All rights reserved. NursingCenter Blog. Continuing Education More. May 25 by Myrna B. Share this on. In a previous blog post, we discussed preload and afterload. You may recall, preload is the amount of ventricular stretch at the end of diastole. Afterload is the pressure the myocardial muscle must overcome to push blood out of the heart during systole.
The left ventricle ejects blood through the aortic valve against the high pressure of the systemic circulation, also known as systemic vascular resistance SVR. For example, if the blood vessels tighten or constrict, SVR increases, resulting in diminished ventricular compliance, reduced stroke volume and ultimately a drop in cardiac output.
For this reason, the above relationship is expressed as a proportionality to highlight how pressure, radius and wall thickness contribute to afterload. The pressure that the ventricle generates during systolic ejection is very close to aortic pressure unless aortic stenosis is present, in which case the left ventricular pressure during ejection can be much greater than aortic pressure.
At a given intraventricular pressure, wall stress and therefore afterload are increased by an increase in ventricular inside radius ventricular dilation. A hypertrophied ventricle , which has a thickened wall, has less wall stress and reduced afterload. Hypertrophy, therefore can be thought of as a mechanism that permits more parallel muscle fibers actually, sarcomere units to share in the wall tension that is determined at a give pressure and radius.
The thicker the wall, the less tension experienced by each sarcomere unit. Afterload is increased when aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis , and by ventricular dilation. When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.
As shown in the figure, an increase in afterload shifts the Frank-Starling curve down and to the right from point A to B , which decreases stroke volume SV and at the same time increases left ventricular end-diastolic pressure LVEDP. The basis for this is found in the force-velocity relationship for cardiac myocytes. Briefly, an increase in afterload decreases the velocity of fiber shortening. Afterload per se does not alter preload; however, preload changes secondarily to changes in afterload.
Increasing afterload not only reduces stroke volume, but it also increases left ventricular end-diastolic pressure LVEDP i. Systemic vascular resistance SVR is the resistance to blood flow offered by all of the systemic vasculature [2]. An increase in SVR depends on the degree of sympathetic stimulation which itself depends on the degree of sympathetic activation, responsiveness of the vasculature, the number of vascular beds involved and the relative series and parallel arrangement of these beds to each other.
Changes in blood viscosity also affect SVR. SVR is an unreliable indicator of left ventricular afterload [2] since it reflects only peripheral vasomotor tone and not left ventricular systolic wall force.
Discordant changes in left ventricular afterload and SVR can occur during pharmacological interventions as shown by Lang et al. Klabunde, R.
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