HOCM vs aortic stenosis murmur: telling them apart at the bedside
Both murmurs are harsh and systolic. The difference is the obstruction: a fixed valve in aortic stenosis, a dynamic muscle and mitral leaflet in HOCM. The manoeuvres follow from that.
Chapters (11)
Distinguish hypertrophic obstructive cardiomyopathy from aortic stenosis by the outflow mechanism, the murmur's response to Valsalva, standing, squatting and handgrip, and the carotid pulse.
The short version
- Aortic stenosis is a fixed obstruction at the valve, so its murmur follows flow across the valve.
- Hypertrophic obstructive cardiomyopathy (HOCM) is a dynamic obstruction: a thickened septum plus systolic anterior motion of the anterior mitral leaflet, which changes with how full the ventricle is.
- Lower preload (Valsalva strain, standing from a squat) makes the HOCM murmur louder and the aortic stenosis murmur softer; higher preload (squatting, passive leg raise) does the opposite.
- Handgrip raises afterload and softens the HOCM murmur.
- The carotid pulse separates them: weak and slow to rise (pulsus parvus et tardus) in aortic stenosis, brisk and bifid in HOCM.
HOCM vs aortic stenosis murmur: the trap is timing
Picture two patients with the same harsh systolic murmur: a 19-year-old who collapsed during a basketball drill, and a 78-year-old who gets breathless climbing stairs. On paper the murmurs match. At the bedside you can tell them apart.
The trap is that both murmurs happen in systole, as blood leaves the left ventricle through a narrowed path. The HOCM vs aortic stenosis murmur question is therefore not about timing. It is about what is narrowing the path, and whether that narrowing can change.[1][2]
Aortic stenosis: a fixed valve obstruction
In aortic stenosis the obstruction is the valve itself: a stiff, calcified or bicuspid valve that opens poorly. Calcific disease is the usual cause in older adults. Under 70, think bicuspid.[2]
The orifice is fixed. The murmur therefore simply follows flow: more blood across the valve, louder; less blood, softer.[2][5]
Hypertrophic obstructive cardiomyopathy: the muscle is the problem
In hypertrophic cardiomyopathy the valve is fine. The problem is the muscle. It is usually caused by sarcomere gene variants, most often MYBPC3 and MYH7, and a thickened septum bulges into the outflow tract.[1]
During systole the anterior mitral leaflet is pulled toward that bulge. This is systolic anterior motion (SAM), and it narrows the outflow tract further.[1][3]
The obstruction is dynamic: it changes from beat to beat with how full the ventricle is. A smaller, emptier ventricle crowds the septum and the leaflet together, so obstruction and murmur get worse. A fuller ventricle opens the path up, so both get better.[3][4]
Bedside comparison: murmur site, radiation and carotid pulse
| Feature | Aortic stenosis | HOCM |
|---|---|---|
| Obstruction | Fixed, at the valve | Dynamic: septum plus systolic anterior motion |
| Murmur shape | Crescendo–decrescendo | Late-peaking |
| Best heard | Right upper sternal border | Left sternal border |
| Radiation | Carotid arteries | Suprasternal notch, not the carotids |
| Carotid pulse | Weak and slow to rise (parvus et tardus) | Brisk and bifid |
Valsalva, standing, squatting and handgrip: how the manoeuvres change the murmur
Last lesson showed that preload and afterload change murmur intensity. That is the whole trick: for Valsalva, standing and squatting, the two murmurs respond in opposite ways.[4]
| Manoeuvre | Effect | HOCM murmur | Aortic stenosis murmur |
|---|---|---|---|
| Valsalva strain, or standing from a squat | Lower venous return and preload | Louder | Softer |
| Squatting, or passive leg raise | Higher preload | Softer | Louder |
| Handgrip | Higher afterload | Softer | Not covered in this lesson |
- Strain phase of Valsalva lowers venous return, so preload falls.
- Fixed valve: less blood crosses the valve, so the aortic stenosis murmur gets softer.
- Dynamic obstruction: the ventricle is smaller, the septum and leaflet crowd the outflow tract, so the HOCM murmur gets louder.
What this means for treatment of obstructive HCM
The same logic guides treatment. In obstructive hypertrophic cardiomyopathy, avoid dehydration and vasodilators, which shrink the ventricle or lower resistance and worsen the obstruction, and use beta blockers.[1]
Practice question
Original · USMLE styleA 17-year-old boy faints during basketball practice. His paternal uncle died suddenly at age 31. His blood pressure is 118/72 mm Hg and heart rate is 72/min. Cardiac examination shows a harsh systolic murmur at the left lower sternal border and a fourth heart sound. Echocardiography shows an asymmetric septal thickness of 22 mm with systolic anterior motion of the mitral valve.
Common questions
How do you tell HOCM from aortic stenosis at the bedside?
Use the mechanism: aortic stenosis is a fixed valve obstruction with a weak, delayed carotid pulse, while HOCM is a dynamic muscle obstruction with a brisk, bifid carotid pulse. Then check how the murmur responds to Valsalva strain and squatting, which move the two murmurs in opposite directions.[1][2][4]
Why does the HOCM murmur get louder with Valsalva strain?
Valsalva strain lowers venous return and preload. A smaller ventricle crowds the septum and the anterior mitral leaflet together, so the obstruction and the murmur get worse.[4]
Transcript
Read the full narration, by chapter694 words
0:00Two patients, one murmur
A 19-year-old and a 78-year-old both have a harsh systolic murmur. One collapsed during a basketball drill. The other gets breathless climbing stairs. Same murmur on paper. So what can you do, right at the bedside, to tell them apart? By the end of this lesson, you'll separate hypertrophic obstructive cardiomyopathy from aortic stenosis using the outflow mechanism and how each murmur responds to manoeuvres. First, the trap: both murmurs happen in systole,
0:28The trap: both murmurs are systolic
as blood leaves the left ventricle through a narrowed path. Last lesson, we saw that preload and afterload change murmur intensity. That is the whole trick.
0:43Aortic stenosis: a fixed valve obstruction
Start with aortic stenosis. The obstruction is the valve itself, a stiff, calcified or bicuspid valve that opens poorly. Calcific disease is the usual cause in older adults. Under 70, think bicuspid. The orifice is fixed. So the murmur simply follows flow: more blood across the valve, louder. Less blood, softer.
1:09The AS murmur and the carotid pulse
It is a crescendo-decrescendo murmur, heard best at the right upper sternal border, and it radiates to the carotid arteries. Feel the carotid pulse and it is weak and slow to rise: pulsus parvus et tardus.
1:24Hypertrophic cardiomyopathy: the muscle is the problem
Now hypertrophic cardiomyopathy. The valve is fine. The problem is the muscle. It is usually caused by sarcomere gene variants, most often MYBPC three and MYH seven, and a thickened septum bulges into the outflow tract. During systole, the anterior mitral leaflet is pulled toward that bulge. This is systolic anterior motion, and it narrows the outflow tract further.
1:53Dynamic obstruction: preload changes the gap
That obstruction is dynamic. It changes from beat to beat, depending on how full the ventricle is. A smaller, emptier ventricle crowds the septum and leaflet together, so obstruction and murmur get worse. A fuller ventricle opens the path up, so both get better. This murmur is late-peaking,
2:13The HOCM murmur, S4 and the carotid pulse
best heard at the left sternal border, and it radiates toward the suprasternal notch, not the carotids. The carotid pulse is brisk and bifid, and an S four is common, from a stiff, thick ventricle. Now the manoeuvres.
2:29Manoeuvres: Valsalva, standing, squatting, handgrip
Strain phase of Valsalva, or standing up from a squat, drops venous return and preload. In hypertrophic cardiomyopathy, the murmur gets louder. In aortic stenosis, it gets softer. Squatting, or a passive leg raise, raises preload. In hypertrophic cardiomyopathy, the murmur gets softer. In aortic stenosis, it gets louder. Handgrip raises afterload, and softens the hypertrophic cardiomyopathy murmur too. This also guides treatment.
3:02Treatment of obstructive HCM
In obstructive hypertrophic cardiomyopathy, we avoid dehydration and vasodilators, and use beta blockers. Your turn.
3:13Practice question
Pause if you want to work it out. A 17-year-old boy faints during basketball practice. His uncle died suddenly at 31. Blood pressure is 118 over 72, and heart rate is 72. He has a harsh systolic murmur at the left lower sternal border and a fourth heart sound. Echocardiography shows an asymmetric septum 22 millimetres thick, with systolic anterior motion of the mitral valve. Which findings are most likely when he moves from squatting to standing? A, the murmur is louder, with a weak, delayed carotid upstroke. B, louder, with a brisk, bifid carotid upstroke. C, softer, with a brisk, bifid upstroke. D, softer, with a weak, delayed upstroke. E, no change in the murmur, with a normal upstroke. The answer is B. A, the murmur is right, but a weak, delayed upstroke belongs to aortic stenosis, not to this obstruction. C has the pulse right, but standing lowers preload, so this murmur gets louder, not softer. D describes the aortic stenosis pattern, both the softer murmur and the slow pulse. E is wrong, because a dynamic obstruction changes with preload, and the echo shows it. B fits. Standing drops preload, the ventricle shrinks, the leaflet and septum crowd the outflow tract, and the murmur gets louder, with the brisk, bifid pulse of hypertrophic cardiomyopathy.
4:56High-yield recap and next lesson
Quick recap. One: aortic stenosis is a fixed valve obstruction, so its murmur follows flow, with a slow, weak carotid pulse. Two: hypertrophic cardiomyopathy is a dynamic muscle obstruction, so its murmur gets louder with less preload and softer with more. Three: Valsalva and standing separate them, and so does squatting, in opposite directions. Next, we move from the pump to its electrical signal: the ventricular myocyte action potential.
Sources
Numbers in the text, e.g. [1], point here- Hypertrophic Cardiomyopathy. MSD Manual Professional Edition. msdmanuals.com/professional/cardiovascular-disorders/cardiomyopathies/hypertrophic-cardiomyopathy
- Aortic Stenosis. MSD Manual Professional Edition. msdmanuals.com/professional/cardiovascular-disorders/valvular-disorders/aortic-stenosis
- Hypertrophic Cardiomyopathy. Life in the Fast Lane (LITFL). litfl.com/hypertrophic-cardiomyopathy/
- Dynamic Auscultation. Learn the Heart, Healio. healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/dynamic-auscultation
- Aortic Stenosis: Physical Examination. Learn the Heart, Healio. healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/aortic-stenosis/physical-examination
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. All video diagrams (heart schematics, murmur traces, carotid pulse tracings, table) are original and drawn in code; no third-party artwork is used in the video. Murmur and pulse shapes are schematic teaching drawings, not recordings. Thumbnail heart model: "Anatomical Human Heart" by Nexal 3D (BlenderKit).
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-012.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01S2 splitting and heart sounds S1–S4, explained5:26
- EP 02Heart murmurs and dynamic manoeuvres, from preload and afterload5:15
- EP 03HOCM vs aortic stenosis murmur: telling them apart at the bedside5:31
- EP 04Ventricular action potential: phases 0 to 4 and their ion currents5:15
- EP 05SA node pacemaker potential: phase 4 sets the heart rate5:17
- EP 06ECG waves and intervals: what P, PR, QRS, ST and QT mean5:29