What Causes The Second Heart Sound

The second heart sound, often referred to as S2, is an important auscultatory finding during a cardiac examination. It provides valuable information about the function of the heart valves, particularly the aortic and pulmonic valves. Understanding what causes this sound, its components, and variations can aid in the diagnosis of various cardiovascular conditions.

Understanding the Basics of Heart Sounds

Before delving into the specifics of S2, it's helpful to understand the context of heart sounds in general. A normal heartbeat produces two primary sounds, S1 and S2, often described as "lub-dub." These sounds are generated by the closing of the heart valves:

• S1 (First Heart Sound): This sound marks the beginning of systole (the contraction phase of the heart) and is primarily caused by the closure of the mitral and tricuspid valves (the atrioventricular valves).
• S2 (Second Heart Sound): This sound marks the beginning of diastole (the relaxation phase of the heart) and is caused by the closure of the aortic and pulmonic valves (the semilunar valves).

In addition to S1 and S2, other heart sounds (S3 and S4) can be present in certain individuals, often indicating underlying cardiac pathology. These sounds occur during diastole and are usually softer than S1 and S2, making them more difficult to hear.

The Genesis of the Second Heart Sound (S2)

The second heart sound, S2, is generated by the closure of the aortic and pulmonic valves. These valves are located at the exit points of the left and right ventricles, respectively. The aortic valve guards the entrance to the aorta, the main artery carrying oxygenated blood to the body, while the pulmonic valve guards the entrance to the pulmonary artery, which carries deoxygenated blood to the lungs.

Closure of the Aortic and Pulmonic Valves

At the end of systole, the ventricles begin to relax. As the ventricular pressure falls below the pressure in the aorta and pulmonary artery, blood begins to flow backward towards the ventricles. This backward flow forces the aortic and pulmonic valves to snap shut, preventing backflow of blood into the ventricles. The abrupt closure of these valves generates vibrations that are transmitted through the chest wall, producing the second heart sound.

Components of S2: A2 and P2

The second heart sound is actually composed of two distinct components:

• A2 (Aortic Component): This is the component caused by the closure of the aortic valve. A2 is typically louder than P2 and is heard best at the base of the heart, specifically in the second right intercostal space along the sternal border.
• P2 (Pulmonic Component): This component is caused by the closure of the pulmonic valve. P2 is usually softer than A2 and is heard best in the second left intercostal space along the sternal border.

Physiologic Splitting of S2

Under normal circumstances, the aortic and pulmonic valves do not close at exactly the same time. The aortic valve typically closes slightly before the pulmonic valve. This slight difference in timing is due to differences in the pressures and volumes in the left and right sides of the heart, as well as the effects of respiration.

During inspiration (breathing in), the negative intrathoracic pressure increases venous return to the right side of the heart. This increased venous return leads to increased right ventricular volume, which prolongs right ventricular systole. As a result, the pulmonic valve closure is delayed. At the same time, inspiration decreases venous return to the left side of the heart, which can slightly shorten left ventricular systole and cause the aortic valve to close earlier.

The combined effect of these respiratory changes is to widen the interval between A2 and P2 during inspiration, resulting in a phenomenon known as physiologic splitting of S2. During expiration (breathing out), the interval between A2 and P2 narrows, and the two components may fuse into a single sound.

Variations in S2 Splitting: Implications for Diagnosis

The pattern of S2 splitting can provide important clues about underlying cardiovascular abnormalities. Variations from the normal physiologic splitting pattern include:

• Wide Splitting: This occurs when the interval between A2 and P2 is abnormally wide and persists throughout the respiratory cycle. It can be caused by conditions that delay pulmonic valve closure or hasten aortic valve closure, such as:
  • Pulmonic stenosis: Narrowing of the pulmonic valve, which delays pulmonic valve closure.
  • Right bundle branch block: A conduction delay in the right ventricle, which delays pulmonic valve closure.
  • Mitral regurgitation: Backflow of blood from the left ventricle to the left atrium, which shortens left ventricular systole and hastens aortic valve closure.
• Fixed Splitting: This occurs when the interval between A2 and P2 is constant and does not vary with respiration. The most common cause of fixed splitting is:
  • Atrial septal defect (ASD): A hole in the wall between the left and right atria, which equalizes pressures in the two atria and eliminates the respiratory variation in venous return.
• Paradoxical (or Reversed) Splitting: This occurs when P2 occurs before A2. In this case, the split narrows during inspiration and widens during expiration. Paradoxical splitting is caused by conditions that delay aortic valve closure, such as:
  • Aortic stenosis: Narrowing of the aortic valve, which delays aortic valve closure.
  • Left bundle branch block: A conduction delay in the left ventricle, which delays aortic valve closure.
  • Hypertrophic cardiomyopathy: A condition in which the heart muscle is abnormally thick, which can delay aortic valve closure.
• Single S2: In some cases, only one component of S2 is audible, creating a single S2 sound. This can be caused by:
  • Severe aortic stenosis: In severe aortic stenosis, the aortic valve closure may be very soft or inaudible.
  • Severe pulmonic stenosis: Similarly, in severe pulmonic stenosis, the pulmonic valve closure may be very soft or inaudible.
  • Transposition of the great arteries: A congenital heart defect in which the aorta and pulmonary artery are switched.

Other Abnormalities Associated with S2

In addition to abnormalities in splitting, the intensity of S2 and its components (A2 and P2) can also provide clues about underlying cardiovascular conditions.

• Loud A2: A loud A2 component can be caused by systemic hypertension (high blood pressure). The increased pressure in the aorta causes a more forceful closure of the aortic valve, resulting in a louder sound.
• Soft A2: A soft A2 component can be caused by aortic stenosis. The narrowed aortic valve restricts blood flow, resulting in a less forceful closure and a softer sound.
• Loud P2: A loud P2 component can be caused by pulmonary hypertension (high blood pressure in the pulmonary arteries). The increased pressure in the pulmonary artery causes a more forceful closure of the pulmonic valve, resulting in a louder sound.
• Soft P2: A soft P2 component can be caused by pulmonic stenosis. The narrowed pulmonic valve restricts blood flow, resulting in a less forceful closure and a softer sound.

Clinical Significance of S2 Assessment

Careful auscultation of the second heart sound is an essential part of a comprehensive cardiovascular examination. By listening to the timing, splitting pattern, and intensity of S2 and its components, clinicians can gain valuable insights into the function of the heart valves and the presence of underlying cardiac abnormalities.

Abnormalities in S2 can be indicative of a wide range of cardiovascular conditions, including:

• Valvular heart disease (aortic stenosis, pulmonic stenosis, aortic regurgitation, pulmonic regurgitation)
• Congenital heart defects (atrial septal defect, ventricular septal defect, patent ductus arteriosus, transposition of the great arteries)
• Pulmonary hypertension
• Systemic hypertension
• Conduction abnormalities (right bundle branch block, left bundle branch block)
• Cardiomyopathy

Diagnostic Tools Complementing S2 Assessment

While auscultation of S2 is a valuable diagnostic tool, it is important to remember that it is just one piece of the puzzle. Other diagnostic tests, such as electrocardiography (ECG), echocardiography, and cardiac catheterization, are often necessary to confirm a diagnosis and determine the severity of any underlying cardiac condition.

• Electrocardiography (ECG): An ECG records the electrical activity of the heart and can help identify arrhythmias, conduction abnormalities, and evidence of myocardial ischemia or infarction.
• Echocardiography: Echocardiography uses ultrasound to create images of the heart. It can provide detailed information about the structure and function of the heart valves, chambers, and myocardium.
• Cardiac Catheterization: Cardiac catheterization is an invasive procedure in which a catheter is inserted into a blood vessel and guided to the heart. It allows for direct measurement of pressures in the heart chambers and blood vessels, as well as angiography (imaging of the coronary arteries).

Conclusion: The Second Heart Sound as a Diagnostic Window

The second heart sound, S2, is a crucial auscultatory finding that reflects the closure of the aortic and pulmonic valves. Its two components, A2 and P2, normally exhibit physiologic splitting that varies with respiration. Deviations from this normal pattern, as well as changes in the intensity of A2 and P2, can provide valuable clues about underlying cardiovascular abnormalities. By carefully assessing S2 and integrating this information with other clinical findings and diagnostic tests, clinicians can effectively diagnose and manage a wide range of cardiac conditions. Learning to listen to the subtle nuances of the heart sounds is a cornerstone of clinical cardiology and is crucial for providing optimal patient care. It serves as an easily accessible, non-invasive method for initial assessment and can guide further diagnostic evaluations, emphasizing its continued importance in modern medical practice.