The mechanical function of the heart can be described by the pressure, volume, and flow changes that occur within it during a single cardiac cycle. A cardiac cycle is defined as one complete sequence of contraction and relaxation. The normal mechanical events of a cycle of the left heart pump are correlated in Figure 3–1
. This important figure summarizes a great deal of information and should be studied carefully.
Cardiac cycle—left heart pump. Cardiac cycle phases: A, diastole; B, systole that is divided into 3 periods; C, isovolumetric contraction; D, ejection; and E, isovolumetric relaxation.
The diastolic phase1 of the cardiac cycle begins with the opening of the atrioventricular (AV) valves. As shown in Figure 3–1, the mitral valve passively opens when left ventricular pressure falls below left atrial pressure and the period of ventricle filling begins. Blood that had previously accumulated in the atrium behind the closed mitral valve empties rapidly into the ventricle, and this causes an initial drop in atrial pressure. Later, the pressures in both chambers slowly rise together as the atrium and ventricle continue passively filling in unison with blood returning to the heart through the veins.
Proper filling of the ventricles depends on three conditions: (1) the filling pressure of blood returning to the heart and atria, (2) the ability of the AV valves to open fully (not be stenotic), and (3) the ability of the ventricular wall to expand passively with little resistance (ie, to have high compliance). The healthy heart is very compliant during diastole so that filling normally occurs with only small increases in ventricular pressure.
Atrial contraction is initiated near the end of ventricular diastole by the depolarization of the atrial muscle cells, which causes the P wave of the electrocardiogram. As the atrial muscle cells develop tension and shorten, atrial pressure rises and an additional amount of blood is forced into the ventricle. At normal resting heart rates, atrial contraction is not essential for adequate ventricular filling. This is evident in Figure 3–1 from the fact that the ventricle has nearly reached its maximum or end-diastolic volume before atrial contraction begins. Atrial contraction plays an increasingly significant role in ventricular filling as heart rate increases because the time interval between beats for passive filling becomes progressively shorter with increased heart rate. Note that throughout diastole, atrial and ventricular pressures are nearly identical. This is because a normal open mitral valve has very little resistance to flow and thus only a very small atrial–ventricular pressure difference is necessary to produce ventricular filling.
Ventricular systole begins when the action potential passes through the AV node and sweeps over the ventricular muscle—an event heralded by the QRS complex of the electrocardiogram. Contraction of the ventricular muscle cells causes intraventricular pressure to rise above that in the atrium. Because of the valve structure, the increased pressure behind the leaflets in the ventricle causes abrupt closure of the AV valve.
Pressure in the left ventricle continues to rise sharply as the ventricular contraction intensifies. When the left ventricular pressure exceeds that in the aorta, the aortic valve passively opens. The period between mitral valve closure and aortic valve opening is referred to as the isovolumetric contraction phase because during this interval the ventricle is a closed chamber with a fixed volume. Ventricular ejection begins with the opening of the aortic valve. In early ejection, blood enters the aorta rapidly and causes the pressure there to rise. Pressure builds up simultaneously in both the ventricle and the aorta as the ventricular muscle cells continue to contract in early systole. This interval is often called the rapid ejection period.
Left ventricular and aortic pressures ultimately reach a maximum called peak systolic pressure. At this point, the strength of ventricular muscle contraction begins to wane. Muscle shortening and ejection continue, but at a reduced rate. Aortic pressure begins to fall because blood is leaving the aorta and large arteries faster than blood is entering from the left ventricle. Throughout ejection, very small pressure differences exist between the left ventricle and the aorta because the aortic valve orifice is so large that it presents very little resistance to flow.
Eventually, the strength of the ventricular contraction diminishes to the point where intraventricular pressure falls below aortic pressure. Because of the aortic valve structure, the increased pressure behind the leaflets in the aorta causes abrupt closure of the aortic valve. A dip, called the incisura or dicrotic notch, appears in the aortic pressure trace because a small volume of aortic blood must flow backward to fill the space behind the aortic valve leaflets as they close. After aortic valve closure, intraventricular pressure falls rapidly as the ventricular muscle relaxes. For a brief interval, called the isovolumetric relaxation phase, the mitral valve is also closed. Ultimately, intraventricular pressure falls below atrial pressure, the AV valve opens, and a new cardiac cycle begins.
Note that atrial pressure progressively rises during ventricular systole because blood continues to return to the heart and fill the atrium. The elevated atrial pressure at the end of systole promotes rapid ventricular filling once the AV valve opens to begin the next heart cycle.
The ventricle has reached its minimum or end-systolic volume at the time of aortic valve closure. The amount of blood ejected from the ventricle during a single beat, the stroke volume, is equal to ventricular end-diastolic volume minus ventricular end-systolic volume. Note that under normal conditions, the heart ejects only about 60% of its end-diastolic volume.
The aorta distends or balloons out during systole because more blood enters the aorta than leaves it. During diastole, the arterial pressure is maintained by the elastic recoil of walls of the aorta and other large arteries. Nonetheless, aortic pressure gradually falls during diastole as the aorta supplies blood to the systemic vascular beds. The lowest aortic pressure, reached at the end of diastole, is called diastolic pressure. The difference between diastolic and peak systolic pressures in the aorta is called the arterial pulse pressure. Typical values for systolic and diastolic pressures in the aorta are 120 and 80 mm Hg, respectively.
At a normal resting heart rate of approximately 70 beats/min, the heart spends approximately two-thirds of the cardiac cycle in diastole and one-third in systole. When increases in the heart rate occur, both diastolic and systolic intervals become shorter. Action potential durations are shortened and conduction velocity is increased. Contraction and relaxation rates are also enhanced. This shortening of the systolic interval tends to blunt the potential adverse effects of increases in the heart rate on diastolic filling time.
Because the entire heart is served by a single electrical excitation system, similar mechanical events occur essentially simultaneously in both the left and right sides of the heart. Both ventricles have synchronous systolic and diastolic periods, and the valves of the right and left sides of the heart normally open and close nearly in unison. Because the two sides of the heart are arranged in series in the circulation, they must pump the same amount of blood and therefore must have identical stroke volumes.
The major difference between the right and left pumps is in the magnitude of the peak systolic pressure. The pressures developed by the right side of the heart, as shown in Figure 3–2, are considerably lower than those for the left side of the heart (Figure 3–1). This is because the lungs provide considerably less resistance to blood flow than that offered collectively by the systemic organs. Therefore, less arterial pressure is required to drive the cardiac output through the lungs than through the systemic organs. Typical pulmonary artery systolic and diastolic pressures are 24 and 8 mm Hg, respectively.
Cardiac cycle—right heart pump.
The pressure pulsations that occur in the right atrium are transmitted in retrograde fashion to the large veins near the heart. These pulsations, shown on the atrial pressure trace in Figure 3–2, can be visualized in the neck over the jugular veins in a recumbent individual. They are collectively referred to as the jugular venous pulse and can provide clinically useful information about the heart. Atrial contraction produces the first pressure peak called the a wave. The c wave, which follows shortly thereafter, coincides with the onset of ventricular systole and is caused by an initial bulging of the tricuspid valve into the right atrium. Right atrial pressure falls after the c wave because of atrial relaxation and a downward displacement of the tricuspid valve during ventricular emptying. Right atrial pressure then begins to increase toward a third peak, the v wave, as the central veins and right atrium fill behind a closed tricuspid valve with blood returning to the heart from the peripheral organs. With the opening of the tricuspid valve at the conclusion of ventricular systole, right atrial pressure again falls as blood moves into the relaxed right ventricle. Shortly afterward, right atrial pressure begins to rise once more toward the next a wave, as returning blood fills the central veins, the right atrium, and the right ventricle together during diastole.
A phonocardiographic record of the heart sounds, which occur in the cardiac cycle, is included in Figure 3–1
. These sounds are normally heard by auscultation
with a stethoscope placed on the chest. The first heart sound, S1
, occurs at the beginning of systole because of the abrupt closure of the AV valves, which produces vibrations of the cardiac structures and the blood in the ventricular chambers. S1
can be heard most clearly by placing the stethoscope over the apex of the heart. Note that this sound occurs immediately after the QRS complex of the electrocardiogram.
The second heart sound, S2, arises from the closure of the aortic and pulmonic valves at the beginning of the period of isovolumetric relaxation. This sound is heard near the end of the T wave in the electrocardiogram. The pulmonic valve usually closes slightly after the aortic valve. Because this discrepancy is enhanced during the inspiratory phase of the respiratory cycle, inspiration causes what is referred to as the physiological splitting of the second heart sound. The discrepancy in valve closure during inspiration may range from 30 to 60 ms. There are at least two factors that lead to this prolonged ejection time from the right ventricle during inspiration. The first is related to an inspiration-induced decrease in intrathoracic pressure and increased filling of the right side of the heart. This extra volume will be ejected, but a little extra time is required to do so. The second factor is related to the inspiration-induced decrease in pulmonary vascular resistance, which transiently reduces pulmonary artery pressure and right ventricular afterload. With reduced afterload, ventricular ejection can go on for a slightly longer period of time.
The third and fourth heart sounds, shown in Figure 3–1, are not normally present. When they are present, however, they, along with S1 and S2, produce what are called gallop rhythms (resembling the sound of a galloping horse). When present, the third heart sound occurs shortly after S2 during the period of rapid passive ventricular filling and, in combination with heart sounds S1 and S2, produces what is called ventricular gallop rhythm. Although S3 may sometimes be detected in normal children, it is heard more commonly in patients with left ventricular failure. The fourth heart sound, which occasionally is heard shortly before S1, is associated with atrial contraction and rapid active filling of the ventricle. Thus, the combination of S1, S2, and S4 sounds produces what is called an atrial gallop rhythm. The presence of S4 often indicates an increased ventricular diastolic stiffness, which can occur with several cardiac disease states.
There may be other sounds associated with the cardiac cycle that usually indicate abnormal conditions. Murmurs can occur during systole or diastole and usually indicate turbulent flow through cardiac valves that do not fully open or are completely closed. (These are described in more detail in Chapter 5.) Information about other abnormal sounds including rubs, snaps, and clicks can be obtained in more specific clinical references.
Cardiac Cycle Pressure–Volume and Length–Tension Relationships
Intraventricular pressure and volume are intimately linked to the tension and length of the cardiac muscle cells in the ventricular wall through purely geometric and physical laws. Figure 3–3A
shows the correspondence between a ventricular pressure–volume loop and a cardiac muscle length–tension loop during a single cardiac cycle. These two loops indicate that cardiac muscle length–tension behavior is the underlying basis for ventricular function. Note that in Figure 3–3
, each major phase of the ventricular cardiac cycle has a corresponding phase of cardiac muscle length and tension change. During diastolic ventricular filling, for example, the progressive increase in ventricular pressure causes a corresponding increase in muscle tension, which passively stretches the resting cardiac muscle to greater lengths along its resting length–tension curve. End-diastolic ventricular pressure is referred to as ventricular preload
because it sets the end-diastolic ventricular volume and therefore the resting length of the cardiac muscle fibers at the end of diastole.
(A) Left ventricular pressure–volume cycle and (B) corresponding cardiac muscle length–tension cycle.
At the onset of systole, the ventricular muscle cells develop tension isometrically and intraventricular pressure rises accordingly. After the intraventricular pressure rises sufficiently to open the outlet valve, ventricular ejection begins as a consequence of ventricular muscle shortening. Systemic arterial pressure is often referred to as the ventricular afterload because it determines the tension that must be developed by cardiac muscle fibers before they can shorten.2
During cardiac ejection, the cardiac muscle is simultaneously generating active tension and shortening (ie, an afterloaded isotonic contraction). The magnitude of ventricular volume change during ejection (ie, stroke volume) is determined simply by how far ventricular muscle cells are able to shorten during contraction. This, as already discussed, depends on the length–tension relationship of the cardiac muscle cells and the load against which they are shortening. Once shortening ceases and the output valve closes, the cardiac muscle cells relax isometrically. Ventricular wall tension and intraventricular pressure fall in unison during isovolumetric relaxation.
1 The atria and ventricles do not beat simultaneously. Usually, and unless otherwise noted, systole and diastole denote phases of ventricular operation.
2 This designation is somewhat misleading for at least three reasons. First, arterial pressure is more analogous to ventricular total load than to ventricular afterload. Second, because of the law of Laplace, the actual wall tension that needs to be generated to attain a given intraventricular pressure also depends on the ventricular radius (tension = pressure × radius). Thus, the larger the end-diastolic volume, the greater the tension required to develop sufficient intraventricular pressure to open the outflow valve. Third, inertial factors associated with acceleration of blood flow during ejection also contribute to ventricular afterload. We choose, however, to ignore these complications at this time.