Split S2

Wiggers diagram of various events of a cardiac cycle, with 2nd heart sound at bottom.

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 during inspiration. The second heart sound (S2) is caused by the closure of the aortic and pulmonic valves, which causes vibration of the valve leaflets and the adjacent structures. The aortic valve closes slightly before the pulmonic, and this difference is accentuated during inspiration when S2 splits into two distinct components (physiological splitting). During expiration, the pulmonic valve closes at nearly the same time as the aortic, and splitting of S2 cannot be heard.

Exercise increases the intensity of both the aortic and pulmonic components of S2, whereas deep inspiration increases the intensity of the pulmonic component only.

## Contents

* 1 Physiological split
* 1.1 Steps
* 1.2 Analysis of pressure
* 2 Pathological split
* 3 References

## Physiological 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 venae 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 atrium (the blood wants to stay in the lungs because of the vacuum surrounding the lungs, and PVR is lower because of lung expansion). Since there is an increase in blood volume in the right ventricle during inspiration, 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.[citation needed]

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.[citation needed]

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

### 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".[2]

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.[citation needed]

## Pathological split

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

* Split during inspiration: normal.[3] (See above)
* Wide splitting: seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block). Delay in RV emptying causes delayed pulmonic sound (regardless of breath); it is an exaggeration of normal splitting sounds.
* Split during expiration: Reverse splitting (paradoxical splitting) indicates pathology due to delay of aortic valve closing. Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block (LBBB), and a ventricular pacemaker could all cause a reverse splitting of the second heart sound.[4]
* Split during both inspiration and expiration:
* If splitting does not vary with inspiration, it is termed a "fixed split S2" and is usually due to a septal defect,[5] such as an atrial septal defect (ASD). The ASD creates a left to right shunt that increases the blood flow to the right side of the heart, thereby causing the pulmonary valve to close later than the aortic valve independent of inspiration/expiration.
* A bundle branch block either LBBB or RBBB, (although RBBB is known to be associated only with S1 split), will produce continuous splitting but the degree of splitting will still vary with respiration.

When the pulmonary valve closes before the aortic valve, this is known as a "paradoxically split S2".[6] On physical exam, paradoxical splitting is appreciated as increased splitting on expiration relative to inspiration, versus normal splitting where inspiration will increase splitting. It is seen in conditions that delay left ventricular emptying (e.g., aortic stenosis, left bundle branch block).

## References

1. ↑ "The Auscultation Assistant – Split S2". http://www.wilkes.med.ucla.edu/SplitS2main.htm.
2. ↑ 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
3. ↑ Mayra Perez; Lindsay K. Botsford; Winston Liaw (2007). Deja Review: Family Medicine. McGraw Hill Professional. p. 28. ISBN 978-0-07-148568-5. https://books.google.com/books?id=cAakbVN9RU4C&pg=PA28.
4. ↑ Dan Longo. Principles of Internal Medicine. McGraw Hill Medical. pp. 1826–1827. ISBN 978-0-07-174890-2.
5. ↑ Salvatore Mangione (2000). Physical diagnosis secrets. Elsevier Health Sciences. p. 215. ISBN 978-1-56053-164-7. https://books.google.com/books?id=-BmjqujomUMC&pg=PA215.
6. ↑ Ellen Chiocca (2010). Advanced Pediatric Assessment. Lippincott Williams & Wilkins. p. 379. ISBN 978-0-7817-9165-6. https://books.google.com/books?id=3mSTPSG4c5QC&pg=PA379.

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Symptoms and signs relating to the cardiovascular system (R00–R03, 785)

Chest pain|

* Referred pain
* Angina
* Aerophagia

Auscultation|

* Heart sounds
* Split S2
* S3
* S4
* Gallop rhythm
* Heart murmur
* Systolic
* Diastolic
* Continuous
* Pericardial friction rub
* Heart click
* Bruit
* carotid

Pulse|

* Tachycardia
* Bradycardia
* Pulsus tardus et parvus
* Pulsus paradoxus
* doubled
* Pulsus bisferiens
* Dicrotic pulse
* Pulsus bigeminus
* Pulsus alternans
* Pulse deficit

Vascular disease|

* Gangrene

Other|

* Palpitations
* Apex beat
* Cœur en sabot
* Jugular venous pressure
* Cannon A waves
* Hyperaemia

Shock|

* Cardiogenic
* Obstructive
* Hypovolemic
* Distributive
* Septic
* Neurogenic
* Refractory vasodilatory shock

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