The incisura, or notch, on the descending limb of the aortic pressure curve is a result of the closure of the aortic valve. This closure also produces the second heart sound, with some vibrations observed on the atrial pressure curve. The incisura indicates the end of ventricular systole. The period between the closure of the semilunar valves and the opening of the AV valves is known as isovolumic relaxation, characterized by a sudden decrease in ventricular pressure without any change in ventricular volume.

The majority of ventricular filling occurs immediately after the AV valves open. During this time, the blood that returned to the atria during the previous ventricular systole is rapidly released into the relaxing ventricles, resulting in the rapid filling phase. In Fig. 16.39, the beginning of the rapid filling phase is marked by a decrease in left ventricular pressure below left atrial pressure, which leads to the opening of the mitral valve. The rapid flow of blood from the atria to the relaxing ventricles causes transient decreases in atrial and ventricular pressures, as well as a sharp increase in ventricular volume.

Following the rapid ventricular filling phase, there is a phase of slow ventricular filling called diastasis. During diastasis, blood returns from the peripheral veins and flows into the right ventricle, while blood from the lungs flows into the left ventricle. This slow addition to ventricular filling is indicated by gradual increases in atrial, ventricular, and venous pressures, as well as ventricular volume (see Fig. 16.39).

An increase in myocardial contractility, as induced by catecholamines or digitalis in a patient with a failing heart, can decrease residual ventricular volume and increase stroke volume and ejection fraction. In severely hypodynamic and dilated hearts, residual volume can become much greater than stroke volume.

Atrial systole, which occurs soon after the beginning of the P wave (atrial depolarization) of the ECG, completes the period of ventricular filling by transferring blood from the atrium to the ventricle through atrial contraction.

Atrial systole leads to small increases in atrial, ventricular, and venous pressures, as well as ventricular volume (see Fig. 16.39). Throughout ventricular diastole, atrial pressure barely exceeds ventricular pressure, indicating a low-resistance pathway through the open AV valves during ventricular filling.

Due to the absence of valves at the junction of the venae cavae and right atrium, or at the junction of the pulmonary veins and left atrium, atrial contraction may force blood in both directions. However, the inertia of the inflowing blood limits the amount of blood actually pumped back into the venous tributaries during the brief atrial contraction.

The contribution of atrial contraction to ventricular filling is primarily influenced by the heart rate and the position of the AV valves. At slow heart rates, filling nearly ceases towards the end of diastasis, and atrial contraction provides little additional filling. However, during tachycardia, diastasis is shortened, and the contribution of atrial contraction becomes substantial. In cases where tachycardia is severe enough to attenuate the rapid filling phase, atrial contraction becomes crucial in rapidly propelling blood into the ventricle during this brief period of the cardiac cycle. If the period of ventricular relaxation is too short to allow adequate filling, even atrial contraction cannot compensate, resulting in a reduction in cardiac output that may lead to syncope (fainting).
Closure of the aortic valve produces the characteristic incisura (notch) on the descending limb of the aortic pressure curve, and it also produces the second heart sound (with some vibrations evident on the atrial pressure curve). The incisura marks the end of ventricular systole. The period between closure of the semilunar valves and opening of the AV valves is termed isovolumic relaxation. It is characterized by a precipitous fall in ventricular pressure without a change in ventricular volume.
The major portion of ventricular filling occurs immediately after the AV valves open. At this point, the blood that 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
Fig.
16.39 , the onset of the rapid filling phase is indicated by the decrease in left ventricular pressure below left atrial pressure. This pressure reversal opens the mitral valve. The rapid flow of blood from atria to relaxing ventricles produces transient decreases in atrial and ventricular pressures and a sharp increase in ventricular volume.
The rapid ventricular filling phase is followed by a phase of slow ventricular filling called diastasis. During diastasis, blood returning from the peripheral veins flows into the right ventricle and blood from the lungs flows into the left ventricle. This small, slow addition to ventricular filling is indicated by gradual rises in atrial, ventricular, and venous pressures and in ventricular volume (see
Fig. 16.39
Anincreaseinmyocardialcontractility,asproducedbycatecholaminesorbydigitalisinapatientwithafailingheart,maydecreaseresidualventricularvolumeandincreasethestrokevolumeandejectionfraction.Inseverelyhypodynamicanddilatedhearts,residualvolumecanbecomemuchgreaterthanstrokevolume.
The onset of atrial systole occurs soon after the beginning of the P wave (atrial depolarization) of the ECG. The transfer of blood from atrium to ventricle achieved by atrial contraction completes the period of ventricular filling.
Atrial systole is responsible for the small increases in atrial, ventricular, and venous pressure, as well as in ventricular volume (see
Fig. 16.39 ). Throughout ventricular diastole, atrial pressure barely exceeds ventricular pressure. This small pressure difference indicates that the pathway through the open AV valves during ventricular filling has low resistance.
Because there are no valves at the junction of the venae cavae and right atrium or at the junction of the pulmonary veins and left atrium, atrial contraction may force blood in both directions. However, little blood is actually pumped back into the venous tributaries during the brief atrial contraction, mainly because of the inertia of the inflowing blood.
The contribution of atrial contraction to ventricular filling is governed to a great extent by the heart rate and the position of the AV valves. At slow heart rates, filling practically ceases toward the end of diastasis, and atrial contraction contributes little additional filling. During tachycardia, however, diastasis is abbreviated and the atrial contribution can become substantial. Should tachycardia become so severe that the rapid filling phase is attenuated, atrial contraction assumes great importance in rapidly propelling blood into the ventricle during this brief period of the cardiac cycle. If the period of ventricular relaxation is so brief that filling is seriously impaired, even atrial contraction cannot provide adequate ventricular filling. The consequent reduction in cardiac output may result in syncope (fainting).