Common misconceptions

Common mistake
Wrong: Paradoxical splitting of S2 is caused by RBBB.
Right: Paradoxical splitting is caused by delayed aortic valve closure (e.g., LBBB, aortic stenosis), so A2 follows P2 instead of preceding it.
Paradoxical splitting means the normal order of A2 then P2 is reversed — P2 comes first and A2 follows. This happens when aortic valve closure is delayed, as in LBBB (delayed LV depolarization) or severe aortic stenosis (prolonged LV ejection). RBBB delays pulmonic closure, which actually widens physiologic splitting on inspiration — it does not cause paradoxical splitting. The distinction is about which component is delayed: aortic delay = paradoxical; pulmonic delay = wide or fixed splitting.
Common mistake
Wrong: Physiologic splitting of S2 on inspiration is due to earlier pulmonic valve closure.
Right: Inspiration increases RV filling and prolongs RV ejection, delaying pulmonic valve closure (P2) so it follows aortic closure (A2), producing the split.
Physiologic S2 splitting on inspiration is driven by delayed P2, not earlier P2 or earlier A2. Inspiration lowers intrathoracic pressure, increasing venous return to the right heart; the RV takes longer to eject that extra volume, so the pulmonic valve closes later. The aortic valve actually closes slightly earlier on inspiration due to reduced LV preload. The result: A2 and P2 move apart, creating an audible split on inspiration that disappears on expiration.
Common mistake
Wrong: S3 and S4 both occur in early diastole.
Right: S3 occurs in early diastole (rapid ventricular filling) and indicates volume overload; S4 occurs in late diastole (atrial kick) and indicates a stiff, non-compliant ventricle.
S3 and S4 are both diastolic sounds, but they occur at opposite ends of diastole. S3 happens during rapid passive ventricular filling in early diastole — it indicates the ventricle is volume-overloaded and the walls are decelerating blood abruptly (think dilated cardiomyopathy or mitral regurgitation). S4 happens in late diastole during the atrial kick — it indicates a stiff, non-compliant ventricle that requires extra atrial force to fill (think LVH from hypertension or aortic stenosis). S4 cannot occur in atrial fibrillation because there is no atrial kick.
Common mistake
Wrong: The mitral valve closes at the start of isovolumetric relaxation.
Right: The mitral valve closes at the start of isovolumetric contraction (marking S1); the aortic valve closes at the start of isovolumetric relaxation (marking S2).
The two isovolumetric phases are defined by which valve just closed. Isovolumetric contraction begins when the mitral valve closes (S1) — both valves are now shut and the ventricle is building pressure with no volume change. Isovolumetric relaxation begins when the aortic valve closes (S2) — again both valves are shut, but now pressure is dropping before the mitral valve opens. A useful anchor: S1 starts isovolumetric contraction, S2 starts isovolumetric relaxation.
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What the exam tests

  1. Know the ordered phases of the cardiac cycle in sequence: late diastole → isovolumetric contraction → rapid ejection → reduced ejection → isovolumetric relaxation → rapid filling → slow filling → atrial kick — and understand what's happening to pressure and volume in each phase.
  2. Be able to read a Wiggers diagram and identify LV pressure, aortic pressure, LV volume, the ECG trace, and heart sounds simultaneously — the exam will ask what happens to one variable at a specific point in the cycle.
  3. Know the precise timing of S1, S2, S3, and S4 within the cardiac cycle, what valve events or ventricular mechanics generate each sound, and what pathology each extra sound (S3, S4) indicates clinically.

Can you avoid these mistakes?

On the Wiggers diagram, at the moment LV pressure first exceeds aortic pressure, what phase is beginning and which valve just opened? What valve event immediately preceded this?
A patient with poorly controlled hypertension has a new S4 heard best at the apex. What does this sound represent mechanically, and why can this sound never be heard in a patient with atrial fibrillation?
During auscultation, a split S2 is heard that is loudest on expiration and disappears on inspiration. Is this physiologic or paradoxical splitting, and what is the most likely underlying cause?
Walk through what happens to mitral valve status, LV volume, and LV pressure during isovolumetric contraction — then explain why LV volume doesn't change even though the ventricle is actively contracting.

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