The ejection phase of systole follows the tense phase. During the ejection phase, stroke volume is pumped into the aorta. Synonymous with the ejection phase of systole is the term expulsion phase. Valvular defects, such as tricuspid regurgitation, can disrupt the ejection phase and cause pathologic changes in the heart.
What is the ejection fraction?
During the ejection phase, the heart pumps about 80 milliliters of blood into the aorta. The heart is a muscle whose contraction is vital. The hollow organ is the center of blood circulation. In this context, the outflow phase of the heart’s contraction serves to eject blood from the atrium of the heart into the ventricle or to transport blood out of the ventricle into the vascular system. Thus, systole correlates with delivery rate. Between two systoles there is a diastole, i.e. a relaxation phase. Systole consists of a contraction phase and an ejection phase, each of which follows the contraction of the muscle. During the ejection phase, the heart pumps about 80 milliliters of blood into the aorta. This is also referred to as the stroke volume of the heart. Systoles remain constant in duration despite changes in heart rate and amount to about 300 milliseconds in adults. The ejection phase accounts for about 200 milliseconds of this time. Before the contraction phase, blood is present in the ventricles and the leaflet and pocket valves of the ventricle are closed. Cardiac contraction causes the pressure to rise. In the ejection phase, the pressure of the ventricles is higher than that of the pulmonary artery and aorta. Therefore, the pocket valves open and blood flows out into the great vessels.
Function and purpose
In diastole, the heart muscle is relaxed and blood flows into the hollow organ. Systole of the heart forces blood out of the ventricles and transfers it to the vascular system. Systole consists of several parts. A relatively short and mechanical tense phase of the heart muscle is followed by the longer lasting ejection phase of the blood. At rest, the ejection phase of systole lasts about 200 milliseconds. The valves of the heart open at the beginning of the ejection phase. For them to open at all, a lower pressure is required in the left ventricle of the heart than exists in the aorta. The pressure of the right ventricle, on the other hand, must exceed that of the pulmonary artery. Once the ventricles have opened, blood flows out. The outflow of blood targets the aorta and the truncus pulmonalis. The more blood that flows out, the higher the pressure in each ventricle of the heart. The ventricular radius decreases and the wall thickness increases. This relationship is also known as Laplace’s law, which causes the pressure of the ventricles to keep increasing. A large proportion of the total stroke volume is thus ejected from the heart at high velocity. Measurements within the aorta reveal intermittent blood flow rates of about 500 milliliters per second. After the ejection phase, the pressure in the ventricles of the heart drops significantly. As soon as there is less pressure in the ventricles than in the aorta, the pocket valves of the heart are closed again and the ejection phase of systole reaches its end. After the ejection phase, there is a residual volume of about 40 milliliters in the left ventricle. This residual volume is also called end-systolic volume. The ejection fraction is more than 60 percent.
Diseases and medical conditions
Various diseases of the heart show devastating effects on the ejection phase of systole. For example, reflux of blood during the ejection phase is characterized by tricuspid regurgitation. This is a leak in the tricuspid valve that causes blood to flow back into the right atrium during the ejection phase. The condition is one of the most common valve defects in humans. Valve disease of this type is usually the result of other diseases. For example, athletes and young patients with the leak often suffer from enlargement of the heart. The enlargement results from high physical stress, which is accompanied by distension of the valve annulus. Because the leaflets expand during exercise, for example, complete closure of the valve no longer occurs. This leakage results in mild tricuspid regurgitation, which in this case often has no pathologic value. In severe tricuspid regurgitation with pathological value, regurgitation openings of more than 40 mm² are present. The regurgitation volume is usually more than 60 milliliters.This phenomenon can have life-threatening consequences. In the ejection phase, the valve defect causes a substantial increase in pressure in the atrium of the heart. This pressure increase is transmitted to the vena cavae and may result in hepatic congestion and eventually venous congestion. Due to the large backflow of blood, the ejection of the heart into the pulmonary artery is inadequate and the organs become insufficiently perfused. When tricuspid regurgitation develops over a long period of time, compensatory mechanisms occur that affect the heart and upstream veins. Persistent pressure in the atrium causes atrial enlargement. As a result, atrial volume increases, sometimes until it reaches four times its original volume. Changes also occur in the vena cavae or liver. The high volume load enlarges the right ventricle. With this enlargement, either the stroke volume increases via the Frank-Starling mechanism or a cycle is created in that the enlargement of the ventricle disrupts the valve geometry, exacerbating the insufficiency. Other valvular defects may also cause similar effects during the ejection phase of systole.
