | Tamponade, constrictive pericarditis, asthma and COPD | LV filling falls on inspiration |
A murmur gets louder when the patient stands. What are the only two answers, and what separates them?
HCM or MVP: a smaller ventricle means more outflow obstruction and earlier prolapse. Hand grip is the tiebreaker against aortic stenosis, since raising afterload softens both AS and HCM but worsens MR and AR.
How it's tested
Valsalva and standing lower preload, which makes nearly every murmur softer. The two exceptions are hypertrophic cardiomyopathy and mitral valve prolapse, which get louder, because a smaller ventricle means more outflow obstruction and earlier prolapse. So if a question tells you a murmur intensified on standing, the answer is one of those two, and squatting or leg raise will do the reverse. Hand grip is the tiebreaker between them and aortic stenosis, since raising afterload worsens MR and AR but softens AS and HCM.
A new systolic murmur hours to days after a myocardial infarction is mitral regurgitation from papillary muscle rupture, and Mehlman says the exam is obsessed with this pairing. Note the counterintuitive VSD rule, that smaller defects produce louder murmurs, because a small orifice generates more turbulence than a large one, so a quiet murmur in a sick infant is the worrying finding rather than the reassuring one. The pregnancy version is also reliable: second-trimester dyspnea with a diastolic murmur is unmasked mitral stenosis, whereas late third-trimester dyspnea with edema is peripartum cardiomyopathy.
Go deeper
First Aid 2026 — CV/Physiology (p.294-295) · B&B — Murmur maneuvers; heart murmurs · Mehlman — HY Cardio (handgrip/Valsalva/squat, papillary rupture, MS in pregnancy)
High-yield images1
Flashcards for this page
Card 1 of 5 · try-out only, nothing is saved
(...)
You just read one page of 944
The rest of Step 1, written exactly like this.
Rapid Review is the reading layer of a full Step 1 platform: a schedule fitted to your exam date, flashcards for every page, and a mentor a message away.
Every Step 1 system
Written the same way: what to know, how it’s tested, where to go deeper.
A plan built to your exam date
Tell us when you sit, and the schedule fits the whole library and your question bank to it.
Flashcards for every page
Ready-made spaced-repetition decks linked to each topic, so nothing you read gets forgotten.
