1. SECOND HEART SOUND (S2)
INTRODUCTION :
A. History - Rouanet, more than 140 years ago, attributed the second heart sound to closure of the aortic and pulmonary valves.
B. The clinical evaluation of the second heart sound has been called the “KEY TO AUSCULTATION OF THE HEART”
C. The two components- A2 and P2 are best heard with the diaphragm of the stethoscope and over the left second ICS close to the sternal border.
D. S2 is single during expiration, particularly in semi recumbent position. Separation of A2 and P2 occurs in inspiration and the duration is <30 ms.
Physiology of the Normal split of S2
- Normally, pulmonary valve closes after aortic valve closure, hence P2 occurs after A2.
- This is because, the pulmonary vascular resistance is about 1/10th
of that of systemic vascular resistance.
- Therefore, forward flow of blood continues longer in the pulmonary circuit than in the aortic circuit (called the hangout interval).
- Thus, pulmonary closure sound (P2) occurs later than aortic closure sound (A2), producing a normal physiological split of S2.
- This normal split widens physiologically during inspiration due to an early P2 and a late A2.
- This is because, Inspiration lowers intrathoracic pressure, drawing more blood from SVC and IVC, thus increasing RV volume,
which in turn delays the pulmonary valve closure (early P2).
- Inspiration also increases the vascular capacity of the lung, which withholds some amount of blood from reaching the LV,
thus decreasing the LV volume, causing early aortic valve closure (delayed A2).
Wide splitting of S2 :
A wide split is one that is persistent (present during inspiration and expiration)
and widens on inspiration to atleast 60 milliseconds.
Causes :
1. Delayed pulmonic closure
a. Delayed electrical activation of the RV
• Complete RBBB (proximal type)
• LV paced beats
• LV ectopic beats
b. Prolonged RV mechanical systole
• Acute massive PE
• Pulmonary hypertension with right heart failure
• Pulmonary stenosis with intact septum (moderate to severe)
c. Decreased impedence of the pulmonary vascular bed (Increased hangout)
• Normotensive ASD
• Idiopathic pulmonary dilatation of the pulmonary artery
• Pulmonary stenosis (mild)
• ASD, postoperative (70%)
• Unexplained audible expiratory splitting in normal subjects
2. Early aortic closure
• Shortened LV ejection time
• Mitral regurgitation
• VSD
Reversed splitting on S2 :
Identification of reverse split - A split that widens on expiration
and narrows on inspiration implies that the P2 comes first.
Causes :
1. Delayed aortic closure
• Complete LBBB
• RV pacing
• RV ectopics
a. Prolonged LV mechanical systole
• Complete LBBB
• LV outflow tract obstruction – Aortic stenosis
• Hypertensive cardiovascular disease
• Arteriosclerotic heart disease- Chronic IHD,
Angina pectoris
b. Decreased impedence of the systemic vascular bed
(Increased hangout interval)
• Post stenotic dilatation of the aorta secondary to
AS
• PDA
2. Early pulmonic closure
Early electrical activation of the RV
• WPW, type B
Expiratory split of S2 : There are only 3 possibilities if a split is heard in
expiration
a. wide split - widens further on inspiration
b. fixed split - remains the same on inspiration
c. reverse split - decreases on inspiration
Hurst’s The heart 12th
edition, UpToDate, Clinical Methods- NCBI Nikita Mehra nikita.mehra3@gmail.com