CHAPTER 9: The Cardiovascular System

Intro

Introduction

Listening to the heart has come to epitomize the art of bedside diagnosis. Mastering the skills of cardiac examination requires patience, practice, and repetition—a process especially vulnerable to evolving technology and the time constraints of clinical practice.[1]–[4] Many reports attest to the current decline in physical examination skills, well documented for the cardiovascular system at all levels of training.[5]–[12]

As you study this chapter, combining your knowledge of anatomy and physiology with hands-on practice of inspection, palpation, and auscultation brings rewards of proven diagnostic value. Take advantage of the numerous programs for learning cardiac physiology and auscultation that can reinforce your growing clinical acumen, and pursue the emerging literature that compares the effectiveness of different modes of learning these important skills.[13]–[22]

Anatomy and Physiology

Surface Projections of the Heart and Great Vessels

Visualize the underlying structures of the heart as you inspect the anterior chest. Note that the right ventricle (RV) occupies most of the anterior cardiac surface. This chamber and the pulmonary artery form a wedgelike structure behind and to the left of the sternum, outlined in black (Fig. 9-1).

FIGURE 9-1 Chest wall and cardiac anatomy.

Chest wall and cardiac anatomy.

The inferior border of the RV lies below the junction of the sternum and the xiphoid process. The RV narrows superiorly and joins the pulmonary artery at the level of the sternal angle, or “base of the heart,” a clinical term that refers to the superior aspect of the heart at the right and left 2nd interspaces adjacent to the sternum.

The left ventricle, behind the RV and to the left, forms the left lateral margin of the heart (Fig. 9-2). Its tapered inferior tip is often termed the cardiac apex. It is clinically important because it produces the apical impulse, identified during palpation of the precordium as the point of maximal impulse (PMI). This impulse locates the left border of the heart and is normally found in the 5th intercostal space at or just medial to the left midclavicular line (or 7 to 9 cm lateral to the midsternal line). The PMI is not always palpable, even in a healthy patient with a normal heart. Detection is affected by both the patient’s body habitus and position during the examination.

FIGURE 9-2 Cardiac anatomy—major structures.

Cardiac anatomy—major structures.


Rarely, in situs inversus and dextrocardia, the PMI is located on the right side of the chest.


? In supine patients the diameter of the PMI may be as large as a quarter, approximately 1 to 2.5 cm.


A PMI ;2.5 cm is evidence of left ventricular hypertrophy (LVH) from hypertension or aortic stenosis.


? Note that, in some patients, the most prominent precordial impulse may not be at the apex of the left ventricle. For example, in patients with chronic obstructive pulmonary disease (COPD), the most prominent palpable impulse or PMI may be in the xiphoid or epigastric area due to right ventricular hypertrophy.


Displacement of the PMI lateral to the midclavicular line or ;10 cm lateral to the midsternal line occurs in LVH and also in ventricular dilatation from myocardial infarction (MI) or heart failure.


Above the heart lie the great vessels. The pulmonary artery bifurcates quickly into its left and right branches. The aorta curves upward from the left ventricle to the level of the sternal angle, where it arches posteriorly to the left and then downward. On the medial border, the superior and inferior venae cavae channel venous blood from the upper and lower portions of the body into the right atrium.

Cardiac Chambers, Valves, and Circulation

Circulation through the heart is diagrammed below. Identify the cardiac chambers, valves, and direction of blood flow. Because of their location, the mitral and tricuspid valves are often called atrioventricular (AV) valves. The aortic and pulmonic valves are called semilunar valves because the valve leaflets are shaped like half moons.

As the heart valves close, the heart sounds of S1 and S2 arise from vibrations emanating from the leaflets, the adjacent cardiac structures, and the flow of blood. Study carefully the opening and closing of the AV and semilunar valves in relation to events in the cardiac cycle to improve your diagnostic accuracy as you auscultate the heart. In Figure 9-3, note that the aortic and pulmonic valves are closed, and the mitral and tricuspid valves are open, as seen in diastole.

FIGURE 9-3 Cardiac chambers, valves, and circulation.

Cardiac chambers, valves, and circulation.


In most adults over age 40 years, the diastolic sounds of S3 and S4 are pathologic, and are correlated with heart failure and acute myocardial ischemia.19,23,24 In recent studies, an S3 corresponds to an abrupt deceleration of inflow across the mitral valve, and an S4 to increased left ventricular end diastolic stiffness which decreases compliance.25–27


Events in the Cardiac Cycle

The heart serves as a pump that generates varying pressures as its chambers contract and relax. Systole is the period of ventricular contraction. As shown in Figure 9-4, pressure in the left ventricle rises, from less than 5 mm Hg in its resting state, to a normal peak of 120 mm Hg. After the ventricle ejects much of its blood into the aorta, the pressure levels off and starts to fall. Diastole is the period of ventricular relaxation. Ventricular pressure falls further to below 5 mm Hg, and blood flows from atrium to ventricle. Late in diastole, ventricular pressure rises slightly during inflow of blood from atrial contraction.

FIGURE 9-4 Cardiac cycle—left ventricle.

Cardiac cycle—left ventricle.

Note that during systole the aortic valve is open, allowing ejection of blood from the left ventricle into the aorta. The mitral valve is closed, preventing blood from regurgitating back into the left atrium. In contrast, during diastole the aortic valve is closed, preventing regurgitation of blood from the aorta back into the left ventricle. The mitral valve is open, allowing blood to flow from the left atrium into the relaxed left ventricle. At the same time, during systole the pulmonic valve opens and the tricuspid valve closes as blood is ejected from the RV into the pulmonary artery. During diastole, the pulmonic valve closes and the tricuspid valve opens as blood flows into the right atrium.

Understanding the interrelationships of the pressure gradients in the left heart (the left atrium, left ventricle, and aorta), together with the position and movement of the four heart valves, is fundamental to understanding heart sounds. An extensive literature explores how heart sounds are generated. Possible explanations include closure of the valve leaflets; tensing of related structures, leaflet positions, and pressure gradients at the time of atrial and ventricular systole; and the acoustic effects of moving columns of blood.

Trace the changing left ventricular pressures and sounds through one cardiac cycle. Note that S1 and S2 define the duration of systole and diastole. Right heart sounds occur at pressures that are usually lower than those on the left, and are usually less audible. The explanations given here are oversimplified, but retain clinical usefulness.

During diastole, pressure in the blood-filled left atrium slightly exceeds that in the relaxed left ventricle, and blood flows from left atrium to left ventricle across the open mitral valve (Fig. 9-5). Just before the onset of ventricular systole, atrial contraction produces a slight pressure rise in both chambers.

FIGURE 9-5 Cardiac cycle—diastole.

Cardiac cycle—diastole.

During systole, the left ventricle starts to contract and ventricular pressure rapidly exceeds left atrial pressure, closing the mitral valve (Fig. 9-6). Closure of the mitral valve produces the first heart sound, S1.

FIGURE 9-6 Diastole—mitral valve closes.

Diastole—mitral valve closes.

As left ventricular pressure continues to rise, it quickly exceeds the pressure in the aorta and forces the aortic valve open (Fig. 9-7). In some pathologic conditions, an early systolic ejection sound (Ej)accompanies the opening of the aortic valve. Normally, maximal left ventricular pressure corresponds to systolic blood pressure.

FIGURE 9-7 Systole—aortic valve opens.

Systole—aortic valve opens.

As the left ventricle ejects most of its blood, ventricular pressure begins to fall. When left ventricular pressure drops below aortic pressure, the aortic valve closes (Fig. 9-8). Aortic valve closure produces the second heart sound, S2, and another diastole begins.

FIGURE 9-8 Systole—aortic valve closes.

Systole—aortic valve closes.

In diastole, left ventricular pressure continues to drop and falls below left atrial pressure. The mitral valve opens (Fig. 9-9). This event is usually silent, but may be audible as a pathologic opening snap (OS) if valve leaflet motion is restricted, as in mitral stenosis.

FIGURE 9-9 Diastole—mitral valve opens.

Diastole—mitral valve opens.

After the mitral valve opens, there is a period of rapid ventricular filling as blood flows early in diastole from left atrium to left ventricle (Fig. 9-10). In children and young adults, a third heart sound, S3, may arise from rapid deceleration of the column of blood against the ventricular wall. In older adults, an S3, sometimes termed “an S3 gallop,” usually indicates a pathologic change in ventricular compliance.

FIGURE 9-10 Diastole—rapid ventricular filling; S3.

Diastole—rapid ventricular filling; S3.

Finally, although not often heard in normal adults, a fourth heart sound, S4, marks atrial contraction (Fig. 9-11). It immediately precedes S1 of the next beat and can also reflect a pathologic change in ventricular compliance.

FIGURE 9-11 Diastole—atrial contraction; S4.

Diastole—atrial contraction; S4.

The Splitting of Heart Sounds

While these events are occurring on the left side of the heart, similar changes are occurring on the right side, which involves the right atrium, tricuspid valve, RV, pulmonic valve, and pulmonary arteries. Right ventricular and pulmonary arterial pressures are significantly lower than corresponding pressures on the left side. Note that right-sided cardiac events usually occur slightly later than those on the left. Instead of a hearing a single heart sound for S2, you may hear two discernible components, the first from left-sided aortic valve closure, or A2, and the second from right-sided closure of the pulmonic valve, or P2.

The second heart sound, S2, and its two components, A2 and P2, are caused primarily by closure of the aortic and pulmonic valves, respectively. During inspiration, the right heart filling time is increased, which increases right ventricular stroke volume and the duration of right ventricular ejection compared with the neighboring left ventricle. This delays the closure of the pulmonic valve, P2, splitting S2 into its two audible components.

During expiration, these two components fuse into a single sound, S2 (Fig. 9-12). Note that because walls of veins contain less smooth muscle, the venous system has more capacitance than the arterial system and lower systemic pressure. Distensibility and impedance in the pulmonary vascular bed contribute to the “hangout time” that delays P2.[28]

FIGURE 9-12 Spitting of S2 during inspiration.

Spitting of S2 during inspiration.

Of the two components of the S2, A2 is normally louder, reflecting the high pressure in the aorta. It is heard throughout the precordium. In contrast, P2 is relatively soft, reflecting the lower pressure in the pulmonary artery. It is heard best in its own area, the 2nd and 3rd left interspaces close to the sternum. It is here that you should search for the splitting of S2.

S1 also has two components, an earlier mitral and a later tricuspid sound. The mitral sound—the principal component of S1—is much louder, again reflecting the higher pressures on the left side of the heart. It can be heard throughout the precordium and is loudest at the cardiac apex. The softer tricuspid component is heard best at the lower left sternal border; it is here that you may hear a split S1. The earlier louder mitral component may mask the tricuspid sound, however, and splitting is not always detectable. Splitting of S1 does not vary with respiration.

Heart Murmurs

Heart murmurs are distinct heart sounds distinguished by their pitch and their longer duration. They are attributed to turbulent blood flow and are usually diagnostic of valvular heart disease. At times, they may also represent “innocent” flow murmurs, especially in young adults. A stenotic valve has an abnormally narrowed valvular orifice that obstructs blood flow, as in aortic stenosis, and causes a characteristic murmur. So does a valve that fails to fully close, as in aortic regurgitation. Such a valve allows blood to leak backward in a retrograde direction and produces a regurgitant murmur.

To identify murmurs accurately, you must learn where they are best heard on the chest wall, their timing in systole or diastole, and their descriptive qualities. In the Techniques of Examination section, you will learn to integrate location and timing with the murmur’s shape, maximal intensity, direction of radiation, grade of intensity, pitch, and quality (see pp. 373–399).

Relation of Auscultatory Findings to the Chest Wall

The locations on the chest wall where you auscultate heart sounds and murmurs help identify the valve or chamber where they originate.


Chest Wall Location and Origin of Valve Sounds and Murmurs

Chest Wall Location Typical Origin of Sounds and Murmurs
Right 2nd interspace to the apex Aortic valve
Left 2nd and 3rd interspaces close to the sternum, but also at higher or lower levels Pulmonic valve
At or near the lower left sternal border Tricuspid valve
At and around the cardiac apex Mitral valve

These areas overlap, as illustrated in Figure 9-13. Integrating the auscultatory location with the timing of the sound or murmur, either systole or diastole, is an important first step in identifying sounds and murmurs correctly, and often leads to accurate bedside diagnosis when integrated with other cardiac findings.

FIGURE 9-13 Listening areas on the chest wall.

Listening areas on the chest wall.