Recognition of Commonly Heard Murmurs


LSU Physician Champion - Dr. David Tadin



Location:
The location of where you place your stethoscope is very important to hear the intensity and quality of a murmur. In Figure 1, the modified picture shows the location of where the valves are located by color. Furthermore, the picture illustrates where the murmur radiates.

• To best hear the aortic valve, you place the diaphragm of your stethoscope over the 2nd intercostal space at the right upper sternal border.
• To best hear the pulmonic valve, you place the diaphragm of your stethoscope over the 2nd intercostal space at the left upper sternal border.
• To best hear the tricuspid valve, you place the diaphragm of your stethoscope over the 4th intercostal space at the left lower sternal border.
• To best hear the mitral valve, you place the diaphragm of your stethoscope over the 6th intercostal space at the mid clavicular line. If you do not hear the mitral S1 well or to better characterize the murmur better, make sure you locate the point of maximal impulse (PMI) and place the diaphragm of your stethoscope there.


Figure 1
The normal heart sounds consist of an S1 (mitral and tricuspid closure) followed by an S2 (closure of the pulmonic and aortic valve) (See Figure 2).

Figure 2 Normal sounds of the cardiac cycle.

Sometimes an S3 or S4 can be heard. The S3 is a dull, low-pitched sound best heard over the cardiac apex (needs to locate the point of maximum impulse (PMI)) with the patient lying in the left lateral decubitus position with the bell of the stethoscope. It occurs at the beginning of the middle third of diastole, approximately 0.12 to 0.18 seconds after S2 (See figure 3). This produces a rhythm classically compared word "Kentucky" with Ken(S1)tucky(S2-S3). An S3 may be normal in people under 40 years of age, pregnancy and some trained athletes but should disappear before middle age. A pathologic S3 occurs from high left sided filling pressures in which blood from the left atrium during passive filling is rapid and decelerates into wall the left ventricle causing vibratory oscillations. An S3 can be heard over the right ventricle as well. The S4 is a low-pitched sound that results from a forceful atrial kick at the end of diastole during into a ventricle which cannot expand further. S4 occurs ~90 msec before S1 (See figure 3). This sound is best heard over the cardiac apex (needs to locate the point of maximum impulse (PMI)) with the patient lying in the left lateral decubitus position with the bell of the stethoscope. It will become more apparent with exercise or with the patient holding expiration. If the culprit is the right ventricle, the abnormal sound will be most evident on the left lower border of the sternum and will get louder with exercise and deep inspiration. This produces a rhythm classically compared word "Tennessee" with Tennne(S4-S1)see(S2).



Grading of murmurs
When you hear turbulent flow across a valve, you need to describe the intensity of the murmur. See figure 4, which lists the descriptors from grade I/VI to VI/VI. Any systolic murmur greater than a grade II/VI or any grade of diastolic murmur needs to be evaluated by an echocardiogram.


Figure 4 Grading of murmurs.



Figure 5 Quality of Murmurs

Systolic Murmurs
Not only do you have to characterize the intensity of the murmur, but you need to describe the quality of the murmur. This section is a breakdown of systolic and diastolic murmurs.



Mid-systolic murmurs
• Aortic stenosis: Is best heard over the 2nd intercostal space at the right upper sternal border. It is described as mid-systolic murmur that is crescendo-decrescendo (See Figure 5). As the severity of the stenosis increases, the peaking of the crescendo-decrescendo murmur moves from a mid-systolic position to a late peaking position and can even obliterate the S2 component. Also, this murmur can be heard over all the precordium when severe. There is a specific finding in aortic stenosis called Gallavardin phenomenon. This phenomenon is a noisy, harsh musical sound best heard at the cardiac apex. The presence of a murmur at the apex can be misinterpreted as mitral regurgitation. However, the apical murmur of the Gallavardin phenomenon does not radiate to the left axilla and is accentuated by a slowing of the heart rate (such as a compensatory pause after a premature beat) whereas the mitral regurgitation murmur does not change. Sometimes, it is difficult to tell the difference between aortic stenosis and aortic sclerosis (which is also a mid-systolic murmur best heard at the 2nd intercostal space of the right upper sternal border). A helpful hint is that an aortic stenosis murmur is radiating to the neck due to the high velocity jet in the ascending aorta. You can determine this by placing the diaphragm of the stethoscope over the carotids or in the supraclavicular fossa. You should hear the same quality of the aortic stenosis murmur vs a different quality murmur as in carotid stenosis. You can march the diaphragm of your stethoscope from these positions to the 2nd intercostal space at the right upper sternal border and the quality of the sound should be the same but the intensity should increase. Because it takes longer for the left ventricle to eject its load of blood through the stenotic valve, the closure of the aortic valve is delayed. This widens the slight gap between the closure of the aortic and pulmonary valves in S2 to a noticeable degree, and a significant splitting of S2 can be heard in expiration. This is called a paradoxical split (See figure 7B). Finally, maneuvers which increase preload and decrease afterload tend to increase the intensity of the murmur (See Figure 8).
• Pulmonic stenosis: Is best heard over 2nd intercostal space at the left upper sternal border. The murmur can be heard radiating into the neck or the back, has a crescendo-decrescendo, and a harsh quality. Because it takes longer for the right ventricle to eject its load of blood through the stenotic valve, the closure of the pulmonary valve is delayed. This widens the slight gap between the closure of the aortic and pulmonary valves in S2 to a noticeable degree, and a significant splitting of S2 can be heard in inspiration. This is called a wide split (See figure 7C). Finally, maneuvers which increase venous filling and blood flow into the right ventricle, such as deep inspiration, will tend to increase the intensity of the murmur (See figure 8).
• Atrial septal defect: Is best heard over the heard over 2nd intercostal space at the left upper sternal border. Because the pressure in the left atria initially exceeds that in the right, the blood flows in a left to right shunt. This high volume of blood next passes into the right ventricle, and the ejection of the excess blood through a normal pulmonary valve produces the prominent mid-systolic flow murmur.
• Hypertrophic obstructive cardiomyopathy (HOCM): Typically, medium pitched, has a crescendo–decrescendo configuration, and is heard best along the left sternal border (See Figure 5). There is radiation to the base of the neck, but not into the carotid arteries. The murmur is similar in quality to that of aortic valve stenosis, but is somewhat less harsh and slightly higher pitched. The intensity of the murmur is quite variable. Maneuvers that change the murmur is softer with squatting/leg raises, and louder with standing/valsalva by affecting preload. The murmur is softer with handgrip by affecting afterload (See Figure 8).
• Mitral valve prolapse (MVP): Following a normal S1 and briefly quiet systole, the valve suddenly prolapses, resulting in a mid-systolic click (See Figure 5). Immediately after the click, a brief medium pitch crescendo-decrescendo murmur is heard, usually best at the apex – however this is not well illustrated in figure 4. In stark contrast to most other murmurs, MVP is enhanced by Valsalva maneuvers and decreased by squatting. This is because those maneuvers which decrease the volume of the left ventricle (Valsalva, standing) will cause the prolapse to occur sooner and more severely, while those that increase venous return and diastolic filling (squatting) and thereby enhance the ventricular volume, help to maintain tension along the chordae and to keep the valve shut (See Figure 8).




Holosystolic murmurs
• Mitral regurgitation: The quality of this murmur depends if it is acute or chronic. Chronic mitral regurgitation is high pitched, blowing, and best heard at the cardiac apex with radiation to the axilla. It is holosystolic, starting with the first heart sound and extending to and sometimes through the aortic component of the second heart sound. Typically plateau in configuration, the murmur occasionally has late systolic accentuation (See Figure 5). The intensity of classic mitral valve regurgitation is quite variable. The intensity increases with squatting, isometric hand grip exercise, and intravenous administration of alpha-adrenergic agonists. It typically decreases with amyl nitrite inhalation (See Figure 8). Acute mitral regurgitation is typically decrescendo and of variable intensity (usually grade 3 or higher). It begins with the first heart sound and decreases in intensity throughout systole, occasionally terminating before the aortic component of the second heart sound. Best heard at the cardiac apex, the murmur typically radiates to the axilla and may be audible along the cervical spine or at the top of the head in selected cases. The murmur is lower pitched than that of chronic mitral regurgitation, often possessing a harsh quality reminiscent of valvular aortic stenosis.
• Tricuspid regurgitation: High-pitched, blowing, holosystolic, plateau, non-radiating murmur best heard over the heard over 4nd intercostal space at the left upper sternal border. (See Figure 5). The intensity is variable, but tends to increase during inspiration (Carvallo's sign), with passive leg raising, after a post-extrasystole pause, and following amyl nitrite inhalation (See Figure 8).
• Ventricular septal defect: In patients with low pulmonary vascular resistance is a low to medium pitched, holosystolic murmur (See Figure 5). The murmur is heard best over the third and fourth intercostal space at the left sternal border but is widely audible over the entire precordium. The intensity of the murmur is typically grade 3 or higher. Amyl nitrite inhalation causes the murmur of an uncomplicated ventricular septal defect to decrease, whereas alpha-adrenergic agonists cause no change or an increase in intensity.




Diastolic Murmurs:
• Mitral stenosis: Is best heard over the apex. You need to locate the point of maximal impulse (PMI) and place the bell (not diaphragm) of your stethoscope there. This is a low pitch, diastolic rumbling murmur with presystolic accentuation will be heard after the opening snap (See Figure 5). The opening snap can occur either in mid-diastole or late diastole. When the opening snap occurs, depends on the severity of the mitral stenosis. As the pressure in the left atrium increases, the mitral valve opens earlier in ventricular diastole. Also, the duration increases with worsening disease. Maneuvers that transiently increase cardiac output, such as sit-ups, coughing, or squatting, may aid in detection. Valsalva will increase left atrial pressure and move the opening snap earlier in diastole.
• Tricuspid stenosis: Tricuspid stenosis is often inaudible but may produce a soft opening snap and a mid-diastolic rumble with presystolic accentuation at the left lower sternal border of the 4nd intercostal space. Use the bell of the stethoscope to hear this murmur. It is characterized as scratchy and short in duration. The murmur becomes louder and longer with maneuvers that increase venous return (exercise, inspiration, leg-raising) and softer and shorter with maneuvers that decrease venous return (standing, Valsalva maneuver).
• Aortic regurgitation: Decrescendo in intensity for a variable duration of diastole (See Figure 5). The murmur is described as a high-frequency, "blowing" sound, most often heard best usually along the left lower sternal border at the 4th intercostal space (also known as Erb’s point). Although occasionally at 2nd right intercostal space especially if a dilated aorta is present. The murmur may only be heard by listening in one of these areas with the patient sitting, leaning forward in relaxed expiratory apnea. Proper timing of the cardiac cycle is essential. A heart rate of 100 or greater abbreviates diastole so that systolic and diastolic duration are nearly equal. In this situation, even a loud murmur of aortic regurgitation may be mistaken for a systolic murmur. Any bedside maneuver that transiently increases blood pressure may intensify or bring out the murmur. Hand grip or squatting can be useful.
• Pulmonic regurgitation: Is an early diastolic, decrescendo murmur beginning with the pulmonary component of the second sound, best heard along the upper left sternal border (See Figure 5). Auscultatory techniques are like those for aortic regurgitation. The quality of pulmonary valve regurgitation is similar to that of aortic regurgitation, and differentiation may be difficult. The murmur of pulmonary valve regurgitation may increase in intensity with inspiration.
• Austin-Flint murmur: Is a low-pitched rumbling heart murmur which is best heard at the cardiac apex. It can be a mid-diastolic or presystolic murmur. It is associated with severe aortic regurgitation. Classically, it is described as the result of mitral valve anterior leaflet displacement from the aortic insufficiency jet and turbulent mixing of antegrade mitral flow and retrograde aortic flow:



Figure 6 Murmurs of the cardiac cycle

Other Murmurs/Sounds
• Patent ductus arteriosus: Is best heard inferior to the left clavicle. It is a continuous murmur in patients with normal pulmonary vascular resistance. As pulmonary vascular resistance increases, the diastolic portion of the murmur attenuates. With equalization of pressures in the systemic and pulmonary circuits, the systolic component of the murmur remains, extends through the second heart sound, and ends in early diastole (See Figure 5).
• Pericardial rub: Is best heard over the 4nd intercostal space of the left lower sternal border. The sound of a rub is often described as “walking through snow,” as this produces a crunching sound (See Figure 5). The rub can be three or two components. The components of the rub are from the atrial kick, ventricular systole and ventricular diastole.



Splitting
• Physiologic splitting: Normal the S1 component closes together and S2 component closes nearly together. The S2 (defined as the aortic valve (A2) and pulmonic valve (P2)) splits upon inspiration. When increased blood flow to the right ventricle causes the pulmonic valve (P2) to delay. When evaluating this murmur, a supine position increases venous return, lengthens right ventricular systole, and thus widens the physiologic splitting of S2. Conversely, a sitting (or standing) position decreases venous return, shortens right ventricular systole, and narrows the physiologic split (See Figure 7A).
• Paradoxical splitting: Indicates an S2 that becomes audibly split only in exhalation, while remaining single in inspiration. The behavior (opposite to the physiologic inspiratory split of normal subjects—hence, the paradox) usually results from a delay in aortic closure (A2), so that A2 now follows the pulmonic valve (P2). Inspiration will narrow their closure from increased right ventricular venous return delaying of P2, whereas exhalation will widen it (See Figure 7B). Some causes of a paradoxical split is left bundle branch block or aortic stenosis.
• Wide splitting: It is a splitting present throughout respiration, albeit still more marked in inspiration. It occurs because of delayed closure of the pulmonic valve (P2) (See Figure 7C). Causes of delayed pulmonic closure are right bundle branch block and pulmonic stenosis.
• Fixed splitting: It an S2 that remains audibly split throughout respiration, both in the supine and upright positions, and with a consistent interval between its two components. Although encountered in severe ventricular failure, a fixed splitting of S2 should suggest a septal defect (most often atrial but occasionally ventricular), especially if associated with pulmonary hypertension. These patients cannot cope with the increased venous return of inspiration by increasing right ventricular stroke volume. Hence, they maintain their S2 widely and persistently split throughout respiration (See Figure 7D). It is very important to know that decompensated heart failure will cause a fixed split of S2. This occurs because the right ventricle fails to respond to the increased volume produced by inspiration and because the lungs are so congested that impedance to forward flow from the right ventricle barely falls during inspiration. This S2 is usually heard over all the precordium because the of loud S2 occurring from elevated pulmonary artery pressures. Whereas the fixed splitting from an atrial septal defect is heard best over the pulmonic area.



Figure 7 Splitting of the heart sounds



Figure 8 Maneuvers for cardiac murmurs