Common misconceptions

Common mistake
Wrong: S3 and S4 are both caused by a stiff, non-compliant ventricle.
Right: S3 results from rapid passive ventricular filling (dilated, volume-overloaded ventricle); S4 results from atrial contraction against a stiff, non-compliant ventricle.
S4 is caused by atrial contraction pushing blood into a stiff, non-compliant ventricle — so ventricular stiffness is correct for S4. S3, however, occurs during early diastole when blood rushes passively into a dilated or volume-overloaded ventricle, causing the ventricular walls to vibrate — stiffness has nothing to do with it. Keep them separate: S3 = too much volume (think dilated cardiomyopathy, heart failure with reduced EF, MR, AR); S4 = too stiff (think hypertension, hypertrophic cardiomyopathy, aortic stenosis).
Common mistake
Wrong: HCM murmur behaves like other systolic murmurs and increases with increased preload.
Right: HCM murmur increases with decreased preload (standing, Valsalva) because less ventricular filling worsens outflow obstruction.
In HCM, the outflow obstruction is dynamic — it worsens when the ventricle is smaller because the hypertrophied septum gets closer to the anterior mitral leaflet. Increased preload fills the ventricle more, pushing the walls apart and relieving obstruction — so the murmur gets softer with squatting or leg raise. Decreased preload (standing, Valsalva strain) shrinks the ventricle and worsens obstruction, making the murmur louder. This is the opposite of fixed-obstruction murmurs like aortic stenosis.
Common mistake
Wrong: Students classify the mitral stenosis murmur as systolic because it is associated with rheumatic heart disease affecting the mitral valve.
Right: Mitral stenosis produces a mid-to-late diastolic rumble following an opening snap, as the stenotic valve obstructs filling during diastole.
Think about when mitral stenosis causes a problem: the stenotic valve obstructs blood flowing from the left atrium into the left ventricle during diastole (ventricular filling). That obstruction produces turbulence during diastole, not systole. The opening snap is the stiff mitral valve snapping open at the start of diastole, followed by the rumbling murmur as blood struggles through the narrowed orifice. Mitral regurgitation is the systolic mitral murmur — don't let 'mitral' anchor you to systole for both.
Common mistake
Gap: Unaware that Valsalva selectively increases HCM and MVP murmurs by reducing preload while decreasing most other cardiac murmurs
Valsalva strain phase decreases venous return and preload, increasing HCM and MVP murmurs while decreasing most other murmurs.
During Valsalva strain, increased intrathoracic pressure reduces venous return, dropping preload. For most murmurs (aortic stenosis, mitral regurgitation, aortic regurgitation), less preload means less flow and a softer murmur. For HCM, less preload shrinks the ventricle and worsens dynamic outflow obstruction — louder murmur. For MVP, less preload means less ventricular volume, so the mitral leaflets prolapse earlier in systole — the click moves earlier and the murmur lengthens. Knowing WHY these two behave differently from all others lets you reason through any maneuver the exam throws at you.
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What the exam tests

  1. Know the physiologic basis of each heart sound: S1 (mitral/tricuspid closure), S2 (aortic/pulmonic closure), S3 (rapid passive ventricular filling in a volume-overloaded or dilated ventricle), and S4 (atrial kick against a stiff, non-compliant ventricle) — and recognize which clinical conditions produce each.
  2. Classify murmurs correctly as systolic, diastolic, or continuous based on their timing relative to S1 and S2 — including distinguishing specific murmurs like the mid-to-late diastolic rumble of mitral stenosis with opening snap from systolic murmurs like mitral regurgitation or aortic stenosis.
  3. Predict how bedside maneuvers (Valsalva strain, standing, squatting, handgrip, leg raise) change murmur intensity by reasoning through their effects on preload and afterload — especially for HCM and MVP, which behave opposite to most other murmurs.

Can you avoid these mistakes?

A 65-year-old with longstanding hypertension has a new S4 on exam. Your classmate says both S3 and S4 are caused by a stiff ventricle. How do you correct them, and what would you expect to find in a patient with dilated cardiomyopathy instead?
A 22-year-old athlete is found to have a harsh systolic murmur at the left sternal border that gets louder when they stand up quickly. What is the diagnosis, and why does standing increase this murmur while squatting decreases it?
A 35-year-old woman with a history of rheumatic fever has exertional dyspnea. Auscultation reveals a low-pitched rumble after a high-pitched extra sound in early diastole. What are these two findings, what valve is affected, and is this murmur systolic or diastolic?
During Valsalva strain, you hear a systolic murmur get louder. What are the two murmurs that behave this way, and what is the shared mechanism that explains why they both increase while most other murmurs decrease?

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