Heart Murmurs Topic Review

Describing Murmurs | Systolic Murmurs | Diastolic Murmurs | Dynamic Auscultation 


Disease of the cardiac valves and other cardiac structures frequently results in abnormal, turbulent blood flow within the heart, causing murmurs.

Careful auscultation of heart murmurs is an extremely valuable tool in the diagnosis of many cardiac conditions.

When normal laminar blood flow within the heart is disrupted, an audible sound is created by turbulent blood flow. Outside of the heart, audible turbulence is referred to as a bruit, whereas inside the heart it is called a murmur. A pictorial representation of systolic and diastolic murmurs is below. 

There are four major causes of cardiac murmurs.

  1. Valvular stenosis: If blood is forced through a tight area, turbulent blood flow ensues, as is the case in valvular stenosis. Generally, the worse the stenosis, the louder the murmur; however, if heart failure develops, adequate pressures to create turbulent blood flow may not be able to be achieved, and the murmur may lessen or even disappear. Thus, the intensity of a murmur is not used to indicated severity of disease.
  2. Valvular insufficiency: Blood abnormally travels backward through an incompetent valve in valvular insufficiency, causing turbulence when it meets normal, forward blood flow.
  3. Congenital anomaly: If blood is forced through a congenital anomaly from one chamber to another, as in an atrial septal defect or ventricular septal defect, a murmur is produced — again due to turbulence.
  4. Increased blood flow: Yet another cause of cardiac murmurs is increased flow of blood through a normal valve. In high-output states such as anemia, thyrotoxicosis or sepsis, a large volume passes through the cardiac valves, and the normal laminar blood flow may be disturbed. Stills murmur is a normal aortic flow murmur frequently heard in childhood that frequently disappears over time.

Murmurs are described by their timing in the cardiac cycle, intensity, shape, pitch, location, radiation and response to dynamic maneuvers. Using the above, clinicians can accurately characterize the nature of a murmur and communicate their findings in a precise manner.

Describing Heart Murmurs


The timing of a murmur is crucial to accurate diagnosis. A murmur is either systolic, diastolic or continuous throughout systole and diastole. Remember that systole occurs between the S1 and S2 heart sounds, whereas diastole occurs between S2 and S1.

With the knowledge of the possible cardiovascular conditions that cause systolic or diastolic murmurs, the clinician can narrow their differential diagnosis. Thus, it is important to remember which lesions result in systolic murmurs and which result in diastolic murmurs.

Stenosis of the aortic or pulmonic valves will result in a systolic murmur as blood is ejected through the narrowed orifice. Conversely, regurgitation of the same valves will result in a diastolic murmur as blood flows backward through the diseased valve when ventricular pressures drop during relaxation. Regarding the mitral and tricuspid valves, stenosis would result in a diastolic murmur and regurgitation a systolic murmur.

Other murmurs will be discussed in their respective sections below. More in-depth discussion of valvular heart disease can be found elsewhere.

Once it is determined if the murmur is systolic or diastolic, the timing within systole or diastole also becomes important when characterizing the murmur. Systolic murmurs can be classified as either midsystolic (systolic ejection murmurs, or SEM), holosystolic (pansystolic) or late systolic. A midsystolic murmur begins just after the S1 heart sound and terminates just before the P2 heart sound; thus, S1 and S2 will be distinctly audible. Conversely, a holosystolic murmur begins with or immediately after the S1 heart sound and extends up to the S2, making them difficult — if not impossible — to hear. A mid-late systolic murmur begins significantly after S1 and may or may not extend up to the S2.


Systolic murmurs are graded on a scale of 6. This grading is, for the most part, subjective. Grade I murmurs may not be audible to the inexperienced examiner; however, grade 6 murmurs are heard even without the stethoscope on the chest and may actually be visible.

Diastolic murmurs are graded on a scale of 4. This a completely subjective grading scale. Once again, grade I murmurs may not be audible to some, whereas grade IV murmurs are audible very easily.

The intensity of a murmur is primarily determined by the volume/velocity of blood flowing through a defect and the distance between the stethoscope and the lesion. For example, a very thin patient with severe aortic stenosis and a high pressure gradient across the valve (thus, high velocity of blood flow) will have a loud murmur. Conversely, the exact same valvular lesion in a patient with morbid obesity or severe chronic obstructive pulmonary disease, or COPD, and a widened anterior-posterior chest diameter may be inaudible.


The shape of a murmur describes the change of intensity throughout the cardiac cycle. Murmurs are either crescendo, decrescendo, crescendo-decrescendo or uniform.


A murmur will be high pitched if there is a large pressure gradient across the pathologic lesion and low pitched if the pressure gradient is low. For example, the murmur of aortic stenosis is high pitched because there is usually a large pressure gradient between the left ventricle and the aorta. Conversely, the murmur of mitral stenosis is low pitched because there is a lower pressure gradient between the left atrium and the left ventricle during diastole. Remember high-pitched sounds are heard with the diaphragm of the stethoscope, whereas low-pitched sounds are heard with the bell.


The anatomic location where the murmur is best heard is an important factor in determining the etiology of the lesion. The four main “listening posts” on the chest are described below.

A = aortic valve post (right upper sternal border or RUSB)
P = pulmonic valve post (left upper sternal border or LUSB)
T = tricuspid valve post (left lower sternal border or LLSB)
M = mitral valve post (apex)
E = “Erb’s point”

Note that both the aortic and pulmonic listening posts are considered to be near the “base” of the heart.

In general, a murmur will be the most intense over the listening post that corresponds to the diseased valve. Many murmurs will radiate to more than one listening post. For example, the murmur of aortic stenosis is best heard at the LUSB, but it may radiate to the apex. This radiation of the aortic stenosis murmur is called the “Gallavardin dissociation.”


While murmurs are usually most intense at one specific listening post, they often radiate to other listening posts or areas of the body. For example, the murmur of aortic stenosis frequently radiates to the carotid arteries and the murmur of mitral regurgitation radiates to the left axillary region. It is often difficult to distinguish if one murmur is radiating to multiple sites or if there are multiple murmurs present from many different causes. Dynamic auscultation and echocardiography are helpful in determining the exact lesion present.

Systolic Heart Murmurs

Midsystolic Murmurs

Midsystolic murmurs — also known as systolic ejection murmurs, or SEM — include the murmurs of aortic stenosis, pulmonic stenosis, hypertrophic obstructive cardiomyopathy and atrial septal defects. A midsystolic murmur begins just after the S1 heart sound and terminates just before the P2 heart sound, thus S1 and S2 will be distinctly audible. The term midsystolic is preferred to SEM because many lesions that produce midsystolic murmurs are unrelated to systolic ejection.

Aortic stenosis (AS)

The classic murmur of aortic stenosis is a high-pitched, crescendo-decrescendo (diamond shaped), midsystolic murmur located at the aortic listening post and radiating toward the neck.

The radiation of the AS murmur is often mistaken for a carotid bruit. The AS murmur is also known to radiate to the cardiac apex on occasion, making it difficult to distinguish if mitral regurgitation is also present. This radiation of the AS murmur to the apex is known as “Gallavardin dissociation.” Determining if coexisting mitral regurgitation is the cause of the apical murmur in a patient with AS requires dynamic auscultation or echocardiography.

The intensity of the murmur of AS is not a good indicator as to the severity of disease. As AS worsens, the LV begins to fail, and the ejection fraction declines to the point where sufficient force to create turbulent flow is no longer produced, resulting in a decrease in the intensity of the murmur.

While the intensity of the murmur may not be an accurate determinant of aortic stenosis severity, the shape of the murmur can be very helpful. As aortic stenosis worsens, it takes longer for blood to eject through the valve, so the peak of the crescendo-decrescendo murmur moves to later in systole. Therefore, mild aortic stenosis would have a murmur that peaks early in systole, whereas the murmur of severe aortic stenosis would peak later.

Remember from the Heart Sounds Topic Review that the delay in aortic valve closure can cause a paradoxically split S2 heart sound and, as the aortic valve becomes more heavily calcified, the intensity of the S2 heart sound declines. Also, in patients with bicuspid aortic valves, an ejection click may be heard just before the murmur begins.

Pulmonic stenosis (PS)

The murmur of pulmonic stenosis is very similar to that of aortic stenosis. It is a midsystolic, high-pitched, crescendo-decrescendo murmur heard best at the pulmonic listening post and radiating slightly toward the neck; however, the murmur of pulmonic stenosis does not radiate as widely as that of aortic stenosis. The murmur of pulmonic stenosis peaks early if the disease is mild and peaks later as the disease progresses. Also, this murmur demonstrates increased intensity during inspiration due to the increased venous return to the right heart, resulting in greater flow across the pulmonic valve.

Compared with the murmur of aortic stenosis that extends up to the A2 heart sound, the murmur of pulmonic stenosis extends through the A2 sound up to the P2 heart sound. Severe PS results in decreased mobility of the pulmonic valve leaflets, and thus a softer P2 sound. Also, as the PS worsens, the closure of the pulmonic valve is delayed, because more time is required to eject blood through the stenotic valve; this results in a widely split S2 heart sound that still exhibits inspiratory delay. Note that the murmur of an ASD, discussed below, is also midsystolic; however, it has a fixed split S2.

Atrial septal defect (ASD)

The murmur produced by an atrial septal defect is due to increased flow through the pulmonic valve, making it remarkably similar to that of PS. The difference lies in the intensity and splitting pattern of the S2 heart sound. The intensity of S2 should remain unchanged and may, in fact, be accentuated if pulmonary hypertension develops. The S2 is fixed-split in a patient with an ASD. This differs from the widened split S2, seen in severe PS. Also, the murmur of an ASD does not increase in intensity with inspiration.

Hypertrophic obstructive cardiomyopathy (HOCM)

The murmur of hypertrophic obstructive cardiomyopathy is important to detect due to its clinical implications; see Hypertrophic Obstructive Cardiomyopathy Topic Review. The murmur is high-pitched, crescendo-decrescendo, midsystolic murmur heard best at the left lower sternal border. The murmur of HOCM does not radiate to the carotids like that of AS. The important auscultatory features of HOCM that distinguish it from AS relate to dynamic auscultation, discussed in the respective section below.

Holosystolic Murmurs

Holotsystolic murmurs — also known as pansystolic — include the murmurs of mitral regurgitation, tricuspid regurgitation and ventricular septal defects. Because the intensity of these murmurs is high immediately after the onset of S1, and extends to just before the S2, the S1 and S2 sounds are often overwhelmed by the murmur and may be difficult to hear.

Mitral regurgitation (MR)

The murmur of mitral regurgitation is described as a high-pitched, “blowing” holosystolic murmur best heard at the apex. Although the direction of radiation of the murmur depends on the nature of the mitral valve disease, it usually radiates to the axilla. The intensity of the murmur of MR does not increase with inspiration, helping to distinguish it from the murmur of tricuspid regurgitation.

Tricuspid regurgitation (TR)

The murmur of tricuspid regurgitation is similar to that of MR in that it is high pitched and holosystolic; however, it is best heard at the left lower sternal border, and it radiates to the right lower sternal border. The intensity significantly increases with inspiration, helping to distinguish it from MR. This inspiratory enhancement of the TR murmur is called “Carvallos sign.”

Ventricular septal defect (VSD)

A ventricular septal defect produces yet another holosystolic murmur. Blood abnormally flows from the LV (high pressure) to the RV (low pressure), thereby creating turbulent blood flow and a holosystolic murmur heard best at “Erb’s point.” The smaller the VSD, the louder the murmur.

Late Systolic Murmurs

The murmur of mitral or tricuspid valve prolapse is the only significant late systolic murmur. Tricuspid valve prolapse is relatively rare and usually not clinically significant.

Mitral valve prolapse (MVP)

Mitral valve prolapse produces a midsystolic click, typically followed by a uniform, high-pitched murmur. The murmur is actually due to MR that accompanies the mitral valve prolapse; thus, it is heard best at the cardiac apex. Mitral valve prolapse responds to dynamic auscultation.

 Summary of Systolic Murmurs

Diastolic Heart Murmurs

Diastolic murmurs include aortic and pulmonic regurgitation (early diastolic) and mitral or tricuspid stenosis (mid- to late-diastolic). Tricuspid stenosis is very rare and is discussed further in the Tricuspid Stenosis Topic Review.

Early Diastolic

Aortic regurgitation (AR)

The murmur of aortic regurgitation is a soft, high-pitched, early diastolic, decrescendo murmur usually heard best at the third intercostal space on the left (Erbs point) at end expiration with the patient sitting up and leaning forward. However, if the aortic regurgitation is due to aortic root disease, the murmur will be best heard at the right upper sternal border — not at Erbs point. As AR worsens in severity, the pressure between the LV and the aorta equalize much faster, and the murmur becomes significantly shorter.

In patients with AR, an early diastolic rumble may also be heard at the apex due to the regurgitant jet striking the anterior leaflet of the mitral valve and causing it to vibrate. This murmur is termed the Austin-Flint murmur.

In addition to the above two murmurs, a systolic ejection murmur may be present in patients with severe aortic regurgitation at the right upper sternal border simply due to the large stroke volume passing through the aortic valve with each systolic contraction of the LV.

Pulmonic regurgitation (PR)

Pulmonic regurgitation produces a murmur that is often indistinguishable from that of AR. PR produces a soft, high-pitched, early diastolic decrescendo murmur heard best at the pulmonic listening post (LUSB). The murmur of PR increases in intensity during inspiration, unlike that of AR. The murmur of PR is classically referred to as the Graham-Steele murmur, after the experts that initially described the sound.

Mid- to Late-diastolic

Mitral stenosis

Mitral stenosis results in a uniquely-shaped, low-pitched, diastolic murmur best heard at the cardiac apex. The opening of the mitral valve produces an “opening snap” due to the high left atrial pressures, immediately followed by a decrescendo murmur as blood flows passively from the left atrium to the left ventricle through the stenosed mitral valve, creating turbulence. Immediately before the S1 sound, active left ventricular filling occurs when the LA contracts and forces more blood through the stenosed mitral valve, creating a late diastolic, crescendo murmur. In the presence of atrial fibrillation, the active left ventricular filling phase does not take place, and the latter part of the mitral stenosis murmur disappears.

As mitral stenosis worsens, left atrial pressure increases, forcing the mitral valve open earlier in diastole. Thus, in severe mitral stenosis, the opening snap occurs earlier — as does the initial decrescendo part of the murmur. The opening snap and murmur of mitral stenosis also respond to dynamic auscultation.

Continuous Murmurs

The murmur of a patent ductus arteriosus, or PDA, is continuous throughout systole and diastole. Often, the S2 heart sound is difficult to detect. The murmur begins just after S1 and crescendos, peaking at S2, then decrescendos to S1.

Summary of Diastolic Murmurs

Dynamic Auscultation of Heart Murmurs

Dynamic auscultation refers to using maneuvers to alter hemodynamic parameters during cardiac auscultation in order to diagnose the etiology of a heart sound or murmur.

Valsalva Maneuver

The Valsalva maneuver is performed by having a patient “bear down” — as if they are going to have a bowel movement, exhaling forcefully with the airway closed. The hemodynamic changes that occur are complex; however, the ultimate result is a decrease in left ventricular preload.

The most important use of the Valsalva maneuver is to distinguish the murmur of aortic stenosis from hypertrophic obstructive cardiomyopathy — or simply to bring forth the murmur of HOCM. Aortic stenosis will soften or not change, whereas the murmur of HOCM becomes quite loud with Valsalva.

The Valsalva maneuver is also performed during routine echocardiographic examinations to see if a patient with grade II or worse diastolic function can decrease his or her left ventricular filling pressures adequately. If the Valsalva maneuver fails to reduce the left ventricular pressure in the setting of diastolic heart failure, then grade IV diastolic dysfunction is said to be present — indicating a poor prognosis.

Squatting from a Standing Position

Squatting forces the blood volume that was stored in the legs to return to the heart, increasing preload and thus increasing left ventricular filling.

This maneuver will decrease the murmur of HOCM, as the increased left ventricular volume helps displace the hypertrophied interventricular septum, causing less outflow tract obstruction.

This maneuver causes the click of MVP to move later in systole.

Standing from a Squatting Position

Standing quickly from a squatting position causes blood to move from the central body to the legs, resulting in less blood returning to the heart and decreasing left ventricular preload — similar to the effect seen with the Valsalva maneuver.

This maneuver will increase the murmur of HOCM and decrease that of aortic stenosis.

This maneuver causes the click of MVP to move earlier in systole.

Leg Raising

Passive leg raising is done simply by raising the legs high in a patient lying supine. This results in blood that was pooled in the legs returning to the heart, increasing left ventricular filling and preload — similar to the effect seen with squatting from a standing position.

This maneuver will decrease the murmur of HOCM, as the increased left ventricular volume helps displace the hypertrophied interventricular septum, causing less outflow tract obstruction.

This maneuver causes the click of MVP to move later in systole.

Handgrip Exercise

Isometric handgrip exercises are performed by having a patient squeeze hard repetitively. This results in increased blood pressure, similar to exercise, and thus increased afterload. Elderly individuals may have a hard time with this maneuver, and transient arterial occlusion (described below) can be used instead.

This maneuver will increase the intensity of left-sided regurgitant murmurs including MR and AR. However, handgrip exercises will have no effect on the murmur of AS, which helps distinguish the presence of coexistent MR from Galliverdin phenomenon.

Transient Arterial Occlusion

This maneuver is performed by placing a blood pressure cuff on both arms and inflating it to 20 to 40 mmHg above the systolic blood pressure for 20 seconds — effectively resulting in increased afterload.

This maneuver will increase the intensity of left-sided regurgitant murmurs including MR and AR and is especially useful in elderly individuals who are unable to perform adequate handgrip exercises.

Amyl Nitrate Inhalation

Amyl nitrate decreases left ventricular afterload by dilating the peripheral arteries and would decrease the murmur of MR.

When the afterload is decreased, there is less resistance to blood flow from the LV through the aortic valve; this means less blood regurgitates through the mitral valve, thereby decreasing the intensity of the murmur.

Amyl nitrate can be given via inhalation to reduce afterload for diagnostic purposes in the cardiac catheterization laboratory (to invoke a LV outflow tract gradient in patients with HOCM) or as a diagnostic tool during cardiac physical examination. Due to the advancement of echocardiography, it is not commonly used any longer.