AND VENTRICLES CONSTITUTE THE CARDIAC CYCLE
The sequence of electrical changes, pressures, and mechanical events within the heart and great vessels leading to and away from the heart during each beat is known as the cardiac cycle. Knowledge of the cardiac cycle is critical to understanding the physiologic regu-lation of cardiac output and for the clinician, for whom it is necessary in assessing cardiac function.
During unchanging physiologic conditions, the events of the cardiac cycle are the same on each beat, but the cycle is often represented as beginning midway through diastole, as in Figure 4-13. In general, the car-diac cycle consists of a period of carcar-diac muscle relax-ation, known as diastole, and a period of contraction, known as systole. Contraction of the ventricles is referred to as ventricular systole. The cardiac output (CO) is equal to the product of heart rate (HR) and stroke volume (SV), which is the output of the left ventricle on each stroke, or cycle. The SV of the left ventricle, which is ejected into the aorta during the ejection phase of the cardiac cycle, is simply the differ-ence between the end-diastolic volume (EDV) and the end-systolic volume (ESV). Stroke volume into the
aorta is determined by strength and velocity of the left ventricular contraction. Thus, myocardial contractil-ity (i.e., excitation-contraction coupling processes), preload (sarcomere length), and afterload are impor-tant determinants of stroke volume, because these fac-tors determine the strength and velocity of the myocardial contraction.
Ventricular Systole Isovolumic Contraction
The onset of ventricular contraction coincides with the peak of the R wave of the electrocardiogram and the initial vibration of the first heart sound. It is indicated
on the ventricular pressure curve as the earliest rise in ventricular pressure after atrial contraction. The phase between the start of ventricular systole and the opening of the semilunar valves (when ventricular pressure rises abruptly) is termed isovolumic contraction because ventricular volume is constant during this brief period (see Figure 4-13).
The increment in ventricular pressure during iso-volumic contraction is transmitted across the closed valves. Isovolumic contraction has also been referred to as “isometric contraction.” However, some fibers shorten and others lengthen, as evidenced by changes in ventricular shape; it is, therefore, not a true isomet-ric contraction.
LengthForce (gm) Velocity of shortening (mm/sec)10
0
Time (s) Force (gm)
1 2
0 5
10 NE Control 15
3 Fo
Vo
Velocity of shortening is slope of initial length change
a b c
a b
c
B C
A
FIGURE 4-12 n The velocity of shortening of cardiac muscle depends on the afterload.
Velocity of shortening is increased by norepinephrine (NE). A and B, Experiment to measure the effect of afterload on shortening velocity. a: A preload, stop, and small afterload are added. b: The muscle is stimulated to contract. It contracts isometrically at first, until it generates enough force to lift the afterload. c: When the muscle gener-ates sufficient force to lift the afterload, muscle shortening can occur. The velocity of shortening is the slope of the initial length change. C, Force-velocity (F/V) curve. Veloc-ity of shortening decreases monotonically as the afterload is increased, up to a level, F0, that the muscle cannot lift. The velocity of shortening is increased at all forces by increasing contractility, as through the action of norepinephrine (NE).
FIGURE 4-13 n Left atrial, aortic, and left ventricular pres-sure pulses correlated in time with aortic flow, ventricular volume, heart sounds, venous pulse, and the electrocar-diogram for a complete cardiac cycle in a human subject.
Isovol., isovolemic; relax., relaxation.
Reduced ejection Rapid ventricular filling Reduced ventr
icular filling— diastasis
Atrial systole Isovol. contract. Rapid ejection Isovol. relax.
1
Aortic valve closes
Ejection
Opening of the semilunar valves marks the onset of the ejection phase, which may be subdivided into an earlier, shorter phase (rapid ejection) and a later, longer phase (reduced ejection). The rapid ejection phase is distinguished from the reduced ejection phase by (1) the sharp rise in ventricular and aortic pressures that terminate at the peak ventricular and aortic pres-sures; (2) a more abrupt decrease in ventricular vol-ume; and (3) a greater aortic blood flow (see Figure 4-13). The sharp decrease in the left atrial pressure curve at the onset of ejection results from the descent of the base of the heart and stretch of the atria. During the reduced ejection period, blood flow from the aorta to the periphery exceeds ventricular output, and therefore aortic pressure declines. Throughout ven-tricular systole, the blood returning to the atria pro-duces a progressive increase in atrial pressure. Note that during approximately the first third of the ejec-tion period, left ventricular pressure slightly exceeds aortic pressure and flow accelerates (continues to increase), whereas during the last two thirds of ven-tricular ejection, the reverse holds true. This reversal of the ventricular-aortic pressure gradient in the pres-ence of continued flow of blood from the left ventricle to the aorta (caused by the momentum of the forward blood flow) is the result of the storage of potential energy in the stretched arterial walls, which produces a deceleration of blood flow into the aorta (see Chap-ter 7). The peak of the flow curve coincides in time with the point at which the left ventricular pressure curve intersects the aortic pressure curve during ejec-tion. Thereafter, flow decelerates (continues to decrease) because the pressure gradient has been reversed.
With right ventricular ejection, there is shortening of the free wall of the right ventricle (descent of the
tricuspid valve ring) and lateral compression of the chamber. However, with left ventricular ejection, there is very little shortening of the base-to-apex axis, and ejection is accomplished chiefly by compression of the left ventricular chamber.
The effect of ventricular systole on left ventricular diameter is shown in an echocardiogram in Figure 4-14. During ventricular systole, the septum and the free wall of the left ventricle become thicker and move closer to each other.
The venous pulse curve shown in Figure 4-13 has been taken from a jugular vein. The a wave is caused by atrial contraction, the c wave by the impact of the adja-cent common carotid artery and to some extent by transmission of a pressure wave produced by the abrupt closure of the tricuspid valve in early ventricular sys-tole, and the v wave by the pressure of blood returning from the peripheral vessels and the abrupt opening of the tricuspid valve. Note that except for the c wave, the venous pulse closely follows the atrial pressure curve.
At the end of ejection, a volume of blood approxi-mately equal to that ejected during systole remains in the ventricular cavities. This residual volume (end-systolic volume) is fairly constant in normal hearts but is smaller with increased heart rate or reduced outflow resistance and larger when the opposite conditions prevail.
In addition to serving as a small adjustable blood reservoir, the residual volume to a limited degree can permit transient disparities between the outputs of the two ventricles.
CLINICAL BOX
In heart failure, the preload can be increased substan-tially because of the poor ventricular ejection and an increased blood volume caused by fluid retention. In essential hypertension, the high peripheral resistance augments the afterload by decreasing the peripheral runoff of the blood from the arterial system.
LV
LA
A
Peri
AV
ALMV RV
CS
B
IVS
PLMV
LVPW dAo
aAo
FIGURE 4-14 n Two-dimensional echocardiographic images of a normal human heart (young adult male) taken from the parasternal long-axis view. A, During diastole, the left atrium (LA) communicates freely with the cavity of the left ventricle (LV). The ante-rior leaflet (ALMV) and the posteante-rior leaflet (PLMV, shown in B) of the mitral valve (MV) are open; the leaflets of the aortic valve (AV) are closed. B, During systole, the left ventricular (LV) interventricular septum (IVS), and posterolateral wall (LVPW) wall thicken; the LV cavity diminishes in volume. The LV cavity is open to the ascending aorta (aAo); the AV is open and the MV is closed. Also evident in the echocardiograms are the descending aorta (dAo), the coronary sinus (CS), the right ventricle cavity (RV), and the RV free wall. The pericardium (Peri) is evident as a very bright structure; a reverberation artifact is present. (Courtesy of Dr. Peter Schulman.).
Ventricular Diastole
Isovolumic Relaxation Aortic valve closure pro-duces the incisura on the descending limb of the aortic pressure curve and the second heart sound (with some vibrations evident on the atrial pressure curve) and marks the end of ventricular systole. The phase between the closure of the semilunar valves and the opening of the AV valves, termed isovolumic relax-ation, is characterized by a precipitous fall in ventricu-lar pressure without a change in ventricuventricu-lar volume.
Rapid Filling Phase The major part of the ventricu-lar filling occurs immediately on opening of the AV valves, when the blood that had returned to the atria during the previous ventricular systole is abruptly released into the relaxing ventricles. This period of ventricular filling is called the rapid filling phase. In Figure 4-13 the onset of the rapid filling phase is indi-cated by the decrease in left ventricular pressure below left atrial pressure, resulting in the opening of the mitral valve. The rapid flow of blood from atria to relaxing ventricles produces a decrease in atrial and ventricular pressures and a sharp increase in ventricu-lar volume.
Diastasis The rapid filling phase is followed by a phase of slow filling called diastasis. During diastasis, blood returning from the periphery flows into the right ventricle and blood from the lungs into the left ventricle.
This small, slow addition to ventricular filling is indi-cated by a gradual rise in atrial, ventricular, and venous pressures and in ventricular volume (see Figure 4-13).
Atrial Systole The onset of atrial systole occurs soon after the beginning of the P wave of the electro-cardiogram (atrial depolarization), and the transfer of blood from atrium to ventricle made by the peristalsis-like wave of atrial contraction completes the period of ventricular filling. Atrial systole is responsible for the small increases in atrial, ventricular, and venous (a wave) pressures as well as in ventricular volume shown in Figure 4-13. Throughout ventricular dias-tole, atrial pressure barely exceeds ventricular pres-sure, indicating a low-resistance pathway across the open AV valves during ventricular filling.
Atrial contraction can force blood in both direc-tions because there are no valves at the juncdirec-tions of the venae cavae and right atrium or at the junctions of the pulmonary veins and left atrium. Actually, little blood is pumped back into the venous tributaries during the
brief atrial contraction, mainly because of the inertia of the inflowing blood.
Atrial contraction is not essential for ventricular fill-ing, as can be observed in atrial fibrillation or complete heart block. However, its contribution is governed to a great extent by the heart rate and the structure of the AV valves. At slow heart rates, filling practically ceases toward the end of diastasis, and atrial contraction con-tributes little additional filling. During tachycardia, diastasis is abbreviated, and the atrial contribution can become substantial, especially if it occurs immediately after the rapid filling phase, when the AV pressure gra-dient is maximal. Should tachycardia become so great as to encroach on the rapid filling phase, atrial contraction becomes very important in rapidly propelling blood to fill the ventricle during this brief period of the cardiac cycle. Of course, if the period of ventricular relaxation is so brief that filling is seriously impaired, even atrial con-traction cannot prevent inadequate ventricular filling.
The consequent reduction in cardiac output may result in syncope. Obviously, if atrial contraction occurs simultaneously with ventricular contraction, no atrial contribution to ventricular filling can occur.
Echocardiography Reveals Movement of the Ventricular Walls and of the Valves
Echocardiography consists of sending short pulses of high-frequency sound waves (ultrasound) through the chest tissues and the heart and recording the echoes reflected from the various structures. The timing and pattern of the reflected waves provide such informa-tion as the diameter of the heart, the ventricular wall thickness, and the magnitude and direction of the movements of various components of the heart. In Figure 4-14 the echocardiograph depicts the left heart in diastole (see Figure 4-14A) and in systole (see Fig-ure 4-14B). During diastole, the mitral valve leaflets are open, allowing the cavity of the left atrium to be continuous with the cavity of the left ventricle. The
CLINICAL BOX
With slow, progressive, and sustained enlargement of the heart, as occurs in cardiac hypertrophy, or with a slow progressive increase in pericardial fluid, as occurs in pericarditis with pericardial effusion, the intact pericardium is gradually stretched.
anterior leaflet of the mitral valve is directed toward the interventricular septum, and the posterior leaflet is positioned along the inferolateral wall of the left ven-tricle. The open mitral valve is a funnel for the transfer of blood from atrium to ventricle. The aortic valve is closed. During systole, the aortic valve is open and the mitral valve is closed (see Figure 4-14B). The left ven-tricular wall and the intervenven-tricular septum are thick-ened as the ventricle contracts to eject blood into the aorta. The cavity of the left ventricle is diminished in volume.
The Two Major Heart Sounds Are Produced Mainly by Closure of the Cardiac Valves
Four sounds are usually produced by the heart, but only two are ordinarily audible through a stethoscope.
With electronic amplification, the less intense sounds can be detected and recorded graphically as a phono-cardiogram. This means of registering heart sounds that may be inaudible to the human ear helps to delin-eate the precise timing of the heart sounds relative to other events in the cardiac cycle.
A normal phonocardiogram taken simultaneously with an electrocardiogram is illustrated in Figure 4-15.
The first heart sound is initiated at the onset of ventricular systole and consists of a series of vibra-tions of mixed, unrelated, low frequencies (a noise). It is the loudest and longest of the heart sounds, has a crescendo-decrescendo quality, and is heard best over the apical region of the heart. The tricuspid valve sounds are heard best in the fifth intercostal space just to the left of the sternum; the mitral sounds are heard best in the fifth intercostal space at the cardiac apex.
The first heart sound is chiefly caused by oscillation of blood in the ventricular chambers and vibration of the chamber walls. The vibrations are engendered in part by the abrupt rise of ventricular pressure with acceleration of blood back toward the atria, but pri-marily by sudden tension and recoil of the AV valves and adjacent structures with deceleration of the blood resulting from closure of the AV valves. The vibrations of the ventricles and the contained blood are transmit-ted through surrounding tissues and reach the chest wall, where they may be heard or recorded. The inten-sity of the first sound is a function of the force of
ventricular contraction and of the distance between the valve leaflets. The first sound is loudest when the leaflets are farthest apart, as occurs when the interval between atrial and ventricular systoles is prolonged (AV valve leaflets float apart) or when ventricular sys-tole immediately follows atrial syssys-tole.
The second heart sound, which occurs with closure of the semilunar valves, is composed of higher- frequency vibrations (higher pitch), is of shorter duration and lower intensity, and has a more snap-ping quality than the first heart sound. The second sound is caused by abrupt closure of the semilunar valves, which initiates oscillations of the columns of blood and the tensed vessel walls by the stretch and recoil of the closed valve. The second sound caused by closure of the pulmonic valve is heard best in the sec-ond thoracic interspace just to the left of the sternum, whereas that caused by closure of the aortic valve is heard best in the same intercostal space but to the right of the sternum. Conditions that bring about a more rapid closure of the semilunar valves, such as rises in pulmonary artery or aortic pressure (e.g., pul-monary or systemic hypertension), increase the inten-sity of the second heart sound. In adults the aortic valve sound is usually louder than the pulmonic, but in cases of pulmonary hypertension the reverse is often true.
P R
T
1 2
PhonocardiogramElectrocardiogram
0 0 . 2 0 . 4 0 . 6 0 . 8 1 . 0 1 . 2 1 . 4 1 . 6 Time (s)
FIGURE 4-15 n Phonocardiogram illustrating the first (1) and second (2) heart sounds and their relationship to the P, R, and T waves of the electrocardiogram.
Note that the first sound, which starts just beyond the peak of the R wave, is composed of irregular waves and is of greater intensity and duration than the second sound, which appears at the end of the T wave. The third and fourth heart sounds do not appear on this record.
The third heart sound, which is sometimes heard in children with thin chest walls or in patients with left ventricular failure, consists of a few intensity, low-frequency vibrations heard best in the region of the apex. It occurs in early diastole and is believed to be the result of vibrations of the ventricular walls caused by abrupt cessation of ventricular distention and deceleration of blood entering the ventricles.
A fourth, or atrial, sound, consisting of a few low-frequency oscillations, is occasionally heard in normal individuals. It is caused by oscillation of blood and cardiac chambers created by atrial contraction.
Differences in the time of vibration of the two AV valves or two semilunar valves can sometimes be detected with the stethoscope because the onset and termination of right and left ventricular systoles are not precisely synchronous. Such asynchrony of valve vibrations, which may sometimes indicate abnormal cardiac function, is manifested as a split sound over the apex of the heart for the AV valves and over the base of the heart for the semilunar valves.