5 Heart Sounds and Murmurs

Learning Objectives

  • Describe the underlying events that produce the normal heart sounds, S1 to S4.
  • Relate the timing and structure of a heart murmur to the underlying pathophysiology.

As unintrusive as the ECG is, listening to the heart is a cheap, quick, and informative clinical test. We will cover the basic structure, causes, and common pathologies of heart murmurs as a companion guide to clinical skills classes on auscultation of the chest. A good understanding of the cardiac cycle would be beneficial.

Heart Sounds

The first and second sounds (S1 and S2) are the fundamental heart sounds.

All figures include a large line labeled M1 and a line half the size labeled T1. Normal S1: T1 is centered above M1 with a small space between. RBBB: T1 is centered above M1 with a large space between. LBBB S1: T1 centered directly on top of M1
Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1).

S1 occurs at the beginning of isovolumetric contraction. The ventricle is beginning to contract, so ventricular pressure quickly rises above atrial pressure and the atrioventricular (tricuspid and mitral) valves close, producing the S1 sound. The mitral valve normally closes slightly (0.04 seconds) before the tricuspid, causing S1 to be “split” (i.e., actually being two sounds, M1 and T1 (figure 5.1)), but the time gap is too short with a normal heart to be detectable with a stethoscope. The reasons for M1 preceding T1 are not clear, but may be due to the force generation of the left ventricle being slightly faster than that of the right ventricle. The splitting of S1 can be more pronounced and audible in the presence of a right bundle branch block (figure 5.1) that causes left ventricular contraction (and mitral valve closure) to markedly precede contraction of the right ventricle. Conversely, in the case of a left bundle branch block, the normal splitting of S1 may be absent (figure 5.1) as M1 is delayed and so occurs in synchrony with T1.


All figures include a large line labeled A2 and a line half the size labeled P2. S2 during expiration: P2 is centered directly on top of A2. S2 during inspiration: P2 is centered over A2 with a large space between
Figure 5.2: Normal splitting of S2 with inspiration.

S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation when ventricular pressure falls below pulmonary and aortic pressure. As aortic pressure (80 mmHg) is far greater than pulmonary artery pressure (10 mmHg), S2 is normally split with two components (A2 and P2) relating to the closure of the aortic and pulmonic valves, respectively. How split A2 and P2 are depend on physiological conditions, primarily the phase of breathing that influences the pulmonary artery pressure. In expiration pulmonary artery pressure is higher, so the pulmonic valve closes earlier and P2 occurs closer to A2. Conversely, during inspiration pulmonary artery pressure falls, so pulmonic valve closing occurs later and A2 and P2 occur further apart (figure 5.2). This physiological splitting can be heard with a stethoscope, but can be further influenced by diseases as listed in table 5.1.


Changes in S2 splitting and possible underlying causes
Abnormally wide splitting - Right ventricle (RV) volume overload (e.g., atrial septal defect)
- RV outflow obstruction (e.g., pulmonary stenosis)
Narrow splitting - Pulmonary hypertension
- Mild to moderate aortic stenosis
Single S2 - One semilunar valve is absent (e.g., truncus arteriosus, valvular atresia)
- Large ventricular septal defect (equal ventricular pressures)
- Pulmonary hypertension with equal ventricular pressures
Paradoxical splitting (P2 before A2) - Severe aortic stenosis

Table 5.1: Changes in S2 splitting and possible underlying causes.


S3 is associated with the rapid filling phase of the ventricle (when the AV valves open), about 0.14 to 0.16 seconds after S2 (closure of the aortic and pulmonic valves). The exact cause of the sound is unclear, but a normal S3 occurs as a brief, low-frequency vibration. Previously thought to be an intracardiac sound arising from vibrations in the valve cusps or ventricular wall, more recent studies suggest the sound may be due to the filling ventricular wall hitting the inner chest wall, or it may arise from the ventricular apex as it hits a limitation of its longitudinal expansion.

Common causes of abnormal S3
Dilated cardiomyopathy
Chronic mitral valve regurgitation
Diastolic heart failure
Pregnancy (not pathological sign)
Athletes (not pathological sign)

Table 5.2: Common causes of abnormal S3.

As S3 is a filling sound, an abnormal S3 (higher pitch and referred to as a ventricular gallop) is an important clue to heart failure or volume overload (see table 5.2). The absence of an abnormal S3 does not rule out heart failure, but its presence is a sensitive indicator of ventricular dysfunction. Constriction around the heart (e.g., constrictive pericarditis) may cause an early S3, or “pericardial knock.”


S4 is abnormal and is associated with poor ventricular compliance (e.g., ventricular hypertrophy). It occurs during atrial contraction and is associated with the atrial pressure pulse. The sound is thought to be caused by reverberation of the stiffened ventricular wall as blood is propelled into the ventricle from the atrium (hence it is also known as an atrial gallop). S4 and raised end-diastolic ventricular pressure (EDVP) commonly occur together as both are caused by poor ventricular compliance, so S4 tends to be associated with conditions that cause pressure overload (see table 5.3).

Common causes of abnormal S4
Hypertensive heart disease
Aortic stenosis
Hypertrophic cardiomyopathy
Acute phase of myocardial infarction
Acute and severe mitral or aortic regurgitation

Table 5.3: Common causes of abnormal S4.

Ejection Sounds (Clicks)

As S1 and S2 occur during closure of heart valves, pathological conditions can lead to the valves producing a high-frequency “clicking” sound when they open during chamber ejection—hence they can be referred to as ejection sounds and they are pathological.

Aortic ejection sounds usually occur 0.12–0.14 seconds after the Q-wave of the ECG (i.e., after ventricular pressure has risen to exceed aortic pressure). Because of its timing, the “click” produced can be misinterpreted as a split S1. The abnormal opening of the aortic valve is usually caused by a deformed but mobile valve leaflet or aortic root dilation that may be caused by the conditions listed in table 5.4.

Pulmonary ejection sounds occur a little earlier (0.09–0.11 seconds) after the Q-wave as the pulmonary valve opens a little earlier (figure 5.1). It can also be distinguished by the fact that its intensity is diminished during inspiration as increased venous return during inspiration augments the effect of atrial contraction and causes a “gentler” opening of the valve. As with the aortic ejection sounds, pulmonary ejection sounds are associated with deformed valves or pulmonary arterial dilation.

A click occurring in diastole is associated with abnormal opening of either the mitral or tricuspid valve. Similar to systolic clicks, a diastolic click can be misinterpreted as a split S2. The most common cause of diastolic clicks is valvular stenosis of an AV valve.

Aortic Pulmonary
- Aortic stenosis
- Bicuspid aortic valve
- Aortic regurgitation
- Aneurysm in ascending aorta
- Pulmonary stenosis
- Pulmonary arterial dilation
- Pulmonary hypertension

Table 5.4: Common causes of ejection "clicks."

Heart Murmurs

A murmur is the sound of turbulence associated with abnormal blood flow through a valve or chamber. The turbulent flow produces low-frequency audible sounds that are distinct from heart sounds associated with valve closures. Murmurs can be divided into those caused by valvular defects and those caused by abnormal interchamber flow. Depending on the defect involved, the murmur may occur during diastole and systole, hence distinguishing whether a murmur is diastolic or systolic is a useful first diagnostic step.

Classification of a murmur includes the intensity (Grades 1–6, faintest to loudest), the pitch (high or low), configuration, location, and timing. The timing refers to the onset and duration of the murmur, and the classifications are shown in table 5.5 with some common causes listed there and below.

  • Aortic stenosis produces a midsystolic murmur that has a crescendo–decrescendo pattern (intensity builds up, then fades). This pattern relates to the level of turbulent flow through the narrowed valve—slow at first as the resistance is overcome, then fading away as blood flow decreases.
  • Mitral/tricuspid regurgitation produces a holosystolic murmur as the incompetent valve allows a constant turbulent (and reverse) flow from the ventricle back to the atria.
  • Mitral valve prolapse produces a late-systolic murmur often proceeded by a midsystolic click. The click is caused by tensioning of the chordae tendineae as ventricular pressure increases and the murmur builds up as regurgitation is established.
  • Ventricular septal defect produces a holosystolic murmur when severe. Turbulent flow through the defect is constant as the left ventricular pressure is higher than right ventricular pressure throughout systole—hence a continuous left–right shunt is established.
  • Aortic regurgitation produces a “blowing” diastolic murmur that is usually decrescendo. This early diastolic murmur is short because rapidly rising ventricular pressure (due to atrial and aortic contributions) ends the reverse flow from the aorta. In cases when the aortic pressure is high, the regurgitation may be sustained and the murmur becomes pandiastolic.
  • Mitral stenosis produces a diastolic murmur that starts late as the stenosed valve prevents atria-to-ventricular flow until high atrial pressures are established. The murmur may be preceded by a middiastolic click as the atrial pressure finally “flings” the valve open.
Classification Description Possible cause
Early-systolic Obscures S1 and extends for a variable length in systole but does not extend up to S2 The table includes graphic description of seven types of heart murmurs. In each the cardiac cycle is represented by vertical lines that denote normal heart sounds. The onset of systole is represented by two adjacent, center-aligned vertical lines, one long and pink labelled M1 and one shorter an red labelled T1. The end of systole and onset of diastole is represented by two adjacent center-aligned vertical lines that are spaced away from M1 and T1, these lines include a long brown line labelled A2 and a shorter black line labelled P2. There is then a space denoting the duration of diastole, followed by the another set of M1 and T1 lines denoting the start of the next systole. 

Heart murmurs are displayed as series of parallel vertical white lines that are center-aligned and sized to represent their volume (longer = louder). 

Early systolic murmur is depicted as a series of progressively shorter white vertical lines. The series starts at the beginning of systole and stop with the shortest one about halfway to the onset of diastole. Small ventricular septal defect
Midsystolic Begins after S1 and ends before A2 or P2. Both S1 and S2 are audible A midsystolic murmur is represented by a series of white vertical lines than span the duration of systole and become progressively longer until half way through systole, when they start to become progressively shorter again and stop at the onset of diastole. Aortic stenosis

(a.k.a. pansystolic)

Starts with S1 and extends up to A2 or P2, obscuring both S1 and S2 A holosystolic murmur (or pan systolic murmur) is represented by parallel, vertical white lines that have consistent length and the series of lines spans the duration of systole. Ventricular septal defect or AV valve regurgitation
Late-systolic Starts after S1 and obscures A2 or P2 A late systolic murmur is represented by a series of parallel, vertical white lines that begin about half way through systole and get progressively larger until the series stops at the beginning of diastole. Mitral valve prolapse
Early-diastolic Starts with A2 or P2 and extends into diastole for a variable duration An early diastolic murmur is depicted as a series of parallel, vertical lines that begins at the start of diastole and become progressively shorter until the series stops about halfway through diastole. Aortic regurgitation
Middiastolic Starts after S2 and terminates before S1 A mid diastolic is represented by a series of vertical, parallel white lines that begins at the onset of diastole, becoming progressively longer until a third of diastole is reached whereupon they shorten again and the series stops about two-thirds of the way through diastole. Atrial septal defect
Late-diastolic Starts well after S2 and extends up to the mitral component or to the tricuspid component of S1 A late diastolic murmur is represented  by a series of vertical, parallel white lines that start half way through diastole with the lines becoming progressively longer until he series stops at the end of diastole. Mitral stenosis

Table 5.5: Classifications of heart murmurs.

References, resources, and further reading


Dornbush, Sean, and Andre E. Turnquest. Physiology, Heart Sounds. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK541010, CC BY 4.0.

Kulkarni, Vivek T., and Leonard S. Lilly. “The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 2. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.

Thomas, Seth L., Joseph Heaton, and Amgad N. Makaryus. Physiology, Cardiovascular Murmurs. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK525958, CC BY 4.0.


Figure 5.1: Normal and abnormal differences in the components of S1 (M1 and T1). Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.1_20220113

Figure 5.2: Normal splitting of S2 with inspiration. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.2_20220113

Table 5.5: Classifications of heart murmurs. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/5.5_20220113



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