The first-time appearance of a murmur in an adolescent can create a substantial amount of anxiety in the parents and the teenager. The appropriate evaluation and diagnosis is very important in decision-making regarding sports participation in this population. Accurate identification of the innocent murmurs can obviate the need for echocardiography. Identification of a pathologic murmur may reduce morbidity and, possibly, mortality in critical lesions such as hypertrophic cardiomyopathy. This article discusses the physiology and characteristics of different murmurs, and outlines an approach to cardiac murmurs in adolescents.
Key points
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A heart murmur may be innocent without any pathologic significance or may present as the first or only sign of valvular, congenital, or other structural heart diseases.
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Proper evaluation of murmurs along with history and physical examination should help physicians in deciding the need for further referral.
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Referral to a pediatric cardiologist is recommended when a murmur is suspected to be pathologic or when diagnostic uncertainty remains.
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This article discusses physiologic and clinical aspects of innocent and pathologic murmurs and outlines an approach to cardiac murmurs in adolescents.
Introduction
Heart murmurs constitute the most common cause of pediatric cardiology referrals. Most of these murmurs are innocent; less than 1% of murmurs are a result of congenital heart defects in all pediatric age groups. In children and adolescents, as age advances, the number of referrals identifying undiagnosed congenital heart disease decreases. However, the incidence of identifying acquired heart disease, such as mitral valve prolapse (MVP), increases. In certain congenital lesions, such as bicuspid aortic valve, valvular dysfunction may progress as age advances. In a large-scale study involving 17-year-old adolescents, the most prevalent cardiac diagnoses were congenital valvular heart disease; syncope, including neurocardiogenic; MVP; and nonvalvular congenital heart diseases. Therefore, the first-time appearance of a murmur in an adolescent is always a concern. Moreover, finding a murmur creates a substantial amount of anxiety in both parents and teenagers. The appropriate evaluation and diagnosis of a murmur is very important in decision-making regarding sports participation in this population. A vital aspect of cardiovascular examination is an ability to identify different types of murmurs and relate them to other clinical findings. Accurate identification of the innocent murmurs can obviate the need for echocardiography and provide an opportunity to educate and reassure patients and their family. More importantly, identification of a pathologic murmur allows appropriate management in timely fashion and reduces morbidity and, possibly, mortality in critical lesions such as hypertrophic cardiomyopathy (HCM). This article discusses the physiology and characteristics of murmurs, and outlines an approach to cardiac murmurs in adolescents.
What is a murmur?
An organized movement of molecules in a medium caused by a vibrating body is defined as a sound. Murmurs are the sounds produced by the vibrations caused by turbulence of the blood flow in the heart. The most comprehensive mechanism of murmur origin is the direct impact of the jet-producing vibration. Several other mechanisms have been proposed as producing vessel vibrations, such as vibrations from Bernoulli effect, eddy currents, and bubbles of vapor. The amount of turbulence-causing vibrations and, hence, the intensity of the murmur depends on blood volume and pressure differences (which determine blood flow velocity) across the site, in addition to the size of the orifice.
Cardiac cycle
The classification of heart murmurs is based on their timing. Therefore, knowledge of the timing of the events in the cardiac cycle is crucial for a better understanding of various murmurs. Fig. 1 shows the phases of the cardiac cycle and its relationship with heart sounds. The relationship of pressure and blood volume between chambers and/or arteries determines characteristic heart sounds and murmurs. Systole is comprised of isovolumetric contraction, rapid ejection, and reduced ejection phases; whereas diastole includes isovolumetric relaxation, early filling (rapid filling), and reduced filling followed by atrial contraction.
Atrial Contraction
The atria contract during the terminal period of diastole. This atrial systole augments ventricular filling just before the onset of the next ventricular contraction.
Isovolumetric Contraction
As ventricular muscle contracts, ventricular pressure increases rapidly, accompanied by closure of the atrioventricular (AV) valves, producing the first heart sound (S1). Clinically, S1 denotes the beginning of systole. During this short period of isovolumic contraction, pressure builds within the ventricle without change in the ventricular volume.
Rapid Ejection Phase
The rapid ejection phase begins with the opening of semilunar valves. During this period, the ventricles eject blood into the aorta and pulmonary artery. Approximately two-thirds of the blood in the ventricles is ejected during the rapid ejection phase.
Reduced Ejection Phase
During the reduced ejection phase, a lesser volume is pumped out of the ventricles. As ventricular contraction ceases, pressure drops in the ventricles leading to closure of the semilunar valves producing the second heart sound (S2). Clinically, S2 denotes the end of systole.
Isovolumetric Relaxation
During isovolumetric relaxation, pressure decreases rapidly in the ventricles without a change in the volume. When the ventricular pressure drops below the atrial pressure, the AV valves open, ending the isovolumetric relaxation phase.
Rapid Filling Phase
The rapid inflow phase occurs immediately after the opening of the AV valves. The blood accumulated in the atria during systole rushes into the ventricles. Most ventricular filling occurs during this phase.
Reduced Filling Phase
During the reduced filling phase, venous blood returning from the body continues to flow through the atria into the ventricles at a slower rate.
Characteristics of murmur
Each murmur should be determined and described based on the characteristics listed later. It is crucial to identify these characteristics for proper diagnosis of murmurs.
Timing and Duration
Murmurs are classified based on their timing in relation to cardiac cycle (ie, systole or diastole). Duration is the length of a murmur from beginning to end. Compared with infants and young children, timings and duration can be defined more precisely in adolescents due to their slower heart rate and better cooperation.
Intensity
Intensity is graded with the Levine grading system :
Grade I: very faint, heard with intense concentration, may not be heard in all positions
Grade II: faint, but heard immediately and in all positions
Grade III: intermediate intensity, easily heard
Grade IV: loud, with a palpable thrill (murmurs with a thrill are always abnormal)
Grade V: very loud, heard with stethoscope partly off the chest, with a palpable thrill
Grade VI: loudest, heard with stethoscope just above the precordium completely off the chest, with a palpable thrill.
Of note, murmurs of grades IV to VI have a palpable thrill.
Location
In classic auscultation, the precordium is divided into four areas : (1) mitral, located at the cardiac apex in the fifth intercostal space (ICS) along the midclavicular line; (2) tricuspid, located in the left fourth or fifth ICS along the left sternal border; (3) pulmonary, located in the left second ICS near the left sternal border; and (4) aortic, located in the right second ICS along the right sternal border. In addition to these areas, auscultation of the precordium in between these areas is very important to avoid missing pathologic murmurs. For example, the murmur of a small, muscular ventricular septal defect may be heard best in between pulmonary and tricuspid areas. Similarly, the murmur of a coronary fistulae is heard best at the lower right sternal border. In dextrocardia, heart sounds and murmurs are better heard over the right precordium. After auscultating the entire precordium, an area with the highest intensity of murmur should be identified carefully to localize the origin of a murmur. Loud murmurs may be heard in multiple areas. However, the “location” of a murmur describes the area where it is the loudest.
Configuration
The descriptor “configuration” indicates a change in the murmur intensity during different phases of cardiac cycle. Various configurations of murmurs include
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Crescendo: increasing intensity from beginning to end
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Decrescendo: decreasing intensity from beginning to end
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Crescendo-decrescendo: increasing and then decreasing intensity
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Decrescendo-crescendo: decreasing and then increasing intensity
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Plateau: constant intensity.
Quality
The tonal qualities of murmurs often have somewhat subjective descriptions, which may be characterized as harsh, blowing, or musical. In general, a blowing quality is thought to be specific for regurgitant murmurs.
Pitch
The pitch can be low, medium, or high. Pitch often reflects the pressure gradient across the site of murmur origin, with higher pitches usually corresponding to higher gradients.
Quality and pitch are often combined when describing murmurs.
Radiation
Murmurs usually radiate in the direction of the blood flow. Additional areas should be auscultated for complete evaluation of murmurs. The typical areas for describing radiation are the back or the neck. For example, in mitral regurgitation, the murmur radiates to axilla; murmurs from the pulmonary valve or arteries radiate to the back; and murmurs from aortic valve and left ventricle radiate to the neck.
Murmur classification
Murmurs are classified into two major categories based on their timing: systolic and diastolic. Fig. 2 is a schematic presentation of various murmurs. Murmurs may be pathologic or innocent based on their cause. Common pathologic murmurs produced by various congenital and acquired heart diseases presenting in teenage are summarized in Box 1 . See later discussion on innocent murmurs.
Systolic murmurs
Holosystolic (pansystolic)
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Mitral regurgitation (MR)
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Congenital: cleft mitral valve, postsurgical (after AV canal defect repair)
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Acquired: rheumatic carditis, Infective endocarditis, Kawasaki disease
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Functional: left ventricular dysfunction, annular dilatation
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Tricuspid regurgitation (TR)
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Congenital: Ebstein anomaly, congenitally corrected transposition of great arteries
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Acquired: infective endocarditis, trauma
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Functional: Eisenmenger syndrome, pulmonary hypertension, annular dilatation
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Left-to-right shunt from ventricular septal defect (VSD)
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Early systolic
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Most likely from small muscular VSD in adolescents
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Ejection systolic (midsystolic)
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Aortic
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Obstructive
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Congenital-bicuspid aortic valve, congenitally dysplastic aortic valve, supravalvular aortic stenosis, coarctation of the aorta
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Acquired-discrete, tunnel-type subaortic membrane, hypertrophic cardiomyopathy, rheumatic heart disease
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Increased flow
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Severe aortic regurgitation (AR)
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Large patent ductus arteriosus (PDA), systemic arteriovenous malformation
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Complete heart block
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Hyperkinetic state
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Pulmonary
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Obstructive
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Congenital-pulmonic valve stenosis, pulmonary artery stenosis, branch stenosis, double chamber right ventricle in presence of membranous VSD
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Functional-compression in pectus excavatum, kyphoscoliosis
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Increased flow
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Atrial septal defect (ASD)
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Anomalous pulmonary venous return
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Severe pulmonary regurgitation
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Hyperkinetic state
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Midsystolic to late systolic
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Mitral-MVP, HCM
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Tricuspid-tricuspid valve prolapse
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Diastolic murmurs
Early diastolic
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AR—high-pitched due to higher difference between aortic and left ventricular diastolic pressures
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Congenital: bicuspid valve, after valvuloplasty, after Ross procedure, aortic cusp prolapse in presence of membranous VSD and subaortic membrane
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Acquired: rheumatic, infective endocarditis
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Functional: dilation of annulus—Marfan syndrome, connective tissue disease
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Pulmonic regurgitation—medium to low pitch due to lower difference between pulmonary artery and right ventricular diastolic pressure
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Congenital; after valvulotomy, after valvuloplasty, after transannular patch in tetralogy of Fallot
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Acquired: endocarditis, rheumatic heart disease, carcinoid
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Functional: dilatation of annulus—Marfan syndrome, connective tissue disease
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Mid-diastolic
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Mitral
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Mitral stenosis
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Congenital: dysplastic mitral valve, parachute mitral valve
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Acquired: rheumatic heart disease
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Functional: left atrial myxoma
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Carey Coombs murmur (mid-diastolic apical murmur in acute rheumatic fever)
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Increased flow across nonstenotic mitral valve (eg, MR, VSD, PDA, high-output states, complete heart block)
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Severe or eccentric AR (Austin Flint murmur)
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Tricuspid
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Tricuspid stenosis—congenital after repair
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Increased flow across nonstenotic tricuspid valve (eg, TR, ASD, and anomalous pulmonary venous return)
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Right atrial myxoma
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Late diastolic
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Presystolic accentuation of true mitral stenosis murmur
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Continuous murmurs
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Arterial:
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Aortopulmonary shunts such as PDA, surgical shunts, aortopulmonary window
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Arteriovenous fistula, coronary fistula
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Ruptured sinus of Valsalva aneurysm
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Turbulent flow in arteries
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Anomalous left coronary artery
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Proximal coronary artery stenosis
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Coarctation of aorta
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Severe branch pulmonary artery stenosis
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Bronchial collateral circulation
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Venous:
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Turbulent flow in veins—obstructed total anomalous pulmonary venous return
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