Afterload
As afterload (engl. Afterload ) those forces are referred to by the contraction of the muscles of the ventricles to counter and thus the ejection of blood from the ventricles into the blood vessel system limit. It reaches its maximum shortly after the opening of the aortic valve at the end of the systole . The afterload is mainly determined by two factors: the arterial blood pressure and the stiffness ( low compliance ) of the arteries. Often the afterload is equated with the arterial peripheral resistance . The opposite is the preload .
The wall tension of the heart chambers and thus the afterload cannot be measured directly. It can be reliably derived from the impedance of the aorta (pressure in the aorta divided by the blood flow at a given point in time). The impedance can only be measured invasively, however, approximately also by means of transesophageal echocardiography . Clinically, the afterload can also be estimated using the arterial blood pressure, as long as there is no significant aortic stenosis or change in vascular stiffness.
The afterload can be influenced pharmacologically and can, for example, be reduced by using arterial vasodilators (e.g. calcium antagonists of the dihydropyridine type) or beta blockers . ACE inhibitors , diuretics and nitroglycerin reduce the preload and also the afterload.
See also
Individual evidence
- ^ A b Hugo Aken et al: Intensive care medicine . Georg Thieme Verlag, 2nd edition 2007, ISBN 9783131148728 , p. 948.