In addition to the inherent contractility of the ventricular myocardium and the heart rate at which the ventricle performs its pumping function, the major determinant of its stroke output is the end-diastolic volume, which is essentially the preload. The end-diastolic pressure achieved prior to the onset of systolic contraction will primarily depend on the diastolic function reflecting both ventricular relaxation and compliance. These have been discussed in relation to the heart sounds S3 and S4. Once systole is set in motion by electrical depolarization of the ventricular myocardium, the excitation-contraction coupling leads to actin-myosin bridge formation. As the ventricular contraction proceeds, more and more of the myofibrils are recruited into contraction, resulting in rise of the ventricular pressure. The force exerted by the contracting ventricle on the blood mass it contains imparts energy to it. Once the inertial resistance offered by the blood mass is overcome, the blood mass begins to accelerate and move toward the low-pressure area of the mitral region where it gets decelerated because of the closure of the mitral valve. The energy dissipated when deceleration occurs results in the production of the M1. After this event, continued ventricular contraction during the isovolumic phase (extending from the time of mitral valve closure to the time when the aortic valve opens) produces further rise in the ventricular pressure. When the ventricular pressure exceeds the aortic pressure, the aortic valve opens and ejection begins. Similar events occur on the right side as well. By this time the blood mass has gained significant momentum, which aids its forward movement. The forces that operate to oppose this forward flow have been called impedance (see Chapter 6). These include the vascular capacity, the viscosity of the blood, and the resistance of the systemic arterial and the pulmonary vascular beds. To this one can also add the proximal aortic and pulmonary artery distensibility or compliance. The momentum gained by the blood mass will keep it moving forward into the aorta and the pulmonary artery, even during the later part of systole when the ventricular pressure begins to fall below that of the aorta and the pulmonary artery, respectively (9). However, with the falling ventricular pressure, the opposing impedance will prevent further forward flow. The blood mass close to the aortic and the pulmonary valves will suddenly tend to reverse its flow direction toward the ventricle, which presents a low-pressure area because of the falling ventricular pressure. This will close the aortic and the pulmonary valves. Deceleration of the column of blood in the aorta against the closed aortic valve generates the A2, and similar deceleration against the pulmonary valve results in P2. Because the impedance in the pulmonary circuit is lower, this deceleration occurs later. These have been discussed previously under S2.
During the ejection phase, the left ventricular pressure remains slightly higher than the aortic pressure in the early to mid part of systole. This pressure gradient, which has been measured by catheter-tip microsensors, has been termed the impulse gradient (Fig. 3). The peak flow acceleration and peak impulse gradients occur very early in systole (9). The aortic flow velocity peaks slightly later, with a slow return to zero flow at the end of
Fig. 3. Simultaneous recording of the left ventricular (LV) and the aortic (AO) pressures through catheters placed in the LV and AO, respectively, showing a small but discernible pressure gradient, "the impulse gradient" between the LV and the AO.
ejection. A smaller right-sided impulse gradient has also been shown between the right ventricle and the pulmonary artery (9).
With exercise the cardiac output is increased because of the increased venous return. There is a significant increase in heart rate in untrained individuals, and the stroke output may or may not be increased. With trained athletes, the heart rate increases slowly. The increased cardiac output is achieved by the increased stroke volume. With exercise, the ejection time shortens, particularly when the heart rate increases. The stroke output, whether increased or normal, is accomplished over a shorter ejection time. This has been shown to be accompanied by an increase in the impulse gradient and an increase in flow acceleration (9).
The flow through normal ventricular outflow tracts and the semilunar valves is still smooth and laminar in most instances. Conditions that lead to an increase in the velocity of flow or actual increase in volume of flow, particularly in the presence of anatomical abnormalities of the outflow tract, are all likely to result in turbulent flow.
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