I. Problem/Condition.

Heart murmurs result from disturbed or turbulent blood flow, and can be caused by higher than usual flow, or lower than usual viscosity (e.g., anemia). Murmurs can be present at birth (congenital) or develop later in life. As many as 30-75% of children prior to age 18 have been noted to have a murmur. A heart murmur is a clinical finding, not a disease, but murmurs may indicate an underlying heart problem.

Murmurs can be physiological (functional) or pathological (organic). Functional murmurs, such as venous hum in healthy children or mammary souffle in pregnancy, are caused by high flow. Organic murmurs are caused by structural abnormalities of the heart or circulation, such as a stenotic valve or a communication from one chamber or vessel to another (such as a ventricular septal defect). Recognizing whether a murmur is functional or organic has implications for patient safety for cardiac or non-cardiac surgery, risk of pregnancy to the mother and fetus, necessity for prophylaxis for endocarditis and evaluation of chest pain, dyspnea and syncope.

The ability to distinguish benign from pathologic causes of heart murmurs depends upon examination skills that include noting the location, timing, and character of the murmur (with its intensity a lower priority). Referring all murmurs to echocardiogram or a specialist (cardiologist) for evaluation can needlessly increase expenses, and if not readily available, may unnecessarily delay needed care when the underlying condition is critical.

Continue Reading

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

Differential diagnosis of murmurs is broad. All murmurs are either systolic, diastolic or continuous. Functional systolic murmurs are innocent or physiologic (i.e. related to increased cardiac output, such as anemia, thyrotoxicosis, fever and following exercise). Pathological murmurs may be present at birth (congenital) or develop later in life because of rheumatic fever, coronary heart disease, hypertension, infective endocarditis or aging.

Pathologic systolic murmurs result from valvar stenosis (aortic and pulmonic), valvar regurgitation (mitral and tricuspid) or septal defects (atrial and ventricular). All diastolic murmurs are pathological and result from semilunar valvar incompetence (aortic or pulmonic) or atrioventricular valvar stenosis (i.e. mitral or tricuspid).

Continuous murmurs result from communication between high pressure and low pressure chamber (e.g., congenital heart diseases like patent ductus arteriosus).

B. Describe a diagnostic approach/method to the patient with this problem.

When examining the patient, physician should note seven characteristics of murmur:

  • Timing

  • Shape

  • Intensity

  • Location

  • Radiation

  • Pitch

  • Quality

1.Timing refers to determing whether the murmur is systolic or diastolic or continuous. Once it is clear whether the murmur is systolic or diastolic, it is necessary to classify further whether the murmur is early, mid, late or holo in systole or diastole. Early systolic murmurs are often the result of acute severe mitral regurgitation. Midsystolic murmurs are most often ejection murmurs, resulting from stenosis of the semilunar valves. Late systolic murmurs are most often heard in mitral valve prolapse with mitral regurgitation. Holosystolic murmurs are heard in mitral and tricuspid regurgitation and VSD.

The murmur of hypertrophic cardiomyopathy may be any of these systolic murmurs. Early diastolic murmurs result from semilunar valve regurgitation (pulmonic or aortic regurgitation). Mid-diastolic murmurs are produced most often by stenosis of A-V valves (i.e. tricuspid or mitral stenosis). Late diastolic murmurs are produced by atrial contraction in the presence of tricuspid or mitral stenosis.

2. Shape of the murmur refers to the contour. Crescendo murmurs progressively increase in intensity. Decrescendo murmurs progressively decrease in intensity. Crescendo-decrescendo murmurs have a progressive increase in intensity followed by a progressive decrease in intensity. Plateau murmurs maintain a relatively constant intensity. Systolic ejection murmurs are crescendo-decrescendo while regurgitant/holosystolic murmurs are most often plateau.

3. Intensity of the murmur refers to its loudness and it is directly related to the degree of turbulence. Using the 1-6 grading protocol provides a systematic and consistent method of evaluating intensity of heart murmurs:

Grade 1 is the faintest murmur that is barely heard (after several seconds of listening), under optimal conditions (i.e the room is quiet and the patient is relaxed).

Grade 2 is a soft but readily audible murmur even under noisy conditions.

Grade 3 is a moderately loud murmur, easily heard and prominent. Any murmur of grade 3 intensity should stimulate a careful search for cardiac disease.

Grade 4 is a very loud murmur that is palpable (thrill).

Grade 5 is a murmur heard with stethoscope partly off the chest wall (with thrill).

Grade 6 is a murmur heard with stethoscope completely (5-10 mm) off the chest wall (with thrill).

4. Location of the murmur refers to areas of the chest where murmurs are heard best. The 2nd right intercostal space (2nd RICS) is known as the “aortic area”; the 2nd left intercostal space (2nd LICS) is the “pulmonary area”; the left lower sternal border (LLSB) is the “tricuspid area” and the apex is the “mitral area”. However, this is an oversimplified approach to location of valvar lesions, and there are exceptions in which some valvar lesions can be heard at other listening locations as well. Systematic auscultation to all areas of the chest is imperative to finding the location where murmur is heard best.

5. Radiation refers to the area to which murmurs transmit. Radiation and transmission patters are related to the intensity of the murmur. Loud murmurs transmit widely, while soft ones do not.

6. Pitch refers to the frequency of a heart murmur and can be high, medium or low in frequency. High pitched murmurs usually result from high blood flow and/or large gradients (e.g., murmurs of aortic and mitral regurgitation or pulmonary regurgitation secondary to pulmonary hypertension. Low-pitched murmurs usually result from low blood flow and/or small gradients (e.g., rumbling murmur of mitral stenosis). Very harsh murmurs (e.g., murmurs of aortic valve stenosis) are mixture of high and medium frequencies.

7. Quality refers to the tonal effects of the murmurs. Most frequently used descriptors are blowing, harsh, rumbling, honking, squeaking or musical. Most harsh holosystolic murmurs at the left lower sternal border are VSDs. Most harsh midsystolic murmurs at 2nd right intercostal space are aortic stenosis. Most harsh machine-like continuous murmurs at the high left sternal border are consistent with PDA (patent ductus arteriosus). A rumbling distant subclavicular murmur heard best with standing and disappearing with a change in position is a venous hum.

1. Historical information important in the diagnosis of this problem.

Innocent murmurs do not have any symptoms.

Pathological murmurs might have these symptoms:

  • Cyanosis i.e. blue fingertips and lips

  • Shortness of breath

  • Dyspnea on exertion

  • Decreased exercise tolerance

  • Chest pain

  • Dizziness

  • Syncope/fainting

  • Poor appetite

  • Failure to grow normally (infants and children)

  • Weight gain (adults and children)

  • Elevated neck veins

Risk factors

There are no risk factors for developing innocent heart murmur.

Family history of a heart defect increases the likelihood of developing congential heart disease.

Pregnancy: Having illnesses during pregnancy (uncontrolled diabetes, rubella and other infections) increases the likelihood for developing congenital heart diseases.

Medications and illicit drugs: Taking Class C or D medication during pregnancy or using alcohol or ilicit drugs may contribute in developing congential heart diseases for the fetus.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

1. Respiration: On inspiration, the intrathoracic pressure decreases, pulmonary capacitance increases and ejection time increases. As a result, right heart blood flow is augmented and left heart blood flow is diminished. Accordingly, right-sided murmurs are louder with inspiration while left-sided murmurs are louder with expiration. This finding, also called Carvallo’s maneuver, has been found to have sensitivity of 100% and a specificity of 80-88% in detecting murmurs originating in the right heart. Exception are patients with pulmonary hypertension and severe right sided heart failure who may not demonstrate inspiratory increase in right sided murmurs due to little or no increase in venous return to the right heart with inspiration.

2. Postural changes: When patients move from a recumbent to a sitting or a standing position, systemic venous return is abruptly reduced, left ventricular filling and stroke volume are decreased and this results in an immediate increase in heart rate and systemic vascular resistance. Thus, as the patient goes from a recumbent to a sitting or standing position, intensity of all murmurs originating from the right as well as the left heart decreases, except for those systolic murmurs of hypertrophic cardiomyopathy (HCM) and mitral valve prolapse (MVP).

When patients move from standing to a squatting position, there is an initial large increase in venous return first to the right and then to the left side of the heart. Thus, systolic murmur of HCM frequently dissapears with squatting and becomes quite loud with resumption of the upright position. Right-sided heart murmurs, murmurs of mitral regurgitation, aortic stenosis and regurgitation increase with squatting.

3. Valsalva maneuveris helpful to differentiate right-sided from left-sided systolic murmurs. During strain phase of the Valsalva maneuver, systolic venous return is decreased; as a result, cardiac output and systemic arterial pressure are decreased and heart rate is reflexively, increased. Most murmurs are decreased during the strain phase of the Valsalva except murmurs of hypertrophic cardiomyopathy (HCM) and mitral valve prolapse (MVP).

4. Isometric handgrip for 20-30 secondsincreases cardiac contractility, cardiac output and arterial pressure, without significant change in size of the ventricular chamber. These murmurs are increased with isometric handgrip: murmur of mitral regurgitation, mitral stenosis, aortic regurgitation and ventricular septal defect. Right-sided murmurs and murmurs of aortic stenosis and hypertrophic cardiomyopathy generally are unchanged or decreased during isometric handgrip.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

Ancillary tests are useful in evaluation of murmurs, but should be ordered with an understanding that each test has limitations. CXR and electrocardiogram (ECG) are good screening tools in evaluating murmurs. An echocardiogram is helpful but should not be used as a screening tool.

  • Chest roengenogram (CXR)can confirm cardiac enlargement (atrial or right or left ventricular), demonstrate prominent pulmonary vasculature or increased pulmonary vascularity. Valvar regurgitation usually increases the overall cardiac size. Valvar stenosis may cause little if any cardiac enlargement. Calcification of aortic or mitral valve or annulus can also be seen on the CXR.

  • Electrocardiogram (ECG)can reveal cardiac hypertrophy, atrial or ventricular enlargement, axis deviation, bundle branch blocks or arrythmias. Wolf-Parkinson-White syndrome is seen in patients with Ebstein anomaly. Intra-atrial rentrant tachycardiac is found in patients with tetralogy of Fallot. Atrial fibrilation occurs in patients with mitral stenosis and aortic stenosis and tetralogy of Fallot; Ventricular tachycardia is present in patients with Tetralogy of Fallot and aortic stenosis. Sinus bradycardia can be seen in patients with sinus venosus ASD.

  • Transthoracic echocardiography (TTE)reveals valve function, assesses leaflets and subvalvular apparatus, determines valve area and mean transvalvar gradient, estimates pulmonary artery (PA pressures) and evaluates cardiac wall motion and overall cardiac size adn function. Echo can also reveal etiology of valvar disease (like mitral stenosis or bicuspid aortic stenosis).

  • Transesophageal echocardiography (TEE)is helpful in assessing presence or abscence of clot and severity of valvar lesion (mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation). TEE also better visualizes valves and clarifies underlying pathology. TEE has better sensitivity and specificity for detecting aortic dissection and valvar vegetations (endocarditis) or root abscess. In patients with prosthetic valves, TEE provides better visualization (prosthetic i.e. aortic valve).

  • Exercise echocardiographycan be helpful in clarifying functional capacity in some lesions (mitral stenosis, aortic stenosis). It can also be helpful in patients with aortic stenosis who are asymptomatic or in whom symptoms are unclear.

  • Cardiac catheterizationrecords intracardiac pressures and flow and is almost always combined with cineangiography. Given risks associated with cardiac catheterization, this invasive procedure is almost always reserved for patients who are candidates for valve surgery. In addition, cardiac catheterization is also helpful in determining severity of valvar lesions when clinical and echo assessments are discordant. If patient with moderate aortic stenosis and chest pain (angina), and those undergoing valve replacements, cardiac catheterization is performed to evaluate for coronary artery disease (CAD). Right heart catheterization is helpful in evaluating pulmonary hypertension in patients with chronic severe MR.

  • Nuclear studiesmight be helpful in assessing ejection fraction (EF) in patients with severe MR when TTE is technically difficult and unable to provide adequate assessment of EF.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Most murmurs are innocent (harmless) and do not need treatment. The biggest challenge for a clinician is to distinguish innocent (physiologic, flow, innocent) versus pathologic (i.e. organic) murmur. Since innocent flow murmurs are very common in normal population, physicians have great responsibility to determine whether a murmur is pathologic or not.

There are few criteria that absolutely identify murmur as pathologic:

  • All diastolic murmurs are pathologic

  • All holosystolic and late systolic murmurs are pathologic

  • All continuous murmurs are pathologic

  • Very loud murmurs are usually pathologic

Innocent, functional or flow murmurs are the most common murmurs heard in clinical practice. Those murmurs may result from turbulence created by anxiety, anemia, fever, tachycardia, pregnancy, thyrotoxicosis or exertion. They are best heard along the left sternal border at the 2nd to 4th intercoastal space. They do not radiate into the neck but can be heard throught the precordium. They are usually low or moderate in intensity 1-2/6, crescendo-decrescendo in shape, low to medium in frequency.

I. SYSTOLIC MURMURSare classified as ejection or regurgitant.

IA. Systolic ejection murmursare innocent or pathological.

IA1. Innocent, functional or flow murmurs are the most common murmurs heard in clinical practice. They are best heard along the left sternal border at the 2nd to 4th intercoastal space. They do not radiate into the neck but can be heard throughout the precordium. They are usually low or moderate in intensity 1-2/6, crescendo-decrescendo in shape, low to medium in frequency.

Functional systolic murmurs include pulmonic flow murmurs in patients with either normal or increased pulmonary artery or aortic flow. Functional systolic murmur may also result from hyperdynamic blood flow over a normal pulmonic or aortic valve. Those murmurs may result from turbulence created by anxiety, anemia, fever, tachycardia, pregnancy, thyrotoxicosis, arteriovenous fistula, beri-beri or exertion.

IA2. Pathological or significant systolic ejection murmurs include aortic stenosis, and pulmonic stenosis.

IA2a. Aortic stenosis

IA2b. Pulmonic stenosis

IB. Systolic regurgitant murmursare murmurs of mitral regurgitation, tricuspid valve regurgitation and ventricular septal defect.


IIA. Aortic Regurgitation

IIB. Pulmonary Regurgitation

IIC. Mitral Stenosis

IID.Tricuspid Stenosis


Patent ductus arteriosus





IVD. Eisenmenger syndrome

IVE. Ebstein’s anomaly

IVF. Coarctation of aorta

IVG. Tetralogy of Fallot

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Use of echocardiograms is rising faster than the growth in aging population. Number of echocardiograms ordered increased from 11 million in 1996 to 21 million in 2003 with an estimated annual cost of $16 billion. In practice, echo should aid and not replace bedside physical examination skills.

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Murmur.

Treatment for heart murmurs depends on the cause. Innocent murmurs do not need treatment. Depending on the murmur etiology some patients might need prophylactic antibiotics prior to dental work or some kind of surgery (mitral valve prolpapse), diuretics, vasodilators, anticoagulants for thrombus prevention (mitral stenosis), antiarrhythmic medications, antihypertensive medications, beta-adrenergic blockers to control rapid heart rate. In some patients surgery may be needed to repair a heart defect or to repair or replace a damaged heart valve.

Life Threatening diagnoses

Acute aortic regurgitation: the most common causes of acute regurgitation are bacterial endocarditis, trauma and a dissection of the ascending aorta involving the aortic valve. Since condition is acute, there is no enough time for compensatory mechanisms, i.e. left ventricular dilatation and distensibility to develop. As a result of an increased heart rate, stroke volume may increase minimally but the cardiac output falls. The volume of regurgitant blood causes an extreme elevation of left ventricular diastolic pressure and symptoms of left ventricular failure, i.e. dyspnea, orthopnea and paroxysmal nocturnal dyspnea. These symptoms often develop and progress rapidly to pulmonary edema.

If the etiology of acute aortic regurgitation is infective valve endocarditis, blood cultures should be obtained and antibiotics started as soon as possible. If the patient develops congestive heart failure, diuretics, digitalis and vasodilator therapy should be instituted. If the patient continues to have clinical deterioration, despite medical therapy, the patient needs an urgent valve replacement. Delay in operation in the patient who is deteriorating causes a great mortality. If acute aortic regurgitation is due to trauma or aortic dissection, the patient should first be stabilized medically, and then taken to cardiac catheterized to define the severity of aortic regurgitation and an immediate replacement of the aortic valve is needed.

Acute mitral regurgitation: often leads to pulmonary vascular congestion and pulmonary edema and is a life threatening event. It occurs due to:

  • rupture of papillary muscle

  • rupture of chordae tendineae;

  • acute bacterial endocarditis or

  • trauma.

The patient with acute mitral regurgitation presents with severe dyspnea, orthopnea and proxysmal nocturnal dyspnea. The patient with acute severe mitral regurgitation tolerates the condition poorly and requires initial stabilization wtih inotropic agents, vasodilators (if tolerated) and intraaortic baloon counterpulsation. As soon as the patient is stabilized, he should undergo emergency cardiac catheterization and coronary angiography followed by an emergent valve replacement. If surgery is delayed beyond 12-24 hours, mortality is significantly increased.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

Common pitfalls:

  • Mistaking systolic for diastolic murmur

  • Mistaking diastolic for systolic murmur

  • Calling midsystolic murmur holosystolic

  • Calling holosystolic murmur midsystolic

  • Missing atrial fibrilation in the setting of mitral stenosis

  • Note entry: RRR, no mrg

IV. What's the evidence?

Vukanovic-Criley, JM, Criley, SR, Warde, CM. “Competency in cardiac examination skills in medical students, trainees, physicians, and faculty”. Arch Intern Med. vol. 166. 2006. pp. 610-616.

Criley, JM, Criley, DG, Criley, SR.. “The Physiological Origins of Heart SoundsMurmurs: The Unique Interactive Guide to Cardiac Auscultation”. Blaufuss Mulitmedia. 2009..

Zoneraich, S, Spodick, DH.. “Bedside science reduces laboratory art”. Circulation. vol. 92. 1995. -2762.

Criley, JM, Siegel, RJ.. “New techniques should enhance, not replace, bedside diagnostic skills in cardiology, Part 1”. Mod Concepts Cardiovasc Dis. vol. 59. 1990. pp. 19-24.

Roldan, CA, Shively, BK, Crawford, MH.. ” Value of the cardiovascular physical examination for detecting valvular heart disease in asymptomatic subjects”. Am J Cardiol. vol. 77. 1996. pp. 1327-1331..

Criley, JM, Siegel, RJ. “New techniques should enhance, not replace, bedside diagnostic skills in cardiology, Part 2”. Mod Concepts Cardiovasc Dis. vol. 59. 1990. pp. 25-30.

“Echocardiography or auscultation? How to evaluate systolic murmurs”. Can Fam Physician. vol. 49. 2003. pp. 163-167.