Physiology 5th Ed.

CARDIAC CYCLE

Figure 4-25 illustrates the mechanical and electrical events that occur during a single cardiac cycle. The cycle is divided into seven phases (Fig. 4-25, letters A through G), which are separated by vertical lines in the figure. The ECG marks the electrical events of the cardiac cycle. Left ventricular pressure and volume, aortic and left atrial pressures, venous pulse, and heart sounds are all plotted simultaneously. The points at which the mitral and aortic valves open and close are shown by arrows.

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Figure 4–25 The cardiac cycle. The mechanical and electrical events that occur during one cycle are shown. Atrial systole (A); isovolumetric ventricular contraction (B); rapid ventricular ejection (C); reduced ventricular ejection (D); isovolumetric ventricular relaxation (E); rapid ventricular filling (F); reduced ventricular filling (diastasis) (G).

Video: The cardiac cycle

Figure 4-25 is best studied vertically, one phase at a time, so that all of the cardiovascular parameters in a given phase of the cycle can be correlated. The ECG can be used as a time/event marker. The cycle begins with depolarization and contraction of the atria. Table 4-5 can be used in conjunction with Figure 4-25 to learn the events of the cardiac cycle.

Table 4–5 Events of the Cardiac Cycle

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*Lettered phases of cardiac cycle correspond to phases in Figure 4-25.

Atrial Systole (A)

Atrial systole is atrial contraction. It is preceded by the P wave on the ECG, which marks depolarization of the atria. Contraction of the left atrium causes an increase in left atrial pressure. When this increase in atrial pressure is reflected back to the veins, it appears on the venous pulse record as the a wave. The left ventricle is relaxed during this phase, and because the mitral valve (AV valve of the left side of the heart) is open, the ventricle is filling with blood from the atrium, even prior to atrial systole. Atrial systole causes a further increase in ventricular volume as blood is actively ejected from the left atrium to the left ventricle through the open mitral valve. The corresponding “blip” in left ventricular pressure reflects this additional volume added to the ventricle from atrial systole. The fourth heart sound(S4) is not audible in normal adults, although it may be heard in ventricular hypertrophy, where ventricular compliance is decreased. When present, S4 coincides with atrial contraction. The sound is caused by the atrium contracting against, and trying to fill, a stiffened ventricle.

Isovolumetric Ventricular Contraction (B)

Isovolumetric ventricular contraction begins during the QRS complex, which represents the electrical activation of the ventricles. When the left ventricle contracts, left ventricular pressure begins to increase. As soon as left ventricular pressure exceeds left atrial pressure, the mitral valve closes. (In the right heart, the tricuspid valve closes.) Closure of the AV valves produces the first heart sound (S1), which may be split because the mitral valve closes slightly before the tricuspid valve. Ventricular pressure increases dramatically during this phase, but ventricular volume remains constant because all valves are closed (the aortic valve has remained closed from the previous cycle).

Rapid Ventricular Ejection (C)

The ventricle continues to contract, and ventricular pressure reaches its highest value. When ventricular pressure becomes greater than aortic pressure, the aortic valve opens. Now blood is rapidly ejected from the left ventricle into the aorta through the open aortic valve, driven by the pressure gradient between the left ventricle and the aorta. Most of the stroke volume is ejected during rapid ventricular ejection, dramatically decreasing ventricular volume. Concomitantly, aortic pressure increases as a result of the large volume of blood that is suddenly added to the aorta. During this phase, atrial filling begins and left atrial pressure slowly increases as blood is returned to the left heart from the pulmonary circulation. This blood will, of course, be ejected from the left heart in the next cycle. The end of this phase coincides with the end of the ST segment (or the beginning of the T wave) on the ECG and with the end of ventricular contraction.

Reduced Ventricular Ejection (D)

During reduced ventricular ejection, the ventricles begin to repolarize, which is marked by the beginning of the T wave on the ECG. Ventricular pressure falls because the ventricles are no longer contracting. Because the aortic valve is still open, blood continues to be ejected from the left ventricle into the aorta, albeit at a reduced rate; ventricular volume also continues to fall, but at a reduced rate. Even though blood continues to be added to the aorta from the left ventricle, blood is “running off” into the arterial tree at an even faster rate, causing aortic pressure to fall. Left atrial pressure continues to increase as blood returns to the left heart from the lungs.

Isovolumetric Ventricular Relaxation (E)

Isovolumetric ventricular relaxation begins after the ventricles are fully repolarized, marked by the end of the T wave on the ECG. Because the left ventricle is relaxed, left ventricular pressure decreases dramatically. When left ventricular pressure falls below aortic pressure, the aortic valve closes. The aortic valve closes slightly before the pulmonic valve, producing the second heart sound (S2). Inspiration delays closure of the pulmonic valve and causes splitting of the second heart sound; that is, during inspiration, the pulmonic valve closes distinctly after the aortic valve. Splitting occurs during inspiration because the associated decrease in intrathoracic pressure produces an increase in venous return to the right side of the heart. The resulting increase in right ventricular end-diastolic volume causes an increase in right ventricular stroke volume by the Frank-Starling mechanism and prolongs right ventricular ejection time; the prolongation of ejection time delays closure of the pulmonic valve relative to the aortic valve. At the point where the aortic valve closes, the aortic pressure curve shows a “blip,” called the dicrotic notchor incisura. Because all valves are closed again, no blood can be ejected from the left ventricle, nor can the left ventricle fill with blood from the atria. Therefore, during this phase, ventricular volume is constant (isovolumetric).

Rapid Ventricular Filling (F)

When ventricular pressure falls to its lowest level (and slightly below left atrial pressure), the mitral valve opens. Once the mitral valve opens, the ventricle begins to fill with blood from the left atrium, and ventricular volume increases rapidly. Ventricular pressure remains low, however, because the ventricle is still relaxed and compliant. (The high compliance of the ventricle means that volume can be added to it without changing pressure.) The rapid flow of blood from the atria to the ventricles produces the third heart sound (S3), which is normal in children but is not heard in normal adults; in middle-aged or older adults, the presence of S3 indicates volume overload, as in congestive heart failure or advanced mitral or tricuspid regurgitation. During this phase (and for the remainder of the cardiac cycle), aortic pressure decreases as blood runs off from the aorta into the arterial tree, to the veins, and then back to the heart.

Reduced Ventricular Filling (Diastasis) (G)

Reduced ventricular filling, or diastasis, is the longest phase of the cardiac cycle and includes the final portion of ventricular filling, which occurs at a slower rate than in the previous phase. Atrial systole marks the end of diastole, at which point ventricular volume is equal to end-diastolic volume.

Changes in heart rate alter the time available for diastasis because it is the longest phase of the cardiac cycle. For example, increases in heart rate reduce the time interval before the next P wave (i.e., the next cycle) and reduce, or even eliminate, this final portion of ventricular filling. If diastasis is reduced by such an increase in heart rate, ventricular filling will be compromised, end-diastolic volume will be reduced, and, as a consequence, stroke volume also will be reduced (recall the Frank-Starling relationship).