Afterload corresponds to the resistance that works against the contraction of the heart muscle, limiting the ejection of blood from the heart. The heart‘s afterload increases in the setting of hypertension or valvular stenosis, for example. Compensatory to this, the heart muscle may hypertrophy and promote heart failure.
What is afterload?
Afterload corresponds to the resistance that works against the contraction of the heart muscle, limiting the ejection of blood from the heart. The heart is a muscle that pumps blood into the circulatory system by alternating contraction and relaxation, and thus is involved in supplying nutrients, messengers, and oxygen to body tissues. To limit the ejection of blood from the ventricles, the so-called afterload counteracts the contraction of the ventricles. All forces that oppose the ejection of blood from the cardiac ventricles into the vascular system are summarized as afterload. The ventricular myocardium has a certain wall tension. Under physiological conditions, the wall tension at the beginning of systole (blood ejection phase) can be understood as the afterload of the heart. In a healthy body, the wall tension of the ventricular myocardium overcomes the end-diastolic aortic pressure or pulmonary pressure and thus initiates the ejection phase. The afterload in terms of wall tension reaches its maximum shortly after the opening of the aortic valve. The value of afterload is determined by both arterial blood pressure and arterial stiffness. The latter factor is also known as compliance. To be distinguished from afterload is preload. It corresponds to all the forces that stretch the contractile muscle fibers of the cardiac ventricles toward the end of diastole (relaxation phase of the heart muscle).
Function and purpose
Afterload is the resistance that the left ventricle must overcome to expel blood from the heart shortly after the aortic valve opens. Thus, the wall stress at the beginning of systole regulates blood ejection. In medicine, systole is the contraction phase of the heart. The ventricular systole consists of a tension phase and an ejection phase. Systole thus serves to eject blood from the atrium into the ventricle or from the ventricle into the vascular system. Thus, the delivery rate of the heart depends on systole, with two systoles each being interrupted by a diastole. Systole is around 400 ms at a rate of around 60/min. The resistance to be overcome in the expulsion phase of the blood is the afterload, whereby the force for systole depends on the ventricular volume as part of the so-called Frank-Starling mechanism. Furthermore, the stroke volume of the heart results from the peripheral resistance. The Frank-Starling mechanism corresponds to the interrelationships between the filling and ejection of the heart, which adjust cardiac activity to short-term variations in pressure and volume and allow both ventricles to eject the same stroke volume. For example, when preload increases, resulting in an increased end-diastolic filling volume of the ventricle, the Frank-Starling mechanism shifts the reference point on the resting strain curve to the right. Thus, the curve of support maxima also shifts to the right. The increased filling allows for larger isobaric and isovolumetric maxima. The ejected stroke volume increases and the end-systolic volume increases slightly. An increase in preload thus increases the pressure-volume work of the heart. The afterload increases. This increased ejection resistance depends on the mean aortic pressure. With increased afterload, the heart must reach a higher pressure to the pocket valve opening during the tension phase. Due to the increased contraction force, stroke volume and end-systolic volume decrease. At the same time, the end-diastolic volume increases. The subsequent contraction, in turn, increases preload.
Diseases and conditions
Clinically, blood pressure is usually used to estimate afterload or wall stress. However, determination of blood pressure at the beginning of the expulsion phase at the myocardium (heart muscle) allows only an approximation of the actual afterload values. The exact determination of impedance is not possible. As an approximation, afterload is sometimes estimated in clinical practice by transesophageal echocardiography. In heart failure, the systolic force of the myocardium no longer matches the diastolic filling volume.As a result, the blood pressure no longer responds appropriately to stress situations. This phenomenon initially characterizes exercise-induced heart failure, which in the course of time may become resting insufficiency. In severe heart failure, it is no longer possible to maintain resting blood pressure, and cardiac hypotension develops, i.e., a loss of tone. Hypertension in the sense of increased tone, on the other hand, causes the afterload to rise. The heart must increase its ejection capacity in the event of such an increase in tone, but it can only meet this requirement to the extent that its power development capabilities are sufficient. In coronary heart disease, oxygen supply and, in cardiomyopathy, muscle strength counteract this aspect as a limiting factor. Excessive afterload accompanies numerous cardiac diseases. The increase in afterload can be regulated to a certain extent by medication. Therapeutic afterload reducers include AT1 blockers. ACE inhibitors, diuretics, and nitroglycerin lower afterload in addition to preload. In addition, arterial vasodilators such as dihydropyridine-type calcium antagonists can lower cardiac afterload. Vasodilators cause the vascular muscles to relax and increase the lumen of the vessels. ACE inhibitors, in turn, lower blood pressure and in this way reduce the afterload on the heart’s work. For this reason, they are often used to treat heart failure, although they are also used in coronary heart disease. AT1 blockers are competitive inhibitors and act selectively at the so-called AT1 receptor, where they antagonize the cardiovascular action of angiotensin II. In this way, they primarily lower blood pressure and correspondingly reduce afterload. Afterload increases not only due to hypertension, but also in the context of valve stenosis. According to Laplace’s law, the ventricular muscles increase in size to compensate for a chronically increased afterload, in order to counter-regulate and reduce the increased wall tension. As a consequence, dilatation of the affected ventricle may occur, from which heart failure in turn develops.
