Auscultation of diastolic and continuous murmurs in adults

INTRODUCTION — 

Cardiac auscultation is one of the most useful bedside diagnostic tools to detect alterations in cardiovascular anatomy and physiology. Valvular heart disease, congenital heart disease, and other cardiovascular disorders are often first suspected upon auscultation of a murmur.

This topic will review auscultation of diastolic and continuous murmurs in adults.

Related subjects are discussed separately:

●(See "Auscultation of cardiac murmurs in adults: General concepts and systolic murmurs".)

●(See "Auscultation of heart sounds".)

●(See "Approach to the infant or child with a cardiac murmur" and "Common causes of cardiac murmurs in infants and children".)

MURMUR DESCRIPTION — 

Cardiac murmurs arise from turbulent blood flow. The character of a murmur is described by several features, including intensity (grade), pitch (frequency), configuration, timing, quality, location, and radiation.

A murmur's intensity is primarily determined by blood flow turbulence (which is related to the rate of blood flow and the pressure gradient across narrow cardiac structures, such as a regurgitant orifice [1-3]) and transmission of sound. The pressure gradient across an orifice is inversely related to the orifice size.

Six grades are used to classify the intensity of a systolic murmur (table 1). The first four of these grades (I through IV) are commonly used for diastolic murmurs since louder diastolic murmurs are very rare.

DIASTOLIC MURMURS

Early diastolic murmurs — Early diastolic murmurs, most often due to aortic or pulmonary regurgitation, typically start at the time of semilunar valve closure, and their onset coincides with S2. An aortic regurgitation (AR) murmur begins with A2; pulmonary regurgitation begins with P2.

Aortic regurgitation — Discovery of a diastolic murmur is essential for the diagnosis of AR. In a review of the literature, the presence of an early diastolic murmur was the most useful finding for establishing the presence of AR (positive likelihood ratio 8.8 [ie, the odds of AR are increased 8.8-fold]) and its absence the most useful finding for eliminating the presence of AR (negative likelihood ratio 0.2 to 0.3 [ie, the odds of disease are reduced by a factor of 0.2 to 0.3]) [4]. Among patients with end-stage kidney disease, a transient murmur of AR may be induced by the effects of volume overload; thus, such patients should be reexamined after dialysis, when the excess fluid has been removed [4].

The murmur of AR is best heard with the diaphragm of the stethoscope. Low-intensity, high-pitched AR murmurs may not be heard unless firm pressure is applied with the diaphragm of the stethoscope over the left sternal border or over the right second interspace, while the patient sits and leans forward with the breath held in full expiration (movie 1 and movie 2).

The radiation of an AR murmur is toward the cardiac apex, and the location of maximum intensity may vary considerably. It can be best heard in some patients over the mid precordium, along the lower left sternal border, or even over the cardiac apex (movie 3). Radiation of the murmur to the right sternal border is more common in AR caused by aortic root or aortic cusp anomalies [5].

The configuration of the AR murmur is usually decrescendo because the magnitude of regurgitation progressively declines. The murmur is high-frequency and has a "blowing" character. Occasionally the murmur can be musical in quality (diastolic whoop); this has been attributed to a flail everted aortic cusp. The "whoop" can be mid-, late-, or pandiastolic [6].

The duration of the murmur is variable but usually terminates before S1. The duration of the murmur does not always correlate with the severity of AR, although mild AR is usually associated with a murmur of brief duration. The murmur may also be short with acute severe AR because of a rapid increase in left ventricular (LV) diastolic pressure, which equalizes with aortic diastolic pressure soon after the onset of diastole. If the aortic pressure remains higher than LV pressure throughout diastole, a pandiastolic murmur may be present, even when the severity of AR is only moderate. Bedside evaluation of the severity of AR should be primarily based upon a determination of the hemodynamic consequences. (See "Examination of the arterial pulse".)

An Austin Flint murmur is usually associated with significant AR (see 'Austin Flint murmur' below). A decreased intensity of S2 does not necessarily suggest significant AR; however, reversed splitting of S2, which in the absence of left bundle branch block results from increased LV forward stroke volume, indirectly suggests significant AR. Changes in the intensity of S1 should be noted, since a reduced intensity is usually associated with an elevated LV end-diastolic pressure, which is more likely to occur in severe AR. Physical findings of pulmonary venous, arterial hypertension, and right-sided heart failure indicate hemodynamically significant AR. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Assessment of LV function is important, particularly with respect to the timing of surgery. A hyperdynamic LV impulse is associated with a relatively normal ejection fraction. On the other hand, a sustained impulse and S3 gallop may indicate a reduced LV ejection fraction.

The onset of heart failure can modify many of the physical findings that suggest significant AR. The pulse pressure that was initially high may decrease, and the arterial diastolic pressure that was low may increase. The duration of the regurgitant murmur may decrease as the LV diastolic pressure increases.

The hemodynamic consequences of acute, severe AR differ considerably from those of chronic AR, explaining the differences in physical findings. (See "Acute aortic regurgitation in adults".)

●Sudden severe volume overload in a nondilated LV causes a rapid increase in diastolic pressure and often equalization of LV and aortic root pressures in middiastole. Thus, the regurgitant murmur can be of short duration.

●S1 is soft or absent due to a reduced intensity of the mitral component of S1 and premature closure of the mitral valve [7].

●The P2 of S2 is frequently accentuated due to postcapillary pulmonary hypertension. The A2 component of S2 is often attenuated due to incomplete leaflet coaptation.

Pulmonic regurgitation — A small amount of pulmonic regurgitation is normal and occasionally can be heard in thin subjects.

Pathologic pulmonic regurgitation is most frequently a result of pulmonic hypertension (Graham-Steell murmur) or residual after tetralogy of Fallot repair in adults [8]. The murmur of pulmonic regurgitation associated with pulmonary hypertension is high-pitched and "blowing." It begins with an accentuated P2 of S2 and can be of variable duration. It may occupy all of diastole if there is a pandiastolic gradient between the pulmonary artery and the right ventricular diastolic pressure. The murmur has a decrescendo configuration like that of AR; differentiation is difficult if not impossible by auscultation alone. The murmur may increase in intensity during inspiration and can be more localized. It is best heard over the left second and third interspaces.

In contrast, the murmur of residual pulmonic regurgitation after Tetralogy of Fallot repair typically is low pitched and soft because pulmonary pressures are normal, so there is only a small diastolic pressure difference between the pulmonary artery and right ventricle. A to-and-fro murmur over the left second intercostal space may be noted or there may be no audible murmur with severe pulmonic regurgitation.

Pulmonic regurgitation can occur in the absence of pulmonary hypertension, as in patients with idiopathic dilatation of the pulmonary artery, after pulmonic valvulotomy, with right-sided endocarditis, and with congenital absence of the pulmonic valve. In these conditions, the pulmonary artery diastolic pressure is normal or low and there is a lower rate of regurgitant flow; the regurgitant murmur is of low to medium pitch.

In congenital absence of the pulmonic valve, P2 is absent and there is a silent interval between A2 and the onset of the regurgitant murmur. A loud to-and-fro murmur may be heard in these patients.

Left anterior descending artery stenosis — Left anterior descending coronary artery stenosis very rarely causes a diastolic murmur similar to AR (Dock murmur) [9]. The murmur is not widespread like that of AR and usually is best heard over the left second or third interspace, a little lateral to the left sternal border. The murmur may be long or short. It is caused by turbulent flow across the coronary artery stenosis and usually indicates moderately severe stenosis. Coronary artery bypass surgery or percutaneous coronary intervention abolishes the murmur.

Middiastolic murmurs — Middiastolic murmurs result from turbulent flow across the atrioventricular valves during the rapid filling phase because of mitral or tricuspid valve stenosis and an abnormal pattern of flow across these valves.

Mitral stenosis — The middiastolic murmur of mitral stenosis has a rumbling character and is best heard with the bell of the stethoscope over the LV impulse with the patient in the left lateral decubitus position (movie 4 and movie 5). The murmur originates in the LV cavity, explaining its location of maximum intensity.

The murmur is present both in sinus rhythm and in atrial fibrillation. It characteristically starts with an opening snap. Its duration, which correlates with the duration of the diastolic pressure gradient across the mitral valve, is a reasonably good guide to assess the severity of mitral stenosis [10]. In patients with sinus rhythm, there is frequently a presystolic accentuation of the diastolic murmur. The longer the duration of the murmur, the more severe is the mitral stenosis, provided the diastolic interval is not too short (absence of tachycardia). If the murmur extends up to S1 during a longer diastolic interval, it can be assumed that the pressure gradient is still present at end-diastole, which implies severe mitral stenosis.

The murmur of mitral stenosis may be of very brief duration or even absent (so-called silent mitral stenosis), even in the presence of severe mitral stenosis, when the flow across the mitral valve is markedly reduced. This may occur in the setting of right-sided heart failure and pulmonary hypertension. Conversely, with enhanced flow across the valve, as in the high-output state of pregnancy, the intensity and duration of the murmur increase even with less severe stenosis. In these circumstances, one cannot rely on the duration of the murmur to assess the severity of mitral stenosis; other ancillary investigations, particularly echocardiographic studies, are necessary. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

Prosthetic mitral valve — A diastolic murmur is usually not appreciated in patients with normal functioning bioprosthetic and mechanical mitral valves. A diastolic murmur may become evident over time due the progressive degeneration of the bioprosthetic valve. An absent mechanical mitral valve closing click (S1) and medium to long diastolic murmur is characteristic of a thrombosed mechanical mitral valve (in the setting of inadequate anticoagulation).

Tricuspid stenosis — Tricuspid stenosis may be associated with a middiastolic rumble that is best heard along the left sternal border. The most characteristic feature is the increase in intensity of the murmur with inspiration (Carvallo sign or Rivero-Carvallo sign) [11]. The middiastolic rumble may be associated with a tricuspid opening snap and wide splitting of S1 due to delayed closure of the tricuspid valve. Most patients with tricuspid stenosis are in atrial fibrillation and the murmur is middiastolic when the transvalvular pressure gradient is maximum. In sinus rhythm, the murmur may occur only in late diastole, resulting from an increased flow due to right atrial systole.

Tricuspid stenosis most frequently occurs in association with mitral stenosis. Isolated tricuspid stenosis is uncommon; when suspected, carcinoid heart disease and right atrial myxoma should be investigated as possible etiologies.

Atrial myxoma — Atrial myxoma may cause obstruction of the atrioventricular valves and a middiastolic murmur. In left atrial myxoma, the auscultatory findings can be similar to those of mitral stenosis. The murmur is frequently presystolic and crescendo in configuration; it appears to occur with the onset of ventricular systole when the tumor is moved toward the left atrium through the mitral orifice, and when the flow across the valve is still continuing.

It is difficult to distinguish between a left atrial myxoma and mitral stenosis at the bedside. However, the character and intensity of the murmur due to an atrial myxoma may change with alterations of position [12]. Sinus rhythm, changing intensity and character of the murmur, and a "tumor plop" sound favor the diagnosis of left atrial myxoma. Nevertheless, echocardiographic evaluation is necessary and is always recommended in a patient with suspected mitral stenosis.

Right atrial myxoma is far less common than left atrial myxoma. Auscultatory findings may be similar to those of tricuspid stenosis. (See "Cardiac tumors".)

Increased flow across the atrioventricular valve — An early diastolic rumbling murmur can be appreciated at the apex in the presence of complete heart block when atrial contraction coincides with rapid early diastolic filling. Middiastolic murmurs may occur in the presence of normal atrioventricular valves when the flow across the valve is markedly increased in middiastole (flow murmurs). In pure severe mitral regurgitation (MR), a larger volume of blood (due to the regurgitant volume) moves from the left atrium to the LV during diastole; the etiology is a partial closing movement of the mitral valve, which occurs after it opens widely at the beginning of diastole. The rapid flow to the LV continues, and thus "functional mitral stenosis" occurs, explaining the middiastolic rumble. In some patients, a middiastolic pressure gradient has been demonstrated [13-15].

With a left-to-right shunt across a ventricular septal defect or patent ductus arteriosus, antegrade blood flow across the mitral valve increases during diastole, which may be associated with a middiastolic murmur. The mechanism may be similar to that seen in MR. When the etiology is an atrial septal defect or anomalous pulmonary venous drainage, a tricuspid flow murmur can also be heard along the lower left sternal border; this is due to a partial closing movement of the tricuspid valve after its full opening in early diastole and functional tricuspid stenosis at middiastole [16]. The intensity of the tricuspid flow murmur tends to increase during inspiration.

Carey-Coombs murmur — In acute rheumatic fever, a middiastolic murmur over the LV impulse, a Carey-Coombs murmur, has been attributed to acute mitral valvulitis. However, first-degree atrioventricular block (prolonged PR interval) is common in rheumatic carditis and an increased flow due to earlier atrial systole coinciding with the rapid filling phase may contribute to a Carey-Coombs murmur.

Austin Flint murmur — An apical diastolic rumbling murmur has been described in patients with pure AR [17,18]. Several mechanisms have been proposed to explain the genesis of this murmur, including fluttering of the mitral valve from the impingement by the AR jet, relative (functional) mitral stenosis, and regurgitant jets directed against the LV free wall [17-19].

Mitral fluttering is not the mechanism of the Austin Flint murmur, since fluttering occurs in early diastole with the onset of regurgitation, while the rumble occurs in mid or late diastole. A second proposed mechanism was premature partial closing movement of the mitral valve at middiastole due to the regurgitant flow, leading to functional mitral stenosis. However, use of M-mode and two-dimensional echocardiography, color flow Doppler, and cine magnetic resonance imaging has shown that the murmur arises from the regurgitant jets that are directed at the LV free wall, thus excluding functional mitral stenosis as the etiology [19].

If the Austin Flint murmur is not recognized, a mistaken diagnosis of organic mitral stenosis might occur occur. The presence of an opening snap suggests organic mitral stenosis.

Left-to-right shunts — Flow murmurs due to a large left-to-right shunt are usually middiastolic in timing. Occasionally, they can extend to late diastole.

Late diastolic murmurs — Presystolic murmurs occur in late diastole and extend up to S1. They usually have a crescendo configuration. The murmurs result from increased flow across the mitral or tricuspid valve and are most frequently observed in the presence of normal sinus rhythm. However, crescendo presystolic murmurs can occur in the presence of atrial fibrillation in the absence of atrial systole; mitral valve closure, resulting in a reduction of an effective mitral orifice, begins before the onset of isovolumic systole and S1 and during this period antegrade flow across the mitral valve continues [20].

Mitral stenosis — Atrial contraction increases the pressure gradient and flow at end-diastole when mitral stenosis is present, generating the presystolic murmur. When a middiastolic rumble accompanies a presystolic murmur, the intensity of the middiastolic murmur frequently decreases before the onset of the presystolic murmur. The presence of only a presystolic murmur associated with increased intensity of S1 suggests mild mitral stenosis.

Tricuspid stenosis — In tricuspid stenosis with sinus rhythm, the murmur is usually presystolic because the transvalvular gradient is maximum during this period [11]. The intensity of the presystolic murmur of tricuspid stenosis also increases during inspiration, which is associated with an increased venous return to the right atrium. Increased right atrial volume is associated with more forceful right atrial contraction and, therefore, an increased pressure gradient during this interval and accentuation of the murmur.

Myxoma — Presystolic murmurs may occur with left or right atrial myxomas. This is due to obstruction of the atrioventricular valves.

Complete heart block — In complete atrioventricular block with a slow idioventricular rhythm, a short late diastolic murmur can occasionally be heard and recorded (Rytand murmur). The precise mechanism of Rytand murmur has not been elucidated; diastolic MR has been postulated [21,22]. Diastolic MR appears to depend upon the timing of the P wave and atrial systole relative to ventricular diastole. (See "Acquired third-degree (complete) atrioventricular block".)

CONTINUOUS MURMURS — 

Continuous murmurs are defined as murmurs that begin in systole and extend up to diastole without interruption. They do not necessarily need to occupy the total duration of systole and diastole. Continuous murmurs result from blood flow from a higher pressure chamber or vessel to a lower system associated with a persistent pressure gradient between these areas during systole and diastole. These murmurs may occur due to aortopulmonary connections, arteriovenous communication, and disturbances in the flow patterns in the arteries or veins (table 2 and figure 1) [23-26].

Patent ductus arteriosus — Patent ductus arteriosus is a relatively common cause of a continuous murmur in adults. Aortic pressure is higher than pulmonary artery pressure during both systole and diastole; blood flow from the high pressure descending thoracic aorta to the low pressure pulmonary artery causes the continuous murmur (Gibson murmur or machinery murmur).

The maximum intensity of the murmur usually occurs at S2. The duration of the murmur depends upon the pressure difference between aorta and pulmonary artery. With pulmonary hypertension, pulmonary artery diastolic pressure increases; when it approaches systemic level, the diastolic portion of the continuous murmur becomes shorter and ultimately absent [27]. With more severe pulmonary hypertension, pulmonary artery systolic pressure can equalize with aortic systolic pressure and the systolic component of the murmur may also be absent (silent ductus). Differential cyanosis due to the reversal of the shunt and signs of pulmonary hypertension with or without evidence of right-sided heart failure are the only physical findings that are recognizable at the bedside in these circumstances.

Aortopulmonary window — Continuous murmurs may be present with an aortopulmonary window. However, because of the large size of the communication, pulmonary vascular resistance and pulmonary artery diastolic pressure tend to be higher, which is associated with a shorter duration of the diastolic component of the continuous murmur.

Shunts — A left-to-right shunt through a small atrial septal defect in the presence of mitral valve obstruction, known as Lutembacher syndrome, may occasionally cause a continuous murmur [28]. Total anomalous pulmonary venous drainage, a small atrial septal defect without mitral valve obstruction, and mitral stenosis with a persistent left superior vena cava are very rare causes of continuous murmurs.

Arteriovenous fistulas — Congenital or acquired arteriovenous fistulas also cause continuous murmurs.

●Coronary arteriovenous fistulas may produce a continuous murmur; the location, duration, and character of the murmur depend upon the anatomical type of fistulas. As an example, the right coronary and right atrial, or coronary sinus, communication produces continuous murmurs that are usually located along the parasternal areas. The murmur of a circumflex coronary artery and coronary sinus communication are usually located in the left axilla. The configuration of the murmur and the intensity of the systolic and diastolic components are variable. Marked systolic compression of the abnormal vessels reduces the systolic flow; thus, the systolic component of the murmur may be very soft. On the other hand, an increased systolic gradient may result from the partial compression of the intramural communication, which will tend to increase the intensity of the systolic portion of the murmur.

●Fistulous connection between an internal mammary graft and the pulmonary vasculature or left anterior descending vein are rare causes of continuous murmurs [29].

●A communication between the sinus of Valsalva and the right atrium or right ventricle produces continuous murmurs that may appear as to-and-fro murmurs due to the increased intensity of both the systolic and diastolic components and a softer intensity around S2.

●Systemic and pulmonary arteriovenous fistulas are also associated with continuous murmurs. Although a systemic arteriovenous communication usually produces a loud murmur, the murmur of pulmonary arteriovenous fistulas is softer and may be primarily systolic. The major pressure gradient occurs in systole, and the diastolic gradient is usually very small. Pulmonary arteriovenous fistulas usually involve the lower left or right middle lobe; the location of the murmurs corresponds to these areas. (See "Pulmonary arteriovenous malformations: Epidemiology, etiology, and pathology in adults".)

●A large dialysis fistula can be associated with a continuous murmur that can radiate to the infraclavicular area.

Coarctation of the aorta — In coarctation of the aorta, a continuous murmur can be heard in the back overlying the area of constriction. Continuous murmurs may originate in large tortuous collateral arteries in coarctation of the aorta, which are also heard in the back over the interscapular regions. Sometimes, large, tortuous intercostal vessels are visible when the shoulders are rotated medially and forward to separate the scapulas (Suzman sign) [30]. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)

Other causes of continuous murmurs

●Constriction in the systemic or pulmonary arteries can be associated with continuous murmurs due to a persistent pressure gradient across the narrowed segment of the vessel.

Pulmonary artery branch stenosis and a partial occlusion of the pulmonary artery due to pulmonary embolism may also cause continuous murmurs.

●Rapid flow through tortuous collateral vessels, as in coarctation of the aorta, may cause a continuous murmur. Bronchial arterial collateral vessels develop in certain types of cyanotic congenital heart disease (tricuspid atresia, pulmonary atresia with ventricular septal defect) and loud continuous murmurs may be heard along the parasternal area.

●The "mammary souffle" associated with pregnancy may be systolic or continuous. These innocent murmurs are usually of higher frequency (high pitched) and louder in systole.

●A venous hum, which results from altered flow in the veins, can also cause an innocent continuous murmur. The venous hum is heard with the patient in the sitting position (usually in the supraclavicular fossa) and frequently disappears when the patient moves to the supine position. The hum tends to be louder in diastole and can be completely abolished by compression of the ipsilateral internal jugular vein. A loud, left-sided venous hum transmitted below the clavicle should not be mistaken for the murmur of patent ductus arteriosus. Venous hum is not heard in the supine position, and pressure on the internal jugular vein abolishes the venous hum. In contrast, the murmur of patent ductus arteriosus persists in the supine position and despite pressure on the internal jugular vein.

Differential diagnosis — A pericardial friction rub may be confused with a continuous murmur. It is heard best at the left lower sternal border, and sounds more scratchy and swishing than continuous.

ROLE OF ECHOCARDIOGRAPHY — 

In clinical practice, echocardiography is the standard for establishing the cause of a murmur. As noted in major society guidelines, an echocardiogram is indicated for the diagnosis and evaluation of patients with known or suspected valve disease [2,3]. Echocardiography is not needed in asymptomatic patients with a benign flow murmur but is appropriate in patients with cardiac symptoms and any cardiac murmur. It is also indicated in asymptomatic patients with a diastolic murmur, a grade 2 or greater systolic murmur, or a systolic murmur in association with other abnormal examination findings, such as a systolic click or reduced carotid upstroke.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Heart murmurs (The Basics)")

SUMMARY

●Murmur characteristics – A murmur is characterized by its intensity (grade), timing, configuration (time course), frequency (pitch), and location. (See 'Murmur description' above.)

Six grades are used to classify the intensity of a systolic murmur (table 1). The first four of these grades (I through IV) are commonly used for diastolic murmurs since louder diastolic murmurs are very rare.

●Diastolic murmurs

•An early diastolic murmur is usually due to aortic or pulmonic regurgitation. (See 'Early diastolic murmurs' above.)

•Mitral stenosis causes a middiastolic murmur, a late diastolic murmur, or both. (See 'Mitral stenosis' above and 'Mitral stenosis' above.)

•Tricuspid stenosis with sinus rhythm causes a late diastolic murmur while tricuspid stenosis with atrial fibrillation causes a middiastolic murmur. (See 'Tricuspid stenosis' above and 'Tricuspid stenosis' above.)

•A myxoma causes a mid- or late-diastolic murmur. (See 'Atrial myxoma' above and 'Myxoma' above.)

●Continuous murmurs – Causes of a continuous murmur include patent ductus arteriosus, aortopulmonary window, some shunts, arteriovenous fistulas, and coarctation of the aorta. (See 'Continuous murmurs' above.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledge Catherine M Otto, MD, who contributed to earlier versions of this topic review.