The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 31

Home , Aortic pressure, Cardiac cycle, Continuous murmurs, Fourth heart sound, Heart sounds, Right atrial pressure

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CHAPTER

The Cardiac Cycle: Mechanisms of Heart 2 Sounds and Murmurs Nicole Martin Leonard S. Lilly

CARDIAC CYCLE MURMURS HEART SOUNDS Systolic Murmurs Diastolic Murmurs First Heart Sound (S1) Continuous Murmurs Second Heart Sound (S2) Extra Systolic Heart Sounds Extra Diastolic Heart Sounds

Cardiac diseases often cause abnormal CARDIAC CYCLE findings on physical examination, includ- ing pathologic heart sounds and murmurs. The cardiac cycle consists of precisely timed These findings are clues to the underlying electrical and mechanical events that are re- pathophysiology, and proper interpreta- sponsible for rhythmic atrial and ventricu- tion is essential for successful diagnosis lar contractions. Figure 2.1 displays the pres- Fig. 1 and disease management. This chapter de- sure relationships between the left-sided scribes heart sounds in the context of the cardiac chambers during the normal cardiac normal cardiac cycle and then focuses on cycle and serves as a platform for describing the origins of pathologic heart sounds and key events. Mechanical systole refers to ven- murmurs. tricular contraction, and diastole to ven- Many cardiac diseases are mentioned tricular relaxation and filling. Throughout briefly in this chapter as examples of abnor- the cardiac cycle, the right and left atria mal heart sounds and murmurs. Because accept blood returning to the heart from each of these conditions is described in the systemic veins and from the pulmonary greater detail later in the book, it is not nec- veins, respectively. During diastole, blood essary to memorize the examples presented passes from the atria into the ventricles here. Rather, it is preferable to understand across the open tricuspid and mitral valves, the mechanisms by which the abnormal causing a gradual increase in ventricular di- sounds are produced, so that their descrip- astolic pressures. In late diastole, atrial con- tions will make sense in later chapters. traction propels a final bolus of blood into

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30 Chapter Two

ECG the mitral component slightly precedes that of the tricuspid valve because of the earlier AV c electrical stimulation of left ventricular con- AV traction (see Chapter 4). As the right and left ventricular pressures ) 100 g

H rapidly rise further, they soon exceed the Aorta m diastolic pressures within the pulmonary m (

e artery and aorta, forcing the pulmonic and r u

s aortic valves to open, and blood is ejected

s LV e

r into the pulmonary and systemic circula-

P 50 tions. The ventricular pressures continue to MV MV c increase during contraction, and because the pulmonic and aortic valves are open, the aortic and pulmonary artery pressures rise, par- LA v a c allel to those of the corresponding ventricles. Time At the conclusion of ventricular ejection, the ventricular pressures fall below those of the pulmonary artery and aorta (the pulmonary artery and aorta are elastic struc- S1 S2 tures that maintain their pressures longer), DIASTOLESYSTOLE DIASTOLE such that the pulmonic and aortic valves are forced to close, producing the second heart Figure 2.1. The normal cardiac cycle, showing pressure relationships between the left-sided heart sound, S2. Like the first heart sound (S1), this chambers. During diastole, the mitral valve (MV) is sound consists of two parts: the aortic (A2) open, so that the left atrial (LA) and left ventricular (LV) component normally precedes the pulmonic pressures are equal. In late diastole, LA contraction causes a small rise in pressure in both the LA and LV (the (P2) because the diastolic pressure gradient a wave). During systolic contraction, the LV pressure between the aorta and left ventricle is rises; when it exceeds the LA pressure, the MV closes, greater than that between the pulmonary contributing to the first heart sound (S1). As LV pressure rises above the aortic pressure, the aortic valve (AV) artery and right ventricle, forcing the aortic opens, which is a silent event. As the ventricle begins to valve to shut more readily. The ventricular relax and its pressure falls below that of the aorta, the pressures fall rapidly during the subsequent AV closes, contributing to the second heart sound (S2). As LV pressure falls further, below that of the LA, the relaxation phase. As they drop below the MV opens, which is silent in the normal heart. In addi- pressures in the right and left atria, the tri- tion to the a wave, the LA pressure curve displays two cuspid and mitral valves open, followed by positive deflections: the c wave represents a small rise in LA pressure as the MV closes and bulges toward the diastolic ventricular filling and repetition of atrium, and the v wave is the result of passive filling of this cycle. the LA from the pulmonary veins during systole, when Notice in Figure 2.1 that in addition to the MV is closed. the a wave, the atrial pressure curve displays two other positive deflections during the cardiac cycle: The c wave represents a small each ventricle, an action that produces a rise in atrial pressure as the tricuspid and mi- brief further rise in atrial and ventricle pres- tral valves close and bulge into their respec- sures, termed the a wave (see Fig. 2.1). tive atria. The v wave is the result of passive Contraction of the ventricles follows, sig- filling of the atria from the systemic and naling the onset of mechanical systole. As pulmonary veins during systole, a period the ventricles start to contract, the pressures during which blood accumulates in the atria within them rapidly exceed atrial pressures. because the tricuspid and mitral valves are This results in the forced closure of the tri- closed. cuspid and mitral valves, which produces At the bedside, systole can be approxi-

the ﬁrst heart sound, termed S1. This sound mated by the period from S1 to S2, and dias-

has two nearly superimposed components: tole from S2 to the next S1. Although the du- 10090-02_CH02.qxd 8/24/06 5:41 PM Page 31

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 31

ration of systole remains constant from beat the left side of the heart. Equivalent events to beat, the length of diastole varies with the occur simultaneously in the right side of the heart rate: the faster the heart rate, the shorter heart in the right atrium, right ventricle,

the diastolic phase. The main sounds, S1 and and pulmonary artery. At the bedside, clues

S2, provide a framework from which all other to right-heart function can be ascertained by heart sounds and murmurs can be timed. examining the jugular venous pulse, which The pressure relationships and events de- is representative of the right atrial pressure picted in Figure 2.1 are those that occur in (see Box 2.1). Box 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 internal jugular (IJ) veins and the superior vena cava and right atrium (RA), the height of the IJ venous 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- a nous pulse during the cardiac cycle, man- ifested by oscillations in the overlying v skin, are shown in the figure (notice the similarity to the left atrial pressure tracing y in Fig. 2.1). There are two major upward x components, the a and v waves, followed 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) at the time of tricuspid valve closure, but that is usually not distinguishable in the JVP. The a wave represents transient venous distension caused by back pressure from RA contraction. The v wave corresponds to passive filling of the RA from the systemic veins during systole, when the tricuspid valve is closed. Opening of the tricuspid valve in early diastole allows blood to rapidly empty from the RA into the right ventricle; that fall in RA pressure corresponds to the y descent. Conditions that abnormally raise right-sided cardiac pressures (e.g., heart failure, tricuspid valve disease, pulmonic stenosis, pericardial diseases) elevate the JVP, while reduced intravascular volume (e.g., dehydration) decreases it. In addition, specific disease states can influence the individual components of the JVP, examples of which are listed here for reference and explained in subsequent chapters: Prominent a: right ventricular hypertrophy, tricuspid stenosis Prominent v: tricuspid regurgitation Prominent 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 sternal angle is located approximately 5 cm above the center of the RA, the JVP is calculated 10090-02_CH02.qxd 8/24/06 5:41 PM Page 32

32 Chapter Two

at the bedside by adding 5 cm to the vertical height of the top of the IJ venous column above the sternal angle. The right IJ vein is usually the easiest to evaluate because it extends directly upward from the RA and superior vena cava. First, observe the pulsations in the skin overlying the IJ with the patient supine and the head of the bed at about a 45° angle. Shining a light obliquely across the neck helps to visualize the pulsations. Be sure to examine the IJ, not the 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 typically easier to see, it does not accurately reflect RA pressure because it contains valves that interfere 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 such situations, the head of the bed must be lowered or raised, respectively, so that the top of the 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 angle of the head of the bed. Sometimes it can be difficult to distinguish the jugular venous pulsations from the neighboring 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 seated position or during inspiration.

HEART SOUNDS ates only a single sound. An exception occurs in patients with right bundle branch Typical stethoscopes contain two chest pieces block (see Chapter 4), in whom these com- for auscultation of the heart. The concave ponents may be audibly split because of de- “bell” chest piece, meant to be applied lightly layed closure of the tricuspid valve. to the skin, accentuates low-frequency sounds. Three factors determine the intensity of S1: Conversely, the flat “diaphragm” chest piece (1) the distance separating the leaflets of the should be pressed firmly against the skin to open valves at the onset of ventricular con- eliminate low frequencies and therefore ac- traction; (2) the mobility of the leaflets (nor- centuate high-frequency sounds and mur- mal, or rigid because of stenosis); and (3) the murs. Some modern stethoscopes incorpo- rate of rise of ventricular pressure (Table 2.1). Tab. 1 rate both the bell and diaphragm functions into a single chest piece; in these models, placing the piece lightly on the skin brings out the low-frequency sounds, while firm pressure accentuates the high-frequency ones.

First Heart Sound (S1)

S1 is produced by closure of the mitral and tricuspid valves in early systole and is loud- Fig. 2 est near the apex of the heart (Fig. 2.2). It is a high-frequency sound, best heard with the diaphragm of the stethoscope. Although mitral closure usually precedes tricuspid closure, they are separated by only about Figure 2.2. Standard positions of stethoscope place- 0.01 sec, such that the human ear appreci- ment for cardiac auscultation. 10090-02_CH02.qxd 8/24/06 5:41 PM Page 33

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 33

a diminished S1 results from an abnormally TABLE 2.1. Causes of Altered Intensity of First prolonged PR interval, which delays the Heart Sound (S ) 1 onset of ventricular contraction. Following

Accentuated S1 atrial contraction, the mitral and tricuspid valves have additional time to ﬂoat back to- 1. Shortened PR interval gether so that the leaﬂets are forced closed 2. Mild mitral stenosis 3. High cardiac output states or tachycardia from only a small distance apart. (e.g., exercise or anemia) In patients with mitral regurgitation (see

Chapter 8), S1 is often diminished in inten- Diminished S1 sity because the mitral leaflets may not come 1. Lengthened PR interval: first-degree AV nodal into full contact with one another as they block close. In severe mitral stenosis, the leaflets are 2. Mitral regurgitation 3. Severe mitral stenosis nearly fixed in position throughout the car- 4. “Stiff” left ventricle (e.g., systemic hypertension) diac cycle, and that reduced movement lessens the intensity of S1. AV, atrioventricular. In patients with a “stiffened” left ventricle (e.g., a hypertrophied chamber), atrial The distance between the open valve leaf- contraction results in a higher-than-normal lets at the onset of ventricular contraction pressure at the end of diastole. This greater relates to the electrocardiographic PR inter- pressure causes the mitral leaflets to drift to- val (see Chapter 4), the period between the gether more rapidly, forcing them closed onset of atrial and ventricular activation. from a smaller-than-normal distance when Atrial contraction at the end of diastole ventricular contraction begins and thus re- forces the tricuspid and mitral valve leaflets ducing the intensity of S1. apart. As they start to drift back together, ventricular contraction forces them shut, Second Heart Sound (S2) from whatever position they are at, as soon as the ventricular pressure exceeds that in The second heart sound results from the clo-

the atrium. An accentuated S1 results when sure of the aortic and pulmonic valves and the PR interval is shorter than normal be- therefore has aortic (A2) and pulmonic (P2)

cause the valve leaﬂets do not have sufﬁ- components. Unlike S1, which is usually cient time to drift back together and are heard as a single sound, the components of

therefore forced shut from a relatively wide S2 vary with the respiratory cycle: they are distance. normally fused as one sound during expira- Similarly, in mild mitral stenosis (see tion but become audibly separated during Chapter 8) a prolonged diastolic pressure inspiration, a situation termed normal or gradient exists between the left atrium and physiologic splitting (Fig. 2.3). Fig. 3 ventricle, which keeps the mobile portions One explanation for normal splitting of

of the mitral leaﬂets farther apart than nor- S2 is as follows. Expansion of the chest dur- mal during diastole. Because the leaﬂets are ing inspiration causes the intrathoracic pres- relatively wide apart at the onset of systole, sure to become more negative. The negative they are forced shut loudly when the left pressure transiently increases the capaci- ventricle contracts. tance (and reduces the impedance) of the in-

S1 also may be accentuated when the trathoracic pulmonary vessels. As a result, heart rate is more rapid than normal (i.e., there is a temporary delay in the diastolic tachycardia) because diastole is shortened “back pressure” of the pulmonary artery re- and the leaﬂets have insufﬁcient time to drift sponsible for closure of the pulmonic valve.

back together before the ventricles contract. Thus, P2 is delayed; that is, it occurs later

Conditions that reduce the intensity of S1 during inspiration than during expiration.

are also listed in Table 2.1. In ﬁrst-degree Inspiration has the opposite effect on A2. atrioventricular (AV) block (see Chapter 12), Because the capacity of the intrathoracic 10090-02_CH02.qxd 8/24/06 5:41 PM Page 34

34 Chapter Two

A. Physiologic (normal) P2 splitting

B. Widened splitting P2

P C. Fixed splitting 2

P D. Paradoxical splitting 2

(Note reversed position of A2 and P2)

Figure 2.3. Splitting patterns of the second heart sound (S2). A2, aortic component; P2, pulmonic component of S2; S1, ﬁrst heart sound. 10090-02_CH02.qxd 8/24/06 5:41 PM Page 35

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 35

pulmonary veins is increased by the nega- that condition, chronic volume overload of tive pressure generated by inspiration, the the right-sided circulation results in a high- venous return to the left atrium and ventri- capacitance, low-resistance pulmonary vas- cle temporarily decreases. Reduced ﬁlling of cular system. This alteration in pulmonary the LV causes a reduced stroke volume dur- artery hemodynamics delays the back pres- ing the next systolic contraction and there- sure responsible for closure of the pulmonic

fore shortens the time required for LV emp- valve. Thus, P2 occurs later than normal,

tying. Therefore, aortic valve closure (A2) even during expiration, such that there is

occurs slightly earlier in inspiration than wider than normal separation of A2 and P2. during expiration. The combination of an The pattern of splitting does not change (i.e.,

earlier A2 and delayed P2 during inspiration it is ﬁxed) during the respiratory cycle be- causes audible separation of the two com- cause (1) inspiration does not substantially ponents. Since these components are high- increase further the already elevated pul- frequency sounds, they are best heard with monary vascular capacitance, and (2) aug- the diaphragm of the stethoscope, and split- mented ﬁlling of the right atrium from the

ting of S2 is usually most easily appreciated systemic veins during inspiration is counter- near the second left intercostal space next to balanced by a reciprocal decrease in the left- the sternum (the pulmonic area). to-right transatrial shunt, eliminating respi-

Abnormalities of S2 include alterations in ratory variations in right ventricular ﬁlling. its intensity and changes in the pattern of Paradoxical splitting (or reversed split-

splitting. The intensity of S2 depends on the ting) refers to audible separation of A2 and P2 velocity of blood coursing back toward the during expiration that disappears on inspira- valves from the aorta and pulmonary artery tion, the opposite of the normal situation. It after the completion of ventricular contrac- reﬂects an abnormal delay in the closure of

tion, and the suddenness with which that the aortic valve such that P2 precedes A2. In motion is arrested by the closing valves. In adults, the most common cause is left bun- systemic hypertension or pulmonary arte- dle branch block (LBBB). In LBBB, the spread rial hypertension, the diastolic pressure in of electrical activity through the left ventri- the respective great artery is higher than cle is impaired, resulting in delayed ventric- normal, such that the velocity of the blood ular contraction and late closure of the aor-

surging toward the valve is elevated and S2 is tic valve such that it follows P2. During accentuated. Conversely, in severe aortic or inspiration, as in the normal case, the pul- pulmonic valve stenosis, the valve commis- monic valve closure sound is delayed and sures are nearly ﬁxed in position, such that the aortic valve closure sound moves earlier.

the contribution of the stenotic valve to S2 is This results in narrowing and often superim- diminished. position of the two sounds; thus, there is no

Widened splitting of S2 refers to an in- apparent split at the height of inspiration

crease in the time interval between A2 and P2, (see Fig. 2.3). In addition to LBBB, paradoxi- such that the two components are audibly cal splitting may be observed under circum- separated even during expiration and become stances in which left ventricular ejection is more widely separated in inspiration (see Fig. greatly prolonged, such as aortic stenosis. 2.3). This pattern is usually the result of delayed closure of the pulmonic valve, which Extra Systolic Heart Sounds occurs in right bundle branch block and pulmonic valve stenosis. Extra systolic heart sounds may occur in

Fixed splitting of S2 is an abnormally early, mid-, or late systole.

widened interval between A2 and P2 that per- sists unchanged through the respiratory Early Extra Systolic Heart Sounds cycle (see Fig. 2.3). The most common ab-

normality that causes ﬁxed splitting of S2 is Abnormal early systolic sounds, or ejection

an atrial septal defect (see Chapter 16). In clicks, occur shortly after S1 and coincide with 10090-02_CH02.qxd 8/24/06 5:41 PM Page 36

36 Chapter Two

the opening of the aortic or pulmonic valves the aortic or pulmonic root with the onset Fig. 4 (Fig. 2.4). These sounds have a sharp, high- of blood ﬂow into the vessel. The aortic ejec- pitched quality, so they are heard best with tion click is heard at both the base and the the diaphragm of the stethoscope placed apex of the heart and does not vary with res- over the aortic and pulmonic areas. Ejection piration. In contrast, the pulmonic ejection clicks indicate the presence of aortic or pul- click is heard only at the base and its inten- monic valve stenosis or dilatation of the pul- sity diminishes during inspiration (see Chap- monary artery or aorta. In stenosis of the aor- ter 16). tic or pulmonic valve, the sound occurs as the valve leaﬂets reach their maximal level of Mid- or Late Extra Systolic Heart Sounds ascent into the great artery, just prior to blood ejection. At that moment, the rapidly Clicks occurring in mid- or late systole are ascending valve reaches its elastic limit and usually the result of systolic prolapse of decelerates abruptly, an action thought to re- the mitral or tricuspid valves, in which sult in the sound generation. In dilatation of the leaflets bulge abnormally from the ven- the root of the aorta or pulmonary artery, the tricular side of the atrioventricular junction sound is associated with sudden tensing of into the atrium during ventricular contraction, often accompanied by valvular regurgitation. They are loudest over the mitral or tricuspid auscultatory regions, respectively. ECG

Extra Diastolic Heart Sounds Extra heart sounds in diastole include the Aorta opening snap (OS), the third heart sound

(S3), the fourth heart sound (S4), and the LV pericardial knock.

MV opens Opening Snap Opening of the mitral and tricuspid valves is LA normally silent, but mitral or tricuspid valvular stenosis (usually the result of rheumatic heart disease; see Chapter 8) produces a sound, termed a snap, when the affected valve opens. It is a sharp, high-pitched sound, and S S1 S2 S its timing does not vary signiﬁcantly with 4 OS 3 Ejection respiration. In mitral stenosis (which is much click more common than tricuspid valve steno- Figure 2.4. Timing of extra systolic sis), the OS is heard best between the apex and diastolic heart sounds. S4 is produced by atrial contraction into a “stiff” and the left sternal border, just after the aor- left ventricle (LV). An ejection click fol- tic closure sound (A2), when the left ventric- lows the opening of the aortic or pul- ular pressure falls below that of the left monic valve in cases of valve stenosis or dilatation of the corresponding great atrium (see Fig. 2.4). artery. S3 occurs during the period of Because of its proximity to A2, the A2–OS rapid ventricular filling; it is normal in sequence can be confused with a widely young people, but its presence in adults implies LV contractile dysfunction. The split second heart sound. However, careful timing of an opening snap (OS) is placed auscultation at the pulmonic area during for comparison, but it is not likely that all inspiration reveals three sounds occurring of these sounds would appear in the same person. LA, left atrium; MV, mitral in rapid succession (Fig. 2.5), which corre- Fig. 5 valve. spond to aortic closure (A2), pulmonic clo- 10090-02_CH02.qxd 8/24/06 5:41 PM Page 37

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 37

mitral stenosis, the opening snap is widely

separated from A2, whereas in more severe

stenosis, the A2–OS interval is narrower.

Expiration Third Heart Sound (S3) OS When present, an S3 occurs in early diastole, following the opening of the atrioventricular valves, during the ventricular rapid ﬁll- ing phase (see Fig. 2.4). It is a dull, low- pitched sound best heard with the bell of S1 S2 the stethoscope. A left-sided S3 is typically loudest over the cardiac apex while the patient lies in the left lateral decubitus posi-

tion. A right-sided S3 is better appreciated at the lower-left sternal border. Production

of the S3 appears to result from tensing of the chordae tendineae during rapid ﬁlling and expansion of the ventricle. A third heart sound is a normal ﬁnding in Inspiration children and young adults. In these groups, OS an S3 implies the presence of a supple ventricle capable of normal rapid expansion in early diastole. Conversely, when heard in

middle-aged or older adults, an S3 is often a sign of disease, indicating volume overload A2P2 owing to congestive heart failure, or the in- Figure 2.5. Timing of the opening snap (OS) in mitral creased transvalvular ﬂow that accompanies stenosis does not change with respiration. On inspi- advanced mitral or tricuspid regurgitation. ration, normal splitting of the second heart sound (S2) is A pathologic S3 is sometimes referred to as a observed so that three sounds are heard. A2, aortic component; P2, pulmonic component of S2; S1, ﬁrst heart ventricular gallop. sound.

Fourth Heart Sound (S4)

sure (P2), and then the opening snap (OS). When an S4 is present, it occurs in late di- The three sounds become two on expiration astole and coincides with contraction of

because A2 and P2 normally fuse. the atria (see Fig. 2.4). This sound is gener- The severity of stenosis can be approxi- ated by the left (or right) atrium vigorously

mated by the time interval between A2 and contracting against a stiffened ventricle.

the opening snap: the more advanced the Thus, an S4 usually indicates the presence stenosis, the shorter the interval. This oc- of cardiac disease—specifically, a decrease curs because the degree of left atrial pressure in ventricular compliance typically result- elevation corresponds to the severity of mi- ing from ventricular hypertrophy or myo-

tral stenosis. When the ventricle relaxes in cardial ischemia. Like an S3, the S4 is a dull, diastole, the greater the left atrial pressure, low-pitched sound and is best heard with the earlier the mitral valve opens. Com- the bell of the stethoscope. In the case

pared with severe stenosis, mild disease is of the more common left-sided S4, the marked by a less elevated left atrial pressure sound is loudest at the apex, with the pa- is less elevated, lengthening the time it tient lying in the left lateral decubitus

takes for the left ventricular pressure to fall position. S4 is sometimes referred to as an below that of the atrium. Therefore, in mild atrial gallop. 10090-02_CH02.qxd 8/24/06 5:41 PM Page 38

38 Chapter Two

Quadruple Rhythm or Summation Gallop Murmurs are described by their timing, intensity, pitch, shape, location, radiation, In a patient with both an S and S , those 3 4 and response to maneuvers. Timing refers to sounds, in conjunction with S and S , pro- 1 2 whether the murmur occurs during systole duce a quadruple beat. If a patient with a or diastole or is continuous (i.e., begins in quadruple rhythm develops tachycardia, di- systole and continues into diastole). The in- astole becomes shorter in duration, the S 3 tensity of the murmur is typically quantiﬁed and S coalesce, and a summation gallop 4 by a grading system. In the case of systolic results. The summation of S and S is heard 3 4 murmurs: as a long middiastolic, low-pitched sound,

often louder than S1 and S2.

Grade 1/6 (or I/VI): Barely audible (i.e., med- Pericardial Knock ical students may not hear it!) A pericardial knock is an uncommon, high- Grade 2/6 (or II/VI): Faint but immediately pitched sound that occurs in patients with audible severe constrictive pericarditis (see Chapter Grade 3/6 (or III/VI): Easily heard 14). It appears early in diastole soon after Grade 4/6 (or IV/VI): Easily heard and asso-

S2 and can be confused with an opening ciated with a palpable

snap or an S3. However, the knock appears thrill slightly later in diastole than the timing of Grade 5/6 (or V/VI): Very loud; heard with an opening snap and is louder and occurs stethoscope lightly on earlier than the ventricular gallop. It results chest Grade 6/6 (or VI/VI): Audible without the from the abrupt cessation of ventricular ﬁll- stethoscope directly on ing in early diastole, which is the hallmark the chest wall of constrictive pericarditis.

MURMURS And in the case of diastolic murmurs: A murmur is the sound generated by turbulent blood flow. Under normal conditions, the movement of blood through the vascular Grade 1/4 (or I/IV): Barely audible bed is laminar, smooth and silent. However, Grade 2/4 (or II/IV): Faint but immediately as a result of hemodynamic and/or structural audible changes, laminar flow can become disturbed Grade 3/4 (or III/IV): Easily heard Grade 4/4 (or IV/IV): Very loud and produce an audible noise. Murmurs result from any of the following mechanisms: 1. Flow across a partial obstruction (e.g., aortic stenosis) Pitch refers to the frequency of the murmur, ranging from high to low. High-frequency 2. Increased flow through normal structures murmurs are caused by large pressure gra- (e.g., aortic systolic murmur associated dients between chambers (e.g., aortic steno- with a high-output state, such as anemia) sis) and are best appreciated using the di- 3. Ejection into a dilated chamber (e.g., aphragm chest piece of the stethoscope. aortic systolic murmur associated with Low-frequency murmurs imply less of a pres- aneurysmal dilatation of the aorta) sure gradient between chambers (e.g., mitral 4. Regurgitant flow across an incompetent stenosis) and are best heard using the stetho- valve (e.g., mitral regurgitation) scope’s bell piece. 5. Abnormal shunting of blood from one Shape describes how the murmur changes vascular chamber to a lower-pressure in intensity from its onset to its comple- chamber (e.g., ventricular septal defect) tion. For example, a crescendo–decrescendo 10090-02_CH02.qxd 8/24/06 5:41 PM Page 39

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 39

(or “diamond-shaped”) murmur first rises right, Valsalva (forceful expiration against a and then falls off in intensity. Other shapes closed airway), or clenching of the fists, each include decrescendo (i.e., the murmur begins of which alters the heart’s loading condi- at its maximum intensity and grows softer) tions and can affect the intensity of many and uniform (the intensity of the murmur murmurs. Examples of the effects of maneu- does not change). vers on specific murmurs are presented in Location refers to the murmur’s region of Chapter 8. maximum intensity and is usually described When reporting a murmur, some or all of in terms of specific auscultatory areas (see these descriptors are mentioned. For exam- Fig. 2.2): ple, you might describe a particular patient’s murmur of aortic stenosis as “A grade III/ VI high-pitched, crescendo–decrescendo systolic murmur, heard best at the upper-right Aortic area: Second to third right inter- sternal border, radiating toward the neck.” costal spaces, next to sternum Pulmonic area: Second to third left intercostal spaces, next to sternum Systolic Murmurs Tricuspid area: Lower-left sternal border Mitral area: Cardiac apex Systolic murmurs are subdivided into systolic ejection murmurs, pansystolic murmurs, and late systolic murmurs (Fig. 2.6). A Fig. 6 systolic ejection murmur is typical of aor- From their primary locations, murmurs are tic or pulmonic valve stenosis. It begins after often heard to radiate to other areas of the the first heart sound and terminates before

chest, and such patterns of transmission re- or during S2, depending on its severity and late to the direction of the turbulent flow. whether the obstruction is of the aortic or Finally, similar types of murmurs can be pulmonic valve. The shape of the murmur is distinguished from one another by simple of the crescendo–decrescendo type (i.e., its bedside maneuvers, such as standing up- intensity rises and then falls).

Click

Figure 2.6. Classiﬁcation of systolic murmurs. Ejection murmurs are crescendo–decrescendo in conﬁguration, whereas pansystolic murmurs are uniform throughout systole. A late systolic murmur often follows a midsystolic click and suggests mitral (or tricuspid) valve prolapse. 10090-02_CH02.qxd 8/24/06 5:41 PM Page 40

40 Chapter Two

The ejection murmur of aortic stenosis be-

gins in systole after S1, from which it is sep- Fig. 7 arated by a short audible gap (Fig. 2.7). This gap corresponds to the period of isovolu- metric contraction of the left ventricle (the period after the mitral valve has closed but before the aortic valve has opened). The S A P murmur becomes more intense as flow in- 1 2 2 creases across the aortic valve during the rise in left ventricular pressure (crescendo). Then, as the ventricle relaxes, forward ﬂow decreases, and the murmur lessens in intensity (decrescendo) and ﬁnally ends prior

to the aortic component of S2. The murmur may be immediately preceded by an ejection click, especially in mild forms of aortic stenosis. S A P Although the intensity of the murmur 1 2 2 does not correlate well with the severity of aortic stenosis, other features do. For example, the more severe the stenosis, the longer it takes to force blood across the valve, and the Fig. 8 later the murmur peaks in systole (Fig. 2.8). Also, as shown in Figure 2.8, as the severity of

S1 P2

Figure 2.8. The severity of aortic stenosis affects the shape of the systolic murmur and the heart sounds. A. In mild stenosis, an ejection click (EJ) is often present, followed by an early peaking crescendo– decrescendo murmur and a normal aortic component of

S2 (A2). B. As stenosis becomes more severe, the peak of the murmur becomes more delayed in systole and the

intensity of A2 lessens. The prolonged ventricular ejection time delays A2 so that it merges with or occurs after the pulmonic component of S2 (P2); the ejection click may not be heard. C. In severe stenosis, the murmur

peaks very late in systole, and A2 is usually absent because of immobility of the valve leaflets. S1, first heart sound; S2, second heart sound.

stenosis increases, the aortic component of S2 softens because the leaflets become more rigidly fixed in place. Aortic stenosis causes a high-frequency murmur, reflecting the sizable pressure gra- S1 S2 dient across the valve. It is best heard in the “aortic area” at the second and third right Figure 2.7. Systolic ejection murmur of aortic steno- intercostal spaces close to the sternum. The sis. There is a short delay between the first heart sound murmur typically radiates toward the neck (S1) and the onset of the murmur. LV, left ventricle; S2, second heart sound. (the direction of turbulent blood flow) but 10090-02_CH02.qxd 8/24/06 5:41 PM Page 41

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 41

often can be heard in a wide distribution, in- Tricuspid valve regurgitation is best heard cluding the cardiac apex. along the left lower sternal border. It gener- The murmur of pulmonic stenosis also be- ally radiates to the right of the sternum and

gins after S1, it may be preceded by an ejec- is high pitched and blowing in quality. The tion click, but unlike aortic stenosis, it may intensity of the murmur increases with

extend beyond A2. That is, if the stenosis is inspiration because the negative intratho- severe, it will result in a very prolonged right racic pressure induced during inspiration ventricular ejection time, elongating the enhances venous return to the heart. The

murmur, which will continue beyond A2 latter augments right ventricular stroke vol- and end just before closure of the pulmonic ume, thereby increasing the amount of re-

valve (P2). Pulmonic stenosis is usually loud- gurgitated blood. est at the second to third left intercostal The murmur of a ventricular septal defect is spaces close to the sternum. It does not ra- heard best at the fourth to sixth left inter- diate as widely as aortic stenosis, but some- costal spaces, is high pitched, and may be as- times it is transmitted to the neck or left sociated with a palpable thrill. The intensity shoulder. of the murmur does not increase with in- Young adults often have benign systolic spiration, nor does it radiate to the axilla, ejection murmurs owing to increased systolic which helps distinguish it from tricuspid flow across normal aortic and pulmonic and mitral regurgitation, respectively. Of valves. This type of murmur often becomes note, the smaller the VSD, the greater the softer or disappears when the patient sits turbulence of blood flow between the left upright. and right ventricles and the louder the mur- Pansystolic (also termed holosystolic) mur. Some of the loudest murmurs ever murmurs are caused by regurgitation of heard are those associated with small VSDs. blood across an incompetent mitral or tri- Late systolic murmurs begin in mid-to- cuspid valve or through a ventricular septal late systole and continue to the end of sys- defect (VSD; see Fig. 2.6). These murmurs tole. The most common example is mitral are characterized by a uniform intensity regurgitation caused by mitral valve prolapse— throughout systole. In mitral and tricuspid bowing of abnormally redundant and elon- valve regurgitation, as soon as ventricular gated valve leaflets into the left atrium dur-

pressure exceeds atrial pressure (i.e., when S1 ing ventricular contraction (see Fig. 2.6). occurs), there is immediate retrograde ﬂow This murmur is usually preceded by a across the regurgitant valve. Thus, there is midsystolic click and is described further in

no gap between S1 and the onset of these Chapter 8. pansystolic murmurs, in contrast to the systolic ejection murmurs discussed earlier. Diastolic Murmurs Similarly, there is no signiﬁcant gap be-

tween S1 and the onset of the systolic Diastolic murmurs are divided into early de- murmur of a VSD, because left ventricular crescendo murmurs and mid-to-late rum- systolic pressure exceeds right ventricular bling murmurs (Fig. 2.9). Early diastolic Fig. 9 systolic pressure (and ﬂow occurs) quickly murmurs result from regurgitant flow after the onset of contraction. through either the aortic or pulmonic valve, The pansystolic murmur of advanced mi- with the former being much more common tral regurgitation continues through the aor- in adults. If produced by aortic valve regurgi-

tic closure sound because left ventricular tation, the murmur begins at A2, has a de- pressure remains greater than that in the left crescendo shape, and terminates before the

atrium at the time of aortic closure. The next S1. Because diastolic relaxation of the murmur is heard best at the apex, is high left ventricle is rapid, a pressure gradient de- pitched and “blowing” in quality, and often velops immediately between the aorta and radiates toward the left axilla; its intensity lower-pressured left ventricle in aortic re- does not change with respiration. gurgitation, and the murmur therefore dis- 10090-02_CH02.qxd 8/24/06 5:41 PM Page 42

42 Chapter Two

• Aortic regurgitation • Pulmonic regurgitation

S1 S2 S1

• Mild mitral or tricuspid stenosis

S1 S2 S1

• Severe mitral or tricuspid stenosis

S1 S2 S1

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

plays its maximum intensity at its onset. begins after S2 and is preceded by an open- Thereafter in diastole, as the aortic pressure ing snap. The shape of this murmur is falls and the LV pressure increases (as blood unique. Following the opening snap, the fills the ventricle), the gradient between the murmur is at its loudest because the pres- two chambers diminishes and the murmur sure gradient between the atrium and ven- decreases in intensity. Aortic regurgitation is tricle is at its maximum. The murmur then a high-pitched murmur, best heard using decrescendos or disappears totally during the diaphragm of the stethoscope along the diastole as the transvalvular gradient de- left sternal border with the patient sitting, creases. The degree to which the murmur leaning forward, and exhaling. fades depends on the severity of the steno- Pulmonic regurgitation in adults is usually sis. If the stenosis is severe, the murmur owing to the presence of pulmonary arterial is prolonged; if the stenosis is mild, the hypertension. It has an early diastolic de- murmur disappears in mid-to-late diastole. crescendo murmur profile similar to that of Whether the stenosis is mild or severe, the aortic regurgitation, but it is best heard in murmur intensifies at the end of diastole in the pulmonic area and its intensity may in- patients in normal sinus rhythm, when crease with inspiration. atrial contraction augments flow across the Mid-to-late diastolic murmurs result valve (see Fig. 2.9). The murmur of mitral from either turbulent flow across a stenotic stenosis is low pitched and is heard best mitral or tricuspid valve or less commonly with the bell of the stethoscope at the apex, from abnormally increased flow across a while the patient lies in the left lateral de- normal mitral or tricuspid valve (see Fig. cubitus position. The much less common 2.9). If resulting from stenosis, the murmur murmur of tricuspid stenosis is better aus- 1 LINE SHORT 10090-02_CH02.qxd 8/24/06 5:41 PM Page 43

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 43

cultated at the lower sternum, near the xi- begins in early systole, crescendos to its

phoid process. maximum at S2, then decrescendos until the

Hyperdynamic states such as fever, ane- next S1 (Fig. 2.10). Fig. 10 mia, hyperthyroidism, and exercise cause The “to-and-fro” combined murmur in a increased ﬂow across the normal tricuspid patient with both aortic stenosis and aortic and mitral valves and can therefore result in regurgitation could be mistaken for a con- a diastolic murmur. In patients with ad- tinuous murmur (see Fig. 2.10). During sys- vanced mitral regurgitation, the expected tole, there is a diamond-shaped ejection systolic murmur can be accompanied by an murmur, and during diastole a decrescendo additional diastolic murmur owing to the murmur. However, in the case of a to-and- increased volume of blood that must return fro murmur, the sound does not extend

across the valve to the left ventricle in dias- through S2 because it has discrete systolic tole. Similarly, patients with either tricuspid and diastolic components. regurgitation or an atrial septal defect (see Chapter 16) may display a diastolic flow murmur across the tricuspid valve. SUMMARY Abnormal heart sounds and murmurs are Continuous Murmurs common in acquired and congenital heart disease and can be predicted by the underly- Continuous murmurs are heard throughout ing pathology. Although it may seem diffi- the cardiac cycle without an audible hiatus cult to remember even the basic features pre- between systole and diastole. Such murmurs sented here, it will become easier as you learn result from conditions in which there is a more about the pathophysiology of these persistent pressure gradient between two conditions, and as your experience in physi- structures during systole and diastole. An cal diagnoses grows. For now, just remember example is the murmur of patent ductus ar- that the information is here, and refer to it as teriosus, in which there is an abnormal com- needed. Tables 2.2 and 2.3 and Figure 2.11 Tab. 2, munication between the aorta and pul- summarize features of the heart sounds and Tab. 3, monary artery (see Chapter 16). During murmurs described in this chapter. Fig. 11 systole, blood flows from the high-pressure ascending aorta through the ductus into the lower-pressure pulmonary artery. During di- Acknowledgments astole, the aortic pressure remains greater Contributors to the previous editions of this chapter than that in the pulmonary artery and flow were Oscar Benavidez, MD; Bradley S. Marino, MD; continues across the ductus. This murmur Allan Goldblatt, MD; and Leonard S. Lilly, MD.

• Patent ductus arteriosus

S1 S2 S1

• Aortic stenosis and regurgitation • Pulmonic stenosis and regurgitation

S1 S2 S1

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- 1 LINE SHORT ponent, separated by S2. S1, ﬁrst heart sound. 10090-02_CH02.qxd 8/24/06 5:41 PM Page 44

44 Chapter Two

TABLE 2.2. Common Heart Sounds

Sound Location Pitch Signiﬁcance

S1 Apex High Normal closure of mitral and tricuspid valves

S2 Base High Normal closure of aortic (A2) and

pulmonic (P2) valves Extra systolic sounds Ejection clicks Aortic: apex and base High Aortic or pulmonic stenosis, or dilata- Pulmonic: base High tion of aortic root or pulmonary artery Mid-to-late click Mitral: apex High Mitral or tricuspid valve prolapse Tricuspid: LLSB High Extra diastolic sounds Opening snap Apex High Mitral stenosis

S3 Left-sided: apex Low Normal in children Abnormal in adults: indicates heart failure or volume overload state

S4 Left-sided: apex Low Reduced ventricular compliance

LLSB, lower left sternal border.

TABLE 2.3. Common Murmurs

Murmur Type Example Location and Radiation

Systolic ejection Aortic stenosis 2nd right intercostal space → neck (but may radiate widely) Pulmonic stenosis 2nd–3rd left intercostal spaces

Pansystolic Mitral regurgitation Apex → axilla Tricuspid regurgitation Left lower sternal border → right lower sternal border

Late systolic Mitral valve prolapse Apex → axilla

Early diastolic Aortic regurgitation Along left side of sternum Pulmonic regurgitation Upper left side of sternum

Mid- or late diastolic Mitral stenosis Apex 10090-02_CH02.qxd 8/24/06 5:41 PM Page 45

The Cardiac Cycle: Mechanisms of Heart Sounds and Murmurs 45

Aortic area Pulmonic area Ejection-type murmur Ejection-type murmur • Aortic stenosis • Pulmonic stenosis • Flow murmur • Flow murmur

Left sternal border Early diastolic murmur • Aortic regurgitation • Pulmonic regurgitation

Mitral area Tricuspid area Pansystolic murmur Pansystolic murmur • Mitral regurgitation • Tricuspid regurgitation Mid-to-late diastolic murmur • Ventricular septal defect • Mitral stenosis

Mid-to-late diastolic murmur • Tricuspid stenosis • Atrial septal defect Figure 2.11. Locations of maximum intensity of common murmurs.

Additional Reading LeBlond RF, DeGowin RL, Brown DD. DeGowin’s Diagnostic Examination. 7th Ed. New York: Bickley LS. Bates’ Guide to Physical Examination McGraw-Hill, 2004. and History Taking. 8th Ed. Philadelphia: Lippin- Orient JM, Sapira JD. Sapira’s Art and Science of Bed- cott Williams & Wilkins, 2003. side Diagnosis. 3rd Ed. Philadelphia: Lippincott Constant J. Essentials of Bedside Cardiology. 2nd Ed. Williams & Wilkins, 2005. Totowa, NJ: Humana Press, 2003.