Split S2

A split S2 is a finding upon auscultation of the S2 heart sound.[1]

It is caused when the closure of the aortic valve (A2) and the closure of the pulmonary valve (P2) are not synchronized.[2]

Contents

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Physiologic split

During inspiration, the chest wall expands and causes the intrathoracic pressure to become more negative (think of a vacuum). The increased negative pressure allows the lungs to fill with air and expand. While doing so, it also induces an increase in venous blood return from the body into the right atrium via the superior and inferior vena cavae, and into the right ventricle by increasing the pressure gradient (blood is being pulled by the vacuum from the body and towards the right side of the heart). Simultaneously, there is a reduction in blood volume returning from the lungs into the left ventricle (the blood wants to stay in the lungs because of the vacuum surrounding the lungs). Since there is an increase in blood volume in the right ventricle, the pulmonary valve (P2 component of S2) stays open longer during ventricular systole due to an increase in ventricular emptying time, whereas the aortic valve (A2 component of S2) closes slightly earlier due to a reduction in left ventricular volume and ventricular emptying time. Thus the P2 component of S2 is delayed relative to that of the A2 component. This delay in P2 versus A2 is heard as a slight broadening or even "splitting" of the second heart sound; though it is usually only heard in the pulmonic area of the chest because the P2 is soft and not heard in other areas. During expiration, the chest wall collapses and decreases the negative intrathoracic pressure (compared to inspiration). Therefore, there is no longer an increase in blood return to the right ventricle versus the left ventricle and the right ventricle volume is no longer increased. This allows the pulmonary valve to close earlier such that it overlaps the closing of the aortic valve, and the split is no longer heard.

It is physiologically normal to hear a "splitting" of the second heart tone in younger people, during inspiration and in the "pulmonary area", i.e. the 2nd ICS (intercostal space) at the left edge of the sternum.

Steps

  1. Chest wall expands during inspiration
  2. Intrathoracic pressure becomes more negative to form a vacuum
  3. Venous return from the body to the right heart increases, venous return from the lungs to the left heart decreases
  4. Right ventricular volume and emptying time increases, left ventricular volume and emptying time decreases
  5. Pulmonic valve closure is delayed, aortic valve closure is advanced
  6. S2 splits into A2 and P2 respectively
  7. Expiration equalizes filling and emptying times on both sides of the heart eliminating the splitting of S2

Analysis of pressure

According to Harrison's Principles of Internal Medicine, "Normally, blood pressure falls during inspiration (equal or less than 10 mmHg), due to an increase in blood flow into the right ventricle with displacement of the interventricular septum to the left, decreasing left ventricular filling and cardiac output".[3]

The pressure in the right ventricle tries to open the pulmonary valve. The pressure in the pulmonary artery tries to close the pulmonary valve. Remember that the higher pressure will "win". Hence, the closure of the pulmonary valve (P2) will be delayed since the pressure in the right ventricle is increased in inspiration, opposing the pressure in the pulmonary artery and keeping it open longer than in expiration. The change in A2 is not that evident. Thus P2 appears after A2 in inspiration.

Pathologic split

The different types of split S2 can be associated with medical conditions:

When the pulmonary valve closes before the aortic valve, this is known as a "paradoxically split S2".[6]

References

  1. ^ "The Auscultation Assistant - Split S2". http://www.wilkes.med.ucla.edu/SplitS2main.htm. Retrieved 2009-01-09. 
  2. ^ "casemed.case.edu". http://casemed.case.edu/cardiacexam/sounds/splitS2.htm. Retrieved 2009-01-09. 
  3. ^ Loscalzo, Joseph; Charles M. Wiener; Bloomfield, Gerald T.; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's principles of internal medicine: self-assessment and board review. McGraw-Hill Medical. ISBN 0-07-149619-X.  Question 29 disorders of the cardiovascular system
  4. ^ Mayra Perez; Lindsay K. Botsford; Winston Liaw (18 October 2007). Deja Review: Family Medicine. McGraw Hill Professional. pp. 28–. ISBN 9780071485685. http://books.google.com/books?id=cAakbVN9RU4C&pg=PA28. Retrieved 11 November 2010. 
  5. ^ Salvatore Mangione (2000). Physical diagnosis secrets. Elsevier Health Sciences. pp. 215–. ISBN 9781560531647. http://books.google.com/books?id=-BmjqujomUMC&pg=PA215. Retrieved 11 November 2010. 
  6. ^ Ellen Chiocca (1 March 2010). Advanced Pediatric Assessment. Lippincott Williams & Wilkins. pp. 379–. ISBN 9780781791656. http://books.google.com/books?id=3mSTPSG4c5QC&pg=PA379. Retrieved 11 November 2010.