CARDIAC CYCLE

HEART SOUNDSFirst Heart Sound (S1)Second Heart Sound (S2)Extra Systolic Heart SoundsExtra Diastolic Heart Sounds

MURMURSSystolic MurmursDiastolic MurmursContinuous Murmurs

29

C H A P T E R

2The Cardiac Cycle:Mechanisms of HeartSounds and MurmursNicole MartinLeonard S. Lilly

Cardiac diseases often cause abnormal findings on physical examination, includ-ing pathologic heart sounds and murmurs.These findings are clues to the underlyingpathophysiology, and proper interpreta-tion is essential for successful diagnosis and disease management. This chapter de-scribes heart sounds in the context of thenormal cardiac cycle and then focuses onthe origins of pathologic heart sounds andmurmurs.

Many cardiac diseases are mentionedbriefly in this chapter as examples of abnor-mal heart sounds and murmurs. Becauseeach of these conditions is described ingreater detail later in the book, it is not nec-essary to memorize the examples presentedhere. Rather, it is preferable to understandthe mechanisms by which the abnormalsounds are produced, so that their descrip-tions will make sense in later chapters.

CARDIAC CYCLE

The cardiac cycle consists of precisely timedelectrical and mechanical events that are re-sponsible for rhythmic atrial and ventricu-lar contractions. Figure 2.1 displays the pres-sure relationships between the left-sidedcardiac chambers during the normal cardiaccycle and serves as a platform for describingkey events. Mechanical systole refers to ven-tricular contraction, and diastole to ven-tricular relaxation and filling. Throughoutthe cardiac cycle, the right and left atria accept blood returning to the heart from the systemic veins and from the pulmonaryveins, respectively. During diastole, bloodpasses from the atria into the ventriclesacross the open tricuspid and mitral valves,causing a gradual increase in ventricular di-astolic pressures. In late diastole, atrial con-traction propels a final bolus of blood into

Fig. 1

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each ventricle, an action that produces abrief further rise in atrial and ventricle pres-sures, termed the a wave (see Fig. 2.1).

Contraction of the ventricles follows, sig-naling the onset of mechanical systole. Asthe ventricles start to contract, the pressureswithin them rapidly exceed atrial pressures.This results in the forced closure of the tri-cuspid and mitral valves, which producesthe first heart sound, termed S1. This soundhas two nearly superimposed components:

the mitral component slightly precedes thatof the tricuspid valve because of the earlierelectrical stimulation of left ventricular con-traction (see Chapter 4).

As the right and left ventricular pressuresrapidly rise further, they soon exceed the diastolic pressures within the pulmonaryartery and aorta, forcing the pulmonic andaortic valves to open, and blood is ejectedinto the pulmonary and systemic circula-tions. The ventricular pressures continue toincrease during contraction, and because thepulmonic and aortic valves are open, the aor-tic and pulmonary artery pressures rise, par-allel to those of the corresponding ventricles.

At the conclusion of ventricular ejection,the ventricular pressures fall below those ofthe pulmonary artery and aorta (the pul-monary artery and aorta are elastic struc-tures that maintain their pressures longer),such that the pulmonic and aortic valves areforced to close, producing the second heartsound, S2. Like the first heart sound (S1), thissound consists of two parts: the aortic (A2)component normally precedes the pulmonic(P2) because the diastolic pressure gradientbetween the aorta and left ventricle isgreater than that between the pulmonaryartery and right ventricle, forcing the aorticvalve to shut more readily. The ventricularpressures fall rapidly during the subsequentrelaxation phase. As they drop below thepressures in the right and left atria, the tri-cuspid and mitral valves open, followed bydiastolic ventricular filling and repetition ofthis cycle.

Notice in Figure 2.1 that in addition tothe a wave, the atrial pressure curve displaystwo other positive deflections during thecardiac cycle: The c wave represents a smallrise in atrial pressure as the tricuspid and mi-tral valves close and bulge into their respec-tive atria. The v wave is the result of passivefilling of the atria from the systemic andpulmonary veins during systole, a periodduring which blood accumulates in the atriabecause the tricuspid and mitral valves areclosed.

At the bedside, systole can be approxi-mated by the period from S1 to S2, and dias-tole from S2 to the next S1. Although the du-

30 Chapter Two

Figure 2.1. The normal cardiac cycle, showing pres-sure relationships between the left-sided heartchambers. During diastole, the mitral valve (MV) isopen, so that the left atrial (LA) and left ventricular (LV)pressures are equal. In late diastole, LA contractioncauses a small rise in pressure in both the LA and LV (thea wave). During systolic contraction, the LV pressurerises; when it exceeds the LA pressure, the MV closes,contributing to the first heart sound (S1). As LV pressurerises above the aortic pressure, the aortic valve (AV)opens, which is a silent event. As the ventricle begins torelax and its pressure falls below that of the aorta, theAV closes, contributing to the second heart sound (S2).As LV pressure falls further, below that of the LA, theMV opens, which is silent in the normal heart. In addi-tion to the a wave, the LA pressure curve displays twopositive deflections: the c wave represents a small rise inLA pressure as the MV closes and bulges toward theatrium, and the v wave is the result of passive filling ofthe LA from the pulmonary veins during systole, whenthe MV is closed.

AV opens

Pre

ssur

e (m

m H

g)

MV opens

AV closes

MV closes

DIASTOLE DIASTOLESYSTOLE

a c v

Time

S1 S2

LV

ECG

100

50

LA

Aorta

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 31

ration of systole remains constant from beatto beat, the length of diastole varies with theheart rate: the faster the heart rate, the shorterthe diastolic phase. The main sounds, S1 andS2, provide a framework from which all otherheart sounds and murmurs can be timed.

The pressure relationships and events de-picted in Figure 2.1 are those that occur in

the left side of the heart. Equivalent eventsoccur simultaneously in the right side of theheart in the right atrium, right ventricle,and pulmonary artery. At the bedside, cluesto right-heart function can be ascertained byexamining the jugular venous pulse, whichis representative of the right atrial pressure(see Box 2.1).

Box 2.1 Jugular Venous Pulsations and Assessment of Right-Heart Function

Bedside observation of jugular venous pulsations in the neck is a vital part of the car-diovascular examination. With no structures impeding blood flow between the internaljugular (IJ) veins and the superior vena cava and right atrium (RA), the height of the IJvenous column (termed the jugular venous pressure, or JVP) is an accurate representa-tion of the RA pressure. Thus, the JVP provides an easily obtainable measure of right-heart function.

Typical fluctuations in the jugular ve-nous pulse during the cardiac cycle, man-ifested by oscillations in the overlyingskin, are shown in the figure (notice thesimilarity to the left atrial pressure tracingin Fig. 2.1). There are two major upwardcomponents, the a and v waves, fol-lowed by two descents, termed x and y.The x descent, which represents the pressure decline following the a wave, may be inter-rupted by a small upward deflection (the c wave, denoted in the figure by the arrow) atthe time of tricuspid valve closure, but that is usually not distinguishable in the JVP. The awave represents transient venous distension caused by back pressure from RA contrac-tion. The v wave corresponds to passive filling of the RA from the systemic veins duringsystole, when the tricuspid valve is closed. Opening of the tricuspid valve in early diastoleallows blood to rapidly empty from the RA into the right ventricle; that fall in RA pressurecorresponds to the y descent.

Conditions that abnormally raise right-sided cardiac pressures (e.g., heart failure, tri-cuspid valve disease, pulmonic stenosis, pericardial diseases) elevate the JVP, while re-duced intravascular volume (e.g., dehydration) decreases it. In addition, specific diseasestates can influence the individual components of the JVP, examples of which are listedhere for reference and explained in subsequent chapters:

Prominent a: right ventricular hypertrophy, tricuspid stenosisProminent v: tricuspid regurgitationProminent y: constrictive pericarditis

Technique of Measurement

The JVP is measured as the maximum vertical height of the internal jugular vein (in cm)above the center of the right atrium, and in a normal person is ≤9 cm. Because the ster-nal angle is located approximately 5 cm above the center of the RA, the JVP is calculated

a

x

v

y

Box 1

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32 Chapter Two

at the bedside by adding 5 cm to the vertical height of the top of the IJ venous columnabove the sternal angle.

The right IJ vein is usually the easiest to evaluate because it extends directly upwardfrom the RA and superior vena cava. First, observe the pulsations in the skin overlying theIJ with the patient supine and the head of the bed at about a 45° angle. Shining a lightobliquely across the neck helps to visualize the pulsations. Be sure to examine the IJ, notthe external jugular vein. The former is medial to, or behind, the sternocleidomastoid mus-cle, while the external jugular is usually more lateral. Although the external jugular is typ-ically easier to see, it does not accurately reflect RA pressure because it contains valves thatinterfere with venous return to the heart.

If the top of the IJ column is not visible at 45°, the column of blood is either too low(below the clavicle) or too high (above the jaw) to be measured in that position. In suchsituations, the head of the bed must be lowered or raised, respectively, so that the top ofthe column becomes visible. As long as the top can be ascertained, the vertical height of the JVP above the sternal angle will accurately reflect RA pressure, no matter the angleof the head of the bed.

Sometimes it can be difficult to distinguish the jugular venous pulsations from theneighboring carotid artery. Unlike the carotid, the JVP is usually not palpable, it has a dou-ble rather than a single upstroke, and it declines in most patients by assuming the seatedposition or during inspiration.

HEART SOUNDS

Typical stethoscopes contain two chest piecesfor auscultation of the heart. The concave“bell” chest piece, meant to be applied lightlyto the skin, accentuates low-frequency sounds.Conversely, the flat “diaphragm” chest pieceshould be pressed firmly against the skin toeliminate low frequencies and therefore ac-centuate high-frequency sounds and mur-murs. Some modern stethoscopes incorpo-rate both the bell and diaphragm functionsinto a single chest piece; in these models,placing the piece lightly on the skin bringsout the low-frequency sounds, while firmpressure accentuates the high-frequencyones.

First Heart Sound (S1)

S1 is produced by closure of the mitral andtricuspid valves in early systole and is loud-est near the apex of the heart (Fig. 2.2). It isa high-frequency sound, best heard with thediaphragm of the stethoscope. Although mitral closure usually precedes tricuspid closure, they are separated by only about0.01 sec, such that the human ear appreci-

ates only a single sound. An exception oc-curs in patients with right bundle branchblock (see Chapter 4), in whom these com-ponents may be audibly split because of de-layed closure of the tricuspid valve.

Three factors determine the intensity of S1:(1) the distance separating the leaflets of theopen valves at the onset of ventricular con-traction; (2) the mobility of the leaflets (nor-mal, or rigid because of stenosis); and (3) therate of rise of ventricular pressure (Table 2.1).

Figure 2.2. Standard positions of stethoscope place-ment for cardiac auscultation.

Fig. 2

Tab. 1

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 33

The distance between the open valve leaf-lets at the onset of ventricular contractionrelates to the electrocardiographic PR inter-val (see Chapter 4), the period between theonset of atrial and ventricular activation.Atrial contraction at the end of diastoleforces the tricuspid and mitral valve leafletsapart. As they start to drift back together,ventricular contraction forces them shut,from whatever position they are at, as soonas the ventricular pressure exceeds that inthe atrium. An accentuated S1 results whenthe PR interval is shorter than normal be-cause the valve leaflets do not have suffi-cient time to drift back together and aretherefore forced shut from a relatively widedistance.

Similarly, in mild mitral stenosis (seeChapter 8) a prolonged diastolic pressuregradient exists between the left atrium andventricle, which keeps the mobile portionsof the mitral leaflets farther apart than nor-mal during diastole. Because the leaflets arerelatively wide apart at the onset of systole,they are forced shut loudly when the leftventricle contracts.

S1 also may be accentuated when theheart rate is more rapid than normal (i.e.,tachycardia) because diastole is shortenedand the leaflets have insufficient time to driftback together before the ventricles contract.

Conditions that reduce the intensity of S1

are also listed in Table 2.1. In first-degreeatrioventricular (AV) block (see Chapter 12),

a diminished S1 results from an abnormallyprolonged PR interval, which delays theonset of ventricular contraction. Followingatrial contraction, the mitral and tricuspidvalves have additional time to float back to-gether so that the leaflets are forced closedfrom only a small distance apart.

In patients with mitral regurgitation (seeChapter 8), S1 is often diminished in inten-sity because the mitral leaflets may not comeinto full contact with one another as theyclose. In severe mitral stenosis, the leaflets arenearly fixed in position throughout the car-diac cycle, and that reduced movementlessens the intensity of S1.

In patients with a “stiffened” left ventri-cle (e.g., a hypertrophied chamber), atrialcontraction results in a higher-than-normalpressure at the end of diastole. This greaterpressure causes the mitral leaflets to drift to-gether more rapidly, forcing them closedfrom a smaller-than-normal distance whenventricular contraction begins and thus re-ducing the intensity of S1.

Second Heart Sound (S2)

The second heart sound results from the clo-sure of the aortic and pulmonic valves andtherefore has aortic (A2) and pulmonic (P2)components. Unlike S1, which is usuallyheard as a single sound, the components ofS2 vary with the respiratory cycle: they arenormally fused as one sound during expira-tion but become audibly separated duringinspiration, a situation termed normal orphysiologic splitting (Fig. 2.3).

One explanation for normal splitting ofS2 is as follows. Expansion of the chest dur-ing inspiration causes the intrathoracic pres-sure to become more negative. The negativepressure transiently increases the capaci-tance (and reduces the impedance) of the in-trathoracic pulmonary vessels. As a result,there is a temporary delay in the diastolic“back pressure” of the pulmonary artery re-sponsible for closure of the pulmonic valve.Thus, P2 is delayed; that is, it occurs laterduring inspiration than during expiration.

Inspiration has the opposite effect on A2.Because the capacity of the intrathoracic

TABLE 2.1. Causes of Altered Intensity of FirstHeart Sound (S1)

Accentuated S1

1. Shortened PR interval2. Mild mitral stenosis3. High cardiac output states or tachycardia

(e.g., exercise or anemia)

Diminished S1

1. Lengthened PR interval: first-degree AV nodalblock

2. Mitral regurgitation3. Severe mitral stenosis4. “Stiff” left ventricle (e.g., systemic hypertension)

AV, atrioventricular.

Fig. 3

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34 Chapter Two

P2

P2

P2

P2

A. Physiologic (normal)splitting

B. Widened splitting

C. Fixed splitting

D. Paradoxical splitting

(Note reversed position ofA2 and P2)

Figure 2.3. Splitting patterns of the second heart sound (S2). A2, aortic component; P2, pulmonic componentof S2; S1, first heart sound.

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 35

pulmonary veins is increased by the nega-tive pressure generated by inspiration, thevenous return to the left atrium and ventri-cle temporarily decreases. Reduced filling ofthe LV causes a reduced stroke volume dur-ing the next systolic contraction and there-fore shortens the time required for LV emp-tying. Therefore, aortic valve closure (A2)occurs slightly earlier in inspiration thanduring expiration. The combination of anearlier A2 and delayed P2 during inspirationcauses audible separation of the two com-ponents. Since these components are high-frequency sounds, they are best heard withthe diaphragm of the stethoscope, and split-ting of S2 is usually most easily appreciatednear the second left intercostal space next tothe sternum (the pulmonic area).

Abnormalities of S2 include alterations inits intensity and changes in the pattern ofsplitting. The intensity of S2 depends on thevelocity of blood coursing back toward thevalves from the aorta and pulmonary arteryafter the completion of ventricular contrac-tion, and the suddenness with which thatmotion is arrested by the closing valves. Insystemic hypertension or pulmonary arte-rial hypertension, the diastolic pressure inthe respective great artery is higher thannormal, such that the velocity of the bloodsurging toward the valve is elevated and S2 isaccentuated. Conversely, in severe aortic orpulmonic valve stenosis, the valve commis-sures are nearly fixed in position, such thatthe contribution of the stenotic valve to S2 isdiminished.

Widened splitting of S2 refers to an in-crease in the time interval between A2 and P2,such that the two components are audiblyseparated even during expiration and becomemore widely separated in inspiration (see Fig.2.3). This pattern is usually the result of de-layed closure of the pulmonic valve, whichoccurs in right bundle branch block and pul-monic valve stenosis.

Fixed splitting of S2 is an abnormallywidened interval between A2 and P2 that per-sists unchanged through the respiratorycycle (see Fig. 2.3). The most common ab-normality that causes fixed splitting of S2 isan atrial septal defect (see Chapter 16). In

that condition, chronic volume overload ofthe right-sided circulation results in a high-capacitance, low-resistance pulmonary vas-cular system. This alteration in pulmonaryartery hemodynamics delays the back pres-sure responsible for closure of the pulmonicvalve. Thus, P2 occurs later than normal,even during expiration, such that there iswider than normal separation of A2 and P2.The pattern of splitting does not change (i.e.,it is fixed) during the respiratory cycle be-cause (1) inspiration does not substantiallyincrease further the already elevated pul-monary vascular capacitance, and (2) aug-mented filling of the right atrium from thesystemic veins during inspiration is counter-balanced by a reciprocal decrease in the left-to-right transatrial shunt, eliminating respi-ratory variations in right ventricular filling.

Paradoxical splitting (or reversed split-ting) refers to audible separation of A2 and P2

during expiration that disappears on inspira-tion, the opposite of the normal situation. Itreflects an abnormal delay in the closure ofthe aortic valve such that P2 precedes A2. Inadults, the most common cause is left bun-dle branch block (LBBB). In LBBB, the spreadof electrical activity through the left ventri-cle is impaired, resulting in delayed ventric-ular contraction and late closure of the aor-tic valve such that it follows P2. Duringinspiration, as in the normal case, the pul-monic valve closure sound is delayed andthe aortic valve closure sound moves earlier.This results in narrowing and often superim-position of the two sounds; thus, there is noapparent split at the height of inspiration(see Fig. 2.3). In addition to LBBB, paradoxi-cal splitting may be observed under circum-stances in which left ventricular ejection isgreatly prolonged, such as aortic stenosis.

Extra Systolic Heart Sounds

Extra systolic heart sounds may occur inearly, mid-, or late systole.

Early Extra Systolic Heart Sounds

Abnormal early systolic sounds, or ejectionclicks, occur shortly after S1 and coincide with

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the opening of the aortic or pulmonic valves(Fig. 2.4). These sounds have a sharp, high-pitched quality, so they are heard best withthe diaphragm of the stethoscope placedover the aortic and pulmonic areas. Ejectionclicks indicate the presence of aortic or pul-monic valve stenosis or dilatation of the pul-monary artery or aorta. In stenosis of the aor-tic or pulmonic valve, the sound occurs asthe valve leaflets reach their maximal level ofascent into the great artery, just prior toblood ejection. At that moment, the rapidlyascending valve reaches its elastic limit anddecelerates abruptly, an action thought to re-sult in the sound generation. In dilatation ofthe root of the aorta or pulmonary artery, thesound is associated with sudden tensing of

the aortic or pulmonic root with the onsetof blood flow into the vessel. The aortic ejec-tion click is heard at both the base and theapex of the heart and does not vary with res-piration. In contrast, the pulmonic ejectionclick is heard only at the base and its inten-sity diminishes during inspiration (see Chap-ter 16).

Mid- or Late Extra Systolic Heart Sounds

Clicks occurring in mid- or late systole areusually the result of systolic prolapse of the mitral or tricuspid valves, in which the leaflets bulge abnormally from the ven-tricular side of the atrioventricular junctioninto the atrium during ventricular contrac-tion, often accompanied by valvular regur-gitation. They are loudest over the mitral ortricuspid auscultatory regions, respectively.

Extra Diastolic Heart Sounds

Extra heart sounds in diastole include theopening snap (OS), the third heart sound(S3), the fourth heart sound (S4), and thepericardial knock.

Opening Snap

Opening of the mitral and tricuspid valves isnormally silent, but mitral or tricuspid valvu-lar stenosis (usually the result of rheumaticheart disease; see Chapter 8) produces asound, termed a snap, when the affected valveopens. It is a sharp, high-pitched sound, andits timing does not vary significantly withrespiration. In mitral stenosis (which is muchmore common than tricuspid valve steno-sis), the OS is heard best between the apexand the left sternal border, just after the aor-tic closure sound (A2), when the left ventric-ular pressure falls below that of the leftatrium (see Fig. 2.4).

Because of its proximity to A2, the A2–OSsequence can be confused with a widelysplit second heart sound. However, carefulauscultation at the pulmonic area during inspiration reveals three sounds occurringin rapid succession (Fig. 2.5), which corre-spond to aortic closure (A2), pulmonic clo-

36 Chapter Two

MV opens

S1 S2

LV

ECG

LA

Aorta

S4Ejection

clickOS

S3

Figure 2.4. Timing of extra systolicand diastolic heart sounds. S4 is pro-duced by atrial contraction into a “stiff”left ventricle (LV). An ejection click fol-lows the opening of the aortic or pul-monic valve in cases of valve stenosis ordilatation of the corresponding greatartery. S3 occurs during the period ofrapid ventricular filling; it is normal inyoung people, but its presence in adultsimplies LV contractile dysfunction. Thetiming of an opening snap (OS) is placedfor comparison, but it is not likely that allof these sounds would appear in thesame person. LA, left atrium; MV, mitralvalve.

Fig. 4

Fig. 5

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 37

sure (P2), and then the opening snap (OS).The three sounds become two on expirationbecause A2 and P2 normally fuse.

The severity of stenosis can be approxi-mated by the time interval between A2 andthe opening snap: the more advanced thestenosis, the shorter the interval. This oc-curs because the degree of left atrial pressureelevation corresponds to the severity of mi-tral stenosis. When the ventricle relaxes indiastole, the greater the left atrial pressure,the earlier the mitral valve opens. Com-pared with severe stenosis, mild disease ismarked by a less elevated left atrial pressureis less elevated, lengthening the time ittakes for the left ventricular pressure to fallbelow that of the atrium. Therefore, in mild

mitral stenosis, the opening snap is widelyseparated from A2, whereas in more severestenosis, the A2–OS interval is narrower.

Third Heart Sound (S3)

When present, an S3 occurs in early diastole,following the opening of the atrioventricu-lar valves, during the ventricular rapid fill-ing phase (see Fig. 2.4). It is a dull, low-pitched sound best heard with the bell ofthe stethoscope. A left-sided S3 is typicallyloudest over the cardiac apex while the pa-tient lies in the left lateral decubitus posi-tion. A right-sided S3 is better appreciated at the lower-left sternal border. Productionof the S3 appears to result from tensing ofthe chordae tendineae during rapid fillingand expansion of the ventricle.

A third heart sound is a normal finding inchildren and young adults. In these groups,an S3 implies the presence of a supple ven-tricle capable of normal rapid expansion inearly diastole. Conversely, when heard inmiddle-aged or older adults, an S3 is often asign of disease, indicating volume overloadowing to congestive heart failure, or the in-creased transvalvular flow that accompaniesadvanced mitral or tricuspid regurgitation.A pathologic S3 is sometimes referred to as aventricular gallop.

Fourth Heart Sound (S4)

When an S4 is present, it occurs in late di-astole and coincides with contraction ofthe atria (see Fig. 2.4). This sound is gener-ated by the left (or right) atrium vigorouslycontracting against a stiffened ventricle.Thus, an S4 usually indicates the presenceof cardiac disease—specifically, a decreasein ventricular compliance typically result-ing from ventricular hypertrophy or myo-cardial ischemia. Like an S3, the S4 is a dull,low-pitched sound and is best heard withthe bell of the stethoscope. In the case of the more common left-sided S4, thesound is loudest at the apex, with the pa-tient lying in the left lateral decubitus position. S4 is sometimes referred to as anatrial gallop.

Expiration

OS

OS

S1 S2

A2P2

Inspiration

Figure 2.5. Timing of the opening snap (OS) in mitralstenosis does not change with respiration. On inspi-ration, normal splitting of the second heart sound (S2) isobserved so that three sounds are heard. A2, aortic com-ponent; P2, pulmonic component of S2; S1, first heartsound.

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Quadruple Rhythm or Summation Gallop

In a patient with both an S3 and S4, thosesounds, in conjunction with S1 and S2, pro-duce a quadruple beat. If a patient with aquadruple rhythm develops tachycardia, di-astole becomes shorter in duration, the S3

and S4 coalesce, and a summation gallopresults. The summation of S3 and S4 is heardas a long middiastolic, low-pitched sound,often louder than S1 and S2.

Pericardial Knock

A pericardial knock is an uncommon, high-pitched sound that occurs in patients withsevere constrictive pericarditis (see Chapter14). It appears early in diastole soon after S2 and can be confused with an openingsnap or an S3. However, the knock appearsslightly later in diastole than the timing ofan opening snap and is louder and occursearlier than the ventricular gallop. It resultsfrom the abrupt cessation of ventricular fill-ing in early diastole, which is the hallmarkof constrictive pericarditis.

MURMURS

A murmur is the sound generated by turbu-lent blood flow. Under normal conditions,the movement of blood through the vascularbed is laminar, smooth and silent. However,as a result of hemodynamic and/or structuralchanges, laminar flow can become disturbedand produce an audible noise. Murmurs re-sult from any of the following mechanisms:

1. Flow across a partial obstruction (e.g., aortic stenosis)

2. Increased flow through normal structures(e.g., aortic systolic murmur associatedwith a high-output state, such as anemia)

3. Ejection into a dilated chamber (e.g.,aortic systolic murmur associated withaneurysmal dilatation of the aorta)

4. Regurgitant flow across an incompetentvalve (e.g., mitral regurgitation)

5. Abnormal shunting of blood from onevascular chamber to a lower-pressurechamber (e.g., ventricular septal defect)

Murmurs are described by their timing, intensity, pitch, shape, location, radiation,and response to maneuvers. Timing refers towhether the murmur occurs during systoleor diastole or is continuous (i.e., begins insystole and continues into diastole). The in-tensity of the murmur is typically quantifiedby a grading system. In the case of systolicmurmurs:

38 Chapter Two

Grade 1/6 (or I/VI): Barely audible (i.e., med-ical students may nothear it!)

Grade 2/6 (or II/VI): Faint but immediatelyaudible

Grade 3/6 (or III/VI): Easily heardGrade 4/6 (or IV/VI): Easily heard and asso-

ciated with a palpablethrill

Grade 5/6 (or V/VI): Very loud; heard withstethoscope lightly onchest

Grade 6/6 (or VI/VI): Audible without thestethoscope directly onthe chest wall

Grade 1/4 (or I/IV): Barely audibleGrade 2/4 (or II/IV): Faint but immediately

audibleGrade 3/4 (or III/IV): Easily heardGrade 4/4 (or IV/IV): Very loud

And in the case of diastolic murmurs:

Pitch refers to the frequency of the murmur,ranging from high to low. High-frequencymurmurs are caused by large pressure gra-dients between chambers (e.g., aortic steno-sis) and are best appreciated using the di-aphragm chest piece of the stethoscope.Low-frequency murmurs imply less of a pres-sure gradient between chambers (e.g., mitralstenosis) and are best heard using the stetho-scope’s bell piece.

Shape describes how the murmur changesin intensity from its onset to its comple-tion. For example, a crescendo–decrescendo

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 39

(or “diamond-shaped”) murmur first risesand then falls off in intensity. Other shapesinclude decrescendo (i.e., the murmur beginsat its maximum intensity and grows softer)and uniform (the intensity of the murmurdoes not change).

Location refers to the murmur’s region ofmaximum intensity and is usually describedin terms of specific auscultatory areas (seeFig. 2.2):

right, Valsalva (forceful expiration against aclosed airway), or clenching of the fists, eachof which alters the heart’s loading condi-tions and can affect the intensity of manymurmurs. Examples of the effects of maneu-vers on specific murmurs are presented inChapter 8.

When reporting a murmur, some or all ofthese descriptors are mentioned. For exam-ple, you might describe a particular patient’smurmur of aortic stenosis as “A grade III/VI high-pitched, crescendo–decrescendo sys-tolic murmur, heard best at the upper-rightsternal border, radiating toward the neck.”

Systolic Murmurs

Systolic murmurs are subdivided into sys-tolic ejection murmurs, pansystolic mur-murs, and late systolic murmurs (Fig. 2.6). Asystolic ejection murmur is typical of aor-tic or pulmonic valve stenosis. It begins afterthe first heart sound and terminates beforeor during S2, depending on its severity andwhether the obstruction is of the aortic orpulmonic valve. The shape of the murmur isof the crescendo–decrescendo type (i.e., itsintensity rises and then falls).

Aortic area: Second to third right inter-costal spaces, next to sternum

Pulmonic area: Second to third left intercostalspaces, next to sternum

Tricuspid area: Lower-left sternal borderMitral area: Cardiac apex

From their primary locations, murmurs areoften heard to radiate to other areas of thechest, and such patterns of transmission re-late to the direction of the turbulent flow.Finally, similar types of murmurs can bedistinguished from one another by simplebedside maneuvers, such as standing up-

Click

Figure 2.6. Classification of systolic murmurs. Ejection murmurs arecrescendo–decrescendo in configuration, whereas pansystolic murmurs areuniform throughout systole. A late systolic murmur often follows a midsys-tolic click and suggests mitral (or tricuspid) valve prolapse.

Fig. 6

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The ejection murmur of aortic stenosis be-gins in systole after S1, from which it is sep-arated by a short audible gap (Fig. 2.7). Thisgap corresponds to the period of isovolu-metric contraction of the left ventricle (theperiod after the mitral valve has closed butbefore the aortic valve has opened). Themurmur becomes more intense as flow in-creases across the aortic valve during therise in left ventricular pressure (crescendo).Then, as the ventricle relaxes, forward flowdecreases, and the murmur lessens in in-tensity (decrescendo) and finally ends priorto the aortic component of S2. The murmurmay be immediately preceded by an ejec-tion click, especially in mild forms of aorticstenosis.

Although the intensity of the murmurdoes not correlate well with the severity ofaortic stenosis, other features do. For exam-ple, the more severe the stenosis, the longer ittakes to force blood across the valve, and thelater the murmur peaks in systole (Fig. 2.8).Also, as shown in Figure 2.8, as the severity of

stenosis increases, the aortic component of S2

softens because the leaflets become morerigidly fixed in place.

Aortic stenosis causes a high-frequencymurmur, reflecting the sizable pressure gra-dient across the valve. It is best heard in the“aortic area” at the second and third rightintercostal spaces close to the sternum. Themurmur typically radiates toward the neck(the direction of turbulent blood flow) but

40 Chapter Two

S1 S2

Figure 2.7. Systolic ejection murmur of aortic steno-sis. There is a short delay between the first heart sound(S1) and the onset of the murmur. LV, left ventricle; S2,second heart sound.

S1 A2 P2

S1 A2 P2

S1 P2

Figure 2.8. The severity of aortic stenosis affectsthe shape of the systolic murmur and the heartsounds. A. In mild stenosis, an ejection click (EJ) is oftenpresent, followed by an early peaking crescendo–decrescendo murmur and a normal aortic component ofS2 (A2). B. As stenosis becomes more severe, the peak ofthe murmur becomes more delayed in systole and theintensity of A2 lessens. The prolonged ventricular ejec-tion time delays A2 so that it merges with or occurs afterthe pulmonic component of S2 (P2); the ejection clickmay not be heard. C. In severe stenosis, the murmurpeaks very late in systole, and A2 is usually absent be-cause of immobility of the valve leaflets. S1, first heartsound; S2, second heart sound.

Fig. 7

Fig. 8

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 41

often can be heard in a wide distribution, in-cluding the cardiac apex.

The murmur of pulmonic stenosis also be-gins after S1, it may be preceded by an ejec-tion click, but unlike aortic stenosis, it mayextend beyond A2. That is, if the stenosis issevere, it will result in a very prolonged rightventricular ejection time, elongating themurmur, which will continue beyond A2

and end just before closure of the pulmonicvalve (P2). Pulmonic stenosis is usually loud-est at the second to third left intercostalspaces close to the sternum. It does not ra-diate as widely as aortic stenosis, but some-times it is transmitted to the neck or leftshoulder.

Young adults often have benign systolicejection murmurs owing to increased systolicflow across normal aortic and pulmonicvalves. This type of murmur often becomessofter or disappears when the patient sitsupright.

Pansystolic (also termed holosystolic)murmurs are caused by regurgitation ofblood across an incompetent mitral or tri-cuspid valve or through a ventricular septaldefect (VSD; see Fig. 2.6). These murmursare characterized by a uniform intensitythroughout systole. In mitral and tricuspidvalve regurgitation, as soon as ventricularpressure exceeds atrial pressure (i.e., when S1

occurs), there is immediate retrograde flowacross the regurgitant valve. Thus, there isno gap between S1 and the onset of thesepansystolic murmurs, in contrast to the systolic ejection murmurs discussed earlier.Similarly, there is no significant gap be-tween S1 and the onset of the systolic murmur of a VSD, because left ventricularsystolic pressure exceeds right ventricularsystolic pressure (and flow occurs) quicklyafter the onset of contraction.

The pansystolic murmur of advanced mi-tral regurgitation continues through the aor-tic closure sound because left ventricularpressure remains greater than that in the leftatrium at the time of aortic closure. Themurmur is heard best at the apex, is highpitched and “blowing” in quality, and oftenradiates toward the left axilla; its intensitydoes not change with respiration.

Tricuspid valve regurgitation is best heardalong the left lower sternal border. It gener-ally radiates to the right of the sternum andis high pitched and blowing in quality. Theintensity of the murmur increases with inspiration because the negative intratho-racic pressure induced during inspirationenhances venous return to the heart. Thelatter augments right ventricular stroke vol-ume, thereby increasing the amount of re-gurgitated blood.

The murmur of a ventricular septal defect isheard best at the fourth to sixth left inter-costal spaces, is high pitched, and may be as-sociated with a palpable thrill. The intensityof the murmur does not increase with in-spiration, nor does it radiate to the axilla,which helps distinguish it from tricuspidand mitral regurgitation, respectively. Ofnote, the smaller the VSD, the greater theturbulence of blood flow between the leftand right ventricles and the louder the mur-mur. Some of the loudest murmurs everheard are those associated with small VSDs.

Late systolic murmurs begin in mid-to-late systole and continue to the end of sys-tole. The most common example is mitralregurgitation caused by mitral valve prolapse—bowing of abnormally redundant and elon-gated valve leaflets into the left atrium dur-ing ventricular contraction (see Fig. 2.6).This murmur is usually preceded by amidsystolic click and is described further inChapter 8.

Diastolic Murmurs

Diastolic murmurs are divided into early de-crescendo murmurs and mid-to-late rum-bling murmurs (Fig. 2.9). Early diastolicmurmurs result from regurgitant flowthrough either the aortic or pulmonic valve,with the former being much more commonin adults. If produced by aortic valve regurgi-tation, the murmur begins at A2, has a de-crescendo shape, and terminates before thenext S1. Because diastolic relaxation of theleft ventricle is rapid, a pressure gradient de-velops immediately between the aorta andlower-pressured left ventricle in aortic re-gurgitation, and the murmur therefore dis-

Fig. 9

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plays its maximum intensity at its onset.Thereafter in diastole, as the aortic pressurefalls and the LV pressure increases (as bloodfills the ventricle), the gradient between thetwo chambers diminishes and the murmurdecreases in intensity. Aortic regurgitation isa high-pitched murmur, best heard usingthe diaphragm of the stethoscope along theleft sternal border with the patient sitting,leaning forward, and exhaling.

Pulmonic regurgitation in adults is usuallyowing to the presence of pulmonary arterialhypertension. It has an early diastolic de-crescendo murmur profile similar to that ofaortic regurgitation, but it is best heard inthe pulmonic area and its intensity may in-crease with inspiration.

Mid-to-late diastolic murmurs resultfrom either turbulent flow across a stenoticmitral or tricuspid valve or less commonlyfrom abnormally increased flow across anormal mitral or tricuspid valve (see Fig.2.9). If resulting from stenosis, the murmur

begins after S2 and is preceded by an open-ing snap. The shape of this murmur isunique. Following the opening snap, themurmur is at its loudest because the pres-sure gradient between the atrium and ven-tricle is at its maximum. The murmur thendecrescendos or disappears totally duringdiastole as the transvalvular gradient de-creases. The degree to which the murmurfades depends on the severity of the steno-sis. If the stenosis is severe, the murmur is prolonged; if the stenosis is mild, themurmur disappears in mid-to-late diastole.Whether the stenosis is mild or severe, themurmur intensifies at the end of diastole inpatients in normal sinus rhythm, whenatrial contraction augments flow across thevalve (see Fig. 2.9). The murmur of mitralstenosis is low pitched and is heard bestwith the bell of the stethoscope at the apex,while the patient lies in the left lateral de-cubitus position. The much less commonmurmur of tricuspid stenosis is better aus-

42 Chapter Two

S1 S2 S1

S1 S2 S1

S1 S2 S1

• Aortic regurgitation• Pulmonic regurgitation

• Mild mitral or tricuspid stenosis

• Severe mitral or tricuspid stenosis

Figure 2.9. Classification of diastolic murmurs. A. An early diastolic decrescendo murmur is typi-cal of aortic or pulmonic valve regurgitation. B. Mid-to-late low-frequency rumbling murmurs are usu-ally the result of mitral or tricuspid valve stenosis, which follows a sharp opening snap (OS). Presystolicaccentuation of the murmur occurs in patients in normal sinus rhythm because of the transient rise inatrial pressure during atrial contraction. C. In more severe mitral or tricuspid valve stenosis, the open-ing snap and diastolic murmur occur earlier and the murmur is prolonged. S1, first heart sound; S2, sec-ond heart sound.

1 LINE SHORT

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 43

cultated at the lower sternum, near the xi-phoid process.

Hyperdynamic states such as fever, ane-mia, hyperthyroidism, and exercise causeincreased flow across the normal tricuspidand mitral valves and can therefore result ina diastolic murmur. In patients with ad-vanced mitral regurgitation, the expectedsystolic murmur can be accompanied by anadditional diastolic murmur owing to theincreased volume of blood that must returnacross the valve to the left ventricle in dias-tole. Similarly, patients with either tricuspidregurgitation or an atrial septal defect (seeChapter 16) may display a diastolic flowmurmur across the tricuspid valve.

Continuous Murmurs

Continuous murmurs are heard throughoutthe cardiac cycle without an audible hiatusbetween systole and diastole. Such murmursresult from conditions in which there is apersistent pressure gradient between twostructures during systole and diastole. Anexample is the murmur of patent ductus ar-teriosus, in which there is an abnormal com-munication between the aorta and pul-monary artery (see Chapter 16). Duringsystole, blood flows from the high-pressureascending aorta through the ductus into thelower-pressure pulmonary artery. During di-astole, the aortic pressure remains greaterthan that in the pulmonary artery and flowcontinues across the ductus. This murmur

begins in early systole, crescendos to itsmaximum at S2, then decrescendos until thenext S1 (Fig. 2.10).

The “to-and-fro” combined murmur in apatient with both aortic stenosis and aorticregurgitation could be mistaken for a con-tinuous murmur (see Fig. 2.10). During sys-tole, there is a diamond-shaped ejectionmurmur, and during diastole a decrescendomurmur. However, in the case of a to-and-fro murmur, the sound does not extendthrough S2 because it has discrete systolicand diastolic components.

SUMMARY

Abnormal heart sounds and murmurs arecommon in acquired and congenital heartdisease and can be predicted by the underly-ing pathology. Although it may seem diffi-cult to remember even the basic features pre-sented here, it will become easier as you learnmore about the pathophysiology of theseconditions, and as your experience in physi-cal diagnoses grows. For now, just rememberthat the information is here, and refer to it asneeded. Tables 2.2 and 2.3 and Figure 2.11summarize features of the heart sounds andmurmurs described in this chapter.

Acknowledgments

Contributors to the previous editions of this chapterwere Oscar Benavidez, MD; Bradley S. Marino, MD;Allan Goldblatt, MD; and Leonard S. Lilly, MD.

S1 S2 S1

S1 S2 S1

• Aortic stenosis and regurgitation• Pulmonic stenosis and regurgitation

• Patent ductus arteriosus

Figure 2.10. A continuous murmur peaks at, and extends through, the second heart sound (S2).A to-and-fro murmur is not continuous; rather, there is a systolic component and a distinct diastolic com-ponent, separated by S2. S1, first heart sound.1 LINE SHORT

Fig. 10

Tab. 2,Tab. 3,Fig. 11

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44 Chapter Two

TABLE 2.2. Common Heart Sounds

Sound Location Pitch Significance

S1

S2

Extra systolic soundsEjection clicks

Mid-to-late click

Extra diastolic soundsOpening snapS3

S4

LLSB, lower left sternal border.

High

High

HighHighHighHigh

HighLow

Low

Apex

Base

Aortic: apex and basePulmonic: baseMitral: apexTricuspid: LLSB

ApexLeft-sided: apex

Left-sided: apex

Normal closure of mitral and tricuspidvalves

Normal closure of aortic (A2) and pulmonic (P2) valves

Aortic or pulmonic stenosis, or dilata-tion of aortic root or pulmonary artery

Mitral or tricuspid valve prolapse

Mitral stenosisNormal in childrenAbnormal in adults: indicates heart

failure or volume overload stateReduced ventricular compliance

TABLE 2.3. Common Murmurs

Murmur Type Example Location and Radiation

Systolic ejection

Pansystolic

Late systolic

Early diastolic

Mid- or late diastolic

Aortic stenosis

Pulmonic stenosis

Mitral regurgitationTricuspid regurgitation

Mitral valve prolapse

Aortic regurgitationPulmonic regurgitation

Mitral stenosis

2nd right intercostal space →neck (but may radiatewidely)

2nd–3rd left intercostal spaces

Apex → axillaLeft lower sternal border →

right lower sternal border

Apex → axilla

Along left side of sternumUpper left side of sternum

Apex

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The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 45

Additional Reading

Bickley LS. Bates’ Guide to Physical Examinationand History Taking. 8th Ed. Philadelphia: Lippin-cott Williams & Wilkins, 2003.

Constant J. Essentials of Bedside Cardiology. 2nd Ed.Totowa, NJ: Humana Press, 2003.

LeBlond RF, DeGowin RL, Brown DD. DeGowin’s Diagnostic Examination. 7th Ed. New York: McGraw-Hill, 2004.

Orient JM, Sapira JD. Sapira’s Art and Science of Bed-side Diagnosis. 3rd Ed. Philadelphia: LippincottWilliams & Wilkins, 2005.

Pulmonic areaEjection-type murmur• Pulmonic stenosis• Flow murmur

Mitral areaPansystolic murmur• Mitral regurgitation

Tricuspid areaPansystolic murmur• Tricuspid regurgitation• Ventricular septal defect

Mid-to-late diastolicmurmur• Tricuspid stenosis• Atrial septal defect

Aortic areaEjection-type murmur• Aortic stenosis• Flow murmur

Mid-to-late diastolic murmur• Mitral stenosis

Left sternal borderEarly diastolic murmur• Aortic regurgitation• Pulmonic regurgitation

Figure 2.11. Locations of maximum intensity of common murmurs.

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