Aortic valve disease: effects of hemodynamic in the narrowing and opening of the valve

In aortic stenosis, the correlation with the left ventricle is not properly emptied, whereas, in aortic reflux, blood flows back to the left ventricle from the aorta after the left ventricle pumps blood into the artery. motherboard. Then, in both cases, the heart's blood supply is reduced.

The amount of compensation taking place can improve the severity of the circulatory defects. Some of the compensation mechanisms are described in the following sections.

Left ventricular hypertrophy

In both aortic stenosis and openness, the muscles of the ventricles enlarge because of an increase in the working volume of the ventricles.

In an artery, the left ventricle enlarges to keep blood from backing up from the aorta. Sometimes left ventricular volume increases 4 to 5 times, creating a very large area on the left side of the heart.

When the aortic valve is severely narrowed, the enlarged muscles allow the left ventricle to rise with a pressure of about 400 mmHg at the apex of the systole.

In people with severe aortic regurgitation, sometimes enlarged muscle allows the left ventricle to pump a very large amount of blood about 250 ml, although three-quarters of this blood returns to the ventricles during diastole, and only a quarter pass through the aorta to the body.

Increased blood volume

An effect on reduced blood pumping due to increased volume of blood volume in the ventricles. This leads to an increase in the number that results from (1) an initial slight decrease in arterial pressure, plus (2) peripheral circulation reflexes reduced by pressure drop. Together these mechanisms reduce the amount of urine in the kidneys, causing an increase in blood volume and a normal return of arterial pressure. Despite this, the volume of red blood cells is even increased because of a slight lack of oxygen in the tissues. The increase in circulating volume tends to flow through the veins back to the heart, which, in turn, causes the left ventricle to pump more power to overcome abnormal pumps.

Aortic valve damage may be associated with coronary anaemia

When a person has aortic stenosis, the right ventricle muscles develop vigorously to create the high pressure in the ventricles required to pass blood through the narrowed valve. The ventricles work harder and consume more oxygen, so coronary blood flow must be increased to meet oxygen demand. The walls of the ventricles are very tense, thus causing a significant decrease in blood flow during systole, especially in the pericardial vessels. Diastolic pressure also increases as the aortic valve narrows, and this increase in pressure can compress the inner layers of the heart muscle and decrease coronary blood flow. Thus, severe aortic stenosis often causes ischemia of the myocardium.

With aortic regurgitation, pressure in the ventricles increases diastole, squeezing the inner layers of the heart muscle and reducing coronary blood flow. The aortic diastolic pressure is reduced, which can also decrease coronary blood flow and this also causes myocardial ischemia.

Eventually causes left ventricular failure and develops into pulmonary oedema. In the early stages of aortic stenosis and aortic reflux, the ability in the left ventricle itself to adapt increases the load to prevent abnormal signs of circulatory function in humans during rest, otherwise with the need to increase the required workload in the left ventricle. Consequently, significant levels of aortic stenosis or reflux often occur before the person learns that he or she has cardiovascular disease (for example, in people with left ventricular systolic pressure at a time) rest about 200mmHg or with a workload that's twice as high in people with aortic openings).

In addition, at a critical stage in aortic valve damage, the left ventricle eventually fails to respond to work demands. As a result, the left ventricle relaxes and cardiac output begins to decrease; blood simultaneously hits the left atrium and enters the lung after the left ventricle fails. The left atrial pressure gradually increased, and the mean left atrial pressure ranged from 25 to 40 mmHg, and severe oedema appeared in the lungs.