S2: The Second Heart Sound

S2 is where cardiac auscultation gets interesting. While S1 mainly tells you about AV valve function and timing, S2 gives you insights into the semilunar valves, pulmonary pressures, and ventricular conduction. Understanding S2 splitting patterns is one of the most diagnostically powerful skills you'll develop.

Here's a question to consider as you read: S2 has two components that can be heard separately during breathing. Why would respiration affect the timing of valve closure in the heart?

What Creates S2?

S2 marks the end of systole and the beginning of diastole. It's created by the closure of the aortic and pulmonic valves as the ventricles finish contracting and begin to relax.

Two Components: A2 and P2

Unlike S1, where the two components usually blend together, S2's components are often audibly separate. A2 (aortic closure) usually comes first and is louder—best heard at the right upper sternal border and apex. P2 (pulmonic closure) comes slightly after A2 and is best heard at the left upper sternal border in the 2nd intercostal space.

Why A2 is Normally Louder Than P2

The aortic valve closes under much higher pressure than the pulmonic valve—systemic pressure around 120 mmHg versus pulmonary pressure around 25 mmHg. Higher pressure creates more forceful valve closure and thus a louder sound. It's like comparing a door slamming in a windstorm versus a gentle breeze.

Physiologic Splitting of S2

In healthy young people, S2 normally splits during inspiration and becomes single during expiration. Understanding why this happens will help you recognize abnormal splitting patterns.

The Mechanism

During inspiration, negative intrathoracic pressure increases venous return to the right heart. The right ventricle takes longer to eject this increased volume, so the pulmonic valve closes later—P2 delays. Simultaneously, blood pools in the pulmonary vasculature, decreasing return to the left heart. The left ventricle ejects less volume and finishes faster, so the aortic valve closes slightly earlier—A2 comes earlier. The result: A2 and P2 move apart, and you hear two distinct sounds.

During expiration, venous return normalizes. Both ventricles eject similar volumes with similar timing, so A2 and P2 occur nearly simultaneously—you hear a single S2.

How to Assess Splitting

The best location to assess splitting is the left upper sternal border (2nd left intercostal space)—this is where P2 is heard best. Have the patient breathe normally rather than deeply, since deep breathing exaggerates splitting and can be misleading. Listen through several respiratory cycles, focusing on whether S2 is single or split and whether the splitting varies with respiration.

Abnormal Splitting Patterns

Abnormal splitting patterns tell you about specific cardiac pathologies. Before we dive in, test yourself:

If something delays right ventricular ejection (like pulmonic stenosis or RBBB), what would happen to S2 splitting?

Wide Splitting

In wide splitting, A2 and P2 are widely separated, but the split still varies with respiration—widening with inspiration and narrowing with expiration. Anything that delays right ventricular ejection or shortens left ventricular ejection will widen the gap between A2 and P2.

Right bundle branch block (RBBB) is the most common cause—delayed RV activation leads to delayed RV ejection and late P2. Pulmonic stenosis causes the RV to take longer to eject through the narrowed valve. Mitral regurgitation causes the LV to empty faster since some blood regurgitates into the LA, producing early A2. Ventricular septal defects shunt blood left-to-right, increasing RV volume and delaying P2.

The key point: wide splitting still varies with respiration, so you know both ventricles are responding normally to respiratory changes.

Fixed Splitting

In fixed splitting, A2 and P2 are split, but the splitting does NOT change with respiration—it's the same in inspiration and expiration. This happens when atrial pressures are equalized, so respiratory changes in venous return don't affect ventricular filling differently.

The classic cause is atrial septal defect (ASD). Blood shunts from LA to RA through the defect. During inspiration, RA pressure drops normally and would increase venous return, but blood also shunts from LA to RA through the ASD, maintaining consistent RA filling. During expiration, the opposite happens. The net result: RV receives similar volume throughout the respiratory cycle, and P2 stays in the same position relative to A2 regardless of respiration.

Paradoxical Splitting

Paradoxical splitting is backwards—S2 splits during expiration and becomes single during inspiration. This is the opposite of normal. It happens when anything significantly delays left ventricular ejection, causing A2 to come after P2 instead of before.

Left bundle branch block (LBBB) is the most common cause—delayed LV activation creates a very late A2. Severe aortic stenosis causes the LV to take much longer to eject through the narrowed valve. Right ventricular pacing causes the LV to depolarize late.

The respiratory effect works like this: during inspiration, P2 delays (normal response), but A2 is already so delayed that P2 "catches up"—the sounds merge into a single S2. During expiration, P2 comes earlier (normal), creating a bigger gap from the delayed A2—you hear the split. If S2 splits when the patient breathes OUT, it's paradoxical.

Single S2

When you hear only one component of S2 throughout the respiratory cycle, consider several causes. In severe aortic stenosis, A2 becomes very soft or absent because the calcified valve barely moves. In pulmonary hypertension, a very loud P2 masks A2. In Tetralogy of Fallot, P2 is absent or soft. In older patients, decreased physiologic splitting is common and benign. And of course, poor technique—not listening at the right spot or patient not breathing normally—can make splitting undetectable.

Loud P2: The Sign of Pulmonary Hypertension

Normally, A2 is louder than P2 everywhere except possibly at the pulmonic area. If P2 becomes loud and palpable, suspect pulmonary hypertension.

You'll find a loud, palpable P2 at the left upper sternal border, with P2 equal to or louder than A2. This is often accompanied by a right ventricular heave (the RV is working harder against elevated pulmonary pressures). You may also hear a tricuspid regurgitation murmur since pulmonary hypertension dilates the RV and tricuspid annulus.

Causes of pulmonary hypertension include chronic lung disease, left heart failure, recurrent pulmonary emboli, primary pulmonary hypertension, mitral stenosis, and chronic hypoxemia.

Summary: S2 Splitting Patterns

Quick Recall

Test yourself on the table above:

1. S2 splitting that doesn't change with respiration—split in both inspiration and expiration. What is this pattern called and what is the classic cause?

2. S2 splits during expiration and becomes single during inspiration. What is this called?

3. Which conduction abnormality causes wide splitting of S2?

4. A patient has a single S2 throughout the respiratory cycle. Name two causes.

Clinical Scenarios

For each scenario, think about what you would suspect before revealing the answer.

Case 1: The Young Athlete

Findings: S2 splits with inspiration, single with expiration. P2 normal intensity.

Case 2: Post-MI Patient

Findings: New onset wide splitting that varies with respiration. New holosystolic murmur at apex.

Case 3: Child with Murmur

Findings: Fixed split S2 that doesn't change with breathing. Soft systolic murmur at left upper sternal border.

Case 4: Elderly Man with Syncope

Findings: Paradoxical S2 splitting (splits on expiration). Harsh systolic murmur at right upper sternal border. Delayed carotid upstroke.

Getting Better at S2 Assessment

Developing skill at hearing S2 splitting takes deliberate practice. Start by listening to every young patient's S2 at the left upper sternal border during normal breathing—learn what physiologic splitting sounds like before trying to recognize abnormal patterns. When you think you hear wide or fixed splitting, have your attending confirm it and discuss the findings.

Remember that subtle splitting is normal; wide, fixed, and paradoxical patterns are pathologic. If you're unsure whether splitting is truly fixed, have the patient take a few deep breaths—if it's truly fixed, it won't change even with exaggerated breathing. Some echo machines have phonocardiogram displays that can help you visualize the splitting pattern.

Mastering S2 splitting is one of the most valuable auscultation skills you can develop. It gives you real-time diagnostic information about cardiac structure and function without any imaging. Practice this skill relentlessly—it's worth it.