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What in the Murmur?

An Approach to Aortic Stenosis

Mohamed Adam, PGY-3 Internal Medicine

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Scan to join the poll!

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Case 1: Lightheaded on the stairs

A 78-year-old man is admitted with pneumonia.

He mentions two episodes of lightheadedness climbing stairs over the past three months.

Vitals: BP 118/86, HR 78, afebrile on antibiotics.

Exam: a loud harsh systolic murmur at the right upper sternal border

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Question 1

Which additional finding would best suggest his AS is severe?

A Grade 4/6 murmur

B Late-peaking murmur with a soft S2

C Murmur also heard at the apex

D Radiating to both carotids

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Aortic Stenosis

Narrowing of the aortic valve that obstructs outflow from the left ventricle. A fixed outflow obstruction.

Causes

Calcific degeneration: most common, usually over 65
Bicuspid valve: congenital, presents younger (50s to 60s)
Rheumatic: rare in Canada, usually with mitral disease

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Consequences of a fixed obstruction

1. Narrow valve: pressure overload on the LV

2. The LV thickens to keep wall stress normal

3. Early – stage remodelling: stiff LV, more O2 demand, less coronary reserve

4. Late – stage remodelling: the LV dilates and EF falls

Normal LV

LV Concentric Hypertrophy

LV Dilation

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Symptoms of AS

Symptom	Mechanism
Angina	Hypertrophy raises demand and limits coronary flow, even with normal coronaries
Exertional syncope	Output cannot rise across a fixed valve while muscle vasodilates; arrhythmia
Exertional dyspnea, heart failure	Stiff LV, high filling pressure; late LV failure

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Systolic Murmur on Exam

1. Where is it loudest, and where does it go?

2. What shape is it?

3. What do S2 and the carotid pulse tell you?

4. Any change with maneuvers?

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Examination: The murmur in detail

Timing: mid-systolic, ends before S2

Shape: crescendo-decrescendo

Where: right 2nd intercostal space

Radiates: both carotids

Quality: harsh, use the diaphragm

Best heard: leaning forward, end-expiration

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Further Exam Findings

S2: soft, may split paradoxically

S4: stiff, thick ventricle

Apex: sustained, not displaced

Carotid pulse: slow-rising, low volume “Pulsus parvus et tardus”

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Assessing Severity of AS (without an echo!)

Suggests severe

Late-peaking murmur
Soft or absent S2
Slow, weak carotid upstroke
S4

Misleading

Loudness alone
A quiet murmur with low gradient due to reduced EF

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Question 1

Which additional finding would best suggest his AS is severe?

A Grade 4/6 murmur

B Late-peaking murmur with a soft S2

C Murmur also heard at the apex

D Radiating to both carotids

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Question 1

Which additional finding would best suggest his AS is severe?

A Grade 4/6 murmur

B Late-peaking murmur with a soft S2

C Murmur also heard at the apex

D Radiating to both carotids

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Investigations

ECG: LVH with strain, LA enlargement, conduction disease
CXR: Features of pulmonary edema, enlarged heart
BNP: risk marker in asymptomatic severe AS
Exercise test: *asymptomatic only, to unmask symptoms

Echocardiogram: the key test for anatomy, severity and LV function

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Echocardiogram to grade severity

	Mild	Moderate	Severe
Peak velocity (m/s)	2.6 – 2.9	3.0 – 3.9	≥4.0
Mean gradient (mm Hg)	<20	20 – 39	≥40
Valve area (cm²)	>1.5	1.0 – 1.5	≤1.0

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Case 1, six months later

78-year-old man returns to your clinic. He now has exertional dyspnea and ankle swelling.

BP: 128/74 at the time of the echo.

Echo: LVEF 62%. Small, thick LV.

Valve: area 0.8 cm². Mean gradient 28 mm Hg. Peak velocity 3.4 m/s.

Stroke volume index: 30 mL/m².

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Question 2

What is the best next step?

A Dobutamine stress echo

B Refer for valve replacement now

C CT aortic valve calcium score

D Repeat echo in 6 to 12 months

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Low-flow, low-gradient severe AS

Reduced EF (classic)

A weak LV cannot push enough flow to open the valve or build a gradient

Dobutamine stress echo:

True severe: gradient rises to ≥40 mm Hg, valve area stays ≤1.0 cm²
Pseudo-severe: valve area opens above 1.0 cm², gradient stays low
No contractile reserve: worse prognosis, still consider AVR

Preserved EF (paradoxical)

A small, thick, stiff LV ejects a low stroke volume despite a normal EF
Stroke volume index <35 mL/m²
Confirm with CT calcium score, since dobutamine rarely helps here
Exclude measurement error and uncontrolled hypertension first

Valve area ≤1.0 cm² but mean gradient <40 mm Hg, because flow is low

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Question 2

What is the best next step?

A Dobutamine stress echo

B Refer for valve replacement now

C CT aortic valve calcium score

D Repeat echo in 6 to 12 months

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Question 2

What is the best next step?

A Dobutamine stress echo

B Refer for valve replacement now

C CT aortic valve calcium score

D Repeat echo in 6 to 12 months

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Management of Aortic Stenosis

Medical Therapy: No drug slows AS progression.
Hypertension management: In severe AS, avoid hypotension and aggressive vasodilators.
Statins have been studied, but prospective data found they do not affect outcomes

Valve replacement is the only definitive treatment.

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Class I Indications for Aortic Valve Replacement

1. Symptomatic severe AS

2. Asymptomatic severe AS with LVEF below 50%

3. Severe AS in a patient having other heart surgery

4. Symptomatic low-flow, low-gradient AS, once confirmed severe (reduced or normal EF)

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Bonus: TAVR or SAVR?

	Favours SAVR	Favours TAVR
Age	Under 65	Over 80 (65 to 80: shared decision)
Life expectancy	More than 20 years	Less than 10 years
Surgical risk	Low	High or prohibitive
Anatomy	Bicuspid valve, aortic dilation, poor femoral access	Tricuspid valve, good femoral access
Other heart surgery	CABG or other valve surgery needed	Isolated AS
Other factors		Frailty, prior chest radiation

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Case 2: Dizzy on the soccer field

A 22-year-old university student nearly faints during a soccer game.

His father passed away at age 45 due to a drowning accident.

Exam: a 2/6 systolic murmur at the left lower sternal border. It does not radiate to the carotids. The carotid upstroke is brisk.

Maneuver: the murmur gets louder when he bears down.

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Question 3

Which other maneuver will also make his murmur louder?

A Squatting

B Handgrip

C Passive leg raise

D Squat to stand

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Hypertrophic cardiomyopathy

LV wall ≥15 mm without another cause such as hypertension, AS or infiltrative disease
Autosomal dominant sarcomere mutations; about 1 in 500
Usually asymmetric septal hypertrophy

LVOT obstruction: the key concern

Septal bulge plus SAM of the mitral leaflet narrows the outflow tract
Peak gradient ≥30 mm Hg, at rest or provoked
Dynamic: worse with less preload or afterload, or increased contractility
Causes the murmur and much of the symptom burden

Insert an image of asymmetric septal hypertrophy with SAM in the right-hand box.

Diagnosis: wall thickness of 15 mm or more anywhere in the LV, or 13 mm or more with a family history or a known pathogenic variant, without another cause that explains it.

Genetics: autosomal dominant, so first-degree relatives have a 50% chance of carrying the variant. MYH7 and MYBPC3 are the most common genes. Many patients have no variant found on testing. Screen first-degree relatives with ECG and echo.

Patterns: asymmetric septal hypertrophy is classic. Concentric and apical forms also occur.

Obstruction: a peak LVOT gradient of 30 mm Hg or more defines obstructive HCM. Roughly a third of patients obstruct at rest, a third only with provocation such as Valsalva or exercise, and a third never. That is why you provoke the murmur at the bedside.

Why it matters for today: the obstruction is dynamic. That is the physiology behind the maneuvers in Case 2.

Source: 2024 AHA/ACC HCM guideline; CardioGuide overview.

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AS or HCM?

Aortic stenosis

Right upper sternal border, to the carotids
Slow, weak carotid upstroke
Soft or single S2
Softer with Valsalva
Older patient

HCM

Left lower sternal border, not to the carotids
Brisk, sometimes bifid upstroke
Normal S2
Louder with Valsalva
Young, family history of sudden death

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Question 3

Which other maneuver will also make his murmur louder?

A Squatting

B Handgrip

C Passive leg raise

D Squat to stand

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Question 3

Which other maneuver will also make his murmur louder?

A Squatting

B Handgrip

C Passive leg raise

D Squat to stand

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Case 3: Sudden dyspnea after MI

A 64-year-old man had a stent for an inferior STEMI two days ago.

Overnight, he becomes suddenly short of breath and cannot tolerate lying flat.

Vitals: BP 84/50, HR 122, RR 32, SpO2 86% on 6 L.

Exam: crackles to the mid lung fields. Cool peripheries.

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Question 4

What would you expect to hear?

A Loud holosystolic apical murmur to the axilla

B Soft, decrescendo early systolic murmur

C Mid-systolic click, late systolic murmur

D Crescendo-decrescendo murmur at the base

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Acute mitral regurgitation

A life-threatening emergency. Sudden volume overload of an unprepared left atrium and ventricle causes pulmonary congestion and low cardiac output.

Causes

Leaflet perforation or rupture (e.g., endocarditis)
Papillary muscle rupture (e.g., after myocardial infarction)
Spontaneous chordal rupture (e.g., myxomatous mitral valve disease)

Chronic MR is a different disease process. The atrium dilates over time, and that is where you hear the classic holosystolic murmur.

Acute MR: the left atrium is small and non-compliant, so its pressure rises sharply. That pressure goes straight back to the lungs, causing flash pulmonary edema. Forward stroke volume falls, causing hypotension and shock.

The murmur is often soft, short and early, and can be absent, because LA and LV pressures equalize early in systole. Do not let a quiet chest reassure you in a post-MI patient with sudden pulmonary edema or hypotension.

Papillary muscle rupture classically follows an inferior MI and involves the posteromedial papillary muscle, which has a single blood supply. Contrast with post-MI ventricular septal rupture, which usually gives a loud holosystolic murmur, often with a thrill.

Management: urgent echo (TEE if TTE is unclear), afterload reduction as blood pressure allows, mechanical support if needed, and early cardiac surgery referral.

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AS or chronic MR?

Aortic stenosis

Right upper sternal border, to the carotids
Diamond, ends before S2
Softer with handgrip
Louder after a PVC

Chronic MR

Apex, to the axilla
Holosystolic, runs into S2
Louder with handgrip
No change after a PVC

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Question 4

What would you expect to hear?

A Loud holosystolic apical murmur to the axilla

B Soft, decrescendo early systolic murmur

C Mid-systolic click, late systolic murmur

D Crescendo-decrescendo murmur at the base

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Question 4

What would you expect to hear?

A Loud holosystolic apical murmur to the axilla

B Soft, decrescendo early systolic murmur

C Mid-systolic click, late systolic murmur

D Crescendo-decrescendo murmur at the base

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Reference table

	Aortic stenosis	LVOT obstruction	Mitral regurgitation
Loudest at	RUSB	LLSB to apex	Apex
Radiates to	Carotids	Not to carotids	Axilla
Shape	Crescendo- decrescendo	Crescendo-decrescendo	Holosystolic
Carotid pulse	Slow and weak	Brisk, may be bifid	Brisk
S2	Soft or single	Normal	Normal, may have S3
Valsalva or standing	Softer	Louder	Softer
Squatting	Louder	Softer	Louder
Handgrip	Softer	Softer	Louder

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Final Question

You ask the previous 3 patients to do the handgrip maneuver. What happens to each?

A AS louder, LVOTO softer, MR louder

B AS softer, LVOTO softer, MR louder

C AS softer, LVOTO louder, MR softer

D No change in any of them

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Answer: B. Afterload goes up.

	Aortic stenosis	LVOT obstruction	Mitral regurgitation
Loudest at	RUSB	LLSB to apex	Apex
Radiates to	Carotids	Not to carotids	Axilla
Shape	Crescendo- decrescendo	Crescendo-decrescendo	Holosystolic
Carotid pulse	Slow and weak	Brisk, may be bifid	Brisk
S2	Soft or single	Normal	Normal, may have S3
Valsalva or standing	Softer	Louder	Softer
Squatting	Louder	Softer	Louder
Handgrip	Softer	Softer	Louder
Beat after a PVC	Louder	Louder	No change

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Thank You!