The Ejection phase the systole follows on from the tension phase. In the ejection phase, the stroke volume is pumped into the aorta. The term is synonymous with the ejection phase of the systole Expulsion phase used. Heart valve defects, such as tricuspid regurgitation, can disrupt the ejection phase and pathologically change the heart.
What is the ejection phase?
The heart is a muscle whose contraction is vital. The hollow organ is the center of the blood circulation. In this context, the outflow phase of the heart contraction serves to eject blood from the atrium of the heart into the chamber or transports blood out of the heart chamber into the vascular system.
The systole thus correlates with the delivery rate. Between two systoles there is a diastole, i.e. a relaxation phase. The systole consists of a tension phase and an expulsion phase, which each follow the contraction of the muscle. During the ejection phase, the heart pumps around 80 milliliters of blood into the aorta. The stroke volume of the heart is also mentioned.
Systoles remain constant in their duration despite changes in the heart rate and are around 300 milliseconds in adults. The ejection phase makes up about 200 milliseconds of this. Before the tension phase, blood is present in the chambers and the leaflet and pocket flaps of the chamber are closed. The contraction of the heart causes the pressure to rise. In the ejection phase, the pressure of the chambers is higher than that of the pulmonary artery and aorta. As a result, the pocket flaps open and blood flows out into the large vessels.
Function & task
During diastole, the heart muscle is relaxed and blood flows into the hollow organ. The systole of the heart presses the blood out of the heart chambers and transfers it into the vascular system. The systole consists of several parts. A relatively short and mechanical tension phase of the heart muscle is followed by the longer-lasting outflow phase of the blood. At rest, the ejection phase of the systole lasts about 200 milliseconds. The heart's pocket flaps open at the beginning of the ejection phase. In order for them to open at all, a lower pressure is required in the left heart ventricle than in the aorta. The pressure of the right ventricle, on the other hand, must exceed that of the pulmonary artery.
As soon as the chambers open, blood flows out. The target of the blood flow is the aorta and the pulmonary trunk. The more blood flows out, the higher the pressure in the individual ventricles 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 in the ventricles to keep increasing.
A large proportion of the total stroke volume is ejected from the heart at high speed. Measurements within the aorta occasionally show blood flow rates of around 500 milliliters per second.
After the ejection phase, the pressure in the ventricles of the heart drops significantly. As soon as the pressure in the ventricles is lower than that in the aorta, the pocket valves of the heart are closed again and the ejection phase of the systole comes to an end.
After the ejection phase, there is a residual volume of around 40 milliliters in the left ventricle. This residual volume is also called the end-systolic volume. The proportion of ejection is over 60 percent.
Illnesses & ailments
Various diseases of the heart have devastating effects on the ejection phase of systole. For example, tricuspid regurgitation is characterized by a backflow of blood during the ejection phase. This is a leak in the tricuspid valve that causes blood to flow back into the right atrium during the ejection phase. The appearance is one of the most common valve defects in humans.
Valve diseases of this type are usually the result of other diseases. For example, athletes and young patients with the leak often suffer from an enlarged heart. The enlargement is caused by high physical stress, which is associated with an expansion of the valve ring. Because the sails expand during training, for example, the flap no longer closes completely. This leakage results in a slight tricuspid regurgitation, which in this case often remains without pathological value.
In the case of severe tricuspid insufficiency with disease value, there are regurgitation openings of over 40 mm². The regurgitation volume is usually over 60 milliliters. This phenomenon can have life-threatening consequences. In the ejection phase, the valve defect causes a significant increase in pressure in the atrium of the heart. This increase in pressure is transmitted to the vena cava and can cause liver congestion and ultimately venous congestion. Due to the large return flow of blood, the ejection capacity of the heart into the pulmonary artery is insufficient and the organs are insufficiently supplied with blood. If the tricuspid valve regurgitation develops over a long period of time, compensation mechanisms that affect the heart and the upstream veins occur. The persistent pressure in the atrium causes an enlargement of the atrium. As part of this, the atrial volume increases until it has risen to four times the volume.
Changes also take place in the vena cava or the liver. The high volume loading enlarges the right ventricle. With this enlargement, either the stroke volume increases via the Frank Starling mechanism or a circulation is created in which the expansion of the ventricle disrupts the valve geometry and thus increases the insufficiency. Other heart valve defects can also cause similar effects in the ejection phase of the systole.
