10090-02_CH02.qxd 8/24/06 5:41 PM Page 29 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 29 10090-02_CH02.qxd 8/24/06 5:41 PM Page 30 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 aor- tic 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 pul- monary 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 pres- sure 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, 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) 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 contrac- tion. 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, tri- cuspid valve disease, pulmonic stenosis, pericardial diseases) elevate the JVP, while re- duced 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 ster- nal 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.