Definitions

continuous murmur

Heart murmur

Murmurs are abnormal heart sounds that are produced as a result of turbulent blood flow which is sufficient to produce audible noise. This most commonly results from narrowing or leaking of valves or the presence of abnormal passages through which blood flows in or near the heart. Murmurs are not usually part of the normal cardiac physiology and thus warrant further investigations. However, they sometimes result from harmless flow characteristics of no clinical significance.

Murmurs can be classified by seven different characteristics: timing, shape, location, radiation, intensity, pitch and quality. Timing refers to whether the murmur is a systolic or diastolic murmur. Shape refers to the intensity over time; murmurs can be crescendo, decrescendo or crescendo-decrescendo. Location refers to where the heart murmur is auscultated best. There are 6 places on the anterior chest to listen for heart murmurs; the first five out of six are adjacent to the sternum. Each of these locations roughly correspond to a specific part of the heart. The locations are: 2nd right intercostal space, 2nd - 5th left intercostal spaces, and 5th mid-clavicular intercostal space. Radiation refers to where the sound of the murmur radiates. The general rule of thumb is that the sound radiates in the direction of the blood flow. Intensity refers to the loudness of the murmur, and is graded on a scale from 0-6/6. The pitch of a murmur is low, medium or high and is determined by whether it can be auscultated best with the bell or diaphragm of a stethoscope. Some examples of the quality of a murmur are: blowing, harsh, rumbling and musical.

For this article, heart murmurs will be primarily organized by timing.

Systolic murmurs

Mid-systolic ejection murmurs

Mid-systolic ejection murmurs are due to blood flow through the semilunar valves. They occur at the start of blood ejection — which starts after S1 — and ends with the cessation of the blood flow — which is before S2.* Therefore, the onset of a midsystolic ejection murmur is separated from S1 by the isovolumic contraction phase; the cessation of the murmur and the S2 interval is the aortic or pulmonary hangout time. The resultant configuration of this murmur is a crescendo-decrescendo murmur. Causes of midsystolic ejection murmurs include outflow obstruction, increased flow through normal semilunar valves, dilation of aortic root or pulmonary trunk, or structural changes in the semilunar valves without obstruction.

  • Aortic outflow obstruction. Can be due to aortic valve stenosis or hypertrophic cardiomyopathy (HCM), with a harsh and rough quality.
    • Valvular aortic stenosis can produce a harsh, or even a musical murmur over the right second intercostal space which radiates into the neck over the two carotid arteries. The most common cause of AS (Aortic Stenosis) is calcified valves due to aging followed by congenital bicuspid aortic valves (normal valve is tricuspid). The distinguishing feature between these two causes is that bicuspid AS has little or no radiation. It can be confirmed if it also has an aortic ejection sound, a short early diastolic murmur, and normal carotid pulse. The murmur in valvular AS decreases with standing and straining with Valsalva maneuver.
    • Supravalvular aortic stenosis is loudest at a point slightly higher than in that of valvular AS and may radiate more to the right carotid artery.
    • Subvalvular aortic stenosis is usually due to hypertrophic cardiomyopathy (HCM), with murmur loudest over the left sternal border or the apex. The murmur in HCM increases in intensity with a standing position as well as straining with Valsalva maneuver.
  • Pulmonic outflow obstruction. A harsh murmur usually on left second intercostal space radiating to left neck and accompanied by palpable thrill. It can be distinguished from a VSD (Ventricular septal defect) by listening to the S2, which is normal in VSD but it is widely split in pulmonary stenosis. However, VSD is almost always pansystolic where the murmur of pulmonary stenosis is diamond-shaped and ends clearly before S2. Many innocent murmurs also arise from this location but S1 and S2 must split normally.
  • Dilation of aortic root or pulmonary artery. Produces an ejection sound, with a short ejection systolic murmur and a relatively wide split S2. There is no hemodynamic abnormality. This is similar to pulmonary hypertension except the latter has hemodynamic instabilities.
  • Increased semilunar blood flow. This can occur in situations such as anemia, pregnancy, or hyperthyroidism.
  • Aortic valve sclerosis. This is due to degenerative thickening of the roots of the aortic cusps but produces no obstruction and no hemodynamic instability and thus should be differentiated from aortic stenosis. It is heard over right second intercostal space with a normal carotid pulse and normal S2.
  • Innocent midsystolic murmurs. These murmurs are not accompanied by other abnormal findings. One example of a benign paediatric heart murmur is Still's murmur in children.

Late systolic murmurs

Late systolic murmurs starts after S1 and, if left sided, extends up to S2, usually in a crescendo manner. Causes include mitral valve prolapse, tricuspid valve prolapse and papillary muscle dysfunction.

  • Mitral valve prolapse. This is the most common cause of late systolic murmurs. It can be heard best over the apex of the heart, usually preceded by clicks. The most common cause of mitral valve prolapse is "floppy" valve (Barlow's) syndrome. If the prolapse becomes severe enough, mitral regurgitation may occur. Any maneuver that decreases left ventricular volume — such as standing, sitting, Valsalva maneuver, and amyl nitrate inhalation — can produce earlier onset of clicks, longer murmur duration, and decreased murmur intensity. Any maneuver that increases left ventricular volume — such as squatting, elevation of legs, hand grip, and phenylephrine — can delay the onset of clicks, shorten murmur duration, and increase murmur intensity.
  • Tricuspid valve prolapse. Uncommon without concomitant mitral valve prolapse. Best heard over left lower sternal border.
  • Papillary muscle dysfunction. Usually due to acute myocardial infarction or ischemia, which causes mild mitral regurgitation.

Holosystolic (pansystolic) murmurs

Usually due to regurgitation in cases such as mitral regurgitation, tricuspid regurgitation, or ventricular septal defect (VSD). These murmurs start at S1 and extends up to S2.

  • Mitral regurgitation. In the presence of incompetent mitral valve, the pressure in the L ventricle becomes greater than that in the L atrium at the onset of isovolumic contraction, which corresponds to the closing of the mitral valve (S1). This explains why the murmur in MR starts at the same time as S1. This difference in pressure extends throughout systole and can even continue after the aortic valve has closed, explaining how it can sometimes drown the sound of S2. The murmur in MR is high pitched and best heard at the apex with diaphragm of the stethoscope with patient in the lateral decubitus position. Left ventricular function can be assessed by determining the apical impulse. A normal or hyperdynamic apical impulse suggests good ejection fraction and primary MR. A displaced and sustained apical impulse suggests decreased ejection fraction and chronic and severe MR.
  • Tricuspid insufficiency. Can be best heard over the fourth left sternal border. The intensity can be accentuated following inspiration (Carvallo's sign) due to increased regurgitant flow in right ventricular volume. Tricuspid regurgitation is most often secondary to pulmonary hypertension. Primary tricuspid regurgitation is less common and can be due to bacterial endocarditis following IV drug use, Ebstein's anomaly, carcinoid disease, or prior right ventricular infarction.
  • Ventricular septal defect. VSD is a defect in the ventricular wall, producing a shunt between the left and right ventricles. Since the L ventricle has a higher pressure than the R ventricle, flow during systole occurs from the L to R ventricle, producing the holosystolic murmur. It can be best heard over the left third and fourth intercostal spaces and along the sternal border. It is associated with nomal pulmonary artery pressure and thus S2 is normal. This fact can be used to distinguish from pulmonary stenosis, which has a wide splitting S2. When the shunt becomes reversed ("Eisenmenger syndrome"), the murmur may be absent and S2 can become markedly accentuated and single.

Diastolic murmurs

Diastolic murmurs start at or after S2 and ends before or at S1.

Early diastolic murmurs

They start at the same time as S2 with the close of the semilunar valves and typically ends before S1. Common causes include aortic or pulmonary regurgitation and left anterior descending artery stenosis.

Aortic regurgitation. The murmur is low intensity, high-pitched, best heard over the left sternal border or over the right second intercostal space, especially if the patient leans forward and holds breath in full expiration. The radiation is typically toward the apex. The configuration is usually decrescendo and has a blowing character. The presence of this murmur is a good positive predictor for AR and the absence of this murmur strongly suggests the absence of AR. An Austin Flint murmur is usually associated with significant aortic regurgitation.

Pulmonary regurgitation. Pulmonary regurgitation is most commonly due to pulmonary hypertension (Graham-Steell murmur). It is a high-pitched and blowing murmur with a decrescendo configuration. It may increase in intensity during inspiration and best heard over left second and third intercostal spaces. The murmur usually does not extend to S1.

Left anterior descending artery stenosis. This murmur, also known as Dock's murmur, is similar to that of aortic regurgitation and is heard at the left second or third intercostal space. A Coronary artery bypass surgery can eliminate the murmur.

Mid-diastolic murmurs

These murmurs start after S2 and end before S1. They are due to turbulent flow across the atrioventricular valves during the rapid filling phase from mitral or tricuspid stenosis.

Mitral stenosis. This murmur has a rumbling character and is best heard with the bell of the stethoscope in the left ventricular impulse area with the patient in the lateral decubitus position. It usually starts with an opening snap. In general, the longer the duration, the more severe the mitral stenosis. However, this rule can be misleading in situations where the stenosis is so severe that the flow becomes reduced, or during high-output situations such as pregnancy where a less severe stenosis may still produce a strong murmur.

Tricuspid stenosis. Best heard over the left sternal border with rumbling character and tricuspid opening snap with wide splitting S1. May increase in intensity with inspiration (Carvallo's sign). Tricuspid stenosis often occurs in association with mitral stenosis. Isolated TS are often associated with carcinoid disease and right atrial myxoma.

Atrial myxoma. Atrial myxomas are benign tumors of the heart. Left myxomas are far more common than right myxomas and those may cause obstruction of the mitral valve producing a mid-diastolic murmur similar to that of mitral stenosis. An echocardiographic evaluation is necessary.

Increased flow across the atrioventricular valve. This can also produce a mid-diastolic murmur, such as in severe mitral regurgitation where a large regurgitant volume in the left atrium can lead to "functional mitral stenosis."

Austin Flint murmur. An apical diastolic rumbling murmur in patients with pure aortic regurgitation. This can be mistaken with the murmur in mitral stenosis and should be noted by the fact that an Austin Flint murmur does not have an opening snap that is found in mitral stenosis.

Carey-Coombs murmur. A mid-diastolic murmur over the left ventricular impulse due to mitral valvulitis from acute rheumatic fever.

Late diastolic (presystolic) murmurs

These murmurs start after S2 and extends up to S1 and have a crescendo configuration. They include mitral stenosis, tricupsid stenosis, myxoma, and complete heart block.

Complete heart block. A short late diastolic murmur can occasionally be heard (Rytand's murmur).

Continuous murmurs

These murmurs are due to blood flow from a high pressure chamber or vessel to a lower pressure system.

Patent ductus arteriosus. PDA is an abnormal connection between the aorta and the pulmonary artery, which normally should be closed in infancy. Since aortic pressure is higher than pulmonary pressure, a continuous murmur occurs, which is often described as a machinery murmur, or Gibson's murmur.

Aortopulmonary window.

shunts. Usually a left to right shunt through a small atrial septal defect in the presence of mitral valve obstruction.

Gradations of Murmurs

Gradations of Murmurs
Grade Description
Grade 1 Very faint, heard only after listener has "tuned in"; may not be heard in all positions.
Grade 2 Quiet, but heard immediately after placing the stethoscope on the chest.
Grade 3 Moderately loud.
Grade 4 Loud, with palpable thrill (ie, a tremor or vibration felt on palpation)
Grade 5 Very loud, with thrill. May be heard when stethoscope is partly off the chest.
Grade 6 Very loud, with thrill. May be heard with stethoscope entirely off the chest.

Interventions that change murmur sounds

  • inspiration will increase the amount of blood filling into the right ventricle, thereby prolonging ejection time. This will affect the closure of the pulmonary valve. This finding, also called Carvallo's Maneuver has been found by studies to have a sensitivity of 100% and a specificity of 80% to 88% in detecting murmurs originating in the right heart .
  • abrupt standing
  • squatting
  • valsalva maneuver. One study found the valsalva maneuver to have a sensitivity of 65%, specificity of 96% in detecting Hypertrophic obstructive cardiomyopathy (HOCM) .
  • hand grip
  • post ectopic potentiation
  • amyl nitrite
  • methoxamine
  • positioning of the patient. ie. positioning patients in the left lateral position will allow a murmur in the mitral area to be more pronounced.

See also

References

External links

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