Cardiac diseases often cause abnormal findings on physical examination, including pathologic heart sounds and murmurs. These findings are clues to the underlying pathophysiology, and proper interpretation is essential for successful diagnosis and disease management. This chapter describes heart sounds in the context of the normal cardiac cycle and then focuses on the origins of pathologic heart sounds and murmurs.
Many cardiac diseases are mentioned briefly in this chapter as examples of abnormal heart sounds and murmurs. Because each of these conditions is described in greater detail later in the book, it is not necessary to memorize the examples presented here. Rather, the goal of this chapter is to explain the mechanisms by which the abnormal sounds are produced, so that their descriptions will make sense in later chapters.
The cardiac cycle consists of precisely timed electrical and mechanical events that are responsible for rhythmic atrial and ventricular contractions. Figure 2.1 displays the pressure relationships between the left-sided cardiac chambers during the normal cardiac cycle and serves as a platform for describing key events. Mechanical systole refers to the phase of ventricular contraction, and diastole refers to the phase of ventricular relaxation and filling. Throughout the cardiac cycle, the right and left atria accept blood returning to the heart from the systemic veins and from the pulmonary veins, respectively. During diastole, blood passes from the atria into the ventricles across the open tricuspid and mitral valves, causing a gradual increase in ventricular diastolic pressures. In late diastole, atrial contraction propels a final bolus of blood into each ventricle, an action that produces a brief further rise in atrial and ventricle pressures, termed the a wave (see Fig. 2.1).
Figure 2.1.The normal cardiac cycle, showing pressure relationships between the left-sided heart chambers.
During diastole, the mitral valve (MV) is open, so that the left atrial (LA) and left ventricular (LV) pressures are equal. In late diastole, LA contraction causes a small rise in pressure in both the LA and LV (the a wave). During systolic contraction, the LV pressure rises; when it exceeds the LA pressure, the MV closes, contributing to the first heart sound (S1). As LV pressure rises above the aortic pressure, the aortic valve (AV) opens, which is a silent event. As the ventricle begins to relax and its pressure falls below that of the aorta, the AV closes, contributing to the second heart sound (S2). As LV pressure falls further, below that of the LA, the MV opens, which is silent in the normal heart. In addition to the a wave, the LA pressure curve displays two positive deflections: the c wave represents a small rise in LA pressure as the MV closes and bulges toward the atrium, and the v wave is the result of passive filling of the LA from the pulmonary veins during systole, when the MV is closed.
Contraction of the ventricles follows, signaling the onset of mechanical systole. As the ventricles start to contract, the pressures within them rapidly exceed atrial pressures. This results in the forced closure of the tricuspid and mitral valves, which produces the first heart sound, termed S1. This sound has two nearly superimposed components: the mitral component slightly precedes that of the tricuspid valve because of the earlier electrical activation of the left ventricle (see Chapter 4).
As the right and left ventricular pressures rapidly rise further, they soon exceed the diastolic pressures within the pulmonary artery and aorta, forcing the pulmonic and aortic valves to open, and blood is ejected into the pulmonary and systemic circulations. The ventricular pressures continue to increase during the initial portion of this ejection phase, and then decline as ventricular relaxation commences. Since the pulmonic and aortic valves are open during this phase, the aortic and pulmonary artery pressures rise and fall in parallel to those of the corresponding ventricles.
At the conclusion of ventricular ejection, the ventricular pressures decline below those of the pulmonary artery and aorta (the pulmonary artery and aorta are elastic structures that maintain their pressures longer), such that the pulmonic and aortic valves are forced to close, producing the second heart sound, S2. Like the first heart sound (S1), this sound consists of two parts: the aortic (A2) component normally precedes the pulmonic (P2) because the diastolic pressure gradient between the aorta and left ventricle is greater than that between the pulmonary artery and the right ventricle, forcing the aortic valve to shut more readily. The ventricular pressures fall rapidly during the subsequent relaxation phase. As they drop below the pressures in the right and left atria, the tricuspid and mitral valves open, followed by diastolic ventricular filling and then repetition of this cycle.
Notice in Figure 2.1 that in addition to the a wave, the atrial pressure curve displays two other positive deflections during the cardiac cycle: the c wave represents a small rise in atrial pressure as the tricuspid and mitral valves close and bulge into their respective atria. The v wave is the result of passive filling of the atria from the systemic and pulmonary veins during systole, a period during which blood accumulates in the atria because the tricuspid and mitral valves are closed.
At the bedside, systole can be approximated as the period from S1 to S2, and diastole from S2 to the next S1. Although the duration of systole remains constant from beat to beat, the length of diastole varies with the heart rate: the faster the heart rate, the shorter the diastolic phase. The main sounds, S1 and S2, provide a framework from which all other heart sounds and murmurs can be timed.
The pressure relationships and events depicted in Figure 2.1 are those that occur in the left side of the heart. Equivalent events occur simultaneously in the right side of the heart in the right atrium, right ventricle, and pulmonary artery. At the bedside, clues to right-heart function can be ascertained by examining the jugular venous pulse, which is 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 cardiovascular 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 representation of the RA pressure. Thus, the JVP provides an easily obtainable measure of right-heart function.
Typical fluctuations in the jugular venous pulse during the cardiac cycle, manifested by oscillations in the overlying skin, are shown in the figure (notice the similarity to the left atrial pressure tracing in Fig. 2.1). There are two major upward 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 interrupted by a small upward deflection (the c wave) 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 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 muscle, whereas 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 pulsatile to palpation, it has a double rather than a single upstroke, and it declines in most patients by assuming the seated position or during inspiration.
Commonly used stethoscopes contain two chest pieces for auscultation of the heart. The concave “bell” chest piece, meant to be applied lightly to the skin, accentuates low-frequency sounds. Conversely, the flat “diaphragm” chest piece is designed to be pressed firmly against the skin to eliminate low frequencies and therefore accentuate high-frequency sounds and murmurs. Some modern stethoscopes incorporate 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. The sections below describe when, and where on the chest, to listen for high- versus low-frequency sounds.
First Heart Sound (S1)
S1 is produced by the closure of the mitral and tricuspid valves in early systole and is loudest 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 0.01 sec, such that the human ear appreciates only a single sound. An exception occurs in patients with right bundle branch block (see Chapter 4), in whom these components may be audibly split because of delayed right ventricular contraction and late closure of the tricuspid valve.
Figure 2.2.Standard positions of stethoscope placement for cardiac auscultation
Three factors determine the intensity of S1: (1) the distance separating the leaflets of the open valves at the onset of ventricular contraction; (2) the mobility of the leaflets (normal, or rigid because of stenosis); and (3) the rate of rise of ventricular pressure ( Table 2.1).
Table 2.1.Causes of Altered Intensity of First Heart Sound (S1)
The distance between the open valve leaflets at the onset of ventricular contraction relates to the electrocardiographic PR interval (see Chapter 4), the period between the onset of atrial and ventricular activation. Atrial contraction at the end of diastole forces the tricuspid and mitral valve leaflets apart. As they start to drift back together, ventricular contraction forces them shut, from whatever position they are at, as soon as the ventricular pressure exceeds that in the atrium. An accentuated S1 results when the PR interval is shorter than normal because the valve leaflets do not have sufficient time to drift back together and are therefore forced shut from a relatively wide distance.
Similarly, in mild mitral stenosis (see Chapter 8), a prolonged diastolic pressure gradient exists between the left atrium and ventricle, which keeps the mobile portions of the mitral leaflets farther apart than normal during diastole. Because the leaflets are relatively wide apart at the onset of systole, they are forced shut loudly when the left ventricle contracts.
S1 may also be accentuated when the heart rate is more rapid than normal (i.e., tachycardia) because diastole is shortened and the leaflets have insufficient time to drift back together before the ventricles contract.
Conditions that reduce the intensity of S1 are also listed in Table 2.1. In first-degree atrioventricular (AV) block (see Chapter 12), a diminished S1 results from an abnormally prolonged PR interval, which delays the onset of ventricular contraction. Consequently, following atrial contraction, the mitral and tricuspid valves have additional time to float back together so that the leaflets are forced closed from only a small distance apart and the sound is softened.
In patients with mitral regurgitation (see Chapter 8), S1 is often diminished in intensity because the mitral leaflets may not come into full contact with one another as they close. In severe mitral stenosis, the leaflets are nearly fixed in position throughout the cardiac cycle, and that reduced movement lessens the intensity of S1.
In patients with a “stiffened” left ventricle (e.g., a hypertrophied chamber), atrial contraction results in a higher-than-normal pressure at the end of diastole. This greater pressure causes the mitral leaflets to drift together more rapidly, so that they are forced closed from a smaller-than-normal distance when ventricular contraction begins, thus reducing the intensity of S1.