The production of murmurs results from turbulent flow across valves. Three main factors have been attributed to cause a murmur: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve. [30, 1, 31] When evaluating a heart murmur, it is important to know the timing of the murmur in the cardiac cycle, the location, the duration, character, configuration, radiation, aggravating maneuvers, and diminishing maneuvers. Recognizing the periodicity of murmur helps to narrow the differential diagnoses and often guides further diagnostic evaluation. For example, all diastolic murmurs and any systolic murmur above grade 2 in severity requires further evaluation with echocardiography. [30] The timing of the murmur is determined by palpating the carotid pulse while listening to the murmur. The carotid upstroke corresponds to the onset of systole. The factors to focus on while evaluating a murmur are discussed briefly below. Intensity: The intensity of the murmur depends on the volume of blood flow across the valve and the pressure gradient across which the blood flow occurs. The intensity is graded into 6 different grades, as follows:
The grade of the murmur is important, as any diastolic murmur and a systolic murmur above grade II/VI in severity warrants echocardiographic evaluation as per ACC/AHA guidelines. Timing: Depending on when they are best heard in the cardiac cycle, the murmurs can be systolic (holosystolic, early/middle/late systolic), diastolic (early/middle/late) or continuous (ie, present in both systole and diastole). Location: This is the area of the heart where the murmur is heard the loudest. While auscultating, one should concentrate on the apex, pulmonary area, tricuspid, and aortic areas, in addition to the axilla, base of the heart, and left fourth ICS for evidence of radiation of murmur. As shown in Table 3, the location and timing help in determining whether the murmur is arising from the right or the left side of the heart. In addition, the position can help in locating the involved valves. Quality/character: Different murmurs have different qualities, such as harsh, blowing, rumbling, musical, or cooing. See Table 3. Pitch: This can be high or low pitched depending on the frequency of the murmur. The high-pitched sounds are best audible with a diaphragm and the low-pitched sounds with the bell. Radiation: Murmurs tend to radiate to certain specific areas that are often characteristic of a particular murmur. The murmur of MR radiates to the axilla or base of the heart, depending on which leaflet is involved. In the case of AS, the murmur radiates in the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly, the aortic regurgitant murmur tends to radiate along the left sternal border. Configuration: This corresponds to the shape of murmur intensity over time. It can be a plateau, decrescendo, crescendo-decrescendo, or crescendo murmur. Dynamic auscultation involves certain specific maneuvers that affect the blood flow through the valves and can aid in recognition and differentiation of heart murmurs. Inspiration: Inspiration leads to a decrease in the intrathoracic pressure with an increase in venous return to the right side of the heart. The murmurs generated from the right side of the heart increase in intensity with inspiration. Expiration: Expiration has the opposite effect as inspiration. There is an increase in the intrathoracic pressure and a decrease in venous return to the right side of the heart. Blood in the lung is “forced” into the left heart. Hence, murmurs arising from the left side of the heart become more prominent with expiration. Standing up: This causes a peripheral pooling of blood and a net decrease in venous return. Most murmurs are thus decreased in intensity upon standing, except that of hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which become more prominent. Squatting: Squatting causes an increase in the afterload and venous return (ie, preload). The net effect is an increase in intensity of all the murmurs, except those associated with MVP and HOCM, which become less prominent with squatting. Straight leg raising: Passive straight leg raising increases venous return (ie, preload) and has an effect similar to brisk squatting. All murmurs increase in intensity except those of HOCM and MVP, which decrease in intensity with this maneuver. Hand grip: Hand grip is a form of isometric exercise and increases the afterload, arterial pressure, LV volume, and LV pressure. The net effect of these changes is complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip, while those of HOCM and MVP become less prominent. Valsalva maneuver: Valsalva maneuver involves asking the patient to strain, which increases the intrathoracic pressure, thus causing a net decrease in preload. Most heart murmurs decrease in intensity with Valsalva, except those of HOCM and MVP, which become more prominent. Amyl nitrate inhalation: Amyl nitrate is an arteriolar vasodilator and initially causes decreased afterload followed by reflex tachycardia. During the initial phase, because of reduced afterload, the murmurs of AR, MR, and VSD diminish, while those of AS are accentuated. Later on, during the tachycardic phase, the murmur of MS is accentuated. Table 1. Effect of Different Maneuvers on Some Common Murmurs (Open Table in a new window)
Table 2. Differential Diagnoses of Cardiac Murmur [32] (Open Table in a new window)
Systolic murmurs occur during the ventricular contraction. They can result from (1) leakage across the abnormal atrioventricular valves (tricuspid or mitral) or interventricular septal defects or (2) ventricular outflow tract obstruction, which can be valvular, supravalvular, or subvalvular. In some cases, the systolic murmurs can be audible owing to an abnormal amount of blood flow across normal valves, as can occur in hyperdynamic states. Systolic murmurs can be holosystolic, early systolic, late systolic, or mid-systolic in their timing. As per the ACC/AHA guidelines, any patient with a holosystolic, early systolic, late systolic, or a mid-systolic murmur greater than II/VI in severity or with evidence of cardiac compromise due to valvular disease should be further evaluated with echocardiography. [30] Early systolic murmurs Early systolic murmurs are produced by acute MR or TR or in VSD with pulmonary hypertension. They are blowing in nature and decrescendo in character. Blood flows rapidly from the ventricle into an unprepared atrium, leading to rapid equalization of the pressures and early systolic murmur. Acute MR can occur in the setting of an acute MI, infective endocarditis, chordal rupture in patients with MVP, or blunt chest wall trauma. In the acute setting, the LA does not have sufficient time to dilate in response to the high-volume regurgitant jet. Thus, the LA and LV pressures equalize in the early part of systole, confining the murmur to early systole. When acute, the murmur of MR is accompanied by an S4. MI can damage the papillary muscles, resulting in acute MR. This usually occurs on day 2-7 post–acute MI, and the posteromedial muscle is involved more often than the anterolateral muscle. The murmur of acute MR must be differentiated from a murmur of ventricular septal rupture, which is usually holosystolic and associated with a palpable systolic thrill. Nevertheless, any newly onset systolic murmur following MI should be evaluated with echocardiography. Infective endocarditis can directly damage the valve leaflets, the chordae, or both, producing MR. Blunt chest wall trauma can damage the papillary muscle and/or cause chordal rupture or valvular leaflet avulsion, leading to acute MR. Chordal rupture due to myxomatous degeneration caused by MVP or other associated connective tissue disease worsens the severity of a pre-existing murmur. A small muscular VSD alone and a large VSD with pulmonary hypertension can also produce an early systolic murmur. These murmurs are soft and blowing and audible at the left lower sternal border. In case of a muscular VSD, the septal defect closes during septal contraction in systole, thus limiting the murmur to the early part of systole. In the presence of pulmonary hypertension with VSD, the pressure gradient is maintained between the left and the right ventricle only in the early part of systole. This confines the murmur to early systole. Acute TR can occur in the setting of infective endocarditis. The murmur is usually soft, blowing, and decrescendo and is not associated with signs of right heart failure. It is often accompanied by a right-sided S4 and a diastolic flow rumble. Mid to late systolic murmurs These murmurs are usually associated with ventricular outflow tract obstruction (which can be valvular, supravalvular, or subvalvular) or an abnormal amount of blood flow across normal valves as can happen in hyperdynamic states (hyperthyroidism, fever, pregnancy, anemia, renal failure). The murmur associated with valvular stenosis (AS or PS) is usually a harsh murmur which is crescendo- decrescendo in configuration and high pitched. AS-associated murmurs are most audible at the right upper sternal border/right third ICS with the patient in the upright position and breath held at end expiration. In some cases, it is audible at the apex, in which case it can be confused with the murmur of MR. Some of the findings that help delineate the murmur of MR from that of AS include an audible S1, forceful apex, radiation to carotids, changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usually radiates to the carotid arteries. An S4 is audible with severe AS. The time to peak of murmur often depends on the severity of valvular obstruction. The later the murmur peak, the more severe the obstruction. The exact location of the murmur varies depending on whether the murmur is valvular, subvalvular, or supravalvular. A valvular murmur is most prominent at the right second ICS, while a supravalvular stenosis produces a murmur that is located slightly higher than the valvular murmur. Refer to the audio example below. The mid-systolic harsh crescendo-decrescendo murmur of aortic stenosis best audible at the right upper sternal border. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3) The murmur of PS is best audible at the left second ICS just to the left of sternum. It is late peaking, is crescendo-decrescendo in configuration, and may be associated with a systolic click that becomes softer with inspiration. The P2 is usually soft and S2 usually split, with the split directly proportional to the degree of stenosis. The split depends on the severity of the murmur. As the severity increases, the P2 component of the S2 is delayed to the extent that a severe stenotic murmur can overshadow the sound generated by aortic valve closure. In severe PS, a right-sided S4 is often audible. The murmur of HOCM is most audible at the left lower sternal border, left fourth ICS. It is harsh and crescendo-decrescendo in character. The murmur of HOCM is dynamic, and its intensity varies with the changes in left ventricular outflow tract (LVOT). An increase in LV volume leads to a decrease in the severity of outflow tract obstruction, thus leading to a decrease in the intensity of HOCM murmur. This can happen during leg raising, during squatting, or with handgrip. Similarly, any decrease in the LV volume leads to an increase in outflow tract obstruction, increasing the intensity of HOCM murmur. This can be seen with Valsalva maneuver and sudden standing. MVP produces a mid- to late systolic murmur that is preceded by a nonejection click. [33] The murmur is blowing and high pitched in nature. The murmur is increased in intensity upon sudden standing and Valsalva. Squatting, hand grip, and bradycardia decrease the intensity of MVP murmur. Holosystolic murmurs These murmurs last throughout ventricular systole. They usually start at S1 and proceed through S2; the intensity of the murmur may overshadow both valve closure sounds. These murmurs are typically produced by emptying of the high-pressure ventricle during systole into chambers that have lower pressure at that time (the atria with MR or TR or the right ventricle in the case of VSD). At the start of isovolumetric ventricular contraction, the ventricular pressure rapidly exceeds the atrial pressure. The abnormal AV valves cannot prevent the regurgitation of blood from ventricle to atrium. As a result, the high-pressure ventricle empties into the low pressure atria. This marks the beginning of the holosystolic murmur, in which the sound of murmur onset often muffles S1. The regurgitant murmur can also muffle S2, as the ventricular pressure continues to exceed atrial pressure for a short period after closure of the aortic/pulmonary valve. The murmur of MR is blowing and high pitched and is best heard at the apex with radiation to the axilla or the base of the heart. It is usually plateau in configuration. The MR murmur is increased during expiration, passive leg raising, squatting, and handgrip and decreased in intensity with inspiration, Valsalva, and standing. The radiation of the murmur depends on which leaflet is involved. A murmur generated by the deformity of anterior leaflet radiates more toward the axilla, thoracic spine, and scapula, while a murmur arising from posterior leaflet involvement radiates to the base of the heart. [34] The presence of S3 with valvular MR indicates a more severe and hemodynamically significant lesion. The association of signs of pulmonary hypertension and right heart failure also indicate hemodynamically significant MR. Refer to the audio example below. The holosystolic, blowing murmur from mitral regurgitation audible best at the apex. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3) The murmur of TR is best heard at the left lower sternal border. It is a blowing high-pitched murmur heard that increases in intensity with inspiration (Carvallo sign). It can result primarily from involvement of the tricuspid valve or secondarily from pulmonary hypertension. When due to pulmonary hypertension, it is associated with a loud P2. In VSD with normal pulmonary arterial pressures, a holosystolic murmur can be heard over the left lower sternal border at the level of the third and fourth ICSs. This murmur depends on the orifice size of the septal defect. The smaller the defect, the greater the intensity of the murmur. With a larger orifice size, RV and pulmonary pressure increase, confining the murmur to early systole. Subsequently, once pressure equalization occurs, blood flow is absent. This is associated with pulmonary hypertension and is a bad prognostic sign, as it indicates progression of disease. Thus, the presence of holosystolic murmur in VSD indicates early disease and, depending on clinical setting, carries a better prognosis than the absence of a murmur in the presence of VSD. Refer to the audio example below. The murmur from ventricular septal defect, best audible at the left lower sternal border. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3) Innocent murmurs and functional systolic ejection murmurs Innocent murmurs are mid- to late-systolic, medium- to high-pitched ejection murmurs audible at the left lower sternal border or the left second ICS, depending on origin from the LV or RV outflow tract. These murmurs are usually blowing in character and grade I or II/VI in intensity. They can vary in intensity with the body’s positioning and always end before the closure of the semilunar valves. Murmurs are categorized as innocent only if examination of the cardiovascular system reveals normal findings. Functional systolic ejection murmurs are associated with increased blood flow across the semilunar valves (aortic/pulmonary). Some of the conditions associated with functional murmurs include anemia, thyrotoxicosis, pregnancy, fever, exercise, arteriovenous fistula, and complete heart block. With complete heart block, there is beat-to-beat variation in the murmur intensity. Diastolic murmurs are audible during ventricular diastole and caused by either (1) regurgitation across the aortic or pulmonary valve or (2) stenotic AV valves. Early diastolic murmurs Early diastolic murmurs are produced by either AR or pulmonary regurgitation. The AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is most audible at the left sternal border or the right second ICS just to the right of sternum, with the patient leaning forward at end expiration. The murmur radiates to the left lower sternal border if it is due to primary valve disease. In patients with aortic root disease, the murmur may radiate to the right sternal border. The murmur increases in intensity during expiration and decreases in intensity with hand grip, squatting, Valsalva, and amyl nitrate inhalation. The S2 is usually muffled with AR, and there is an audible wide physiologic split. Refer to the audio example below. The early diastolic decrescendo murmur from aortic regurgitation. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3) The murmur of pulmonary regurgitation is best audible at the pulmonary area. The character, quality, and pitch of the murmur vary depending on the presence or absence of pulmonary hypertension. In the presence of pulmonary hypertension, it is a high-pitched, decrescendo murmur also known as a Graham Steell murmur. S2 is usually loud in association with pulmonary regurgitation. In the absence of pulmonary hypertension, it is a low-pitched crescendo-decrescendo murmur. Mid- to late diastolic murmurs These murmurs are produced by the blood flow across stenotic AV valves. MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation, best heard with the bell of the stethoscope placed over the cardiac apex with the patient in the left lateral position. S1 is loud. The murmur usually follows an OS, and the interval between the A2 and OS is inversely proportional to the severity of obstruction. The murmur of MS is increased in intensity with expiration and maneuvers that increase cardiac output, such as exercise. The presystolic accentuation results from atrial contraction in late diastole and is absent in patients with atrial fibrillation. The duration of murmur corresponds to the period in which the LA-LV diastolic pressure gradient is maintained. This duration correlates with the severity of obstruction; the longer the murmur duration, the more severe the MS (provided the diastolic filling time is not shortened, as may happen in tachycardia). The duration of murmur does not correlate to the severity of MS in high-output states, such as pregnancy, as the murmur is long-lasting owing to increased blood flow. Similarly, in the presence of pulmonary hypertension or right heart failure, the flow across the mitral valve is decreased, and, even in severe MS, the duration of murmur may be shortened. Refer to the audio example below. The mid to late diastolic, low-pitched, rumbling murmur from mitral stenosis. Murmur is best audible at the apex with the bell of the stethoscope. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3) TS produces a low-pitched, mid-systolic rumbling murmur best audible at the left third ICS/left sternal border and xiphoid process. The murmur increases in intensity with inspiration (Carvallo sign) and decreases in intensity during expiration and with Valsalva maneuver. Atrial myxoma can produce a diastolic murmur that is very similar to that associated with MS or TS. This murmur is also low pitched, mid-diastolic, and rumbling with presystolic accentuation. An OS is absent and is replaced by a “tumor plop.” It is difficult to clinically differentiate the murmur of atrial myxoma from that of MS, but the murmur of atrial tumors changes in intensity as the patient changes positions. Austin Flint murmur: This is an early diastolic rumbling murmur associated with valvular AR. This murmur arises from aortic regurgitant jets abutting the LV free wall and causing premature closure of the MV. [35] The Austin Flint murmur decreases in intensity with maneuvers that would decrease the intensity of AR, such as afterload reduction with amyl nitrate. On the other hand, amyl nitrate inhalation would increase the intensity of MS. This can potentially differentiate Austin Flint murmur from MS murmur. Carey Coombs murmur: This is a mid-diastolic murmur audible during acute rheumatic fever over the apical impulse. It is attributed to acute mitral valvulitis due to rheumatic fever. States of increased flow across AV valves can also produce diastolic rumbling murmurs. Patients with MR have an increased amount of diastolic blood flow across the mitral valve. There is a partial closure of the mitral valve in mid diastole after wide opening of the valve leaflets during early diastole. This, combined with increased blood flow, causes a functional MS murmur. [36] Similarly, ASD with left-to-right shunt can produce a mid-diastolic rumbling murmur over the tricuspid area. These murmurs are audible in systole and diastole, although their intensity usually varies during systole and diastole. They result from a communication between a high-pressure arterial and low-pressure venous chamber or vessel. Some of the causes of continuous murmurs are listed in Table 2. The continuous murmurs produced by patent ductus arteriosus (PDA) result from an abnormal communication between the aorta and the pulmonary artery. The aortic pressure is always higher than that of the pulmonary artery and results in a continuous murmur, with peak flow occurring during the end of systole (ie, at S2). The murmur is blowing, high pitched, and best audible at the left upper sternal border near the left second ICS. If the communication is large, pulmonary arterial pressure eventually rises, leading to pulmonary hypertension. This may cause the diastolic component of the murmur to become muffled; in severe pulmonary hypertension, it may lead to reversal of flow during diastole and differential cyanosis. The continuous murmur of PDA may be confused with the murmur associated with AS with coexisting AR. In the case of AS with AR, the murmur is least intense around S2, while, in PDA, the murmur is most pronounced at S2. The continuous murmur from anomalous origin of left coronary artery from the pulmonary artery (so called Bland-Garland-White syndrome) can produce a continuous murmur best audible around the left sternal border. In this case, the collateral vessels from the right coronary artery to the left coronary artery give rise to the continuous murmur. Rupture of a sinus of Valsalva into the RA or RV can produce a continuous murmur best audible over the lower left sternal border and the xiphoid. These murmurs are more pronounced during diastole, a fact that differentiates them from the murmur of PDA. Coronary artery fistulas emptying in the RA can produce a continuous murmur audible at the right or left sternal area. These murmurs are more prominent in diastole, as the flow in the coronary arteries occurs during diastole. A continuous murmur due to coarctation of aorta is best audible at the level of coarctation, usually between the shoulder blades. Table 3. Summary of Characteristics of Some Common Murmurs (Open Table in a new window)
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You wish to listen in the mitral valve area. to do this, you place the stethoscope at the:
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