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Propaedeutics · Cardiovascular system

Splitting and bifurcation of heart sounds

Splitting of heart sounds is an important auscultatory phenomenon in which the main valvular components of a heart sound are heard separately. The pathophysiological basis of this phenomenon is asynchrony, which is the non-simultaneous closure of valves. Most commonly, it is caused by differences in the duration of the right and left ventricular systole, resulting from changes in blood pressure or volume within the pulmonary and systemic circulations.

Effect of respirationA deep inspiration increases blood return to the right heart, delaying the closure of the pulmonary valve.
ASDFixed splitting of the second heart sound is a pathognomonic sign of an atrial septal defect.
Auscultation pointPhysiological splitting is best heard over the pulmonary artery (in the 2nd intercostal space).
Conduction disordersBundle branch blocks lead to pathological splitting due to delayed ventricular systole.
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Physiological splitting of the second heart sound

Normally, minor splitting of the second heart sound is closely related to the phases of respiration and is heard primarily at the base of the heart in the second intercostal space.

  • Hemodynamic mechanism: During a deep inspiration, venous return to the right heart increases. The right ventricle must eject this increased blood volume, which physiologically prolongs its systole.
  • Auscultatory picture: Due to the prolonged systole, the pulmonary valve closes slightly later. First, the aortic component is heard, followed shortly by the pulmonary component.

This phenomenon is best detected in young individuals directly over the pulmonary artery. However, splitting is not heard over the aorta itself, because the pulmonary sound component is too weak to be transmitted to that auscultation point.

Pathological variants of second sound splitting

The nature of pathological splitting depends on the state of the myocardial conduction system and hemodynamic features. Several key clinical scenarios are distinguished:

  1. Delayed closure of the pulmonary valve. It occurs due to delayed blood ejection or impaired electrical impulse conduction. The main causes are right ventricular dilation (characteristic of pulmonary stenosis) and intraventricular blocks (e.g., right bundle branch block).
  2. Fixed splitting of the second heart sound. The key feature of this phenomenon is the complete absence of respiratory variability. The interval between the sound components changes neither during inspiration nor expiration. This is a strictly pathognomonic diagnostic sign of an atrial septal defect (ASD). Due to a persistent pathological left-to-right shunt, a chronic volume overload of the pulmonary circulation and the right chambers of the heart develops.
  3. Features in pulmonary hypertension. In chronic lung diseases, the right ventricle undergoes hypertrophy because it has to work against high pressure. Since pressure overload occurs rather than volume overload (unlike dilation), no significant prolongation of systole takes place. As a result, the splitting sounds less distinct.
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Features of first sound splitting

Splitting of the first heart sound is less common and can be caused by both physiological factors and serious pathology. Graphically (on diagrams and phonocardiograms), this process appears as the division of the first sound into two separate components while the second sound remains completely intact.

  • Normal variant. Normal splitting can be heard along the left sternal border, where the sound of tricuspid valve closure is well transmitted, and sometimes at the apex of the heart. In some cases, the auscultatory picture is supplemented by the presence of a fourth heart sound or an early systolic click, also known as an ejection sound.
  • Pathological splitting. The main cause is intraventricular conduction disturbances, namely bundle branch blocks. In this case, the electrical signal is delayed in one of the ventricles, its systole is delayed, which naturally leads to asynchronous closure of the atrioventricular valves.

Briefly: answers to topical questions

How to auscultatorily distinguish second sound splitting from a mitral opening snap (opening click)?

The main auscultatory difference is the point of maximum auscultation of the sound phenomenon and the nature of the resulting sound.

SignSplitting of the second heart soundMitral opening snap
LocalizationHeard over the pulmonary artery (base of the heart)Heard at the apex of the heart
Nature of the soundAsynchronous closure of the aortic and pulmonary valves (components of a single sound)Appearance of an extra sound in diastole
MechanismDifferent duration of ventricular systoleSharp tension of fused mitral valve leaflets
How to memorize

Respiration rule: Inspiration increases blood return to the right heart → Right ventricle works longer → Pulmonary valve closes later than the aortic valve.

Class and exam questions

Why is physiological splitting of the second heart sound not heard over the aorta?

The pulmonary component of the second heart sound (pulmonary valve closure) sounds too weak, so it is not transmitted to the aortic auscultation point.

What does "fixed" sound splitting mean?

This is splitting in which the interval between the two sound components remains completely unchanged during both inspiration and expiration. This is a hallmark sign of an atrial septal defect.

Why is splitting less pronounced in chronic lung diseases?

In pulmonary hypertension, the right ventricle is hypertrophied due to pressure overload. Unlike volume overload, there is no significant prolongation of systole here, so the valve leaflets are not significantly delayed.

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What else to study on this topic

  • Pathogenesis of atrial septal defect (ASD)
  • Changes in heart sounds during bundle branch blocks
  • Mechanisms of early systolic click (ejection sound) formation
  • Graphical representation of heart sounds on a phonocardiogram
  • Pulmonary circulation hemodynamics in pulmonary hypertension

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